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The Changing Standard of Care for Spinal Immobilization
Prehospital spinal immobilization has long been the standard of care (SOC) to prevent spinal cord injury in trauma patients, but utilizing the best data currently available, some professional societies recently released new recommendations that question this practice. Guidelines released in 2014 from the National Association of EMS Physicians (NAEMSP) and the American College of Surgeons Committee on Trauma (ACS-COT) support limited application of spinal immobilization.1 These guidelines note, “Given the rarity of unstable spinal injuries in EMS trauma patients, the number that might benefit from immobilization to prevent secondary injury is likely extremely small. For each patient who has potential benefit, hundreds to thousands of patients must undergo immobilization with no potential benefit.” Further, they advise “utilization of backboards for spinal immobilization during transport should be judicious, so that potential benefits outweigh risks.”1 Spinal immobilization should not be used at all in patients with penetrating trauma who do not present with obvious neurological injury and should be selective, based on objective findings of injury or the high potential for same.1
Questioning a Long-standing Practice
Fear of the consequences of spinal cord injury from significant vertebral fractures has dictated prehospital spinal immobilization to manage injured trauma patients for decades. For almost 50 years, it has been the SOC. However, increasing evidence that spinal immobilization is not only unnecessary, but may even cause harm has resulted in questioning this paradigm, which has lead to promoting a change in the SOC.
Spinal immobilization dates back to the mid-1960s, when Geisler et al2 reported on a cohort of patients who suffered long-term paralysis from what was believed to be improper handling and failure to discover spinal injuries. Soon after, Farrington3,4 developed and published a systematic approach to spinal immobilization during extrication following blunt force trauma, supporting the widespread acceptance of backboards and cervical collars to immobilize the spine in injured trauma patients. Logic dictated that an unstable spine fracture could be worsened, or a cord injury could result, by unnecessary movement during extrication, transport, and initial evaluation in the ED, resulting in avoidable injury. This fear of potential secondary injury grew as more papers were published examining the link between prehospital handling of blunt force trauma patients and delayed paralysis. This resulted in the use of spinal immobilization on the majority of trauma patients, regardless of mechanism of injury or presenting symptoms.5,6
One review estimated that over 50% of trauma patients with no complaint of neck or back pain were transported with full spinal immobilization.7 This immobilization on uncomfortable long backboards typically continued in the ED for prolonged periods, until the spine could be cleared by physical examination and/or imaging studies. Yet a 2001 Cochrane review found that despite increasing use of spinal immobilization, no prospective, randomized controlled trial of the appropriate use of spinal immobilization or patient outcomes had ever been conducted.8
What the Evidence Says
How much evidence exists that supports the benefits of spinal immobilization? Not much. Studies on healthy volunteers and cadavers evaluating spinal motion with immobilization have been contradictory.9 One study found there was less motion with a cervical collar in place than without,10 whereas others found that the use of a cervical collar did not effectively reduce motion in an unstable spine.11,12 Perry et al13 studied the effectiveness of different head immobilization techniques and found that none could eliminate head and neck motion during emergency medical services (EMS) transport. Still other reports, including two biomechanical studies, demonstrated increased neck motion when using conventional extrication techniques (cervical collar with backboard) versus controlled self-extrication with cervical collar only.14,15
An Abundance of Literature on the Risks
Whereas data regarding the actual benefits of spinal immobilization is lacking, an abundance of literature details the risks. One of the most frequently cited studies is also one of the most controversial. Hauswald et al16 compared the outcomes of two groups of patients with blunt force trauma who were either immobilized during transport (in New Mexico) or non-immobilized (in Malaysia) and found that the risk of disability was higher in the immobilized group (odds ratio, 2.03). Although these environments are very different, the authors noted that mechanism of injury, resources, and the size of the hospitals were similar.16
Studies of spinal immobilization in patients with penetrating trauma report even worse outcomes. In separate studies, Haut et al17 and Vanderlan et al18 demonstrated increased mortality when immobilization led to increased transport times and interference with other resuscitative measures. These and other studies have led the American College of Emergency Physicians, NAEMSP, ACS-COT, the Prehospital Trauma Life Support Executive Committee, and other national organizations to recommend no spinal immobilization in patients with penetrating neck trauma.1,19,20
Many trauma patients arrive with complaints of pain at one or more sites. Some of these complaints, particularly back pain, may be secondary to the use of the backboard itself, especially in cases of prolonged transport.21,22 In a study of healthy volunteers who were immobilized on a backboard for 30 minutes, all of them reported pain, along with headaches, most often involving the occipital and sacral regions.23 A 1996 study compared spinal immobilization utilizing a backboard versus a vacuum mattress in 37 healthy volunteers with no history of back pain or spinal disease.24 Compared to those immobilized with the vacuum mattress, patients immobilized with a backboard for 30 minutes were 3.1 times more likely to have symptoms, 7.9 times more likely to complain of occipital pain, and 4.3 times more likely to have lumbosacral pain.24
Increased pain complaints in the setting of trauma can result in increased imaging, leading to increased costs and unnecessary radiation exposure.25 Prolonged backboard times can also result in sacral pressure ulcers.26 A recent study has shown that patients who undergo computed tomography (CT) scans with automatic tube current modulation (as most modern multidetector row CT systems utilize) while on a backboard may be exposed to a significant increase in radiation dose.27
Spinal immobilization has also been linked to respiratory compromise, particularly with the use of straps across the chest, even when not applied tightly. One study found worse lung function test results in healthy immobilized volunteers.28 Other studies have shown that older patients (even when healthy) and those with lung or chest injury have an even larger degree of restriction and respiratory compromise.29,30
Risks from immobilization are not isolated to backboards. The use of cervical collars alone also carries potential risks. (See “What About Cervical Collars?”8,31-39)
Risk of Secondary Neurological Deterioration Is Low
Many EMS systems have already adopted the new standards calling for less use of spinal immobilization. Though the evidence is compelling, not all EMS systems have adopted these standards due to strongly rooted beliefs and fears of long-term patient disability and subsequent litigation. However, these fears do not appear justified.
A recent review by Oto et al40 found only 42 cases of early secondary neurological deterioration after blunt trauma in all of the indexed medical literature. They noted, “In twelve cases the authors did attribute deterioration to temporally associated precipitants, seven of which were possibly iatrogenic; these included removal of a cervical collar, placement of a halo device, patient agitation, performance of flexion/extension films, ‘unintentional manipulation,’ falling in or near the ED, and forced collar application in patients with ankylosing spondylitis.” Thirteen of these cases occurred during prehospital care, none of them sudden and movement-provoked, and all reported by a single study.” This review highlights the rarity of secondary deterioration.
When Should Immobilization Be Used?
So what’s the next step for spinal immobilization in the field? How do we appropriately protect trauma patients during transport? As always seems to be the case in medicine, more evidence is needed. Oteir et al41 recently published a review of new literature on the epidemiology and current practice of prehospital spine management. They reported that early (8-24 hours) transfer of patients with spinal injury to spinal care units, along with effective resuscitation, was the most important determinant of better neurological outcomes.41 This review reaffirms the need for more data evaluating the relationship between spinal immobilization and neurological outcomes.
Currently, recommendations call for selective spinal immobilization to decrease unnecessary application and potential harm. Use of backboards for spinal immobilization should be limited to the following types of patients:1,20
- Blunt trauma and altered level of consciousness;
- Spinal pain or tenderness;
- Neurological complaint (eg, numbness or motor weakness);
- Anatomic deformity of the spine;
- High-energy mechanism of injury and:
- Drug or alcohol intoxication;
- Inability to communicate; and/or
- Distracting injury.
Patients for whom immobilization on a backboard is not necessary include those with all of the following:
- Normal level of consciousness (GCS 15);
- No spine tenderness or anatomic abnormality;
- No neurological findings or complaints;
- No distracting injury;
- No intoxication.
Cervical collars alone are still recommended for use in patients who do not meet validated clinical rules, such as the NEXUS or Canadian C spine rules.1,20,42,43 As these rules are well validated, they can be safely used to determine who should have a cervical collar placed, with or without a backboard. In a retrospective review, selective spinal immobilization was found to be 99% sensitive in identifying patients with cervical injuries.44
Clearly, there is still work to be done. Due to the relative rarity of actual spinal cord injury with the consequences of neurological injury, prospective trials in this area are rare and very difficult to safely design. However, there is growing confidence that selective spinal protocols, together with the inclusion of validated clinical rules, can effectively limit exposure to unnecessary spinal immobilization. As the current evidence continues to mount for the potential harm in indiscriminate backboard and cervical collar use, it seems clear we should strive to decrease the overuse of prehospital and early spinal immobilization consistent with current position statements and validated clinical rules.
1. White CC, Domeier RM, Millin MG. EMS spinal precautions and the use of the long backboard - resource document to the position statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care. 2014;18(2):306-314.
2. Geisler WO, Wynne-Jones M, Jousse AT. Early management of patients with trauma to the spinal cord. Med Serv J Can. 1966;22(7):512–523.
3. Farrington JD. Death in a ditch. Bulletin of the American College of Surgeons. 1967;52(3):121-130.
4. Farrington JD. Extrication of victims- surgical principles. J Trauma. 1968;8(4):493-512.
5. Riggins RS, Kraus JF. The risk of neurologic damage with fractures of the vertebrae. J Trauma. 1977;17(2):126-133.
6. Soderstrom CA, Brumback RJ. Early care of the patient with cervical spine injury. Orthop Clin North Am. 1986;17(1):3-13.
7. McHugh TP, Taylor JP. Unnecessary out-of-hospital use of full spinal immobilization. Acad Emerg Med. 1998;5(3):278-280.
8. Kwan I, Bunn F, Roberts I. Spinal immobilisation for trauma patients. Cochrane Database Syst Rev. 2001;(2):CD002803.
9. Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital use of cervical collars in trauma patients: a critical review. J Neurotrauma. 2014;31(6):531-540.
10. Conrad BP, Rechtine G, Weight M, Clarke J, Horodyski M. Motion in the unstable cervical spine during hospital bed transfers. J Trauma. 2010;69,432-436.
11. Horodyski M, DiPaola CP, Conrad BP, Rechtine GR. Cervical collars are insufficient for immobilizing an unstable cervical spine injury. J Emerg Med. 2011;41(5):513-519.
12. Hughes SJ. How effective is the Newport/Aspen collar? A prospective radiographic evaluation in healthy adult volunteers. J Trauma. 1998;45(2):374-378.
13. Perry SD, McLellan B, McIlroy WE, Maki BE, Schwartz M, Fernie GR. The efficacy of head immobilization techniques during simulated vehicle motion. Spine (Phil Pa 1976). 1999;24(17):1839-1844.
14. Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS. Cervical spine motion during extrication. J Emerg Med. 2013;44(1):122-127.
15. Dixon M, O’Halloran J, Cummins NM. Biomechanical analysis of spinal immobilization during prehospital extrication—a proof of concept study. Emerg Med J. 2014;31(9):745-749.
16. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998;5(3):214-219.
17. Haut ER, Kalish BT, Efron DT, et al. Spine immobilization in penetrating trauma: more harm than good? J Trauma. 2010;68(1):115-120.
18. Vanderlan WB, Tew BE, McSwain NE. Increased risk of death with cervical spine immobilization in penetrating cervical trauma. Injury. 2009;40(8):880-883.
19. Stuke LE, Pons PT, Guy JS, Chapleau WP, Butler FK, McSwain NE. Prehospital spine immobilization for penetrating trauma—review and recommendations from the Prehospital Trauma Life Support Executive Committee. J Trauma. 2011;71(3):763–769.
20. American College of Emergency Physicians. Policy Statement- EMS Management of Patients with Potential Spinal Injury. 2015. Available at: http://www.acep.org/Physician-Resources/Policies/Policy-Statements/EMS-Management-of-Patients-with-Potential-Spinal-Injury. Accessed February 9, 2016.
21. Barney RN, Cordell WH, Miller E. Pain associated with immobilization on rigid spine boards. Ann Emerg Med. 1989;18:918.
22. Cooney DR, Wallus H, Asaly M, Wojcik S. Backboard time for patients receiving spinal immobilization by emergency medical services. Int J Emerg Med. 2013;6(1):17.
23. Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994;23(1):48-51.
24. Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med, 1996;14(3):293-298.
25. March J, Ausband S, Brown L. Changes in physical examination caused by use of spinal immobilization. Prehosp Emerg Care. 2002;6(4):421-424.
26. Berg G, Nyberg S, Harrison P, Baumchen J, Gurss E, Hennes E. Near-infrared spectroscopy measurement of sacral tissue oxygen saturation in healthy volunteers immobilized on rigid spine boards. Prehosp Emerg Care. 2010;14(4):419-424.
27. Lee AY, Elojeimy S, Kanal KM, Gunn ML. The effect of trauma backboards on computed tomography radiation dose. Clin Radiol. 2016. Epub ahead of print.
28. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy, nonsmoking man. Ann Emerg Med. 1988;17(9):915-918.
29. Walsh M, Grant T, Mickey S. Lung function compromised by spinal immobilization. Ann Emerg Med. 1990;19(5):615-616.
30. Totten VY, Sugarman DB. Respiratory effects of spinal immobilization. Prehosp Emerg Care. 1999; 3(4):347-352.
31. Goutcher CM, Lochhead V. Reduction in mouth opening with semi-rigid cervical collars. Br J Anaesth. 2005;95(3):344-348.
32. Davies G, Deakin C, Wilson A. The effect of a rigid collar on intracranial pressure. Injury. 1996;27(9):647-649.
33. Dunham CM, Brocker BP, Collier BD, Gemmel DJ. Risks associated with magnetic resonance imaging and cervical collar in comatose, blunt trauma patients with negative comprehensive cervical spine computed tomography and no apparent spinal deficit. Crit Care. 2008;12(4):R89.
34. Mobbs RJ, Stoodley MA, Fuller J. Effect of cervical hard collar on intracranial pressure after head injury. ANZ J Surg. 2002;72(6):389-391.
35. Stone MB, Tubridy CM, Curran R. The effect of rigid cervical collars on internal jugular vein dimensions. Acad Emerg Med. 2010;17(1):100-102.
36. Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010;69(2):447-450.
37. Podolsky SM, Hoffman JR, Pietrafesa CA. Neurologic complications following immobilization of cervical spine fracture in a patient with ankylosing spondylitis. Ann Emerg Med. 1983;12(9):578-580.
38. Papadopoulos MC, Chakraborty A, Waldron G, Bell BA. Exacerbating cervical spine injury by applying a hard collar. BMJ. 1999;319(7203):171-172.
39. Thumbikat P, Hariharan RP, Ravichandran G, Mcclelland MR, Mathew KM. Spinal cord injury in patients with ankylosing spondylitis: a 10-year review. Spine (Phila Pa 1976). 2007;32(26):2989-2995.
40. Oto B, Corey DJ, Oswald J, Sifford D, Walsh B. Early secondary neurologic deterioration after blunt spinal trauma: a review of the literature. Acad Emerg Med. 2015;22(10):1200-1212.
41. Oteir AO, Smith K, Jennings PA, Stoelwinder JU. The prehospital management of suspected spinal cord injury: an update. Prehosp Disaster Med. 2014;29(4):399-402.
42. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000;343(2):94-99.
43. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001;286(15):1841–1848.
44. Stroh G, Braude D. Can an out-of-hospital cervical spine clearance protocol identify all patients with injuries? An argument for selective immobilization. Ann Emerg Med. 2001;37(6):609-615.
Prehospital spinal immobilization has long been the standard of care (SOC) to prevent spinal cord injury in trauma patients, but utilizing the best data currently available, some professional societies recently released new recommendations that question this practice. Guidelines released in 2014 from the National Association of EMS Physicians (NAEMSP) and the American College of Surgeons Committee on Trauma (ACS-COT) support limited application of spinal immobilization.1 These guidelines note, “Given the rarity of unstable spinal injuries in EMS trauma patients, the number that might benefit from immobilization to prevent secondary injury is likely extremely small. For each patient who has potential benefit, hundreds to thousands of patients must undergo immobilization with no potential benefit.” Further, they advise “utilization of backboards for spinal immobilization during transport should be judicious, so that potential benefits outweigh risks.”1 Spinal immobilization should not be used at all in patients with penetrating trauma who do not present with obvious neurological injury and should be selective, based on objective findings of injury or the high potential for same.1
Questioning a Long-standing Practice
Fear of the consequences of spinal cord injury from significant vertebral fractures has dictated prehospital spinal immobilization to manage injured trauma patients for decades. For almost 50 years, it has been the SOC. However, increasing evidence that spinal immobilization is not only unnecessary, but may even cause harm has resulted in questioning this paradigm, which has lead to promoting a change in the SOC.
Spinal immobilization dates back to the mid-1960s, when Geisler et al2 reported on a cohort of patients who suffered long-term paralysis from what was believed to be improper handling and failure to discover spinal injuries. Soon after, Farrington3,4 developed and published a systematic approach to spinal immobilization during extrication following blunt force trauma, supporting the widespread acceptance of backboards and cervical collars to immobilize the spine in injured trauma patients. Logic dictated that an unstable spine fracture could be worsened, or a cord injury could result, by unnecessary movement during extrication, transport, and initial evaluation in the ED, resulting in avoidable injury. This fear of potential secondary injury grew as more papers were published examining the link between prehospital handling of blunt force trauma patients and delayed paralysis. This resulted in the use of spinal immobilization on the majority of trauma patients, regardless of mechanism of injury or presenting symptoms.5,6
One review estimated that over 50% of trauma patients with no complaint of neck or back pain were transported with full spinal immobilization.7 This immobilization on uncomfortable long backboards typically continued in the ED for prolonged periods, until the spine could be cleared by physical examination and/or imaging studies. Yet a 2001 Cochrane review found that despite increasing use of spinal immobilization, no prospective, randomized controlled trial of the appropriate use of spinal immobilization or patient outcomes had ever been conducted.8
What the Evidence Says
How much evidence exists that supports the benefits of spinal immobilization? Not much. Studies on healthy volunteers and cadavers evaluating spinal motion with immobilization have been contradictory.9 One study found there was less motion with a cervical collar in place than without,10 whereas others found that the use of a cervical collar did not effectively reduce motion in an unstable spine.11,12 Perry et al13 studied the effectiveness of different head immobilization techniques and found that none could eliminate head and neck motion during emergency medical services (EMS) transport. Still other reports, including two biomechanical studies, demonstrated increased neck motion when using conventional extrication techniques (cervical collar with backboard) versus controlled self-extrication with cervical collar only.14,15
An Abundance of Literature on the Risks
Whereas data regarding the actual benefits of spinal immobilization is lacking, an abundance of literature details the risks. One of the most frequently cited studies is also one of the most controversial. Hauswald et al16 compared the outcomes of two groups of patients with blunt force trauma who were either immobilized during transport (in New Mexico) or non-immobilized (in Malaysia) and found that the risk of disability was higher in the immobilized group (odds ratio, 2.03). Although these environments are very different, the authors noted that mechanism of injury, resources, and the size of the hospitals were similar.16
Studies of spinal immobilization in patients with penetrating trauma report even worse outcomes. In separate studies, Haut et al17 and Vanderlan et al18 demonstrated increased mortality when immobilization led to increased transport times and interference with other resuscitative measures. These and other studies have led the American College of Emergency Physicians, NAEMSP, ACS-COT, the Prehospital Trauma Life Support Executive Committee, and other national organizations to recommend no spinal immobilization in patients with penetrating neck trauma.1,19,20
Many trauma patients arrive with complaints of pain at one or more sites. Some of these complaints, particularly back pain, may be secondary to the use of the backboard itself, especially in cases of prolonged transport.21,22 In a study of healthy volunteers who were immobilized on a backboard for 30 minutes, all of them reported pain, along with headaches, most often involving the occipital and sacral regions.23 A 1996 study compared spinal immobilization utilizing a backboard versus a vacuum mattress in 37 healthy volunteers with no history of back pain or spinal disease.24 Compared to those immobilized with the vacuum mattress, patients immobilized with a backboard for 30 minutes were 3.1 times more likely to have symptoms, 7.9 times more likely to complain of occipital pain, and 4.3 times more likely to have lumbosacral pain.24
Increased pain complaints in the setting of trauma can result in increased imaging, leading to increased costs and unnecessary radiation exposure.25 Prolonged backboard times can also result in sacral pressure ulcers.26 A recent study has shown that patients who undergo computed tomography (CT) scans with automatic tube current modulation (as most modern multidetector row CT systems utilize) while on a backboard may be exposed to a significant increase in radiation dose.27
Spinal immobilization has also been linked to respiratory compromise, particularly with the use of straps across the chest, even when not applied tightly. One study found worse lung function test results in healthy immobilized volunteers.28 Other studies have shown that older patients (even when healthy) and those with lung or chest injury have an even larger degree of restriction and respiratory compromise.29,30
Risks from immobilization are not isolated to backboards. The use of cervical collars alone also carries potential risks. (See “What About Cervical Collars?”8,31-39)
Risk of Secondary Neurological Deterioration Is Low
Many EMS systems have already adopted the new standards calling for less use of spinal immobilization. Though the evidence is compelling, not all EMS systems have adopted these standards due to strongly rooted beliefs and fears of long-term patient disability and subsequent litigation. However, these fears do not appear justified.
A recent review by Oto et al40 found only 42 cases of early secondary neurological deterioration after blunt trauma in all of the indexed medical literature. They noted, “In twelve cases the authors did attribute deterioration to temporally associated precipitants, seven of which were possibly iatrogenic; these included removal of a cervical collar, placement of a halo device, patient agitation, performance of flexion/extension films, ‘unintentional manipulation,’ falling in or near the ED, and forced collar application in patients with ankylosing spondylitis.” Thirteen of these cases occurred during prehospital care, none of them sudden and movement-provoked, and all reported by a single study.” This review highlights the rarity of secondary deterioration.
When Should Immobilization Be Used?
So what’s the next step for spinal immobilization in the field? How do we appropriately protect trauma patients during transport? As always seems to be the case in medicine, more evidence is needed. Oteir et al41 recently published a review of new literature on the epidemiology and current practice of prehospital spine management. They reported that early (8-24 hours) transfer of patients with spinal injury to spinal care units, along with effective resuscitation, was the most important determinant of better neurological outcomes.41 This review reaffirms the need for more data evaluating the relationship between spinal immobilization and neurological outcomes.
Currently, recommendations call for selective spinal immobilization to decrease unnecessary application and potential harm. Use of backboards for spinal immobilization should be limited to the following types of patients:1,20
- Blunt trauma and altered level of consciousness;
- Spinal pain or tenderness;
- Neurological complaint (eg, numbness or motor weakness);
- Anatomic deformity of the spine;
- High-energy mechanism of injury and:
- Drug or alcohol intoxication;
- Inability to communicate; and/or
- Distracting injury.
Patients for whom immobilization on a backboard is not necessary include those with all of the following:
- Normal level of consciousness (GCS 15);
- No spine tenderness or anatomic abnormality;
- No neurological findings or complaints;
- No distracting injury;
- No intoxication.
Cervical collars alone are still recommended for use in patients who do not meet validated clinical rules, such as the NEXUS or Canadian C spine rules.1,20,42,43 As these rules are well validated, they can be safely used to determine who should have a cervical collar placed, with or without a backboard. In a retrospective review, selective spinal immobilization was found to be 99% sensitive in identifying patients with cervical injuries.44
Clearly, there is still work to be done. Due to the relative rarity of actual spinal cord injury with the consequences of neurological injury, prospective trials in this area are rare and very difficult to safely design. However, there is growing confidence that selective spinal protocols, together with the inclusion of validated clinical rules, can effectively limit exposure to unnecessary spinal immobilization. As the current evidence continues to mount for the potential harm in indiscriminate backboard and cervical collar use, it seems clear we should strive to decrease the overuse of prehospital and early spinal immobilization consistent with current position statements and validated clinical rules.
Prehospital spinal immobilization has long been the standard of care (SOC) to prevent spinal cord injury in trauma patients, but utilizing the best data currently available, some professional societies recently released new recommendations that question this practice. Guidelines released in 2014 from the National Association of EMS Physicians (NAEMSP) and the American College of Surgeons Committee on Trauma (ACS-COT) support limited application of spinal immobilization.1 These guidelines note, “Given the rarity of unstable spinal injuries in EMS trauma patients, the number that might benefit from immobilization to prevent secondary injury is likely extremely small. For each patient who has potential benefit, hundreds to thousands of patients must undergo immobilization with no potential benefit.” Further, they advise “utilization of backboards for spinal immobilization during transport should be judicious, so that potential benefits outweigh risks.”1 Spinal immobilization should not be used at all in patients with penetrating trauma who do not present with obvious neurological injury and should be selective, based on objective findings of injury or the high potential for same.1
Questioning a Long-standing Practice
Fear of the consequences of spinal cord injury from significant vertebral fractures has dictated prehospital spinal immobilization to manage injured trauma patients for decades. For almost 50 years, it has been the SOC. However, increasing evidence that spinal immobilization is not only unnecessary, but may even cause harm has resulted in questioning this paradigm, which has lead to promoting a change in the SOC.
Spinal immobilization dates back to the mid-1960s, when Geisler et al2 reported on a cohort of patients who suffered long-term paralysis from what was believed to be improper handling and failure to discover spinal injuries. Soon after, Farrington3,4 developed and published a systematic approach to spinal immobilization during extrication following blunt force trauma, supporting the widespread acceptance of backboards and cervical collars to immobilize the spine in injured trauma patients. Logic dictated that an unstable spine fracture could be worsened, or a cord injury could result, by unnecessary movement during extrication, transport, and initial evaluation in the ED, resulting in avoidable injury. This fear of potential secondary injury grew as more papers were published examining the link between prehospital handling of blunt force trauma patients and delayed paralysis. This resulted in the use of spinal immobilization on the majority of trauma patients, regardless of mechanism of injury or presenting symptoms.5,6
One review estimated that over 50% of trauma patients with no complaint of neck or back pain were transported with full spinal immobilization.7 This immobilization on uncomfortable long backboards typically continued in the ED for prolonged periods, until the spine could be cleared by physical examination and/or imaging studies. Yet a 2001 Cochrane review found that despite increasing use of spinal immobilization, no prospective, randomized controlled trial of the appropriate use of spinal immobilization or patient outcomes had ever been conducted.8
What the Evidence Says
How much evidence exists that supports the benefits of spinal immobilization? Not much. Studies on healthy volunteers and cadavers evaluating spinal motion with immobilization have been contradictory.9 One study found there was less motion with a cervical collar in place than without,10 whereas others found that the use of a cervical collar did not effectively reduce motion in an unstable spine.11,12 Perry et al13 studied the effectiveness of different head immobilization techniques and found that none could eliminate head and neck motion during emergency medical services (EMS) transport. Still other reports, including two biomechanical studies, demonstrated increased neck motion when using conventional extrication techniques (cervical collar with backboard) versus controlled self-extrication with cervical collar only.14,15
An Abundance of Literature on the Risks
Whereas data regarding the actual benefits of spinal immobilization is lacking, an abundance of literature details the risks. One of the most frequently cited studies is also one of the most controversial. Hauswald et al16 compared the outcomes of two groups of patients with blunt force trauma who were either immobilized during transport (in New Mexico) or non-immobilized (in Malaysia) and found that the risk of disability was higher in the immobilized group (odds ratio, 2.03). Although these environments are very different, the authors noted that mechanism of injury, resources, and the size of the hospitals were similar.16
Studies of spinal immobilization in patients with penetrating trauma report even worse outcomes. In separate studies, Haut et al17 and Vanderlan et al18 demonstrated increased mortality when immobilization led to increased transport times and interference with other resuscitative measures. These and other studies have led the American College of Emergency Physicians, NAEMSP, ACS-COT, the Prehospital Trauma Life Support Executive Committee, and other national organizations to recommend no spinal immobilization in patients with penetrating neck trauma.1,19,20
Many trauma patients arrive with complaints of pain at one or more sites. Some of these complaints, particularly back pain, may be secondary to the use of the backboard itself, especially in cases of prolonged transport.21,22 In a study of healthy volunteers who were immobilized on a backboard for 30 minutes, all of them reported pain, along with headaches, most often involving the occipital and sacral regions.23 A 1996 study compared spinal immobilization utilizing a backboard versus a vacuum mattress in 37 healthy volunteers with no history of back pain or spinal disease.24 Compared to those immobilized with the vacuum mattress, patients immobilized with a backboard for 30 minutes were 3.1 times more likely to have symptoms, 7.9 times more likely to complain of occipital pain, and 4.3 times more likely to have lumbosacral pain.24
Increased pain complaints in the setting of trauma can result in increased imaging, leading to increased costs and unnecessary radiation exposure.25 Prolonged backboard times can also result in sacral pressure ulcers.26 A recent study has shown that patients who undergo computed tomography (CT) scans with automatic tube current modulation (as most modern multidetector row CT systems utilize) while on a backboard may be exposed to a significant increase in radiation dose.27
Spinal immobilization has also been linked to respiratory compromise, particularly with the use of straps across the chest, even when not applied tightly. One study found worse lung function test results in healthy immobilized volunteers.28 Other studies have shown that older patients (even when healthy) and those with lung or chest injury have an even larger degree of restriction and respiratory compromise.29,30
Risks from immobilization are not isolated to backboards. The use of cervical collars alone also carries potential risks. (See “What About Cervical Collars?”8,31-39)
Risk of Secondary Neurological Deterioration Is Low
Many EMS systems have already adopted the new standards calling for less use of spinal immobilization. Though the evidence is compelling, not all EMS systems have adopted these standards due to strongly rooted beliefs and fears of long-term patient disability and subsequent litigation. However, these fears do not appear justified.
A recent review by Oto et al40 found only 42 cases of early secondary neurological deterioration after blunt trauma in all of the indexed medical literature. They noted, “In twelve cases the authors did attribute deterioration to temporally associated precipitants, seven of which were possibly iatrogenic; these included removal of a cervical collar, placement of a halo device, patient agitation, performance of flexion/extension films, ‘unintentional manipulation,’ falling in or near the ED, and forced collar application in patients with ankylosing spondylitis.” Thirteen of these cases occurred during prehospital care, none of them sudden and movement-provoked, and all reported by a single study.” This review highlights the rarity of secondary deterioration.
When Should Immobilization Be Used?
So what’s the next step for spinal immobilization in the field? How do we appropriately protect trauma patients during transport? As always seems to be the case in medicine, more evidence is needed. Oteir et al41 recently published a review of new literature on the epidemiology and current practice of prehospital spine management. They reported that early (8-24 hours) transfer of patients with spinal injury to spinal care units, along with effective resuscitation, was the most important determinant of better neurological outcomes.41 This review reaffirms the need for more data evaluating the relationship between spinal immobilization and neurological outcomes.
Currently, recommendations call for selective spinal immobilization to decrease unnecessary application and potential harm. Use of backboards for spinal immobilization should be limited to the following types of patients:1,20
- Blunt trauma and altered level of consciousness;
- Spinal pain or tenderness;
- Neurological complaint (eg, numbness or motor weakness);
- Anatomic deformity of the spine;
- High-energy mechanism of injury and:
- Drug or alcohol intoxication;
- Inability to communicate; and/or
- Distracting injury.
Patients for whom immobilization on a backboard is not necessary include those with all of the following:
- Normal level of consciousness (GCS 15);
- No spine tenderness or anatomic abnormality;
- No neurological findings or complaints;
- No distracting injury;
- No intoxication.
Cervical collars alone are still recommended for use in patients who do not meet validated clinical rules, such as the NEXUS or Canadian C spine rules.1,20,42,43 As these rules are well validated, they can be safely used to determine who should have a cervical collar placed, with or without a backboard. In a retrospective review, selective spinal immobilization was found to be 99% sensitive in identifying patients with cervical injuries.44
Clearly, there is still work to be done. Due to the relative rarity of actual spinal cord injury with the consequences of neurological injury, prospective trials in this area are rare and very difficult to safely design. However, there is growing confidence that selective spinal protocols, together with the inclusion of validated clinical rules, can effectively limit exposure to unnecessary spinal immobilization. As the current evidence continues to mount for the potential harm in indiscriminate backboard and cervical collar use, it seems clear we should strive to decrease the overuse of prehospital and early spinal immobilization consistent with current position statements and validated clinical rules.
1. White CC, Domeier RM, Millin MG. EMS spinal precautions and the use of the long backboard - resource document to the position statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care. 2014;18(2):306-314.
2. Geisler WO, Wynne-Jones M, Jousse AT. Early management of patients with trauma to the spinal cord. Med Serv J Can. 1966;22(7):512–523.
3. Farrington JD. Death in a ditch. Bulletin of the American College of Surgeons. 1967;52(3):121-130.
4. Farrington JD. Extrication of victims- surgical principles. J Trauma. 1968;8(4):493-512.
5. Riggins RS, Kraus JF. The risk of neurologic damage with fractures of the vertebrae. J Trauma. 1977;17(2):126-133.
6. Soderstrom CA, Brumback RJ. Early care of the patient with cervical spine injury. Orthop Clin North Am. 1986;17(1):3-13.
7. McHugh TP, Taylor JP. Unnecessary out-of-hospital use of full spinal immobilization. Acad Emerg Med. 1998;5(3):278-280.
8. Kwan I, Bunn F, Roberts I. Spinal immobilisation for trauma patients. Cochrane Database Syst Rev. 2001;(2):CD002803.
9. Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital use of cervical collars in trauma patients: a critical review. J Neurotrauma. 2014;31(6):531-540.
10. Conrad BP, Rechtine G, Weight M, Clarke J, Horodyski M. Motion in the unstable cervical spine during hospital bed transfers. J Trauma. 2010;69,432-436.
11. Horodyski M, DiPaola CP, Conrad BP, Rechtine GR. Cervical collars are insufficient for immobilizing an unstable cervical spine injury. J Emerg Med. 2011;41(5):513-519.
12. Hughes SJ. How effective is the Newport/Aspen collar? A prospective radiographic evaluation in healthy adult volunteers. J Trauma. 1998;45(2):374-378.
13. Perry SD, McLellan B, McIlroy WE, Maki BE, Schwartz M, Fernie GR. The efficacy of head immobilization techniques during simulated vehicle motion. Spine (Phil Pa 1976). 1999;24(17):1839-1844.
14. Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS. Cervical spine motion during extrication. J Emerg Med. 2013;44(1):122-127.
15. Dixon M, O’Halloran J, Cummins NM. Biomechanical analysis of spinal immobilization during prehospital extrication—a proof of concept study. Emerg Med J. 2014;31(9):745-749.
16. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998;5(3):214-219.
17. Haut ER, Kalish BT, Efron DT, et al. Spine immobilization in penetrating trauma: more harm than good? J Trauma. 2010;68(1):115-120.
18. Vanderlan WB, Tew BE, McSwain NE. Increased risk of death with cervical spine immobilization in penetrating cervical trauma. Injury. 2009;40(8):880-883.
19. Stuke LE, Pons PT, Guy JS, Chapleau WP, Butler FK, McSwain NE. Prehospital spine immobilization for penetrating trauma—review and recommendations from the Prehospital Trauma Life Support Executive Committee. J Trauma. 2011;71(3):763–769.
20. American College of Emergency Physicians. Policy Statement- EMS Management of Patients with Potential Spinal Injury. 2015. Available at: http://www.acep.org/Physician-Resources/Policies/Policy-Statements/EMS-Management-of-Patients-with-Potential-Spinal-Injury. Accessed February 9, 2016.
21. Barney RN, Cordell WH, Miller E. Pain associated with immobilization on rigid spine boards. Ann Emerg Med. 1989;18:918.
22. Cooney DR, Wallus H, Asaly M, Wojcik S. Backboard time for patients receiving spinal immobilization by emergency medical services. Int J Emerg Med. 2013;6(1):17.
23. Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994;23(1):48-51.
24. Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med, 1996;14(3):293-298.
25. March J, Ausband S, Brown L. Changes in physical examination caused by use of spinal immobilization. Prehosp Emerg Care. 2002;6(4):421-424.
26. Berg G, Nyberg S, Harrison P, Baumchen J, Gurss E, Hennes E. Near-infrared spectroscopy measurement of sacral tissue oxygen saturation in healthy volunteers immobilized on rigid spine boards. Prehosp Emerg Care. 2010;14(4):419-424.
27. Lee AY, Elojeimy S, Kanal KM, Gunn ML. The effect of trauma backboards on computed tomography radiation dose. Clin Radiol. 2016. Epub ahead of print.
28. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy, nonsmoking man. Ann Emerg Med. 1988;17(9):915-918.
29. Walsh M, Grant T, Mickey S. Lung function compromised by spinal immobilization. Ann Emerg Med. 1990;19(5):615-616.
30. Totten VY, Sugarman DB. Respiratory effects of spinal immobilization. Prehosp Emerg Care. 1999; 3(4):347-352.
31. Goutcher CM, Lochhead V. Reduction in mouth opening with semi-rigid cervical collars. Br J Anaesth. 2005;95(3):344-348.
32. Davies G, Deakin C, Wilson A. The effect of a rigid collar on intracranial pressure. Injury. 1996;27(9):647-649.
33. Dunham CM, Brocker BP, Collier BD, Gemmel DJ. Risks associated with magnetic resonance imaging and cervical collar in comatose, blunt trauma patients with negative comprehensive cervical spine computed tomography and no apparent spinal deficit. Crit Care. 2008;12(4):R89.
34. Mobbs RJ, Stoodley MA, Fuller J. Effect of cervical hard collar on intracranial pressure after head injury. ANZ J Surg. 2002;72(6):389-391.
35. Stone MB, Tubridy CM, Curran R. The effect of rigid cervical collars on internal jugular vein dimensions. Acad Emerg Med. 2010;17(1):100-102.
36. Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010;69(2):447-450.
37. Podolsky SM, Hoffman JR, Pietrafesa CA. Neurologic complications following immobilization of cervical spine fracture in a patient with ankylosing spondylitis. Ann Emerg Med. 1983;12(9):578-580.
38. Papadopoulos MC, Chakraborty A, Waldron G, Bell BA. Exacerbating cervical spine injury by applying a hard collar. BMJ. 1999;319(7203):171-172.
39. Thumbikat P, Hariharan RP, Ravichandran G, Mcclelland MR, Mathew KM. Spinal cord injury in patients with ankylosing spondylitis: a 10-year review. Spine (Phila Pa 1976). 2007;32(26):2989-2995.
40. Oto B, Corey DJ, Oswald J, Sifford D, Walsh B. Early secondary neurologic deterioration after blunt spinal trauma: a review of the literature. Acad Emerg Med. 2015;22(10):1200-1212.
41. Oteir AO, Smith K, Jennings PA, Stoelwinder JU. The prehospital management of suspected spinal cord injury: an update. Prehosp Disaster Med. 2014;29(4):399-402.
42. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000;343(2):94-99.
43. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001;286(15):1841–1848.
44. Stroh G, Braude D. Can an out-of-hospital cervical spine clearance protocol identify all patients with injuries? An argument for selective immobilization. Ann Emerg Med. 2001;37(6):609-615.
1. White CC, Domeier RM, Millin MG. EMS spinal precautions and the use of the long backboard - resource document to the position statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care. 2014;18(2):306-314.
2. Geisler WO, Wynne-Jones M, Jousse AT. Early management of patients with trauma to the spinal cord. Med Serv J Can. 1966;22(7):512–523.
3. Farrington JD. Death in a ditch. Bulletin of the American College of Surgeons. 1967;52(3):121-130.
4. Farrington JD. Extrication of victims- surgical principles. J Trauma. 1968;8(4):493-512.
5. Riggins RS, Kraus JF. The risk of neurologic damage with fractures of the vertebrae. J Trauma. 1977;17(2):126-133.
6. Soderstrom CA, Brumback RJ. Early care of the patient with cervical spine injury. Orthop Clin North Am. 1986;17(1):3-13.
7. McHugh TP, Taylor JP. Unnecessary out-of-hospital use of full spinal immobilization. Acad Emerg Med. 1998;5(3):278-280.
8. Kwan I, Bunn F, Roberts I. Spinal immobilisation for trauma patients. Cochrane Database Syst Rev. 2001;(2):CD002803.
9. Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital use of cervical collars in trauma patients: a critical review. J Neurotrauma. 2014;31(6):531-540.
10. Conrad BP, Rechtine G, Weight M, Clarke J, Horodyski M. Motion in the unstable cervical spine during hospital bed transfers. J Trauma. 2010;69,432-436.
11. Horodyski M, DiPaola CP, Conrad BP, Rechtine GR. Cervical collars are insufficient for immobilizing an unstable cervical spine injury. J Emerg Med. 2011;41(5):513-519.
12. Hughes SJ. How effective is the Newport/Aspen collar? A prospective radiographic evaluation in healthy adult volunteers. J Trauma. 1998;45(2):374-378.
13. Perry SD, McLellan B, McIlroy WE, Maki BE, Schwartz M, Fernie GR. The efficacy of head immobilization techniques during simulated vehicle motion. Spine (Phil Pa 1976). 1999;24(17):1839-1844.
14. Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS. Cervical spine motion during extrication. J Emerg Med. 2013;44(1):122-127.
15. Dixon M, O’Halloran J, Cummins NM. Biomechanical analysis of spinal immobilization during prehospital extrication—a proof of concept study. Emerg Med J. 2014;31(9):745-749.
16. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998;5(3):214-219.
17. Haut ER, Kalish BT, Efron DT, et al. Spine immobilization in penetrating trauma: more harm than good? J Trauma. 2010;68(1):115-120.
18. Vanderlan WB, Tew BE, McSwain NE. Increased risk of death with cervical spine immobilization in penetrating cervical trauma. Injury. 2009;40(8):880-883.
19. Stuke LE, Pons PT, Guy JS, Chapleau WP, Butler FK, McSwain NE. Prehospital spine immobilization for penetrating trauma—review and recommendations from the Prehospital Trauma Life Support Executive Committee. J Trauma. 2011;71(3):763–769.
20. American College of Emergency Physicians. Policy Statement- EMS Management of Patients with Potential Spinal Injury. 2015. Available at: http://www.acep.org/Physician-Resources/Policies/Policy-Statements/EMS-Management-of-Patients-with-Potential-Spinal-Injury. Accessed February 9, 2016.
21. Barney RN, Cordell WH, Miller E. Pain associated with immobilization on rigid spine boards. Ann Emerg Med. 1989;18:918.
22. Cooney DR, Wallus H, Asaly M, Wojcik S. Backboard time for patients receiving spinal immobilization by emergency medical services. Int J Emerg Med. 2013;6(1):17.
23. Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994;23(1):48-51.
24. Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med, 1996;14(3):293-298.
25. March J, Ausband S, Brown L. Changes in physical examination caused by use of spinal immobilization. Prehosp Emerg Care. 2002;6(4):421-424.
26. Berg G, Nyberg S, Harrison P, Baumchen J, Gurss E, Hennes E. Near-infrared spectroscopy measurement of sacral tissue oxygen saturation in healthy volunteers immobilized on rigid spine boards. Prehosp Emerg Care. 2010;14(4):419-424.
27. Lee AY, Elojeimy S, Kanal KM, Gunn ML. The effect of trauma backboards on computed tomography radiation dose. Clin Radiol. 2016. Epub ahead of print.
28. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy, nonsmoking man. Ann Emerg Med. 1988;17(9):915-918.
29. Walsh M, Grant T, Mickey S. Lung function compromised by spinal immobilization. Ann Emerg Med. 1990;19(5):615-616.
30. Totten VY, Sugarman DB. Respiratory effects of spinal immobilization. Prehosp Emerg Care. 1999; 3(4):347-352.
31. Goutcher CM, Lochhead V. Reduction in mouth opening with semi-rigid cervical collars. Br J Anaesth. 2005;95(3):344-348.
32. Davies G, Deakin C, Wilson A. The effect of a rigid collar on intracranial pressure. Injury. 1996;27(9):647-649.
33. Dunham CM, Brocker BP, Collier BD, Gemmel DJ. Risks associated with magnetic resonance imaging and cervical collar in comatose, blunt trauma patients with negative comprehensive cervical spine computed tomography and no apparent spinal deficit. Crit Care. 2008;12(4):R89.
34. Mobbs RJ, Stoodley MA, Fuller J. Effect of cervical hard collar on intracranial pressure after head injury. ANZ J Surg. 2002;72(6):389-391.
35. Stone MB, Tubridy CM, Curran R. The effect of rigid cervical collars on internal jugular vein dimensions. Acad Emerg Med. 2010;17(1):100-102.
36. Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010;69(2):447-450.
37. Podolsky SM, Hoffman JR, Pietrafesa CA. Neurologic complications following immobilization of cervical spine fracture in a patient with ankylosing spondylitis. Ann Emerg Med. 1983;12(9):578-580.
38. Papadopoulos MC, Chakraborty A, Waldron G, Bell BA. Exacerbating cervical spine injury by applying a hard collar. BMJ. 1999;319(7203):171-172.
39. Thumbikat P, Hariharan RP, Ravichandran G, Mcclelland MR, Mathew KM. Spinal cord injury in patients with ankylosing spondylitis: a 10-year review. Spine (Phila Pa 1976). 2007;32(26):2989-2995.
40. Oto B, Corey DJ, Oswald J, Sifford D, Walsh B. Early secondary neurologic deterioration after blunt spinal trauma: a review of the literature. Acad Emerg Med. 2015;22(10):1200-1212.
41. Oteir AO, Smith K, Jennings PA, Stoelwinder JU. The prehospital management of suspected spinal cord injury: an update. Prehosp Disaster Med. 2014;29(4):399-402.
42. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000;343(2):94-99.
43. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001;286(15):1841–1848.
44. Stroh G, Braude D. Can an out-of-hospital cervical spine clearance protocol identify all patients with injuries? An argument for selective immobilization. Ann Emerg Med. 2001;37(6):609-615.
A Click Is Not a Clunk: Developmental Dysplasia of the Hip in a Newborn
IN THIS ARTICLE
- Diagnosis
- Management
- Newborn hip evaluation algorithm
Developmental dysplasia of the hip (DDH), previously known as congenital dislocation of the hip, follows a spectrum of irregular anatomic hip development spanning from acetabular dysplasia to irreducible dislocation at birth. Early detection is critical to improve the overall prognosis. Prompt diagnosis requires understanding of potential risk factors, proficiency in physical examination techniques, and implementation of appropriate screening tools when indicated. Although current guidelines direct timing for physical exam screenings, imaging, and treatment, it is ultimately up to the provider to determine the best course of action on a case-by-case basis. This article provides a review of these topics and more.
CURRENT GUIDELINES
In 2000, the American Academy of Pediatrics (AAP) developed guidelines for detection of hip dysplasia, including recommendation of relevant physical exam screenings for all newborns.1 In 2007, the Pediatric Orthopaedic Society of North America (POSNA) encouraged providers to follow the AAP guidelines with a continued recommendation to perform newborn screening for hip instability and routine follow-up evaluations until the child achieves walking.2 The American Academy of Orthopaedic Surgeons (AAOS) also established clinical guidelines in 2014 that are endorsed by both AAP and POSNA.3 These guidelines support routine clinical screening; research evaluated infants up to 6 months old, however, limiting the recommendations to that age-group.
Failure to treat DDH early has been associated with serious negative sequelae that include chronic pain, degenerative arthritis, postural scoliosis, and early gait disturbances.4 Primary care providers are expected to perform thorough newborn hip exams with associated specialized tests (ie, Ortolani and Barlow, which are discussed in “Physical exam”) at each routine follow-up. Heightened clinical suspicion and risk factor awareness are key for primary care providers to promptly identify patients requiring orthopedic referral. With early diagnosis, a removable soft abduction brace can be applied as the initial treatment. When treatment is delayed, however, closed reduction under anesthesia or complex surgical intervention may be required.
EPIDEMIOLOGY
The etiology for DDH remains unknown. Hip dysplasia typically presents unilaterally but can also occur bilaterally. DDH is more likely to affect the left hip than the right.5
Reported incidence varies, ranging from 0.06 to 76.1 per 1,000 live births, and is largely affected by race and geographic location.5 Incidence is higher in countries where routine screening is required, by either physical examination or ultrasound (1.6 to 28.5 and 34.0 to 60.3 per 1,000, respectively), compared with countries not requiring routine screening (1.3 per 1,000). This may suggest that the majority of hip dysplasia cases are transient and resolve spontaneously without treatment.6,7
RISK FACTORS AND PATIENT HISTORY
Known risk factors for DDH include breech presentation (see Figure 1), positive family history, and female gender.5,8-10 Female infants are eight times more likely than males to develop DDH.10 Firstborn status is also recognized as an associated risk factor, which may be attributable to space constraints in utero. This hypothesis is further supported by the relative DDH-protective effect of prematurity and low birth weight. Other potential risk factors include advanced maternal age, birth weight that is high for gestational age, decreased hip abduction, and joint laxity. However, the majority of patients with hip dysplasia have no identifiable risk factors.3,5,9,11,12
Swaddling, which often maintains the hips in an adducted and/or extended position, has also been strongly associated with hip dysplasia.5,13 Multiple organizations, including the AAOS,AAP, POSNA, and the International Hip Dysplasia Institute, have developed or endorsed hip-healthy swaddling recommendations to minimize the risk for DDH in swaddled infants.13-15 Such practices allow the infant’s legs to bend up and out at the hips, promoting free hip movement, flexion, and abduction.13,15 Swaddling has demonstrated multiple benefits (including improved sleep and relief of excessive crying13) and continues to be recommended by many US providers; however, those caring for infants at risk for DDH should avoid traditional swaddling and/or practice hip-healthy swaddling techniques.10,13,14 Early diagnosis starts with the clinician’s knowledge of DDH risk factors and the recommended screening protocols. The presence of multiple risk factors will increase the likelihood of this condition and should lower the clinician’s threshold for ordering additional screening, regardless of hip exam findings.
PHYSICAL EXAM
Both AAP and AAOS guidelines recommend clinical screening for DDH with physical exam in all newborns.1,3 A head-to-toe musculoskeletal exam is warranted during the initial evaluation of every newborn in order to assess for any known DDH-associated conditions, which may include neuromuscular disorders, torticollis, and metatarsus adductus.5
Initial evaluation of an infant with DDH may reveal nonspecific findings, including asymmetric skin folds and limb-length inequality. The Galeazzi sign should be sought by aligning flexed knees with the child in the supine position and assessing for uneven knee heights (see Figure 2). Unilateral posterior hip dislocation or femoral shortening represents a positive Galeazzi sign.16 Joint laxity and limited hip abduction have also been associated with DDH.1,10
Barlow and Ortolani exams are more specific to DDH and should be completed at newborn screening and each subsequent well-baby exam.1 The Barlow maneuver is a provocative test with flexion, adduction, and posterior pressure through the infant’s hip (Figure 3). A palpable clunk during the Barlow maneuver indicates positive instability with posterior displacement. The Ortolani test is a reductive maneuver requiring abduction with posterior pressure to lift the greater trochanter (Figure 4). A clunk sensation with this test is positive for reduction of the hip.
The infant’s diaper should be removed during the hip evaluation. These exams are more reliable when each hip is evaluated separately with the pelvis stabilized.10 All physical exam findings must be carefully documented at each encounter.1,17
It is critical for the examiner to understand the appropriate technique and potential results when conducting each of these specialized hip exams. A true positive finding is the clunking sensation that occurs with the dislocation or relocation of the affected hip; this finding is better felt than heard. In contrast, a benign hip click with these maneuvers is a more subtle sensation—typically, a soft-tissue snapping or catching—and is not diagnostic of DDH. A click is not a clunk and is not indicative of DDH.1,3
DDH may present later in infancy or early childhood; therefore, DDH should remain within the differential diagnosis for gait asymmetry, unequal hip motion, or limb-length discrepancy. It may be beneficial to continue to evaluate for these developments during routine exams as part of a thorough pediatric musculoskeletal assessment, particularly in patients with documented risk factors for DDH.1,3,4 Delay in diagnosis of DDH, it should be noted, is a relatively common complaint in pediatric medical malpractice lawsuits; until the early 2000s, this condition represented about 75% of claims in one medical malpractice database.The decrease in claims has been attributed to better awareness and earlier diagnosis of DDH. 17
Continue for the diagnosis >>
DIAGNOSIS
A positive Ortolani or Barlow sign is diagnostic and warrants prompt orthopedic referral (Figure 5). If physical examination results are equivocal or inconclusive, follow-up at two weeks is recommended, with continued routine follow-up until walking is achieved. Patients with persistent equivocal findings at the two-week follow-up warrant ultrasound at age 3 to 4 weeks or orthopedic referral. Infants with significant risk factors, particularly breech presentation at birth, should also undergo imaging.18 AAP recommends ultrasound at age 6 weeks or radiograph after 4 months of age.1,18 AAOS recommends performing an imaging study before age 6 months when at least one of the following risk factors is present: breech presentation, positive family history of DDH, or previous clinical instability (moderate level of evidence).3
IMAGING
Ultrasound is the diagnostic test of choice for infants because radiographs have limited value until the femoral heads begin to ossify at age 4 to 6 months.18 Ultrasonography allows for visualization of the cartilaginous portion of the acetabulum and femoral head.1 Dynamic stressing is performed during ultrasound to assess the level of hip stability. A provider trained in ultrasound will measure the depth of the acetabulum and identify any potential laxity or instability of the hip joint. Accuracy of these findings is largely dependent on the experience and skill of the examiner.
Ultrasound evaluation is not recommended until after age 3 to 4 weeks. Earlier findings may include mild laxity and immature morphology of the acetabulum, which often resolve spontaneously.1,18 Use of ultrasound is currently recommended only to confirm diagnostic suspicion, based on clinical findings, or for infants with significant risk factors.18 Universal ultrasound screening in newborns is not recommended and would incur unnecessary costs.1,3,9 Plain radiographs are used after age 4 months to confirm a diagnosis of DDH or to assess for residual dysplasia.3,18
Continue for management >>
MANAGEMENT
Once hip dysplasia is suggested by physical exam or imaging study, the child’s subsequent care should be provided by an orthopedic specialist with experience in treating this condition. Treatment is preferably initiated before age 6 weeks.12 The specifics of treatment are largely based on age at diagnosis and the severity of dysplasia.
The goal of treatment is to maintain the hips in a stable position with the femoral head well covered by the acetabulum. This will improve anatomic development and function. Early clinical diagnosis is often sufficient to justify initiating conservative treatment; additionally, early detection of DDH can considerably reduce the need for surgical intervention.12 Although the potential for spontaneous resolution is high, the consequences associated with delay in care can be significant.
Preferred initial management, which can be initiated before confirmation of DDH by ultrasound, involves implementation of soft abduction support.19 The Pavlik harness is the support design of choice (Figure 6).12 This harness maintains hip flexion and abduction, creating concentric reduction of the femoral head. The brace is highly successful when its use is initiated early. Treatment in a Pavlik harness requires nearly full-time wear and close monitoring by a clinician. Unlikely potential risks associated with this treatment include avascular necrosis and femoral nerve palsy.4
Ultrasonography is used to further monitor treatment and to determine length of wear. Long-term results suggest a success rate exceeding 90%.20,21 However, this rate may be falsely elevated due to the number of hips that likely would have improved spontaneously without treatment.6,19
The Pavlik harness becomes less effective with increasing age, and a more rigid abduction brace may be considered in infants older than 6 months.20 Overall outcomes improve once the femoral head is consistently maintained in the acetabulum. Delay in treatment is associated with an increase in the long-term complications associated with residual hip dysplasia.22
Once an infant is undergoing treatment for DDH in a Pavlik harness, there is no need for primary care providers to continue to perform provocative testing, such as the Ortolani or Barlow test, at routine well-baby checks. Unnecessary stress to the hips is not beneficial, and any new results will not change the treatment being provided by the orthopedic specialist. Adjustments to the fit of the harness should be made only by the orthopedist, unless femoral nerve palsy is noted on exam. This development warrants immediate discontinuation of harness use until symptoms resolve.21
Abduction bracing may not be suitable for all cases of hip dysplasia. Newborns with irreducible hips, more advanced dysplasia, or associated neuromuscular or syndromic disorder may require closed versus open reduction and casting. More invasive surgical options may also be considered in advanced dysplasia in order to reshape the joint and improve function.20,22
Continue for patient education >>
PATIENT EDUCATION
Parents should be fully educated on the options for managing hip dysplasia. Once DDH is diagnosed, prompt referral to an orthopedic specialist is critical in order to weigh the treatment options and to develop the appropriate individualized plan for each child. Once treatment is initiated, parental compliance is essential; frequent meetings between parents and the specialist are important.
Parents of infants with known risk factors for and/or suspicion of hip dysplasia should also be educated on hip-healthy swaddling to allow for free motion of the hips and knees.10,13 Advise them that some commercial baby carriers and slings may maintain the hips in an undesirable extended position. In both swaddling and with baby carriers, care should be taken to allow for hip abduction and flexion. Caution should also be taken during diaper changes to avoid lifting the legs and thereby causing unnecessary stress to the hips.
CONCLUSION
Developmental dysplasia of the hip can be a disabling pediatric condition. Early diagnosis improves the likelihood of successful treatment during infancy and can prevent serious complications. If untreated, DDH can lead to joint degeneration and premature arthritis. Recognition and treatment within the first six weeks of life is crucial to the overall outcome.
The role of a primary care provider is to identify hip dysplasia risk factors and recognize associated physical exam findings in order to refer to an orthopedic specialist in a timely manner. Guidelines from the AAP, POSNA, and AAOS help direct this process in order to effectively identify infants at risk and in need of treatment.
REFERENCES
1. American Academy of Pediatrics. Committee on Quality Improvement, Subcommittee on Developmental Dysplasia of the Hip. Clinical practice guideline: early detection of developmental dysplasia of the hip. Pediatrics. 2000;105(4 pt 1):896-905.
2. Schwend RM, Schoenecker P, Richards BS, et al. Screening the newborn for developmental dysplasia of the hip: now what do we do? J Pediatr Orthop. 2007;27(6):607-610.
3. Mulpuri K, Song KM, Goldberg MJ, Sevarino K. Detection and nonoperative management of pediatric developmental dysplasia of the hip in infants up to six months of age. J Am Acad Orthop Surg. 2015;23(3):202-205.
4. Thomas SRYW. A review of long-term outcomes for late presenting developmental hip dysplasia. Bone Joint J. 2015;97-B(6):729-733.
5. Loder RT, Skopelja EN. The epidemiology and demographics of hip dysplasia. ISRN Orthop. 2011;2011:238607.
6. US Preventive Services Task Force. Screening for developmental dysplasia of the hip: recommendation statement. Pediatrics. 2006;117(3):898-902.
7. Shorter D, Hong T, Osborn DA. Screening programmes for developmental dysplasia of the hip in newborn infants. Cochrane Database Syst Rev. 2011;(9):CD004595.
8. Loder RT, Shafer C. The demographics of developmental hip dysplasia in the Midwestern United States (Indiana). J Child Orthop. 2015;9(1):93-98.
9. Paton RW, Hinduja K, Thomas CD. The significance of at-risk factors in ultrasound surveillance of developmental dysplasia of the hip: a ten-year prospective study. J Bone Joint Surg Br. 2005;87(9):1264-1266.
10. Alsaleem M, Set KK, Saadeh L. Developmental dysplasia of hip: a review. Clin Pediatr (Phila). 2015;54(10):921-928.
11. Chan A, McCaul KA, Cundy PJ, et al. Perinatal risk factors for developmental dysplasia of the hip. Arch Dis Child. 1997;76(2):F94-F100.
12. Godley DR. Assessment, diagnosis, and treatment of developmental dysplasia of the hip. JAAPA. 2013;26(3):54-58.
13. Van Sleuwen BE, Engelberts AC, Boere-Boonekamp MM, et al. Swaddling: a systematic review. Pediatrics. 2007;120(4):e1097-e1106.
14. American Academy of Orthopaedic Surgeons, American Association of Orthopaedic Surgeons. Position statement: swaddling and developmental hip dysplasia. www.aaos.org/uploadedFiles/PreProduction/About/Opinion_Statements/position/1186%20Swaddling%20and%20Developmental%20Hip%20Dysplasia.pdf. Accessed January 22, 2016.
15. Clarke NM. Swaddling and hip dysplasia: an orthopaedic perspective. Arch Dis Child. 2014;99(1):5-6.
16. Storer SK, Skaggs DL. Developmental dysplasia of the hip. Am Fam Physician. 2006;74(8):1310-1316.
17. McAbee GN, Donn SM, Mendelson RA, et al. Medical diagnoses commonly associated with pediatric malpractice lawsuits in the United States. Pediatrics. 2008;122(6):e1282-e1286.
18. Imrie M, Scott V, Stearns P, et al. Is ultrasound screening for DDH in babies born breech sufficient? J Child Orthop. 2010;4(1):3-8.
19. Chen HW, Chang CH, Tsai ST, et al. Natural progression of hip dysplasia in newborns: a reflection of hip ultrasonographic screenings in newborn nurseries. J Pediatr Orthop B. 2010;19(5):418-423.
20. Gans I, Flynn JM, Sankar WN. Abduction bracing for residual acetabular dysplasia in infantile DDH. J Pediatr Orthop. 2013;33(7):714-718.
21. Murnaghan ML, Browne RH, Sucato DJ, Birch J. Femoral nerve palsy in Pavlik harness treatment for developmental dysplasia of the hip. J Bone Joint Surg Am. 2011;93(5):493-499.
22. Dezateux C, Rosendahl K. Developmental dysplasia of the hip. Lancet. 2007;369(9572):1541-1552.
IN THIS ARTICLE
- Diagnosis
- Management
- Newborn hip evaluation algorithm
Developmental dysplasia of the hip (DDH), previously known as congenital dislocation of the hip, follows a spectrum of irregular anatomic hip development spanning from acetabular dysplasia to irreducible dislocation at birth. Early detection is critical to improve the overall prognosis. Prompt diagnosis requires understanding of potential risk factors, proficiency in physical examination techniques, and implementation of appropriate screening tools when indicated. Although current guidelines direct timing for physical exam screenings, imaging, and treatment, it is ultimately up to the provider to determine the best course of action on a case-by-case basis. This article provides a review of these topics and more.
CURRENT GUIDELINES
In 2000, the American Academy of Pediatrics (AAP) developed guidelines for detection of hip dysplasia, including recommendation of relevant physical exam screenings for all newborns.1 In 2007, the Pediatric Orthopaedic Society of North America (POSNA) encouraged providers to follow the AAP guidelines with a continued recommendation to perform newborn screening for hip instability and routine follow-up evaluations until the child achieves walking.2 The American Academy of Orthopaedic Surgeons (AAOS) also established clinical guidelines in 2014 that are endorsed by both AAP and POSNA.3 These guidelines support routine clinical screening; research evaluated infants up to 6 months old, however, limiting the recommendations to that age-group.
Failure to treat DDH early has been associated with serious negative sequelae that include chronic pain, degenerative arthritis, postural scoliosis, and early gait disturbances.4 Primary care providers are expected to perform thorough newborn hip exams with associated specialized tests (ie, Ortolani and Barlow, which are discussed in “Physical exam”) at each routine follow-up. Heightened clinical suspicion and risk factor awareness are key for primary care providers to promptly identify patients requiring orthopedic referral. With early diagnosis, a removable soft abduction brace can be applied as the initial treatment. When treatment is delayed, however, closed reduction under anesthesia or complex surgical intervention may be required.
EPIDEMIOLOGY
The etiology for DDH remains unknown. Hip dysplasia typically presents unilaterally but can also occur bilaterally. DDH is more likely to affect the left hip than the right.5
Reported incidence varies, ranging from 0.06 to 76.1 per 1,000 live births, and is largely affected by race and geographic location.5 Incidence is higher in countries where routine screening is required, by either physical examination or ultrasound (1.6 to 28.5 and 34.0 to 60.3 per 1,000, respectively), compared with countries not requiring routine screening (1.3 per 1,000). This may suggest that the majority of hip dysplasia cases are transient and resolve spontaneously without treatment.6,7
RISK FACTORS AND PATIENT HISTORY
Known risk factors for DDH include breech presentation (see Figure 1), positive family history, and female gender.5,8-10 Female infants are eight times more likely than males to develop DDH.10 Firstborn status is also recognized as an associated risk factor, which may be attributable to space constraints in utero. This hypothesis is further supported by the relative DDH-protective effect of prematurity and low birth weight. Other potential risk factors include advanced maternal age, birth weight that is high for gestational age, decreased hip abduction, and joint laxity. However, the majority of patients with hip dysplasia have no identifiable risk factors.3,5,9,11,12
Swaddling, which often maintains the hips in an adducted and/or extended position, has also been strongly associated with hip dysplasia.5,13 Multiple organizations, including the AAOS,AAP, POSNA, and the International Hip Dysplasia Institute, have developed or endorsed hip-healthy swaddling recommendations to minimize the risk for DDH in swaddled infants.13-15 Such practices allow the infant’s legs to bend up and out at the hips, promoting free hip movement, flexion, and abduction.13,15 Swaddling has demonstrated multiple benefits (including improved sleep and relief of excessive crying13) and continues to be recommended by many US providers; however, those caring for infants at risk for DDH should avoid traditional swaddling and/or practice hip-healthy swaddling techniques.10,13,14 Early diagnosis starts with the clinician’s knowledge of DDH risk factors and the recommended screening protocols. The presence of multiple risk factors will increase the likelihood of this condition and should lower the clinician’s threshold for ordering additional screening, regardless of hip exam findings.
PHYSICAL EXAM
Both AAP and AAOS guidelines recommend clinical screening for DDH with physical exam in all newborns.1,3 A head-to-toe musculoskeletal exam is warranted during the initial evaluation of every newborn in order to assess for any known DDH-associated conditions, which may include neuromuscular disorders, torticollis, and metatarsus adductus.5
Initial evaluation of an infant with DDH may reveal nonspecific findings, including asymmetric skin folds and limb-length inequality. The Galeazzi sign should be sought by aligning flexed knees with the child in the supine position and assessing for uneven knee heights (see Figure 2). Unilateral posterior hip dislocation or femoral shortening represents a positive Galeazzi sign.16 Joint laxity and limited hip abduction have also been associated with DDH.1,10
Barlow and Ortolani exams are more specific to DDH and should be completed at newborn screening and each subsequent well-baby exam.1 The Barlow maneuver is a provocative test with flexion, adduction, and posterior pressure through the infant’s hip (Figure 3). A palpable clunk during the Barlow maneuver indicates positive instability with posterior displacement. The Ortolani test is a reductive maneuver requiring abduction with posterior pressure to lift the greater trochanter (Figure 4). A clunk sensation with this test is positive for reduction of the hip.
The infant’s diaper should be removed during the hip evaluation. These exams are more reliable when each hip is evaluated separately with the pelvis stabilized.10 All physical exam findings must be carefully documented at each encounter.1,17
It is critical for the examiner to understand the appropriate technique and potential results when conducting each of these specialized hip exams. A true positive finding is the clunking sensation that occurs with the dislocation or relocation of the affected hip; this finding is better felt than heard. In contrast, a benign hip click with these maneuvers is a more subtle sensation—typically, a soft-tissue snapping or catching—and is not diagnostic of DDH. A click is not a clunk and is not indicative of DDH.1,3
DDH may present later in infancy or early childhood; therefore, DDH should remain within the differential diagnosis for gait asymmetry, unequal hip motion, or limb-length discrepancy. It may be beneficial to continue to evaluate for these developments during routine exams as part of a thorough pediatric musculoskeletal assessment, particularly in patients with documented risk factors for DDH.1,3,4 Delay in diagnosis of DDH, it should be noted, is a relatively common complaint in pediatric medical malpractice lawsuits; until the early 2000s, this condition represented about 75% of claims in one medical malpractice database.The decrease in claims has been attributed to better awareness and earlier diagnosis of DDH. 17
Continue for the diagnosis >>
DIAGNOSIS
A positive Ortolani or Barlow sign is diagnostic and warrants prompt orthopedic referral (Figure 5). If physical examination results are equivocal or inconclusive, follow-up at two weeks is recommended, with continued routine follow-up until walking is achieved. Patients with persistent equivocal findings at the two-week follow-up warrant ultrasound at age 3 to 4 weeks or orthopedic referral. Infants with significant risk factors, particularly breech presentation at birth, should also undergo imaging.18 AAP recommends ultrasound at age 6 weeks or radiograph after 4 months of age.1,18 AAOS recommends performing an imaging study before age 6 months when at least one of the following risk factors is present: breech presentation, positive family history of DDH, or previous clinical instability (moderate level of evidence).3
IMAGING
Ultrasound is the diagnostic test of choice for infants because radiographs have limited value until the femoral heads begin to ossify at age 4 to 6 months.18 Ultrasonography allows for visualization of the cartilaginous portion of the acetabulum and femoral head.1 Dynamic stressing is performed during ultrasound to assess the level of hip stability. A provider trained in ultrasound will measure the depth of the acetabulum and identify any potential laxity or instability of the hip joint. Accuracy of these findings is largely dependent on the experience and skill of the examiner.
Ultrasound evaluation is not recommended until after age 3 to 4 weeks. Earlier findings may include mild laxity and immature morphology of the acetabulum, which often resolve spontaneously.1,18 Use of ultrasound is currently recommended only to confirm diagnostic suspicion, based on clinical findings, or for infants with significant risk factors.18 Universal ultrasound screening in newborns is not recommended and would incur unnecessary costs.1,3,9 Plain radiographs are used after age 4 months to confirm a diagnosis of DDH or to assess for residual dysplasia.3,18
Continue for management >>
MANAGEMENT
Once hip dysplasia is suggested by physical exam or imaging study, the child’s subsequent care should be provided by an orthopedic specialist with experience in treating this condition. Treatment is preferably initiated before age 6 weeks.12 The specifics of treatment are largely based on age at diagnosis and the severity of dysplasia.
The goal of treatment is to maintain the hips in a stable position with the femoral head well covered by the acetabulum. This will improve anatomic development and function. Early clinical diagnosis is often sufficient to justify initiating conservative treatment; additionally, early detection of DDH can considerably reduce the need for surgical intervention.12 Although the potential for spontaneous resolution is high, the consequences associated with delay in care can be significant.
Preferred initial management, which can be initiated before confirmation of DDH by ultrasound, involves implementation of soft abduction support.19 The Pavlik harness is the support design of choice (Figure 6).12 This harness maintains hip flexion and abduction, creating concentric reduction of the femoral head. The brace is highly successful when its use is initiated early. Treatment in a Pavlik harness requires nearly full-time wear and close monitoring by a clinician. Unlikely potential risks associated with this treatment include avascular necrosis and femoral nerve palsy.4
Ultrasonography is used to further monitor treatment and to determine length of wear. Long-term results suggest a success rate exceeding 90%.20,21 However, this rate may be falsely elevated due to the number of hips that likely would have improved spontaneously without treatment.6,19
The Pavlik harness becomes less effective with increasing age, and a more rigid abduction brace may be considered in infants older than 6 months.20 Overall outcomes improve once the femoral head is consistently maintained in the acetabulum. Delay in treatment is associated with an increase in the long-term complications associated with residual hip dysplasia.22
Once an infant is undergoing treatment for DDH in a Pavlik harness, there is no need for primary care providers to continue to perform provocative testing, such as the Ortolani or Barlow test, at routine well-baby checks. Unnecessary stress to the hips is not beneficial, and any new results will not change the treatment being provided by the orthopedic specialist. Adjustments to the fit of the harness should be made only by the orthopedist, unless femoral nerve palsy is noted on exam. This development warrants immediate discontinuation of harness use until symptoms resolve.21
Abduction bracing may not be suitable for all cases of hip dysplasia. Newborns with irreducible hips, more advanced dysplasia, or associated neuromuscular or syndromic disorder may require closed versus open reduction and casting. More invasive surgical options may also be considered in advanced dysplasia in order to reshape the joint and improve function.20,22
Continue for patient education >>
PATIENT EDUCATION
Parents should be fully educated on the options for managing hip dysplasia. Once DDH is diagnosed, prompt referral to an orthopedic specialist is critical in order to weigh the treatment options and to develop the appropriate individualized plan for each child. Once treatment is initiated, parental compliance is essential; frequent meetings between parents and the specialist are important.
Parents of infants with known risk factors for and/or suspicion of hip dysplasia should also be educated on hip-healthy swaddling to allow for free motion of the hips and knees.10,13 Advise them that some commercial baby carriers and slings may maintain the hips in an undesirable extended position. In both swaddling and with baby carriers, care should be taken to allow for hip abduction and flexion. Caution should also be taken during diaper changes to avoid lifting the legs and thereby causing unnecessary stress to the hips.
CONCLUSION
Developmental dysplasia of the hip can be a disabling pediatric condition. Early diagnosis improves the likelihood of successful treatment during infancy and can prevent serious complications. If untreated, DDH can lead to joint degeneration and premature arthritis. Recognition and treatment within the first six weeks of life is crucial to the overall outcome.
The role of a primary care provider is to identify hip dysplasia risk factors and recognize associated physical exam findings in order to refer to an orthopedic specialist in a timely manner. Guidelines from the AAP, POSNA, and AAOS help direct this process in order to effectively identify infants at risk and in need of treatment.
REFERENCES
1. American Academy of Pediatrics. Committee on Quality Improvement, Subcommittee on Developmental Dysplasia of the Hip. Clinical practice guideline: early detection of developmental dysplasia of the hip. Pediatrics. 2000;105(4 pt 1):896-905.
2. Schwend RM, Schoenecker P, Richards BS, et al. Screening the newborn for developmental dysplasia of the hip: now what do we do? J Pediatr Orthop. 2007;27(6):607-610.
3. Mulpuri K, Song KM, Goldberg MJ, Sevarino K. Detection and nonoperative management of pediatric developmental dysplasia of the hip in infants up to six months of age. J Am Acad Orthop Surg. 2015;23(3):202-205.
4. Thomas SRYW. A review of long-term outcomes for late presenting developmental hip dysplasia. Bone Joint J. 2015;97-B(6):729-733.
5. Loder RT, Skopelja EN. The epidemiology and demographics of hip dysplasia. ISRN Orthop. 2011;2011:238607.
6. US Preventive Services Task Force. Screening for developmental dysplasia of the hip: recommendation statement. Pediatrics. 2006;117(3):898-902.
7. Shorter D, Hong T, Osborn DA. Screening programmes for developmental dysplasia of the hip in newborn infants. Cochrane Database Syst Rev. 2011;(9):CD004595.
8. Loder RT, Shafer C. The demographics of developmental hip dysplasia in the Midwestern United States (Indiana). J Child Orthop. 2015;9(1):93-98.
9. Paton RW, Hinduja K, Thomas CD. The significance of at-risk factors in ultrasound surveillance of developmental dysplasia of the hip: a ten-year prospective study. J Bone Joint Surg Br. 2005;87(9):1264-1266.
10. Alsaleem M, Set KK, Saadeh L. Developmental dysplasia of hip: a review. Clin Pediatr (Phila). 2015;54(10):921-928.
11. Chan A, McCaul KA, Cundy PJ, et al. Perinatal risk factors for developmental dysplasia of the hip. Arch Dis Child. 1997;76(2):F94-F100.
12. Godley DR. Assessment, diagnosis, and treatment of developmental dysplasia of the hip. JAAPA. 2013;26(3):54-58.
13. Van Sleuwen BE, Engelberts AC, Boere-Boonekamp MM, et al. Swaddling: a systematic review. Pediatrics. 2007;120(4):e1097-e1106.
14. American Academy of Orthopaedic Surgeons, American Association of Orthopaedic Surgeons. Position statement: swaddling and developmental hip dysplasia. www.aaos.org/uploadedFiles/PreProduction/About/Opinion_Statements/position/1186%20Swaddling%20and%20Developmental%20Hip%20Dysplasia.pdf. Accessed January 22, 2016.
15. Clarke NM. Swaddling and hip dysplasia: an orthopaedic perspective. Arch Dis Child. 2014;99(1):5-6.
16. Storer SK, Skaggs DL. Developmental dysplasia of the hip. Am Fam Physician. 2006;74(8):1310-1316.
17. McAbee GN, Donn SM, Mendelson RA, et al. Medical diagnoses commonly associated with pediatric malpractice lawsuits in the United States. Pediatrics. 2008;122(6):e1282-e1286.
18. Imrie M, Scott V, Stearns P, et al. Is ultrasound screening for DDH in babies born breech sufficient? J Child Orthop. 2010;4(1):3-8.
19. Chen HW, Chang CH, Tsai ST, et al. Natural progression of hip dysplasia in newborns: a reflection of hip ultrasonographic screenings in newborn nurseries. J Pediatr Orthop B. 2010;19(5):418-423.
20. Gans I, Flynn JM, Sankar WN. Abduction bracing for residual acetabular dysplasia in infantile DDH. J Pediatr Orthop. 2013;33(7):714-718.
21. Murnaghan ML, Browne RH, Sucato DJ, Birch J. Femoral nerve palsy in Pavlik harness treatment for developmental dysplasia of the hip. J Bone Joint Surg Am. 2011;93(5):493-499.
22. Dezateux C, Rosendahl K. Developmental dysplasia of the hip. Lancet. 2007;369(9572):1541-1552.
IN THIS ARTICLE
- Diagnosis
- Management
- Newborn hip evaluation algorithm
Developmental dysplasia of the hip (DDH), previously known as congenital dislocation of the hip, follows a spectrum of irregular anatomic hip development spanning from acetabular dysplasia to irreducible dislocation at birth. Early detection is critical to improve the overall prognosis. Prompt diagnosis requires understanding of potential risk factors, proficiency in physical examination techniques, and implementation of appropriate screening tools when indicated. Although current guidelines direct timing for physical exam screenings, imaging, and treatment, it is ultimately up to the provider to determine the best course of action on a case-by-case basis. This article provides a review of these topics and more.
CURRENT GUIDELINES
In 2000, the American Academy of Pediatrics (AAP) developed guidelines for detection of hip dysplasia, including recommendation of relevant physical exam screenings for all newborns.1 In 2007, the Pediatric Orthopaedic Society of North America (POSNA) encouraged providers to follow the AAP guidelines with a continued recommendation to perform newborn screening for hip instability and routine follow-up evaluations until the child achieves walking.2 The American Academy of Orthopaedic Surgeons (AAOS) also established clinical guidelines in 2014 that are endorsed by both AAP and POSNA.3 These guidelines support routine clinical screening; research evaluated infants up to 6 months old, however, limiting the recommendations to that age-group.
Failure to treat DDH early has been associated with serious negative sequelae that include chronic pain, degenerative arthritis, postural scoliosis, and early gait disturbances.4 Primary care providers are expected to perform thorough newborn hip exams with associated specialized tests (ie, Ortolani and Barlow, which are discussed in “Physical exam”) at each routine follow-up. Heightened clinical suspicion and risk factor awareness are key for primary care providers to promptly identify patients requiring orthopedic referral. With early diagnosis, a removable soft abduction brace can be applied as the initial treatment. When treatment is delayed, however, closed reduction under anesthesia or complex surgical intervention may be required.
EPIDEMIOLOGY
The etiology for DDH remains unknown. Hip dysplasia typically presents unilaterally but can also occur bilaterally. DDH is more likely to affect the left hip than the right.5
Reported incidence varies, ranging from 0.06 to 76.1 per 1,000 live births, and is largely affected by race and geographic location.5 Incidence is higher in countries where routine screening is required, by either physical examination or ultrasound (1.6 to 28.5 and 34.0 to 60.3 per 1,000, respectively), compared with countries not requiring routine screening (1.3 per 1,000). This may suggest that the majority of hip dysplasia cases are transient and resolve spontaneously without treatment.6,7
RISK FACTORS AND PATIENT HISTORY
Known risk factors for DDH include breech presentation (see Figure 1), positive family history, and female gender.5,8-10 Female infants are eight times more likely than males to develop DDH.10 Firstborn status is also recognized as an associated risk factor, which may be attributable to space constraints in utero. This hypothesis is further supported by the relative DDH-protective effect of prematurity and low birth weight. Other potential risk factors include advanced maternal age, birth weight that is high for gestational age, decreased hip abduction, and joint laxity. However, the majority of patients with hip dysplasia have no identifiable risk factors.3,5,9,11,12
Swaddling, which often maintains the hips in an adducted and/or extended position, has also been strongly associated with hip dysplasia.5,13 Multiple organizations, including the AAOS,AAP, POSNA, and the International Hip Dysplasia Institute, have developed or endorsed hip-healthy swaddling recommendations to minimize the risk for DDH in swaddled infants.13-15 Such practices allow the infant’s legs to bend up and out at the hips, promoting free hip movement, flexion, and abduction.13,15 Swaddling has demonstrated multiple benefits (including improved sleep and relief of excessive crying13) and continues to be recommended by many US providers; however, those caring for infants at risk for DDH should avoid traditional swaddling and/or practice hip-healthy swaddling techniques.10,13,14 Early diagnosis starts with the clinician’s knowledge of DDH risk factors and the recommended screening protocols. The presence of multiple risk factors will increase the likelihood of this condition and should lower the clinician’s threshold for ordering additional screening, regardless of hip exam findings.
PHYSICAL EXAM
Both AAP and AAOS guidelines recommend clinical screening for DDH with physical exam in all newborns.1,3 A head-to-toe musculoskeletal exam is warranted during the initial evaluation of every newborn in order to assess for any known DDH-associated conditions, which may include neuromuscular disorders, torticollis, and metatarsus adductus.5
Initial evaluation of an infant with DDH may reveal nonspecific findings, including asymmetric skin folds and limb-length inequality. The Galeazzi sign should be sought by aligning flexed knees with the child in the supine position and assessing for uneven knee heights (see Figure 2). Unilateral posterior hip dislocation or femoral shortening represents a positive Galeazzi sign.16 Joint laxity and limited hip abduction have also been associated with DDH.1,10
Barlow and Ortolani exams are more specific to DDH and should be completed at newborn screening and each subsequent well-baby exam.1 The Barlow maneuver is a provocative test with flexion, adduction, and posterior pressure through the infant’s hip (Figure 3). A palpable clunk during the Barlow maneuver indicates positive instability with posterior displacement. The Ortolani test is a reductive maneuver requiring abduction with posterior pressure to lift the greater trochanter (Figure 4). A clunk sensation with this test is positive for reduction of the hip.
The infant’s diaper should be removed during the hip evaluation. These exams are more reliable when each hip is evaluated separately with the pelvis stabilized.10 All physical exam findings must be carefully documented at each encounter.1,17
It is critical for the examiner to understand the appropriate technique and potential results when conducting each of these specialized hip exams. A true positive finding is the clunking sensation that occurs with the dislocation or relocation of the affected hip; this finding is better felt than heard. In contrast, a benign hip click with these maneuvers is a more subtle sensation—typically, a soft-tissue snapping or catching—and is not diagnostic of DDH. A click is not a clunk and is not indicative of DDH.1,3
DDH may present later in infancy or early childhood; therefore, DDH should remain within the differential diagnosis for gait asymmetry, unequal hip motion, or limb-length discrepancy. It may be beneficial to continue to evaluate for these developments during routine exams as part of a thorough pediatric musculoskeletal assessment, particularly in patients with documented risk factors for DDH.1,3,4 Delay in diagnosis of DDH, it should be noted, is a relatively common complaint in pediatric medical malpractice lawsuits; until the early 2000s, this condition represented about 75% of claims in one medical malpractice database.The decrease in claims has been attributed to better awareness and earlier diagnosis of DDH. 17
Continue for the diagnosis >>
DIAGNOSIS
A positive Ortolani or Barlow sign is diagnostic and warrants prompt orthopedic referral (Figure 5). If physical examination results are equivocal or inconclusive, follow-up at two weeks is recommended, with continued routine follow-up until walking is achieved. Patients with persistent equivocal findings at the two-week follow-up warrant ultrasound at age 3 to 4 weeks or orthopedic referral. Infants with significant risk factors, particularly breech presentation at birth, should also undergo imaging.18 AAP recommends ultrasound at age 6 weeks or radiograph after 4 months of age.1,18 AAOS recommends performing an imaging study before age 6 months when at least one of the following risk factors is present: breech presentation, positive family history of DDH, or previous clinical instability (moderate level of evidence).3
IMAGING
Ultrasound is the diagnostic test of choice for infants because radiographs have limited value until the femoral heads begin to ossify at age 4 to 6 months.18 Ultrasonography allows for visualization of the cartilaginous portion of the acetabulum and femoral head.1 Dynamic stressing is performed during ultrasound to assess the level of hip stability. A provider trained in ultrasound will measure the depth of the acetabulum and identify any potential laxity or instability of the hip joint. Accuracy of these findings is largely dependent on the experience and skill of the examiner.
Ultrasound evaluation is not recommended until after age 3 to 4 weeks. Earlier findings may include mild laxity and immature morphology of the acetabulum, which often resolve spontaneously.1,18 Use of ultrasound is currently recommended only to confirm diagnostic suspicion, based on clinical findings, or for infants with significant risk factors.18 Universal ultrasound screening in newborns is not recommended and would incur unnecessary costs.1,3,9 Plain radiographs are used after age 4 months to confirm a diagnosis of DDH or to assess for residual dysplasia.3,18
Continue for management >>
MANAGEMENT
Once hip dysplasia is suggested by physical exam or imaging study, the child’s subsequent care should be provided by an orthopedic specialist with experience in treating this condition. Treatment is preferably initiated before age 6 weeks.12 The specifics of treatment are largely based on age at diagnosis and the severity of dysplasia.
The goal of treatment is to maintain the hips in a stable position with the femoral head well covered by the acetabulum. This will improve anatomic development and function. Early clinical diagnosis is often sufficient to justify initiating conservative treatment; additionally, early detection of DDH can considerably reduce the need for surgical intervention.12 Although the potential for spontaneous resolution is high, the consequences associated with delay in care can be significant.
Preferred initial management, which can be initiated before confirmation of DDH by ultrasound, involves implementation of soft abduction support.19 The Pavlik harness is the support design of choice (Figure 6).12 This harness maintains hip flexion and abduction, creating concentric reduction of the femoral head. The brace is highly successful when its use is initiated early. Treatment in a Pavlik harness requires nearly full-time wear and close monitoring by a clinician. Unlikely potential risks associated with this treatment include avascular necrosis and femoral nerve palsy.4
Ultrasonography is used to further monitor treatment and to determine length of wear. Long-term results suggest a success rate exceeding 90%.20,21 However, this rate may be falsely elevated due to the number of hips that likely would have improved spontaneously without treatment.6,19
The Pavlik harness becomes less effective with increasing age, and a more rigid abduction brace may be considered in infants older than 6 months.20 Overall outcomes improve once the femoral head is consistently maintained in the acetabulum. Delay in treatment is associated with an increase in the long-term complications associated with residual hip dysplasia.22
Once an infant is undergoing treatment for DDH in a Pavlik harness, there is no need for primary care providers to continue to perform provocative testing, such as the Ortolani or Barlow test, at routine well-baby checks. Unnecessary stress to the hips is not beneficial, and any new results will not change the treatment being provided by the orthopedic specialist. Adjustments to the fit of the harness should be made only by the orthopedist, unless femoral nerve palsy is noted on exam. This development warrants immediate discontinuation of harness use until symptoms resolve.21
Abduction bracing may not be suitable for all cases of hip dysplasia. Newborns with irreducible hips, more advanced dysplasia, or associated neuromuscular or syndromic disorder may require closed versus open reduction and casting. More invasive surgical options may also be considered in advanced dysplasia in order to reshape the joint and improve function.20,22
Continue for patient education >>
PATIENT EDUCATION
Parents should be fully educated on the options for managing hip dysplasia. Once DDH is diagnosed, prompt referral to an orthopedic specialist is critical in order to weigh the treatment options and to develop the appropriate individualized plan for each child. Once treatment is initiated, parental compliance is essential; frequent meetings between parents and the specialist are important.
Parents of infants with known risk factors for and/or suspicion of hip dysplasia should also be educated on hip-healthy swaddling to allow for free motion of the hips and knees.10,13 Advise them that some commercial baby carriers and slings may maintain the hips in an undesirable extended position. In both swaddling and with baby carriers, care should be taken to allow for hip abduction and flexion. Caution should also be taken during diaper changes to avoid lifting the legs and thereby causing unnecessary stress to the hips.
CONCLUSION
Developmental dysplasia of the hip can be a disabling pediatric condition. Early diagnosis improves the likelihood of successful treatment during infancy and can prevent serious complications. If untreated, DDH can lead to joint degeneration and premature arthritis. Recognition and treatment within the first six weeks of life is crucial to the overall outcome.
The role of a primary care provider is to identify hip dysplasia risk factors and recognize associated physical exam findings in order to refer to an orthopedic specialist in a timely manner. Guidelines from the AAP, POSNA, and AAOS help direct this process in order to effectively identify infants at risk and in need of treatment.
REFERENCES
1. American Academy of Pediatrics. Committee on Quality Improvement, Subcommittee on Developmental Dysplasia of the Hip. Clinical practice guideline: early detection of developmental dysplasia of the hip. Pediatrics. 2000;105(4 pt 1):896-905.
2. Schwend RM, Schoenecker P, Richards BS, et al. Screening the newborn for developmental dysplasia of the hip: now what do we do? J Pediatr Orthop. 2007;27(6):607-610.
3. Mulpuri K, Song KM, Goldberg MJ, Sevarino K. Detection and nonoperative management of pediatric developmental dysplasia of the hip in infants up to six months of age. J Am Acad Orthop Surg. 2015;23(3):202-205.
4. Thomas SRYW. A review of long-term outcomes for late presenting developmental hip dysplasia. Bone Joint J. 2015;97-B(6):729-733.
5. Loder RT, Skopelja EN. The epidemiology and demographics of hip dysplasia. ISRN Orthop. 2011;2011:238607.
6. US Preventive Services Task Force. Screening for developmental dysplasia of the hip: recommendation statement. Pediatrics. 2006;117(3):898-902.
7. Shorter D, Hong T, Osborn DA. Screening programmes for developmental dysplasia of the hip in newborn infants. Cochrane Database Syst Rev. 2011;(9):CD004595.
8. Loder RT, Shafer C. The demographics of developmental hip dysplasia in the Midwestern United States (Indiana). J Child Orthop. 2015;9(1):93-98.
9. Paton RW, Hinduja K, Thomas CD. The significance of at-risk factors in ultrasound surveillance of developmental dysplasia of the hip: a ten-year prospective study. J Bone Joint Surg Br. 2005;87(9):1264-1266.
10. Alsaleem M, Set KK, Saadeh L. Developmental dysplasia of hip: a review. Clin Pediatr (Phila). 2015;54(10):921-928.
11. Chan A, McCaul KA, Cundy PJ, et al. Perinatal risk factors for developmental dysplasia of the hip. Arch Dis Child. 1997;76(2):F94-F100.
12. Godley DR. Assessment, diagnosis, and treatment of developmental dysplasia of the hip. JAAPA. 2013;26(3):54-58.
13. Van Sleuwen BE, Engelberts AC, Boere-Boonekamp MM, et al. Swaddling: a systematic review. Pediatrics. 2007;120(4):e1097-e1106.
14. American Academy of Orthopaedic Surgeons, American Association of Orthopaedic Surgeons. Position statement: swaddling and developmental hip dysplasia. www.aaos.org/uploadedFiles/PreProduction/About/Opinion_Statements/position/1186%20Swaddling%20and%20Developmental%20Hip%20Dysplasia.pdf. Accessed January 22, 2016.
15. Clarke NM. Swaddling and hip dysplasia: an orthopaedic perspective. Arch Dis Child. 2014;99(1):5-6.
16. Storer SK, Skaggs DL. Developmental dysplasia of the hip. Am Fam Physician. 2006;74(8):1310-1316.
17. McAbee GN, Donn SM, Mendelson RA, et al. Medical diagnoses commonly associated with pediatric malpractice lawsuits in the United States. Pediatrics. 2008;122(6):e1282-e1286.
18. Imrie M, Scott V, Stearns P, et al. Is ultrasound screening for DDH in babies born breech sufficient? J Child Orthop. 2010;4(1):3-8.
19. Chen HW, Chang CH, Tsai ST, et al. Natural progression of hip dysplasia in newborns: a reflection of hip ultrasonographic screenings in newborn nurseries. J Pediatr Orthop B. 2010;19(5):418-423.
20. Gans I, Flynn JM, Sankar WN. Abduction bracing for residual acetabular dysplasia in infantile DDH. J Pediatr Orthop. 2013;33(7):714-718.
21. Murnaghan ML, Browne RH, Sucato DJ, Birch J. Femoral nerve palsy in Pavlik harness treatment for developmental dysplasia of the hip. J Bone Joint Surg Am. 2011;93(5):493-499.
22. Dezateux C, Rosendahl K. Developmental dysplasia of the hip. Lancet. 2007;369(9572):1541-1552.
Homelessness, HIV, and HCV
According to researchers from Columbia University in New York City, McMaster University in Hamilton, Ontario, Canada, and Ontario HIV Treatment Network, in Canada, homelessness and unstable housing situations are associated with higher rates of HIV and hepatitis C infection (HCV). They reviewed 152 studies involving 139,757 participants who had HIV or were co-infected with HCV. The researchers found “strong evidence” that the lack of stable, secure, adequate housing is a significant barrier to consistent and appropriate medical care, adherence to treatment, sustained viral suppression, and reduction of risk behaviors.
Research data showed that the worse the housing status, the less the engagement and utilization of HIV medical care. Homeless patients had more emergency department (ED) admissions; homeless males had longer hospital stays; and homeless injection-drug users were more often hospitalized than were people with HIV in high socioeconomic neighborhoods.
In another study, homelessness was significantly associated with baseline HCV-positive status. Twenty-five studies reported that homelessness or unstable housing was associated with significantly poorer outcomes on 1 or more indications of physical or mental health functioning and quality of life, mental health symptoms or diagnosis, or diagnosed physical health comorbidities, such as HCV and tuberculosis. The studies also showed the impact of having a home on both treatment and adherence to treatment. One study of co-infected patients who were on antiretroviral therapy (ART) or beginning HCV treatment found that good housing conditions reduced the risk of nonadherence to ART, regardless of the treatment of HCV. Stable housing also doubled the odds of ART use.
Data from another study also found participants with a fixed address were more likely to stop abusing drugs. Obtaining stable housing was also associated with using an outpatient setting rather than the ED as the usual source of care.
“Housing first” interventions are receiving growing attention, the researchers note, as a potential health care cost-containment strategy. As interventions for people with complex health conditions, changing housing status is “both possible and promising.”
Source:
Aidala AA, Wilson MG, Shubert V, et al. Am J Public Health. 2016;106(1):e1-e23
doi: 10.2105/AJPH.2015.302905.
According to researchers from Columbia University in New York City, McMaster University in Hamilton, Ontario, Canada, and Ontario HIV Treatment Network, in Canada, homelessness and unstable housing situations are associated with higher rates of HIV and hepatitis C infection (HCV). They reviewed 152 studies involving 139,757 participants who had HIV or were co-infected with HCV. The researchers found “strong evidence” that the lack of stable, secure, adequate housing is a significant barrier to consistent and appropriate medical care, adherence to treatment, sustained viral suppression, and reduction of risk behaviors.
Research data showed that the worse the housing status, the less the engagement and utilization of HIV medical care. Homeless patients had more emergency department (ED) admissions; homeless males had longer hospital stays; and homeless injection-drug users were more often hospitalized than were people with HIV in high socioeconomic neighborhoods.
In another study, homelessness was significantly associated with baseline HCV-positive status. Twenty-five studies reported that homelessness or unstable housing was associated with significantly poorer outcomes on 1 or more indications of physical or mental health functioning and quality of life, mental health symptoms or diagnosis, or diagnosed physical health comorbidities, such as HCV and tuberculosis. The studies also showed the impact of having a home on both treatment and adherence to treatment. One study of co-infected patients who were on antiretroviral therapy (ART) or beginning HCV treatment found that good housing conditions reduced the risk of nonadherence to ART, regardless of the treatment of HCV. Stable housing also doubled the odds of ART use.
Data from another study also found participants with a fixed address were more likely to stop abusing drugs. Obtaining stable housing was also associated with using an outpatient setting rather than the ED as the usual source of care.
“Housing first” interventions are receiving growing attention, the researchers note, as a potential health care cost-containment strategy. As interventions for people with complex health conditions, changing housing status is “both possible and promising.”
Source:
Aidala AA, Wilson MG, Shubert V, et al. Am J Public Health. 2016;106(1):e1-e23
doi: 10.2105/AJPH.2015.302905.
According to researchers from Columbia University in New York City, McMaster University in Hamilton, Ontario, Canada, and Ontario HIV Treatment Network, in Canada, homelessness and unstable housing situations are associated with higher rates of HIV and hepatitis C infection (HCV). They reviewed 152 studies involving 139,757 participants who had HIV or were co-infected with HCV. The researchers found “strong evidence” that the lack of stable, secure, adequate housing is a significant barrier to consistent and appropriate medical care, adherence to treatment, sustained viral suppression, and reduction of risk behaviors.
Research data showed that the worse the housing status, the less the engagement and utilization of HIV medical care. Homeless patients had more emergency department (ED) admissions; homeless males had longer hospital stays; and homeless injection-drug users were more often hospitalized than were people with HIV in high socioeconomic neighborhoods.
In another study, homelessness was significantly associated with baseline HCV-positive status. Twenty-five studies reported that homelessness or unstable housing was associated with significantly poorer outcomes on 1 or more indications of physical or mental health functioning and quality of life, mental health symptoms or diagnosis, or diagnosed physical health comorbidities, such as HCV and tuberculosis. The studies also showed the impact of having a home on both treatment and adherence to treatment. One study of co-infected patients who were on antiretroviral therapy (ART) or beginning HCV treatment found that good housing conditions reduced the risk of nonadherence to ART, regardless of the treatment of HCV. Stable housing also doubled the odds of ART use.
Data from another study also found participants with a fixed address were more likely to stop abusing drugs. Obtaining stable housing was also associated with using an outpatient setting rather than the ED as the usual source of care.
“Housing first” interventions are receiving growing attention, the researchers note, as a potential health care cost-containment strategy. As interventions for people with complex health conditions, changing housing status is “both possible and promising.”
Source:
Aidala AA, Wilson MG, Shubert V, et al. Am J Public Health. 2016;106(1):e1-e23
doi: 10.2105/AJPH.2015.302905.
Excessive Bleeding After Cardiac Surgery
Cardiac surgery patients have a high risk of excessive postoperative bleeding as a consequence of procoagulant blood products, vasoconstrictors, and poor organ perfusion. Researchers who conducted a study at University Hospital in São Paulo, Brazil, say that for clinicians to be prepared for timely interventions, it helps to know which patients to watch and when to identify the risk factors.
In their prospective study of 323 patients, episodes of excessive bleeding were concentrated in the first and second postoperative hours, and 21% of complications required interventions, such as vasoactive medication titration, protamine supplementation, and transfusions of blood products. During the immediate postoperative time, 105 patients developed excessive bleeding with 39 in the first hour, followed by 36 patients in the second hour, and 8 in the third hour.
The researchers found that other risk factors for excessive bleeding were chronic hypertension, greater height, body mass index (BMI) < 26.35 kg/m2, higher hematocrit, and intraoperative heparin dose > 312.5 mg without subsequent platelet transfusion. The researchers say platelet transfusions may have been protective. Certain variables, such as lower BMI and male gender, may have been explained by greater clot strength and faster rate of fibrin formation in women.
Patients at risk for excessive bleeding also had lower preoperative platelet count, although the mean value was within the normal range. But given that more than half the study group used aspirin and 11% used an adenosine diphosphate-receptor blocker, the researchers say they may have had a higher prevalence of unknown platelet dysfunctions.
Source:
Lopes CT, Brunori EFR, Cavalcante AMRZ, et al. Heart Lung. 2016;45(1):64-69.e2.
doi: 10.1016/j.hrtlng.2015.09.
Cardiac surgery patients have a high risk of excessive postoperative bleeding as a consequence of procoagulant blood products, vasoconstrictors, and poor organ perfusion. Researchers who conducted a study at University Hospital in São Paulo, Brazil, say that for clinicians to be prepared for timely interventions, it helps to know which patients to watch and when to identify the risk factors.
In their prospective study of 323 patients, episodes of excessive bleeding were concentrated in the first and second postoperative hours, and 21% of complications required interventions, such as vasoactive medication titration, protamine supplementation, and transfusions of blood products. During the immediate postoperative time, 105 patients developed excessive bleeding with 39 in the first hour, followed by 36 patients in the second hour, and 8 in the third hour.
The researchers found that other risk factors for excessive bleeding were chronic hypertension, greater height, body mass index (BMI) < 26.35 kg/m2, higher hematocrit, and intraoperative heparin dose > 312.5 mg without subsequent platelet transfusion. The researchers say platelet transfusions may have been protective. Certain variables, such as lower BMI and male gender, may have been explained by greater clot strength and faster rate of fibrin formation in women.
Patients at risk for excessive bleeding also had lower preoperative platelet count, although the mean value was within the normal range. But given that more than half the study group used aspirin and 11% used an adenosine diphosphate-receptor blocker, the researchers say they may have had a higher prevalence of unknown platelet dysfunctions.
Source:
Lopes CT, Brunori EFR, Cavalcante AMRZ, et al. Heart Lung. 2016;45(1):64-69.e2.
doi: 10.1016/j.hrtlng.2015.09.
Cardiac surgery patients have a high risk of excessive postoperative bleeding as a consequence of procoagulant blood products, vasoconstrictors, and poor organ perfusion. Researchers who conducted a study at University Hospital in São Paulo, Brazil, say that for clinicians to be prepared for timely interventions, it helps to know which patients to watch and when to identify the risk factors.
In their prospective study of 323 patients, episodes of excessive bleeding were concentrated in the first and second postoperative hours, and 21% of complications required interventions, such as vasoactive medication titration, protamine supplementation, and transfusions of blood products. During the immediate postoperative time, 105 patients developed excessive bleeding with 39 in the first hour, followed by 36 patients in the second hour, and 8 in the third hour.
The researchers found that other risk factors for excessive bleeding were chronic hypertension, greater height, body mass index (BMI) < 26.35 kg/m2, higher hematocrit, and intraoperative heparin dose > 312.5 mg without subsequent platelet transfusion. The researchers say platelet transfusions may have been protective. Certain variables, such as lower BMI and male gender, may have been explained by greater clot strength and faster rate of fibrin formation in women.
Patients at risk for excessive bleeding also had lower preoperative platelet count, although the mean value was within the normal range. But given that more than half the study group used aspirin and 11% used an adenosine diphosphate-receptor blocker, the researchers say they may have had a higher prevalence of unknown platelet dysfunctions.
Source:
Lopes CT, Brunori EFR, Cavalcante AMRZ, et al. Heart Lung. 2016;45(1):64-69.e2.
doi: 10.1016/j.hrtlng.2015.09.
How to Make Your Patient With Sleep Apnea a Super User of Positive Airway Pressure Therapy
Adherence to positive airway pressure (PAP) therapy is a difficult patient management issue. Clinicians at the John D. Dingell VA Medical Center in Detroit (VAMC Detroit) developed the O’Brien criteria and extensive patient education materials to increase patient adherence. The importance of PAP therapy and the reasons veterans should sleep with a PAP machine for 7 to 9 hours each night are stressed (many sleep only 4 to 5 hours). Several recent studies have confirmed widely varying PAP therapy adherence rates (30%-84%).1-13 A majority of patients indicated that mask discomfort is the primary reason for nonadherence.1
Adherence is affected by many factors, including heated humidity, patient education, mask type, and type of PAP machine (eg, continuous PAP [CPAP] vs bilevel PAP [BPAP]; auto-PAP vs CPAP). Other factors, such as race and economic status, also affect adherence.14 The Wisconsin Sleep Cohort Study found that patients with moderate-to-severe untreated obstructive sleep apnea (OSA) were 4 to 5 times more likely to die of a cardiovascular event and 3 times more likely to die of any cause.15 The morbidity and mortality associated with severe untreated OSA led the clinicians to intensify treatment efforts.16In this article, the authors summarize the initiative at the VAMC Detroit to enhance PAP therapy adherence in patients with sleep apnea. The goal was to motivate patients to maximize PAP machine use. This article is a guide that federal health care providers and their civilian counterparts in the private sector can use to maximize PAP machine use. Working toward that goal, a set of PAP “super user” criteria was developed and used to create a 5-point method for encouraging patients to maximize adherence to PAP therapy.
Background
Positive airway pressure is the room air pressure, measured in centimeters of H2O, which splints open the airway to prevent snoring, apneas, and hypopneas. An apnea is a 90%-plus airway obstruction that lasts longer than 10 seconds and is seen with sleep study polysomnography. A hypopnea is a 30%-plus airway obstruction that lasts longer than 10 seconds and is accompanied by a 3% drop in pulse oximetry (SpO2).
A CPAP device delivers pressure continuously through a medical air compressor or flow generator called a PAP machine. The BPAP machine has separate inspiratory pressure and expiratory pressure. Auto-PAP machines give minimum pressure and maximum pressure usually between the range of 4 cm H2O to 20 cm H2O. This machine finds the user’s median pressure (90th percentile) and maximum pressure and averages pressure over a specified period of use. The auto-PAP can then be set to CPAP mode and the pressure fixed or set to the 90th percentile.
O’Brien Criteria
The O’Brien criteria for PAP super-user status (Table 1) were developed for maximizing PAP machine use and presented at the 2013 John D. Dingell Sleep and Wake Disorders Center Symposium. There is no other published reference or criteria proposed for maximizing PAP machine adherence. A recent study on sleep time criteria suggested that a higher percentage of patients achieved normal functioning with longer duration nightly CPAP therapy, which is in line with the authors’ recommended PAP machine use duration.17
Positive airway pressure therapy is eligible for insurance reimbursement by Medicare and third-party payers for adult patients who have OSA and achieve 4 hours of nightly use for 70% of nights over 30 days. Coverage for CPAP therapy is initially limited to 12 weeks during which beneficiaries with an OSA diagnosis can be identified and any therapy benefits documented. Subsequent CPAP therapy is covered only for those OSA patients who benefit during the 12-week period.18At VAMC Detroit, the data covering the previous 30 days of use is downloaded. Medicare allows for the best 30-day period out of the 12-week window. The hospital, along with Harper Hospital and the Detroit Medical Centers in conjunction with the Wayne State University sleep program, is an Academic Center of Distinction, which follows the sleep guidelines and practice parameters for Medicare, third-party insurance companies, and the American Academy of Sleep Medicine.
The sleep clinic clinicians follow the clinical guidelines for evaluation, management, and long-term care of adults with OSA.19,20 Follow-up visits are scheduled and made on a consultation basis up to 90 days for the required download or as necessary for PAP therapy. In this initiative, practitioners offer veteran-specific patient care with PAP therapy that exceeds Medicare guidelines. The success of this process yielded a growing cohort of PAP super users at VAMC Detroit. These patients exceed the Medicare criterion of 4 hours of nightly use for 70% of nights over 30 days. Thus, 4 hours of nightly use for 100% of nights over the same period was proposed as another criterion.
The super-user criteria, which provide motivation to reach the top, stimulate many patients to achieve the Medicare criteria. All 5 criteria must be satisfied to attain super-user status, and becoming a super user is not easy. In fact, the expectation is that, if an adherence data study is conducted, it will show that only a small percentage of all users meet the criteria. Maximum adherence is expected to be the tail (3%-4%) of a bell-shaped curve.
PAP Super-User Status
At the initial evaluation, practitioners create a self-fulfilling prophecy that, as first described by Merton, sets expectations.21 A self-fulfilling prophecy is a prediction that directly or indirectly causes the prediction to become true as a result of the positive feedback between belief and behavior.21 The personnel at VAMC Detroit sleep clinic set a tone that enables patients to meet and exceed the Medicare sleep guidelines and their expectations. Patients are encouraged to make it their personal mission to achieve the goal of becoming a PAP super user. The patients receive the O’Brien criteria for PAP super-user status—guidelines thought to contribute to higher quality of life.
The Medicare criterion emphasized is the minimum required for full adherence. The goal is to reduce sleepiness and increase well-being. The literature shows that increasing duration of sleep results in lower daytime sleepiness.22 Inadequate sleep has many detrimental effects. According to a recent study, insufficient sleep contributes to weight gain.22 Desired patient outcomes are increased sleep time without arousals, increased slow-wave sleep (SWS), consolidation of memories and rapid eye movement (REM), and improvement in emotional and procedural skill memories.23 Patients are informed that using a PAP machine for 7 to 9 hours can reduce excessive daytime sleepiness and allow for more SWS and REM sleep, which help improve memory, judgment, and concentration. Many other studies have shown how 7 to 9 hours of sleep benefit adults. Thus, 7 to 9 hours became the criterion for maximizing PAP sleep time.
Initial Evaluation and Sleep Study
A primary care provider can enroll a patient into the clinic for a sleep study by requesting an evaluation. The consultation is then triaged using the STOP-BANG (Snoring, Tiredness, Observed apnea, high blood Pressure–Body mass index > 35, Age > 50, Neck circumference > 40 cm, Gender male) questionnaire. The STOP-BANG has a high sensitivity for predicting moderate-to-severe (87.0%) and severe (70.4%) sleep-disordered breathing.24 More than 3 affirmative answers indicate a high risk for sleep-disordered breathing and is cause for ordering a sleep study.
CPAP Group Class
Patients with a diagnosis of sleep apnea subsequently receive their CPAP machines when they attend a 2-hour group class taught by a respiratory therapist. Group education sessions increase the chance of issuing more machines and providing better education.25 One study found that “attendance in a group clinic designed to encourage compliance with CPAP therapy provided a simple and effective means of improving treatment of OSA.”25
In class, the respiratory therapist briefly assesses each patient’s CPAP prescription, describes the patient’s type of sleep apnea and final diagnosis, and reviews the CPAP machine’s features. Veterans are then instructed to take their CPAP machines home to use all night, every night for 4 weeks. All night is defined as a period of 7.5 to 8 hours, as population-based study results have shown that sleep of this duration is associated with lowest cardiovascular morbidity and mortality. After the initial 4-plus weeks of machine use, patients with all their CPAP equipment are seen in the sleep clinic.
First Sleep Clinic Follow-Up Visit
At first follow-up, patients are asked for a subjective evaluation of their sleep. Most state they are “better” with PAP therapy. Each patient’s mask is checked and refitted with the patient’s prescribed pressure.
Patients are informed of their PAP settings and requirements from the sleep study and told their particular “magic pressure.” Patients understand that a person’s magic pressure, determined in the laboratory, is the pressure of room air blown into the nose, mouth, or both that eliminates not only snoring, but also partial and complete airway obstructions (hypopneas, apneas). Patients are asked to remember their particular magic pressure and their AHI and told their OSA status (mild, moderate, or severe) as assessed by the laboratory study.26 Extensive education on sleep apnea and treatment are also addressed. Education and training are among the most important tenets of PAP therapy, and these are incorporated into all encounters.25,26
PAP Data Report and Leak
The CPAP data are downloaded and printed. If adherence is suboptimal, clinician and patient discuss increasing adherence and possibly becoming a super user. The patient receives a copy of the report, which can be compared with the patient’s adherence statistics and with the adherence statistics of similar patients who are super users. A few blacked-out names are posted on the board in front of the provider’s computer station. Patients can thus easily see that attaining super-user status is very difficult but possible. Some patients maximize their therapy and are designated PAP super users. These patients are proud to receive this designation, and they strive to keep it.
Data downloads are crucial for adherence. In a recent study, the American Thoracic Society stated, “Providers need to be able to interpret adherence systems.”27
The clinic provides a summary report on each patient’s adherence. A provider interpretation is added, and the report is copied into the Computer Patient Record System.
After the report is downloaded, the provider checks for correct pressure and then for a large leak. A large leak is an unintentional leak (the total amount that leaks but not including leak from the mask) > 5% of the night. A leak of > 15 minutes was added to the super-user criteria, because some software provides the average time of a large leak per day in minutes.28 Many veterans sleep only 4 to 5 hours nightly (300 minutes × 5% = 15 minutes). Therefore, the leak should not be more than 5% or 15 minutes for a veteran sleeping 5 hours.
The machine indicates a percentage of leak on the patient self-check LED screen for adherence. There is no standardized leak criterion used by all flow-generator manufacturers. Every mask has venting designed to leak intentionally so that the patient does not rebreathe air CO2. The main concern is unintentional leaks above the intentional leak or venting threshold.
The ResMed CPAP (ResMed Corp, San Diego, CA) maximum intentional leak is 24 L/min.29 Above that level is large leak. The exact leak amount varies by interface (mask) based on pressure and mask type.2,12
The larger the interface surface area, the larger the leak. Unintentional leak is higher with the full-face mask than with the nasal mask, most likely because there is more opportunity for leakage with the larger surface area of the full-face mask. Nasal pillows seem to leak less because of their smaller surface area, but more studies on mask interfaces are needed to validate this finding.
Chin Strap
Adding a chin strap improved patient adherence, nightly duration of use, residual AHI, and leak in patients with sleep apnea.30 Other investigators reported reduced OSA, confirmed by polysomnography and nasopharyngolaryngoscopy, with use of only a chin strap.31 When a nasal mask with chin strap is used, the strap should be made to fit properly over the chin, not on the throat. Properly used chin straps significantly reduce leakage and residual AHI.30
A chin strap most likely reduces large leak and dry mouth.30 Dry mouth can result from mouth leak, which is commonly caused by nasal congestion or high pressure and mouth breathing. The nasal turbinates help humidify, warm, and cool the air. Heated humidification of PAP can help prevent dry mouth.
Asking the Right Questions
The clinician should ask several key questions at the first follow-up: How is it going with your PAP machine? Do you feel PAP therapy is helping you sleep? Do you feel better with PAP therapy? To a patient who states he or she is not doing well with therapy, the clinician should ask, What type of problems are you having? In many cases, poor adherence is attributable to a large leak from a poorly fitting mask. A large leak can also increase residual AHI and cause frequent arousals.30
Some machines cannot maintain the pressure of a large leak and will shut off and trigger an alarm that wakes the patient to readjust the mask. This situation causes some patients to discontinue CPAP/BPAP use. The mask leak must be adjusted. Another common complaint is morning dry mouth. This extreme dryness—a significant clue pointing to mouth leak caused in part by the mouth dropping open during sleep with PAP—should be addressed by fitting the patient with a chin strap.30 Dry mouth also can be caused by low humidity; increasing the humidity setting usually resolves the problem. However, as one study found, use of controlled heated humidification did not improve adherence or quality of life.32 In the same study, the nasopharyngeal dryness that resulted from CPAP therapy without humidification was reduced immediately and during the first weeks of treatment.All current PAP machines feature heated humidification.
Mouth breathing can also result from nasal congestion, allergic or vasomotor rhinitis, nasal turbinate hypertrophy, obstruction from a deviated septum, polyps, or air hunger/insufficient PAP pressure. Chronic rhinosinusitis is a problem that affects up to 12.5% of the U.S. population.33
Adherence is also increased with the elimination of leak and associated arousals. Patients are shown how to use their PAP machine’s heated humidity settings to obtain desired comfort levels. The clinician explains that the nasal turbinates heat and cool the air and that they can become swollen and irritated with PAP therapy. A heated hose may be prescribed to provide optimal humidification without condensation or water dripping into the hose (rainout).
A full-face mask is used only when the patient cannot breathe out the nose adequately or when PAP becomes too high. A 2013 study found no significant differences among ResMed, Respironics, and Fisher & Paykel CPAP interfaces (Fisher & Paykel Healthcare, Irvine, CA).34 The clinician determines which mask is comfortable for a patient and tries to stay with that mask for that patient.
Adherence Report
A therapy data summary is downloaded and reviewed with the patient.28 A pattern of use report that shows daily use with times over the month is also reviewed.28 The software’s sleep therapy long-term trend report lists important statistics. The adherence data summary and the CPAP summary are also reviewed (Table 2).28 This page is printed and given to patients to reieiw their progress. For some it represents a reward for using the CPAP/BPAP machine as well as a congratulatory note.
In the Example 1 summary download (Table 2), a patient used a PAP machine 4 hours or more on 93.3% of the 30 days the machine was used.28 Residual AHI was low, 2.1, and there was no appreciable leak. The PAP of 11.2 cm H2O was in the 90th percentile. The patient was fixed to 12 cm H2O with expiratory pressure relief (EPR) of 1. The EPR is a comfort feature that reduces pressure from 1 cm H2O to 3 cm H2O to make it easier for the patient to exhale. (A flow generator that produces EPR of > 3 cm H2O is a BPAP machine.)
This patient was not a super user. Overall use was low—5 hours, 28 minutes—which could indicate behaviorally insufficient sleep syndrome. Sleep time is controversial, but the National Sleep Foundation recommends 7 to 9 hours of sleep per night.
A different patient used a PAP machine 4 hours or more on 100% (28/28) of the days when the machine was used (Table 3).29 Residual AHI was low (0.6), median use was 8 hours, 47 minutes, and there was no appreciable leak. The patient was using autoset mode with a minimum pressure of 13 cm H2O and maximum pressure of 18 cm H2O. The 95th percentile pressure was 13.6 cm H2O. The patient’s pressure was changed to 14 cm H2O with EPR of 3. This patient was a super user.
Sleep Hygiene Discussion
Providers must discuss sleep hygiene (good sleep habits) with veterans. If needed, AASM pamphlets on sleep hygiene and other educational materials can be provided. The bedroom should be cool, comfortable, quiet, and dark and should not include a television or computer. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration and tells the brain it is time to wake up.34
Patients are asked about the number of arousals they have per night. At first follow-up, providers must determine what is causing a patient to arouse while on CPAP/BPAP therapy. Some causes are air leak resulting in unresolved OSA, nocturia (may be triggered by unresolved OSA), dry mouth (indicating need for chin strap), nightmares (suggestive of unresolved OSA in REM sleep), posttraumatic stress disorder (PTSD), environmental noise, and claustrophobia. The provider should have thought-out answers to these problems in advance.
Epworth Sleepiness Scale
The Epworth Sleepiness Scale (ESS) is administered as part of the baseline comprehensive examination and at every sleep clinic follow-up after issuing a CPAP/BPAP machine.35 The first evaluation after the machine is issued should show a reduction in ESS. No reduction in ESS indicates that a problem needs to be addressed. The most common reason for insufficient reduction in ESS is suboptimal PAP therapy adherence, usually because of a large leak. Some cases of poor adherence may be attributable to restless legs syndrome, periodic limb movement disorder, chronic musculoskeletal pain, and sleep fragmentation caused by alcohol, smoking, caffeine, or cocaine. Excessive daytime sleepiness may persist from use of pain medications or other sedating medications. One study found a correlation between sleep duration with CPAP therapy and reduction in ESS.36 In addition to administering the ESS, patients are asked how they doing with PAP therapy, and the answer is documented. Treatment changes are made if needed to reduce excessive daytime sleepiness.
Ear-Nose-Throat Examination
A quick look into the nose with a nasal speculum is a crucial component of a thorough examination. The clinician looks for a deviated septum, swollen turbinates, obstruction, polyps, bleeding, infection, septal perforation, and discharge. In addition, the patient is checked for airflow amount, nasal congestion, and obstruction; if necessary a nasal steroid spray or a nasal saline spray is prescribed. In some cases, saline spray can be added to the steroid spray to help reduce or eliminate nasal congestion.37
Treatment of congestion requires education, as many patients improperly use these sprays. The steroid spray is not an instant vasoconstrictor; a week of regular use is needed to reduce inflammation and congestion. Saline spray and saline irrigation can be used as a treatment adjunct for symptoms of chronic rhinosinusitis.37If the steroid and saline sprays fail after a 2-month trial, consider an ear-nose-throat (ENT) consultation. A recent study found that adherence rates increased after septoplasty in patients with nasal obstruction.38 The throat is examined for macroglossia or scalloping of the tongue.39 Macroglossic Mallampati IV tongues are platterlike. They are big, long, and wide and often have impressions or scalloping along the outside from a molding of the teeth. The patient is shown a Mallampati diagram and given a Mallampati score.
Creating a Sense of Mission
The sleep physician assistant (PA)at the Detroit VAMC is a retired U.S. Army colonel who ensures that the language the physician uses aligns with the language veterans use. Behavioral techniques are used to create a common culture that helps overcome obstacles—allowing patients to understand the benefits of and need for full CPAP/BPAP therapy adherence. One technique reinforces their sense of mission accomplishment, their military pride, and their interservice rivalry to increase adherence. The mission with each patient is to “work until success is achieved...but the patient can’t quit.” The mantra given to a patient with a difficult case is, “We will not let you fail with CPAP/BPAP therapy,” which echoes a familiar military motto, “We will not leave you behind.” Also, the goal of the physician is: Never give up on the patient.
Behavioral and Psychological Principles
The behavioral and psychological principles for success with PAP super users should be studied to validate better outcomes with longer duration PAP machine use. Patients who are motivated to succeed and to participate in their care can make great strides in changing their behavior to get more and better sleep. Obese patients can get referrals to the MOVE! weight loss program. Some veterans simply follow instructions, pay attention to detail, and do what they are told regarding sleep, PAP education, and good sleep hygiene. Many veterans have poor sleep hygiene and insomnia because they watch television or play games on electronic devices right before bedtime. Many patients develop behaviorally insufficient sleep syndrome. Their behavior prevents them from going to bed at a time that will allow sufficient sleep. Some veterans smoke or drink caffeinated beverages or al cohol immediately before sleep time and then wonder why they have insomnia.
Veterans with insomnia may be referred to the insomnia clinic psychologist for cognitive behavioral therapy for insomnia.40 Referral to this psychologist can be very helpful in the treatment of insomnia after the patient’s OSA has been treated. Veterans are encouraged to follow good sleep hygiene principles and permanently discontinue detrimental sleep behaviors.
For veterans with PTSD, imagery rehearsal before sleep has been effective in resolving disturbing nightmares and excluding their violent details.41 Clinicians recommend that these veterans rehearse a pleasant dream before sleep time. Cartwright and Lamberg performed extensive research on dreams and nightmares, and their book may provide insight into reducing nightmares for veterans with severe PTSD.42 Persistent nightmares associated with PTSD also can be reduced with use of prazosin. 43
Sleep Clinic Economics
The economic impact of OSA is substantial because of increased risk of cardiovascular disease and risk of motor vehicle accidents and decreased quality of life and productivity. Results of cost-effectiveness analyses support the value of diagnosing and treating OSA. Studies have provided estimates from a payer perspective, ranging from $2,000 to $11,000 per quality-adjusted life year over 5 years for treating moderate-to-severe OSA. The Sleep Heart Health Study showed that OSA was associated with an 18% increase in predicted health care utilization based on medication use.44,45 Moreover, CPAP therapy was found to be clinically more effective than no treatment: Therapy increased life expectancy in males and females, and effective treatment of OSA was associated with lower health care and disability costs and fewer missed workdays.
The authors’ initiatives to improve PAP therapy adherence required adding a PA and a registered respiratory therapist (RT) to the staff of 2 full-time equivalent (FTE) board-certified sleep physicians. The sleep physicians trained the PA to initiate and complete all the recommendations described, and the PA attended an AASM-sponsored review course for additional training. The PA is responsible for performing comprehensive face-to-face clinical evaluations in 4 half-day clinic sessions each week, as well as providing follow-up care in 4 additional half-day clinic sessions each week.
During these sessions, the PA provides education about sleep apnea and treatment. Thirty-minute follow-up clinic appointments are reserved for downloading CPAP data, providing interpretation, and educating patients to maximize PAP therapy and become super users. The remaining clinic sessions are run by 3 sleep fellows under the supervision of the sleep physicians. During all visits, providers encourage patients to maintain good sleep hygiene. Nonadherent patients are scheduled to be seen in a separate clinic session during which the RT troubleshoots and corrects PAP machine and mask-related problems.
Setting up the CPAP group classes and follow-up clinics required adding an FTE RT at a cost of $44,000 to $48,000 per year. By recruiting an FTE PA starting at GS-12 and $75,542 instead of another board-certified sleep physician, VAMC Detroit was able to provide increased access to patient care (8 clinics) at sizable financial savings (estimate, $75,000/y). A 0.5 FTE clinical psychologist provided cognitive behavioral therapy for insomnia and PAP therapy nonadherence and helped achieve the initiative’s goals.
The sleep center projects that the overall cost-effectiveness of these initiatives in terms of admission rates, life expectancy, and productivity would not be dissimilar to that reported in the peer-reviewed literature, as noted earlier. The center’s upcoming research projects will provide more data specific to its population. Educating patients requires that only motivated providers give patients instructions during a 30-minute follow-up clinic visit—there is no additional expense. This model of intensive care can be adopted at other VAMCs.
Conclusion
Maximizing PAP machine use is a unique approach that stimulates veterans to attain the highest level of adherence. This approach is based on clinical observation and patient encounters, and treatment recommendations over 8 years.
Showing enthusiasm with patients is crucial. Enthusiasm is contagious. Clinicians who are also PAP machine users should let patients know of their PAP super-user status and add that many others have attained this status, too. The benefits of optimal treatment are reviewed with patients: increased energy, lower risk of cardiovascular disease, lower blood pressure, better insulin sensitivity, and overall reduced mortality. Some patients have difficulty using the nasal mask and chin strap and understanding and adhering to PAP therapy. These impediments can be overcome with further education and follow-up. Sleep clinic clinicians take the time to show patients how to use the machine’s self-adherence check and leak functions. Patients can then monitor their progress daily.
To motivate patients, clinicians should set expectations early, invest time in providing education at follow-up; be diligent with respect to mask fitting and download evaluation. Sleep clinic providers should also speak the veterans’ language, create a self-fulfilling prophesy for success, and schedule a follow-up sleep clinic appointment if a patient is not fulfilling the Medicare adherence criterion of 4 hours’ nightly use for 70% of nights over 30 days.
PAP therapy coaching and persistent education with provider contact and enthusiasm can improve adherence. Encouragement and praise can help patients exceed Medicare’s minimum PAP therapy criterion and improve their overall PAP experience. The sleep team should tell patients they are proud of their accomplishments with such a difficult treatment. Being genuine and caring and showing concern about their evaluation, treatment, and follow-up is important. This helps reduce their OSA-related morbidity, lessen their depression, and improves their daily well-being and quality of life.
“The variation in responses to CPAP and acceptance of CPAP suggest that focused interventions, rather than one-size-fits-all interventions, may have a greater effect on the overall outcome of CPAP adherence,” wrote Weaver and Sawyer.46
Finally, one cannot equate spending on veteran care with spending in other areas of the national budget. The real cost of not giving veterans appropriate care will be a loss of trust, given that the overarching mission is “to care for him who shall have borne the battle and for his widow and his orphan.”
1. Boyaci H, Gacar K, Baris SA, Basyigit I, Yildiz F. Positive airway pressure device compliance of patients with obstructive sleep apnea syndrome. Adv Clin Exp Med. 2013;22(6):809-815.
2. Bachour A, Vitikainen P, Virkkula P, Maasilta P. CPAP interface: satisfaction and side effects. Sleep Breath. 2013;17(2):667-672.
3. Wimms AJ, Richards GN, Genjafield AV. Assessment of the impact on compliance of a new CPAP system in obstructive sleep apnea. Sleep Breath. 2013;17(1):69-76.
4. Smith I, Nadig V, Lasserson TJ. Educational, supportive and behavioral interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnea. Cochrane Database Syst Rev. 2009;(2):CD007736.
5. Beecroft J, Zanon S, Lukic D, Hanly P. Oral continuous positive airway pressure for sleep apnea: effectiveness, patient preference, and adherence. Chest. 2003;124(6):2200-2208.
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7. Nilius G, Happel A, Domanski U, Ruhle KH. Pressure-relief continuous positive airway pressure vs constant continuous positive airway pressure: a comparison of efficacy and compliance. Chest. 2006;130(4):1018-1024.
8. Ballard RD, Gay PC, Strollo PJ. Interventions to improve compliance in sleep apnea patients previously non-compliant with continuous positive airway pressure. J Clin Sleep Med. 2007;3(7):706-712.
9. Sin DD, Mayers I, Man GC, Pawluk L. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest. 2002;121(2):430-435.
10. Mortimore IL, Whittle AT, Douglas NJ. Comparison of nose and face mask CPAP therapy for sleep apnoea. Thorax. 1998;53(4):290-292.
11. Haniffa M, Lasserson TJ, Smith I. Interventions to improve compliance with continuous positive airway pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2004;(4):CD003531.
12. Kushida CA, Berry RB, Blau, A, et al. Positive airway pressure initiation: a randomized controlled trial to assess the impact of therapy mode and titration process on efficacy, adherence, and outcomes. Sleep. 2011;34(8):1083-1092.
13. Gentina T, Fortin F, Douay B, et al. Auto bi-level with pressure relief during exhalation as a rescue therapy for optimally treated obstructive sleep apnoea patients with poor compliance to continuous positive airways pressure therapy--a pilot study. Sleep Breath. 2011;15(1):21-27.
14. Billings, ME, Auckley D, Benca R, et al. Race and residential socioeconomics as predictors of CPAP adherence. Sleep. 2011;34(12):1653-1658.
15. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin Sleep Cohort. Sleep. 2008;31(8):1071-1078.
16. Centers for Disease Control and Prevention. Effect of short sleep duration on daily activities--United States, 2005-2008. MMWR Morb Mortal Wkly Rep. 2011;60(8):239-242.
17. Antic NA, Catcheside P, Buchan C, et al. The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA. Sleep. 2011;34(1):111-119.
18. Phurrough S, Jacques L, Spencer F, Stiller J, Brechner R. Coverage decision memorandum for continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) (CAG-00093R2). Centers for Medicare & Medicaid Services Website. https://www.cms.gov/medicare-coverage-database/details/nca-decision-memo.aspx?NCAId=204&fromdb=true. Accessed February 5, 2016.
19. Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2009;5(3):263-276.
20. Berry RB, Chediak A, Brown LK, et al; NPPV Titration Task Force of the American Academy of Sleep Medicine. Best clinical practices for the sleep center adjustment of noninvasive positive pressure ventilation (NPPV) in stable chronic alveolar hypoventilation syndromes. J Clin Sleep Med. 2010;6(5):491-509.
21. Merton RK. Social Theory and Social Structure. New York, NY: Free Press; 1968.
22. Chaput JP, McNeil J, Després JP, Bouchard C, Tremblay A. Seven to eight hours of sleep a night is associated with a lower prevalence of the metabolic syndrome and reduced overall cardiometabolic risk in adults. PLoS One. 2013;8(9):e72832.
23. Born J, Wagner U. Sleep, hormones, and memory. Obstet Gynecol Clin North Am. 2009;36(4):809-829, x.
24. Silva GE, Vana KD, Goodwin JL, Sherrill DL, Quan SF. Identification of patients with sleep disordered breathing: comparing the four-variable screening tool, STOP, STOP-Bang, and Epworth Sleepiness Scales. J Clin Sleep Med. 2011;7(5):467-472.
25. Soares Pires F, Drummond M, Marinho A, et al. Effectiveness of a group education session on adherence with APAP in obstructive sleep apnea--a randomized controlled study. Sleep Breath. 2013;17(3):993-1001.
26. Berry RB, Budhiraja R, Gottlieb DJ, et al; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
27. Schwab RJ, Badr SM, Epstein LJ, et al; ATS Subcommittee on CPAP Adherence Tracking Systems. An official American Thoracic Society statement: continuous positive airway pressure adherence tracking systems. The optimal monitoring strategies and outcome measures in adults. Am J Respir Crit Care Med. 2013;188(5):613-620.
28. Respironics Encore Pro and Encore Pro 2 [computer program]. Philips, Inc; May 12, 2013.
29. ResMed. Version 04.01.013. San Diego, CA.
30. Knowles SR, O'Brien DT, Zhang S, Devara A, Rowley JA. Effect of addition of chin strap on PAP compliance, nightly duration of use, and other factors. J Clin Sleep Med. 2014;10(4):377-383.
31. Vorona RD, Ware JC, Sinacori JT, Ford ML 3rd, Cross JP. Treatment of severe obstructive sleep apnea syndrome with a chinstrap. J Clin Sleep Med. 2007;3(7):729-730.
32. Ruhle KH, Franke KJ, Domanski U, Nilius G. Quality of life, compliance, sleep and nasopharyngeal side effects during CPAP therapy with and without controlled heated humidification. Sleep Breath. 2011;15(3):479-485.
33. Hamilos DL. Chronic rhinosinusitis: epidemiology and medical management. J Allergy Clin Immunol. 2011;128(4):693-707.
34. Gooley JJ, Chamberlain K, Smith KA, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. J Clin Endocrinol Metab. 2011;96(3):E463-E472.
35. Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545.
36. Bednarek M, Zgierska A, Pływaczewski R, Zielinski J. The effect of CPAP treatment on excessive daytime somnolence in patients with obstructive sleep apnea [in Polish]. Pneumonol Alergol Pol. 1999;67(5-6):237-244.
37. Harvey R, Hannan SA, Badia L, Scadding G. Nasal saline irrigations for the symptoms of chronic rhinosinusitis. Cochrane Database Syst Rev. 2007;(3):CD006394.
38. Poirier J, George C, Rotenberg B. The effect of nasal surgery on nasal continuous positive airway pressure compliance. Laryngoscope. 2014;124(1):317-319.
39. Law JA. From the journal archives: Mallampati in two millennia: its impact then and implications now. Can J Anaesth. 2014;61(5):480-484.
40. Hood HK, Rogojanski J, Moss TG. Cognitive-behavioral therapy for chronic insomnia. Curr Treat Options Neurol. 2014;16(12):321.
41. Harb GC, Thompson R, Ross RJ, Cook JM. Combat-related PTSD nightmares and imagery rehearsal: nightmare characteristics and relation to treatment outcome. J Trauma Stress. 2012;25(5):511-518.
42. Cartwright R, Lamberg L. Crisis Dreaming: Using Your Dreams to Solve Your Problems.. New York, NY: HarperCollins;1992.
43.Writer BW, Meyer EG, Schillerstrom JE. Prazosin for military combat-related PTSD nightmares: a critical review. J Neuropsychiatry Clin Neurosci. 2014;26(1):24-33.
44. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-554.
45. Kapur V, Blough DK, Sandblom RE, et al. The medical cost of undiagnosed sleep apnea. Sleep. 1999;22(6):749-755.
46. Weaver TE, Sawyer AM. Adherence to continuous positive airway pressure treatment for obstructive sleep apnoea: implications for future interventions. Indian J Med Res. 2010;131:245-258.
Adherence to positive airway pressure (PAP) therapy is a difficult patient management issue. Clinicians at the John D. Dingell VA Medical Center in Detroit (VAMC Detroit) developed the O’Brien criteria and extensive patient education materials to increase patient adherence. The importance of PAP therapy and the reasons veterans should sleep with a PAP machine for 7 to 9 hours each night are stressed (many sleep only 4 to 5 hours). Several recent studies have confirmed widely varying PAP therapy adherence rates (30%-84%).1-13 A majority of patients indicated that mask discomfort is the primary reason for nonadherence.1
Adherence is affected by many factors, including heated humidity, patient education, mask type, and type of PAP machine (eg, continuous PAP [CPAP] vs bilevel PAP [BPAP]; auto-PAP vs CPAP). Other factors, such as race and economic status, also affect adherence.14 The Wisconsin Sleep Cohort Study found that patients with moderate-to-severe untreated obstructive sleep apnea (OSA) were 4 to 5 times more likely to die of a cardiovascular event and 3 times more likely to die of any cause.15 The morbidity and mortality associated with severe untreated OSA led the clinicians to intensify treatment efforts.16In this article, the authors summarize the initiative at the VAMC Detroit to enhance PAP therapy adherence in patients with sleep apnea. The goal was to motivate patients to maximize PAP machine use. This article is a guide that federal health care providers and their civilian counterparts in the private sector can use to maximize PAP machine use. Working toward that goal, a set of PAP “super user” criteria was developed and used to create a 5-point method for encouraging patients to maximize adherence to PAP therapy.
Background
Positive airway pressure is the room air pressure, measured in centimeters of H2O, which splints open the airway to prevent snoring, apneas, and hypopneas. An apnea is a 90%-plus airway obstruction that lasts longer than 10 seconds and is seen with sleep study polysomnography. A hypopnea is a 30%-plus airway obstruction that lasts longer than 10 seconds and is accompanied by a 3% drop in pulse oximetry (SpO2).
A CPAP device delivers pressure continuously through a medical air compressor or flow generator called a PAP machine. The BPAP machine has separate inspiratory pressure and expiratory pressure. Auto-PAP machines give minimum pressure and maximum pressure usually between the range of 4 cm H2O to 20 cm H2O. This machine finds the user’s median pressure (90th percentile) and maximum pressure and averages pressure over a specified period of use. The auto-PAP can then be set to CPAP mode and the pressure fixed or set to the 90th percentile.
O’Brien Criteria
The O’Brien criteria for PAP super-user status (Table 1) were developed for maximizing PAP machine use and presented at the 2013 John D. Dingell Sleep and Wake Disorders Center Symposium. There is no other published reference or criteria proposed for maximizing PAP machine adherence. A recent study on sleep time criteria suggested that a higher percentage of patients achieved normal functioning with longer duration nightly CPAP therapy, which is in line with the authors’ recommended PAP machine use duration.17
Positive airway pressure therapy is eligible for insurance reimbursement by Medicare and third-party payers for adult patients who have OSA and achieve 4 hours of nightly use for 70% of nights over 30 days. Coverage for CPAP therapy is initially limited to 12 weeks during which beneficiaries with an OSA diagnosis can be identified and any therapy benefits documented. Subsequent CPAP therapy is covered only for those OSA patients who benefit during the 12-week period.18At VAMC Detroit, the data covering the previous 30 days of use is downloaded. Medicare allows for the best 30-day period out of the 12-week window. The hospital, along with Harper Hospital and the Detroit Medical Centers in conjunction with the Wayne State University sleep program, is an Academic Center of Distinction, which follows the sleep guidelines and practice parameters for Medicare, third-party insurance companies, and the American Academy of Sleep Medicine.
The sleep clinic clinicians follow the clinical guidelines for evaluation, management, and long-term care of adults with OSA.19,20 Follow-up visits are scheduled and made on a consultation basis up to 90 days for the required download or as necessary for PAP therapy. In this initiative, practitioners offer veteran-specific patient care with PAP therapy that exceeds Medicare guidelines. The success of this process yielded a growing cohort of PAP super users at VAMC Detroit. These patients exceed the Medicare criterion of 4 hours of nightly use for 70% of nights over 30 days. Thus, 4 hours of nightly use for 100% of nights over the same period was proposed as another criterion.
The super-user criteria, which provide motivation to reach the top, stimulate many patients to achieve the Medicare criteria. All 5 criteria must be satisfied to attain super-user status, and becoming a super user is not easy. In fact, the expectation is that, if an adherence data study is conducted, it will show that only a small percentage of all users meet the criteria. Maximum adherence is expected to be the tail (3%-4%) of a bell-shaped curve.
PAP Super-User Status
At the initial evaluation, practitioners create a self-fulfilling prophecy that, as first described by Merton, sets expectations.21 A self-fulfilling prophecy is a prediction that directly or indirectly causes the prediction to become true as a result of the positive feedback between belief and behavior.21 The personnel at VAMC Detroit sleep clinic set a tone that enables patients to meet and exceed the Medicare sleep guidelines and their expectations. Patients are encouraged to make it their personal mission to achieve the goal of becoming a PAP super user. The patients receive the O’Brien criteria for PAP super-user status—guidelines thought to contribute to higher quality of life.
The Medicare criterion emphasized is the minimum required for full adherence. The goal is to reduce sleepiness and increase well-being. The literature shows that increasing duration of sleep results in lower daytime sleepiness.22 Inadequate sleep has many detrimental effects. According to a recent study, insufficient sleep contributes to weight gain.22 Desired patient outcomes are increased sleep time without arousals, increased slow-wave sleep (SWS), consolidation of memories and rapid eye movement (REM), and improvement in emotional and procedural skill memories.23 Patients are informed that using a PAP machine for 7 to 9 hours can reduce excessive daytime sleepiness and allow for more SWS and REM sleep, which help improve memory, judgment, and concentration. Many other studies have shown how 7 to 9 hours of sleep benefit adults. Thus, 7 to 9 hours became the criterion for maximizing PAP sleep time.
Initial Evaluation and Sleep Study
A primary care provider can enroll a patient into the clinic for a sleep study by requesting an evaluation. The consultation is then triaged using the STOP-BANG (Snoring, Tiredness, Observed apnea, high blood Pressure–Body mass index > 35, Age > 50, Neck circumference > 40 cm, Gender male) questionnaire. The STOP-BANG has a high sensitivity for predicting moderate-to-severe (87.0%) and severe (70.4%) sleep-disordered breathing.24 More than 3 affirmative answers indicate a high risk for sleep-disordered breathing and is cause for ordering a sleep study.
CPAP Group Class
Patients with a diagnosis of sleep apnea subsequently receive their CPAP machines when they attend a 2-hour group class taught by a respiratory therapist. Group education sessions increase the chance of issuing more machines and providing better education.25 One study found that “attendance in a group clinic designed to encourage compliance with CPAP therapy provided a simple and effective means of improving treatment of OSA.”25
In class, the respiratory therapist briefly assesses each patient’s CPAP prescription, describes the patient’s type of sleep apnea and final diagnosis, and reviews the CPAP machine’s features. Veterans are then instructed to take their CPAP machines home to use all night, every night for 4 weeks. All night is defined as a period of 7.5 to 8 hours, as population-based study results have shown that sleep of this duration is associated with lowest cardiovascular morbidity and mortality. After the initial 4-plus weeks of machine use, patients with all their CPAP equipment are seen in the sleep clinic.
First Sleep Clinic Follow-Up Visit
At first follow-up, patients are asked for a subjective evaluation of their sleep. Most state they are “better” with PAP therapy. Each patient’s mask is checked and refitted with the patient’s prescribed pressure.
Patients are informed of their PAP settings and requirements from the sleep study and told their particular “magic pressure.” Patients understand that a person’s magic pressure, determined in the laboratory, is the pressure of room air blown into the nose, mouth, or both that eliminates not only snoring, but also partial and complete airway obstructions (hypopneas, apneas). Patients are asked to remember their particular magic pressure and their AHI and told their OSA status (mild, moderate, or severe) as assessed by the laboratory study.26 Extensive education on sleep apnea and treatment are also addressed. Education and training are among the most important tenets of PAP therapy, and these are incorporated into all encounters.25,26
PAP Data Report and Leak
The CPAP data are downloaded and printed. If adherence is suboptimal, clinician and patient discuss increasing adherence and possibly becoming a super user. The patient receives a copy of the report, which can be compared with the patient’s adherence statistics and with the adherence statistics of similar patients who are super users. A few blacked-out names are posted on the board in front of the provider’s computer station. Patients can thus easily see that attaining super-user status is very difficult but possible. Some patients maximize their therapy and are designated PAP super users. These patients are proud to receive this designation, and they strive to keep it.
Data downloads are crucial for adherence. In a recent study, the American Thoracic Society stated, “Providers need to be able to interpret adherence systems.”27
The clinic provides a summary report on each patient’s adherence. A provider interpretation is added, and the report is copied into the Computer Patient Record System.
After the report is downloaded, the provider checks for correct pressure and then for a large leak. A large leak is an unintentional leak (the total amount that leaks but not including leak from the mask) > 5% of the night. A leak of > 15 minutes was added to the super-user criteria, because some software provides the average time of a large leak per day in minutes.28 Many veterans sleep only 4 to 5 hours nightly (300 minutes × 5% = 15 minutes). Therefore, the leak should not be more than 5% or 15 minutes for a veteran sleeping 5 hours.
The machine indicates a percentage of leak on the patient self-check LED screen for adherence. There is no standardized leak criterion used by all flow-generator manufacturers. Every mask has venting designed to leak intentionally so that the patient does not rebreathe air CO2. The main concern is unintentional leaks above the intentional leak or venting threshold.
The ResMed CPAP (ResMed Corp, San Diego, CA) maximum intentional leak is 24 L/min.29 Above that level is large leak. The exact leak amount varies by interface (mask) based on pressure and mask type.2,12
The larger the interface surface area, the larger the leak. Unintentional leak is higher with the full-face mask than with the nasal mask, most likely because there is more opportunity for leakage with the larger surface area of the full-face mask. Nasal pillows seem to leak less because of their smaller surface area, but more studies on mask interfaces are needed to validate this finding.
Chin Strap
Adding a chin strap improved patient adherence, nightly duration of use, residual AHI, and leak in patients with sleep apnea.30 Other investigators reported reduced OSA, confirmed by polysomnography and nasopharyngolaryngoscopy, with use of only a chin strap.31 When a nasal mask with chin strap is used, the strap should be made to fit properly over the chin, not on the throat. Properly used chin straps significantly reduce leakage and residual AHI.30
A chin strap most likely reduces large leak and dry mouth.30 Dry mouth can result from mouth leak, which is commonly caused by nasal congestion or high pressure and mouth breathing. The nasal turbinates help humidify, warm, and cool the air. Heated humidification of PAP can help prevent dry mouth.
Asking the Right Questions
The clinician should ask several key questions at the first follow-up: How is it going with your PAP machine? Do you feel PAP therapy is helping you sleep? Do you feel better with PAP therapy? To a patient who states he or she is not doing well with therapy, the clinician should ask, What type of problems are you having? In many cases, poor adherence is attributable to a large leak from a poorly fitting mask. A large leak can also increase residual AHI and cause frequent arousals.30
Some machines cannot maintain the pressure of a large leak and will shut off and trigger an alarm that wakes the patient to readjust the mask. This situation causes some patients to discontinue CPAP/BPAP use. The mask leak must be adjusted. Another common complaint is morning dry mouth. This extreme dryness—a significant clue pointing to mouth leak caused in part by the mouth dropping open during sleep with PAP—should be addressed by fitting the patient with a chin strap.30 Dry mouth also can be caused by low humidity; increasing the humidity setting usually resolves the problem. However, as one study found, use of controlled heated humidification did not improve adherence or quality of life.32 In the same study, the nasopharyngeal dryness that resulted from CPAP therapy without humidification was reduced immediately and during the first weeks of treatment.All current PAP machines feature heated humidification.
Mouth breathing can also result from nasal congestion, allergic or vasomotor rhinitis, nasal turbinate hypertrophy, obstruction from a deviated septum, polyps, or air hunger/insufficient PAP pressure. Chronic rhinosinusitis is a problem that affects up to 12.5% of the U.S. population.33
Adherence is also increased with the elimination of leak and associated arousals. Patients are shown how to use their PAP machine’s heated humidity settings to obtain desired comfort levels. The clinician explains that the nasal turbinates heat and cool the air and that they can become swollen and irritated with PAP therapy. A heated hose may be prescribed to provide optimal humidification without condensation or water dripping into the hose (rainout).
A full-face mask is used only when the patient cannot breathe out the nose adequately or when PAP becomes too high. A 2013 study found no significant differences among ResMed, Respironics, and Fisher & Paykel CPAP interfaces (Fisher & Paykel Healthcare, Irvine, CA).34 The clinician determines which mask is comfortable for a patient and tries to stay with that mask for that patient.
Adherence Report
A therapy data summary is downloaded and reviewed with the patient.28 A pattern of use report that shows daily use with times over the month is also reviewed.28 The software’s sleep therapy long-term trend report lists important statistics. The adherence data summary and the CPAP summary are also reviewed (Table 2).28 This page is printed and given to patients to reieiw their progress. For some it represents a reward for using the CPAP/BPAP machine as well as a congratulatory note.
In the Example 1 summary download (Table 2), a patient used a PAP machine 4 hours or more on 93.3% of the 30 days the machine was used.28 Residual AHI was low, 2.1, and there was no appreciable leak. The PAP of 11.2 cm H2O was in the 90th percentile. The patient was fixed to 12 cm H2O with expiratory pressure relief (EPR) of 1. The EPR is a comfort feature that reduces pressure from 1 cm H2O to 3 cm H2O to make it easier for the patient to exhale. (A flow generator that produces EPR of > 3 cm H2O is a BPAP machine.)
This patient was not a super user. Overall use was low—5 hours, 28 minutes—which could indicate behaviorally insufficient sleep syndrome. Sleep time is controversial, but the National Sleep Foundation recommends 7 to 9 hours of sleep per night.
A different patient used a PAP machine 4 hours or more on 100% (28/28) of the days when the machine was used (Table 3).29 Residual AHI was low (0.6), median use was 8 hours, 47 minutes, and there was no appreciable leak. The patient was using autoset mode with a minimum pressure of 13 cm H2O and maximum pressure of 18 cm H2O. The 95th percentile pressure was 13.6 cm H2O. The patient’s pressure was changed to 14 cm H2O with EPR of 3. This patient was a super user.
Sleep Hygiene Discussion
Providers must discuss sleep hygiene (good sleep habits) with veterans. If needed, AASM pamphlets on sleep hygiene and other educational materials can be provided. The bedroom should be cool, comfortable, quiet, and dark and should not include a television or computer. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration and tells the brain it is time to wake up.34
Patients are asked about the number of arousals they have per night. At first follow-up, providers must determine what is causing a patient to arouse while on CPAP/BPAP therapy. Some causes are air leak resulting in unresolved OSA, nocturia (may be triggered by unresolved OSA), dry mouth (indicating need for chin strap), nightmares (suggestive of unresolved OSA in REM sleep), posttraumatic stress disorder (PTSD), environmental noise, and claustrophobia. The provider should have thought-out answers to these problems in advance.
Epworth Sleepiness Scale
The Epworth Sleepiness Scale (ESS) is administered as part of the baseline comprehensive examination and at every sleep clinic follow-up after issuing a CPAP/BPAP machine.35 The first evaluation after the machine is issued should show a reduction in ESS. No reduction in ESS indicates that a problem needs to be addressed. The most common reason for insufficient reduction in ESS is suboptimal PAP therapy adherence, usually because of a large leak. Some cases of poor adherence may be attributable to restless legs syndrome, periodic limb movement disorder, chronic musculoskeletal pain, and sleep fragmentation caused by alcohol, smoking, caffeine, or cocaine. Excessive daytime sleepiness may persist from use of pain medications or other sedating medications. One study found a correlation between sleep duration with CPAP therapy and reduction in ESS.36 In addition to administering the ESS, patients are asked how they doing with PAP therapy, and the answer is documented. Treatment changes are made if needed to reduce excessive daytime sleepiness.
Ear-Nose-Throat Examination
A quick look into the nose with a nasal speculum is a crucial component of a thorough examination. The clinician looks for a deviated septum, swollen turbinates, obstruction, polyps, bleeding, infection, septal perforation, and discharge. In addition, the patient is checked for airflow amount, nasal congestion, and obstruction; if necessary a nasal steroid spray or a nasal saline spray is prescribed. In some cases, saline spray can be added to the steroid spray to help reduce or eliminate nasal congestion.37
Treatment of congestion requires education, as many patients improperly use these sprays. The steroid spray is not an instant vasoconstrictor; a week of regular use is needed to reduce inflammation and congestion. Saline spray and saline irrigation can be used as a treatment adjunct for symptoms of chronic rhinosinusitis.37If the steroid and saline sprays fail after a 2-month trial, consider an ear-nose-throat (ENT) consultation. A recent study found that adherence rates increased after septoplasty in patients with nasal obstruction.38 The throat is examined for macroglossia or scalloping of the tongue.39 Macroglossic Mallampati IV tongues are platterlike. They are big, long, and wide and often have impressions or scalloping along the outside from a molding of the teeth. The patient is shown a Mallampati diagram and given a Mallampati score.
Creating a Sense of Mission
The sleep physician assistant (PA)at the Detroit VAMC is a retired U.S. Army colonel who ensures that the language the physician uses aligns with the language veterans use. Behavioral techniques are used to create a common culture that helps overcome obstacles—allowing patients to understand the benefits of and need for full CPAP/BPAP therapy adherence. One technique reinforces their sense of mission accomplishment, their military pride, and their interservice rivalry to increase adherence. The mission with each patient is to “work until success is achieved...but the patient can’t quit.” The mantra given to a patient with a difficult case is, “We will not let you fail with CPAP/BPAP therapy,” which echoes a familiar military motto, “We will not leave you behind.” Also, the goal of the physician is: Never give up on the patient.
Behavioral and Psychological Principles
The behavioral and psychological principles for success with PAP super users should be studied to validate better outcomes with longer duration PAP machine use. Patients who are motivated to succeed and to participate in their care can make great strides in changing their behavior to get more and better sleep. Obese patients can get referrals to the MOVE! weight loss program. Some veterans simply follow instructions, pay attention to detail, and do what they are told regarding sleep, PAP education, and good sleep hygiene. Many veterans have poor sleep hygiene and insomnia because they watch television or play games on electronic devices right before bedtime. Many patients develop behaviorally insufficient sleep syndrome. Their behavior prevents them from going to bed at a time that will allow sufficient sleep. Some veterans smoke or drink caffeinated beverages or al cohol immediately before sleep time and then wonder why they have insomnia.
Veterans with insomnia may be referred to the insomnia clinic psychologist for cognitive behavioral therapy for insomnia.40 Referral to this psychologist can be very helpful in the treatment of insomnia after the patient’s OSA has been treated. Veterans are encouraged to follow good sleep hygiene principles and permanently discontinue detrimental sleep behaviors.
For veterans with PTSD, imagery rehearsal before sleep has been effective in resolving disturbing nightmares and excluding their violent details.41 Clinicians recommend that these veterans rehearse a pleasant dream before sleep time. Cartwright and Lamberg performed extensive research on dreams and nightmares, and their book may provide insight into reducing nightmares for veterans with severe PTSD.42 Persistent nightmares associated with PTSD also can be reduced with use of prazosin. 43
Sleep Clinic Economics
The economic impact of OSA is substantial because of increased risk of cardiovascular disease and risk of motor vehicle accidents and decreased quality of life and productivity. Results of cost-effectiveness analyses support the value of diagnosing and treating OSA. Studies have provided estimates from a payer perspective, ranging from $2,000 to $11,000 per quality-adjusted life year over 5 years for treating moderate-to-severe OSA. The Sleep Heart Health Study showed that OSA was associated with an 18% increase in predicted health care utilization based on medication use.44,45 Moreover, CPAP therapy was found to be clinically more effective than no treatment: Therapy increased life expectancy in males and females, and effective treatment of OSA was associated with lower health care and disability costs and fewer missed workdays.
The authors’ initiatives to improve PAP therapy adherence required adding a PA and a registered respiratory therapist (RT) to the staff of 2 full-time equivalent (FTE) board-certified sleep physicians. The sleep physicians trained the PA to initiate and complete all the recommendations described, and the PA attended an AASM-sponsored review course for additional training. The PA is responsible for performing comprehensive face-to-face clinical evaluations in 4 half-day clinic sessions each week, as well as providing follow-up care in 4 additional half-day clinic sessions each week.
During these sessions, the PA provides education about sleep apnea and treatment. Thirty-minute follow-up clinic appointments are reserved for downloading CPAP data, providing interpretation, and educating patients to maximize PAP therapy and become super users. The remaining clinic sessions are run by 3 sleep fellows under the supervision of the sleep physicians. During all visits, providers encourage patients to maintain good sleep hygiene. Nonadherent patients are scheduled to be seen in a separate clinic session during which the RT troubleshoots and corrects PAP machine and mask-related problems.
Setting up the CPAP group classes and follow-up clinics required adding an FTE RT at a cost of $44,000 to $48,000 per year. By recruiting an FTE PA starting at GS-12 and $75,542 instead of another board-certified sleep physician, VAMC Detroit was able to provide increased access to patient care (8 clinics) at sizable financial savings (estimate, $75,000/y). A 0.5 FTE clinical psychologist provided cognitive behavioral therapy for insomnia and PAP therapy nonadherence and helped achieve the initiative’s goals.
The sleep center projects that the overall cost-effectiveness of these initiatives in terms of admission rates, life expectancy, and productivity would not be dissimilar to that reported in the peer-reviewed literature, as noted earlier. The center’s upcoming research projects will provide more data specific to its population. Educating patients requires that only motivated providers give patients instructions during a 30-minute follow-up clinic visit—there is no additional expense. This model of intensive care can be adopted at other VAMCs.
Conclusion
Maximizing PAP machine use is a unique approach that stimulates veterans to attain the highest level of adherence. This approach is based on clinical observation and patient encounters, and treatment recommendations over 8 years.
Showing enthusiasm with patients is crucial. Enthusiasm is contagious. Clinicians who are also PAP machine users should let patients know of their PAP super-user status and add that many others have attained this status, too. The benefits of optimal treatment are reviewed with patients: increased energy, lower risk of cardiovascular disease, lower blood pressure, better insulin sensitivity, and overall reduced mortality. Some patients have difficulty using the nasal mask and chin strap and understanding and adhering to PAP therapy. These impediments can be overcome with further education and follow-up. Sleep clinic clinicians take the time to show patients how to use the machine’s self-adherence check and leak functions. Patients can then monitor their progress daily.
To motivate patients, clinicians should set expectations early, invest time in providing education at follow-up; be diligent with respect to mask fitting and download evaluation. Sleep clinic providers should also speak the veterans’ language, create a self-fulfilling prophesy for success, and schedule a follow-up sleep clinic appointment if a patient is not fulfilling the Medicare adherence criterion of 4 hours’ nightly use for 70% of nights over 30 days.
PAP therapy coaching and persistent education with provider contact and enthusiasm can improve adherence. Encouragement and praise can help patients exceed Medicare’s minimum PAP therapy criterion and improve their overall PAP experience. The sleep team should tell patients they are proud of their accomplishments with such a difficult treatment. Being genuine and caring and showing concern about their evaluation, treatment, and follow-up is important. This helps reduce their OSA-related morbidity, lessen their depression, and improves their daily well-being and quality of life.
“The variation in responses to CPAP and acceptance of CPAP suggest that focused interventions, rather than one-size-fits-all interventions, may have a greater effect on the overall outcome of CPAP adherence,” wrote Weaver and Sawyer.46
Finally, one cannot equate spending on veteran care with spending in other areas of the national budget. The real cost of not giving veterans appropriate care will be a loss of trust, given that the overarching mission is “to care for him who shall have borne the battle and for his widow and his orphan.”
Adherence to positive airway pressure (PAP) therapy is a difficult patient management issue. Clinicians at the John D. Dingell VA Medical Center in Detroit (VAMC Detroit) developed the O’Brien criteria and extensive patient education materials to increase patient adherence. The importance of PAP therapy and the reasons veterans should sleep with a PAP machine for 7 to 9 hours each night are stressed (many sleep only 4 to 5 hours). Several recent studies have confirmed widely varying PAP therapy adherence rates (30%-84%).1-13 A majority of patients indicated that mask discomfort is the primary reason for nonadherence.1
Adherence is affected by many factors, including heated humidity, patient education, mask type, and type of PAP machine (eg, continuous PAP [CPAP] vs bilevel PAP [BPAP]; auto-PAP vs CPAP). Other factors, such as race and economic status, also affect adherence.14 The Wisconsin Sleep Cohort Study found that patients with moderate-to-severe untreated obstructive sleep apnea (OSA) were 4 to 5 times more likely to die of a cardiovascular event and 3 times more likely to die of any cause.15 The morbidity and mortality associated with severe untreated OSA led the clinicians to intensify treatment efforts.16In this article, the authors summarize the initiative at the VAMC Detroit to enhance PAP therapy adherence in patients with sleep apnea. The goal was to motivate patients to maximize PAP machine use. This article is a guide that federal health care providers and their civilian counterparts in the private sector can use to maximize PAP machine use. Working toward that goal, a set of PAP “super user” criteria was developed and used to create a 5-point method for encouraging patients to maximize adherence to PAP therapy.
Background
Positive airway pressure is the room air pressure, measured in centimeters of H2O, which splints open the airway to prevent snoring, apneas, and hypopneas. An apnea is a 90%-plus airway obstruction that lasts longer than 10 seconds and is seen with sleep study polysomnography. A hypopnea is a 30%-plus airway obstruction that lasts longer than 10 seconds and is accompanied by a 3% drop in pulse oximetry (SpO2).
A CPAP device delivers pressure continuously through a medical air compressor or flow generator called a PAP machine. The BPAP machine has separate inspiratory pressure and expiratory pressure. Auto-PAP machines give minimum pressure and maximum pressure usually between the range of 4 cm H2O to 20 cm H2O. This machine finds the user’s median pressure (90th percentile) and maximum pressure and averages pressure over a specified period of use. The auto-PAP can then be set to CPAP mode and the pressure fixed or set to the 90th percentile.
O’Brien Criteria
The O’Brien criteria for PAP super-user status (Table 1) were developed for maximizing PAP machine use and presented at the 2013 John D. Dingell Sleep and Wake Disorders Center Symposium. There is no other published reference or criteria proposed for maximizing PAP machine adherence. A recent study on sleep time criteria suggested that a higher percentage of patients achieved normal functioning with longer duration nightly CPAP therapy, which is in line with the authors’ recommended PAP machine use duration.17
Positive airway pressure therapy is eligible for insurance reimbursement by Medicare and third-party payers for adult patients who have OSA and achieve 4 hours of nightly use for 70% of nights over 30 days. Coverage for CPAP therapy is initially limited to 12 weeks during which beneficiaries with an OSA diagnosis can be identified and any therapy benefits documented. Subsequent CPAP therapy is covered only for those OSA patients who benefit during the 12-week period.18At VAMC Detroit, the data covering the previous 30 days of use is downloaded. Medicare allows for the best 30-day period out of the 12-week window. The hospital, along with Harper Hospital and the Detroit Medical Centers in conjunction with the Wayne State University sleep program, is an Academic Center of Distinction, which follows the sleep guidelines and practice parameters for Medicare, third-party insurance companies, and the American Academy of Sleep Medicine.
The sleep clinic clinicians follow the clinical guidelines for evaluation, management, and long-term care of adults with OSA.19,20 Follow-up visits are scheduled and made on a consultation basis up to 90 days for the required download or as necessary for PAP therapy. In this initiative, practitioners offer veteran-specific patient care with PAP therapy that exceeds Medicare guidelines. The success of this process yielded a growing cohort of PAP super users at VAMC Detroit. These patients exceed the Medicare criterion of 4 hours of nightly use for 70% of nights over 30 days. Thus, 4 hours of nightly use for 100% of nights over the same period was proposed as another criterion.
The super-user criteria, which provide motivation to reach the top, stimulate many patients to achieve the Medicare criteria. All 5 criteria must be satisfied to attain super-user status, and becoming a super user is not easy. In fact, the expectation is that, if an adherence data study is conducted, it will show that only a small percentage of all users meet the criteria. Maximum adherence is expected to be the tail (3%-4%) of a bell-shaped curve.
PAP Super-User Status
At the initial evaluation, practitioners create a self-fulfilling prophecy that, as first described by Merton, sets expectations.21 A self-fulfilling prophecy is a prediction that directly or indirectly causes the prediction to become true as a result of the positive feedback between belief and behavior.21 The personnel at VAMC Detroit sleep clinic set a tone that enables patients to meet and exceed the Medicare sleep guidelines and their expectations. Patients are encouraged to make it their personal mission to achieve the goal of becoming a PAP super user. The patients receive the O’Brien criteria for PAP super-user status—guidelines thought to contribute to higher quality of life.
The Medicare criterion emphasized is the minimum required for full adherence. The goal is to reduce sleepiness and increase well-being. The literature shows that increasing duration of sleep results in lower daytime sleepiness.22 Inadequate sleep has many detrimental effects. According to a recent study, insufficient sleep contributes to weight gain.22 Desired patient outcomes are increased sleep time without arousals, increased slow-wave sleep (SWS), consolidation of memories and rapid eye movement (REM), and improvement in emotional and procedural skill memories.23 Patients are informed that using a PAP machine for 7 to 9 hours can reduce excessive daytime sleepiness and allow for more SWS and REM sleep, which help improve memory, judgment, and concentration. Many other studies have shown how 7 to 9 hours of sleep benefit adults. Thus, 7 to 9 hours became the criterion for maximizing PAP sleep time.
Initial Evaluation and Sleep Study
A primary care provider can enroll a patient into the clinic for a sleep study by requesting an evaluation. The consultation is then triaged using the STOP-BANG (Snoring, Tiredness, Observed apnea, high blood Pressure–Body mass index > 35, Age > 50, Neck circumference > 40 cm, Gender male) questionnaire. The STOP-BANG has a high sensitivity for predicting moderate-to-severe (87.0%) and severe (70.4%) sleep-disordered breathing.24 More than 3 affirmative answers indicate a high risk for sleep-disordered breathing and is cause for ordering a sleep study.
CPAP Group Class
Patients with a diagnosis of sleep apnea subsequently receive their CPAP machines when they attend a 2-hour group class taught by a respiratory therapist. Group education sessions increase the chance of issuing more machines and providing better education.25 One study found that “attendance in a group clinic designed to encourage compliance with CPAP therapy provided a simple and effective means of improving treatment of OSA.”25
In class, the respiratory therapist briefly assesses each patient’s CPAP prescription, describes the patient’s type of sleep apnea and final diagnosis, and reviews the CPAP machine’s features. Veterans are then instructed to take their CPAP machines home to use all night, every night for 4 weeks. All night is defined as a period of 7.5 to 8 hours, as population-based study results have shown that sleep of this duration is associated with lowest cardiovascular morbidity and mortality. After the initial 4-plus weeks of machine use, patients with all their CPAP equipment are seen in the sleep clinic.
First Sleep Clinic Follow-Up Visit
At first follow-up, patients are asked for a subjective evaluation of their sleep. Most state they are “better” with PAP therapy. Each patient’s mask is checked and refitted with the patient’s prescribed pressure.
Patients are informed of their PAP settings and requirements from the sleep study and told their particular “magic pressure.” Patients understand that a person’s magic pressure, determined in the laboratory, is the pressure of room air blown into the nose, mouth, or both that eliminates not only snoring, but also partial and complete airway obstructions (hypopneas, apneas). Patients are asked to remember their particular magic pressure and their AHI and told their OSA status (mild, moderate, or severe) as assessed by the laboratory study.26 Extensive education on sleep apnea and treatment are also addressed. Education and training are among the most important tenets of PAP therapy, and these are incorporated into all encounters.25,26
PAP Data Report and Leak
The CPAP data are downloaded and printed. If adherence is suboptimal, clinician and patient discuss increasing adherence and possibly becoming a super user. The patient receives a copy of the report, which can be compared with the patient’s adherence statistics and with the adherence statistics of similar patients who are super users. A few blacked-out names are posted on the board in front of the provider’s computer station. Patients can thus easily see that attaining super-user status is very difficult but possible. Some patients maximize their therapy and are designated PAP super users. These patients are proud to receive this designation, and they strive to keep it.
Data downloads are crucial for adherence. In a recent study, the American Thoracic Society stated, “Providers need to be able to interpret adherence systems.”27
The clinic provides a summary report on each patient’s adherence. A provider interpretation is added, and the report is copied into the Computer Patient Record System.
After the report is downloaded, the provider checks for correct pressure and then for a large leak. A large leak is an unintentional leak (the total amount that leaks but not including leak from the mask) > 5% of the night. A leak of > 15 minutes was added to the super-user criteria, because some software provides the average time of a large leak per day in minutes.28 Many veterans sleep only 4 to 5 hours nightly (300 minutes × 5% = 15 minutes). Therefore, the leak should not be more than 5% or 15 minutes for a veteran sleeping 5 hours.
The machine indicates a percentage of leak on the patient self-check LED screen for adherence. There is no standardized leak criterion used by all flow-generator manufacturers. Every mask has venting designed to leak intentionally so that the patient does not rebreathe air CO2. The main concern is unintentional leaks above the intentional leak or venting threshold.
The ResMed CPAP (ResMed Corp, San Diego, CA) maximum intentional leak is 24 L/min.29 Above that level is large leak. The exact leak amount varies by interface (mask) based on pressure and mask type.2,12
The larger the interface surface area, the larger the leak. Unintentional leak is higher with the full-face mask than with the nasal mask, most likely because there is more opportunity for leakage with the larger surface area of the full-face mask. Nasal pillows seem to leak less because of their smaller surface area, but more studies on mask interfaces are needed to validate this finding.
Chin Strap
Adding a chin strap improved patient adherence, nightly duration of use, residual AHI, and leak in patients with sleep apnea.30 Other investigators reported reduced OSA, confirmed by polysomnography and nasopharyngolaryngoscopy, with use of only a chin strap.31 When a nasal mask with chin strap is used, the strap should be made to fit properly over the chin, not on the throat. Properly used chin straps significantly reduce leakage and residual AHI.30
A chin strap most likely reduces large leak and dry mouth.30 Dry mouth can result from mouth leak, which is commonly caused by nasal congestion or high pressure and mouth breathing. The nasal turbinates help humidify, warm, and cool the air. Heated humidification of PAP can help prevent dry mouth.
Asking the Right Questions
The clinician should ask several key questions at the first follow-up: How is it going with your PAP machine? Do you feel PAP therapy is helping you sleep? Do you feel better with PAP therapy? To a patient who states he or she is not doing well with therapy, the clinician should ask, What type of problems are you having? In many cases, poor adherence is attributable to a large leak from a poorly fitting mask. A large leak can also increase residual AHI and cause frequent arousals.30
Some machines cannot maintain the pressure of a large leak and will shut off and trigger an alarm that wakes the patient to readjust the mask. This situation causes some patients to discontinue CPAP/BPAP use. The mask leak must be adjusted. Another common complaint is morning dry mouth. This extreme dryness—a significant clue pointing to mouth leak caused in part by the mouth dropping open during sleep with PAP—should be addressed by fitting the patient with a chin strap.30 Dry mouth also can be caused by low humidity; increasing the humidity setting usually resolves the problem. However, as one study found, use of controlled heated humidification did not improve adherence or quality of life.32 In the same study, the nasopharyngeal dryness that resulted from CPAP therapy without humidification was reduced immediately and during the first weeks of treatment.All current PAP machines feature heated humidification.
Mouth breathing can also result from nasal congestion, allergic or vasomotor rhinitis, nasal turbinate hypertrophy, obstruction from a deviated septum, polyps, or air hunger/insufficient PAP pressure. Chronic rhinosinusitis is a problem that affects up to 12.5% of the U.S. population.33
Adherence is also increased with the elimination of leak and associated arousals. Patients are shown how to use their PAP machine’s heated humidity settings to obtain desired comfort levels. The clinician explains that the nasal turbinates heat and cool the air and that they can become swollen and irritated with PAP therapy. A heated hose may be prescribed to provide optimal humidification without condensation or water dripping into the hose (rainout).
A full-face mask is used only when the patient cannot breathe out the nose adequately or when PAP becomes too high. A 2013 study found no significant differences among ResMed, Respironics, and Fisher & Paykel CPAP interfaces (Fisher & Paykel Healthcare, Irvine, CA).34 The clinician determines which mask is comfortable for a patient and tries to stay with that mask for that patient.
Adherence Report
A therapy data summary is downloaded and reviewed with the patient.28 A pattern of use report that shows daily use with times over the month is also reviewed.28 The software’s sleep therapy long-term trend report lists important statistics. The adherence data summary and the CPAP summary are also reviewed (Table 2).28 This page is printed and given to patients to reieiw their progress. For some it represents a reward for using the CPAP/BPAP machine as well as a congratulatory note.
In the Example 1 summary download (Table 2), a patient used a PAP machine 4 hours or more on 93.3% of the 30 days the machine was used.28 Residual AHI was low, 2.1, and there was no appreciable leak. The PAP of 11.2 cm H2O was in the 90th percentile. The patient was fixed to 12 cm H2O with expiratory pressure relief (EPR) of 1. The EPR is a comfort feature that reduces pressure from 1 cm H2O to 3 cm H2O to make it easier for the patient to exhale. (A flow generator that produces EPR of > 3 cm H2O is a BPAP machine.)
This patient was not a super user. Overall use was low—5 hours, 28 minutes—which could indicate behaviorally insufficient sleep syndrome. Sleep time is controversial, but the National Sleep Foundation recommends 7 to 9 hours of sleep per night.
A different patient used a PAP machine 4 hours or more on 100% (28/28) of the days when the machine was used (Table 3).29 Residual AHI was low (0.6), median use was 8 hours, 47 minutes, and there was no appreciable leak. The patient was using autoset mode with a minimum pressure of 13 cm H2O and maximum pressure of 18 cm H2O. The 95th percentile pressure was 13.6 cm H2O. The patient’s pressure was changed to 14 cm H2O with EPR of 3. This patient was a super user.
Sleep Hygiene Discussion
Providers must discuss sleep hygiene (good sleep habits) with veterans. If needed, AASM pamphlets on sleep hygiene and other educational materials can be provided. The bedroom should be cool, comfortable, quiet, and dark and should not include a television or computer. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration and tells the brain it is time to wake up.34
Patients are asked about the number of arousals they have per night. At first follow-up, providers must determine what is causing a patient to arouse while on CPAP/BPAP therapy. Some causes are air leak resulting in unresolved OSA, nocturia (may be triggered by unresolved OSA), dry mouth (indicating need for chin strap), nightmares (suggestive of unresolved OSA in REM sleep), posttraumatic stress disorder (PTSD), environmental noise, and claustrophobia. The provider should have thought-out answers to these problems in advance.
Epworth Sleepiness Scale
The Epworth Sleepiness Scale (ESS) is administered as part of the baseline comprehensive examination and at every sleep clinic follow-up after issuing a CPAP/BPAP machine.35 The first evaluation after the machine is issued should show a reduction in ESS. No reduction in ESS indicates that a problem needs to be addressed. The most common reason for insufficient reduction in ESS is suboptimal PAP therapy adherence, usually because of a large leak. Some cases of poor adherence may be attributable to restless legs syndrome, periodic limb movement disorder, chronic musculoskeletal pain, and sleep fragmentation caused by alcohol, smoking, caffeine, or cocaine. Excessive daytime sleepiness may persist from use of pain medications or other sedating medications. One study found a correlation between sleep duration with CPAP therapy and reduction in ESS.36 In addition to administering the ESS, patients are asked how they doing with PAP therapy, and the answer is documented. Treatment changes are made if needed to reduce excessive daytime sleepiness.
Ear-Nose-Throat Examination
A quick look into the nose with a nasal speculum is a crucial component of a thorough examination. The clinician looks for a deviated septum, swollen turbinates, obstruction, polyps, bleeding, infection, septal perforation, and discharge. In addition, the patient is checked for airflow amount, nasal congestion, and obstruction; if necessary a nasal steroid spray or a nasal saline spray is prescribed. In some cases, saline spray can be added to the steroid spray to help reduce or eliminate nasal congestion.37
Treatment of congestion requires education, as many patients improperly use these sprays. The steroid spray is not an instant vasoconstrictor; a week of regular use is needed to reduce inflammation and congestion. Saline spray and saline irrigation can be used as a treatment adjunct for symptoms of chronic rhinosinusitis.37If the steroid and saline sprays fail after a 2-month trial, consider an ear-nose-throat (ENT) consultation. A recent study found that adherence rates increased after septoplasty in patients with nasal obstruction.38 The throat is examined for macroglossia or scalloping of the tongue.39 Macroglossic Mallampati IV tongues are platterlike. They are big, long, and wide and often have impressions or scalloping along the outside from a molding of the teeth. The patient is shown a Mallampati diagram and given a Mallampati score.
Creating a Sense of Mission
The sleep physician assistant (PA)at the Detroit VAMC is a retired U.S. Army colonel who ensures that the language the physician uses aligns with the language veterans use. Behavioral techniques are used to create a common culture that helps overcome obstacles—allowing patients to understand the benefits of and need for full CPAP/BPAP therapy adherence. One technique reinforces their sense of mission accomplishment, their military pride, and their interservice rivalry to increase adherence. The mission with each patient is to “work until success is achieved...but the patient can’t quit.” The mantra given to a patient with a difficult case is, “We will not let you fail with CPAP/BPAP therapy,” which echoes a familiar military motto, “We will not leave you behind.” Also, the goal of the physician is: Never give up on the patient.
Behavioral and Psychological Principles
The behavioral and psychological principles for success with PAP super users should be studied to validate better outcomes with longer duration PAP machine use. Patients who are motivated to succeed and to participate in their care can make great strides in changing their behavior to get more and better sleep. Obese patients can get referrals to the MOVE! weight loss program. Some veterans simply follow instructions, pay attention to detail, and do what they are told regarding sleep, PAP education, and good sleep hygiene. Many veterans have poor sleep hygiene and insomnia because they watch television or play games on electronic devices right before bedtime. Many patients develop behaviorally insufficient sleep syndrome. Their behavior prevents them from going to bed at a time that will allow sufficient sleep. Some veterans smoke or drink caffeinated beverages or al cohol immediately before sleep time and then wonder why they have insomnia.
Veterans with insomnia may be referred to the insomnia clinic psychologist for cognitive behavioral therapy for insomnia.40 Referral to this psychologist can be very helpful in the treatment of insomnia after the patient’s OSA has been treated. Veterans are encouraged to follow good sleep hygiene principles and permanently discontinue detrimental sleep behaviors.
For veterans with PTSD, imagery rehearsal before sleep has been effective in resolving disturbing nightmares and excluding their violent details.41 Clinicians recommend that these veterans rehearse a pleasant dream before sleep time. Cartwright and Lamberg performed extensive research on dreams and nightmares, and their book may provide insight into reducing nightmares for veterans with severe PTSD.42 Persistent nightmares associated with PTSD also can be reduced with use of prazosin. 43
Sleep Clinic Economics
The economic impact of OSA is substantial because of increased risk of cardiovascular disease and risk of motor vehicle accidents and decreased quality of life and productivity. Results of cost-effectiveness analyses support the value of diagnosing and treating OSA. Studies have provided estimates from a payer perspective, ranging from $2,000 to $11,000 per quality-adjusted life year over 5 years for treating moderate-to-severe OSA. The Sleep Heart Health Study showed that OSA was associated with an 18% increase in predicted health care utilization based on medication use.44,45 Moreover, CPAP therapy was found to be clinically more effective than no treatment: Therapy increased life expectancy in males and females, and effective treatment of OSA was associated with lower health care and disability costs and fewer missed workdays.
The authors’ initiatives to improve PAP therapy adherence required adding a PA and a registered respiratory therapist (RT) to the staff of 2 full-time equivalent (FTE) board-certified sleep physicians. The sleep physicians trained the PA to initiate and complete all the recommendations described, and the PA attended an AASM-sponsored review course for additional training. The PA is responsible for performing comprehensive face-to-face clinical evaluations in 4 half-day clinic sessions each week, as well as providing follow-up care in 4 additional half-day clinic sessions each week.
During these sessions, the PA provides education about sleep apnea and treatment. Thirty-minute follow-up clinic appointments are reserved for downloading CPAP data, providing interpretation, and educating patients to maximize PAP therapy and become super users. The remaining clinic sessions are run by 3 sleep fellows under the supervision of the sleep physicians. During all visits, providers encourage patients to maintain good sleep hygiene. Nonadherent patients are scheduled to be seen in a separate clinic session during which the RT troubleshoots and corrects PAP machine and mask-related problems.
Setting up the CPAP group classes and follow-up clinics required adding an FTE RT at a cost of $44,000 to $48,000 per year. By recruiting an FTE PA starting at GS-12 and $75,542 instead of another board-certified sleep physician, VAMC Detroit was able to provide increased access to patient care (8 clinics) at sizable financial savings (estimate, $75,000/y). A 0.5 FTE clinical psychologist provided cognitive behavioral therapy for insomnia and PAP therapy nonadherence and helped achieve the initiative’s goals.
The sleep center projects that the overall cost-effectiveness of these initiatives in terms of admission rates, life expectancy, and productivity would not be dissimilar to that reported in the peer-reviewed literature, as noted earlier. The center’s upcoming research projects will provide more data specific to its population. Educating patients requires that only motivated providers give patients instructions during a 30-minute follow-up clinic visit—there is no additional expense. This model of intensive care can be adopted at other VAMCs.
Conclusion
Maximizing PAP machine use is a unique approach that stimulates veterans to attain the highest level of adherence. This approach is based on clinical observation and patient encounters, and treatment recommendations over 8 years.
Showing enthusiasm with patients is crucial. Enthusiasm is contagious. Clinicians who are also PAP machine users should let patients know of their PAP super-user status and add that many others have attained this status, too. The benefits of optimal treatment are reviewed with patients: increased energy, lower risk of cardiovascular disease, lower blood pressure, better insulin sensitivity, and overall reduced mortality. Some patients have difficulty using the nasal mask and chin strap and understanding and adhering to PAP therapy. These impediments can be overcome with further education and follow-up. Sleep clinic clinicians take the time to show patients how to use the machine’s self-adherence check and leak functions. Patients can then monitor their progress daily.
To motivate patients, clinicians should set expectations early, invest time in providing education at follow-up; be diligent with respect to mask fitting and download evaluation. Sleep clinic providers should also speak the veterans’ language, create a self-fulfilling prophesy for success, and schedule a follow-up sleep clinic appointment if a patient is not fulfilling the Medicare adherence criterion of 4 hours’ nightly use for 70% of nights over 30 days.
PAP therapy coaching and persistent education with provider contact and enthusiasm can improve adherence. Encouragement and praise can help patients exceed Medicare’s minimum PAP therapy criterion and improve their overall PAP experience. The sleep team should tell patients they are proud of their accomplishments with such a difficult treatment. Being genuine and caring and showing concern about their evaluation, treatment, and follow-up is important. This helps reduce their OSA-related morbidity, lessen their depression, and improves their daily well-being and quality of life.
“The variation in responses to CPAP and acceptance of CPAP suggest that focused interventions, rather than one-size-fits-all interventions, may have a greater effect on the overall outcome of CPAP adherence,” wrote Weaver and Sawyer.46
Finally, one cannot equate spending on veteran care with spending in other areas of the national budget. The real cost of not giving veterans appropriate care will be a loss of trust, given that the overarching mission is “to care for him who shall have borne the battle and for his widow and his orphan.”
1. Boyaci H, Gacar K, Baris SA, Basyigit I, Yildiz F. Positive airway pressure device compliance of patients with obstructive sleep apnea syndrome. Adv Clin Exp Med. 2013;22(6):809-815.
2. Bachour A, Vitikainen P, Virkkula P, Maasilta P. CPAP interface: satisfaction and side effects. Sleep Breath. 2013;17(2):667-672.
3. Wimms AJ, Richards GN, Genjafield AV. Assessment of the impact on compliance of a new CPAP system in obstructive sleep apnea. Sleep Breath. 2013;17(1):69-76.
4. Smith I, Nadig V, Lasserson TJ. Educational, supportive and behavioral interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnea. Cochrane Database Syst Rev. 2009;(2):CD007736.
5. Beecroft J, Zanon S, Lukic D, Hanly P. Oral continuous positive airway pressure for sleep apnea: effectiveness, patient preference, and adherence. Chest. 2003;124(6):2200-2208.
6. Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(4):CD005308.
7. Nilius G, Happel A, Domanski U, Ruhle KH. Pressure-relief continuous positive airway pressure vs constant continuous positive airway pressure: a comparison of efficacy and compliance. Chest. 2006;130(4):1018-1024.
8. Ballard RD, Gay PC, Strollo PJ. Interventions to improve compliance in sleep apnea patients previously non-compliant with continuous positive airway pressure. J Clin Sleep Med. 2007;3(7):706-712.
9. Sin DD, Mayers I, Man GC, Pawluk L. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest. 2002;121(2):430-435.
10. Mortimore IL, Whittle AT, Douglas NJ. Comparison of nose and face mask CPAP therapy for sleep apnoea. Thorax. 1998;53(4):290-292.
11. Haniffa M, Lasserson TJ, Smith I. Interventions to improve compliance with continuous positive airway pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2004;(4):CD003531.
12. Kushida CA, Berry RB, Blau, A, et al. Positive airway pressure initiation: a randomized controlled trial to assess the impact of therapy mode and titration process on efficacy, adherence, and outcomes. Sleep. 2011;34(8):1083-1092.
13. Gentina T, Fortin F, Douay B, et al. Auto bi-level with pressure relief during exhalation as a rescue therapy for optimally treated obstructive sleep apnoea patients with poor compliance to continuous positive airways pressure therapy--a pilot study. Sleep Breath. 2011;15(1):21-27.
14. Billings, ME, Auckley D, Benca R, et al. Race and residential socioeconomics as predictors of CPAP adherence. Sleep. 2011;34(12):1653-1658.
15. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin Sleep Cohort. Sleep. 2008;31(8):1071-1078.
16. Centers for Disease Control and Prevention. Effect of short sleep duration on daily activities--United States, 2005-2008. MMWR Morb Mortal Wkly Rep. 2011;60(8):239-242.
17. Antic NA, Catcheside P, Buchan C, et al. The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA. Sleep. 2011;34(1):111-119.
18. Phurrough S, Jacques L, Spencer F, Stiller J, Brechner R. Coverage decision memorandum for continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) (CAG-00093R2). Centers for Medicare & Medicaid Services Website. https://www.cms.gov/medicare-coverage-database/details/nca-decision-memo.aspx?NCAId=204&fromdb=true. Accessed February 5, 2016.
19. Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2009;5(3):263-276.
20. Berry RB, Chediak A, Brown LK, et al; NPPV Titration Task Force of the American Academy of Sleep Medicine. Best clinical practices for the sleep center adjustment of noninvasive positive pressure ventilation (NPPV) in stable chronic alveolar hypoventilation syndromes. J Clin Sleep Med. 2010;6(5):491-509.
21. Merton RK. Social Theory and Social Structure. New York, NY: Free Press; 1968.
22. Chaput JP, McNeil J, Després JP, Bouchard C, Tremblay A. Seven to eight hours of sleep a night is associated with a lower prevalence of the metabolic syndrome and reduced overall cardiometabolic risk in adults. PLoS One. 2013;8(9):e72832.
23. Born J, Wagner U. Sleep, hormones, and memory. Obstet Gynecol Clin North Am. 2009;36(4):809-829, x.
24. Silva GE, Vana KD, Goodwin JL, Sherrill DL, Quan SF. Identification of patients with sleep disordered breathing: comparing the four-variable screening tool, STOP, STOP-Bang, and Epworth Sleepiness Scales. J Clin Sleep Med. 2011;7(5):467-472.
25. Soares Pires F, Drummond M, Marinho A, et al. Effectiveness of a group education session on adherence with APAP in obstructive sleep apnea--a randomized controlled study. Sleep Breath. 2013;17(3):993-1001.
26. Berry RB, Budhiraja R, Gottlieb DJ, et al; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
27. Schwab RJ, Badr SM, Epstein LJ, et al; ATS Subcommittee on CPAP Adherence Tracking Systems. An official American Thoracic Society statement: continuous positive airway pressure adherence tracking systems. The optimal monitoring strategies and outcome measures in adults. Am J Respir Crit Care Med. 2013;188(5):613-620.
28. Respironics Encore Pro and Encore Pro 2 [computer program]. Philips, Inc; May 12, 2013.
29. ResMed. Version 04.01.013. San Diego, CA.
30. Knowles SR, O'Brien DT, Zhang S, Devara A, Rowley JA. Effect of addition of chin strap on PAP compliance, nightly duration of use, and other factors. J Clin Sleep Med. 2014;10(4):377-383.
31. Vorona RD, Ware JC, Sinacori JT, Ford ML 3rd, Cross JP. Treatment of severe obstructive sleep apnea syndrome with a chinstrap. J Clin Sleep Med. 2007;3(7):729-730.
32. Ruhle KH, Franke KJ, Domanski U, Nilius G. Quality of life, compliance, sleep and nasopharyngeal side effects during CPAP therapy with and without controlled heated humidification. Sleep Breath. 2011;15(3):479-485.
33. Hamilos DL. Chronic rhinosinusitis: epidemiology and medical management. J Allergy Clin Immunol. 2011;128(4):693-707.
34. Gooley JJ, Chamberlain K, Smith KA, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. J Clin Endocrinol Metab. 2011;96(3):E463-E472.
35. Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545.
36. Bednarek M, Zgierska A, Pływaczewski R, Zielinski J. The effect of CPAP treatment on excessive daytime somnolence in patients with obstructive sleep apnea [in Polish]. Pneumonol Alergol Pol. 1999;67(5-6):237-244.
37. Harvey R, Hannan SA, Badia L, Scadding G. Nasal saline irrigations for the symptoms of chronic rhinosinusitis. Cochrane Database Syst Rev. 2007;(3):CD006394.
38. Poirier J, George C, Rotenberg B. The effect of nasal surgery on nasal continuous positive airway pressure compliance. Laryngoscope. 2014;124(1):317-319.
39. Law JA. From the journal archives: Mallampati in two millennia: its impact then and implications now. Can J Anaesth. 2014;61(5):480-484.
40. Hood HK, Rogojanski J, Moss TG. Cognitive-behavioral therapy for chronic insomnia. Curr Treat Options Neurol. 2014;16(12):321.
41. Harb GC, Thompson R, Ross RJ, Cook JM. Combat-related PTSD nightmares and imagery rehearsal: nightmare characteristics and relation to treatment outcome. J Trauma Stress. 2012;25(5):511-518.
42. Cartwright R, Lamberg L. Crisis Dreaming: Using Your Dreams to Solve Your Problems.. New York, NY: HarperCollins;1992.
43.Writer BW, Meyer EG, Schillerstrom JE. Prazosin for military combat-related PTSD nightmares: a critical review. J Neuropsychiatry Clin Neurosci. 2014;26(1):24-33.
44. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-554.
45. Kapur V, Blough DK, Sandblom RE, et al. The medical cost of undiagnosed sleep apnea. Sleep. 1999;22(6):749-755.
46. Weaver TE, Sawyer AM. Adherence to continuous positive airway pressure treatment for obstructive sleep apnoea: implications for future interventions. Indian J Med Res. 2010;131:245-258.
1. Boyaci H, Gacar K, Baris SA, Basyigit I, Yildiz F. Positive airway pressure device compliance of patients with obstructive sleep apnea syndrome. Adv Clin Exp Med. 2013;22(6):809-815.
2. Bachour A, Vitikainen P, Virkkula P, Maasilta P. CPAP interface: satisfaction and side effects. Sleep Breath. 2013;17(2):667-672.
3. Wimms AJ, Richards GN, Genjafield AV. Assessment of the impact on compliance of a new CPAP system in obstructive sleep apnea. Sleep Breath. 2013;17(1):69-76.
4. Smith I, Nadig V, Lasserson TJ. Educational, supportive and behavioral interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnea. Cochrane Database Syst Rev. 2009;(2):CD007736.
5. Beecroft J, Zanon S, Lukic D, Hanly P. Oral continuous positive airway pressure for sleep apnea: effectiveness, patient preference, and adherence. Chest. 2003;124(6):2200-2208.
6. Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(4):CD005308.
7. Nilius G, Happel A, Domanski U, Ruhle KH. Pressure-relief continuous positive airway pressure vs constant continuous positive airway pressure: a comparison of efficacy and compliance. Chest. 2006;130(4):1018-1024.
8. Ballard RD, Gay PC, Strollo PJ. Interventions to improve compliance in sleep apnea patients previously non-compliant with continuous positive airway pressure. J Clin Sleep Med. 2007;3(7):706-712.
9. Sin DD, Mayers I, Man GC, Pawluk L. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest. 2002;121(2):430-435.
10. Mortimore IL, Whittle AT, Douglas NJ. Comparison of nose and face mask CPAP therapy for sleep apnoea. Thorax. 1998;53(4):290-292.
11. Haniffa M, Lasserson TJ, Smith I. Interventions to improve compliance with continuous positive airway pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2004;(4):CD003531.
12. Kushida CA, Berry RB, Blau, A, et al. Positive airway pressure initiation: a randomized controlled trial to assess the impact of therapy mode and titration process on efficacy, adherence, and outcomes. Sleep. 2011;34(8):1083-1092.
13. Gentina T, Fortin F, Douay B, et al. Auto bi-level with pressure relief during exhalation as a rescue therapy for optimally treated obstructive sleep apnoea patients with poor compliance to continuous positive airways pressure therapy--a pilot study. Sleep Breath. 2011;15(1):21-27.
14. Billings, ME, Auckley D, Benca R, et al. Race and residential socioeconomics as predictors of CPAP adherence. Sleep. 2011;34(12):1653-1658.
15. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin Sleep Cohort. Sleep. 2008;31(8):1071-1078.
16. Centers for Disease Control and Prevention. Effect of short sleep duration on daily activities--United States, 2005-2008. MMWR Morb Mortal Wkly Rep. 2011;60(8):239-242.
17. Antic NA, Catcheside P, Buchan C, et al. The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA. Sleep. 2011;34(1):111-119.
18. Phurrough S, Jacques L, Spencer F, Stiller J, Brechner R. Coverage decision memorandum for continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) (CAG-00093R2). Centers for Medicare & Medicaid Services Website. https://www.cms.gov/medicare-coverage-database/details/nca-decision-memo.aspx?NCAId=204&fromdb=true. Accessed February 5, 2016.
19. Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2009;5(3):263-276.
20. Berry RB, Chediak A, Brown LK, et al; NPPV Titration Task Force of the American Academy of Sleep Medicine. Best clinical practices for the sleep center adjustment of noninvasive positive pressure ventilation (NPPV) in stable chronic alveolar hypoventilation syndromes. J Clin Sleep Med. 2010;6(5):491-509.
21. Merton RK. Social Theory and Social Structure. New York, NY: Free Press; 1968.
22. Chaput JP, McNeil J, Després JP, Bouchard C, Tremblay A. Seven to eight hours of sleep a night is associated with a lower prevalence of the metabolic syndrome and reduced overall cardiometabolic risk in adults. PLoS One. 2013;8(9):e72832.
23. Born J, Wagner U. Sleep, hormones, and memory. Obstet Gynecol Clin North Am. 2009;36(4):809-829, x.
24. Silva GE, Vana KD, Goodwin JL, Sherrill DL, Quan SF. Identification of patients with sleep disordered breathing: comparing the four-variable screening tool, STOP, STOP-Bang, and Epworth Sleepiness Scales. J Clin Sleep Med. 2011;7(5):467-472.
25. Soares Pires F, Drummond M, Marinho A, et al. Effectiveness of a group education session on adherence with APAP in obstructive sleep apnea--a randomized controlled study. Sleep Breath. 2013;17(3):993-1001.
26. Berry RB, Budhiraja R, Gottlieb DJ, et al; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
27. Schwab RJ, Badr SM, Epstein LJ, et al; ATS Subcommittee on CPAP Adherence Tracking Systems. An official American Thoracic Society statement: continuous positive airway pressure adherence tracking systems. The optimal monitoring strategies and outcome measures in adults. Am J Respir Crit Care Med. 2013;188(5):613-620.
28. Respironics Encore Pro and Encore Pro 2 [computer program]. Philips, Inc; May 12, 2013.
29. ResMed. Version 04.01.013. San Diego, CA.
30. Knowles SR, O'Brien DT, Zhang S, Devara A, Rowley JA. Effect of addition of chin strap on PAP compliance, nightly duration of use, and other factors. J Clin Sleep Med. 2014;10(4):377-383.
31. Vorona RD, Ware JC, Sinacori JT, Ford ML 3rd, Cross JP. Treatment of severe obstructive sleep apnea syndrome with a chinstrap. J Clin Sleep Med. 2007;3(7):729-730.
32. Ruhle KH, Franke KJ, Domanski U, Nilius G. Quality of life, compliance, sleep and nasopharyngeal side effects during CPAP therapy with and without controlled heated humidification. Sleep Breath. 2011;15(3):479-485.
33. Hamilos DL. Chronic rhinosinusitis: epidemiology and medical management. J Allergy Clin Immunol. 2011;128(4):693-707.
34. Gooley JJ, Chamberlain K, Smith KA, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. J Clin Endocrinol Metab. 2011;96(3):E463-E472.
35. Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545.
36. Bednarek M, Zgierska A, Pływaczewski R, Zielinski J. The effect of CPAP treatment on excessive daytime somnolence in patients with obstructive sleep apnea [in Polish]. Pneumonol Alergol Pol. 1999;67(5-6):237-244.
37. Harvey R, Hannan SA, Badia L, Scadding G. Nasal saline irrigations for the symptoms of chronic rhinosinusitis. Cochrane Database Syst Rev. 2007;(3):CD006394.
38. Poirier J, George C, Rotenberg B. The effect of nasal surgery on nasal continuous positive airway pressure compliance. Laryngoscope. 2014;124(1):317-319.
39. Law JA. From the journal archives: Mallampati in two millennia: its impact then and implications now. Can J Anaesth. 2014;61(5):480-484.
40. Hood HK, Rogojanski J, Moss TG. Cognitive-behavioral therapy for chronic insomnia. Curr Treat Options Neurol. 2014;16(12):321.
41. Harb GC, Thompson R, Ross RJ, Cook JM. Combat-related PTSD nightmares and imagery rehearsal: nightmare characteristics and relation to treatment outcome. J Trauma Stress. 2012;25(5):511-518.
42. Cartwright R, Lamberg L. Crisis Dreaming: Using Your Dreams to Solve Your Problems.. New York, NY: HarperCollins;1992.
43.Writer BW, Meyer EG, Schillerstrom JE. Prazosin for military combat-related PTSD nightmares: a critical review. J Neuropsychiatry Clin Neurosci. 2014;26(1):24-33.
44. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-554.
45. Kapur V, Blough DK, Sandblom RE, et al. The medical cost of undiagnosed sleep apnea. Sleep. 1999;22(6):749-755.
46. Weaver TE, Sawyer AM. Adherence to continuous positive airway pressure treatment for obstructive sleep apnoea: implications for future interventions. Indian J Med Res. 2010;131:245-258.
Complete Atrioventricular Nodal Block Due to Malignancy-Related Hypercalcemia
Complete atrioventricular (AV) block can occur due to structural or functional causes. Common structural etiologies include sclerodegenerative disease of the conduction system, ischemic heart disease in the acute or chronic setting, infiltrative myocardial disease, congenital heart disease, and cardiac surgery. Reversible etiologies of complete AV block include drug overdose and electrolyte abnormalities. In the following case study, the authors present a rare case of complete AV block caused by severe hypercalcemia related to malignancy that completely normalized after treatment of the hypercalcemia.
Case Report
A 63-year-old African-American man with metastatic carcinoma of the lungs (Figure 1) with unknown primary cancer was found to have a serum calcium level of 17.5 mg/dL (reference range:8.4-10.2 mg/dL) on routine preoperative laboratory testing prior to placement of a surgical port for chemotherapy. The patient also was noted to have a slow heart rate, and his electrocardiogram revealed a third-degree AV block with an escape rhythm at 29 bpm with a prolonged corrected QT (QTc) of 556 ms (Figure 2).
Although the patient reported nonspecific symptoms of fatigue, anorexia, dysphagia, and weight loss for 3 months, there were no new symptoms of dizziness, chest discomfort, or syncope. His past medical history included hypertension, hyperlipidemia, chronic kidney disease, obstructive sleep apnea, and the recently discovered bilateral lung metastasis. The patient reported no prior history of cardiac arrhythmias, coronary artery disease, or structural heart defects. His outpatient medications included aspirin, amlodipine, bupropion, hydralazine, and simvastatin.
At the physical examination the patient was cachectic but in no apparent distress. His heart rate escape rhythm was 29 bpm, with no murmurs and mildly reduced breath sounds. The patient’s blood pressure was 110/70. After correction for albumin, the serum calcium level was 17.8 mg/dL; ionized calcium level was 8.6 mg/dL; parathyroid hormone was 7.6 pg/mL (normal range, 12-88 pg/mL); parathyroid hormone-related protein was 6.4 pmol/L (normal range, < 2.0 pmol/L); potassium was 3.4 mmol/L (normal range, 3.5 – 5.1 mmol/L); and magnesium was 2.01 mg/dL. The patient’s thyroid stimulating hormone level was normal, and serial cardiac enzymes stayed within the reference range.
The patient was admitted to a cardiac care unit. A temporary transvenous pacemaker was placed, and the hypercalcemia was treated with aggressive fluid hydration, calcitonin, and zoledronic acid. Serum calcium gradually decreased to 14.6 mg/dL the following day and 9.6 mg/dL the subsequent day. The normalization of calcium resulted in resolution of complete heart block (Figure 3). The patient did not experience recurrence of AV nodal dysfunction and eventually died 3 months later due to his advanced metastatic disease.
Discussion
The reported cardiovascular effects of hypercalcemia include hypertension, arrhythmias, increased myocardial contractility at serum calcium level below 15 mg/dL, and myocardial depression above that level. Electrocardiographic manifestations of hypercalcemia include a shortened ST segment leading to a short corrected QT interval (QTc), slight increase in T wave duration, and rarely, Osborn waves or J waves.1-3 However, its influence on the AV node is less clear.
One small study assessed the prevalence of cardiac arrhythmias and conduction disturbances in 20 patients with hyperparathyroidism and moderate hypercalcemia and found no increase in the frequency of arrhythmias or high grade AV block.4
There are reports of conduction abnormality secondary to experimentally induced hypercalcemia in the literature. Hoff and colleagues described findings of AV block generated by the injection of IV calcium in dogs.5 In 2 human subjects, sinus bradycardia was precipitated after they received IV infusion of calcium gluconate.6 Shah and colleagues described 2 patients with sinus node dysfunction attributed to hypercalcemia secondary to hyperparathyroidism.7
Case reports of AV nodal dysfunction provoked by hypercalcemia have primarily occurred in the setting of primary hyperparathyroidism.8,9 Milk-alkali syndrome and vitamin D related hypercalcemia also have been reported to cause complete heart block.10,11 Reports of malignancy-related hypercalcemia causing conduction abnormalities are rare. The authors also found one case report of marked sinus bradycardia due to hypercalcemia related to breast cancer.12The case study presented in this report is rare because the patient developed complete AV block due to malignancy-related hypercalcemia that resolved completely with resolution of hypercalcemia. The prolongation of the QTc interval was another unique electrocardiographic change observed in this case. Calcium levels are inversely proportional to the QTc interval, and hypercalcemia is typically associated with a shortened QTc interval. However, this patient had a prolonged QTc without any other clear-cut cause. His hypokalemia was of a mild degree and not severe enough to produce such a long QTc interval. A possible explanation of QTc prolongation may be an increase in the T wave width associated with a serum calcium level above 16 mg/dL.
The pathophysiology of hypercalcemia-induced AV nodal conduction system disease is unknown. Calcium deposition in AV nodes of elderly patients has been associated with paroxysmal 2:1 AV block.8 It could be postulated that elevated serum calcium levels predispose to calcium deposition in cardiac conduction tissue, leading to progressive dysfunction. Although this theory may be applicable in a chronic setting, the mechanism in an acute setting likely relates to elevated serum levels of calcium that causes an alteration in electrochemical gradients. These elevated serum levels also increase intracellular calcium. This rise may result in increased calmodulin activation on the intracellular portion of the myocyte cell membrane and consequent enhanced sodium channel activation, which may then inhibit AV nodal conduction.13
Conclusion
Physicians should be aware that severe hypercalcemia can cause significant conduction system alterations, including complete AV block. A short QTc interval is typical, but a prolonged QTc interval also may be seen. While temporary support with a transvenous pacemaker may be needed, the conduction system abnormality is expected to resolve by treatment of the underlying hypercalcemia.
1. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol. 1979;44(2):243-248.
2. Bronsky D, Dubin A, Waldstein SS, Kushner DS. Calcium and the electrocardiogram II. The electrocardiographic manifestations of hyperparathyroidism and of marked hypercalcemia from various other etiologies. Am J Cardiol. 1961;7(6):833-839.
3. Otero J, Lenihan DJ. The "normothermic" Osborn wave induced by severe hypercalcemia. Tex Heart Inst J. 2000;27(3):316-317.
4. Rosenqvist M, Nordenström J, Andersson M, Edhag OK. Cardiac conduction inpatients with hypercalcaemia due to primary hyperparathyroidism. Clin Endocrinol (Oxf). 1992;37(1):29-33.
5. Hoff H, Smith P, Winkler A. Electrocardiographic changes and concentration of calcium in serum following injection of calcium chloride. Am J Physiol. 1939;125:162-171.
6. Howard JE, Hopkins TR, Connor TB. The use of intravenous calcium as a measure of activity of the parathyroid glands. Trans Assoc Am Physicians. 1952;65:351-358.
7. Shah AP, Lopez A, Wachsner RY, Meymandi SK, El-Bialy AK, Ichiuji AM. Sinus node dysfunction secondary to hyperparathyroidism. J Cardiovasc Pharmacol Ther. 2004;9(2):145-147.
8. Vosnakidis A, Polymeropoulos K, Zaragoulidis P, Zarifis I. Atrioventricular nodal dysfunction secondary to hyperparathyroidism. J Thoracic Dis. 2013;5(3):E90-E92.
9. Crum WB, Till HJ. Hyperparathyroidism with Wenckebach's phenomenon. Am J Cardiol. 1960;6:838-840.
10. Ginsberg H, Schwarz KV. Letter: hypercalcemia and complete heart block. Ann Intern Med. 1973;79(6):903.
11. Garg G, Khadgwat R, Khandelwal D, Gupta N. Vitamin D toxicity presenting as hypercalcemia and complete heart block: an interesting case report. Indian J Endocrinol Metab. 2012;16 (suppl 2):S423-S425.
12. Badertscher E, Warnica JW, Ernst DS. Acute hypercalcemia and severe bradycardia in a patient with breast cancer. CMAJ. 1993;148(9):1506-1508.
13. Potet F, Chagot B, Anghelescu M, et al. Functional interactions between distinct sodium channel cytoplasmic domains through the action of calmodulin. J Biol Chem. 2009;284(13):8846-8854.
Complete atrioventricular (AV) block can occur due to structural or functional causes. Common structural etiologies include sclerodegenerative disease of the conduction system, ischemic heart disease in the acute or chronic setting, infiltrative myocardial disease, congenital heart disease, and cardiac surgery. Reversible etiologies of complete AV block include drug overdose and electrolyte abnormalities. In the following case study, the authors present a rare case of complete AV block caused by severe hypercalcemia related to malignancy that completely normalized after treatment of the hypercalcemia.
Case Report
A 63-year-old African-American man with metastatic carcinoma of the lungs (Figure 1) with unknown primary cancer was found to have a serum calcium level of 17.5 mg/dL (reference range:8.4-10.2 mg/dL) on routine preoperative laboratory testing prior to placement of a surgical port for chemotherapy. The patient also was noted to have a slow heart rate, and his electrocardiogram revealed a third-degree AV block with an escape rhythm at 29 bpm with a prolonged corrected QT (QTc) of 556 ms (Figure 2).
Although the patient reported nonspecific symptoms of fatigue, anorexia, dysphagia, and weight loss for 3 months, there were no new symptoms of dizziness, chest discomfort, or syncope. His past medical history included hypertension, hyperlipidemia, chronic kidney disease, obstructive sleep apnea, and the recently discovered bilateral lung metastasis. The patient reported no prior history of cardiac arrhythmias, coronary artery disease, or structural heart defects. His outpatient medications included aspirin, amlodipine, bupropion, hydralazine, and simvastatin.
At the physical examination the patient was cachectic but in no apparent distress. His heart rate escape rhythm was 29 bpm, with no murmurs and mildly reduced breath sounds. The patient’s blood pressure was 110/70. After correction for albumin, the serum calcium level was 17.8 mg/dL; ionized calcium level was 8.6 mg/dL; parathyroid hormone was 7.6 pg/mL (normal range, 12-88 pg/mL); parathyroid hormone-related protein was 6.4 pmol/L (normal range, < 2.0 pmol/L); potassium was 3.4 mmol/L (normal range, 3.5 – 5.1 mmol/L); and magnesium was 2.01 mg/dL. The patient’s thyroid stimulating hormone level was normal, and serial cardiac enzymes stayed within the reference range.
The patient was admitted to a cardiac care unit. A temporary transvenous pacemaker was placed, and the hypercalcemia was treated with aggressive fluid hydration, calcitonin, and zoledronic acid. Serum calcium gradually decreased to 14.6 mg/dL the following day and 9.6 mg/dL the subsequent day. The normalization of calcium resulted in resolution of complete heart block (Figure 3). The patient did not experience recurrence of AV nodal dysfunction and eventually died 3 months later due to his advanced metastatic disease.
Discussion
The reported cardiovascular effects of hypercalcemia include hypertension, arrhythmias, increased myocardial contractility at serum calcium level below 15 mg/dL, and myocardial depression above that level. Electrocardiographic manifestations of hypercalcemia include a shortened ST segment leading to a short corrected QT interval (QTc), slight increase in T wave duration, and rarely, Osborn waves or J waves.1-3 However, its influence on the AV node is less clear.
One small study assessed the prevalence of cardiac arrhythmias and conduction disturbances in 20 patients with hyperparathyroidism and moderate hypercalcemia and found no increase in the frequency of arrhythmias or high grade AV block.4
There are reports of conduction abnormality secondary to experimentally induced hypercalcemia in the literature. Hoff and colleagues described findings of AV block generated by the injection of IV calcium in dogs.5 In 2 human subjects, sinus bradycardia was precipitated after they received IV infusion of calcium gluconate.6 Shah and colleagues described 2 patients with sinus node dysfunction attributed to hypercalcemia secondary to hyperparathyroidism.7
Case reports of AV nodal dysfunction provoked by hypercalcemia have primarily occurred in the setting of primary hyperparathyroidism.8,9 Milk-alkali syndrome and vitamin D related hypercalcemia also have been reported to cause complete heart block.10,11 Reports of malignancy-related hypercalcemia causing conduction abnormalities are rare. The authors also found one case report of marked sinus bradycardia due to hypercalcemia related to breast cancer.12The case study presented in this report is rare because the patient developed complete AV block due to malignancy-related hypercalcemia that resolved completely with resolution of hypercalcemia. The prolongation of the QTc interval was another unique electrocardiographic change observed in this case. Calcium levels are inversely proportional to the QTc interval, and hypercalcemia is typically associated with a shortened QTc interval. However, this patient had a prolonged QTc without any other clear-cut cause. His hypokalemia was of a mild degree and not severe enough to produce such a long QTc interval. A possible explanation of QTc prolongation may be an increase in the T wave width associated with a serum calcium level above 16 mg/dL.
The pathophysiology of hypercalcemia-induced AV nodal conduction system disease is unknown. Calcium deposition in AV nodes of elderly patients has been associated with paroxysmal 2:1 AV block.8 It could be postulated that elevated serum calcium levels predispose to calcium deposition in cardiac conduction tissue, leading to progressive dysfunction. Although this theory may be applicable in a chronic setting, the mechanism in an acute setting likely relates to elevated serum levels of calcium that causes an alteration in electrochemical gradients. These elevated serum levels also increase intracellular calcium. This rise may result in increased calmodulin activation on the intracellular portion of the myocyte cell membrane and consequent enhanced sodium channel activation, which may then inhibit AV nodal conduction.13
Conclusion
Physicians should be aware that severe hypercalcemia can cause significant conduction system alterations, including complete AV block. A short QTc interval is typical, but a prolonged QTc interval also may be seen. While temporary support with a transvenous pacemaker may be needed, the conduction system abnormality is expected to resolve by treatment of the underlying hypercalcemia.
Complete atrioventricular (AV) block can occur due to structural or functional causes. Common structural etiologies include sclerodegenerative disease of the conduction system, ischemic heart disease in the acute or chronic setting, infiltrative myocardial disease, congenital heart disease, and cardiac surgery. Reversible etiologies of complete AV block include drug overdose and electrolyte abnormalities. In the following case study, the authors present a rare case of complete AV block caused by severe hypercalcemia related to malignancy that completely normalized after treatment of the hypercalcemia.
Case Report
A 63-year-old African-American man with metastatic carcinoma of the lungs (Figure 1) with unknown primary cancer was found to have a serum calcium level of 17.5 mg/dL (reference range:8.4-10.2 mg/dL) on routine preoperative laboratory testing prior to placement of a surgical port for chemotherapy. The patient also was noted to have a slow heart rate, and his electrocardiogram revealed a third-degree AV block with an escape rhythm at 29 bpm with a prolonged corrected QT (QTc) of 556 ms (Figure 2).
Although the patient reported nonspecific symptoms of fatigue, anorexia, dysphagia, and weight loss for 3 months, there were no new symptoms of dizziness, chest discomfort, or syncope. His past medical history included hypertension, hyperlipidemia, chronic kidney disease, obstructive sleep apnea, and the recently discovered bilateral lung metastasis. The patient reported no prior history of cardiac arrhythmias, coronary artery disease, or structural heart defects. His outpatient medications included aspirin, amlodipine, bupropion, hydralazine, and simvastatin.
At the physical examination the patient was cachectic but in no apparent distress. His heart rate escape rhythm was 29 bpm, with no murmurs and mildly reduced breath sounds. The patient’s blood pressure was 110/70. After correction for albumin, the serum calcium level was 17.8 mg/dL; ionized calcium level was 8.6 mg/dL; parathyroid hormone was 7.6 pg/mL (normal range, 12-88 pg/mL); parathyroid hormone-related protein was 6.4 pmol/L (normal range, < 2.0 pmol/L); potassium was 3.4 mmol/L (normal range, 3.5 – 5.1 mmol/L); and magnesium was 2.01 mg/dL. The patient’s thyroid stimulating hormone level was normal, and serial cardiac enzymes stayed within the reference range.
The patient was admitted to a cardiac care unit. A temporary transvenous pacemaker was placed, and the hypercalcemia was treated with aggressive fluid hydration, calcitonin, and zoledronic acid. Serum calcium gradually decreased to 14.6 mg/dL the following day and 9.6 mg/dL the subsequent day. The normalization of calcium resulted in resolution of complete heart block (Figure 3). The patient did not experience recurrence of AV nodal dysfunction and eventually died 3 months later due to his advanced metastatic disease.
Discussion
The reported cardiovascular effects of hypercalcemia include hypertension, arrhythmias, increased myocardial contractility at serum calcium level below 15 mg/dL, and myocardial depression above that level. Electrocardiographic manifestations of hypercalcemia include a shortened ST segment leading to a short corrected QT interval (QTc), slight increase in T wave duration, and rarely, Osborn waves or J waves.1-3 However, its influence on the AV node is less clear.
One small study assessed the prevalence of cardiac arrhythmias and conduction disturbances in 20 patients with hyperparathyroidism and moderate hypercalcemia and found no increase in the frequency of arrhythmias or high grade AV block.4
There are reports of conduction abnormality secondary to experimentally induced hypercalcemia in the literature. Hoff and colleagues described findings of AV block generated by the injection of IV calcium in dogs.5 In 2 human subjects, sinus bradycardia was precipitated after they received IV infusion of calcium gluconate.6 Shah and colleagues described 2 patients with sinus node dysfunction attributed to hypercalcemia secondary to hyperparathyroidism.7
Case reports of AV nodal dysfunction provoked by hypercalcemia have primarily occurred in the setting of primary hyperparathyroidism.8,9 Milk-alkali syndrome and vitamin D related hypercalcemia also have been reported to cause complete heart block.10,11 Reports of malignancy-related hypercalcemia causing conduction abnormalities are rare. The authors also found one case report of marked sinus bradycardia due to hypercalcemia related to breast cancer.12The case study presented in this report is rare because the patient developed complete AV block due to malignancy-related hypercalcemia that resolved completely with resolution of hypercalcemia. The prolongation of the QTc interval was another unique electrocardiographic change observed in this case. Calcium levels are inversely proportional to the QTc interval, and hypercalcemia is typically associated with a shortened QTc interval. However, this patient had a prolonged QTc without any other clear-cut cause. His hypokalemia was of a mild degree and not severe enough to produce such a long QTc interval. A possible explanation of QTc prolongation may be an increase in the T wave width associated with a serum calcium level above 16 mg/dL.
The pathophysiology of hypercalcemia-induced AV nodal conduction system disease is unknown. Calcium deposition in AV nodes of elderly patients has been associated with paroxysmal 2:1 AV block.8 It could be postulated that elevated serum calcium levels predispose to calcium deposition in cardiac conduction tissue, leading to progressive dysfunction. Although this theory may be applicable in a chronic setting, the mechanism in an acute setting likely relates to elevated serum levels of calcium that causes an alteration in electrochemical gradients. These elevated serum levels also increase intracellular calcium. This rise may result in increased calmodulin activation on the intracellular portion of the myocyte cell membrane and consequent enhanced sodium channel activation, which may then inhibit AV nodal conduction.13
Conclusion
Physicians should be aware that severe hypercalcemia can cause significant conduction system alterations, including complete AV block. A short QTc interval is typical, but a prolonged QTc interval also may be seen. While temporary support with a transvenous pacemaker may be needed, the conduction system abnormality is expected to resolve by treatment of the underlying hypercalcemia.
1. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol. 1979;44(2):243-248.
2. Bronsky D, Dubin A, Waldstein SS, Kushner DS. Calcium and the electrocardiogram II. The electrocardiographic manifestations of hyperparathyroidism and of marked hypercalcemia from various other etiologies. Am J Cardiol. 1961;7(6):833-839.
3. Otero J, Lenihan DJ. The "normothermic" Osborn wave induced by severe hypercalcemia. Tex Heart Inst J. 2000;27(3):316-317.
4. Rosenqvist M, Nordenström J, Andersson M, Edhag OK. Cardiac conduction inpatients with hypercalcaemia due to primary hyperparathyroidism. Clin Endocrinol (Oxf). 1992;37(1):29-33.
5. Hoff H, Smith P, Winkler A. Electrocardiographic changes and concentration of calcium in serum following injection of calcium chloride. Am J Physiol. 1939;125:162-171.
6. Howard JE, Hopkins TR, Connor TB. The use of intravenous calcium as a measure of activity of the parathyroid glands. Trans Assoc Am Physicians. 1952;65:351-358.
7. Shah AP, Lopez A, Wachsner RY, Meymandi SK, El-Bialy AK, Ichiuji AM. Sinus node dysfunction secondary to hyperparathyroidism. J Cardiovasc Pharmacol Ther. 2004;9(2):145-147.
8. Vosnakidis A, Polymeropoulos K, Zaragoulidis P, Zarifis I. Atrioventricular nodal dysfunction secondary to hyperparathyroidism. J Thoracic Dis. 2013;5(3):E90-E92.
9. Crum WB, Till HJ. Hyperparathyroidism with Wenckebach's phenomenon. Am J Cardiol. 1960;6:838-840.
10. Ginsberg H, Schwarz KV. Letter: hypercalcemia and complete heart block. Ann Intern Med. 1973;79(6):903.
11. Garg G, Khadgwat R, Khandelwal D, Gupta N. Vitamin D toxicity presenting as hypercalcemia and complete heart block: an interesting case report. Indian J Endocrinol Metab. 2012;16 (suppl 2):S423-S425.
12. Badertscher E, Warnica JW, Ernst DS. Acute hypercalcemia and severe bradycardia in a patient with breast cancer. CMAJ. 1993;148(9):1506-1508.
13. Potet F, Chagot B, Anghelescu M, et al. Functional interactions between distinct sodium channel cytoplasmic domains through the action of calmodulin. J Biol Chem. 2009;284(13):8846-8854.
1. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol. 1979;44(2):243-248.
2. Bronsky D, Dubin A, Waldstein SS, Kushner DS. Calcium and the electrocardiogram II. The electrocardiographic manifestations of hyperparathyroidism and of marked hypercalcemia from various other etiologies. Am J Cardiol. 1961;7(6):833-839.
3. Otero J, Lenihan DJ. The "normothermic" Osborn wave induced by severe hypercalcemia. Tex Heart Inst J. 2000;27(3):316-317.
4. Rosenqvist M, Nordenström J, Andersson M, Edhag OK. Cardiac conduction inpatients with hypercalcaemia due to primary hyperparathyroidism. Clin Endocrinol (Oxf). 1992;37(1):29-33.
5. Hoff H, Smith P, Winkler A. Electrocardiographic changes and concentration of calcium in serum following injection of calcium chloride. Am J Physiol. 1939;125:162-171.
6. Howard JE, Hopkins TR, Connor TB. The use of intravenous calcium as a measure of activity of the parathyroid glands. Trans Assoc Am Physicians. 1952;65:351-358.
7. Shah AP, Lopez A, Wachsner RY, Meymandi SK, El-Bialy AK, Ichiuji AM. Sinus node dysfunction secondary to hyperparathyroidism. J Cardiovasc Pharmacol Ther. 2004;9(2):145-147.
8. Vosnakidis A, Polymeropoulos K, Zaragoulidis P, Zarifis I. Atrioventricular nodal dysfunction secondary to hyperparathyroidism. J Thoracic Dis. 2013;5(3):E90-E92.
9. Crum WB, Till HJ. Hyperparathyroidism with Wenckebach's phenomenon. Am J Cardiol. 1960;6:838-840.
10. Ginsberg H, Schwarz KV. Letter: hypercalcemia and complete heart block. Ann Intern Med. 1973;79(6):903.
11. Garg G, Khadgwat R, Khandelwal D, Gupta N. Vitamin D toxicity presenting as hypercalcemia and complete heart block: an interesting case report. Indian J Endocrinol Metab. 2012;16 (suppl 2):S423-S425.
12. Badertscher E, Warnica JW, Ernst DS. Acute hypercalcemia and severe bradycardia in a patient with breast cancer. CMAJ. 1993;148(9):1506-1508.
13. Potet F, Chagot B, Anghelescu M, et al. Functional interactions between distinct sodium channel cytoplasmic domains through the action of calmodulin. J Biol Chem. 2009;284(13):8846-8854.
Peer Technical Consultant: Veteran-Centric Technical Support Model for VA Home-Based Telehealth Programs
With an increasing demand for mental health services for veterans in rural clinics, telehealth can deliver services to veterans at home or in other nonclinic settings. Telehealth can reduce demands on VA clinic space and staff required for traditional videoconferencing.
Clinic-based telemental health started at the VA in 2003 and has provided access to more than 1 million appointments.1 Despite the great strides in accessibility, logistic barriers limit expansion of clinic-based telehealth appointments. A VA staff member at the patient site must be available to “greet and seat” the veteran; scheduling requires 2 separate appointments (on patient and provider sites); and limited telehealth equipment and clinic space need to be reserved ahead of time.
The first known use of telehealth technologies to deliver mental health services within the VA network information technology system to at-home veterans occurred in 2009 at the VA Portland Health Care System (VAPORHCS) in Oregon. Between 2010 and 2013, the VAPORHCS Home-Based Telemental Health (HBTMH) pilot served about 82 veterans through about 740 appointments. The HBTMH pilot transitioned from a single facility to a regional implementation model under an Office of Innovation Grant Innovation #669: Home-Based Telemental Health (Innovation), which served about 84 veterans from 2013 to 2014.
In 2014, about 4,200 veterans accessed some health care via the national Clinical Video Telehealth–Into the Home (CVT-IH) program, with all 21 VISNs participating (John Peters, e-mail communication, February 2014). In all 3 implementation models (HBTMH pilot, Innovation, and CVT-IH), the veteran can receive health services via videoconferencing in real time, on personal or loaned computers, at home or in another nonclinic setting.
As the VA’s use of telehealth services grows in non-VA settings, technical support remains a significant challenge.2 Increased use of CVT-IH through veterans’ personal computers and devices has generated a corresponding need for technical support. The National Telehealth Technical Help Desk (NTTHD), which supports the national CVT-IH program, does not provide technical support directly to veterans. Instead, recommendations are given to the providers who are expected to transmit and implement the technical solutions with the veterans. Similarly, HBTMH pilot providers were initially responsible for all technical issues for home-based telehealth work, including helping patients with software installation and subsequent troubleshooting.
Providers participating in the HBTMH pilot project encountered veterans with all levels of comfort and skill with the required technology. Some veterans have never used a personal computer, e-mail, and/or webcam. Addressing technical issues often required up to 15 to 20 minutes during an HBTMH pilot session; some cases took hours spread over several days. In VISN 20, providers in Oregon and Washington have reported discontinuation of treatment of veterans enrolled in CVT-IH for technical reasons, including poor connections, lack of timely technical support, and incompatibility of veteran-owned computers with VA-approved third-party software (Anders Goranson, Sara Smucker Barnwell, Kathleen Woodside, e-mail communication, December 2013).
A peer technical consultant (PTC) who directly serves patients and providers may be better positioned to meet the technical needs of everyone involved in a home-based telehealth program. The PTC role was developed for the HBTMH Pilot and expanded during the Innovation program. The authors describe the role of the PTC, outline key responsibilities, and highlight how the PTC can provide effective technical support and improve provider and patient access and engagement with nonclinic-based telehealth services.
Methods
Lessons from the initial phases of the HBTMH pilot strongly suggested that technical barriers had to be reduced. In 2010, a former patient in the HBTMH pilot who had a background in information technology and computer systems and interest in helping other veterans contacted Dr. Peter Shore. They developed the novel role of a PTC, focused on delivering technical support with compassion (Table 1). A functional statement and position description were submitted to volunteer services at the VAPORHCS (Appendix). With the regionwide expansion of the HBTMH pilot into the Innovation program, the PTC was hired as a full-time contract employee to increase the availability of technical support.
The PTC assumed responsibility for installations and troubleshooting for both providers and veterans enrolled in the HBTMH pilot. The PTC, who was based at the VAPORHCS, received referrals, contacted veterans by telephone, addressed technical problems, and reported the result to the provider. No face-to-face contact occurred between the PTC and the veterans. The PTC received regular supervision from the project director. Starting in mid-2012, local providers who were using the national CVT-IH program also requested PTC services. The PTC was able to add technical support for veterans beyond the NTTHD model, allowing for immediate in-session attention in some cases.
For the Innovation program, which loaned devices (netbooks or iPads) and connectivity (mobile broadband Internet access) to veterans who needed them, the role of PTC expanded to become a technology concierge, helping to set up and manage all mobile telecommunication devices. The PTC phoned veterans when they received their device and provided a virtual tour, helped familiarize them with the technology by using test calls, and guided them in the use of relevant mobile applications installed on the device. During treatment, the PTC called enrolled veterans to follow up and to answer additional questions. The PTC also provided assistance to veterans interested in enrolling in the patient online portal My HealtheVet to access health information, communicate with providers, and request medication refills.
The VAPORHCS received institutional review board approval to present HBTMH pilot research data and program evaluation data for Innovation (as a quality improvement project). An initial evaluation of the position was completed through review of PTC workload and productivity, informal feedback from telehealth providers, and veteran and provider surveys during and after treatment.
Results
From March 2010 through April 2012, the PTC logged more than 2,500 hours of volunteer service on behalf of the HBTMH pilot (before the Innovation expansion). The dropout rate due to nonclinical reasons for veterans enrolled in the HBTMH pilot was 11%.3 During the HBTMH pilot, 78% of veterans reported that they had enough technical support (ie, from the volunteer PTC), whereas among veterans receiving clinic-based videoconferencing sessions, 61% reported having adequate technical support (ie, from telehealth clinical technicians employed by the VA).3
During 2013 to 2014, veterans and providers were surveyed during and after Innovation program treatment. Eighty percent of participants stated that the PTC was prompt in resolving any issues (20% reported “neutral”). One hundred percent of providers indicated that the PTC was able to resolve the technical issues and that they were “very likely” to continue participating in HBTMH if the PTC was involved. Eighty-nine percent of veterans reported they felt there was enough technical support, and 11% responded “neutral” to this question. Table 2 describes typical PTC services provided during the Innovation program.
Informal summary observations from the PTC confirmed that the most frequent interventions were device and software orientation, assessment of audio and/or video disruptions during sessions, and software log-in configuration and support. Common technical issues included audio and video bandwidth limitations and the need to clean up veterans’ personal computers to restore functionality or improve performance (eg, problems due to malware and viruses; e-mail communication, various dates, William Cannon).
Troubleshooting was performed immediately during a session about half the time (vs between sessions) and initiated by veterans about half the time (vs by providers on their behalf) according to informal observations. The average length of a technical support appointment was about 30 minutes for veterans who were comfortable with technology; in contrast, appointments with veterans who were unfamiliar with technology averaged about 90 minutes.
The task logs recorded instances where flexibility and availability were needed for optimal task completion. Although many tasks seemed to be routine, others showed considerable use of the PTC’s time or direct participation during a session.
One PTC noted, “Client called around 9:30 and had me put [provider’s name] info into Jabber. Also Jabber had an issue of being stuck but forced a call and issue cleared up. 15 min. Stayed online with client to ensure appointment connection went well. 5 min.”
Malware, although not the most common issue, seemed to be time consuming. A task that required 4 hours for resolution of multiple issues was described as “requested outside assist due to drivers. Troubleshooting discovered 240 plus malware and numerous Trojan [horses].”
Another time-consuming issue involved software or updates to existing software interfering with the videoconferencing program, with the following example logged for 90 minutes: “Jabber will not store contacts. Updated IOS. Deleted games. Deleted and reinstalled Jabber. Re-updated Jabber. Problem finally resolved” (December 19, 2014). Other patients simply needed more time to familiarize themselves with the technology, as in this example: “2.5 hours of training and using the iPad” (November 25, 2014).
Informal feedback from providers as well as formal feedback from a program audit indicated appreciation for the PTC’s ability to facilitate engagement and surmount technical hurdles. One provider reflected on a particular instance in which the PTC worked with both the veteran and the provider over the phone and webchat to teach them to use the equipment. “[Veteran] and the peer technician developed a friendly rapport and [veteran] expressed gratitude for the team’s efforts to deliver treatment that he would not have had otherwise.” Another provider commented, “The [National] Help Desk is almost too general. You have to explain who you are each time, and never get to explain who [the] veteran is. … They are aware of national problems. Otherwise, they can’t help out much.”
In 2012, the Office of Telehealth Services completed its Conditions of Participation review of all VISN 20 Telehealth programs and in their final report commended the practices of the HBTMH program, highlighting the associated peer-to-peer volunteer program.4
Discussion
The number of technical issues addressed by the PTC demonstrates the versatility and potential impact of this role. In each case, the PTC accommodates the specific needs of the veteran and any factors that might impact their technology use (eg, low cognitive functioning, hyperarousal, slowed processing speed, low frustration tolerance, or paranoia). This model could be expanded within or outside the VA, although due to the limited scope of the evaluation and the unique qualifications of the individual who filled the PTC role, generalizability remains to be established.
By providing direct support, the PTC attempts to meet veterans where they are and helps them become comfortable with the technology so they are not preoccupied with technical problems while receiving health care. In doing so, engagement in telehealth care is enhanced for patients and providers, and dropouts due to technologic problems may be prevented. Initial program evaluation of this role also suggests considerable provider and veteran satisfaction.
The PTC’s interactions help minimize potential frustrations related to technology use for the delivery of mental health care. Frequently, veterans using in-home telehealth have little experience with technology. Moreover, technology use has been found to be lower for rural dwelling adults.5 Other populations (eg, geriatric) may have greater technology challenges and need additional support.6 When patients start CVT services, there is a potential for dropout if there are initial connection problems, particularly among patients who may have low stress tolerance. The PTC can develop an ongoing relationship with veterans who have a history of technologic difficulties and help monitor them.
Technology barriers and limited support are also a documented barrier to provider engagement.7 Given the inherent limitations and reported provider discouragement with the NTTHD model, more directed technical support may enhance provider engagement and efficiency. With the immediate and one-on-one support given by the PTC, this concern has been assertively addressed. In VISN 20 some mental health care providers elected not to use the CVT-IH program technical support system of the and chose instead to work with the Innovation PTC.
Programmatically, the PTC role is consistent with the VA Office of Mental Health Services and the VA Central Office initiative to increase involvement of peer support programs. From a recovery model perspective, the role of the PTC goes beyond technical support in connecting veterans to other veterans who are encouraged to take control of their health care by making self-directed choices. They can experience empowerment through interactions with another veteran who may share some of their experiences. Further investigation into the effects of using a peer technical support system on veterans, providers, and PTCs compared with the existing national VA technical support help desk system might be useful, particularly with regard to rates of initiation of care or dropouts.
Integration of this role should be done in a purposeful and direct manner, defining peer roles and establishing clear policies and practices. Logistically, the transition of the PTC from a volunteer to a contract employee afforded increased credentialing to allow for improved integration with the other HBTMH team members. The PTC was able to effectively coordinate with clinical, support and administrative staff to share information, resolve issues collaboratively, and bridge gaps in technology knowledge.
Conclusion
Between the HBTMH pilot and the Innovation program, the authors have demonstrated the growing need for personalized and attentive technical support for patients enrolled in home-based telehealth services. Under a current call center help desk model, satisfaction and services may be inadequate for some veterans’ needs. The authors contend that the PTC is an effective way to deliver the necessary specialized technical assistance to veterans and providers and encourage further implementation and evaluation of this approach.
There is preliminary evidence suggesting that this support can have a beneficial impact on provider and veteran engagement in telehealth services. The PTC offers much needed support to providers who frequently do not have the time or knowledge to address all the technical issues that arise during telehealth care. Veterans helping veterans is a powerful alternative deserving of national resources and policy change. Although this case developed in a very VA-specific context, peer technical support may be applicable to other organizations as well.
Acknowledgements
Being the first to do anything in the VA takes courage, tenacity, and luck. The following individuals greatly assisted with the HBTMH pilot and the subsequent Innovation: William “Bear” Cannon, David Greaves, Tracy Dekelboum, William Minium, Sean O’Connor, Joe Ronzio, Kit Teague, and Mark Ward. For assistance with data entry and analysis, the authors thank Athalia White. For help with administrative approvals, the authors thank Bradford Felker and Carol Simons.
This article is dedicated to William “Bear” Cannon, who reinvented himself while serving as the PTC and saved his life along the way. His unwavering commitment to serve his fellow veterans is unheralded. May he be the shining light to those who follow him.
1. Darkins A. The growth of telehealth services in the Veterans Health Administration between 1994 and 2014: a study in the diffusion of innovation. Telemed J E Health. 2014;20(9):761-768.
2. Ronzio JL, Tuerk PW, Shore P. Technology and clinical videoconferencing infrastructures: a guide to selecting appropriate system. In: Tuerk PW, Shore P, eds. Clinical Video Teleconferencing: Program Development and Practice. New York, NY: Springer;2015:3-22.
3. Shore P, Goranson A, Ward MF, Lu MW. Meeting veterans where they're @: a VA home-based telemental health (HBTMH) pilot program. Int J Psychiatry Med. 2014;48(1):5-17.
4. U.S. Department of Veterans Affairs, Veterans Health Administration. Telehealth Conditions of Participation: Final Core and Modality-Specific Standards. Washington, DC: Veterans Health Administration; 2014.
5. Calvert JF Jr, Kaye J, Leahy M, Hexem K, Carlson N. Technology use by rural and urban oldest old. Technol Health Care. 2009;17(1):1-11.
6. Kang HG, Mahoney DF, Hoenig H, et al; Center for Integration of Medicine and Innovative Technology Working Group on Advanced Approaches to Physiologic Monitoring for the Aged. In situ monitoring of health in older adults: technologies and issues. J Am Geriatr Soc. 2010;58(8):1579-1586.
7. Brooks E, Turvey C, Augusterfer EF. Provider barriers to telemental health: obstacles overcome, obstacles remain. Telemed J E Health. 2013;19(6):433-437.
With an increasing demand for mental health services for veterans in rural clinics, telehealth can deliver services to veterans at home or in other nonclinic settings. Telehealth can reduce demands on VA clinic space and staff required for traditional videoconferencing.
Clinic-based telemental health started at the VA in 2003 and has provided access to more than 1 million appointments.1 Despite the great strides in accessibility, logistic barriers limit expansion of clinic-based telehealth appointments. A VA staff member at the patient site must be available to “greet and seat” the veteran; scheduling requires 2 separate appointments (on patient and provider sites); and limited telehealth equipment and clinic space need to be reserved ahead of time.
The first known use of telehealth technologies to deliver mental health services within the VA network information technology system to at-home veterans occurred in 2009 at the VA Portland Health Care System (VAPORHCS) in Oregon. Between 2010 and 2013, the VAPORHCS Home-Based Telemental Health (HBTMH) pilot served about 82 veterans through about 740 appointments. The HBTMH pilot transitioned from a single facility to a regional implementation model under an Office of Innovation Grant Innovation #669: Home-Based Telemental Health (Innovation), which served about 84 veterans from 2013 to 2014.
In 2014, about 4,200 veterans accessed some health care via the national Clinical Video Telehealth–Into the Home (CVT-IH) program, with all 21 VISNs participating (John Peters, e-mail communication, February 2014). In all 3 implementation models (HBTMH pilot, Innovation, and CVT-IH), the veteran can receive health services via videoconferencing in real time, on personal or loaned computers, at home or in another nonclinic setting.
As the VA’s use of telehealth services grows in non-VA settings, technical support remains a significant challenge.2 Increased use of CVT-IH through veterans’ personal computers and devices has generated a corresponding need for technical support. The National Telehealth Technical Help Desk (NTTHD), which supports the national CVT-IH program, does not provide technical support directly to veterans. Instead, recommendations are given to the providers who are expected to transmit and implement the technical solutions with the veterans. Similarly, HBTMH pilot providers were initially responsible for all technical issues for home-based telehealth work, including helping patients with software installation and subsequent troubleshooting.
Providers participating in the HBTMH pilot project encountered veterans with all levels of comfort and skill with the required technology. Some veterans have never used a personal computer, e-mail, and/or webcam. Addressing technical issues often required up to 15 to 20 minutes during an HBTMH pilot session; some cases took hours spread over several days. In VISN 20, providers in Oregon and Washington have reported discontinuation of treatment of veterans enrolled in CVT-IH for technical reasons, including poor connections, lack of timely technical support, and incompatibility of veteran-owned computers with VA-approved third-party software (Anders Goranson, Sara Smucker Barnwell, Kathleen Woodside, e-mail communication, December 2013).
A peer technical consultant (PTC) who directly serves patients and providers may be better positioned to meet the technical needs of everyone involved in a home-based telehealth program. The PTC role was developed for the HBTMH Pilot and expanded during the Innovation program. The authors describe the role of the PTC, outline key responsibilities, and highlight how the PTC can provide effective technical support and improve provider and patient access and engagement with nonclinic-based telehealth services.
Methods
Lessons from the initial phases of the HBTMH pilot strongly suggested that technical barriers had to be reduced. In 2010, a former patient in the HBTMH pilot who had a background in information technology and computer systems and interest in helping other veterans contacted Dr. Peter Shore. They developed the novel role of a PTC, focused on delivering technical support with compassion (Table 1). A functional statement and position description were submitted to volunteer services at the VAPORHCS (Appendix). With the regionwide expansion of the HBTMH pilot into the Innovation program, the PTC was hired as a full-time contract employee to increase the availability of technical support.
The PTC assumed responsibility for installations and troubleshooting for both providers and veterans enrolled in the HBTMH pilot. The PTC, who was based at the VAPORHCS, received referrals, contacted veterans by telephone, addressed technical problems, and reported the result to the provider. No face-to-face contact occurred between the PTC and the veterans. The PTC received regular supervision from the project director. Starting in mid-2012, local providers who were using the national CVT-IH program also requested PTC services. The PTC was able to add technical support for veterans beyond the NTTHD model, allowing for immediate in-session attention in some cases.
For the Innovation program, which loaned devices (netbooks or iPads) and connectivity (mobile broadband Internet access) to veterans who needed them, the role of PTC expanded to become a technology concierge, helping to set up and manage all mobile telecommunication devices. The PTC phoned veterans when they received their device and provided a virtual tour, helped familiarize them with the technology by using test calls, and guided them in the use of relevant mobile applications installed on the device. During treatment, the PTC called enrolled veterans to follow up and to answer additional questions. The PTC also provided assistance to veterans interested in enrolling in the patient online portal My HealtheVet to access health information, communicate with providers, and request medication refills.
The VAPORHCS received institutional review board approval to present HBTMH pilot research data and program evaluation data for Innovation (as a quality improvement project). An initial evaluation of the position was completed through review of PTC workload and productivity, informal feedback from telehealth providers, and veteran and provider surveys during and after treatment.
Results
From March 2010 through April 2012, the PTC logged more than 2,500 hours of volunteer service on behalf of the HBTMH pilot (before the Innovation expansion). The dropout rate due to nonclinical reasons for veterans enrolled in the HBTMH pilot was 11%.3 During the HBTMH pilot, 78% of veterans reported that they had enough technical support (ie, from the volunteer PTC), whereas among veterans receiving clinic-based videoconferencing sessions, 61% reported having adequate technical support (ie, from telehealth clinical technicians employed by the VA).3
During 2013 to 2014, veterans and providers were surveyed during and after Innovation program treatment. Eighty percent of participants stated that the PTC was prompt in resolving any issues (20% reported “neutral”). One hundred percent of providers indicated that the PTC was able to resolve the technical issues and that they were “very likely” to continue participating in HBTMH if the PTC was involved. Eighty-nine percent of veterans reported they felt there was enough technical support, and 11% responded “neutral” to this question. Table 2 describes typical PTC services provided during the Innovation program.
Informal summary observations from the PTC confirmed that the most frequent interventions were device and software orientation, assessment of audio and/or video disruptions during sessions, and software log-in configuration and support. Common technical issues included audio and video bandwidth limitations and the need to clean up veterans’ personal computers to restore functionality or improve performance (eg, problems due to malware and viruses; e-mail communication, various dates, William Cannon).
Troubleshooting was performed immediately during a session about half the time (vs between sessions) and initiated by veterans about half the time (vs by providers on their behalf) according to informal observations. The average length of a technical support appointment was about 30 minutes for veterans who were comfortable with technology; in contrast, appointments with veterans who were unfamiliar with technology averaged about 90 minutes.
The task logs recorded instances where flexibility and availability were needed for optimal task completion. Although many tasks seemed to be routine, others showed considerable use of the PTC’s time or direct participation during a session.
One PTC noted, “Client called around 9:30 and had me put [provider’s name] info into Jabber. Also Jabber had an issue of being stuck but forced a call and issue cleared up. 15 min. Stayed online with client to ensure appointment connection went well. 5 min.”
Malware, although not the most common issue, seemed to be time consuming. A task that required 4 hours for resolution of multiple issues was described as “requested outside assist due to drivers. Troubleshooting discovered 240 plus malware and numerous Trojan [horses].”
Another time-consuming issue involved software or updates to existing software interfering with the videoconferencing program, with the following example logged for 90 minutes: “Jabber will not store contacts. Updated IOS. Deleted games. Deleted and reinstalled Jabber. Re-updated Jabber. Problem finally resolved” (December 19, 2014). Other patients simply needed more time to familiarize themselves with the technology, as in this example: “2.5 hours of training and using the iPad” (November 25, 2014).
Informal feedback from providers as well as formal feedback from a program audit indicated appreciation for the PTC’s ability to facilitate engagement and surmount technical hurdles. One provider reflected on a particular instance in which the PTC worked with both the veteran and the provider over the phone and webchat to teach them to use the equipment. “[Veteran] and the peer technician developed a friendly rapport and [veteran] expressed gratitude for the team’s efforts to deliver treatment that he would not have had otherwise.” Another provider commented, “The [National] Help Desk is almost too general. You have to explain who you are each time, and never get to explain who [the] veteran is. … They are aware of national problems. Otherwise, they can’t help out much.”
In 2012, the Office of Telehealth Services completed its Conditions of Participation review of all VISN 20 Telehealth programs and in their final report commended the practices of the HBTMH program, highlighting the associated peer-to-peer volunteer program.4
Discussion
The number of technical issues addressed by the PTC demonstrates the versatility and potential impact of this role. In each case, the PTC accommodates the specific needs of the veteran and any factors that might impact their technology use (eg, low cognitive functioning, hyperarousal, slowed processing speed, low frustration tolerance, or paranoia). This model could be expanded within or outside the VA, although due to the limited scope of the evaluation and the unique qualifications of the individual who filled the PTC role, generalizability remains to be established.
By providing direct support, the PTC attempts to meet veterans where they are and helps them become comfortable with the technology so they are not preoccupied with technical problems while receiving health care. In doing so, engagement in telehealth care is enhanced for patients and providers, and dropouts due to technologic problems may be prevented. Initial program evaluation of this role also suggests considerable provider and veteran satisfaction.
The PTC’s interactions help minimize potential frustrations related to technology use for the delivery of mental health care. Frequently, veterans using in-home telehealth have little experience with technology. Moreover, technology use has been found to be lower for rural dwelling adults.5 Other populations (eg, geriatric) may have greater technology challenges and need additional support.6 When patients start CVT services, there is a potential for dropout if there are initial connection problems, particularly among patients who may have low stress tolerance. The PTC can develop an ongoing relationship with veterans who have a history of technologic difficulties and help monitor them.
Technology barriers and limited support are also a documented barrier to provider engagement.7 Given the inherent limitations and reported provider discouragement with the NTTHD model, more directed technical support may enhance provider engagement and efficiency. With the immediate and one-on-one support given by the PTC, this concern has been assertively addressed. In VISN 20 some mental health care providers elected not to use the CVT-IH program technical support system of the and chose instead to work with the Innovation PTC.
Programmatically, the PTC role is consistent with the VA Office of Mental Health Services and the VA Central Office initiative to increase involvement of peer support programs. From a recovery model perspective, the role of the PTC goes beyond technical support in connecting veterans to other veterans who are encouraged to take control of their health care by making self-directed choices. They can experience empowerment through interactions with another veteran who may share some of their experiences. Further investigation into the effects of using a peer technical support system on veterans, providers, and PTCs compared with the existing national VA technical support help desk system might be useful, particularly with regard to rates of initiation of care or dropouts.
Integration of this role should be done in a purposeful and direct manner, defining peer roles and establishing clear policies and practices. Logistically, the transition of the PTC from a volunteer to a contract employee afforded increased credentialing to allow for improved integration with the other HBTMH team members. The PTC was able to effectively coordinate with clinical, support and administrative staff to share information, resolve issues collaboratively, and bridge gaps in technology knowledge.
Conclusion
Between the HBTMH pilot and the Innovation program, the authors have demonstrated the growing need for personalized and attentive technical support for patients enrolled in home-based telehealth services. Under a current call center help desk model, satisfaction and services may be inadequate for some veterans’ needs. The authors contend that the PTC is an effective way to deliver the necessary specialized technical assistance to veterans and providers and encourage further implementation and evaluation of this approach.
There is preliminary evidence suggesting that this support can have a beneficial impact on provider and veteran engagement in telehealth services. The PTC offers much needed support to providers who frequently do not have the time or knowledge to address all the technical issues that arise during telehealth care. Veterans helping veterans is a powerful alternative deserving of national resources and policy change. Although this case developed in a very VA-specific context, peer technical support may be applicable to other organizations as well.
Acknowledgements
Being the first to do anything in the VA takes courage, tenacity, and luck. The following individuals greatly assisted with the HBTMH pilot and the subsequent Innovation: William “Bear” Cannon, David Greaves, Tracy Dekelboum, William Minium, Sean O’Connor, Joe Ronzio, Kit Teague, and Mark Ward. For assistance with data entry and analysis, the authors thank Athalia White. For help with administrative approvals, the authors thank Bradford Felker and Carol Simons.
This article is dedicated to William “Bear” Cannon, who reinvented himself while serving as the PTC and saved his life along the way. His unwavering commitment to serve his fellow veterans is unheralded. May he be the shining light to those who follow him.
With an increasing demand for mental health services for veterans in rural clinics, telehealth can deliver services to veterans at home or in other nonclinic settings. Telehealth can reduce demands on VA clinic space and staff required for traditional videoconferencing.
Clinic-based telemental health started at the VA in 2003 and has provided access to more than 1 million appointments.1 Despite the great strides in accessibility, logistic barriers limit expansion of clinic-based telehealth appointments. A VA staff member at the patient site must be available to “greet and seat” the veteran; scheduling requires 2 separate appointments (on patient and provider sites); and limited telehealth equipment and clinic space need to be reserved ahead of time.
The first known use of telehealth technologies to deliver mental health services within the VA network information technology system to at-home veterans occurred in 2009 at the VA Portland Health Care System (VAPORHCS) in Oregon. Between 2010 and 2013, the VAPORHCS Home-Based Telemental Health (HBTMH) pilot served about 82 veterans through about 740 appointments. The HBTMH pilot transitioned from a single facility to a regional implementation model under an Office of Innovation Grant Innovation #669: Home-Based Telemental Health (Innovation), which served about 84 veterans from 2013 to 2014.
In 2014, about 4,200 veterans accessed some health care via the national Clinical Video Telehealth–Into the Home (CVT-IH) program, with all 21 VISNs participating (John Peters, e-mail communication, February 2014). In all 3 implementation models (HBTMH pilot, Innovation, and CVT-IH), the veteran can receive health services via videoconferencing in real time, on personal or loaned computers, at home or in another nonclinic setting.
As the VA’s use of telehealth services grows in non-VA settings, technical support remains a significant challenge.2 Increased use of CVT-IH through veterans’ personal computers and devices has generated a corresponding need for technical support. The National Telehealth Technical Help Desk (NTTHD), which supports the national CVT-IH program, does not provide technical support directly to veterans. Instead, recommendations are given to the providers who are expected to transmit and implement the technical solutions with the veterans. Similarly, HBTMH pilot providers were initially responsible for all technical issues for home-based telehealth work, including helping patients with software installation and subsequent troubleshooting.
Providers participating in the HBTMH pilot project encountered veterans with all levels of comfort and skill with the required technology. Some veterans have never used a personal computer, e-mail, and/or webcam. Addressing technical issues often required up to 15 to 20 minutes during an HBTMH pilot session; some cases took hours spread over several days. In VISN 20, providers in Oregon and Washington have reported discontinuation of treatment of veterans enrolled in CVT-IH for technical reasons, including poor connections, lack of timely technical support, and incompatibility of veteran-owned computers with VA-approved third-party software (Anders Goranson, Sara Smucker Barnwell, Kathleen Woodside, e-mail communication, December 2013).
A peer technical consultant (PTC) who directly serves patients and providers may be better positioned to meet the technical needs of everyone involved in a home-based telehealth program. The PTC role was developed for the HBTMH Pilot and expanded during the Innovation program. The authors describe the role of the PTC, outline key responsibilities, and highlight how the PTC can provide effective technical support and improve provider and patient access and engagement with nonclinic-based telehealth services.
Methods
Lessons from the initial phases of the HBTMH pilot strongly suggested that technical barriers had to be reduced. In 2010, a former patient in the HBTMH pilot who had a background in information technology and computer systems and interest in helping other veterans contacted Dr. Peter Shore. They developed the novel role of a PTC, focused on delivering technical support with compassion (Table 1). A functional statement and position description were submitted to volunteer services at the VAPORHCS (Appendix). With the regionwide expansion of the HBTMH pilot into the Innovation program, the PTC was hired as a full-time contract employee to increase the availability of technical support.
The PTC assumed responsibility for installations and troubleshooting for both providers and veterans enrolled in the HBTMH pilot. The PTC, who was based at the VAPORHCS, received referrals, contacted veterans by telephone, addressed technical problems, and reported the result to the provider. No face-to-face contact occurred between the PTC and the veterans. The PTC received regular supervision from the project director. Starting in mid-2012, local providers who were using the national CVT-IH program also requested PTC services. The PTC was able to add technical support for veterans beyond the NTTHD model, allowing for immediate in-session attention in some cases.
For the Innovation program, which loaned devices (netbooks or iPads) and connectivity (mobile broadband Internet access) to veterans who needed them, the role of PTC expanded to become a technology concierge, helping to set up and manage all mobile telecommunication devices. The PTC phoned veterans when they received their device and provided a virtual tour, helped familiarize them with the technology by using test calls, and guided them in the use of relevant mobile applications installed on the device. During treatment, the PTC called enrolled veterans to follow up and to answer additional questions. The PTC also provided assistance to veterans interested in enrolling in the patient online portal My HealtheVet to access health information, communicate with providers, and request medication refills.
The VAPORHCS received institutional review board approval to present HBTMH pilot research data and program evaluation data for Innovation (as a quality improvement project). An initial evaluation of the position was completed through review of PTC workload and productivity, informal feedback from telehealth providers, and veteran and provider surveys during and after treatment.
Results
From March 2010 through April 2012, the PTC logged more than 2,500 hours of volunteer service on behalf of the HBTMH pilot (before the Innovation expansion). The dropout rate due to nonclinical reasons for veterans enrolled in the HBTMH pilot was 11%.3 During the HBTMH pilot, 78% of veterans reported that they had enough technical support (ie, from the volunteer PTC), whereas among veterans receiving clinic-based videoconferencing sessions, 61% reported having adequate technical support (ie, from telehealth clinical technicians employed by the VA).3
During 2013 to 2014, veterans and providers were surveyed during and after Innovation program treatment. Eighty percent of participants stated that the PTC was prompt in resolving any issues (20% reported “neutral”). One hundred percent of providers indicated that the PTC was able to resolve the technical issues and that they were “very likely” to continue participating in HBTMH if the PTC was involved. Eighty-nine percent of veterans reported they felt there was enough technical support, and 11% responded “neutral” to this question. Table 2 describes typical PTC services provided during the Innovation program.
Informal summary observations from the PTC confirmed that the most frequent interventions were device and software orientation, assessment of audio and/or video disruptions during sessions, and software log-in configuration and support. Common technical issues included audio and video bandwidth limitations and the need to clean up veterans’ personal computers to restore functionality or improve performance (eg, problems due to malware and viruses; e-mail communication, various dates, William Cannon).
Troubleshooting was performed immediately during a session about half the time (vs between sessions) and initiated by veterans about half the time (vs by providers on their behalf) according to informal observations. The average length of a technical support appointment was about 30 minutes for veterans who were comfortable with technology; in contrast, appointments with veterans who were unfamiliar with technology averaged about 90 minutes.
The task logs recorded instances where flexibility and availability were needed for optimal task completion. Although many tasks seemed to be routine, others showed considerable use of the PTC’s time or direct participation during a session.
One PTC noted, “Client called around 9:30 and had me put [provider’s name] info into Jabber. Also Jabber had an issue of being stuck but forced a call and issue cleared up. 15 min. Stayed online with client to ensure appointment connection went well. 5 min.”
Malware, although not the most common issue, seemed to be time consuming. A task that required 4 hours for resolution of multiple issues was described as “requested outside assist due to drivers. Troubleshooting discovered 240 plus malware and numerous Trojan [horses].”
Another time-consuming issue involved software or updates to existing software interfering with the videoconferencing program, with the following example logged for 90 minutes: “Jabber will not store contacts. Updated IOS. Deleted games. Deleted and reinstalled Jabber. Re-updated Jabber. Problem finally resolved” (December 19, 2014). Other patients simply needed more time to familiarize themselves with the technology, as in this example: “2.5 hours of training and using the iPad” (November 25, 2014).
Informal feedback from providers as well as formal feedback from a program audit indicated appreciation for the PTC’s ability to facilitate engagement and surmount technical hurdles. One provider reflected on a particular instance in which the PTC worked with both the veteran and the provider over the phone and webchat to teach them to use the equipment. “[Veteran] and the peer technician developed a friendly rapport and [veteran] expressed gratitude for the team’s efforts to deliver treatment that he would not have had otherwise.” Another provider commented, “The [National] Help Desk is almost too general. You have to explain who you are each time, and never get to explain who [the] veteran is. … They are aware of national problems. Otherwise, they can’t help out much.”
In 2012, the Office of Telehealth Services completed its Conditions of Participation review of all VISN 20 Telehealth programs and in their final report commended the practices of the HBTMH program, highlighting the associated peer-to-peer volunteer program.4
Discussion
The number of technical issues addressed by the PTC demonstrates the versatility and potential impact of this role. In each case, the PTC accommodates the specific needs of the veteran and any factors that might impact their technology use (eg, low cognitive functioning, hyperarousal, slowed processing speed, low frustration tolerance, or paranoia). This model could be expanded within or outside the VA, although due to the limited scope of the evaluation and the unique qualifications of the individual who filled the PTC role, generalizability remains to be established.
By providing direct support, the PTC attempts to meet veterans where they are and helps them become comfortable with the technology so they are not preoccupied with technical problems while receiving health care. In doing so, engagement in telehealth care is enhanced for patients and providers, and dropouts due to technologic problems may be prevented. Initial program evaluation of this role also suggests considerable provider and veteran satisfaction.
The PTC’s interactions help minimize potential frustrations related to technology use for the delivery of mental health care. Frequently, veterans using in-home telehealth have little experience with technology. Moreover, technology use has been found to be lower for rural dwelling adults.5 Other populations (eg, geriatric) may have greater technology challenges and need additional support.6 When patients start CVT services, there is a potential for dropout if there are initial connection problems, particularly among patients who may have low stress tolerance. The PTC can develop an ongoing relationship with veterans who have a history of technologic difficulties and help monitor them.
Technology barriers and limited support are also a documented barrier to provider engagement.7 Given the inherent limitations and reported provider discouragement with the NTTHD model, more directed technical support may enhance provider engagement and efficiency. With the immediate and one-on-one support given by the PTC, this concern has been assertively addressed. In VISN 20 some mental health care providers elected not to use the CVT-IH program technical support system of the and chose instead to work with the Innovation PTC.
Programmatically, the PTC role is consistent with the VA Office of Mental Health Services and the VA Central Office initiative to increase involvement of peer support programs. From a recovery model perspective, the role of the PTC goes beyond technical support in connecting veterans to other veterans who are encouraged to take control of their health care by making self-directed choices. They can experience empowerment through interactions with another veteran who may share some of their experiences. Further investigation into the effects of using a peer technical support system on veterans, providers, and PTCs compared with the existing national VA technical support help desk system might be useful, particularly with regard to rates of initiation of care or dropouts.
Integration of this role should be done in a purposeful and direct manner, defining peer roles and establishing clear policies and practices. Logistically, the transition of the PTC from a volunteer to a contract employee afforded increased credentialing to allow for improved integration with the other HBTMH team members. The PTC was able to effectively coordinate with clinical, support and administrative staff to share information, resolve issues collaboratively, and bridge gaps in technology knowledge.
Conclusion
Between the HBTMH pilot and the Innovation program, the authors have demonstrated the growing need for personalized and attentive technical support for patients enrolled in home-based telehealth services. Under a current call center help desk model, satisfaction and services may be inadequate for some veterans’ needs. The authors contend that the PTC is an effective way to deliver the necessary specialized technical assistance to veterans and providers and encourage further implementation and evaluation of this approach.
There is preliminary evidence suggesting that this support can have a beneficial impact on provider and veteran engagement in telehealth services. The PTC offers much needed support to providers who frequently do not have the time or knowledge to address all the technical issues that arise during telehealth care. Veterans helping veterans is a powerful alternative deserving of national resources and policy change. Although this case developed in a very VA-specific context, peer technical support may be applicable to other organizations as well.
Acknowledgements
Being the first to do anything in the VA takes courage, tenacity, and luck. The following individuals greatly assisted with the HBTMH pilot and the subsequent Innovation: William “Bear” Cannon, David Greaves, Tracy Dekelboum, William Minium, Sean O’Connor, Joe Ronzio, Kit Teague, and Mark Ward. For assistance with data entry and analysis, the authors thank Athalia White. For help with administrative approvals, the authors thank Bradford Felker and Carol Simons.
This article is dedicated to William “Bear” Cannon, who reinvented himself while serving as the PTC and saved his life along the way. His unwavering commitment to serve his fellow veterans is unheralded. May he be the shining light to those who follow him.
1. Darkins A. The growth of telehealth services in the Veterans Health Administration between 1994 and 2014: a study in the diffusion of innovation. Telemed J E Health. 2014;20(9):761-768.
2. Ronzio JL, Tuerk PW, Shore P. Technology and clinical videoconferencing infrastructures: a guide to selecting appropriate system. In: Tuerk PW, Shore P, eds. Clinical Video Teleconferencing: Program Development and Practice. New York, NY: Springer;2015:3-22.
3. Shore P, Goranson A, Ward MF, Lu MW. Meeting veterans where they're @: a VA home-based telemental health (HBTMH) pilot program. Int J Psychiatry Med. 2014;48(1):5-17.
4. U.S. Department of Veterans Affairs, Veterans Health Administration. Telehealth Conditions of Participation: Final Core and Modality-Specific Standards. Washington, DC: Veterans Health Administration; 2014.
5. Calvert JF Jr, Kaye J, Leahy M, Hexem K, Carlson N. Technology use by rural and urban oldest old. Technol Health Care. 2009;17(1):1-11.
6. Kang HG, Mahoney DF, Hoenig H, et al; Center for Integration of Medicine and Innovative Technology Working Group on Advanced Approaches to Physiologic Monitoring for the Aged. In situ monitoring of health in older adults: technologies and issues. J Am Geriatr Soc. 2010;58(8):1579-1586.
7. Brooks E, Turvey C, Augusterfer EF. Provider barriers to telemental health: obstacles overcome, obstacles remain. Telemed J E Health. 2013;19(6):433-437.
1. Darkins A. The growth of telehealth services in the Veterans Health Administration between 1994 and 2014: a study in the diffusion of innovation. Telemed J E Health. 2014;20(9):761-768.
2. Ronzio JL, Tuerk PW, Shore P. Technology and clinical videoconferencing infrastructures: a guide to selecting appropriate system. In: Tuerk PW, Shore P, eds. Clinical Video Teleconferencing: Program Development and Practice. New York, NY: Springer;2015:3-22.
3. Shore P, Goranson A, Ward MF, Lu MW. Meeting veterans where they're @: a VA home-based telemental health (HBTMH) pilot program. Int J Psychiatry Med. 2014;48(1):5-17.
4. U.S. Department of Veterans Affairs, Veterans Health Administration. Telehealth Conditions of Participation: Final Core and Modality-Specific Standards. Washington, DC: Veterans Health Administration; 2014.
5. Calvert JF Jr, Kaye J, Leahy M, Hexem K, Carlson N. Technology use by rural and urban oldest old. Technol Health Care. 2009;17(1):1-11.
6. Kang HG, Mahoney DF, Hoenig H, et al; Center for Integration of Medicine and Innovative Technology Working Group on Advanced Approaches to Physiologic Monitoring for the Aged. In situ monitoring of health in older adults: technologies and issues. J Am Geriatr Soc. 2010;58(8):1579-1586.
7. Brooks E, Turvey C, Augusterfer EF. Provider barriers to telemental health: obstacles overcome, obstacles remain. Telemed J E Health. 2013;19(6):433-437.
Predictors of VA and Non-VA Health Care Service Use by Homeless Veterans Residing in a Low-Demand Emergency Shelter
In 2009, the VA announced a goal of ending veteran homelessness by 2015.1 The primary focus of this new policy has been housing veterans experiencing chronic homelessness, many of whom languish outside the VA housing system. Since that time, progress has been made with point-in-time enumerations indicating that veteran homelessness has decreased nationally. Despite this progress, however, more than 55,000 veterans are still estimated to experience homelessness each night.2
Historically, the VA has offered an array of services specifically meant to alleviate veteran homelessness (grant, per diem, and other transitional housing programs; vocational rehabilitation, etc).3 The majority of these programs require some period of veteran abstinence as a condition for providing housing services. The recent move toward permanent “housing first” programs with few conditions for enrollment and participation provides new opportunities for housing veterans experiencing chronic homelessness, who are the specific target of the goal of ending veteran homelessness.4
Because veterans experiencing chronic homelessness have additional, substantial need for medical, psychiatric, and substance-abuse services, the VA also offers these services to this population.5-7 Veterans experiencing homelessness also may access parallel non-VA services.8 Information about veterans outside of traditional VA housing services, specifically those housed in low-demand shelters, is needed to develop services for this population and will be critical to success in ending veteran homelessness.
The Behavioral Model of Health Services Use9-11 and its later refinement, the Behavioral Model for Vulnerable Persons,12 have been used to conceptualize health care service use (Figure). In these models, health service use is predicted by 3 types of factors: predisposing factors (eg, age, race, gender, residential history), enabling factors (eg, availability, accessibility, affordability, acceptability), and service need factors (eg, substance-use disorders, mental health problems, physical health problems).
Studies applying these models of health care service use to both general homeless populations and, specifically to populations of veterans experiencing homelessness have found that service use is most influenced by need-based factors (eg, drug abuse, poor health, mental health problems).6,12-20 These same studies indicate that predisposing factors (eg, age, race, and gender) and enabling factors (eg, insurance, use of other services, and usual place of care) are also associated with service use, though less consistently.
Studies focused on veterans experiencing homelessness, however, included only treatment-seeking populations, which are not necessarily representative of the broader population of veterans experiencing homelessness. Additionally, none of these prior studies focused on the unique subset of veterans residing in low-demand shelters (characterized by unlimited duration of stay, no government ID or fee required for entry, and no requirement for service participation). This is a population that seems to be less engaged in services but nevertheless is challenged.21 This study, therefore, is focused on nontreatment seeking veterans residing in a low-demand shelter. The study applied the Behavioral Model of Health Services Use and the Behavioral Model for Vulnerable Persons to examine use of VA and non-VA services.
Study Parameters
This study was conducted in Fort Worth, Texas, the 17th largest city in the U.S. with more than 810,000 residents.22 In 2013, a biennial point-in-time count identified about 2,300 individuals who were homeless in Fort Worth. Most were found in emergency shelters (n = 1,126, 50%) or transitional housing (n = 965, 40%). Slightly more than 10% (n = 281) were found to be unsheltered: sleeping on the streets or in encampments, automobiles, or abandoned buildings.23 Although national estimates identify 12% of all adults who are homeless as veterans,2 only 8% (n = 189) of people experiencing homelessness in Fort Worth reported military service.23
Access to the full array of VA emergency department (ED), inpatient, and outpatient medical, psychiatric, and substance-abuse services are available to veterans experiencing homelessness at the Dallas VA Medical Center (DVAMC), located 35 miles away. Only VA outpatient medical, psychiatric, and substance-related services are available in Fort Worth through the VA Outpatient Clinic and Health Care for the Homeless Veterans (HCHV) program. If veterans experiencing homelessness seek care outside of the VA system, a comprehensive network of emergency, inpatient and outpatient medical, psychiatric, and substance-related services is available in Fort Worth.
Sample
The study sample included 110 adult male veterans randomly recruited as they awaited admission to a private, low-demand emergency shelter. The study excluded veterans with a dishonorable discharge to ensure participants were eligible for VA services. Institutional review board approvals were obtained prior to the study from the University of Texas at Arlington and DVAMC. All participants provided informed consent and were given a $5 gift for their involvement.
Instruments
Through structured interviews, experienced research staff collected demographics, history of homelessness, military service, and substance abuse in the previous 30 days. Data on alcohol and drug problems in the past 12 months were obtained using the Short Michigan Alcohol Screening Test (SMAST) and the Drug Abuse Screening Test. The Veterans RAND 12-Item Health Survey (VR-12) was used to measure physical and mental health functioning in the previous 4 weeks. Finally, participants reported their use of VA or non-VA medical (ED, inpatient, and outpatient), psychiatric (ED, inpatient, and outpatient), and substance abuse-related (inpatient and outpatient) services in the 12 months prior to the interview. These measures have been shown to be valid and reliable with acceptable psychometrics.24-26
Data Analysis
Statistical analysis was completed using IBM SPSS Statistics version 19. Descriptive data were summarized using counts, percentages, means, and standard deviations. A dichotomous variable for alcohol abuse was defined as SMAST score ≥ 3. A variable representing participant’s VR-12 mental component summary scores was used as an indicator of mental health functioning.
McNemar’s test was used to compare the use of VA and non-VA medical, psychiatric, and substance-related services using dichotomous variables for each overall sector as well as respective sector subcomponent services (emergency, inpatient, and outpatient for medical and psychiatric sectors and inpatient and outpatient for the substance-related sector). Statistical significance level was set at α = .05.
Logistic regression was used to predict psychiatric and substance abuse-related service use with separate dependent variables for VA, non-VA, and both VA and non-VA services. Need-based factors included in all models as independent variables were mental health functioning, alcohol abuse, and a dichotomous variable representing cocaine use in the previous 30 days. Independent variables for the other service sectors were included as enabling factors (eg, medical and substance-related problems predicting psychiatric service use), aligning all service use variables in the model to the same provider system (eg, VA service sector independent variables with VA service sector dependent variables).
Results
The sample mean age was 49.2 years (SD = 9.2), and fewer than half (n = 45, 41%) were white. Three-fourths (n = 82, 75%) had ever been married, and few participants (n = 5, 5%) were currently married. Total mean lifetime experience of homelessness was 3.9 years (SD = 4.3). One-third of the samples participants (n = 36, 33%) reported that their current episode of homelessness had lasted 1 year or longer. Most had an adult felony conviction (n = 78, 71%) and a history of incarceration as an adult (n = 104, 95%). All military branches were represented, with 49% serving in the Army, 23% in the Marine Corps, 17% in the Navy, 10% in the Air Force, and 1% in the Coast Guard.
Most of the sample’s veterans served during the Vietnam era (n = 43, 43%) or the post-Vietnam era (n = 49, 45%), but 12 (11%) served during the Persian Gulf era (including Operation Iraqi Freedom and Operation Enduring Freedom). Few received a nonservice connected VA pension (n = 21, 19%) or service-connected disability benefits (n = 20, 18%). The mean income earned in the previous 30 days was $466 (SD = $431). None of these predisposing factors were associated with any service variables.
The sample’s mean VR-12 physical functioning score was 43.8 (SD = 9.1), which was significantly higher (t = 6.2, df = 109, P < .001) than the 38.4 (SD = 12.2) population norm used with the instrument. The sample’s mean mental health functioning score of 39.4 (SD = 14.3) was significantly lower (t = -8.6, df = 109, P < .001) than the population norm (51.1, SD = 11.4).27 Substance-related problems were prevalent, with an identified alcohol problem in 62% (n = 68) and a drug problem in 79% (n = 87) of participants. More than half reported illicit drug use in the past 30 days (n = 61, 56%), especially cocaine (n = 42, 38%) and marijuana (n = 37, 33%).
The majority of veterans (n = 96, 87%) reported using some type of service in the past 12 months (Table 1). Most survey respondents used medical services. About half used psychiatric services, and almost one-third used substance-related services. More veterans used non-VA ED services than used VA ED services. More veterans used VA outpatient medical services than used non-VA outpatient medical services. Examining service sectors indicated that more veterans used VA psychiatric services than used non-VA psychiatric services, especially VA outpatient psychiatric services. More veterans used non-VA substance abuse-related services, especially outpatient services, rather than similar services offered by the VA.
Separate logistic regression models predicted use of psychiatric and substance-abuse services with 3 models (VA, non-VA, or any service use) for each dependent variable from independent variables that reflected need and enabling factors (Tables 2 and 3). Demographic predisposing factors, which were not associated with service use, were not included as covariates in these models. For the model predicting the use of non-VA substance-abuse services, collinearity between the alcohol-abuse and cocaine-abuse variables required separate models for each of the 2 variables.
Medical sector service use predicted psychiatric sector service use in all models. In fact, VA medical service use was the only predictor of use of VA psychiatric services. Lower mental health functioning predicted the use of any (VA or non-VA) psychiatric service use. In addition to the use of medical services, 30-day cocaine use predicted non-VA psychiatric service use.
Any substance-related sector service use was predicted by lower mental health functioning, self-reported alcohol problem, and any medical services utilization. No independent variables included in the model predicted any VA substance-related service use. Non-VA substance abuse service use was predicted by non-VA psychiatric service use and alcohol abuse. In the separate analysis that replaced alcohol problems with 30-day cocaine use variable, only 30-day cocaine use predicted non-VA substance-related service utilization.
Discussion
This study examined the use of medical, psychiatric, and substance-abuse services by randomly sampled veterans from a low-demand emergency shelter. Random selection of the sample and its high (98%) participation rate virtually eliminated potential for bias within this sample. Another strength of this study is its focus on low-demand shelter users—a population that has not been well studied. This low-demand shelter-dwelling population of veterans experiencing homelessness is of interest because more substance-abuse problems and histories of incarceration seem to make them especially disadvantaged and challenged.
The limitation of the sample to users of a low-demand shelter at only 1 location may reduce generalizability to other veteran homeless populations and settings. The study also may not generalize to populations of female veterans experiencing homelessness. Another limitation of the study is that it did not use diagnostic assessments for psychiatric and substance use disorders and objective collateral information such as agency record data. Finally, although the limited size of the sample may have been insufficient to adequately test certain hypotheses, it was a relatively large sample of this population and was large enough to yield significant findings.
This study found that need-based factors predicted the use of some service sectors intended for those needs. For example, mental health functioning appropriately predicted any psychiatric service use, and presence of an alcohol problem appropriately predicted any substance abuse service use. Specifically for non-VA services, both cocaine use and presence of an alcohol problem in separate models predicted substance-abuse service use. However for VA substance-abuse services, neither cocaine use nor presence of an alcohol problem predicted service use. Despite the high need, very few veterans used substance-abuse services, and they rarely used VA substance-abuse services.
For 2 service sectors, need-based factors predicted the use of services intended for other needs. Cocaine use predicted non-VA psychiatric service use, and low mental health functioning predicted substance-abuse service use. One potential explanation for this finding could be that providers or patients incorrectly classified cocaine-related substance use problems as psychiatric. The VR-12 mental health functioning measure also may have incorrectly classified cocaine-related problems as psychiatric.
Three enabling factors predicted service use by sector and type. The first 2 are preference for VA-provided services and the geographic availability of services, which competed for veterans’ selection of service providers. When both VA and non-VA services were present in Fort Worth, a preference for VA-provided services was observed, with the exception of outpatient substance abuse services which were highly underutilized in general. No preference was observed for any non-VA services when both were present. When VA services were not present in Fort Worth, veterans used geographically available non-VA providers for some services, but for other services they used Dallas-based VA and Fort Worth-based non-VA providers equally (Table 3 and Table 4).
The third enabling factor influencing service use was through other service use as an enabling pathway. Those veterans who opted out of locally available services in favor of VA services in Dallas may have been prompted to do so by provider referrals, which were further facilitated by VA and public transportation between Fort Worth and Dallas. The most consistent enabling pathway was medical service use, which predicted all types of psychiatric service use (VA and non-VA combined, VA only, and non-VA only), and any substance-related service use. Psychiatric service use predicted substance abuse service use but only in non-VA settings; no pathways led from VA medical or psychiatric services to VA substance abuse services.
Conclusions
These findings suggest, in large part, the validity of the Andersen and Gelberg models of health care service use. Consistent with prior studies, need-based factors predicted the use of any psychiatric and substance-related sector services as well as the use of non-VA subcomponent services for both sectors. Also consistent with prior studies, enabling factors (medical sector service use) predicted service use, with the exception of VA or non-VA substance-abuse services. Unlike prior studies, however, predisposing factors (eg, age, race, marital status, and income) were not associated with service use.
This study could not determine why veterans underutilized substance-abuse services, even those available locally to them in Fort Worth. One possible barrier to care is that the services are designed or delivered in a manner that does not engage these veterans (eg, expectations regarding abstinence or service involvement). Another barrier could be that referral pathways between VA outpatient medical and psychiatric service providers and VA substance-related services are not sufficiently facilitative. Future investigations could build upon the findings of this study by collecting data that could help assess these potential barriers.
The data from this study suggest 3 opportunities to improve the utilization of services most needed by this population. The first opportunity would be to accurately differentiate between substance abuse and psychiatric problems in clinical assessment and identify the most appropriate type of care. Another opportunity, linked closely to the first, would be to facilitate more effective and efficient referral pathways among VA service sectors, especially from medical and psychiatric services to substance-abuse services. Another strategy to improve referral pathways would be for VA service networks to systematically examine local service systems for factors or processes that may disrupt integrated care and implement program improvements.28 For homeless veterans navigating an inherently complex VA health care system, peer-to-peer and patient navigator programs have helped improve service efficiency and service outcomes.29 The third opportunity to improve utilization of services would be to ensure geographic availability and accessibility by strategic placement of these services.
The results from this study, while informative, point directly to needed areas for further inquiry to inform public health response. Although the low-demand shelter users are a particularly challenging subgroup of veterans experiencing chronic homelessness, other equally challenging populations warrant additional study. For example, veterans outside of both VA and community services (eg, unsheltered populations) are likely to require different approaches to engage in appropriate services. Additionally, changes to the homeless policy implemented in the period after this sample was recruited suggest the need to revisit the service-using behaviors of this population. Finally, interventions developed as part of the national response need to be assessed for their ability to engage these difficult-to-reach veterans.
Acknowledgements
This study was funded by a U.S. Department of Veterans Affairs Office of Academic Affiliations Pre-Doctoral Social Work Research Fellowship award.
1. U.S. Department of Veterans Affairs. Homeless veterans: VA is working to end homelessness among veterans. U.S. Department of Veterans Affairs Website. www.va.gov/homeless/about_the_initiative.asp#one. Updated January 26, 2016. Accessed February 16, 2016.
2. Henry M, Cortes A, Morris S, Abt Associates; U. S. Department of Housing and Urban Development Office of Community Planning and Development. The 2013 Annual Homeless Assessment Report (AHAR) to Congress: Part 1 Point-in-Time Estimates of Homelessness. HUD Exchange Website. https://www.hudexchange.info/resources/documents/ahar-2013-part1.pdf. Published October 2014. Accessed February 16, 2016.
3. U.S. Department of Veterans Affairs. Homeless Veterans: Housing Assistance. U.S. Department of Veterans Affairs Web site. http://www.va.gov/homeless/housing.asp. Updated November 5, 2015. Accessed February 16, 2016.
4. Austin EL, Pollio DE, Holmes S, et al. VA's expansion of supportive housing: successes and challenges on the path to Housing First. Psychiatr Serv. 2014;65(5):641-647.
5. Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460.
6. Wenzel SL, Bakhtiar L, Caskey NH, et al. Homeless veterans utilization of medical, psychiatric, and substance abuse services. Med Care. 1995;33(11):1132-1144.
7. McQuire J, Gelberg L, Blue-Howells J, Rosenheck RA. Access to primary care for homeless veterans with serious mental health illness or substance abuse: a follow-up evaluation of co-located primary care and homeless social services. Adm Policy Ment Health. 2009;36(4):255-264.
8. Tsai J, Mares AS, Rosenheck RA. Do homeless veterans have the same needs and outcomes as non-veterans? Mil Med. 2012;177(1):27-31.
9. Andersen RM. A behavioral model of families use of health services: Research Series No. 25. Chicago, IL: University of Chicago Center for Health Administrative Studies; 1968.
10. Andersen RM. Revisiting the behavioral model and access to medical care: does it matter? J Health Soc Behav. 1995;36(1):1-10.
11. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
12. Gelberg L, Andersen RM, Leake BD. The Behavioral Model for Vulnerable Populations: application to medical care use and outcomes for homeless people. Health Serv Res. 2000;34(6):1273-1302.
13. Padgett D, Struening EL, Andrews H. Factors affecting the use of medical, mental health, alcohol, and drug treatment services by homeless adults. Med Care. 1990;28(9):805-821.
14. Stein JA, Andersen RM, Koegel P, Gelberg L. Predicting health services utilization among homeless adults: a prospective analysis. J Health Care Poor Underserved. 2000;11(2):212-230.
15. Gamache G, Rosenheck RA, Tessler R. Factors predicting choice of provider among homeless veterans with mental illness. Psychiatr Serv. 2000;51(8):1024-1028.
16. Wenzel SL, Audrey Burnam, M, Koegel P, et al. Access to inpatient or residential substance abuse treatment among homeless adults with alcohol or other drug use disorders. Med Care. 2001;39(11):1158-1169.
17. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
18. Solorio MR, Milburn NG, Andersen RM, Trifskin S, Rodríguez MA. Emotional distress and mental health service use among urban homeless adolescents. J Behav Health Serv Res. 2006;33(4):381-393.
19. Stein JA, Andersen RM, Robertson M, Gelberg L. Impact of hepatitis B and C infection on health services utilization in homeless adults: a test of the Gelberg-Anderson Behavioral Model for Vulnerable Populations. Health Psychol. 2012;31(1):20-30.
20. Linton KF, Shafer MS. Factors associated with the health service use of unsheltered, chronically homeless adults. Soc Work Public Health. 2013;29(1):73-80.
21. Petrovich JC, Pollio DE, North CS. Characteristics and service use of homeless veterans and nonveterans residing in a low-demand emergency shelter. Psych Serv. 2014;65(6):751-757.
22. U.S. Census Bureau. State & County Quick Facts: Fort Worth (city), Texas. U.S. Census Bureau Website. http://quickfacts.census.gov/qfd/states/48/4827000.html. Revised December 2, 2015. Accessed February 17, 2016.
23. Tarrant County Homeless Coalition. 2014 point in time count results. Tarrant County Homeless Coalition Website. http://www.ahomewithhope.org/staff/local-data-research/2014-homeless-count/. Accessed February 16, 2016.
24. North CS, Eyrich KM, Pollio DE, Foster DA, Cottler LB, Spitznagel EL. The Homeless Supplement to the Diagnostic Interview Schedule: test-retest analyses. Int J Method Psychiatr Res. 2004;13(3):184-191.
25. Iqbal SU, Rogers W, Selim A, et al. The Veterans RAND 12 Item Health Survey (VR-12): What it is and how it is Used. Washington, DC: Veterans Health Administration; 2009.
26. Fischer J, Corcoran K, eds. Measures for Clinical Practice and Research: A Sourcebook. 4th ed. New York, NY: Oxford University Press; 2013.
27. Selim AJ, Rogers W, Fleishman JA, Qian SX, Finke BG, Rothendler JA, Kazis LE. Updated U.S. population standard for the Veterans RAND 12-Item Health Survey (VR-12). Qual Life Res. 2009;18(1):43-52.
28. Blue-Howells J, McQuire J, Nakashima J. Co-location of health care services for homeless veterans: a case study of innovation in program implementation. Soc Work Health Care. 2008;47(3):219-231.
29. Piette JD, Holtz B, Beard AJ, et al; Ann Arbor PACT Steering Committee. Improving chronic illness care for veterans within the framework of the Patient-Centered Medical Home: experiences from the Ann Arbor Patient-Aligned Care Team Laboratory. Transl Behav Med. 2011;1(4):615-623.
In 2009, the VA announced a goal of ending veteran homelessness by 2015.1 The primary focus of this new policy has been housing veterans experiencing chronic homelessness, many of whom languish outside the VA housing system. Since that time, progress has been made with point-in-time enumerations indicating that veteran homelessness has decreased nationally. Despite this progress, however, more than 55,000 veterans are still estimated to experience homelessness each night.2
Historically, the VA has offered an array of services specifically meant to alleviate veteran homelessness (grant, per diem, and other transitional housing programs; vocational rehabilitation, etc).3 The majority of these programs require some period of veteran abstinence as a condition for providing housing services. The recent move toward permanent “housing first” programs with few conditions for enrollment and participation provides new opportunities for housing veterans experiencing chronic homelessness, who are the specific target of the goal of ending veteran homelessness.4
Because veterans experiencing chronic homelessness have additional, substantial need for medical, psychiatric, and substance-abuse services, the VA also offers these services to this population.5-7 Veterans experiencing homelessness also may access parallel non-VA services.8 Information about veterans outside of traditional VA housing services, specifically those housed in low-demand shelters, is needed to develop services for this population and will be critical to success in ending veteran homelessness.
The Behavioral Model of Health Services Use9-11 and its later refinement, the Behavioral Model for Vulnerable Persons,12 have been used to conceptualize health care service use (Figure). In these models, health service use is predicted by 3 types of factors: predisposing factors (eg, age, race, gender, residential history), enabling factors (eg, availability, accessibility, affordability, acceptability), and service need factors (eg, substance-use disorders, mental health problems, physical health problems).
Studies applying these models of health care service use to both general homeless populations and, specifically to populations of veterans experiencing homelessness have found that service use is most influenced by need-based factors (eg, drug abuse, poor health, mental health problems).6,12-20 These same studies indicate that predisposing factors (eg, age, race, and gender) and enabling factors (eg, insurance, use of other services, and usual place of care) are also associated with service use, though less consistently.
Studies focused on veterans experiencing homelessness, however, included only treatment-seeking populations, which are not necessarily representative of the broader population of veterans experiencing homelessness. Additionally, none of these prior studies focused on the unique subset of veterans residing in low-demand shelters (characterized by unlimited duration of stay, no government ID or fee required for entry, and no requirement for service participation). This is a population that seems to be less engaged in services but nevertheless is challenged.21 This study, therefore, is focused on nontreatment seeking veterans residing in a low-demand shelter. The study applied the Behavioral Model of Health Services Use and the Behavioral Model for Vulnerable Persons to examine use of VA and non-VA services.
Study Parameters
This study was conducted in Fort Worth, Texas, the 17th largest city in the U.S. with more than 810,000 residents.22 In 2013, a biennial point-in-time count identified about 2,300 individuals who were homeless in Fort Worth. Most were found in emergency shelters (n = 1,126, 50%) or transitional housing (n = 965, 40%). Slightly more than 10% (n = 281) were found to be unsheltered: sleeping on the streets or in encampments, automobiles, or abandoned buildings.23 Although national estimates identify 12% of all adults who are homeless as veterans,2 only 8% (n = 189) of people experiencing homelessness in Fort Worth reported military service.23
Access to the full array of VA emergency department (ED), inpatient, and outpatient medical, psychiatric, and substance-abuse services are available to veterans experiencing homelessness at the Dallas VA Medical Center (DVAMC), located 35 miles away. Only VA outpatient medical, psychiatric, and substance-related services are available in Fort Worth through the VA Outpatient Clinic and Health Care for the Homeless Veterans (HCHV) program. If veterans experiencing homelessness seek care outside of the VA system, a comprehensive network of emergency, inpatient and outpatient medical, psychiatric, and substance-related services is available in Fort Worth.
Sample
The study sample included 110 adult male veterans randomly recruited as they awaited admission to a private, low-demand emergency shelter. The study excluded veterans with a dishonorable discharge to ensure participants were eligible for VA services. Institutional review board approvals were obtained prior to the study from the University of Texas at Arlington and DVAMC. All participants provided informed consent and were given a $5 gift for their involvement.
Instruments
Through structured interviews, experienced research staff collected demographics, history of homelessness, military service, and substance abuse in the previous 30 days. Data on alcohol and drug problems in the past 12 months were obtained using the Short Michigan Alcohol Screening Test (SMAST) and the Drug Abuse Screening Test. The Veterans RAND 12-Item Health Survey (VR-12) was used to measure physical and mental health functioning in the previous 4 weeks. Finally, participants reported their use of VA or non-VA medical (ED, inpatient, and outpatient), psychiatric (ED, inpatient, and outpatient), and substance abuse-related (inpatient and outpatient) services in the 12 months prior to the interview. These measures have been shown to be valid and reliable with acceptable psychometrics.24-26
Data Analysis
Statistical analysis was completed using IBM SPSS Statistics version 19. Descriptive data were summarized using counts, percentages, means, and standard deviations. A dichotomous variable for alcohol abuse was defined as SMAST score ≥ 3. A variable representing participant’s VR-12 mental component summary scores was used as an indicator of mental health functioning.
McNemar’s test was used to compare the use of VA and non-VA medical, psychiatric, and substance-related services using dichotomous variables for each overall sector as well as respective sector subcomponent services (emergency, inpatient, and outpatient for medical and psychiatric sectors and inpatient and outpatient for the substance-related sector). Statistical significance level was set at α = .05.
Logistic regression was used to predict psychiatric and substance abuse-related service use with separate dependent variables for VA, non-VA, and both VA and non-VA services. Need-based factors included in all models as independent variables were mental health functioning, alcohol abuse, and a dichotomous variable representing cocaine use in the previous 30 days. Independent variables for the other service sectors were included as enabling factors (eg, medical and substance-related problems predicting psychiatric service use), aligning all service use variables in the model to the same provider system (eg, VA service sector independent variables with VA service sector dependent variables).
Results
The sample mean age was 49.2 years (SD = 9.2), and fewer than half (n = 45, 41%) were white. Three-fourths (n = 82, 75%) had ever been married, and few participants (n = 5, 5%) were currently married. Total mean lifetime experience of homelessness was 3.9 years (SD = 4.3). One-third of the samples participants (n = 36, 33%) reported that their current episode of homelessness had lasted 1 year or longer. Most had an adult felony conviction (n = 78, 71%) and a history of incarceration as an adult (n = 104, 95%). All military branches were represented, with 49% serving in the Army, 23% in the Marine Corps, 17% in the Navy, 10% in the Air Force, and 1% in the Coast Guard.
Most of the sample’s veterans served during the Vietnam era (n = 43, 43%) or the post-Vietnam era (n = 49, 45%), but 12 (11%) served during the Persian Gulf era (including Operation Iraqi Freedom and Operation Enduring Freedom). Few received a nonservice connected VA pension (n = 21, 19%) or service-connected disability benefits (n = 20, 18%). The mean income earned in the previous 30 days was $466 (SD = $431). None of these predisposing factors were associated with any service variables.
The sample’s mean VR-12 physical functioning score was 43.8 (SD = 9.1), which was significantly higher (t = 6.2, df = 109, P < .001) than the 38.4 (SD = 12.2) population norm used with the instrument. The sample’s mean mental health functioning score of 39.4 (SD = 14.3) was significantly lower (t = -8.6, df = 109, P < .001) than the population norm (51.1, SD = 11.4).27 Substance-related problems were prevalent, with an identified alcohol problem in 62% (n = 68) and a drug problem in 79% (n = 87) of participants. More than half reported illicit drug use in the past 30 days (n = 61, 56%), especially cocaine (n = 42, 38%) and marijuana (n = 37, 33%).
The majority of veterans (n = 96, 87%) reported using some type of service in the past 12 months (Table 1). Most survey respondents used medical services. About half used psychiatric services, and almost one-third used substance-related services. More veterans used non-VA ED services than used VA ED services. More veterans used VA outpatient medical services than used non-VA outpatient medical services. Examining service sectors indicated that more veterans used VA psychiatric services than used non-VA psychiatric services, especially VA outpatient psychiatric services. More veterans used non-VA substance abuse-related services, especially outpatient services, rather than similar services offered by the VA.
Separate logistic regression models predicted use of psychiatric and substance-abuse services with 3 models (VA, non-VA, or any service use) for each dependent variable from independent variables that reflected need and enabling factors (Tables 2 and 3). Demographic predisposing factors, which were not associated with service use, were not included as covariates in these models. For the model predicting the use of non-VA substance-abuse services, collinearity between the alcohol-abuse and cocaine-abuse variables required separate models for each of the 2 variables.
Medical sector service use predicted psychiatric sector service use in all models. In fact, VA medical service use was the only predictor of use of VA psychiatric services. Lower mental health functioning predicted the use of any (VA or non-VA) psychiatric service use. In addition to the use of medical services, 30-day cocaine use predicted non-VA psychiatric service use.
Any substance-related sector service use was predicted by lower mental health functioning, self-reported alcohol problem, and any medical services utilization. No independent variables included in the model predicted any VA substance-related service use. Non-VA substance abuse service use was predicted by non-VA psychiatric service use and alcohol abuse. In the separate analysis that replaced alcohol problems with 30-day cocaine use variable, only 30-day cocaine use predicted non-VA substance-related service utilization.
Discussion
This study examined the use of medical, psychiatric, and substance-abuse services by randomly sampled veterans from a low-demand emergency shelter. Random selection of the sample and its high (98%) participation rate virtually eliminated potential for bias within this sample. Another strength of this study is its focus on low-demand shelter users—a population that has not been well studied. This low-demand shelter-dwelling population of veterans experiencing homelessness is of interest because more substance-abuse problems and histories of incarceration seem to make them especially disadvantaged and challenged.
The limitation of the sample to users of a low-demand shelter at only 1 location may reduce generalizability to other veteran homeless populations and settings. The study also may not generalize to populations of female veterans experiencing homelessness. Another limitation of the study is that it did not use diagnostic assessments for psychiatric and substance use disorders and objective collateral information such as agency record data. Finally, although the limited size of the sample may have been insufficient to adequately test certain hypotheses, it was a relatively large sample of this population and was large enough to yield significant findings.
This study found that need-based factors predicted the use of some service sectors intended for those needs. For example, mental health functioning appropriately predicted any psychiatric service use, and presence of an alcohol problem appropriately predicted any substance abuse service use. Specifically for non-VA services, both cocaine use and presence of an alcohol problem in separate models predicted substance-abuse service use. However for VA substance-abuse services, neither cocaine use nor presence of an alcohol problem predicted service use. Despite the high need, very few veterans used substance-abuse services, and they rarely used VA substance-abuse services.
For 2 service sectors, need-based factors predicted the use of services intended for other needs. Cocaine use predicted non-VA psychiatric service use, and low mental health functioning predicted substance-abuse service use. One potential explanation for this finding could be that providers or patients incorrectly classified cocaine-related substance use problems as psychiatric. The VR-12 mental health functioning measure also may have incorrectly classified cocaine-related problems as psychiatric.
Three enabling factors predicted service use by sector and type. The first 2 are preference for VA-provided services and the geographic availability of services, which competed for veterans’ selection of service providers. When both VA and non-VA services were present in Fort Worth, a preference for VA-provided services was observed, with the exception of outpatient substance abuse services which were highly underutilized in general. No preference was observed for any non-VA services when both were present. When VA services were not present in Fort Worth, veterans used geographically available non-VA providers for some services, but for other services they used Dallas-based VA and Fort Worth-based non-VA providers equally (Table 3 and Table 4).
The third enabling factor influencing service use was through other service use as an enabling pathway. Those veterans who opted out of locally available services in favor of VA services in Dallas may have been prompted to do so by provider referrals, which were further facilitated by VA and public transportation between Fort Worth and Dallas. The most consistent enabling pathway was medical service use, which predicted all types of psychiatric service use (VA and non-VA combined, VA only, and non-VA only), and any substance-related service use. Psychiatric service use predicted substance abuse service use but only in non-VA settings; no pathways led from VA medical or psychiatric services to VA substance abuse services.
Conclusions
These findings suggest, in large part, the validity of the Andersen and Gelberg models of health care service use. Consistent with prior studies, need-based factors predicted the use of any psychiatric and substance-related sector services as well as the use of non-VA subcomponent services for both sectors. Also consistent with prior studies, enabling factors (medical sector service use) predicted service use, with the exception of VA or non-VA substance-abuse services. Unlike prior studies, however, predisposing factors (eg, age, race, marital status, and income) were not associated with service use.
This study could not determine why veterans underutilized substance-abuse services, even those available locally to them in Fort Worth. One possible barrier to care is that the services are designed or delivered in a manner that does not engage these veterans (eg, expectations regarding abstinence or service involvement). Another barrier could be that referral pathways between VA outpatient medical and psychiatric service providers and VA substance-related services are not sufficiently facilitative. Future investigations could build upon the findings of this study by collecting data that could help assess these potential barriers.
The data from this study suggest 3 opportunities to improve the utilization of services most needed by this population. The first opportunity would be to accurately differentiate between substance abuse and psychiatric problems in clinical assessment and identify the most appropriate type of care. Another opportunity, linked closely to the first, would be to facilitate more effective and efficient referral pathways among VA service sectors, especially from medical and psychiatric services to substance-abuse services. Another strategy to improve referral pathways would be for VA service networks to systematically examine local service systems for factors or processes that may disrupt integrated care and implement program improvements.28 For homeless veterans navigating an inherently complex VA health care system, peer-to-peer and patient navigator programs have helped improve service efficiency and service outcomes.29 The third opportunity to improve utilization of services would be to ensure geographic availability and accessibility by strategic placement of these services.
The results from this study, while informative, point directly to needed areas for further inquiry to inform public health response. Although the low-demand shelter users are a particularly challenging subgroup of veterans experiencing chronic homelessness, other equally challenging populations warrant additional study. For example, veterans outside of both VA and community services (eg, unsheltered populations) are likely to require different approaches to engage in appropriate services. Additionally, changes to the homeless policy implemented in the period after this sample was recruited suggest the need to revisit the service-using behaviors of this population. Finally, interventions developed as part of the national response need to be assessed for their ability to engage these difficult-to-reach veterans.
Acknowledgements
This study was funded by a U.S. Department of Veterans Affairs Office of Academic Affiliations Pre-Doctoral Social Work Research Fellowship award.
In 2009, the VA announced a goal of ending veteran homelessness by 2015.1 The primary focus of this new policy has been housing veterans experiencing chronic homelessness, many of whom languish outside the VA housing system. Since that time, progress has been made with point-in-time enumerations indicating that veteran homelessness has decreased nationally. Despite this progress, however, more than 55,000 veterans are still estimated to experience homelessness each night.2
Historically, the VA has offered an array of services specifically meant to alleviate veteran homelessness (grant, per diem, and other transitional housing programs; vocational rehabilitation, etc).3 The majority of these programs require some period of veteran abstinence as a condition for providing housing services. The recent move toward permanent “housing first” programs with few conditions for enrollment and participation provides new opportunities for housing veterans experiencing chronic homelessness, who are the specific target of the goal of ending veteran homelessness.4
Because veterans experiencing chronic homelessness have additional, substantial need for medical, psychiatric, and substance-abuse services, the VA also offers these services to this population.5-7 Veterans experiencing homelessness also may access parallel non-VA services.8 Information about veterans outside of traditional VA housing services, specifically those housed in low-demand shelters, is needed to develop services for this population and will be critical to success in ending veteran homelessness.
The Behavioral Model of Health Services Use9-11 and its later refinement, the Behavioral Model for Vulnerable Persons,12 have been used to conceptualize health care service use (Figure). In these models, health service use is predicted by 3 types of factors: predisposing factors (eg, age, race, gender, residential history), enabling factors (eg, availability, accessibility, affordability, acceptability), and service need factors (eg, substance-use disorders, mental health problems, physical health problems).
Studies applying these models of health care service use to both general homeless populations and, specifically to populations of veterans experiencing homelessness have found that service use is most influenced by need-based factors (eg, drug abuse, poor health, mental health problems).6,12-20 These same studies indicate that predisposing factors (eg, age, race, and gender) and enabling factors (eg, insurance, use of other services, and usual place of care) are also associated with service use, though less consistently.
Studies focused on veterans experiencing homelessness, however, included only treatment-seeking populations, which are not necessarily representative of the broader population of veterans experiencing homelessness. Additionally, none of these prior studies focused on the unique subset of veterans residing in low-demand shelters (characterized by unlimited duration of stay, no government ID or fee required for entry, and no requirement for service participation). This is a population that seems to be less engaged in services but nevertheless is challenged.21 This study, therefore, is focused on nontreatment seeking veterans residing in a low-demand shelter. The study applied the Behavioral Model of Health Services Use and the Behavioral Model for Vulnerable Persons to examine use of VA and non-VA services.
Study Parameters
This study was conducted in Fort Worth, Texas, the 17th largest city in the U.S. with more than 810,000 residents.22 In 2013, a biennial point-in-time count identified about 2,300 individuals who were homeless in Fort Worth. Most were found in emergency shelters (n = 1,126, 50%) or transitional housing (n = 965, 40%). Slightly more than 10% (n = 281) were found to be unsheltered: sleeping on the streets or in encampments, automobiles, or abandoned buildings.23 Although national estimates identify 12% of all adults who are homeless as veterans,2 only 8% (n = 189) of people experiencing homelessness in Fort Worth reported military service.23
Access to the full array of VA emergency department (ED), inpatient, and outpatient medical, psychiatric, and substance-abuse services are available to veterans experiencing homelessness at the Dallas VA Medical Center (DVAMC), located 35 miles away. Only VA outpatient medical, psychiatric, and substance-related services are available in Fort Worth through the VA Outpatient Clinic and Health Care for the Homeless Veterans (HCHV) program. If veterans experiencing homelessness seek care outside of the VA system, a comprehensive network of emergency, inpatient and outpatient medical, psychiatric, and substance-related services is available in Fort Worth.
Sample
The study sample included 110 adult male veterans randomly recruited as they awaited admission to a private, low-demand emergency shelter. The study excluded veterans with a dishonorable discharge to ensure participants were eligible for VA services. Institutional review board approvals were obtained prior to the study from the University of Texas at Arlington and DVAMC. All participants provided informed consent and were given a $5 gift for their involvement.
Instruments
Through structured interviews, experienced research staff collected demographics, history of homelessness, military service, and substance abuse in the previous 30 days. Data on alcohol and drug problems in the past 12 months were obtained using the Short Michigan Alcohol Screening Test (SMAST) and the Drug Abuse Screening Test. The Veterans RAND 12-Item Health Survey (VR-12) was used to measure physical and mental health functioning in the previous 4 weeks. Finally, participants reported their use of VA or non-VA medical (ED, inpatient, and outpatient), psychiatric (ED, inpatient, and outpatient), and substance abuse-related (inpatient and outpatient) services in the 12 months prior to the interview. These measures have been shown to be valid and reliable with acceptable psychometrics.24-26
Data Analysis
Statistical analysis was completed using IBM SPSS Statistics version 19. Descriptive data were summarized using counts, percentages, means, and standard deviations. A dichotomous variable for alcohol abuse was defined as SMAST score ≥ 3. A variable representing participant’s VR-12 mental component summary scores was used as an indicator of mental health functioning.
McNemar’s test was used to compare the use of VA and non-VA medical, psychiatric, and substance-related services using dichotomous variables for each overall sector as well as respective sector subcomponent services (emergency, inpatient, and outpatient for medical and psychiatric sectors and inpatient and outpatient for the substance-related sector). Statistical significance level was set at α = .05.
Logistic regression was used to predict psychiatric and substance abuse-related service use with separate dependent variables for VA, non-VA, and both VA and non-VA services. Need-based factors included in all models as independent variables were mental health functioning, alcohol abuse, and a dichotomous variable representing cocaine use in the previous 30 days. Independent variables for the other service sectors were included as enabling factors (eg, medical and substance-related problems predicting psychiatric service use), aligning all service use variables in the model to the same provider system (eg, VA service sector independent variables with VA service sector dependent variables).
Results
The sample mean age was 49.2 years (SD = 9.2), and fewer than half (n = 45, 41%) were white. Three-fourths (n = 82, 75%) had ever been married, and few participants (n = 5, 5%) were currently married. Total mean lifetime experience of homelessness was 3.9 years (SD = 4.3). One-third of the samples participants (n = 36, 33%) reported that their current episode of homelessness had lasted 1 year or longer. Most had an adult felony conviction (n = 78, 71%) and a history of incarceration as an adult (n = 104, 95%). All military branches were represented, with 49% serving in the Army, 23% in the Marine Corps, 17% in the Navy, 10% in the Air Force, and 1% in the Coast Guard.
Most of the sample’s veterans served during the Vietnam era (n = 43, 43%) or the post-Vietnam era (n = 49, 45%), but 12 (11%) served during the Persian Gulf era (including Operation Iraqi Freedom and Operation Enduring Freedom). Few received a nonservice connected VA pension (n = 21, 19%) or service-connected disability benefits (n = 20, 18%). The mean income earned in the previous 30 days was $466 (SD = $431). None of these predisposing factors were associated with any service variables.
The sample’s mean VR-12 physical functioning score was 43.8 (SD = 9.1), which was significantly higher (t = 6.2, df = 109, P < .001) than the 38.4 (SD = 12.2) population norm used with the instrument. The sample’s mean mental health functioning score of 39.4 (SD = 14.3) was significantly lower (t = -8.6, df = 109, P < .001) than the population norm (51.1, SD = 11.4).27 Substance-related problems were prevalent, with an identified alcohol problem in 62% (n = 68) and a drug problem in 79% (n = 87) of participants. More than half reported illicit drug use in the past 30 days (n = 61, 56%), especially cocaine (n = 42, 38%) and marijuana (n = 37, 33%).
The majority of veterans (n = 96, 87%) reported using some type of service in the past 12 months (Table 1). Most survey respondents used medical services. About half used psychiatric services, and almost one-third used substance-related services. More veterans used non-VA ED services than used VA ED services. More veterans used VA outpatient medical services than used non-VA outpatient medical services. Examining service sectors indicated that more veterans used VA psychiatric services than used non-VA psychiatric services, especially VA outpatient psychiatric services. More veterans used non-VA substance abuse-related services, especially outpatient services, rather than similar services offered by the VA.
Separate logistic regression models predicted use of psychiatric and substance-abuse services with 3 models (VA, non-VA, or any service use) for each dependent variable from independent variables that reflected need and enabling factors (Tables 2 and 3). Demographic predisposing factors, which were not associated with service use, were not included as covariates in these models. For the model predicting the use of non-VA substance-abuse services, collinearity between the alcohol-abuse and cocaine-abuse variables required separate models for each of the 2 variables.
Medical sector service use predicted psychiatric sector service use in all models. In fact, VA medical service use was the only predictor of use of VA psychiatric services. Lower mental health functioning predicted the use of any (VA or non-VA) psychiatric service use. In addition to the use of medical services, 30-day cocaine use predicted non-VA psychiatric service use.
Any substance-related sector service use was predicted by lower mental health functioning, self-reported alcohol problem, and any medical services utilization. No independent variables included in the model predicted any VA substance-related service use. Non-VA substance abuse service use was predicted by non-VA psychiatric service use and alcohol abuse. In the separate analysis that replaced alcohol problems with 30-day cocaine use variable, only 30-day cocaine use predicted non-VA substance-related service utilization.
Discussion
This study examined the use of medical, psychiatric, and substance-abuse services by randomly sampled veterans from a low-demand emergency shelter. Random selection of the sample and its high (98%) participation rate virtually eliminated potential for bias within this sample. Another strength of this study is its focus on low-demand shelter users—a population that has not been well studied. This low-demand shelter-dwelling population of veterans experiencing homelessness is of interest because more substance-abuse problems and histories of incarceration seem to make them especially disadvantaged and challenged.
The limitation of the sample to users of a low-demand shelter at only 1 location may reduce generalizability to other veteran homeless populations and settings. The study also may not generalize to populations of female veterans experiencing homelessness. Another limitation of the study is that it did not use diagnostic assessments for psychiatric and substance use disorders and objective collateral information such as agency record data. Finally, although the limited size of the sample may have been insufficient to adequately test certain hypotheses, it was a relatively large sample of this population and was large enough to yield significant findings.
This study found that need-based factors predicted the use of some service sectors intended for those needs. For example, mental health functioning appropriately predicted any psychiatric service use, and presence of an alcohol problem appropriately predicted any substance abuse service use. Specifically for non-VA services, both cocaine use and presence of an alcohol problem in separate models predicted substance-abuse service use. However for VA substance-abuse services, neither cocaine use nor presence of an alcohol problem predicted service use. Despite the high need, very few veterans used substance-abuse services, and they rarely used VA substance-abuse services.
For 2 service sectors, need-based factors predicted the use of services intended for other needs. Cocaine use predicted non-VA psychiatric service use, and low mental health functioning predicted substance-abuse service use. One potential explanation for this finding could be that providers or patients incorrectly classified cocaine-related substance use problems as psychiatric. The VR-12 mental health functioning measure also may have incorrectly classified cocaine-related problems as psychiatric.
Three enabling factors predicted service use by sector and type. The first 2 are preference for VA-provided services and the geographic availability of services, which competed for veterans’ selection of service providers. When both VA and non-VA services were present in Fort Worth, a preference for VA-provided services was observed, with the exception of outpatient substance abuse services which were highly underutilized in general. No preference was observed for any non-VA services when both were present. When VA services were not present in Fort Worth, veterans used geographically available non-VA providers for some services, but for other services they used Dallas-based VA and Fort Worth-based non-VA providers equally (Table 3 and Table 4).
The third enabling factor influencing service use was through other service use as an enabling pathway. Those veterans who opted out of locally available services in favor of VA services in Dallas may have been prompted to do so by provider referrals, which were further facilitated by VA and public transportation between Fort Worth and Dallas. The most consistent enabling pathway was medical service use, which predicted all types of psychiatric service use (VA and non-VA combined, VA only, and non-VA only), and any substance-related service use. Psychiatric service use predicted substance abuse service use but only in non-VA settings; no pathways led from VA medical or psychiatric services to VA substance abuse services.
Conclusions
These findings suggest, in large part, the validity of the Andersen and Gelberg models of health care service use. Consistent with prior studies, need-based factors predicted the use of any psychiatric and substance-related sector services as well as the use of non-VA subcomponent services for both sectors. Also consistent with prior studies, enabling factors (medical sector service use) predicted service use, with the exception of VA or non-VA substance-abuse services. Unlike prior studies, however, predisposing factors (eg, age, race, marital status, and income) were not associated with service use.
This study could not determine why veterans underutilized substance-abuse services, even those available locally to them in Fort Worth. One possible barrier to care is that the services are designed or delivered in a manner that does not engage these veterans (eg, expectations regarding abstinence or service involvement). Another barrier could be that referral pathways between VA outpatient medical and psychiatric service providers and VA substance-related services are not sufficiently facilitative. Future investigations could build upon the findings of this study by collecting data that could help assess these potential barriers.
The data from this study suggest 3 opportunities to improve the utilization of services most needed by this population. The first opportunity would be to accurately differentiate between substance abuse and psychiatric problems in clinical assessment and identify the most appropriate type of care. Another opportunity, linked closely to the first, would be to facilitate more effective and efficient referral pathways among VA service sectors, especially from medical and psychiatric services to substance-abuse services. Another strategy to improve referral pathways would be for VA service networks to systematically examine local service systems for factors or processes that may disrupt integrated care and implement program improvements.28 For homeless veterans navigating an inherently complex VA health care system, peer-to-peer and patient navigator programs have helped improve service efficiency and service outcomes.29 The third opportunity to improve utilization of services would be to ensure geographic availability and accessibility by strategic placement of these services.
The results from this study, while informative, point directly to needed areas for further inquiry to inform public health response. Although the low-demand shelter users are a particularly challenging subgroup of veterans experiencing chronic homelessness, other equally challenging populations warrant additional study. For example, veterans outside of both VA and community services (eg, unsheltered populations) are likely to require different approaches to engage in appropriate services. Additionally, changes to the homeless policy implemented in the period after this sample was recruited suggest the need to revisit the service-using behaviors of this population. Finally, interventions developed as part of the national response need to be assessed for their ability to engage these difficult-to-reach veterans.
Acknowledgements
This study was funded by a U.S. Department of Veterans Affairs Office of Academic Affiliations Pre-Doctoral Social Work Research Fellowship award.
1. U.S. Department of Veterans Affairs. Homeless veterans: VA is working to end homelessness among veterans. U.S. Department of Veterans Affairs Website. www.va.gov/homeless/about_the_initiative.asp#one. Updated January 26, 2016. Accessed February 16, 2016.
2. Henry M, Cortes A, Morris S, Abt Associates; U. S. Department of Housing and Urban Development Office of Community Planning and Development. The 2013 Annual Homeless Assessment Report (AHAR) to Congress: Part 1 Point-in-Time Estimates of Homelessness. HUD Exchange Website. https://www.hudexchange.info/resources/documents/ahar-2013-part1.pdf. Published October 2014. Accessed February 16, 2016.
3. U.S. Department of Veterans Affairs. Homeless Veterans: Housing Assistance. U.S. Department of Veterans Affairs Web site. http://www.va.gov/homeless/housing.asp. Updated November 5, 2015. Accessed February 16, 2016.
4. Austin EL, Pollio DE, Holmes S, et al. VA's expansion of supportive housing: successes and challenges on the path to Housing First. Psychiatr Serv. 2014;65(5):641-647.
5. Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460.
6. Wenzel SL, Bakhtiar L, Caskey NH, et al. Homeless veterans utilization of medical, psychiatric, and substance abuse services. Med Care. 1995;33(11):1132-1144.
7. McQuire J, Gelberg L, Blue-Howells J, Rosenheck RA. Access to primary care for homeless veterans with serious mental health illness or substance abuse: a follow-up evaluation of co-located primary care and homeless social services. Adm Policy Ment Health. 2009;36(4):255-264.
8. Tsai J, Mares AS, Rosenheck RA. Do homeless veterans have the same needs and outcomes as non-veterans? Mil Med. 2012;177(1):27-31.
9. Andersen RM. A behavioral model of families use of health services: Research Series No. 25. Chicago, IL: University of Chicago Center for Health Administrative Studies; 1968.
10. Andersen RM. Revisiting the behavioral model and access to medical care: does it matter? J Health Soc Behav. 1995;36(1):1-10.
11. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
12. Gelberg L, Andersen RM, Leake BD. The Behavioral Model for Vulnerable Populations: application to medical care use and outcomes for homeless people. Health Serv Res. 2000;34(6):1273-1302.
13. Padgett D, Struening EL, Andrews H. Factors affecting the use of medical, mental health, alcohol, and drug treatment services by homeless adults. Med Care. 1990;28(9):805-821.
14. Stein JA, Andersen RM, Koegel P, Gelberg L. Predicting health services utilization among homeless adults: a prospective analysis. J Health Care Poor Underserved. 2000;11(2):212-230.
15. Gamache G, Rosenheck RA, Tessler R. Factors predicting choice of provider among homeless veterans with mental illness. Psychiatr Serv. 2000;51(8):1024-1028.
16. Wenzel SL, Audrey Burnam, M, Koegel P, et al. Access to inpatient or residential substance abuse treatment among homeless adults with alcohol or other drug use disorders. Med Care. 2001;39(11):1158-1169.
17. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
18. Solorio MR, Milburn NG, Andersen RM, Trifskin S, Rodríguez MA. Emotional distress and mental health service use among urban homeless adolescents. J Behav Health Serv Res. 2006;33(4):381-393.
19. Stein JA, Andersen RM, Robertson M, Gelberg L. Impact of hepatitis B and C infection on health services utilization in homeless adults: a test of the Gelberg-Anderson Behavioral Model for Vulnerable Populations. Health Psychol. 2012;31(1):20-30.
20. Linton KF, Shafer MS. Factors associated with the health service use of unsheltered, chronically homeless adults. Soc Work Public Health. 2013;29(1):73-80.
21. Petrovich JC, Pollio DE, North CS. Characteristics and service use of homeless veterans and nonveterans residing in a low-demand emergency shelter. Psych Serv. 2014;65(6):751-757.
22. U.S. Census Bureau. State & County Quick Facts: Fort Worth (city), Texas. U.S. Census Bureau Website. http://quickfacts.census.gov/qfd/states/48/4827000.html. Revised December 2, 2015. Accessed February 17, 2016.
23. Tarrant County Homeless Coalition. 2014 point in time count results. Tarrant County Homeless Coalition Website. http://www.ahomewithhope.org/staff/local-data-research/2014-homeless-count/. Accessed February 16, 2016.
24. North CS, Eyrich KM, Pollio DE, Foster DA, Cottler LB, Spitznagel EL. The Homeless Supplement to the Diagnostic Interview Schedule: test-retest analyses. Int J Method Psychiatr Res. 2004;13(3):184-191.
25. Iqbal SU, Rogers W, Selim A, et al. The Veterans RAND 12 Item Health Survey (VR-12): What it is and how it is Used. Washington, DC: Veterans Health Administration; 2009.
26. Fischer J, Corcoran K, eds. Measures for Clinical Practice and Research: A Sourcebook. 4th ed. New York, NY: Oxford University Press; 2013.
27. Selim AJ, Rogers W, Fleishman JA, Qian SX, Finke BG, Rothendler JA, Kazis LE. Updated U.S. population standard for the Veterans RAND 12-Item Health Survey (VR-12). Qual Life Res. 2009;18(1):43-52.
28. Blue-Howells J, McQuire J, Nakashima J. Co-location of health care services for homeless veterans: a case study of innovation in program implementation. Soc Work Health Care. 2008;47(3):219-231.
29. Piette JD, Holtz B, Beard AJ, et al; Ann Arbor PACT Steering Committee. Improving chronic illness care for veterans within the framework of the Patient-Centered Medical Home: experiences from the Ann Arbor Patient-Aligned Care Team Laboratory. Transl Behav Med. 2011;1(4):615-623.
1. U.S. Department of Veterans Affairs. Homeless veterans: VA is working to end homelessness among veterans. U.S. Department of Veterans Affairs Website. www.va.gov/homeless/about_the_initiative.asp#one. Updated January 26, 2016. Accessed February 16, 2016.
2. Henry M, Cortes A, Morris S, Abt Associates; U. S. Department of Housing and Urban Development Office of Community Planning and Development. The 2013 Annual Homeless Assessment Report (AHAR) to Congress: Part 1 Point-in-Time Estimates of Homelessness. HUD Exchange Website. https://www.hudexchange.info/resources/documents/ahar-2013-part1.pdf. Published October 2014. Accessed February 16, 2016.
3. U.S. Department of Veterans Affairs. Homeless Veterans: Housing Assistance. U.S. Department of Veterans Affairs Web site. http://www.va.gov/homeless/housing.asp. Updated November 5, 2015. Accessed February 16, 2016.
4. Austin EL, Pollio DE, Holmes S, et al. VA's expansion of supportive housing: successes and challenges on the path to Housing First. Psychiatr Serv. 2014;65(5):641-647.
5. Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460.
6. Wenzel SL, Bakhtiar L, Caskey NH, et al. Homeless veterans utilization of medical, psychiatric, and substance abuse services. Med Care. 1995;33(11):1132-1144.
7. McQuire J, Gelberg L, Blue-Howells J, Rosenheck RA. Access to primary care for homeless veterans with serious mental health illness or substance abuse: a follow-up evaluation of co-located primary care and homeless social services. Adm Policy Ment Health. 2009;36(4):255-264.
8. Tsai J, Mares AS, Rosenheck RA. Do homeless veterans have the same needs and outcomes as non-veterans? Mil Med. 2012;177(1):27-31.
9. Andersen RM. A behavioral model of families use of health services: Research Series No. 25. Chicago, IL: University of Chicago Center for Health Administrative Studies; 1968.
10. Andersen RM. Revisiting the behavioral model and access to medical care: does it matter? J Health Soc Behav. 1995;36(1):1-10.
11. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
12. Gelberg L, Andersen RM, Leake BD. The Behavioral Model for Vulnerable Populations: application to medical care use and outcomes for homeless people. Health Serv Res. 2000;34(6):1273-1302.
13. Padgett D, Struening EL, Andrews H. Factors affecting the use of medical, mental health, alcohol, and drug treatment services by homeless adults. Med Care. 1990;28(9):805-821.
14. Stein JA, Andersen RM, Koegel P, Gelberg L. Predicting health services utilization among homeless adults: a prospective analysis. J Health Care Poor Underserved. 2000;11(2):212-230.
15. Gamache G, Rosenheck RA, Tessler R. Factors predicting choice of provider among homeless veterans with mental illness. Psychiatr Serv. 2000;51(8):1024-1028.
16. Wenzel SL, Audrey Burnam, M, Koegel P, et al. Access to inpatient or residential substance abuse treatment among homeless adults with alcohol or other drug use disorders. Med Care. 2001;39(11):1158-1169.
17. Pollio DE, North CS, Eyrich KM, Foster DA, Spitznagel E. Modeling service access in a homeless population. J Psychoactive Drugs. 2003;35(4):487-495.
18. Solorio MR, Milburn NG, Andersen RM, Trifskin S, Rodríguez MA. Emotional distress and mental health service use among urban homeless adolescents. J Behav Health Serv Res. 2006;33(4):381-393.
19. Stein JA, Andersen RM, Robertson M, Gelberg L. Impact of hepatitis B and C infection on health services utilization in homeless adults: a test of the Gelberg-Anderson Behavioral Model for Vulnerable Populations. Health Psychol. 2012;31(1):20-30.
20. Linton KF, Shafer MS. Factors associated with the health service use of unsheltered, chronically homeless adults. Soc Work Public Health. 2013;29(1):73-80.
21. Petrovich JC, Pollio DE, North CS. Characteristics and service use of homeless veterans and nonveterans residing in a low-demand emergency shelter. Psych Serv. 2014;65(6):751-757.
22. U.S. Census Bureau. State & County Quick Facts: Fort Worth (city), Texas. U.S. Census Bureau Website. http://quickfacts.census.gov/qfd/states/48/4827000.html. Revised December 2, 2015. Accessed February 17, 2016.
23. Tarrant County Homeless Coalition. 2014 point in time count results. Tarrant County Homeless Coalition Website. http://www.ahomewithhope.org/staff/local-data-research/2014-homeless-count/. Accessed February 16, 2016.
24. North CS, Eyrich KM, Pollio DE, Foster DA, Cottler LB, Spitznagel EL. The Homeless Supplement to the Diagnostic Interview Schedule: test-retest analyses. Int J Method Psychiatr Res. 2004;13(3):184-191.
25. Iqbal SU, Rogers W, Selim A, et al. The Veterans RAND 12 Item Health Survey (VR-12): What it is and how it is Used. Washington, DC: Veterans Health Administration; 2009.
26. Fischer J, Corcoran K, eds. Measures for Clinical Practice and Research: A Sourcebook. 4th ed. New York, NY: Oxford University Press; 2013.
27. Selim AJ, Rogers W, Fleishman JA, Qian SX, Finke BG, Rothendler JA, Kazis LE. Updated U.S. population standard for the Veterans RAND 12-Item Health Survey (VR-12). Qual Life Res. 2009;18(1):43-52.
28. Blue-Howells J, McQuire J, Nakashima J. Co-location of health care services for homeless veterans: a case study of innovation in program implementation. Soc Work Health Care. 2008;47(3):219-231.
29. Piette JD, Holtz B, Beard AJ, et al; Ann Arbor PACT Steering Committee. Improving chronic illness care for veterans within the framework of the Patient-Centered Medical Home: experiences from the Ann Arbor Patient-Aligned Care Team Laboratory. Transl Behav Med. 2011;1(4):615-623.
A Mysterious Massive Hemorrhage
Faced with a patient who had a massive retroperitoneal hemorrhage, clinicians from Saint Vincent Hospital in Worcester, Massachusetts, had to decide whether the patient had multiple myeloma or plasma cell leukemia,
The patient, a 64-year-old woman, came to the emergency department (ED) with month-long worsening, debilitating lower back pain. She also had a low-grade fever, shortness of breath for about 3 weeks, and weight loss of 10 pounds.
One month earlier, she had visited the ED for right lower quadrant pain and was discharged with the diagnosis of diverticulitis. An abdominal computed tomography (CT) scan revealed incidental splenomegaly. When she next came to the ED, an abdominal examination revealed rigidity, distention, tender splenomegaly, and Grey Turner’s sign. A neurologic examination revealed weakness and numbness with hyperreflexia in her lower legs. Another CT scan showed that the splenomegaly had worsened, and magneting resonance imaging (MRI) showed a compressed spinal cord.
The patient was in severe hemorrhagic shock and was transferred to the intensive care unit. Based on the clinical and laboratory data, the clinicians excluded plasma cell leukemia, since the peripheral blood showed < 20% plasma cells—the major criterion for diagnosing the condition. In the absence of a bleeding disorder, vascular disease, and anticoagulation medications, the authors say their case illustrates a rare and aggressive form of multiple myeloma. The clinical presentation with major spontaneous bleeding is uncommon. In fact, they say, it’s the first time this type of presentation has been reported in the medical literature.
Source: Alawadhi A, Leb L. Case Rep Hematol. 2016;2016:1-3.
doi:10.1155/2016/8206826.
Faced with a patient who had a massive retroperitoneal hemorrhage, clinicians from Saint Vincent Hospital in Worcester, Massachusetts, had to decide whether the patient had multiple myeloma or plasma cell leukemia,
The patient, a 64-year-old woman, came to the emergency department (ED) with month-long worsening, debilitating lower back pain. She also had a low-grade fever, shortness of breath for about 3 weeks, and weight loss of 10 pounds.
One month earlier, she had visited the ED for right lower quadrant pain and was discharged with the diagnosis of diverticulitis. An abdominal computed tomography (CT) scan revealed incidental splenomegaly. When she next came to the ED, an abdominal examination revealed rigidity, distention, tender splenomegaly, and Grey Turner’s sign. A neurologic examination revealed weakness and numbness with hyperreflexia in her lower legs. Another CT scan showed that the splenomegaly had worsened, and magneting resonance imaging (MRI) showed a compressed spinal cord.
The patient was in severe hemorrhagic shock and was transferred to the intensive care unit. Based on the clinical and laboratory data, the clinicians excluded plasma cell leukemia, since the peripheral blood showed < 20% plasma cells—the major criterion for diagnosing the condition. In the absence of a bleeding disorder, vascular disease, and anticoagulation medications, the authors say their case illustrates a rare and aggressive form of multiple myeloma. The clinical presentation with major spontaneous bleeding is uncommon. In fact, they say, it’s the first time this type of presentation has been reported in the medical literature.
Source: Alawadhi A, Leb L. Case Rep Hematol. 2016;2016:1-3.
doi:10.1155/2016/8206826.
Faced with a patient who had a massive retroperitoneal hemorrhage, clinicians from Saint Vincent Hospital in Worcester, Massachusetts, had to decide whether the patient had multiple myeloma or plasma cell leukemia,
The patient, a 64-year-old woman, came to the emergency department (ED) with month-long worsening, debilitating lower back pain. She also had a low-grade fever, shortness of breath for about 3 weeks, and weight loss of 10 pounds.
One month earlier, she had visited the ED for right lower quadrant pain and was discharged with the diagnosis of diverticulitis. An abdominal computed tomography (CT) scan revealed incidental splenomegaly. When she next came to the ED, an abdominal examination revealed rigidity, distention, tender splenomegaly, and Grey Turner’s sign. A neurologic examination revealed weakness and numbness with hyperreflexia in her lower legs. Another CT scan showed that the splenomegaly had worsened, and magneting resonance imaging (MRI) showed a compressed spinal cord.
The patient was in severe hemorrhagic shock and was transferred to the intensive care unit. Based on the clinical and laboratory data, the clinicians excluded plasma cell leukemia, since the peripheral blood showed < 20% plasma cells—the major criterion for diagnosing the condition. In the absence of a bleeding disorder, vascular disease, and anticoagulation medications, the authors say their case illustrates a rare and aggressive form of multiple myeloma. The clinical presentation with major spontaneous bleeding is uncommon. In fact, they say, it’s the first time this type of presentation has been reported in the medical literature.
Source: Alawadhi A, Leb L. Case Rep Hematol. 2016;2016:1-3.
doi:10.1155/2016/8206826.
Diet and Atopic Dermatitis
Atopic dermatitis (AD) is the leading diagnosis among pediatric dermatologists,1 and this condition is commonly seen worldwide by dermatologists and allergists.2 There is a widespread misconception held by many patients and their guardians who believe that AD is caused by a food allergy.3 Although AD is related to and part of the atopic complex of disorders associated with food allergies, the role of diet in AD is not well defined. Previously it was recommended to delay early exposure to foods, but now it is recommended to do the opposite in certain situations. In fact, delaying exposure to certain types of foods can increase the likelihood of food allergies (eg, early exposure to peanut butter lowers the statistical chance of developing peanut allergies). This article reviews recent data on the role of diet in AD regarding disease activity as well as new and emerging data on dietary modifications for prevention and intervention. Emerging data on the relationship between AD and food allergies also are presented.
Pathogenesis of AD
The skin barrier plays a vital role in the prevention of pathogens, allergen exposure, and sensitization. There is no solitary root cause of AD, rather it is a combination of inflammation and barrier dysfunction associated with allergic diathesis (eg, atopy). Many patients with AD, especially those with persistent disease, have an intrinsic barrier dysfunction as part of the root cause of their illness, which may be caused by genetically mediated filaggrin defects or alternative barrier dysfunction such as decreased ceramide content that predisposes to percutaneous and mucosal sensitization.4,5 Another source of percutaneous exposure to allergens is macroscopic breaks in the skin caused by scratching, which allows dendritic termini of Langerhans cells to be exposed to percutaneous antigens4,6 through binding to high-affinity IgE receptors.
Langerhans cells exposed to allergens can trigger either an immediate or delayed-type (type I or type II) reaction (sensitization phase) in the lymph node causing inflammatory activation (elicitation). Inflammatory activity in AD is broad and complex and includes the release of IL-4, elevated IgE levels, and eosinophilia, which trigger the helper T cell TH2 and TH17 cascade of cytokines, including IL-2, IL-4, IL-5, IL-8, IL-10, IL-13, IL-17α, tumor necrosis factor α, and IFN-γ,7-9 with the latter worsening barrier defect via downregulation of intercellular substances (eg, filaggrin) and intercellular adhesion expression (eg, claudin 1).6,7,10
Atopic dermatitis does not exist in isolation. The barrier dysfunction associated with AD allows for sensitization to allergens, including those found in food and/or the environment. The atopic march, which occurs via barrier abnormalities facilitating sensitization, can result in further atopy, such as food allergies, environmental allergies, asthma, and eosinophilic esophagitis.11
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AD and Food Allergies
Many patients and guardians believe AD is caused by a food allergy and that diet restrictions will resolve the disease. Although the latter is not true, in reality many patients with AD do have food allergies. Approximately 40% of infants and young children with moderate to severe AD and 8% of the general population of children will manifest a specific IgE-based food allergy. Food-specific IgE can be triggered or exacerbated by AD through the induction of hives, cutaneous activation of mast cells, increased “spontaneous” basophil histamine release, and food-related lymphocyte-proliferative responses measurable by food patch testing.12 Allergists generally recommend avoidance of or use of heavily denatured food (in the case of a milk/egg allergy) in the setting of documented IgE-mediated allergens.13 Food allergies in AD can manifest with flares, hives, pruritus, and/or other cutaneous symptoms in the absence of flaring AD disease.
Guidelines from the American Academy of Dermatology (AAD)(Table) for the management of AD have recently recommended testing for food allergies in children younger than 5 years who have intractable AD or known food-induced reactions.14 This technique will largely identify children at risk for anaphylaxis but may not yield information contributing to AD improvement. Furthermore, withdrawal of allergens with known IgE-mediated response was classified by the AAD as having consistent good-quality patient-oriented evidence, and asking about allergic reactions as well as acting on a reported allergic history had inconsistent or limited-quality patient-oriented evidence. It is believed that atopy can progress, or march, into a food and/or environmental allergy at any point in life; therefore, testing for a food allergy should be considered in all patients with recent onset of severe and/or persistent AD and/or food-aggravated AD due to a lifetime risk of sensitization.14,15 A food introduction plan may require collaboration with an allergist, especially in high-risk patients (eg, those with known food reactions, family history of food allergies, severe atopy).
Prevention of AD Through Dietary Modification
The National Institute of Allergy and Infectious Diseases consensus group published guidelines on food allergies that affect AD management, including avoidance of proven allergens but not random elimination of food allergens in AD; the group identifies AD and family history of AD as risk factors for food allergies.16 The best data in support of avoidance of documented food allergens to reduce AD severity has been found for egg white allergy and avoidance. Active egg allergy also is linked to staphylococcal superantigen IgE sensitizations,17 but the reason for the link is not yet clear. For the pediatric population, exclusive breastfeeding until 4 to 6 months of age and introduction of solids within the first 4 to 6 months as well as avoidance of maternal dietary restriction during pregnancy and lactation was further endorsed, with use of hydrolyzed formulas as an alternative to exclusive breastfeeding in infants who are not exclusively breastfed (cost permitting).16,18
A Cochrane review of maternal dietary restrictions during pregnancy found no benefit of maternal prenatal dietary restriction on AD prevalence in the first 18 months of life but did note an association with lower mean gestational weight.19
There is currently an effort to produce foods, such as soybeans and corn, that are genetically modified to reduce exposure to the allergenic component, but it is possible that when large-scale challenges occur, these foods also will be allergenic.20,21 In the case of a modified apple, some promising reduction in allergy symptoms has been reported.22 Although genetically modified foods may benefit children with food allergies in the future, they are a source of some controversy.
Complementary and Alternative Medicine
The AAD guidelines do not recommend complementary and alternative medicine (CAM) to treat AD,14 but it remains a commonly used therapy in the United States. A 2014 analysis of data from the 2007 US-based national health interview survey of 9417 children (age range, 0–17 years) demonstrated that 46.9% of children used 1 or more CAM, of which 0.99% used CAM specifically for AD. In this study, herbal therapy, vitamins, homeopathy, diet, and movement techniques were associated with increased prevalence of AD.23 Although some herbals have been shown to be beneficial in AD,24 hepatotoxicity has been reported with some herbal therapies.25 Complementary techniques with evidence-based support include massage therapy,26 relocation to an alternative climate, acupuncture that rivals cetirizine in efficacy, and supportive nutritional advice.24,27
Factors Affecting the Incidence of AD
Atopic dermatitis is of greater prevalence in children in developed wealthy nations such as the United States, supporting the role of enhanced hygiene and overall good health through vaccination as a possible contributor to the rise in AD prevalence in the last 4 decades.28,29 Alternatively, viruses such as respiratory syncytial virus may trigger AD, suggesting vaccination against the virus may reduce the risk for AD.30 Overall, vaccination improves life expectancy and should be conducted on schedule without reservation. Other aspects of hygiene that could conceptually affect prevalence of AD are raw food ingestion and the effects of foodborne microbes on the intestinal microbiome in relationship to AD development. Probiotics have been tested for this purpose.
Probiotics and prebiotics have been theorized to work through a reduction in inflammation; these agents have some evidence in their favor, but they were not endorsed in the AAD guidelines14 despite showing promise in meta-analysis. In particular prenatal and postnatal (maternal and child) supplementation of Lactobacillus rhamnosus shows promise.31-33 Food elimination diets and supplements including vitamin D, selenium, fish oil, borage oil, and zinc were not found to be beneficial and were not recommended in the AAD guidelines.14,34
Percutaneous exposure to peanuts, possibly in household dust, may be the mechanism of peanut sensitization in AD27 via an inherent adjuvant effect of peanut protein.28 The recent LEAP (Learning Early About Peanut Allergy) trial randomized 530 infants aged 4 to 11 months to peanut-avoidant versus peanut-exposed diets for 60 months. The results showed statistically reduced (approximately one-twelfth of the risk) peanut allergy even in infants known to be sensitized (approximately one-third of the risk).35 It is now recommended in countries with a high prevalence of peanut allergies to introduce peanuts to an infant’s diet between 4 and 11 months of age (evidence level 1 [highest level of evidence]), with referral to an allergist for introduction in known sensitization cases and severe AD.36 In the setting of known or documented peanut allergy and for evaluation of potential food allergies, an allergist should be consulted.
Other interventions have been described as promising in mouse models. Those supplements include Lithospermum erythrorhizon,37Platycodon grandiflorus,38Hypsizygus marmoreous,39 fortified ginseng extract,40 polyunsaturated fatty acids,41 and galactooligosaccharide.42 Prebiotic oligosaccharides also are promising for early prevention of AD symptoms in infants, but otherwise these agents have remained largely untested in AD.43 None of these therapies have been endorsed by the AAD, and the long-term safety and efficacy in humans remains to be proven.
Risks of Dietary Restriction
Dietary restrictions in treating AD can have negative consequences, including reduced birth weight when initiated in pregnancy,19 osteomalacia from vitamin D deficiency,44 and nutritional deficiencies (eg, calcium, phosphorus, iron, vitamin K, vitamin D, zinc, vitamin A, B1, B2, B6, niacin, cholesterol, and/or vitamin C deficiencies).45 Excess dietary intake of vegetables in individuals with extensive food allergies can result in carotenemia.46 Protein-restricted diets from use of rice milk or dietary protein restriction can result in kwashiorkorlike protein malnutrition and marasmus.47-49 Nutritional counseling and/or supplementation is recommended for patients with food-restricted diets.
Avoiding Fragrance in Food
Food intolerance often is reported by AD patients. In allergies, food intolerance refers to side effects such as gastrointestinal symptoms; in dermatology, food intolerance can include itching, systemic flares of allergic contact dermatitis (eg, fragrance allergy), or true IgE-mediated allergies such as oral allergy syndrome. Oral allergy syndrome (pollen-food allergy syndrome) is an epitope-spread phenomenon related to an allergy to tree pollen, causing broad allergy to specific groups of fruits and nuts.50 Food triggers in AD include kiwi, milk, apple, tomato, citrus fruits, tree nuts, and peanuts. Oral allergy syndrome is common in food-sensitive AD patients (51.2%) followed by gastrointestinal symptoms (23.5%) and worsening AD (11.4%).51 Sensitization to fragrance can cross-react with foods (eg, balsam of Peru and tomatoes).52 A tomato allergy can be detected either by a skin-prick test or a food patch test in this setting.53 An allergist should be consulted if oral allergy syndrome is suspected.
Conclusion
Food allergies are more common in AD patients and patients should be referred to an allergist for evaluation and management. Strict dietary practice is not recommended, while avoiding proven food allergens in AD could be beneficial. Dermatologists should be aware that patients with dietary restrictions may lack key nutrients, manifesting with nutritional deficiencies in the skin; therefore, nutrition counseling may be needed in the most severe AD/allergy patients. This field is evolving; therefore, ongoing study and evaluation of interventions as they relate to AD will be needed to assess best practices for diet in AD over time.
1. Schachner L, Ling NS, Press S. A statistical analysis of a pediatric dermatology clinic. Pediatr Dermatol. 1983;1:157-164.
2. Kiprono SK, Muchunu JW, Masenga JE. Skin diseases in pediatric patients attending a tertiary dermatology hospital in Northern Tanzania: a cross-sectional study. BMC Dermatol. 2015;15:16.
3. Wensink M, Timmer C, Brand PL. Atopic dermatitis in infants not caused by food allergy [in Dutch]. Ned Tijdschr Geneeskd. 2008;152:4-9.
4. De Benedetto A, Kubo A, Beck LA. Skin barrier disruption: a requirement for allergen sensitization? J Invest Dermatol. 2012;132(3, pt 2):949-963.
5. Margolis DJ, Apter AJ, Gupta J, et al. The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort. J Allergy Clin Immunol. 2012;130:912-917.
6. Hanifin JM. Evolving concepts of pathogenesis in atopic dermatitis and other eczemas. J Invest Dermatol. 2009;129:320-322.
7. Batista DI, Perez L, Orfali RL, et al. Profile of skin barrier proteins (filaggrin, claudins 1 and 4) and Th1/Th2/Th17 cytokines in adults with atopic dermatitis. J Eur Acad Dermatol Venereol. 2015;29:1091-1095.
8. Kondo H, Ichikawa Y, Imokawa G. Percutaneous sensitization with allergens through barrier-disrupted skin elicits a Th2-dominant cytokine response. Eur J Immunol. 1998;28:769-779.
9. Correa da Rosa J, Malajian D, Shemer A, et al. Patients with atopic dermatitis have attenuated and distinct contact hypersensitivity responses to common allergens in skin. J Allergy Clin Immunol. 2015;135:712-720.
10. Paller AS. Latest approaches to treating atopic dermatitis. Chem Immunol Allergy. 2012;96:132-140.
11. Cianferoni A, Spergel J. Eosinophilic esophagitis: a comprehensive review [published online July 22, 2015]. Clin Rev Allergy Immunol. doi:10.1111/all.12846.
12. Sicherer SH, Sampson HA. Food hypersensitivity and atopic dermatitis; pathophysiology, epidemiology, diagnosis, and management. J Allergy Clin Immunol. 1999;104(3, pt 2):S114-S122.
13. Sicherer SH, Sampson HA. Food allergy: epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol. 2014;133:291-307.
14. Sidbury R, Tom WL, Bergman JN, et al. Guidelines of care for the management of atopic dermatitis: section 4. prevention of disease flares and use of adjunctive therapies and approaches. J Am Acad Dermatol. 2014;71:1218-1233.
15. Marenholz I, Rivera VA, Esparza-Gordillo J, et al. Association screening in the epidermal differentiation complex (EDC) identifies an SPRR3 repeat number variant as a risk factor for eczema. J Invest Dermatol. 2011;131:1644-1649.
16. Burks AW, Jones SM, Boyce JA, et al. NIAID-sponsored 2010 guidelines for managing food allergy: applications in the pediatric population. Pediatrics. 2011;128:955-965.
17. Ong PY. Association between egg and staphylococcal superantigen IgE sensitizations in atopic dermatitis. Allergy Asthma Proc. 2014;35:346-348.
18. Botteman M, Detzel P. Cost-effectiveness of partially hydrolyzed whey protein formula in the primary prevention of atopic dermatitis in high-risk urban infants in Southeast Asia. Ann Nutr Metab. 2015;66(suppl 1):26-32.
19. Kramer MS, Kakuma R. Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child. Cochrane Database Syst Rev. 2012;9:CD000133.
20. Yum HY, Lee SY, Lee KE, et al. Genetically modified and wild soybeans: an immunologic comparison. Allergy Asthma Proc. 2005;26:210-216.
21. Mathur C, Kathuria PC, Dahiya P, et al. Lack of detectable allergenicity in genetically modified maize containing “Cry” proteins as compared to native maize based on in silico & in vitro analysis. PLoS One. 2015;10:e0117340.
22. Dubois AE, Pagliarani G, Brouwer RM, et al. First successful reduction of clinical allergenicity of food by genetic modification: Mal d 1-silenced apples cause fewer allergy symptoms than the wild-type cultivar [published online July 24, 2015]. Allergy. 2015;70:1406-1412.
23. Silverberg JI, Lee-Wong M, Silverberg NB. Complementary and alternative medicines and childhood eczema: a US population-based study. Dermatitis. 2014;25:246-254.
24. Pfab F, Schalock PC, Napadow V, et al. Complementary integrative approach for treating pruritus. Dermatol Ther. 2013;26:149-156.
25. Stickel F, Shouval D. Hepatotoxicity of herbal and dietary supplements: an update. Arch Toxicol. 2015;89:851-865.
26. Schachner L, Field T, Hernandez-Reif M, et al. Atopic dermatitis symptoms decreased in children following massage therapy. Pediatr Dermatol. 1998;15:390-395.
27. Pfab F, Schalock PC, Napadow V, et al. Acupuncture for allergic disease therapy–the current state of evidence. Expert Rev Clin Immunol. 2014;10:831-841.
28. Silverberg JI, Hanifin JM. Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. J Allergy Clin Immunol. 2013;132:1132-1138.
29. Silverberg JI, Norowitz KB, Kleiman E, et al. Association between varicella zoster virus infection and atopic dermatitis in early and late childhood: a case-control study. J Allergy Clin Immunol. 2010;126:300-305.
30. Welliver RC, Wong DT, Sun M, et al. The development of respiratory syncytial virus-specific IgE and the release of histamine in nasopharyngeal secretions after infection. N Engl J Med. 1981;305:841-846.
31. Foolad N, Brezinski EA, Chase EP, et al. Effect of nutrient supplementation on atopic dermatitis in children: a systematic review of probiotics, prebiotics, formula, and fatty acids. JAMA Dermatol. 2013;149:350-355.
32. Kalliomäki M, Salminen S, Arvilommi H, et al. Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet. 2001;357:1076-1079.
33. Taylor AL, Dunstan JA, Prescott SL. Probiotic supplementation for the first 6 months of life fails to reduce the risk of atopic dermatitis and increases the risk of allergen sensitization in high-risk children: a randomized controlled trial. J Allergy Clin Immunol. 2007;119:184-191.
34. Bronsnick T, Murzaku EC, Rao BK. Diet in dermatology: part I: atopic dermatitis, acne, and nonmelanoma skin cancer. J Am Acad Dermatol. 2014;71:1039.e1-1039.e12.
35. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372:803-813.
36. Fleischer DM, Sicherer S, Greenhawt M, et al. Consensus communication on early peanut introduction and the prevention of peanut allergy in high-risk infants [published online October 2015]. Allergy. 2015;70:1193-1195.
37. Kim J, Cho Y. Gromwell (Lithospermum erythrorhizon) supplementation enhances epidermal levels of cera-mides, glucosylceramides, β-glucocerebrosidase, and acidicsphingomyelinase in NC/Nga mice. J Med Food. 2013;16:927-933.
38. Choi JH, Jin SW, Han EH, et al. Platycodon grandiflorum root-derived saponins attenuate atopic dermatitis-like skin lesions via suppression of NF-κB and STAT1 and activation of Nrf2/ARE-mediated heme oxygenase-1. Phytomedicine. 2014;21:1053-1061.
39. Kim T, Park K, Jung HS, et al. Evaluation of anti-atopic dermatitis activity of Hypsizigus marmoreus extract. Phytother Res. 2014;28:1539-1546.
40. Kim JR, Choi J, Kim J, et al. 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol-fortified ginseng extract attenuates the development of atopic dermatitis-like symptoms in NC/Nga mice. J Ethnopharmacol. 2014;151:365-371.
41. Weise C, Ernst D, van Tol EA, et al. Dietary polyunsaturated fatty acids and non-digestible oligosaccharides reduce dermatitis in mice. Pediatr Allergy Immunol. 2013;24:361-367.
42. Tanabe S, Hochi S. Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice. Int J Mol Med. 2010;25:331-336.
43. Arslanoglu S, Moro GE, Boehm G, et al. Early neutral prebiotic oligosaccharide supplementation reduces the incidence of some allergic manifestations in the first 5 years of life. J Biol Regul Homeost Agents. 2012;26(3 suppl):49-59.
44. Shikino K, Ikusaka M, Yamashita T. Vitamin D-deficient osteomalacia due to excessive self-restrictions for atopic dermatitis [published online July 4, 2014] . BMJ Case Rep.
45. Kim J, Kwon J, Noh G, et al. The effects of elimination diet on nutritional status in subjects with atopic dermatitis. Nutr Res Pract. 2013;7:488-494.
46. Silverberg NB, Lee-Wong M. Generalized yellow discoloration of the skin. Cutis. 2014;93:E11-E12.
47. Hon KL, Nip SY, Cheung KL. A tragic case of atopic eczema: malnutrition and infections despite multivitamins and supplements. Iran J Allergy Asthma Immunol. 2012;11:267-270.
48. Diamanti A, Pedicelli S, D’Argenio P, et al. Iatrogenic kwashiorkor in three infants on a diet of rice beverages. Pediatr Allergy Immunol. 2011;22:878-879.
49. Pillai K, Acharya S. Iatrogenic kwashiorkar. Indian Pediatr. 2010;47:540-541.
50. Price A, Ramachandran S, Smith GP, et al. Oral allergy syndrome (pollen-food allergy syndrome). Dermatitis. 2015;26:78-88.
51. Mattila L, Kilpeläinen M, Terho EO, et al. Food hypersensitivity among Finnish university students: association with atopic diseases. Clin Exp Allergy. 2003;33:600-606.
52. Paulsen E, Christensen LP, Andersen KE. Tomato contact dermatitis. Contact Dermatitis. 2012;67:321-327.
53. Di Leo E, Nettis E, Cardinale F, et al. Tomato atopy patch test in adult atopic dermatitis: diagnostic value and comparison among different methods. Allergy. 2009;64:659-663.
Atopic dermatitis (AD) is the leading diagnosis among pediatric dermatologists,1 and this condition is commonly seen worldwide by dermatologists and allergists.2 There is a widespread misconception held by many patients and their guardians who believe that AD is caused by a food allergy.3 Although AD is related to and part of the atopic complex of disorders associated with food allergies, the role of diet in AD is not well defined. Previously it was recommended to delay early exposure to foods, but now it is recommended to do the opposite in certain situations. In fact, delaying exposure to certain types of foods can increase the likelihood of food allergies (eg, early exposure to peanut butter lowers the statistical chance of developing peanut allergies). This article reviews recent data on the role of diet in AD regarding disease activity as well as new and emerging data on dietary modifications for prevention and intervention. Emerging data on the relationship between AD and food allergies also are presented.
Pathogenesis of AD
The skin barrier plays a vital role in the prevention of pathogens, allergen exposure, and sensitization. There is no solitary root cause of AD, rather it is a combination of inflammation and barrier dysfunction associated with allergic diathesis (eg, atopy). Many patients with AD, especially those with persistent disease, have an intrinsic barrier dysfunction as part of the root cause of their illness, which may be caused by genetically mediated filaggrin defects or alternative barrier dysfunction such as decreased ceramide content that predisposes to percutaneous and mucosal sensitization.4,5 Another source of percutaneous exposure to allergens is macroscopic breaks in the skin caused by scratching, which allows dendritic termini of Langerhans cells to be exposed to percutaneous antigens4,6 through binding to high-affinity IgE receptors.
Langerhans cells exposed to allergens can trigger either an immediate or delayed-type (type I or type II) reaction (sensitization phase) in the lymph node causing inflammatory activation (elicitation). Inflammatory activity in AD is broad and complex and includes the release of IL-4, elevated IgE levels, and eosinophilia, which trigger the helper T cell TH2 and TH17 cascade of cytokines, including IL-2, IL-4, IL-5, IL-8, IL-10, IL-13, IL-17α, tumor necrosis factor α, and IFN-γ,7-9 with the latter worsening barrier defect via downregulation of intercellular substances (eg, filaggrin) and intercellular adhesion expression (eg, claudin 1).6,7,10
Atopic dermatitis does not exist in isolation. The barrier dysfunction associated with AD allows for sensitization to allergens, including those found in food and/or the environment. The atopic march, which occurs via barrier abnormalities facilitating sensitization, can result in further atopy, such as food allergies, environmental allergies, asthma, and eosinophilic esophagitis.11
|
AD and Food Allergies
Many patients and guardians believe AD is caused by a food allergy and that diet restrictions will resolve the disease. Although the latter is not true, in reality many patients with AD do have food allergies. Approximately 40% of infants and young children with moderate to severe AD and 8% of the general population of children will manifest a specific IgE-based food allergy. Food-specific IgE can be triggered or exacerbated by AD through the induction of hives, cutaneous activation of mast cells, increased “spontaneous” basophil histamine release, and food-related lymphocyte-proliferative responses measurable by food patch testing.12 Allergists generally recommend avoidance of or use of heavily denatured food (in the case of a milk/egg allergy) in the setting of documented IgE-mediated allergens.13 Food allergies in AD can manifest with flares, hives, pruritus, and/or other cutaneous symptoms in the absence of flaring AD disease.
Guidelines from the American Academy of Dermatology (AAD)(Table) for the management of AD have recently recommended testing for food allergies in children younger than 5 years who have intractable AD or known food-induced reactions.14 This technique will largely identify children at risk for anaphylaxis but may not yield information contributing to AD improvement. Furthermore, withdrawal of allergens with known IgE-mediated response was classified by the AAD as having consistent good-quality patient-oriented evidence, and asking about allergic reactions as well as acting on a reported allergic history had inconsistent or limited-quality patient-oriented evidence. It is believed that atopy can progress, or march, into a food and/or environmental allergy at any point in life; therefore, testing for a food allergy should be considered in all patients with recent onset of severe and/or persistent AD and/or food-aggravated AD due to a lifetime risk of sensitization.14,15 A food introduction plan may require collaboration with an allergist, especially in high-risk patients (eg, those with known food reactions, family history of food allergies, severe atopy).
Prevention of AD Through Dietary Modification
The National Institute of Allergy and Infectious Diseases consensus group published guidelines on food allergies that affect AD management, including avoidance of proven allergens but not random elimination of food allergens in AD; the group identifies AD and family history of AD as risk factors for food allergies.16 The best data in support of avoidance of documented food allergens to reduce AD severity has been found for egg white allergy and avoidance. Active egg allergy also is linked to staphylococcal superantigen IgE sensitizations,17 but the reason for the link is not yet clear. For the pediatric population, exclusive breastfeeding until 4 to 6 months of age and introduction of solids within the first 4 to 6 months as well as avoidance of maternal dietary restriction during pregnancy and lactation was further endorsed, with use of hydrolyzed formulas as an alternative to exclusive breastfeeding in infants who are not exclusively breastfed (cost permitting).16,18
A Cochrane review of maternal dietary restrictions during pregnancy found no benefit of maternal prenatal dietary restriction on AD prevalence in the first 18 months of life but did note an association with lower mean gestational weight.19
There is currently an effort to produce foods, such as soybeans and corn, that are genetically modified to reduce exposure to the allergenic component, but it is possible that when large-scale challenges occur, these foods also will be allergenic.20,21 In the case of a modified apple, some promising reduction in allergy symptoms has been reported.22 Although genetically modified foods may benefit children with food allergies in the future, they are a source of some controversy.
Complementary and Alternative Medicine
The AAD guidelines do not recommend complementary and alternative medicine (CAM) to treat AD,14 but it remains a commonly used therapy in the United States. A 2014 analysis of data from the 2007 US-based national health interview survey of 9417 children (age range, 0–17 years) demonstrated that 46.9% of children used 1 or more CAM, of which 0.99% used CAM specifically for AD. In this study, herbal therapy, vitamins, homeopathy, diet, and movement techniques were associated with increased prevalence of AD.23 Although some herbals have been shown to be beneficial in AD,24 hepatotoxicity has been reported with some herbal therapies.25 Complementary techniques with evidence-based support include massage therapy,26 relocation to an alternative climate, acupuncture that rivals cetirizine in efficacy, and supportive nutritional advice.24,27
Factors Affecting the Incidence of AD
Atopic dermatitis is of greater prevalence in children in developed wealthy nations such as the United States, supporting the role of enhanced hygiene and overall good health through vaccination as a possible contributor to the rise in AD prevalence in the last 4 decades.28,29 Alternatively, viruses such as respiratory syncytial virus may trigger AD, suggesting vaccination against the virus may reduce the risk for AD.30 Overall, vaccination improves life expectancy and should be conducted on schedule without reservation. Other aspects of hygiene that could conceptually affect prevalence of AD are raw food ingestion and the effects of foodborne microbes on the intestinal microbiome in relationship to AD development. Probiotics have been tested for this purpose.
Probiotics and prebiotics have been theorized to work through a reduction in inflammation; these agents have some evidence in their favor, but they were not endorsed in the AAD guidelines14 despite showing promise in meta-analysis. In particular prenatal and postnatal (maternal and child) supplementation of Lactobacillus rhamnosus shows promise.31-33 Food elimination diets and supplements including vitamin D, selenium, fish oil, borage oil, and zinc were not found to be beneficial and were not recommended in the AAD guidelines.14,34
Percutaneous exposure to peanuts, possibly in household dust, may be the mechanism of peanut sensitization in AD27 via an inherent adjuvant effect of peanut protein.28 The recent LEAP (Learning Early About Peanut Allergy) trial randomized 530 infants aged 4 to 11 months to peanut-avoidant versus peanut-exposed diets for 60 months. The results showed statistically reduced (approximately one-twelfth of the risk) peanut allergy even in infants known to be sensitized (approximately one-third of the risk).35 It is now recommended in countries with a high prevalence of peanut allergies to introduce peanuts to an infant’s diet between 4 and 11 months of age (evidence level 1 [highest level of evidence]), with referral to an allergist for introduction in known sensitization cases and severe AD.36 In the setting of known or documented peanut allergy and for evaluation of potential food allergies, an allergist should be consulted.
Other interventions have been described as promising in mouse models. Those supplements include Lithospermum erythrorhizon,37Platycodon grandiflorus,38Hypsizygus marmoreous,39 fortified ginseng extract,40 polyunsaturated fatty acids,41 and galactooligosaccharide.42 Prebiotic oligosaccharides also are promising for early prevention of AD symptoms in infants, but otherwise these agents have remained largely untested in AD.43 None of these therapies have been endorsed by the AAD, and the long-term safety and efficacy in humans remains to be proven.
Risks of Dietary Restriction
Dietary restrictions in treating AD can have negative consequences, including reduced birth weight when initiated in pregnancy,19 osteomalacia from vitamin D deficiency,44 and nutritional deficiencies (eg, calcium, phosphorus, iron, vitamin K, vitamin D, zinc, vitamin A, B1, B2, B6, niacin, cholesterol, and/or vitamin C deficiencies).45 Excess dietary intake of vegetables in individuals with extensive food allergies can result in carotenemia.46 Protein-restricted diets from use of rice milk or dietary protein restriction can result in kwashiorkorlike protein malnutrition and marasmus.47-49 Nutritional counseling and/or supplementation is recommended for patients with food-restricted diets.
Avoiding Fragrance in Food
Food intolerance often is reported by AD patients. In allergies, food intolerance refers to side effects such as gastrointestinal symptoms; in dermatology, food intolerance can include itching, systemic flares of allergic contact dermatitis (eg, fragrance allergy), or true IgE-mediated allergies such as oral allergy syndrome. Oral allergy syndrome (pollen-food allergy syndrome) is an epitope-spread phenomenon related to an allergy to tree pollen, causing broad allergy to specific groups of fruits and nuts.50 Food triggers in AD include kiwi, milk, apple, tomato, citrus fruits, tree nuts, and peanuts. Oral allergy syndrome is common in food-sensitive AD patients (51.2%) followed by gastrointestinal symptoms (23.5%) and worsening AD (11.4%).51 Sensitization to fragrance can cross-react with foods (eg, balsam of Peru and tomatoes).52 A tomato allergy can be detected either by a skin-prick test or a food patch test in this setting.53 An allergist should be consulted if oral allergy syndrome is suspected.
Conclusion
Food allergies are more common in AD patients and patients should be referred to an allergist for evaluation and management. Strict dietary practice is not recommended, while avoiding proven food allergens in AD could be beneficial. Dermatologists should be aware that patients with dietary restrictions may lack key nutrients, manifesting with nutritional deficiencies in the skin; therefore, nutrition counseling may be needed in the most severe AD/allergy patients. This field is evolving; therefore, ongoing study and evaluation of interventions as they relate to AD will be needed to assess best practices for diet in AD over time.
Atopic dermatitis (AD) is the leading diagnosis among pediatric dermatologists,1 and this condition is commonly seen worldwide by dermatologists and allergists.2 There is a widespread misconception held by many patients and their guardians who believe that AD is caused by a food allergy.3 Although AD is related to and part of the atopic complex of disorders associated with food allergies, the role of diet in AD is not well defined. Previously it was recommended to delay early exposure to foods, but now it is recommended to do the opposite in certain situations. In fact, delaying exposure to certain types of foods can increase the likelihood of food allergies (eg, early exposure to peanut butter lowers the statistical chance of developing peanut allergies). This article reviews recent data on the role of diet in AD regarding disease activity as well as new and emerging data on dietary modifications for prevention and intervention. Emerging data on the relationship between AD and food allergies also are presented.
Pathogenesis of AD
The skin barrier plays a vital role in the prevention of pathogens, allergen exposure, and sensitization. There is no solitary root cause of AD, rather it is a combination of inflammation and barrier dysfunction associated with allergic diathesis (eg, atopy). Many patients with AD, especially those with persistent disease, have an intrinsic barrier dysfunction as part of the root cause of their illness, which may be caused by genetically mediated filaggrin defects or alternative barrier dysfunction such as decreased ceramide content that predisposes to percutaneous and mucosal sensitization.4,5 Another source of percutaneous exposure to allergens is macroscopic breaks in the skin caused by scratching, which allows dendritic termini of Langerhans cells to be exposed to percutaneous antigens4,6 through binding to high-affinity IgE receptors.
Langerhans cells exposed to allergens can trigger either an immediate or delayed-type (type I or type II) reaction (sensitization phase) in the lymph node causing inflammatory activation (elicitation). Inflammatory activity in AD is broad and complex and includes the release of IL-4, elevated IgE levels, and eosinophilia, which trigger the helper T cell TH2 and TH17 cascade of cytokines, including IL-2, IL-4, IL-5, IL-8, IL-10, IL-13, IL-17α, tumor necrosis factor α, and IFN-γ,7-9 with the latter worsening barrier defect via downregulation of intercellular substances (eg, filaggrin) and intercellular adhesion expression (eg, claudin 1).6,7,10
Atopic dermatitis does not exist in isolation. The barrier dysfunction associated with AD allows for sensitization to allergens, including those found in food and/or the environment. The atopic march, which occurs via barrier abnormalities facilitating sensitization, can result in further atopy, such as food allergies, environmental allergies, asthma, and eosinophilic esophagitis.11
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AD and Food Allergies
Many patients and guardians believe AD is caused by a food allergy and that diet restrictions will resolve the disease. Although the latter is not true, in reality many patients with AD do have food allergies. Approximately 40% of infants and young children with moderate to severe AD and 8% of the general population of children will manifest a specific IgE-based food allergy. Food-specific IgE can be triggered or exacerbated by AD through the induction of hives, cutaneous activation of mast cells, increased “spontaneous” basophil histamine release, and food-related lymphocyte-proliferative responses measurable by food patch testing.12 Allergists generally recommend avoidance of or use of heavily denatured food (in the case of a milk/egg allergy) in the setting of documented IgE-mediated allergens.13 Food allergies in AD can manifest with flares, hives, pruritus, and/or other cutaneous symptoms in the absence of flaring AD disease.
Guidelines from the American Academy of Dermatology (AAD)(Table) for the management of AD have recently recommended testing for food allergies in children younger than 5 years who have intractable AD or known food-induced reactions.14 This technique will largely identify children at risk for anaphylaxis but may not yield information contributing to AD improvement. Furthermore, withdrawal of allergens with known IgE-mediated response was classified by the AAD as having consistent good-quality patient-oriented evidence, and asking about allergic reactions as well as acting on a reported allergic history had inconsistent or limited-quality patient-oriented evidence. It is believed that atopy can progress, or march, into a food and/or environmental allergy at any point in life; therefore, testing for a food allergy should be considered in all patients with recent onset of severe and/or persistent AD and/or food-aggravated AD due to a lifetime risk of sensitization.14,15 A food introduction plan may require collaboration with an allergist, especially in high-risk patients (eg, those with known food reactions, family history of food allergies, severe atopy).
Prevention of AD Through Dietary Modification
The National Institute of Allergy and Infectious Diseases consensus group published guidelines on food allergies that affect AD management, including avoidance of proven allergens but not random elimination of food allergens in AD; the group identifies AD and family history of AD as risk factors for food allergies.16 The best data in support of avoidance of documented food allergens to reduce AD severity has been found for egg white allergy and avoidance. Active egg allergy also is linked to staphylococcal superantigen IgE sensitizations,17 but the reason for the link is not yet clear. For the pediatric population, exclusive breastfeeding until 4 to 6 months of age and introduction of solids within the first 4 to 6 months as well as avoidance of maternal dietary restriction during pregnancy and lactation was further endorsed, with use of hydrolyzed formulas as an alternative to exclusive breastfeeding in infants who are not exclusively breastfed (cost permitting).16,18
A Cochrane review of maternal dietary restrictions during pregnancy found no benefit of maternal prenatal dietary restriction on AD prevalence in the first 18 months of life but did note an association with lower mean gestational weight.19
There is currently an effort to produce foods, such as soybeans and corn, that are genetically modified to reduce exposure to the allergenic component, but it is possible that when large-scale challenges occur, these foods also will be allergenic.20,21 In the case of a modified apple, some promising reduction in allergy symptoms has been reported.22 Although genetically modified foods may benefit children with food allergies in the future, they are a source of some controversy.
Complementary and Alternative Medicine
The AAD guidelines do not recommend complementary and alternative medicine (CAM) to treat AD,14 but it remains a commonly used therapy in the United States. A 2014 analysis of data from the 2007 US-based national health interview survey of 9417 children (age range, 0–17 years) demonstrated that 46.9% of children used 1 or more CAM, of which 0.99% used CAM specifically for AD. In this study, herbal therapy, vitamins, homeopathy, diet, and movement techniques were associated with increased prevalence of AD.23 Although some herbals have been shown to be beneficial in AD,24 hepatotoxicity has been reported with some herbal therapies.25 Complementary techniques with evidence-based support include massage therapy,26 relocation to an alternative climate, acupuncture that rivals cetirizine in efficacy, and supportive nutritional advice.24,27
Factors Affecting the Incidence of AD
Atopic dermatitis is of greater prevalence in children in developed wealthy nations such as the United States, supporting the role of enhanced hygiene and overall good health through vaccination as a possible contributor to the rise in AD prevalence in the last 4 decades.28,29 Alternatively, viruses such as respiratory syncytial virus may trigger AD, suggesting vaccination against the virus may reduce the risk for AD.30 Overall, vaccination improves life expectancy and should be conducted on schedule without reservation. Other aspects of hygiene that could conceptually affect prevalence of AD are raw food ingestion and the effects of foodborne microbes on the intestinal microbiome in relationship to AD development. Probiotics have been tested for this purpose.
Probiotics and prebiotics have been theorized to work through a reduction in inflammation; these agents have some evidence in their favor, but they were not endorsed in the AAD guidelines14 despite showing promise in meta-analysis. In particular prenatal and postnatal (maternal and child) supplementation of Lactobacillus rhamnosus shows promise.31-33 Food elimination diets and supplements including vitamin D, selenium, fish oil, borage oil, and zinc were not found to be beneficial and were not recommended in the AAD guidelines.14,34
Percutaneous exposure to peanuts, possibly in household dust, may be the mechanism of peanut sensitization in AD27 via an inherent adjuvant effect of peanut protein.28 The recent LEAP (Learning Early About Peanut Allergy) trial randomized 530 infants aged 4 to 11 months to peanut-avoidant versus peanut-exposed diets for 60 months. The results showed statistically reduced (approximately one-twelfth of the risk) peanut allergy even in infants known to be sensitized (approximately one-third of the risk).35 It is now recommended in countries with a high prevalence of peanut allergies to introduce peanuts to an infant’s diet between 4 and 11 months of age (evidence level 1 [highest level of evidence]), with referral to an allergist for introduction in known sensitization cases and severe AD.36 In the setting of known or documented peanut allergy and for evaluation of potential food allergies, an allergist should be consulted.
Other interventions have been described as promising in mouse models. Those supplements include Lithospermum erythrorhizon,37Platycodon grandiflorus,38Hypsizygus marmoreous,39 fortified ginseng extract,40 polyunsaturated fatty acids,41 and galactooligosaccharide.42 Prebiotic oligosaccharides also are promising for early prevention of AD symptoms in infants, but otherwise these agents have remained largely untested in AD.43 None of these therapies have been endorsed by the AAD, and the long-term safety and efficacy in humans remains to be proven.
Risks of Dietary Restriction
Dietary restrictions in treating AD can have negative consequences, including reduced birth weight when initiated in pregnancy,19 osteomalacia from vitamin D deficiency,44 and nutritional deficiencies (eg, calcium, phosphorus, iron, vitamin K, vitamin D, zinc, vitamin A, B1, B2, B6, niacin, cholesterol, and/or vitamin C deficiencies).45 Excess dietary intake of vegetables in individuals with extensive food allergies can result in carotenemia.46 Protein-restricted diets from use of rice milk or dietary protein restriction can result in kwashiorkorlike protein malnutrition and marasmus.47-49 Nutritional counseling and/or supplementation is recommended for patients with food-restricted diets.
Avoiding Fragrance in Food
Food intolerance often is reported by AD patients. In allergies, food intolerance refers to side effects such as gastrointestinal symptoms; in dermatology, food intolerance can include itching, systemic flares of allergic contact dermatitis (eg, fragrance allergy), or true IgE-mediated allergies such as oral allergy syndrome. Oral allergy syndrome (pollen-food allergy syndrome) is an epitope-spread phenomenon related to an allergy to tree pollen, causing broad allergy to specific groups of fruits and nuts.50 Food triggers in AD include kiwi, milk, apple, tomato, citrus fruits, tree nuts, and peanuts. Oral allergy syndrome is common in food-sensitive AD patients (51.2%) followed by gastrointestinal symptoms (23.5%) and worsening AD (11.4%).51 Sensitization to fragrance can cross-react with foods (eg, balsam of Peru and tomatoes).52 A tomato allergy can be detected either by a skin-prick test or a food patch test in this setting.53 An allergist should be consulted if oral allergy syndrome is suspected.
Conclusion
Food allergies are more common in AD patients and patients should be referred to an allergist for evaluation and management. Strict dietary practice is not recommended, while avoiding proven food allergens in AD could be beneficial. Dermatologists should be aware that patients with dietary restrictions may lack key nutrients, manifesting with nutritional deficiencies in the skin; therefore, nutrition counseling may be needed in the most severe AD/allergy patients. This field is evolving; therefore, ongoing study and evaluation of interventions as they relate to AD will be needed to assess best practices for diet in AD over time.
1. Schachner L, Ling NS, Press S. A statistical analysis of a pediatric dermatology clinic. Pediatr Dermatol. 1983;1:157-164.
2. Kiprono SK, Muchunu JW, Masenga JE. Skin diseases in pediatric patients attending a tertiary dermatology hospital in Northern Tanzania: a cross-sectional study. BMC Dermatol. 2015;15:16.
3. Wensink M, Timmer C, Brand PL. Atopic dermatitis in infants not caused by food allergy [in Dutch]. Ned Tijdschr Geneeskd. 2008;152:4-9.
4. De Benedetto A, Kubo A, Beck LA. Skin barrier disruption: a requirement for allergen sensitization? J Invest Dermatol. 2012;132(3, pt 2):949-963.
5. Margolis DJ, Apter AJ, Gupta J, et al. The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort. J Allergy Clin Immunol. 2012;130:912-917.
6. Hanifin JM. Evolving concepts of pathogenesis in atopic dermatitis and other eczemas. J Invest Dermatol. 2009;129:320-322.
7. Batista DI, Perez L, Orfali RL, et al. Profile of skin barrier proteins (filaggrin, claudins 1 and 4) and Th1/Th2/Th17 cytokines in adults with atopic dermatitis. J Eur Acad Dermatol Venereol. 2015;29:1091-1095.
8. Kondo H, Ichikawa Y, Imokawa G. Percutaneous sensitization with allergens through barrier-disrupted skin elicits a Th2-dominant cytokine response. Eur J Immunol. 1998;28:769-779.
9. Correa da Rosa J, Malajian D, Shemer A, et al. Patients with atopic dermatitis have attenuated and distinct contact hypersensitivity responses to common allergens in skin. J Allergy Clin Immunol. 2015;135:712-720.
10. Paller AS. Latest approaches to treating atopic dermatitis. Chem Immunol Allergy. 2012;96:132-140.
11. Cianferoni A, Spergel J. Eosinophilic esophagitis: a comprehensive review [published online July 22, 2015]. Clin Rev Allergy Immunol. doi:10.1111/all.12846.
12. Sicherer SH, Sampson HA. Food hypersensitivity and atopic dermatitis; pathophysiology, epidemiology, diagnosis, and management. J Allergy Clin Immunol. 1999;104(3, pt 2):S114-S122.
13. Sicherer SH, Sampson HA. Food allergy: epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol. 2014;133:291-307.
14. Sidbury R, Tom WL, Bergman JN, et al. Guidelines of care for the management of atopic dermatitis: section 4. prevention of disease flares and use of adjunctive therapies and approaches. J Am Acad Dermatol. 2014;71:1218-1233.
15. Marenholz I, Rivera VA, Esparza-Gordillo J, et al. Association screening in the epidermal differentiation complex (EDC) identifies an SPRR3 repeat number variant as a risk factor for eczema. J Invest Dermatol. 2011;131:1644-1649.
16. Burks AW, Jones SM, Boyce JA, et al. NIAID-sponsored 2010 guidelines for managing food allergy: applications in the pediatric population. Pediatrics. 2011;128:955-965.
17. Ong PY. Association between egg and staphylococcal superantigen IgE sensitizations in atopic dermatitis. Allergy Asthma Proc. 2014;35:346-348.
18. Botteman M, Detzel P. Cost-effectiveness of partially hydrolyzed whey protein formula in the primary prevention of atopic dermatitis in high-risk urban infants in Southeast Asia. Ann Nutr Metab. 2015;66(suppl 1):26-32.
19. Kramer MS, Kakuma R. Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child. Cochrane Database Syst Rev. 2012;9:CD000133.
20. Yum HY, Lee SY, Lee KE, et al. Genetically modified and wild soybeans: an immunologic comparison. Allergy Asthma Proc. 2005;26:210-216.
21. Mathur C, Kathuria PC, Dahiya P, et al. Lack of detectable allergenicity in genetically modified maize containing “Cry” proteins as compared to native maize based on in silico & in vitro analysis. PLoS One. 2015;10:e0117340.
22. Dubois AE, Pagliarani G, Brouwer RM, et al. First successful reduction of clinical allergenicity of food by genetic modification: Mal d 1-silenced apples cause fewer allergy symptoms than the wild-type cultivar [published online July 24, 2015]. Allergy. 2015;70:1406-1412.
23. Silverberg JI, Lee-Wong M, Silverberg NB. Complementary and alternative medicines and childhood eczema: a US population-based study. Dermatitis. 2014;25:246-254.
24. Pfab F, Schalock PC, Napadow V, et al. Complementary integrative approach for treating pruritus. Dermatol Ther. 2013;26:149-156.
25. Stickel F, Shouval D. Hepatotoxicity of herbal and dietary supplements: an update. Arch Toxicol. 2015;89:851-865.
26. Schachner L, Field T, Hernandez-Reif M, et al. Atopic dermatitis symptoms decreased in children following massage therapy. Pediatr Dermatol. 1998;15:390-395.
27. Pfab F, Schalock PC, Napadow V, et al. Acupuncture for allergic disease therapy–the current state of evidence. Expert Rev Clin Immunol. 2014;10:831-841.
28. Silverberg JI, Hanifin JM. Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. J Allergy Clin Immunol. 2013;132:1132-1138.
29. Silverberg JI, Norowitz KB, Kleiman E, et al. Association between varicella zoster virus infection and atopic dermatitis in early and late childhood: a case-control study. J Allergy Clin Immunol. 2010;126:300-305.
30. Welliver RC, Wong DT, Sun M, et al. The development of respiratory syncytial virus-specific IgE and the release of histamine in nasopharyngeal secretions after infection. N Engl J Med. 1981;305:841-846.
31. Foolad N, Brezinski EA, Chase EP, et al. Effect of nutrient supplementation on atopic dermatitis in children: a systematic review of probiotics, prebiotics, formula, and fatty acids. JAMA Dermatol. 2013;149:350-355.
32. Kalliomäki M, Salminen S, Arvilommi H, et al. Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet. 2001;357:1076-1079.
33. Taylor AL, Dunstan JA, Prescott SL. Probiotic supplementation for the first 6 months of life fails to reduce the risk of atopic dermatitis and increases the risk of allergen sensitization in high-risk children: a randomized controlled trial. J Allergy Clin Immunol. 2007;119:184-191.
34. Bronsnick T, Murzaku EC, Rao BK. Diet in dermatology: part I: atopic dermatitis, acne, and nonmelanoma skin cancer. J Am Acad Dermatol. 2014;71:1039.e1-1039.e12.
35. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372:803-813.
36. Fleischer DM, Sicherer S, Greenhawt M, et al. Consensus communication on early peanut introduction and the prevention of peanut allergy in high-risk infants [published online October 2015]. Allergy. 2015;70:1193-1195.
37. Kim J, Cho Y. Gromwell (Lithospermum erythrorhizon) supplementation enhances epidermal levels of cera-mides, glucosylceramides, β-glucocerebrosidase, and acidicsphingomyelinase in NC/Nga mice. J Med Food. 2013;16:927-933.
38. Choi JH, Jin SW, Han EH, et al. Platycodon grandiflorum root-derived saponins attenuate atopic dermatitis-like skin lesions via suppression of NF-κB and STAT1 and activation of Nrf2/ARE-mediated heme oxygenase-1. Phytomedicine. 2014;21:1053-1061.
39. Kim T, Park K, Jung HS, et al. Evaluation of anti-atopic dermatitis activity of Hypsizigus marmoreus extract. Phytother Res. 2014;28:1539-1546.
40. Kim JR, Choi J, Kim J, et al. 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol-fortified ginseng extract attenuates the development of atopic dermatitis-like symptoms in NC/Nga mice. J Ethnopharmacol. 2014;151:365-371.
41. Weise C, Ernst D, van Tol EA, et al. Dietary polyunsaturated fatty acids and non-digestible oligosaccharides reduce dermatitis in mice. Pediatr Allergy Immunol. 2013;24:361-367.
42. Tanabe S, Hochi S. Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice. Int J Mol Med. 2010;25:331-336.
43. Arslanoglu S, Moro GE, Boehm G, et al. Early neutral prebiotic oligosaccharide supplementation reduces the incidence of some allergic manifestations in the first 5 years of life. J Biol Regul Homeost Agents. 2012;26(3 suppl):49-59.
44. Shikino K, Ikusaka M, Yamashita T. Vitamin D-deficient osteomalacia due to excessive self-restrictions for atopic dermatitis [published online July 4, 2014] . BMJ Case Rep.
45. Kim J, Kwon J, Noh G, et al. The effects of elimination diet on nutritional status in subjects with atopic dermatitis. Nutr Res Pract. 2013;7:488-494.
46. Silverberg NB, Lee-Wong M. Generalized yellow discoloration of the skin. Cutis. 2014;93:E11-E12.
47. Hon KL, Nip SY, Cheung KL. A tragic case of atopic eczema: malnutrition and infections despite multivitamins and supplements. Iran J Allergy Asthma Immunol. 2012;11:267-270.
48. Diamanti A, Pedicelli S, D’Argenio P, et al. Iatrogenic kwashiorkor in three infants on a diet of rice beverages. Pediatr Allergy Immunol. 2011;22:878-879.
49. Pillai K, Acharya S. Iatrogenic kwashiorkar. Indian Pediatr. 2010;47:540-541.
50. Price A, Ramachandran S, Smith GP, et al. Oral allergy syndrome (pollen-food allergy syndrome). Dermatitis. 2015;26:78-88.
51. Mattila L, Kilpeläinen M, Terho EO, et al. Food hypersensitivity among Finnish university students: association with atopic diseases. Clin Exp Allergy. 2003;33:600-606.
52. Paulsen E, Christensen LP, Andersen KE. Tomato contact dermatitis. Contact Dermatitis. 2012;67:321-327.
53. Di Leo E, Nettis E, Cardinale F, et al. Tomato atopy patch test in adult atopic dermatitis: diagnostic value and comparison among different methods. Allergy. 2009;64:659-663.
1. Schachner L, Ling NS, Press S. A statistical analysis of a pediatric dermatology clinic. Pediatr Dermatol. 1983;1:157-164.
2. Kiprono SK, Muchunu JW, Masenga JE. Skin diseases in pediatric patients attending a tertiary dermatology hospital in Northern Tanzania: a cross-sectional study. BMC Dermatol. 2015;15:16.
3. Wensink M, Timmer C, Brand PL. Atopic dermatitis in infants not caused by food allergy [in Dutch]. Ned Tijdschr Geneeskd. 2008;152:4-9.
4. De Benedetto A, Kubo A, Beck LA. Skin barrier disruption: a requirement for allergen sensitization? J Invest Dermatol. 2012;132(3, pt 2):949-963.
5. Margolis DJ, Apter AJ, Gupta J, et al. The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort. J Allergy Clin Immunol. 2012;130:912-917.
6. Hanifin JM. Evolving concepts of pathogenesis in atopic dermatitis and other eczemas. J Invest Dermatol. 2009;129:320-322.
7. Batista DI, Perez L, Orfali RL, et al. Profile of skin barrier proteins (filaggrin, claudins 1 and 4) and Th1/Th2/Th17 cytokines in adults with atopic dermatitis. J Eur Acad Dermatol Venereol. 2015;29:1091-1095.
8. Kondo H, Ichikawa Y, Imokawa G. Percutaneous sensitization with allergens through barrier-disrupted skin elicits a Th2-dominant cytokine response. Eur J Immunol. 1998;28:769-779.
9. Correa da Rosa J, Malajian D, Shemer A, et al. Patients with atopic dermatitis have attenuated and distinct contact hypersensitivity responses to common allergens in skin. J Allergy Clin Immunol. 2015;135:712-720.
10. Paller AS. Latest approaches to treating atopic dermatitis. Chem Immunol Allergy. 2012;96:132-140.
11. Cianferoni A, Spergel J. Eosinophilic esophagitis: a comprehensive review [published online July 22, 2015]. Clin Rev Allergy Immunol. doi:10.1111/all.12846.
12. Sicherer SH, Sampson HA. Food hypersensitivity and atopic dermatitis; pathophysiology, epidemiology, diagnosis, and management. J Allergy Clin Immunol. 1999;104(3, pt 2):S114-S122.
13. Sicherer SH, Sampson HA. Food allergy: epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol. 2014;133:291-307.
14. Sidbury R, Tom WL, Bergman JN, et al. Guidelines of care for the management of atopic dermatitis: section 4. prevention of disease flares and use of adjunctive therapies and approaches. J Am Acad Dermatol. 2014;71:1218-1233.
15. Marenholz I, Rivera VA, Esparza-Gordillo J, et al. Association screening in the epidermal differentiation complex (EDC) identifies an SPRR3 repeat number variant as a risk factor for eczema. J Invest Dermatol. 2011;131:1644-1649.
16. Burks AW, Jones SM, Boyce JA, et al. NIAID-sponsored 2010 guidelines for managing food allergy: applications in the pediatric population. Pediatrics. 2011;128:955-965.
17. Ong PY. Association between egg and staphylococcal superantigen IgE sensitizations in atopic dermatitis. Allergy Asthma Proc. 2014;35:346-348.
18. Botteman M, Detzel P. Cost-effectiveness of partially hydrolyzed whey protein formula in the primary prevention of atopic dermatitis in high-risk urban infants in Southeast Asia. Ann Nutr Metab. 2015;66(suppl 1):26-32.
19. Kramer MS, Kakuma R. Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child. Cochrane Database Syst Rev. 2012;9:CD000133.
20. Yum HY, Lee SY, Lee KE, et al. Genetically modified and wild soybeans: an immunologic comparison. Allergy Asthma Proc. 2005;26:210-216.
21. Mathur C, Kathuria PC, Dahiya P, et al. Lack of detectable allergenicity in genetically modified maize containing “Cry” proteins as compared to native maize based on in silico & in vitro analysis. PLoS One. 2015;10:e0117340.
22. Dubois AE, Pagliarani G, Brouwer RM, et al. First successful reduction of clinical allergenicity of food by genetic modification: Mal d 1-silenced apples cause fewer allergy symptoms than the wild-type cultivar [published online July 24, 2015]. Allergy. 2015;70:1406-1412.
23. Silverberg JI, Lee-Wong M, Silverberg NB. Complementary and alternative medicines and childhood eczema: a US population-based study. Dermatitis. 2014;25:246-254.
24. Pfab F, Schalock PC, Napadow V, et al. Complementary integrative approach for treating pruritus. Dermatol Ther. 2013;26:149-156.
25. Stickel F, Shouval D. Hepatotoxicity of herbal and dietary supplements: an update. Arch Toxicol. 2015;89:851-865.
26. Schachner L, Field T, Hernandez-Reif M, et al. Atopic dermatitis symptoms decreased in children following massage therapy. Pediatr Dermatol. 1998;15:390-395.
27. Pfab F, Schalock PC, Napadow V, et al. Acupuncture for allergic disease therapy–the current state of evidence. Expert Rev Clin Immunol. 2014;10:831-841.
28. Silverberg JI, Hanifin JM. Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. J Allergy Clin Immunol. 2013;132:1132-1138.
29. Silverberg JI, Norowitz KB, Kleiman E, et al. Association between varicella zoster virus infection and atopic dermatitis in early and late childhood: a case-control study. J Allergy Clin Immunol. 2010;126:300-305.
30. Welliver RC, Wong DT, Sun M, et al. The development of respiratory syncytial virus-specific IgE and the release of histamine in nasopharyngeal secretions after infection. N Engl J Med. 1981;305:841-846.
31. Foolad N, Brezinski EA, Chase EP, et al. Effect of nutrient supplementation on atopic dermatitis in children: a systematic review of probiotics, prebiotics, formula, and fatty acids. JAMA Dermatol. 2013;149:350-355.
32. Kalliomäki M, Salminen S, Arvilommi H, et al. Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet. 2001;357:1076-1079.
33. Taylor AL, Dunstan JA, Prescott SL. Probiotic supplementation for the first 6 months of life fails to reduce the risk of atopic dermatitis and increases the risk of allergen sensitization in high-risk children: a randomized controlled trial. J Allergy Clin Immunol. 2007;119:184-191.
34. Bronsnick T, Murzaku EC, Rao BK. Diet in dermatology: part I: atopic dermatitis, acne, and nonmelanoma skin cancer. J Am Acad Dermatol. 2014;71:1039.e1-1039.e12.
35. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372:803-813.
36. Fleischer DM, Sicherer S, Greenhawt M, et al. Consensus communication on early peanut introduction and the prevention of peanut allergy in high-risk infants [published online October 2015]. Allergy. 2015;70:1193-1195.
37. Kim J, Cho Y. Gromwell (Lithospermum erythrorhizon) supplementation enhances epidermal levels of cera-mides, glucosylceramides, β-glucocerebrosidase, and acidicsphingomyelinase in NC/Nga mice. J Med Food. 2013;16:927-933.
38. Choi JH, Jin SW, Han EH, et al. Platycodon grandiflorum root-derived saponins attenuate atopic dermatitis-like skin lesions via suppression of NF-κB and STAT1 and activation of Nrf2/ARE-mediated heme oxygenase-1. Phytomedicine. 2014;21:1053-1061.
39. Kim T, Park K, Jung HS, et al. Evaluation of anti-atopic dermatitis activity of Hypsizigus marmoreus extract. Phytother Res. 2014;28:1539-1546.
40. Kim JR, Choi J, Kim J, et al. 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol-fortified ginseng extract attenuates the development of atopic dermatitis-like symptoms in NC/Nga mice. J Ethnopharmacol. 2014;151:365-371.
41. Weise C, Ernst D, van Tol EA, et al. Dietary polyunsaturated fatty acids and non-digestible oligosaccharides reduce dermatitis in mice. Pediatr Allergy Immunol. 2013;24:361-367.
42. Tanabe S, Hochi S. Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice. Int J Mol Med. 2010;25:331-336.
43. Arslanoglu S, Moro GE, Boehm G, et al. Early neutral prebiotic oligosaccharide supplementation reduces the incidence of some allergic manifestations in the first 5 years of life. J Biol Regul Homeost Agents. 2012;26(3 suppl):49-59.
44. Shikino K, Ikusaka M, Yamashita T. Vitamin D-deficient osteomalacia due to excessive self-restrictions for atopic dermatitis [published online July 4, 2014] . BMJ Case Rep.
45. Kim J, Kwon J, Noh G, et al. The effects of elimination diet on nutritional status in subjects with atopic dermatitis. Nutr Res Pract. 2013;7:488-494.
46. Silverberg NB, Lee-Wong M. Generalized yellow discoloration of the skin. Cutis. 2014;93:E11-E12.
47. Hon KL, Nip SY, Cheung KL. A tragic case of atopic eczema: malnutrition and infections despite multivitamins and supplements. Iran J Allergy Asthma Immunol. 2012;11:267-270.
48. Diamanti A, Pedicelli S, D’Argenio P, et al. Iatrogenic kwashiorkor in three infants on a diet of rice beverages. Pediatr Allergy Immunol. 2011;22:878-879.
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50. Price A, Ramachandran S, Smith GP, et al. Oral allergy syndrome (pollen-food allergy syndrome). Dermatitis. 2015;26:78-88.
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52. Paulsen E, Christensen LP, Andersen KE. Tomato contact dermatitis. Contact Dermatitis. 2012;67:321-327.
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Practice Points
- Test children younger than 5 years with moderate to severe atopic dermatitis (AD) for food allergies if they have persistently severe AD or known food-induced reactions.
- Food elimination diets are not recommended for management of AD.
- There is not enough evidence supporting the use of complementary and alternative medicine, probiotics/prebiotics, or supplements for the treatment of AD.