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Grand Rounds: Girl, 6, With Facial Weakness
A 6-year-old girl was brought to a pediatric emergency department (ED) in Atlanta by her mother. The mother stated that during the previous hour, she had noticed that her daughter’s face seemed weaker on the right side.
The night before, the child had said, “I can’t blink my eye”; when her mother asked her to demonstrate, the child seemed to be able to blink both eyes appropriately, and she had no further complaints. The next morning, the child complained of the light being too bright and asked to wear her mother’s sunglasses. In the course of the day, she continued to complain of eye discomfort, which she described as “stinging” and “sore.” The mother could see nothing abnormal, but by late afternoon noticed that her daughter’s smile and facial movements were asymmetrical. She immediately took her to the pediatric ED.
The child had no significant medical history and no surgical history. Her vaccination schedule was current, and she denied any recent illnesses. The mother could recall no exposures to infections or tick bites, no rashes, and no trauma to the face or head. The mother and child were visiting Atlanta from northeastern Florida.
The review of systems was negative for headache, fever, chills, rash, earache, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite or disposition. The child was afebrile, and the other vital signs were within normal limits.
Physical examination revealed an alert child who was calm and conversant. Her height was 45” and weight, 43 lb. Otoscopic exam showed normal ears and tympanic membranes with no sign of otitis media or ear pathology. No throat redness, tonsillar enlargement, or lymphadenopathies were noted. Breath sounds were clear, and heart rhythm and rate were regular without murmur.
The patient’s left eye appeared normal, and the right eye was mildly erythematic without drainage or swelling; since corneal abrasion was not suspected, a slit lamp examination was not performed. Upon neurologic examination, right eye ptosis with incomplete lid closure, asymmetrical mouth movement with smile, and a diminished nasal labial fold crease were noted on the right side. When the child was asked to raise her eyebrows and wrinkle her forehead, asymmetrical forehead creases were apparent. All other cranial nerve functions were intact, and motor and sensory responses, including gait and reflexes, were assessed as normal. Unilateral dysfunction of right-sided cranial nerve VII (CN VII), including forehead involvement, was confirmed, consistent with a grade of III to IV on the House-Brackmann (maximum, VI)1,2 facial nerve grading scale.
Based on the rapid onset of unilateral facial nerve paresis (FNP) and an otherwise normal exam, the patient was diagnosed with Bell’s palsy. No further testing was done, and the child was given a dose of oral prednisolone 40 mg in the ED, with a prescription for four more days of oral prednisolone at 15 mg bid. The need for eye protection and lubrication was emphasized to the mother, who was given lubricating eye drops to administer. The mother was also instructed to follow up with the child’s primary care practitioner upon their return to Florida.
The child was seen by her pediatrician three days later. Her facial paresis had not worsened in the interim, and the pediatrician declined to extend the course of corticosteroids or to add an antiviral medication. At the mother’s request, the child was referred to a pediatric otolaryngologist, who saw her the following day and adjusted the treatment plan. The child was prescribed prednisolone elixir 20 mg bid for one week, followed by a tapering dose for the second week. In addition, she was prescribed oral acyclovir 400 mg qid for 10 days. Her mother was instructed to return with the child in one week for audiometry testing.
Discussion
Idiopathic FNP, commonly referred to as Bell’s palsy, is defined as an acute unilateral paresis of the facial nerve without detectable underlying cause.3,4 It most commonly occurs among persons ages 15 to 45, with a prevalence rate of 15 to 30 cases per 100,000 persons. The peak incidence of Bell’s palsy is in the fourth decade of life. Diabetic patients and pregnant women are disproportionately affected by idiopathic FNP.2,5 About 8% to 10% of patients will experience a recurrence of Bell’s palsy within 10 years.2,6
Pediatric FNP can be congenital or acquired. Congenital FNP is most often associated with birth trauma and occurs at a rate of 2.1 cases per 1,000 births. Rare genetic syndromes can also manifest with FNP and will most often present with other syndromic anomalies noted at birth.7
Acquired FNP is two to four times less common in children than adults, with an estimated prevalence of 2.7 per 100,000 patients younger than 10. Children account for only a small proportion of subjects in published studies that address diagnosis and management of FNP.3 While the presentation of FNP is much the same in adults and children, some notable differences in etiology exist.2,3,7-9 Infectious, traumatic, or neoplastic causes of FNP are more common among children than adults and must be distinguished from idiopathic FNP.7,9-11
Decisions regarding diagnostic testing, pharmacologic treatment, and referral must be guided by the history and physical exam, neurologic exam, and clinical judgment. Being able to identify or exclude alarming causes of FNP, such as neoplasm, will aid the primary care practitioner in treatment and referral practices for this condition.
Pathophysiology
CN VII, the facial nerve, has a broad scope of function that incorporates both sensory and motor pathways. The brachial nerve portion of CN VII controls the muscles of voluntary facial expression. CN VII also autonomically innervates the lacrimal gland and submandibular gland and governs sensation from part of the ear as well as taste from the anterior two-thirds of the tongue.4
The precise pathophysiology involved in FNP remains an area of continuing debate, but infectious, vascular, immunologic, and genetic causes have been hypothesized.7,12 Inflammation and subsequent nerve damage along CN VII caused by an infectious process is thought to be the most likely explanation for the pathogenesis of acquired FNP in both adults and children.5,13
Herpes simplex virus 1 (HSV-1) has been suggested as the virus most commonly linked to FNP in both adults and children, but it is unlikely to be the sole cause.5,6,9 Data from a three-year prospective study of FNP cases in children support a relationship between pediatric FNP and HSV-1 infection.14 Other infectious causes implicated in pediatric FNP are Lyme disease, Epstein-Barr, varicella zoster virus, rubella, coxsackie virus, adenovirus, and otitis media.4,7,9
Presentation, History, and Physical Exam
Most children with idiopathic FNP will present with sudden-onset facial asymmetry and may have decreased tearing, loss of the conjunctival reflex (leading to difficulty closing the eye), an inability to hold the lips tightly together, and difficulty keeping food in the mouth. Complaints of otalgia, speech disturbances, hyperacusis, and altered sense of taste are common.2,7 Recent occurrence of an upper respiratory infection is often reported in the history of a pediatric patient with FNP.3,7,15,16
Idiopathic FNP is essentially a diagnosis of exclusion.3,5 A meticulous history must be conducted, including any recent illnesses, trauma to the face or head, vaccines, rashes, and travel. Assessment of the head, eyes, ears, nose, and throat, and a careful neurologic history must be conducted to identify nonidiopathic causes of FNP (see Table 15-7,9). Facial weakness can progress from mild palsy to complete paralysis over one to two weeks5; therefore, a careful history of the progression of facial weakness should be ascertained and documented.5,17
A full neurologic exam is essential. Cranial nerves I through XII should be evaluated; any malfunction of a cranial nerve other than CN VII could be indicative of a tumor or process other than idiopathic FNP. Assessment of facial nerve function is imperative, as this factor is the most important for predicting recovery; it can also aid in formulating a prognosis and directing treatment.5,9,17
The House-Brackmann facial nerve grading system1,2 is considered the gold standard for grading severity of facial paresis9 (see Table 21,2 ). A clear distinction between paresis (partial or incomplete palsy) and paralysis (complete palsy) must be made. Pediatric patients with an incomplete palsy have an improved chance of full recovery.17,18
Any abnormalities in the peripheral neurologic exam should prompt further testing. FNP not involving the forehead musculature, gradual progression of paresis, and weakness in any extremity could be indicative of a central lesion. FNP has been the presenting symptom in various neoplastic processes, including leukemia, cholesteatoma, and astrocytoma.3,7,9
Otitis media is a frequent cause of FNP among children.9-11 Thus, a thorough examination of the ear canal, tympanic membrane, and hearing should be performed. The throat and oropharynx should be inspected, and the parotid gland palpated. Any swelling or abnormalities warrant further investigation.
Lyme disease presenting with FNP is more common in children than adults. This may be related to the increased likelihood for children to be bitten by ticks in the head and neck areas. Frequently, FNP associated with Lyme disease is bilateral—as often as 25% of the time.19 Headache, onset of symptoms during peak Lyme season, or bilateral FNP should raise the clinician’s suspicion for Lyme disease.7,9,19
An accurate assessment of blood pressure is essential, as severe hypertension may be implicated in FNP in children.3,5,7 One literature review reported that hypertension was the origin of FNP in 3% to 17% of affected children.20 Vascular hemorrhage induced by hypertension is thought to cause nerve compression and subsequent FNP.7
A bilateral eye exam is also important. Irritation is likely, and the patient with any suspected corneal abrasion or damage should be referred to an ophthalmologist.6,18
Laboratory Testing and Imaging
Diagnostic testing that facilitates the exclusion of known causes of FNP should be considered, as there is no specific laboratory test to confirm the diagnosis. A complete blood count, Lyme titers, cerebrospinal fluid analysis, CT, and/or MRI may be warranted, based on the clinical presentation.7-9 In children in whom Lyme disease is suspected (ie, those living in tick-endemic areas or with recent tick bites), serologic testing should be performed. Lumbar puncture and an evaluation of cerebrospinal fluid may be necessary in cases in which meningitis cannot be excluded.7,9
Specialized diagnostic tests are not routinely recommended for patients with paresis that is improving. Audiometry and evaluation of the stapedial reflex may help guide treatment decisions for patients whose condition is not improving. In children, the presence or return of the stapedial reflex within three weeks of disease onset is predictive of complete recovery.5 In patients who experience complete paralysis or unimproved paresis, results of electrodiagnostic testing (in particular, evoked facial nerve electroneuronography) can help forecast recovery of facial nerve function.5,17
Treatment and Management
Treatment for FNP in adults is controversial, and even more so for the pediatric patient. Treatment decisions consist of eye care, corticosteroids, antiviral medications, and appropriate referrals.
Eye care. Eye lubrication and protection should be implemented immediately. Protecting the cornea is paramount; thorough lubrication of the eye is the mainstay of treatment.18 Artificial tears should be used frequently during the day, and an ointment should be applied to the eye at night. Use of eye patches is controversial, as they may actually cause corneal injury.7,9 Taping the eye shut at night may prevent trauma during sleep, but this option must be considered carefully.9,18
Corticosteroids. Early initiation of corticosteroids should be considered for all patients with FNP, including children.2,7,9,17 Studies are inconclusive as to whether steroid therapy is beneficial in children with idiopathic FNP. However, two 2010 reviews of pediatric FNP recommend early initiation of steroids for children with acute-onset FNP, particularly when facial paresis is evaluated at a House-Brackmann grade V or VI.7,9 The American Academy of Family Physicians (AAFP) recommends a tapering course of prednisone for all patients, begun as soon as possible.6 The prednisone dosage for pediatric patients is usually 1.0 mg/kg/d, split into two doses, for six days, followed by a tapering dose for four days.5
Antivirals and antibiotic therapy. When an infectious cause of FNP is known, appropriate antibiotic or antiviral therapy should begin. If the patient lives in or has traveled to an area endemic for Lyme disease, empiric treatment may be appropriate. When Ramsay Hunt syndrome is diagnosed or herpetic lesions are visible, antiviral treatment should be initiated.7
Antiviral therapy for idiopathic FNP is the most controversial of the treatment decisions. In 2001, the American Academy of Neurology concluded that no clear benefit from acyclovir could be ascertained, although it might be effective.13 This was affirmed in a recently updated Cochrane review of antiviral therapy for idiopathic FNP.12 Antiviral therapy alone showed no benefit, compared with placebo; however, combined antiviral and corticosteroid therapy was more effective than placebo alone in recovery outcomes. Antivirals may benefit pediatric patients and should be considered early when the cause of FNP is viral or idiopathic.7,9
Referrals. Initial presentation and course of paresis should guide referral patterns for the pediatric patient presenting with FNP. The American Academy of Pediatrics (AAP) recommends referral to an otolaryngologist for any infant or child with FNP.21 The AAFP recommends referral to a specialist for any patient who does not show improvement within two weeks.6
In patients with complete paralysis, early surgical intervention may be considered, and referral should be made promptly for electrodiagnostic testing and surgical consult. In cases in which otitis media causes FNP, myringotomy and tube insertion are indicated, and appropriate referral should be made.7,9
Outcomes
|The prognosis in children with FNP is good, and most will recover completely.2,9-11,22 Idiopathic and infectious etiologies of FNP seem to have the greatest likelihood for complete recovery.10,11,16,17 Recovery appears to be affected by etiology, degree of paresis, and treatment. How these factors coalesce is not fully understood, and up to 20% of children may have mild to moderate residual facial nerve dysfunction.10,11,19,22
The Case Patient
The child’s facial nerve function gradually returned over a three-week period, with no residual deficit (see Figures 1a, 1b, and 1c). Results of the audiometry screening on day 10 were normal, showing a positive stapedial reflex. An MRI, performed four months after the initial paralysis to rule out any tumors, yielded normal results.
This case highlights the differing management of pediatric Bell’s palsy among emergency, pediatric, and specialized providers. This child was managed more aggressively under the care of an otolaryngologist with a two-week course of steroids, antiviral medication for 10 days, and a follow-up MRI to rule out any evidence of a tumor. The need for further research to guide practice in the pediatric patient with Bell’s palsy is apparent.
Conclusion
FNP in the pediatric population is rare and more likely to have an identifiable cause than among adults. Careful examination should reveal differential diagnoses that warrant treatment and referrals. The main causes of FNP that should not be missed are otitis media, hypertension, varicella zoster virus (Ramsay Hunt syndrome), neoplastic processes, and Lyme disease.
Practitioners should have a high index of suspicion for nonidiopathic causes of FNP when a child has a neurologic exam that includes facial paresis of gradual onset, abnormal function of other cranial nerves, lack of forehead muscle weakness, or peripheral abnormalities. In addition to the history and exam, blood work and radiologic imaging can aid the practitioner in ruling in or out nonidiopathic causes of FNP.
Grading of facial palsy severity using the House-Brackmann scale helps guide prognosis and referral choices. Referral to a specialist in otolaryngology is appropriate and recommended by the AAP. Referral should be made to an ophthalmologist if any suspicion of corneal abrasion exists.
Treatment in children should consist of eye care and steroids. Antiviral therapy should be considered on an individualized basis and when evidence of HSV or varicella exists. Parents should be advised about the importance of eye care in a child with FNP (see Table 35-7,9,17,18,22).
The emotional stress associated with FNP can be significant for both children and adults; fear of lifelong facial deformity can be psychologically debilitating. Yet a favorable prognosis for recovery of facial nerve function can be relayed to anxious parents.
1. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2): 146-147.
2. Finsterer J. Management of peripheral facial nerve palsy. Eur Arch Otorhinolaryngol. 2008;265(7):743-752.
3. Lunan R, Nagarajan L. Bell’s palsy: a guideline proposal following a review of practice. J Paediatr Child Health. 2008;44(4):219-220.
4. Blosser CG, Reider-Demer M. Neurologic disorders. In: Burns CE, Dunn AM, Brady MA, et al, eds. Pediatric Primary Care. 4th ed. St. Louis: Saunders Elsevier; 2008:634-672.
5. Singhi P, Jain V. Bell’s palsy in children. Semin Pediatr Neurol. 2003;10(4):289-297.
6. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007;76(7):997-1002.
7. Lorch M, Teach SJ. Facial nerve palsy: Etiology and approach to diagnosis and treatment. Pediatr Emerg Care. 2010;26(10):763-769.
8. El-Hawrani AS, Eng CY, Ahmed SK, et al. General practitioners’ referral pattern for children with acute facial paralysis. J Laryngol Otol. 2005;119(7):540-542.
9. Shargorodsky J, Lin HW, Gopen Q. Facial nerve palsy in the pediatric population. Clin Pediatr (Phila). 2010;49(5):411-417.
10. Wang CH, Chang YC, Shih HM, et al. Facial palsy in children: emergency department management and outcome. Pediatr Emerg Care. 2010;26(2):121-125.
11. Evans AK, Licameli G, Brietzke S, et al. Pediatric facial nerve paralysis: patients, management and outcomes. Int J Pediatr Otorhinolaryngol. 2005;69(11):1521-1528.
12. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2009;(4):CD001869.
13. Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001;56(7):830-836.
14. Khine H, Mayers M, Avner JR, et al. Association between herpes simplex virus-1 infection and idiopathic unilateral facial paralysis in children and adolescents. Pediatr Infect Dis J. 2008;27(5):468-469.
15. Tsai HS, Chang LY, Lu CY, et al. Epidemiology and treatment of Bell’s palsy in children in northern Taiwan. J Microbiol Immunol Infect. 2009;42(4):351-356.
16. Cha CI, Hong CK, Park MS, Yeo SG. Comparison of facial nerve paralysis in adults and children. Yonsei Med J. 2008;49(5):725-734.
17. Linder TE, Abdelkafy W, Cavero-Vanek S. The management of peripheral facial nerve palsy: “paresis” versus “paralysis” and sources of ambiguity in study designs. Otol Neurotol. 2010;31(2):319-327.
18. Rahman I, Sadiq SA. Ophthalmic management of facial nerve palsy: a review. Surv Ophthalmol. 2007;52(2):121-144.
19. Skogman BH, Croner S, Odkvist L. Acute facial palsy in children: a 2-year follow-up with focus on Lyme neuroborreliosis. Int J Pediatr Otorhinolaryngol. 2003;67(6):597-602.
20. Siegler RL, Brewer ED, Corneli HM, Thompson JA. Hypertension first seen as facial paralysis: case reports and review of the literature. Pediatrics. 1991;87(3):387-389.
21. Surgical Advisory Panel, American Academy of Pediatrics. Guidelines for referral to pediatric surgical specialists. Pediatrics. 2002;110(1 pt 1):187-191.
22. Chen WX, Wong V. Prognosis of Bell’s palsy in children: analysis of 29 cases. Brain Dev. 2005; 27(7):504-508.
A 6-year-old girl was brought to a pediatric emergency department (ED) in Atlanta by her mother. The mother stated that during the previous hour, she had noticed that her daughter’s face seemed weaker on the right side.
The night before, the child had said, “I can’t blink my eye”; when her mother asked her to demonstrate, the child seemed to be able to blink both eyes appropriately, and she had no further complaints. The next morning, the child complained of the light being too bright and asked to wear her mother’s sunglasses. In the course of the day, she continued to complain of eye discomfort, which she described as “stinging” and “sore.” The mother could see nothing abnormal, but by late afternoon noticed that her daughter’s smile and facial movements were asymmetrical. She immediately took her to the pediatric ED.
The child had no significant medical history and no surgical history. Her vaccination schedule was current, and she denied any recent illnesses. The mother could recall no exposures to infections or tick bites, no rashes, and no trauma to the face or head. The mother and child were visiting Atlanta from northeastern Florida.
The review of systems was negative for headache, fever, chills, rash, earache, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite or disposition. The child was afebrile, and the other vital signs were within normal limits.
Physical examination revealed an alert child who was calm and conversant. Her height was 45” and weight, 43 lb. Otoscopic exam showed normal ears and tympanic membranes with no sign of otitis media or ear pathology. No throat redness, tonsillar enlargement, or lymphadenopathies were noted. Breath sounds were clear, and heart rhythm and rate were regular without murmur.
The patient’s left eye appeared normal, and the right eye was mildly erythematic without drainage or swelling; since corneal abrasion was not suspected, a slit lamp examination was not performed. Upon neurologic examination, right eye ptosis with incomplete lid closure, asymmetrical mouth movement with smile, and a diminished nasal labial fold crease were noted on the right side. When the child was asked to raise her eyebrows and wrinkle her forehead, asymmetrical forehead creases were apparent. All other cranial nerve functions were intact, and motor and sensory responses, including gait and reflexes, were assessed as normal. Unilateral dysfunction of right-sided cranial nerve VII (CN VII), including forehead involvement, was confirmed, consistent with a grade of III to IV on the House-Brackmann (maximum, VI)1,2 facial nerve grading scale.
Based on the rapid onset of unilateral facial nerve paresis (FNP) and an otherwise normal exam, the patient was diagnosed with Bell’s palsy. No further testing was done, and the child was given a dose of oral prednisolone 40 mg in the ED, with a prescription for four more days of oral prednisolone at 15 mg bid. The need for eye protection and lubrication was emphasized to the mother, who was given lubricating eye drops to administer. The mother was also instructed to follow up with the child’s primary care practitioner upon their return to Florida.
The child was seen by her pediatrician three days later. Her facial paresis had not worsened in the interim, and the pediatrician declined to extend the course of corticosteroids or to add an antiviral medication. At the mother’s request, the child was referred to a pediatric otolaryngologist, who saw her the following day and adjusted the treatment plan. The child was prescribed prednisolone elixir 20 mg bid for one week, followed by a tapering dose for the second week. In addition, she was prescribed oral acyclovir 400 mg qid for 10 days. Her mother was instructed to return with the child in one week for audiometry testing.
Discussion
Idiopathic FNP, commonly referred to as Bell’s palsy, is defined as an acute unilateral paresis of the facial nerve without detectable underlying cause.3,4 It most commonly occurs among persons ages 15 to 45, with a prevalence rate of 15 to 30 cases per 100,000 persons. The peak incidence of Bell’s palsy is in the fourth decade of life. Diabetic patients and pregnant women are disproportionately affected by idiopathic FNP.2,5 About 8% to 10% of patients will experience a recurrence of Bell’s palsy within 10 years.2,6
Pediatric FNP can be congenital or acquired. Congenital FNP is most often associated with birth trauma and occurs at a rate of 2.1 cases per 1,000 births. Rare genetic syndromes can also manifest with FNP and will most often present with other syndromic anomalies noted at birth.7
Acquired FNP is two to four times less common in children than adults, with an estimated prevalence of 2.7 per 100,000 patients younger than 10. Children account for only a small proportion of subjects in published studies that address diagnosis and management of FNP.3 While the presentation of FNP is much the same in adults and children, some notable differences in etiology exist.2,3,7-9 Infectious, traumatic, or neoplastic causes of FNP are more common among children than adults and must be distinguished from idiopathic FNP.7,9-11
Decisions regarding diagnostic testing, pharmacologic treatment, and referral must be guided by the history and physical exam, neurologic exam, and clinical judgment. Being able to identify or exclude alarming causes of FNP, such as neoplasm, will aid the primary care practitioner in treatment and referral practices for this condition.
Pathophysiology
CN VII, the facial nerve, has a broad scope of function that incorporates both sensory and motor pathways. The brachial nerve portion of CN VII controls the muscles of voluntary facial expression. CN VII also autonomically innervates the lacrimal gland and submandibular gland and governs sensation from part of the ear as well as taste from the anterior two-thirds of the tongue.4
The precise pathophysiology involved in FNP remains an area of continuing debate, but infectious, vascular, immunologic, and genetic causes have been hypothesized.7,12 Inflammation and subsequent nerve damage along CN VII caused by an infectious process is thought to be the most likely explanation for the pathogenesis of acquired FNP in both adults and children.5,13
Herpes simplex virus 1 (HSV-1) has been suggested as the virus most commonly linked to FNP in both adults and children, but it is unlikely to be the sole cause.5,6,9 Data from a three-year prospective study of FNP cases in children support a relationship between pediatric FNP and HSV-1 infection.14 Other infectious causes implicated in pediatric FNP are Lyme disease, Epstein-Barr, varicella zoster virus, rubella, coxsackie virus, adenovirus, and otitis media.4,7,9
Presentation, History, and Physical Exam
Most children with idiopathic FNP will present with sudden-onset facial asymmetry and may have decreased tearing, loss of the conjunctival reflex (leading to difficulty closing the eye), an inability to hold the lips tightly together, and difficulty keeping food in the mouth. Complaints of otalgia, speech disturbances, hyperacusis, and altered sense of taste are common.2,7 Recent occurrence of an upper respiratory infection is often reported in the history of a pediatric patient with FNP.3,7,15,16
Idiopathic FNP is essentially a diagnosis of exclusion.3,5 A meticulous history must be conducted, including any recent illnesses, trauma to the face or head, vaccines, rashes, and travel. Assessment of the head, eyes, ears, nose, and throat, and a careful neurologic history must be conducted to identify nonidiopathic causes of FNP (see Table 15-7,9). Facial weakness can progress from mild palsy to complete paralysis over one to two weeks5; therefore, a careful history of the progression of facial weakness should be ascertained and documented.5,17
A full neurologic exam is essential. Cranial nerves I through XII should be evaluated; any malfunction of a cranial nerve other than CN VII could be indicative of a tumor or process other than idiopathic FNP. Assessment of facial nerve function is imperative, as this factor is the most important for predicting recovery; it can also aid in formulating a prognosis and directing treatment.5,9,17
The House-Brackmann facial nerve grading system1,2 is considered the gold standard for grading severity of facial paresis9 (see Table 21,2 ). A clear distinction between paresis (partial or incomplete palsy) and paralysis (complete palsy) must be made. Pediatric patients with an incomplete palsy have an improved chance of full recovery.17,18
Any abnormalities in the peripheral neurologic exam should prompt further testing. FNP not involving the forehead musculature, gradual progression of paresis, and weakness in any extremity could be indicative of a central lesion. FNP has been the presenting symptom in various neoplastic processes, including leukemia, cholesteatoma, and astrocytoma.3,7,9
Otitis media is a frequent cause of FNP among children.9-11 Thus, a thorough examination of the ear canal, tympanic membrane, and hearing should be performed. The throat and oropharynx should be inspected, and the parotid gland palpated. Any swelling or abnormalities warrant further investigation.
Lyme disease presenting with FNP is more common in children than adults. This may be related to the increased likelihood for children to be bitten by ticks in the head and neck areas. Frequently, FNP associated with Lyme disease is bilateral—as often as 25% of the time.19 Headache, onset of symptoms during peak Lyme season, or bilateral FNP should raise the clinician’s suspicion for Lyme disease.7,9,19
An accurate assessment of blood pressure is essential, as severe hypertension may be implicated in FNP in children.3,5,7 One literature review reported that hypertension was the origin of FNP in 3% to 17% of affected children.20 Vascular hemorrhage induced by hypertension is thought to cause nerve compression and subsequent FNP.7
A bilateral eye exam is also important. Irritation is likely, and the patient with any suspected corneal abrasion or damage should be referred to an ophthalmologist.6,18
Laboratory Testing and Imaging
Diagnostic testing that facilitates the exclusion of known causes of FNP should be considered, as there is no specific laboratory test to confirm the diagnosis. A complete blood count, Lyme titers, cerebrospinal fluid analysis, CT, and/or MRI may be warranted, based on the clinical presentation.7-9 In children in whom Lyme disease is suspected (ie, those living in tick-endemic areas or with recent tick bites), serologic testing should be performed. Lumbar puncture and an evaluation of cerebrospinal fluid may be necessary in cases in which meningitis cannot be excluded.7,9
Specialized diagnostic tests are not routinely recommended for patients with paresis that is improving. Audiometry and evaluation of the stapedial reflex may help guide treatment decisions for patients whose condition is not improving. In children, the presence or return of the stapedial reflex within three weeks of disease onset is predictive of complete recovery.5 In patients who experience complete paralysis or unimproved paresis, results of electrodiagnostic testing (in particular, evoked facial nerve electroneuronography) can help forecast recovery of facial nerve function.5,17
Treatment and Management
Treatment for FNP in adults is controversial, and even more so for the pediatric patient. Treatment decisions consist of eye care, corticosteroids, antiviral medications, and appropriate referrals.
Eye care. Eye lubrication and protection should be implemented immediately. Protecting the cornea is paramount; thorough lubrication of the eye is the mainstay of treatment.18 Artificial tears should be used frequently during the day, and an ointment should be applied to the eye at night. Use of eye patches is controversial, as they may actually cause corneal injury.7,9 Taping the eye shut at night may prevent trauma during sleep, but this option must be considered carefully.9,18
Corticosteroids. Early initiation of corticosteroids should be considered for all patients with FNP, including children.2,7,9,17 Studies are inconclusive as to whether steroid therapy is beneficial in children with idiopathic FNP. However, two 2010 reviews of pediatric FNP recommend early initiation of steroids for children with acute-onset FNP, particularly when facial paresis is evaluated at a House-Brackmann grade V or VI.7,9 The American Academy of Family Physicians (AAFP) recommends a tapering course of prednisone for all patients, begun as soon as possible.6 The prednisone dosage for pediatric patients is usually 1.0 mg/kg/d, split into two doses, for six days, followed by a tapering dose for four days.5
Antivirals and antibiotic therapy. When an infectious cause of FNP is known, appropriate antibiotic or antiviral therapy should begin. If the patient lives in or has traveled to an area endemic for Lyme disease, empiric treatment may be appropriate. When Ramsay Hunt syndrome is diagnosed or herpetic lesions are visible, antiviral treatment should be initiated.7
Antiviral therapy for idiopathic FNP is the most controversial of the treatment decisions. In 2001, the American Academy of Neurology concluded that no clear benefit from acyclovir could be ascertained, although it might be effective.13 This was affirmed in a recently updated Cochrane review of antiviral therapy for idiopathic FNP.12 Antiviral therapy alone showed no benefit, compared with placebo; however, combined antiviral and corticosteroid therapy was more effective than placebo alone in recovery outcomes. Antivirals may benefit pediatric patients and should be considered early when the cause of FNP is viral or idiopathic.7,9
Referrals. Initial presentation and course of paresis should guide referral patterns for the pediatric patient presenting with FNP. The American Academy of Pediatrics (AAP) recommends referral to an otolaryngologist for any infant or child with FNP.21 The AAFP recommends referral to a specialist for any patient who does not show improvement within two weeks.6
In patients with complete paralysis, early surgical intervention may be considered, and referral should be made promptly for electrodiagnostic testing and surgical consult. In cases in which otitis media causes FNP, myringotomy and tube insertion are indicated, and appropriate referral should be made.7,9
Outcomes
|The prognosis in children with FNP is good, and most will recover completely.2,9-11,22 Idiopathic and infectious etiologies of FNP seem to have the greatest likelihood for complete recovery.10,11,16,17 Recovery appears to be affected by etiology, degree of paresis, and treatment. How these factors coalesce is not fully understood, and up to 20% of children may have mild to moderate residual facial nerve dysfunction.10,11,19,22
The Case Patient
The child’s facial nerve function gradually returned over a three-week period, with no residual deficit (see Figures 1a, 1b, and 1c). Results of the audiometry screening on day 10 were normal, showing a positive stapedial reflex. An MRI, performed four months after the initial paralysis to rule out any tumors, yielded normal results.
This case highlights the differing management of pediatric Bell’s palsy among emergency, pediatric, and specialized providers. This child was managed more aggressively under the care of an otolaryngologist with a two-week course of steroids, antiviral medication for 10 days, and a follow-up MRI to rule out any evidence of a tumor. The need for further research to guide practice in the pediatric patient with Bell’s palsy is apparent.
Conclusion
FNP in the pediatric population is rare and more likely to have an identifiable cause than among adults. Careful examination should reveal differential diagnoses that warrant treatment and referrals. The main causes of FNP that should not be missed are otitis media, hypertension, varicella zoster virus (Ramsay Hunt syndrome), neoplastic processes, and Lyme disease.
Practitioners should have a high index of suspicion for nonidiopathic causes of FNP when a child has a neurologic exam that includes facial paresis of gradual onset, abnormal function of other cranial nerves, lack of forehead muscle weakness, or peripheral abnormalities. In addition to the history and exam, blood work and radiologic imaging can aid the practitioner in ruling in or out nonidiopathic causes of FNP.
Grading of facial palsy severity using the House-Brackmann scale helps guide prognosis and referral choices. Referral to a specialist in otolaryngology is appropriate and recommended by the AAP. Referral should be made to an ophthalmologist if any suspicion of corneal abrasion exists.
Treatment in children should consist of eye care and steroids. Antiviral therapy should be considered on an individualized basis and when evidence of HSV or varicella exists. Parents should be advised about the importance of eye care in a child with FNP (see Table 35-7,9,17,18,22).
The emotional stress associated with FNP can be significant for both children and adults; fear of lifelong facial deformity can be psychologically debilitating. Yet a favorable prognosis for recovery of facial nerve function can be relayed to anxious parents.
A 6-year-old girl was brought to a pediatric emergency department (ED) in Atlanta by her mother. The mother stated that during the previous hour, she had noticed that her daughter’s face seemed weaker on the right side.
The night before, the child had said, “I can’t blink my eye”; when her mother asked her to demonstrate, the child seemed to be able to blink both eyes appropriately, and she had no further complaints. The next morning, the child complained of the light being too bright and asked to wear her mother’s sunglasses. In the course of the day, she continued to complain of eye discomfort, which she described as “stinging” and “sore.” The mother could see nothing abnormal, but by late afternoon noticed that her daughter’s smile and facial movements were asymmetrical. She immediately took her to the pediatric ED.
The child had no significant medical history and no surgical history. Her vaccination schedule was current, and she denied any recent illnesses. The mother could recall no exposures to infections or tick bites, no rashes, and no trauma to the face or head. The mother and child were visiting Atlanta from northeastern Florida.
The review of systems was negative for headache, fever, chills, rash, earache, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite or disposition. The child was afebrile, and the other vital signs were within normal limits.
Physical examination revealed an alert child who was calm and conversant. Her height was 45” and weight, 43 lb. Otoscopic exam showed normal ears and tympanic membranes with no sign of otitis media or ear pathology. No throat redness, tonsillar enlargement, or lymphadenopathies were noted. Breath sounds were clear, and heart rhythm and rate were regular without murmur.
The patient’s left eye appeared normal, and the right eye was mildly erythematic without drainage or swelling; since corneal abrasion was not suspected, a slit lamp examination was not performed. Upon neurologic examination, right eye ptosis with incomplete lid closure, asymmetrical mouth movement with smile, and a diminished nasal labial fold crease were noted on the right side. When the child was asked to raise her eyebrows and wrinkle her forehead, asymmetrical forehead creases were apparent. All other cranial nerve functions were intact, and motor and sensory responses, including gait and reflexes, were assessed as normal. Unilateral dysfunction of right-sided cranial nerve VII (CN VII), including forehead involvement, was confirmed, consistent with a grade of III to IV on the House-Brackmann (maximum, VI)1,2 facial nerve grading scale.
Based on the rapid onset of unilateral facial nerve paresis (FNP) and an otherwise normal exam, the patient was diagnosed with Bell’s palsy. No further testing was done, and the child was given a dose of oral prednisolone 40 mg in the ED, with a prescription for four more days of oral prednisolone at 15 mg bid. The need for eye protection and lubrication was emphasized to the mother, who was given lubricating eye drops to administer. The mother was also instructed to follow up with the child’s primary care practitioner upon their return to Florida.
The child was seen by her pediatrician three days later. Her facial paresis had not worsened in the interim, and the pediatrician declined to extend the course of corticosteroids or to add an antiviral medication. At the mother’s request, the child was referred to a pediatric otolaryngologist, who saw her the following day and adjusted the treatment plan. The child was prescribed prednisolone elixir 20 mg bid for one week, followed by a tapering dose for the second week. In addition, she was prescribed oral acyclovir 400 mg qid for 10 days. Her mother was instructed to return with the child in one week for audiometry testing.
Discussion
Idiopathic FNP, commonly referred to as Bell’s palsy, is defined as an acute unilateral paresis of the facial nerve without detectable underlying cause.3,4 It most commonly occurs among persons ages 15 to 45, with a prevalence rate of 15 to 30 cases per 100,000 persons. The peak incidence of Bell’s palsy is in the fourth decade of life. Diabetic patients and pregnant women are disproportionately affected by idiopathic FNP.2,5 About 8% to 10% of patients will experience a recurrence of Bell’s palsy within 10 years.2,6
Pediatric FNP can be congenital or acquired. Congenital FNP is most often associated with birth trauma and occurs at a rate of 2.1 cases per 1,000 births. Rare genetic syndromes can also manifest with FNP and will most often present with other syndromic anomalies noted at birth.7
Acquired FNP is two to four times less common in children than adults, with an estimated prevalence of 2.7 per 100,000 patients younger than 10. Children account for only a small proportion of subjects in published studies that address diagnosis and management of FNP.3 While the presentation of FNP is much the same in adults and children, some notable differences in etiology exist.2,3,7-9 Infectious, traumatic, or neoplastic causes of FNP are more common among children than adults and must be distinguished from idiopathic FNP.7,9-11
Decisions regarding diagnostic testing, pharmacologic treatment, and referral must be guided by the history and physical exam, neurologic exam, and clinical judgment. Being able to identify or exclude alarming causes of FNP, such as neoplasm, will aid the primary care practitioner in treatment and referral practices for this condition.
Pathophysiology
CN VII, the facial nerve, has a broad scope of function that incorporates both sensory and motor pathways. The brachial nerve portion of CN VII controls the muscles of voluntary facial expression. CN VII also autonomically innervates the lacrimal gland and submandibular gland and governs sensation from part of the ear as well as taste from the anterior two-thirds of the tongue.4
The precise pathophysiology involved in FNP remains an area of continuing debate, but infectious, vascular, immunologic, and genetic causes have been hypothesized.7,12 Inflammation and subsequent nerve damage along CN VII caused by an infectious process is thought to be the most likely explanation for the pathogenesis of acquired FNP in both adults and children.5,13
Herpes simplex virus 1 (HSV-1) has been suggested as the virus most commonly linked to FNP in both adults and children, but it is unlikely to be the sole cause.5,6,9 Data from a three-year prospective study of FNP cases in children support a relationship between pediatric FNP and HSV-1 infection.14 Other infectious causes implicated in pediatric FNP are Lyme disease, Epstein-Barr, varicella zoster virus, rubella, coxsackie virus, adenovirus, and otitis media.4,7,9
Presentation, History, and Physical Exam
Most children with idiopathic FNP will present with sudden-onset facial asymmetry and may have decreased tearing, loss of the conjunctival reflex (leading to difficulty closing the eye), an inability to hold the lips tightly together, and difficulty keeping food in the mouth. Complaints of otalgia, speech disturbances, hyperacusis, and altered sense of taste are common.2,7 Recent occurrence of an upper respiratory infection is often reported in the history of a pediatric patient with FNP.3,7,15,16
Idiopathic FNP is essentially a diagnosis of exclusion.3,5 A meticulous history must be conducted, including any recent illnesses, trauma to the face or head, vaccines, rashes, and travel. Assessment of the head, eyes, ears, nose, and throat, and a careful neurologic history must be conducted to identify nonidiopathic causes of FNP (see Table 15-7,9). Facial weakness can progress from mild palsy to complete paralysis over one to two weeks5; therefore, a careful history of the progression of facial weakness should be ascertained and documented.5,17
A full neurologic exam is essential. Cranial nerves I through XII should be evaluated; any malfunction of a cranial nerve other than CN VII could be indicative of a tumor or process other than idiopathic FNP. Assessment of facial nerve function is imperative, as this factor is the most important for predicting recovery; it can also aid in formulating a prognosis and directing treatment.5,9,17
The House-Brackmann facial nerve grading system1,2 is considered the gold standard for grading severity of facial paresis9 (see Table 21,2 ). A clear distinction between paresis (partial or incomplete palsy) and paralysis (complete palsy) must be made. Pediatric patients with an incomplete palsy have an improved chance of full recovery.17,18
Any abnormalities in the peripheral neurologic exam should prompt further testing. FNP not involving the forehead musculature, gradual progression of paresis, and weakness in any extremity could be indicative of a central lesion. FNP has been the presenting symptom in various neoplastic processes, including leukemia, cholesteatoma, and astrocytoma.3,7,9
Otitis media is a frequent cause of FNP among children.9-11 Thus, a thorough examination of the ear canal, tympanic membrane, and hearing should be performed. The throat and oropharynx should be inspected, and the parotid gland palpated. Any swelling or abnormalities warrant further investigation.
Lyme disease presenting with FNP is more common in children than adults. This may be related to the increased likelihood for children to be bitten by ticks in the head and neck areas. Frequently, FNP associated with Lyme disease is bilateral—as often as 25% of the time.19 Headache, onset of symptoms during peak Lyme season, or bilateral FNP should raise the clinician’s suspicion for Lyme disease.7,9,19
An accurate assessment of blood pressure is essential, as severe hypertension may be implicated in FNP in children.3,5,7 One literature review reported that hypertension was the origin of FNP in 3% to 17% of affected children.20 Vascular hemorrhage induced by hypertension is thought to cause nerve compression and subsequent FNP.7
A bilateral eye exam is also important. Irritation is likely, and the patient with any suspected corneal abrasion or damage should be referred to an ophthalmologist.6,18
Laboratory Testing and Imaging
Diagnostic testing that facilitates the exclusion of known causes of FNP should be considered, as there is no specific laboratory test to confirm the diagnosis. A complete blood count, Lyme titers, cerebrospinal fluid analysis, CT, and/or MRI may be warranted, based on the clinical presentation.7-9 In children in whom Lyme disease is suspected (ie, those living in tick-endemic areas or with recent tick bites), serologic testing should be performed. Lumbar puncture and an evaluation of cerebrospinal fluid may be necessary in cases in which meningitis cannot be excluded.7,9
Specialized diagnostic tests are not routinely recommended for patients with paresis that is improving. Audiometry and evaluation of the stapedial reflex may help guide treatment decisions for patients whose condition is not improving. In children, the presence or return of the stapedial reflex within three weeks of disease onset is predictive of complete recovery.5 In patients who experience complete paralysis or unimproved paresis, results of electrodiagnostic testing (in particular, evoked facial nerve electroneuronography) can help forecast recovery of facial nerve function.5,17
Treatment and Management
Treatment for FNP in adults is controversial, and even more so for the pediatric patient. Treatment decisions consist of eye care, corticosteroids, antiviral medications, and appropriate referrals.
Eye care. Eye lubrication and protection should be implemented immediately. Protecting the cornea is paramount; thorough lubrication of the eye is the mainstay of treatment.18 Artificial tears should be used frequently during the day, and an ointment should be applied to the eye at night. Use of eye patches is controversial, as they may actually cause corneal injury.7,9 Taping the eye shut at night may prevent trauma during sleep, but this option must be considered carefully.9,18
Corticosteroids. Early initiation of corticosteroids should be considered for all patients with FNP, including children.2,7,9,17 Studies are inconclusive as to whether steroid therapy is beneficial in children with idiopathic FNP. However, two 2010 reviews of pediatric FNP recommend early initiation of steroids for children with acute-onset FNP, particularly when facial paresis is evaluated at a House-Brackmann grade V or VI.7,9 The American Academy of Family Physicians (AAFP) recommends a tapering course of prednisone for all patients, begun as soon as possible.6 The prednisone dosage for pediatric patients is usually 1.0 mg/kg/d, split into two doses, for six days, followed by a tapering dose for four days.5
Antivirals and antibiotic therapy. When an infectious cause of FNP is known, appropriate antibiotic or antiviral therapy should begin. If the patient lives in or has traveled to an area endemic for Lyme disease, empiric treatment may be appropriate. When Ramsay Hunt syndrome is diagnosed or herpetic lesions are visible, antiviral treatment should be initiated.7
Antiviral therapy for idiopathic FNP is the most controversial of the treatment decisions. In 2001, the American Academy of Neurology concluded that no clear benefit from acyclovir could be ascertained, although it might be effective.13 This was affirmed in a recently updated Cochrane review of antiviral therapy for idiopathic FNP.12 Antiviral therapy alone showed no benefit, compared with placebo; however, combined antiviral and corticosteroid therapy was more effective than placebo alone in recovery outcomes. Antivirals may benefit pediatric patients and should be considered early when the cause of FNP is viral or idiopathic.7,9
Referrals. Initial presentation and course of paresis should guide referral patterns for the pediatric patient presenting with FNP. The American Academy of Pediatrics (AAP) recommends referral to an otolaryngologist for any infant or child with FNP.21 The AAFP recommends referral to a specialist for any patient who does not show improvement within two weeks.6
In patients with complete paralysis, early surgical intervention may be considered, and referral should be made promptly for electrodiagnostic testing and surgical consult. In cases in which otitis media causes FNP, myringotomy and tube insertion are indicated, and appropriate referral should be made.7,9
Outcomes
|The prognosis in children with FNP is good, and most will recover completely.2,9-11,22 Idiopathic and infectious etiologies of FNP seem to have the greatest likelihood for complete recovery.10,11,16,17 Recovery appears to be affected by etiology, degree of paresis, and treatment. How these factors coalesce is not fully understood, and up to 20% of children may have mild to moderate residual facial nerve dysfunction.10,11,19,22
The Case Patient
The child’s facial nerve function gradually returned over a three-week period, with no residual deficit (see Figures 1a, 1b, and 1c). Results of the audiometry screening on day 10 were normal, showing a positive stapedial reflex. An MRI, performed four months after the initial paralysis to rule out any tumors, yielded normal results.
This case highlights the differing management of pediatric Bell’s palsy among emergency, pediatric, and specialized providers. This child was managed more aggressively under the care of an otolaryngologist with a two-week course of steroids, antiviral medication for 10 days, and a follow-up MRI to rule out any evidence of a tumor. The need for further research to guide practice in the pediatric patient with Bell’s palsy is apparent.
Conclusion
FNP in the pediatric population is rare and more likely to have an identifiable cause than among adults. Careful examination should reveal differential diagnoses that warrant treatment and referrals. The main causes of FNP that should not be missed are otitis media, hypertension, varicella zoster virus (Ramsay Hunt syndrome), neoplastic processes, and Lyme disease.
Practitioners should have a high index of suspicion for nonidiopathic causes of FNP when a child has a neurologic exam that includes facial paresis of gradual onset, abnormal function of other cranial nerves, lack of forehead muscle weakness, or peripheral abnormalities. In addition to the history and exam, blood work and radiologic imaging can aid the practitioner in ruling in or out nonidiopathic causes of FNP.
Grading of facial palsy severity using the House-Brackmann scale helps guide prognosis and referral choices. Referral to a specialist in otolaryngology is appropriate and recommended by the AAP. Referral should be made to an ophthalmologist if any suspicion of corneal abrasion exists.
Treatment in children should consist of eye care and steroids. Antiviral therapy should be considered on an individualized basis and when evidence of HSV or varicella exists. Parents should be advised about the importance of eye care in a child with FNP (see Table 35-7,9,17,18,22).
The emotional stress associated with FNP can be significant for both children and adults; fear of lifelong facial deformity can be psychologically debilitating. Yet a favorable prognosis for recovery of facial nerve function can be relayed to anxious parents.
1. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2): 146-147.
2. Finsterer J. Management of peripheral facial nerve palsy. Eur Arch Otorhinolaryngol. 2008;265(7):743-752.
3. Lunan R, Nagarajan L. Bell’s palsy: a guideline proposal following a review of practice. J Paediatr Child Health. 2008;44(4):219-220.
4. Blosser CG, Reider-Demer M. Neurologic disorders. In: Burns CE, Dunn AM, Brady MA, et al, eds. Pediatric Primary Care. 4th ed. St. Louis: Saunders Elsevier; 2008:634-672.
5. Singhi P, Jain V. Bell’s palsy in children. Semin Pediatr Neurol. 2003;10(4):289-297.
6. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007;76(7):997-1002.
7. Lorch M, Teach SJ. Facial nerve palsy: Etiology and approach to diagnosis and treatment. Pediatr Emerg Care. 2010;26(10):763-769.
8. El-Hawrani AS, Eng CY, Ahmed SK, et al. General practitioners’ referral pattern for children with acute facial paralysis. J Laryngol Otol. 2005;119(7):540-542.
9. Shargorodsky J, Lin HW, Gopen Q. Facial nerve palsy in the pediatric population. Clin Pediatr (Phila). 2010;49(5):411-417.
10. Wang CH, Chang YC, Shih HM, et al. Facial palsy in children: emergency department management and outcome. Pediatr Emerg Care. 2010;26(2):121-125.
11. Evans AK, Licameli G, Brietzke S, et al. Pediatric facial nerve paralysis: patients, management and outcomes. Int J Pediatr Otorhinolaryngol. 2005;69(11):1521-1528.
12. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2009;(4):CD001869.
13. Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001;56(7):830-836.
14. Khine H, Mayers M, Avner JR, et al. Association between herpes simplex virus-1 infection and idiopathic unilateral facial paralysis in children and adolescents. Pediatr Infect Dis J. 2008;27(5):468-469.
15. Tsai HS, Chang LY, Lu CY, et al. Epidemiology and treatment of Bell’s palsy in children in northern Taiwan. J Microbiol Immunol Infect. 2009;42(4):351-356.
16. Cha CI, Hong CK, Park MS, Yeo SG. Comparison of facial nerve paralysis in adults and children. Yonsei Med J. 2008;49(5):725-734.
17. Linder TE, Abdelkafy W, Cavero-Vanek S. The management of peripheral facial nerve palsy: “paresis” versus “paralysis” and sources of ambiguity in study designs. Otol Neurotol. 2010;31(2):319-327.
18. Rahman I, Sadiq SA. Ophthalmic management of facial nerve palsy: a review. Surv Ophthalmol. 2007;52(2):121-144.
19. Skogman BH, Croner S, Odkvist L. Acute facial palsy in children: a 2-year follow-up with focus on Lyme neuroborreliosis. Int J Pediatr Otorhinolaryngol. 2003;67(6):597-602.
20. Siegler RL, Brewer ED, Corneli HM, Thompson JA. Hypertension first seen as facial paralysis: case reports and review of the literature. Pediatrics. 1991;87(3):387-389.
21. Surgical Advisory Panel, American Academy of Pediatrics. Guidelines for referral to pediatric surgical specialists. Pediatrics. 2002;110(1 pt 1):187-191.
22. Chen WX, Wong V. Prognosis of Bell’s palsy in children: analysis of 29 cases. Brain Dev. 2005; 27(7):504-508.
1. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2): 146-147.
2. Finsterer J. Management of peripheral facial nerve palsy. Eur Arch Otorhinolaryngol. 2008;265(7):743-752.
3. Lunan R, Nagarajan L. Bell’s palsy: a guideline proposal following a review of practice. J Paediatr Child Health. 2008;44(4):219-220.
4. Blosser CG, Reider-Demer M. Neurologic disorders. In: Burns CE, Dunn AM, Brady MA, et al, eds. Pediatric Primary Care. 4th ed. St. Louis: Saunders Elsevier; 2008:634-672.
5. Singhi P, Jain V. Bell’s palsy in children. Semin Pediatr Neurol. 2003;10(4):289-297.
6. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007;76(7):997-1002.
7. Lorch M, Teach SJ. Facial nerve palsy: Etiology and approach to diagnosis and treatment. Pediatr Emerg Care. 2010;26(10):763-769.
8. El-Hawrani AS, Eng CY, Ahmed SK, et al. General practitioners’ referral pattern for children with acute facial paralysis. J Laryngol Otol. 2005;119(7):540-542.
9. Shargorodsky J, Lin HW, Gopen Q. Facial nerve palsy in the pediatric population. Clin Pediatr (Phila). 2010;49(5):411-417.
10. Wang CH, Chang YC, Shih HM, et al. Facial palsy in children: emergency department management and outcome. Pediatr Emerg Care. 2010;26(2):121-125.
11. Evans AK, Licameli G, Brietzke S, et al. Pediatric facial nerve paralysis: patients, management and outcomes. Int J Pediatr Otorhinolaryngol. 2005;69(11):1521-1528.
12. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2009;(4):CD001869.
13. Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001;56(7):830-836.
14. Khine H, Mayers M, Avner JR, et al. Association between herpes simplex virus-1 infection and idiopathic unilateral facial paralysis in children and adolescents. Pediatr Infect Dis J. 2008;27(5):468-469.
15. Tsai HS, Chang LY, Lu CY, et al. Epidemiology and treatment of Bell’s palsy in children in northern Taiwan. J Microbiol Immunol Infect. 2009;42(4):351-356.
16. Cha CI, Hong CK, Park MS, Yeo SG. Comparison of facial nerve paralysis in adults and children. Yonsei Med J. 2008;49(5):725-734.
17. Linder TE, Abdelkafy W, Cavero-Vanek S. The management of peripheral facial nerve palsy: “paresis” versus “paralysis” and sources of ambiguity in study designs. Otol Neurotol. 2010;31(2):319-327.
18. Rahman I, Sadiq SA. Ophthalmic management of facial nerve palsy: a review. Surv Ophthalmol. 2007;52(2):121-144.
19. Skogman BH, Croner S, Odkvist L. Acute facial palsy in children: a 2-year follow-up with focus on Lyme neuroborreliosis. Int J Pediatr Otorhinolaryngol. 2003;67(6):597-602.
20. Siegler RL, Brewer ED, Corneli HM, Thompson JA. Hypertension first seen as facial paralysis: case reports and review of the literature. Pediatrics. 1991;87(3):387-389.
21. Surgical Advisory Panel, American Academy of Pediatrics. Guidelines for referral to pediatric surgical specialists. Pediatrics. 2002;110(1 pt 1):187-191.
22. Chen WX, Wong V. Prognosis of Bell’s palsy in children: analysis of 29 cases. Brain Dev. 2005; 27(7):504-508.
Inhalation of Baby Powder
Emergency Management of Cold-Induced Injuries
Treatment Options for Symptomatic Degenerative Joint Disease Secondary to Legg-Calvé-Perthes Disease
UPDATE ON OBSTETRICS
- How to manage a short cervix to lower the risk of preterm delivery
Joseph R. Wax, MD (May 2010) - When is VBAC appropriate?
Aviva Lee-Parritz, MD (July 2010) - What can be safer than having a baby in the USA? (Commentary)
Louis L. Weinstein, MD (May 2010)
From an evolutionary standpoint, not much has changed in pregnancy and childbirth. From a clinical perspective, however, flux is a constant. Three issues, in particular, have seen notable development over the past year:
- optimal timing of elective delivery
- screening for thrombophilias in women who experience recurrent pregnancy loss, fetal growth restriction, preeclampsia, or placental abruption
- use of magnesium sulfate for fetal neuroprotection.
Of course, in the specialties of obstetrics and perinatal medicine, research continues in a variety of other subject areas, as well. Simulation training, diagnosis and management of gestational diabetes, and rescue steroid treatment are three examples. Other issues being explored include the use of progesterone to prevent prematurity, the use of ultrasonography to measure cervical length, and the safety of vaginal birth after cesarean delivery. The three areas highlighted here are not the only ones “ready for prime time,” but they are areas of considerable interest and debate.
We have a tradition in obstetrics of not embracing change too quickly. We learned this lesson through our experience with diethylstilbestrol (DES) and thalidomide, and we must continue to use caution whenever new technologies or management approaches are proposed.
30 weeks is the rule, provided delivery is truly elective
Tita ATN, Landon MB, Spong CY, et al. Timing of elective cesarean delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
When it comes to elective delivery, no one would argue against the wisdom of continuing pregnancy until at least 39 weeks’ gestation in the absence of complications. But what data form the basis of this wisdom, and when might it be prudent to consider earlier delivery?
In a widely publicized study, Tita and colleagues concluded that elective repeat cesarean delivery before 39 weeks of gestation (i.e., 37 through 38-6/7 weeks) is associated with a higher rate of neonatal respiratory distress and other adverse neonatal outcomes than is delivery at 39 to 40 weeks. Note, however, that the primary outcome of this study was a composite. Therefore, the findings should be interpreted with some caution.
In their report, Tita and coworkers acknowledged that the transient and predominantly minor complications associated with delivery before 39 weeks must be weighed against the risk of fetal death inherent in delaying delivery through 38 full weeks—and an accompanying editorial made the same point.1 Stillbirth occurs at a rate of 1 case for every 1,000 births in the 37- to 39-week gestational age range—a rate that may be higher than the risks associated with delivery. Even so, the risk of stillbirth at 37 to 39 weeks is very small, and that risk is unlikely to be lowered through routine antenatal fetal testing. We should also remember that the risks of neonatal respiratory distress, transient tachypnea, admission to the neonatal intensive care unit (NICU), and even cerebral palsy2 may be increased with delivery at 37 to 38 weeks, or at 42 weeks or later, compared with delivery at 40 weeks.
All truly elective deliveries should occur at or after 39 weeks of gestation. However, when indicated, earlier delivery is acceptable—even essential—if we are to minimize maternal and neonatal morbidity and mortality in high-risk circumstances, such as hypertensive disorders of pregnancy, placenta previa, fetal growth restriction, and other conditions.
Investigations are under way to determine whether there is a role for routine betamethasone administration (regardless of indication or gestational age) in the absence of labor before 39 weeks. Until those data come in, we should continue to follow current practice guidelines for antenatal maternal administration of betamethasone—namely, a single course given between 24 and 34 weeks in women who have an elevated risk of preterm delivery.
Population-based screening for thrombophilias is not recommended
Silver RM, Zhao Y, Spong CY, et al, for the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units (NICHD MFMU) Network. Prothrombin gene G20210A mutation and obstetric complications. Obstet Gynecol. 2010;115(1):14–20.
Said JM, Higgins JR, Moses EK, et al. Inherited thrombophilia polymorphisms and pregnancy outcomes in nulliparous women. Obstet Gynecol. 2010;115(1):5–13.
Since the mid-1990s, screening for thrombophilias has been recommended in the evaluation of a variety of adverse reproductive outcomes, including, but not limited to:
- recurrent pregnancy loss
- unexplained stillbirth
- placental abruption
- preeclampsia
- fetal growth restriction.
When a thrombophilia is detected in these settings, the practitioner faces a dilemma—namely, what to do when the mother is otherwise healthy and asymptomatic. All too often the finding of a thrombophilia leads to the initiation of some anticoagulation regimen, ranging from low-dose aspirin all the way to therapeutic anticoagulation with heparin.
Over the past year, several studies and expert opinions have been published that recast the role of thrombophilia screening in obstetric practice.
Writing for the Maternal-Fetal Medicine Units (MFMU) Network, Silver and colleagues concluded that the prothrombin (PT) gene mutation G20210A was not associated with pregnancy loss, preeclampsia, fetal growth restriction, or placental abruption in a low-risk, prospective cohort.
Said and coworkers reached a similar conclusion. In a blinded, prospective cohort study, they screened for the following mutations in 2,034 healthy nulliparous women before 22 weeks’ gestation:
- factor V Leiden mutation
- PT gene G20210A mutation
- methylenetetrahydrofolate reductase enzyme (MTHFR) C677T
- MTHFR A1298C
- thrombomodulin polymorphism.
The majority of asymptomatic women who carried an inherited thrombophilia polymorphism had a successful pregnancy outcome. In fact, homozygosity of the MTHFR A1298C mutation was found to be protective.
Population-based screening for thrombophilias is not recommended. In fact, some authors have advised against screening for thrombophilias even in the setting of a thrombotic event, suggesting it has limited utility.3
The main reason to screen for a thrombophilia at this time is to explore idiopathic thrombosis or a strong family history of the same. There is no need to screen for thrombophilias when the patient has a history of pregnancy loss, placental abruption, preeclampsia, and fetal growth restriction.
If you give magnesium sulfate for fetal neuroprotection, adhere to a protocol
ACOG Committee Opinion No. 455: Magnesium sulfate before anticipated preterm birth for neuroprotection. Obstet Gynecol. 2010;115(3):669–671.
Magnesium sulfate has a long and glorious history in obstetrics, having been used to prevent eclampsia, to treat preterm uterine contractions, and now, potentially, to reduce the incidence of central nervous system damage among prematurely delivered infants.
Cerebral palsy (CP) is most commonly associated with prematurity and intrauterine fetal infection. Only in the past two decades has there been a shift away from assigning the cause of most cases of CP to intrapartum events. Nevertheless, CP remains an important concern among patients and providers, and research continues to find ways to prevent CP or minimize its effects.
Numerous large trials have explored the use of magnesium sulfate to prevent CP in preterm infants. Although their findings have not been as definitive as researchers had hoped, some data do suggest that magnesium sulfate has a protective effect.
The American Congress of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) urge caution in regard to the use of magnesium sulfate for fetal neuroprotection. The SMFM points out that the reported benefits of magnesium sulfate in this setting have been derived largely from secondary analyses. The SMFM recommends that, if magnesium is used at all, it should be administered according to one of the published protocols (three are cited in the ACOG opinion).
The SMFM goes on to warn against choosing magnesium sulfate as a tocolytic solely because of its possible neuroprotective effects.
In a Committee Opinion published last year, ACOG was a bit more definite. “The Committee on Obstetric Practice and the Society for Maternal-Fetal Medicine recognize that none of the individual studies found a benefit with regard to their primary outcome,” the opinion states. “However, the available evidence suggests that magnesium sulfate given before anticipated early preterm birth reduces the risk of cerebral palsy in surviving infants. Physicians electing to use magnesium sulfate for fetal neuroprotection should develop specific guidelines regarding inclusion criteria, treatment regimens, concurrent tocolysis, and monitoring in concordance with one of the larger trials.”
Recent editorials have cautioned against using magnesium sulfate for fetal neuroprotection until more data become available,4 or have left it up to the individual practitioners (or institution) to decide whether it is advisable.5
The use of magnesium sulfate for fetal neuroprotection when preterm delivery seems likely requires additional research. For now, this practice should be governed strictly by protocol. And it should not be viewed as “standard of care” by our legal colleagues.
When administering magnesium sulfate, avoid giving a cumulative total in excess of 50 g, as this amount may increase the risk of pediatric death.6
We want to hear from you! Tell us what you think.
1. Greene MF. Making small risks even smaller. N Engl J Med. 2009;360(2):183-184.
2. Moster D, Wilcox AJ, Vollset SE, Markestad T, Lie RT. Cerebral palsy among term and postterm births. JAMA. 2010;304(9):976-982.
3. Scifres CM, Macones GA. The utility of thrombophilia testing in pregnant women with thrombosis; fact or fiction? Am J Obstet Gynecol. 2008;199(4):344.e1–7.-
4. Stanley FJ, Crowther C. Antenatal magnesium sulfate for neuroprotection before preterm birth? N Engl J Med. 2008;359(9):962-964.
5. Macones GA. MgSO4 for CP prevention: too good to be true? Am J Obstet Gynecol. 2009;200(6):589.-
6. Mittendorf R, Covert R, Boman J, et al. Is tocolytic magnesium sulfate associated with increased total paediatric mortality? Lancet. 1997;350(9090):1517-1518.
- How to manage a short cervix to lower the risk of preterm delivery
Joseph R. Wax, MD (May 2010) - When is VBAC appropriate?
Aviva Lee-Parritz, MD (July 2010) - What can be safer than having a baby in the USA? (Commentary)
Louis L. Weinstein, MD (May 2010)
From an evolutionary standpoint, not much has changed in pregnancy and childbirth. From a clinical perspective, however, flux is a constant. Three issues, in particular, have seen notable development over the past year:
- optimal timing of elective delivery
- screening for thrombophilias in women who experience recurrent pregnancy loss, fetal growth restriction, preeclampsia, or placental abruption
- use of magnesium sulfate for fetal neuroprotection.
Of course, in the specialties of obstetrics and perinatal medicine, research continues in a variety of other subject areas, as well. Simulation training, diagnosis and management of gestational diabetes, and rescue steroid treatment are three examples. Other issues being explored include the use of progesterone to prevent prematurity, the use of ultrasonography to measure cervical length, and the safety of vaginal birth after cesarean delivery. The three areas highlighted here are not the only ones “ready for prime time,” but they are areas of considerable interest and debate.
We have a tradition in obstetrics of not embracing change too quickly. We learned this lesson through our experience with diethylstilbestrol (DES) and thalidomide, and we must continue to use caution whenever new technologies or management approaches are proposed.
30 weeks is the rule, provided delivery is truly elective
Tita ATN, Landon MB, Spong CY, et al. Timing of elective cesarean delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
When it comes to elective delivery, no one would argue against the wisdom of continuing pregnancy until at least 39 weeks’ gestation in the absence of complications. But what data form the basis of this wisdom, and when might it be prudent to consider earlier delivery?
In a widely publicized study, Tita and colleagues concluded that elective repeat cesarean delivery before 39 weeks of gestation (i.e., 37 through 38-6/7 weeks) is associated with a higher rate of neonatal respiratory distress and other adverse neonatal outcomes than is delivery at 39 to 40 weeks. Note, however, that the primary outcome of this study was a composite. Therefore, the findings should be interpreted with some caution.
In their report, Tita and coworkers acknowledged that the transient and predominantly minor complications associated with delivery before 39 weeks must be weighed against the risk of fetal death inherent in delaying delivery through 38 full weeks—and an accompanying editorial made the same point.1 Stillbirth occurs at a rate of 1 case for every 1,000 births in the 37- to 39-week gestational age range—a rate that may be higher than the risks associated with delivery. Even so, the risk of stillbirth at 37 to 39 weeks is very small, and that risk is unlikely to be lowered through routine antenatal fetal testing. We should also remember that the risks of neonatal respiratory distress, transient tachypnea, admission to the neonatal intensive care unit (NICU), and even cerebral palsy2 may be increased with delivery at 37 to 38 weeks, or at 42 weeks or later, compared with delivery at 40 weeks.
All truly elective deliveries should occur at or after 39 weeks of gestation. However, when indicated, earlier delivery is acceptable—even essential—if we are to minimize maternal and neonatal morbidity and mortality in high-risk circumstances, such as hypertensive disorders of pregnancy, placenta previa, fetal growth restriction, and other conditions.
Investigations are under way to determine whether there is a role for routine betamethasone administration (regardless of indication or gestational age) in the absence of labor before 39 weeks. Until those data come in, we should continue to follow current practice guidelines for antenatal maternal administration of betamethasone—namely, a single course given between 24 and 34 weeks in women who have an elevated risk of preterm delivery.
Population-based screening for thrombophilias is not recommended
Silver RM, Zhao Y, Spong CY, et al, for the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units (NICHD MFMU) Network. Prothrombin gene G20210A mutation and obstetric complications. Obstet Gynecol. 2010;115(1):14–20.
Said JM, Higgins JR, Moses EK, et al. Inherited thrombophilia polymorphisms and pregnancy outcomes in nulliparous women. Obstet Gynecol. 2010;115(1):5–13.
Since the mid-1990s, screening for thrombophilias has been recommended in the evaluation of a variety of adverse reproductive outcomes, including, but not limited to:
- recurrent pregnancy loss
- unexplained stillbirth
- placental abruption
- preeclampsia
- fetal growth restriction.
When a thrombophilia is detected in these settings, the practitioner faces a dilemma—namely, what to do when the mother is otherwise healthy and asymptomatic. All too often the finding of a thrombophilia leads to the initiation of some anticoagulation regimen, ranging from low-dose aspirin all the way to therapeutic anticoagulation with heparin.
Over the past year, several studies and expert opinions have been published that recast the role of thrombophilia screening in obstetric practice.
Writing for the Maternal-Fetal Medicine Units (MFMU) Network, Silver and colleagues concluded that the prothrombin (PT) gene mutation G20210A was not associated with pregnancy loss, preeclampsia, fetal growth restriction, or placental abruption in a low-risk, prospective cohort.
Said and coworkers reached a similar conclusion. In a blinded, prospective cohort study, they screened for the following mutations in 2,034 healthy nulliparous women before 22 weeks’ gestation:
- factor V Leiden mutation
- PT gene G20210A mutation
- methylenetetrahydrofolate reductase enzyme (MTHFR) C677T
- MTHFR A1298C
- thrombomodulin polymorphism.
The majority of asymptomatic women who carried an inherited thrombophilia polymorphism had a successful pregnancy outcome. In fact, homozygosity of the MTHFR A1298C mutation was found to be protective.
Population-based screening for thrombophilias is not recommended. In fact, some authors have advised against screening for thrombophilias even in the setting of a thrombotic event, suggesting it has limited utility.3
The main reason to screen for a thrombophilia at this time is to explore idiopathic thrombosis or a strong family history of the same. There is no need to screen for thrombophilias when the patient has a history of pregnancy loss, placental abruption, preeclampsia, and fetal growth restriction.
If you give magnesium sulfate for fetal neuroprotection, adhere to a protocol
ACOG Committee Opinion No. 455: Magnesium sulfate before anticipated preterm birth for neuroprotection. Obstet Gynecol. 2010;115(3):669–671.
Magnesium sulfate has a long and glorious history in obstetrics, having been used to prevent eclampsia, to treat preterm uterine contractions, and now, potentially, to reduce the incidence of central nervous system damage among prematurely delivered infants.
Cerebral palsy (CP) is most commonly associated with prematurity and intrauterine fetal infection. Only in the past two decades has there been a shift away from assigning the cause of most cases of CP to intrapartum events. Nevertheless, CP remains an important concern among patients and providers, and research continues to find ways to prevent CP or minimize its effects.
Numerous large trials have explored the use of magnesium sulfate to prevent CP in preterm infants. Although their findings have not been as definitive as researchers had hoped, some data do suggest that magnesium sulfate has a protective effect.
The American Congress of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) urge caution in regard to the use of magnesium sulfate for fetal neuroprotection. The SMFM points out that the reported benefits of magnesium sulfate in this setting have been derived largely from secondary analyses. The SMFM recommends that, if magnesium is used at all, it should be administered according to one of the published protocols (three are cited in the ACOG opinion).
The SMFM goes on to warn against choosing magnesium sulfate as a tocolytic solely because of its possible neuroprotective effects.
In a Committee Opinion published last year, ACOG was a bit more definite. “The Committee on Obstetric Practice and the Society for Maternal-Fetal Medicine recognize that none of the individual studies found a benefit with regard to their primary outcome,” the opinion states. “However, the available evidence suggests that magnesium sulfate given before anticipated early preterm birth reduces the risk of cerebral palsy in surviving infants. Physicians electing to use magnesium sulfate for fetal neuroprotection should develop specific guidelines regarding inclusion criteria, treatment regimens, concurrent tocolysis, and monitoring in concordance with one of the larger trials.”
Recent editorials have cautioned against using magnesium sulfate for fetal neuroprotection until more data become available,4 or have left it up to the individual practitioners (or institution) to decide whether it is advisable.5
The use of magnesium sulfate for fetal neuroprotection when preterm delivery seems likely requires additional research. For now, this practice should be governed strictly by protocol. And it should not be viewed as “standard of care” by our legal colleagues.
When administering magnesium sulfate, avoid giving a cumulative total in excess of 50 g, as this amount may increase the risk of pediatric death.6
We want to hear from you! Tell us what you think.
- How to manage a short cervix to lower the risk of preterm delivery
Joseph R. Wax, MD (May 2010) - When is VBAC appropriate?
Aviva Lee-Parritz, MD (July 2010) - What can be safer than having a baby in the USA? (Commentary)
Louis L. Weinstein, MD (May 2010)
From an evolutionary standpoint, not much has changed in pregnancy and childbirth. From a clinical perspective, however, flux is a constant. Three issues, in particular, have seen notable development over the past year:
- optimal timing of elective delivery
- screening for thrombophilias in women who experience recurrent pregnancy loss, fetal growth restriction, preeclampsia, or placental abruption
- use of magnesium sulfate for fetal neuroprotection.
Of course, in the specialties of obstetrics and perinatal medicine, research continues in a variety of other subject areas, as well. Simulation training, diagnosis and management of gestational diabetes, and rescue steroid treatment are three examples. Other issues being explored include the use of progesterone to prevent prematurity, the use of ultrasonography to measure cervical length, and the safety of vaginal birth after cesarean delivery. The three areas highlighted here are not the only ones “ready for prime time,” but they are areas of considerable interest and debate.
We have a tradition in obstetrics of not embracing change too quickly. We learned this lesson through our experience with diethylstilbestrol (DES) and thalidomide, and we must continue to use caution whenever new technologies or management approaches are proposed.
30 weeks is the rule, provided delivery is truly elective
Tita ATN, Landon MB, Spong CY, et al. Timing of elective cesarean delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
When it comes to elective delivery, no one would argue against the wisdom of continuing pregnancy until at least 39 weeks’ gestation in the absence of complications. But what data form the basis of this wisdom, and when might it be prudent to consider earlier delivery?
In a widely publicized study, Tita and colleagues concluded that elective repeat cesarean delivery before 39 weeks of gestation (i.e., 37 through 38-6/7 weeks) is associated with a higher rate of neonatal respiratory distress and other adverse neonatal outcomes than is delivery at 39 to 40 weeks. Note, however, that the primary outcome of this study was a composite. Therefore, the findings should be interpreted with some caution.
In their report, Tita and coworkers acknowledged that the transient and predominantly minor complications associated with delivery before 39 weeks must be weighed against the risk of fetal death inherent in delaying delivery through 38 full weeks—and an accompanying editorial made the same point.1 Stillbirth occurs at a rate of 1 case for every 1,000 births in the 37- to 39-week gestational age range—a rate that may be higher than the risks associated with delivery. Even so, the risk of stillbirth at 37 to 39 weeks is very small, and that risk is unlikely to be lowered through routine antenatal fetal testing. We should also remember that the risks of neonatal respiratory distress, transient tachypnea, admission to the neonatal intensive care unit (NICU), and even cerebral palsy2 may be increased with delivery at 37 to 38 weeks, or at 42 weeks or later, compared with delivery at 40 weeks.
All truly elective deliveries should occur at or after 39 weeks of gestation. However, when indicated, earlier delivery is acceptable—even essential—if we are to minimize maternal and neonatal morbidity and mortality in high-risk circumstances, such as hypertensive disorders of pregnancy, placenta previa, fetal growth restriction, and other conditions.
Investigations are under way to determine whether there is a role for routine betamethasone administration (regardless of indication or gestational age) in the absence of labor before 39 weeks. Until those data come in, we should continue to follow current practice guidelines for antenatal maternal administration of betamethasone—namely, a single course given between 24 and 34 weeks in women who have an elevated risk of preterm delivery.
Population-based screening for thrombophilias is not recommended
Silver RM, Zhao Y, Spong CY, et al, for the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units (NICHD MFMU) Network. Prothrombin gene G20210A mutation and obstetric complications. Obstet Gynecol. 2010;115(1):14–20.
Said JM, Higgins JR, Moses EK, et al. Inherited thrombophilia polymorphisms and pregnancy outcomes in nulliparous women. Obstet Gynecol. 2010;115(1):5–13.
Since the mid-1990s, screening for thrombophilias has been recommended in the evaluation of a variety of adverse reproductive outcomes, including, but not limited to:
- recurrent pregnancy loss
- unexplained stillbirth
- placental abruption
- preeclampsia
- fetal growth restriction.
When a thrombophilia is detected in these settings, the practitioner faces a dilemma—namely, what to do when the mother is otherwise healthy and asymptomatic. All too often the finding of a thrombophilia leads to the initiation of some anticoagulation regimen, ranging from low-dose aspirin all the way to therapeutic anticoagulation with heparin.
Over the past year, several studies and expert opinions have been published that recast the role of thrombophilia screening in obstetric practice.
Writing for the Maternal-Fetal Medicine Units (MFMU) Network, Silver and colleagues concluded that the prothrombin (PT) gene mutation G20210A was not associated with pregnancy loss, preeclampsia, fetal growth restriction, or placental abruption in a low-risk, prospective cohort.
Said and coworkers reached a similar conclusion. In a blinded, prospective cohort study, they screened for the following mutations in 2,034 healthy nulliparous women before 22 weeks’ gestation:
- factor V Leiden mutation
- PT gene G20210A mutation
- methylenetetrahydrofolate reductase enzyme (MTHFR) C677T
- MTHFR A1298C
- thrombomodulin polymorphism.
The majority of asymptomatic women who carried an inherited thrombophilia polymorphism had a successful pregnancy outcome. In fact, homozygosity of the MTHFR A1298C mutation was found to be protective.
Population-based screening for thrombophilias is not recommended. In fact, some authors have advised against screening for thrombophilias even in the setting of a thrombotic event, suggesting it has limited utility.3
The main reason to screen for a thrombophilia at this time is to explore idiopathic thrombosis or a strong family history of the same. There is no need to screen for thrombophilias when the patient has a history of pregnancy loss, placental abruption, preeclampsia, and fetal growth restriction.
If you give magnesium sulfate for fetal neuroprotection, adhere to a protocol
ACOG Committee Opinion No. 455: Magnesium sulfate before anticipated preterm birth for neuroprotection. Obstet Gynecol. 2010;115(3):669–671.
Magnesium sulfate has a long and glorious history in obstetrics, having been used to prevent eclampsia, to treat preterm uterine contractions, and now, potentially, to reduce the incidence of central nervous system damage among prematurely delivered infants.
Cerebral palsy (CP) is most commonly associated with prematurity and intrauterine fetal infection. Only in the past two decades has there been a shift away from assigning the cause of most cases of CP to intrapartum events. Nevertheless, CP remains an important concern among patients and providers, and research continues to find ways to prevent CP or minimize its effects.
Numerous large trials have explored the use of magnesium sulfate to prevent CP in preterm infants. Although their findings have not been as definitive as researchers had hoped, some data do suggest that magnesium sulfate has a protective effect.
The American Congress of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) urge caution in regard to the use of magnesium sulfate for fetal neuroprotection. The SMFM points out that the reported benefits of magnesium sulfate in this setting have been derived largely from secondary analyses. The SMFM recommends that, if magnesium is used at all, it should be administered according to one of the published protocols (three are cited in the ACOG opinion).
The SMFM goes on to warn against choosing magnesium sulfate as a tocolytic solely because of its possible neuroprotective effects.
In a Committee Opinion published last year, ACOG was a bit more definite. “The Committee on Obstetric Practice and the Society for Maternal-Fetal Medicine recognize that none of the individual studies found a benefit with regard to their primary outcome,” the opinion states. “However, the available evidence suggests that magnesium sulfate given before anticipated early preterm birth reduces the risk of cerebral palsy in surviving infants. Physicians electing to use magnesium sulfate for fetal neuroprotection should develop specific guidelines regarding inclusion criteria, treatment regimens, concurrent tocolysis, and monitoring in concordance with one of the larger trials.”
Recent editorials have cautioned against using magnesium sulfate for fetal neuroprotection until more data become available,4 or have left it up to the individual practitioners (or institution) to decide whether it is advisable.5
The use of magnesium sulfate for fetal neuroprotection when preterm delivery seems likely requires additional research. For now, this practice should be governed strictly by protocol. And it should not be viewed as “standard of care” by our legal colleagues.
When administering magnesium sulfate, avoid giving a cumulative total in excess of 50 g, as this amount may increase the risk of pediatric death.6
We want to hear from you! Tell us what you think.
1. Greene MF. Making small risks even smaller. N Engl J Med. 2009;360(2):183-184.
2. Moster D, Wilcox AJ, Vollset SE, Markestad T, Lie RT. Cerebral palsy among term and postterm births. JAMA. 2010;304(9):976-982.
3. Scifres CM, Macones GA. The utility of thrombophilia testing in pregnant women with thrombosis; fact or fiction? Am J Obstet Gynecol. 2008;199(4):344.e1–7.-
4. Stanley FJ, Crowther C. Antenatal magnesium sulfate for neuroprotection before preterm birth? N Engl J Med. 2008;359(9):962-964.
5. Macones GA. MgSO4 for CP prevention: too good to be true? Am J Obstet Gynecol. 2009;200(6):589.-
6. Mittendorf R, Covert R, Boman J, et al. Is tocolytic magnesium sulfate associated with increased total paediatric mortality? Lancet. 1997;350(9090):1517-1518.
1. Greene MF. Making small risks even smaller. N Engl J Med. 2009;360(2):183-184.
2. Moster D, Wilcox AJ, Vollset SE, Markestad T, Lie RT. Cerebral palsy among term and postterm births. JAMA. 2010;304(9):976-982.
3. Scifres CM, Macones GA. The utility of thrombophilia testing in pregnant women with thrombosis; fact or fiction? Am J Obstet Gynecol. 2008;199(4):344.e1–7.-
4. Stanley FJ, Crowther C. Antenatal magnesium sulfate for neuroprotection before preterm birth? N Engl J Med. 2008;359(9):962-964.
5. Macones GA. MgSO4 for CP prevention: too good to be true? Am J Obstet Gynecol. 2009;200(6):589.-
6. Mittendorf R, Covert R, Boman J, et al. Is tocolytic magnesium sulfate associated with increased total paediatric mortality? Lancet. 1997;350(9090):1517-1518.
Postpartum hemorrhage: 11 critical questions, answered by an expert
We know the potentially tragic outcome of postpartum hemorrhage (PPH): Worldwide, more than 140,000 women die every year as a result of PPH—one death every 4 minutes! Lest you dismiss PPH as a concern largely for developing countries, where it accounts for 25% of maternal deaths, consider this: In our highly developed nation, it accounts for nearly 8% of maternal deaths—a troubling statistic, to say the least.
The significant maternal death rate associated with PPH, and questions about how to reduce it, prompted the editors of OBG Management to talk with Haywood L. Brown, MD. Dr. Brown is Roy T. Parker Professor and chair of obstetrics and gynecology at Duke University Medical Center in Durham, NC. He is also a nationally recognized specialist in maternal-fetal medicine. In this interview, he discusses the full spectrum of management of PPH, from proactive assessment of a woman’s risk to determination of the cause to the tactic of last resort, emergent hysterectomy.
Uterine atony is the leading cause of postpartum hemorrhage. When medical management fails to stanch the bleeding, bilateral uterine artery ligation is one surgical option.
1. What is PPH?
OBG Management: Dr. Brown, let’s start with a simple but important aspect of PPH—how do you define it?
Dr. Brown: Obstetric hemorrhage is excessive bleeding that occurs during the intrapartum or postpartum period—specifically, estimated blood loss of 500 mL or more after vaginal delivery or 1,000 mL or more after cesarean delivery.
PPH is characterized as early or late, depending on whether the bleeding occurs within 24 hours of delivery (early, or primary) or between 24 hours and 6 to 12 weeks postpartum (late, or secondary). Primary PPH occurs in 4% to 6% of pregnancies.
Another way to define PPH: a decline of 10% or more in the baseline hematocrit level.
OBG Management: How do you measure blood loss?
Dr. Brown: The estimation of blood loss after delivery is an inexact science and typically yields an underestimation. Most clinicians rely on visual inspection to estimate the amount of blood collected in the drapes after vaginal delivery and in the suction bottles after cesarean delivery. Some facilities weigh lap pads or drapes to get a more accurate assessment of blood loss. In a routine delivery, no specific calorimetric measuring devices are used to estimate blood loss.
At my institution, we make an attempt to estimate blood loss at every delivery—vaginal or cesarean—and record the estimate. By doing this routinely, the clinician improves in accuracy and becomes more adept at identifying excessive bleeding.
OBG Management: Is blood loss the only variable that arouses concern about possible hemorrhage?
Dr. Brown: Because pregnant women experience an increase in blood volume and physiologic cardiovascular changes, the usual sign of significant bleeding can sometimes be masked. Therefore, any changes in maternal vital signs, such as a drop in blood pressure, tachycardia, or sensorial changes, may suggest that more blood has been lost than has been estimated.
Hypotension, dizziness, tachycardia or palpitations, and decreasing urine output will typically occur when more than 10% of maternal blood volume has been lost. In this situation, the patient should be given additional fluids, and a second intravenous line should be started using large-bore, 14-gauge access. In addition, the patient’s hemoglobin and hematocrit levels should be measured. All these actions constitute a first-line strategy to prevent shock and potential irreversible renal failure and cardiovascular collapse.
Low: 500 to 1,000 mL
This level of hemorrhage should be anticipated and can usually be managed with uterine massage and administration of a uterotonic agent, such as oxytocin. Intravenous fluids and careful monitoring of maternal vital signs are also warranted.
Active management of the third stage of labor has been shown to reduce the risk of significant postpartum hemorrhage (PPH). Active management includes:
- administration of a uterotonic agent immediately after delivery of the infant
- early cord clamping and cutting
- gentle cord traction with uterine counter-traction when the uterus is well contracted
- uterine massage.2
If these methods are unsuccessful in correcting the atony, uterotonics such as a prostaglandin (rectally administered misoprostol [800 mg] or intramuscular carboprost tromethamine [Hemabate; 250 μg/mL]) will usually succeed.
Medium: 1,000 to 1,500 mL
Blood loss of this volume is usually accompanied by cardiovascular signs, such as a fall in blood pressure, diaphoresis, and tachycardia. Women with this level of hemorrhage exhibit mild signs of shock.
It is important to correct maternal hypotension with fluids, restabilize vital signs, and resolve the bleeding expeditiously. If uterotonics and massage fail to stanch the bleeding, consider placing a balloon (e.g., Bakri balloon). Once the balloon is placed and inflated, it can be left for as long as 24 hours or until the uterus regains its tone.
Be sure to check hemoglobin and hematocrit levels and transfuse the patient, if necessary, especially if vital signs have not stabilized.
High: 1,500 to 2,000 mL, or greater
This is a medical emergency that must be managed aggressively to prevent morbidity and death. Blood loss of this volume will usually bring significant cardiovascular changes, such as hypotension, tachycardia, restlessness, pallor, oliguria, and cardiovascular collapse from hemorrhagic shock. this degree of blood loss means that the patient has lost 25% to 35% of her blood volume and will need blood-product replacement to prevent coagulation and the cascade of hemorrhage.
If conservative measures are unsuccessful, timely surgical intervention with B-Lynch suture, uterine vessel ligation, or hysterectomy is lifesaving.—HAYWOOD L. BROWN, MD
2. What causes PPH?
OBG Management: Why does PPH occur?
Dr. Brown: The leading cause is uterine atony, a failure of the uterus to contract and undergo resolution following delivery of an infant. Approximately 80% of cases of early PPH are related to uterine atony.
There are other causes of PPH:
- lacerations of the genital tract (perineum, vagina, cervix, or uterus)
- retained fragments of placental tissue
- uterine rupture
- blood clotting abnormalities
- uterine inversion.
3. Is it possible to prepare for PPH?
OBG Management: What is the starting point for management of PPH?
Dr. Brown: Prevention of, and preparation for, hemorrhage begin well before delivery. During the prenatal period, for example, it is important to assess the woman’s level of risk for PPH. Among the variables that increase her risk:
- any situation that leads to overstretching of the uterus, including multiple gestation, whether delivery is vaginal or cesarean
- a history of PPH.
It is important that women with these characteristics maintain adequate hemoglobin and hematocrit levels by taking vitamin and iron supplements in the antepartum period.
In addition, women who have abnormal placental implantation, such as placenta previa, are at risk for bleeding during the antepartum period and during cesarean delivery. They should maintain a hematocrit in the mid-30s because of expected blood loss during delivery.
OBG Management: What preparatory steps should be taken at the time of hospital admission if a woman has an elevated risk of bleeding?
Dr. Brown: When the patient is hospitalized in anticipation of delivery—whether vaginal or cesarean—the team should assess her hemoglobin and hematocrit levels and type and screen for possible transfusion. The patient should also be apprised of her risk and the potential for transfusion.
Last, the anesthesia team should be alerted to her risk factors for postpartum bleeding.
4. What intrapartum variables signal an increased risk of PPH?
OBG Management: During labor and delivery, what variables signal an elevated risk of bleeding?
Dr. Brown: Risk factors for hemorrhage become more apparent during this period. They include prolonged or rapid labor, prolonged use of oxytocin, operative delivery, infections such as chorioamnionitis, and vaginal birth after cesarean delivery (VBAC).
Bleeding with VBAC merits special attention because it could signal uterine rupture. Women who have a low transverse uterine scar and who undergo VBAC have a risk of uterine scar separation during labor of 0.5% to 1%.
OBG Management: What about retained placenta or a placenta that requires manual removal?
Dr. Brown: These intrapartum variables are not as easy to anticipate. They may suggest a condition such as placenta accreta, especially if the patient is undergoing VBAC.
Uterine inversion can also lead to hemorrhage and is a medical emergency.
OBG Management: What steps should be taken at the time of labor to ensure a safe outcome?
Dr. Brown: A type and screen should be available for all women on labor and delivery, and the team should anticipate the need to cross-match for blood if there is a high potential for transfusion. For example, a woman known to have anemia (hematocrit <30%) should have a cross-match performed so that blood can be prepared for transfusion.
In addition, women who are undergoing planned delivery for placental implantation disorders should have blood in the operating room ready for transfusion when cesarean is performed. These women are at great risk of hemorrhage and peripartum hysterectomy.
5. What first-line strategies do you recommend?
OBG Management: Do you recommend oxytocin administration and fundal massage for every patient after delivery of the infant?
Dr. Brown: Yes. These strategies lessen the risk of uterine atony and excessive bleeding after vaginal delivery. At the time of cesarean delivery, expression of the placenta and uterine massage, along with oxytocin administration, reduce the risk of excessive blood loss.
If bleeding continues even after the uterus begins to contract, look for other causes of the bleeding, such as uterine laceration or retained placental fragments.
OBG Management: What uterotonic agents do you use besides oxytocin, and when?
Dr. Brown: Oxytocin is the first-line agent for control of hemorrhage. I give a dosage of 10 to 40 U/L of normal saline or lactated Ringer solution, infused continuously. Alternatively, 10 U can be given intramuscularly (IM). Second-line drugs and their dosages are listed in the TABLE.
Uterotonic agents and how to administer them
| Drug | Dosage and route | Considerations |
|---|---|---|
| FIRST-LINE | ||
| Oxytocin | 10–40 U/L of saline or lactated ringer solution, infused continuously, Or 10 U IM | The preferred drug—often the only one needed |
| SECOND-LINE | ||
| Misoprostol (Cytotec, Prostaglandin e1) | 800–1,000 μg can be given rectally | Often, the second-line drug that is given just after oxytocin because it is easy to administer |
| Methylergonovine (Methergine) | 0.2 mg IM every 2–4 hr | Contraindicated in hypertension |
| Carboprost tromethamine (Hemabate) | 0.25 mg IM every 15–90 minutes (maximum of 8 doses) | Avoid in patients who have asthma. Contra-indicated in hepatic, renal, and cardiac disease |
| Dinoprostone (Prostin e2) | 20 mg suppository can be given vaginally or rectally every 2 hours | Avoid in hypotension |
6. How do you assess the patient once PPH is identified?
OBG Management: How do you assess the patient after hemorrhage begins?
Dr. Brown: We recheck the hemoglobin and hematocrit levels and monitor vital signs for hypotension and tachycardia. We also begin fluid resuscitation and type and cross-match blood and blood products.
A delayed response to hemorrhage raises the risk of maternal morbidity and death.
We notify the anesthesia team when it seems likely that a surgical approach to the hemorrhage will be needed. And we notify interventional radiology if the bleeding may respond to uterine artery embolization.
7. Why is it important to replace blood products?
OBG Management: You’ve been known to say, “The more blood a patient loses, the more blood she loses.” What do you mean by that?
Dr. Brown: Excessive bleeding leads to a loss of critical clotting factors that are made in the liver. Once the clotting factors are depleted, the woman is at risk of coagulopathy or disseminated intravascular coagulation. This depletion potentiates the cycle of hemorrhage. When that occurs, the hemorrhage can be controlled only with transfusion of red blood cells (RBCs) and replacement of clotting factors with fresh frozen plasma, platelets, and cryoprecipitate, along with prompt correction of the process that is causing the bleeding.
OBG Management: What blood products do you administer to a patient with hemorrhage, and when?
Dr. Brown: The first line of defense for blood loss requiring transfusion is packed RBCs. Each unit of packed cells increases the hematocrit by 3% and hemoglobin by 1 g/dL, assuming bleeding is under control. After that, consider:
- Platelets. Depending on the severity of the hemorrhage and the level of platelets once the coagulation status is checked, platelets can be given. A 50-mL unit can raise the platelet count 5,000–10,000/mm3. Platelets should be considered if the count is below 50,000/mm3.
- Fresh frozen plasma should be given to replace clotting factors. Fresh frozen plasma contains fibrinogen, antithrombin III, factor V, and factor VIII. Each unit of fresh frozen plasma increases the fibrinogen level by 10 mg/dL.
- Cryoprecipitate contains fibrinogen, factors VIII and XIII, and von Willebrand factor. Each unit of cryoprecipitate increases fibrinogen by 10 mg/dL.
- Factor VII can be given if the hemorrhage is still active, but it should only be given after fresh frozen plasma and cryo-precipitate have been given to replace clotting factors. Factor VII is ineffective without clotting factor replacement prior to its administration. This medication is associated with a high risk of thromboembolism. It is also expensive.
- Synthetic fibrinogen (RiaSTAP) is available for use in the United States, but it has FDA approval only for the treatment of acute bleeding in patients who have congenital fibrinogen deficiency. It may have potential for use during PPH when essential clotting factors have been depleted.
A woman who is obese has additional risk factors for hemorrhage. Obesity itself is associated with prolonged labor and large-for-gestational-age infants, which, in turn, lead to poor contractility of the uterus and the potential for early postpartum hemorrhage.
Begin by ensuring that the obese or morbidly obese woman has appropriate intravenous access at the time of labor and receives early regional anesthesia (epidural). also alert anesthesia to the risk and assess baseline hemoglobin and hematocrit levels, including a type and screen.
An obese woman undergoing cesarean delivery has a heightened risk of uterine laceration, difficult extraction of the fetus, and uterine atony, especially if prolonged labor preceded the cesarean. Second-stage arrest and prolonged pushing before the cesarean may make extraction of the infant difficult and lead to poor uterine contractility once the placenta is removed.
All obese women, as well as other women at risk of postpartum uterine atony, should have oxytocin infused before the placenta is removed, especially at the time of cesarean delivery. Expressing the placenta at the time of cesarean delivery—as opposed to manual removal—is associated with lower blood loss and allows the uterus to begin contracting before the placenta is removed.—HAYWOOD L. BROWN, MD
8. When do you use the intrauterine balloon?
OBG Management: When is the intrauterine balloon a management option?
Dr. Brown: The balloon offers a way to actively manage hemorrhage and has been associated with decreasing morbidity and a reduced need for surgical intervention, including hysterectomy. It works through a tamponade effect. Once the balloon is inflated with 300 to 500 mL of saline, it compresses the uterine cavity until the uterus develops predelivery tone. It can be left in place as long as 24 hours, need be.
Several balloons are available for use, with the Bakri balloon being the prototype. The balloon may cut off uterine blood flow as a mechanism of action.
Before the advent of manufactured balloons, uterine tamponade was attempted using packing with gauze and a large-bore Foley catheter.
9. How do you proceed when surgery is necessary?
OBG Management: What surgical techniques—aside from hysterectomy—may be useful in stanching hemorrhage?
Dr. Brown: The first-line surgical approach after vaginal delivery is uterine exploration to evacuate uterine clots and check for retained placental fragments. This act alone may impart improved uterine contractility. If retained placental fragments are suspected, a gentle curettage of the uterine cavity, using a large curette, is appropriate.
When it is obvious that atony is the cause of the hemorrhage, and medical management has failed, these surgical steps are appropriate:
- Uterine artery ligation, using the “O’Leary” technique, can be performed bilaterally. The utero-ovarian vessels can also be ligated (but not cut!)
- B-Lynch suture as a technique to compress the uterus. This strategy uses outside, draping, absorbable suture to collapse the uterine cavity. It can be quite successful when combined with the use of uterotonics. One study reported more than 1,000 B-Lynch procedures, with only seven failures.1 Hemostatic multiple-square compression is a surgical technique that works according to a similar principle
- Hypogastric artery ligation can be performed by an experienced surgeon but is rarely employed in severe hemorrhage owing to the risk of complications and lengthy procedure time.
OBG Management: When does hysterectomy become an option?
Dr. Brown: Hysterectomy is the last defense against morbidity and maternal death from hemorrhage due to atony.
Clearly, when hysterectomy is performed, sooner is better than later, especially if uterine artery ligation and B-Lynch suture do not appear to be controlling the hemorrhage and the patient is hemodynamically unstable.
If the patient is a young woman with low parity, the uterus should be preserved, if at all possible, unless the hemorrhage cannot be controlled and the woman’s life is jeopardized.
When a uterine rupture has occurred, usually after a VBAC attempt, it may be prudent to proceed to hysterectomy, especially if the uterus appears to be difficult to repair.
10. When do you call for help?
OBG Management: When do you call in extra help?
Dr. Brown: As soon as hemorrhage occurs, the team should be assembled. It is critical that anesthesia be notified immediately, in the event that the patient requires surgical management. The blood bank should be notified that blood and blood products are likely to be required.
We designate a nursing leader to monitor the patient and another to keep the staff and unit on alert for potential surgical intervention. If uterine rupture or an invasive placental abnormality is suspected, we assemble the surgical team, including any potential consultant surgeon. We also notify the best available surgeons so that they can be ready to perform the necessary techniques. In addition, we notify the OR and surgical intensive care unit, in case they are needed.
OBG Management: How can obstetricians and obstetric units practice the response to OB hemorrhage so that, when a hemorrhage occurs, they are at the top of their game?
Dr. Brown: Obstetric units prepare by performing drills and simulations. These drills are now considered part of most units’ quality and safety programs.
Because obstetric hemorrhage can occur on any unit at any time, the team must be prepared to respond around the clock promptly and effectively to reduce the risk of morbidity and death.
After emergent surgical management of obstetric hemorrhage, the team should be assembled again to discuss what occurred and how they performed or could have performed more effectively as a team.
OBG Management: Should all obstetricians who perform repeat cesarean delivery be able to perform a cesarean hysterectomy in the event that uncontrollable hemorrhage is encountered?
Dr. Brown: It is an absolute must that any clinician who allows VBAC be capable of performing peripartum cesarean hysterectomy and know the indications for hysterectomy, as we have discussed. In fact, any obstetrician who performs cesarean delivery should be capable of performing a cesarean hysterectomy.
11. What do you recommend for practice?
OBG Management: How would you summarize the main points of management of postpartum hemorrhage?
Dr. Brown: I would suggest that the first step is organizing the team (obstetricians, nurses, anesthesiologist), followed by:
- resuscitation of the mother with oxygen and fluids through large-bore intravenous access sites
- notification of the blood bank (with typing and cross-matching) of the possible need for 4 to 6 U of blood for trans-fusion
- liberal assessment of laboratory values, especially coagulation status (International Normalized Ratio [INR], prothrombin time, and partial thromboplastin time) and blood counts (hemoglobin and hematocrit). Values may be lower if there has been significant blood loss and aggressive fluid resuscitation. Blood products such as fresh frozen plasma and cryoprecipitate are indicated, in addition to packed RBCs, if the patient has or is developing a coagulopathy. Also give platelets if the count is low. Once it becomes apparent that surgical intervention will be necessary, begin transfusion and replace clotting factors before beginning the procedure
- monitoring of vital signs and urine output throughout resuscitation and medical and surgical intervention
- elimination of the cause of bleeding as soon as possible by whatever means necessary to prevent maternal death, beginning with conservative medical management and, if necessary, followed by surgical intervention.
Tell us about a challenging case of postpartum hemorrhage and how you managed it.
Go to Send Us Your Letters. Please include your name, city, and state. We’ll publish intriguing “pearls” in an upcoming issue.
1. Allam MS, B-Lynch C. The B-Lynch and other uterine compression techniques. Int J Gynaecol Obstet. 2005;89(3):236-241.
2. Prendiville WJ, Elbourne D, McDonald S. Active versus expectant management in the third stage of labour. Cochrane Database Syst Rev. 2000;(3):CD000007.-
- Activated factor VII proves to be a lifesaver in postpartum hemorrhage
Robert L. Barbieri, MD (February 2007) - Postpartum hemorrhage: Solutions to 2 intractable cases
Michael L. Stitely, MD, and Robert B. Gherman, MD (April 2007) - Give a uterotonic routinely during the third stage of labor
Robert L. Barbieri, MD (May 2007) - Consider retroperitoneal packing for postpartum hemorrhage
Maj. William R. Fulton, DO (July 2008) - You should add the Bakri balloon to your treatments for OB bleeds
Robert L. Barbieri, MD (February 2009) - Planning reduces the risk of maternal death. This tool helps.
Robert L. Barbieri, MD (August 2009) - What you can do to optimize blood conservation in ObGyn practice
Eric J. Bieber, MD, Linda Scott, RN, Corinna Muller, DO, Nancy Nuss, RN, and Edie L. Derian, MD (February 2010)
 | Dr. Brown describes blood product replacement in severe PPH |
Q&A with Haywood L. Brown, MD
Dr. Brown is Roy T. Parker Professor and Chair of the Department of Obstetrics and Gynecology at Duke University Medical Center in Durham, NC.
Dr. Brown serves as a speaker for Alere and Hologic and as an advisor for the Bayer Foundation and Ferring
| Dr. Brown describes blood product replacement in severe PPH |
Q&A with Haywood L. Brown, MD
Dr. Brown is Roy T. Parker Professor and Chair of the Department of Obstetrics and Gynecology at Duke University Medical Center in Durham, NC.
Dr. Brown serves as a speaker for Alere and Hologic and as an advisor for the Bayer Foundation and Ferring
| Dr. Brown describes blood product replacement in severe PPH |
Q&A with Haywood L. Brown, MD
Dr. Brown is Roy T. Parker Professor and Chair of the Department of Obstetrics and Gynecology at Duke University Medical Center in Durham, NC.
Dr. Brown serves as a speaker for Alere and Hologic and as an advisor for the Bayer Foundation and Ferring
We know the potentially tragic outcome of postpartum hemorrhage (PPH): Worldwide, more than 140,000 women die every year as a result of PPH—one death every 4 minutes! Lest you dismiss PPH as a concern largely for developing countries, where it accounts for 25% of maternal deaths, consider this: In our highly developed nation, it accounts for nearly 8% of maternal deaths—a troubling statistic, to say the least.
The significant maternal death rate associated with PPH, and questions about how to reduce it, prompted the editors of OBG Management to talk with Haywood L. Brown, MD. Dr. Brown is Roy T. Parker Professor and chair of obstetrics and gynecology at Duke University Medical Center in Durham, NC. He is also a nationally recognized specialist in maternal-fetal medicine. In this interview, he discusses the full spectrum of management of PPH, from proactive assessment of a woman’s risk to determination of the cause to the tactic of last resort, emergent hysterectomy.
Uterine atony is the leading cause of postpartum hemorrhage. When medical management fails to stanch the bleeding, bilateral uterine artery ligation is one surgical option.
1. What is PPH?
OBG Management: Dr. Brown, let’s start with a simple but important aspect of PPH—how do you define it?
Dr. Brown: Obstetric hemorrhage is excessive bleeding that occurs during the intrapartum or postpartum period—specifically, estimated blood loss of 500 mL or more after vaginal delivery or 1,000 mL or more after cesarean delivery.
PPH is characterized as early or late, depending on whether the bleeding occurs within 24 hours of delivery (early, or primary) or between 24 hours and 6 to 12 weeks postpartum (late, or secondary). Primary PPH occurs in 4% to 6% of pregnancies.
Another way to define PPH: a decline of 10% or more in the baseline hematocrit level.
OBG Management: How do you measure blood loss?
Dr. Brown: The estimation of blood loss after delivery is an inexact science and typically yields an underestimation. Most clinicians rely on visual inspection to estimate the amount of blood collected in the drapes after vaginal delivery and in the suction bottles after cesarean delivery. Some facilities weigh lap pads or drapes to get a more accurate assessment of blood loss. In a routine delivery, no specific calorimetric measuring devices are used to estimate blood loss.
At my institution, we make an attempt to estimate blood loss at every delivery—vaginal or cesarean—and record the estimate. By doing this routinely, the clinician improves in accuracy and becomes more adept at identifying excessive bleeding.
OBG Management: Is blood loss the only variable that arouses concern about possible hemorrhage?
Dr. Brown: Because pregnant women experience an increase in blood volume and physiologic cardiovascular changes, the usual sign of significant bleeding can sometimes be masked. Therefore, any changes in maternal vital signs, such as a drop in blood pressure, tachycardia, or sensorial changes, may suggest that more blood has been lost than has been estimated.
Hypotension, dizziness, tachycardia or palpitations, and decreasing urine output will typically occur when more than 10% of maternal blood volume has been lost. In this situation, the patient should be given additional fluids, and a second intravenous line should be started using large-bore, 14-gauge access. In addition, the patient’s hemoglobin and hematocrit levels should be measured. All these actions constitute a first-line strategy to prevent shock and potential irreversible renal failure and cardiovascular collapse.
Low: 500 to 1,000 mL
This level of hemorrhage should be anticipated and can usually be managed with uterine massage and administration of a uterotonic agent, such as oxytocin. Intravenous fluids and careful monitoring of maternal vital signs are also warranted.
Active management of the third stage of labor has been shown to reduce the risk of significant postpartum hemorrhage (PPH). Active management includes:
- administration of a uterotonic agent immediately after delivery of the infant
- early cord clamping and cutting
- gentle cord traction with uterine counter-traction when the uterus is well contracted
- uterine massage.2
If these methods are unsuccessful in correcting the atony, uterotonics such as a prostaglandin (rectally administered misoprostol [800 mg] or intramuscular carboprost tromethamine [Hemabate; 250 μg/mL]) will usually succeed.
Medium: 1,000 to 1,500 mL
Blood loss of this volume is usually accompanied by cardiovascular signs, such as a fall in blood pressure, diaphoresis, and tachycardia. Women with this level of hemorrhage exhibit mild signs of shock.
It is important to correct maternal hypotension with fluids, restabilize vital signs, and resolve the bleeding expeditiously. If uterotonics and massage fail to stanch the bleeding, consider placing a balloon (e.g., Bakri balloon). Once the balloon is placed and inflated, it can be left for as long as 24 hours or until the uterus regains its tone.
Be sure to check hemoglobin and hematocrit levels and transfuse the patient, if necessary, especially if vital signs have not stabilized.
High: 1,500 to 2,000 mL, or greater
This is a medical emergency that must be managed aggressively to prevent morbidity and death. Blood loss of this volume will usually bring significant cardiovascular changes, such as hypotension, tachycardia, restlessness, pallor, oliguria, and cardiovascular collapse from hemorrhagic shock. this degree of blood loss means that the patient has lost 25% to 35% of her blood volume and will need blood-product replacement to prevent coagulation and the cascade of hemorrhage.
If conservative measures are unsuccessful, timely surgical intervention with B-Lynch suture, uterine vessel ligation, or hysterectomy is lifesaving.—HAYWOOD L. BROWN, MD
2. What causes PPH?
OBG Management: Why does PPH occur?
Dr. Brown: The leading cause is uterine atony, a failure of the uterus to contract and undergo resolution following delivery of an infant. Approximately 80% of cases of early PPH are related to uterine atony.
There are other causes of PPH:
- lacerations of the genital tract (perineum, vagina, cervix, or uterus)
- retained fragments of placental tissue
- uterine rupture
- blood clotting abnormalities
- uterine inversion.
3. Is it possible to prepare for PPH?
OBG Management: What is the starting point for management of PPH?
Dr. Brown: Prevention of, and preparation for, hemorrhage begin well before delivery. During the prenatal period, for example, it is important to assess the woman’s level of risk for PPH. Among the variables that increase her risk:
- any situation that leads to overstretching of the uterus, including multiple gestation, whether delivery is vaginal or cesarean
- a history of PPH.
It is important that women with these characteristics maintain adequate hemoglobin and hematocrit levels by taking vitamin and iron supplements in the antepartum period.
In addition, women who have abnormal placental implantation, such as placenta previa, are at risk for bleeding during the antepartum period and during cesarean delivery. They should maintain a hematocrit in the mid-30s because of expected blood loss during delivery.
OBG Management: What preparatory steps should be taken at the time of hospital admission if a woman has an elevated risk of bleeding?
Dr. Brown: When the patient is hospitalized in anticipation of delivery—whether vaginal or cesarean—the team should assess her hemoglobin and hematocrit levels and type and screen for possible transfusion. The patient should also be apprised of her risk and the potential for transfusion.
Last, the anesthesia team should be alerted to her risk factors for postpartum bleeding.
4. What intrapartum variables signal an increased risk of PPH?
OBG Management: During labor and delivery, what variables signal an elevated risk of bleeding?
Dr. Brown: Risk factors for hemorrhage become more apparent during this period. They include prolonged or rapid labor, prolonged use of oxytocin, operative delivery, infections such as chorioamnionitis, and vaginal birth after cesarean delivery (VBAC).
Bleeding with VBAC merits special attention because it could signal uterine rupture. Women who have a low transverse uterine scar and who undergo VBAC have a risk of uterine scar separation during labor of 0.5% to 1%.
OBG Management: What about retained placenta or a placenta that requires manual removal?
Dr. Brown: These intrapartum variables are not as easy to anticipate. They may suggest a condition such as placenta accreta, especially if the patient is undergoing VBAC.
Uterine inversion can also lead to hemorrhage and is a medical emergency.
OBG Management: What steps should be taken at the time of labor to ensure a safe outcome?
Dr. Brown: A type and screen should be available for all women on labor and delivery, and the team should anticipate the need to cross-match for blood if there is a high potential for transfusion. For example, a woman known to have anemia (hematocrit <30%) should have a cross-match performed so that blood can be prepared for transfusion.
In addition, women who are undergoing planned delivery for placental implantation disorders should have blood in the operating room ready for transfusion when cesarean is performed. These women are at great risk of hemorrhage and peripartum hysterectomy.
5. What first-line strategies do you recommend?
OBG Management: Do you recommend oxytocin administration and fundal massage for every patient after delivery of the infant?
Dr. Brown: Yes. These strategies lessen the risk of uterine atony and excessive bleeding after vaginal delivery. At the time of cesarean delivery, expression of the placenta and uterine massage, along with oxytocin administration, reduce the risk of excessive blood loss.
If bleeding continues even after the uterus begins to contract, look for other causes of the bleeding, such as uterine laceration or retained placental fragments.
OBG Management: What uterotonic agents do you use besides oxytocin, and when?
Dr. Brown: Oxytocin is the first-line agent for control of hemorrhage. I give a dosage of 10 to 40 U/L of normal saline or lactated Ringer solution, infused continuously. Alternatively, 10 U can be given intramuscularly (IM). Second-line drugs and their dosages are listed in the TABLE.
Uterotonic agents and how to administer them
| Drug | Dosage and route | Considerations |
|---|---|---|
| FIRST-LINE | ||
| Oxytocin | 10–40 U/L of saline or lactated ringer solution, infused continuously, Or 10 U IM | The preferred drug—often the only one needed |
| SECOND-LINE | ||
| Misoprostol (Cytotec, Prostaglandin e1) | 800–1,000 μg can be given rectally | Often, the second-line drug that is given just after oxytocin because it is easy to administer |
| Methylergonovine (Methergine) | 0.2 mg IM every 2–4 hr | Contraindicated in hypertension |
| Carboprost tromethamine (Hemabate) | 0.25 mg IM every 15–90 minutes (maximum of 8 doses) | Avoid in patients who have asthma. Contra-indicated in hepatic, renal, and cardiac disease |
| Dinoprostone (Prostin e2) | 20 mg suppository can be given vaginally or rectally every 2 hours | Avoid in hypotension |
6. How do you assess the patient once PPH is identified?
OBG Management: How do you assess the patient after hemorrhage begins?
Dr. Brown: We recheck the hemoglobin and hematocrit levels and monitor vital signs for hypotension and tachycardia. We also begin fluid resuscitation and type and cross-match blood and blood products.
A delayed response to hemorrhage raises the risk of maternal morbidity and death.
We notify the anesthesia team when it seems likely that a surgical approach to the hemorrhage will be needed. And we notify interventional radiology if the bleeding may respond to uterine artery embolization.
7. Why is it important to replace blood products?
OBG Management: You’ve been known to say, “The more blood a patient loses, the more blood she loses.” What do you mean by that?
Dr. Brown: Excessive bleeding leads to a loss of critical clotting factors that are made in the liver. Once the clotting factors are depleted, the woman is at risk of coagulopathy or disseminated intravascular coagulation. This depletion potentiates the cycle of hemorrhage. When that occurs, the hemorrhage can be controlled only with transfusion of red blood cells (RBCs) and replacement of clotting factors with fresh frozen plasma, platelets, and cryoprecipitate, along with prompt correction of the process that is causing the bleeding.
OBG Management: What blood products do you administer to a patient with hemorrhage, and when?
Dr. Brown: The first line of defense for blood loss requiring transfusion is packed RBCs. Each unit of packed cells increases the hematocrit by 3% and hemoglobin by 1 g/dL, assuming bleeding is under control. After that, consider:
- Platelets. Depending on the severity of the hemorrhage and the level of platelets once the coagulation status is checked, platelets can be given. A 50-mL unit can raise the platelet count 5,000–10,000/mm3. Platelets should be considered if the count is below 50,000/mm3.
- Fresh frozen plasma should be given to replace clotting factors. Fresh frozen plasma contains fibrinogen, antithrombin III, factor V, and factor VIII. Each unit of fresh frozen plasma increases the fibrinogen level by 10 mg/dL.
- Cryoprecipitate contains fibrinogen, factors VIII and XIII, and von Willebrand factor. Each unit of cryoprecipitate increases fibrinogen by 10 mg/dL.
- Factor VII can be given if the hemorrhage is still active, but it should only be given after fresh frozen plasma and cryo-precipitate have been given to replace clotting factors. Factor VII is ineffective without clotting factor replacement prior to its administration. This medication is associated with a high risk of thromboembolism. It is also expensive.
- Synthetic fibrinogen (RiaSTAP) is available for use in the United States, but it has FDA approval only for the treatment of acute bleeding in patients who have congenital fibrinogen deficiency. It may have potential for use during PPH when essential clotting factors have been depleted.
A woman who is obese has additional risk factors for hemorrhage. Obesity itself is associated with prolonged labor and large-for-gestational-age infants, which, in turn, lead to poor contractility of the uterus and the potential for early postpartum hemorrhage.
Begin by ensuring that the obese or morbidly obese woman has appropriate intravenous access at the time of labor and receives early regional anesthesia (epidural). also alert anesthesia to the risk and assess baseline hemoglobin and hematocrit levels, including a type and screen.
An obese woman undergoing cesarean delivery has a heightened risk of uterine laceration, difficult extraction of the fetus, and uterine atony, especially if prolonged labor preceded the cesarean. Second-stage arrest and prolonged pushing before the cesarean may make extraction of the infant difficult and lead to poor uterine contractility once the placenta is removed.
All obese women, as well as other women at risk of postpartum uterine atony, should have oxytocin infused before the placenta is removed, especially at the time of cesarean delivery. Expressing the placenta at the time of cesarean delivery—as opposed to manual removal—is associated with lower blood loss and allows the uterus to begin contracting before the placenta is removed.—HAYWOOD L. BROWN, MD
8. When do you use the intrauterine balloon?
OBG Management: When is the intrauterine balloon a management option?
Dr. Brown: The balloon offers a way to actively manage hemorrhage and has been associated with decreasing morbidity and a reduced need for surgical intervention, including hysterectomy. It works through a tamponade effect. Once the balloon is inflated with 300 to 500 mL of saline, it compresses the uterine cavity until the uterus develops predelivery tone. It can be left in place as long as 24 hours, need be.
Several balloons are available for use, with the Bakri balloon being the prototype. The balloon may cut off uterine blood flow as a mechanism of action.
Before the advent of manufactured balloons, uterine tamponade was attempted using packing with gauze and a large-bore Foley catheter.
9. How do you proceed when surgery is necessary?
OBG Management: What surgical techniques—aside from hysterectomy—may be useful in stanching hemorrhage?
Dr. Brown: The first-line surgical approach after vaginal delivery is uterine exploration to evacuate uterine clots and check for retained placental fragments. This act alone may impart improved uterine contractility. If retained placental fragments are suspected, a gentle curettage of the uterine cavity, using a large curette, is appropriate.
When it is obvious that atony is the cause of the hemorrhage, and medical management has failed, these surgical steps are appropriate:
- Uterine artery ligation, using the “O’Leary” technique, can be performed bilaterally. The utero-ovarian vessels can also be ligated (but not cut!)
- B-Lynch suture as a technique to compress the uterus. This strategy uses outside, draping, absorbable suture to collapse the uterine cavity. It can be quite successful when combined with the use of uterotonics. One study reported more than 1,000 B-Lynch procedures, with only seven failures.1 Hemostatic multiple-square compression is a surgical technique that works according to a similar principle
- Hypogastric artery ligation can be performed by an experienced surgeon but is rarely employed in severe hemorrhage owing to the risk of complications and lengthy procedure time.
OBG Management: When does hysterectomy become an option?
Dr. Brown: Hysterectomy is the last defense against morbidity and maternal death from hemorrhage due to atony.
Clearly, when hysterectomy is performed, sooner is better than later, especially if uterine artery ligation and B-Lynch suture do not appear to be controlling the hemorrhage and the patient is hemodynamically unstable.
If the patient is a young woman with low parity, the uterus should be preserved, if at all possible, unless the hemorrhage cannot be controlled and the woman’s life is jeopardized.
When a uterine rupture has occurred, usually after a VBAC attempt, it may be prudent to proceed to hysterectomy, especially if the uterus appears to be difficult to repair.
10. When do you call for help?
OBG Management: When do you call in extra help?
Dr. Brown: As soon as hemorrhage occurs, the team should be assembled. It is critical that anesthesia be notified immediately, in the event that the patient requires surgical management. The blood bank should be notified that blood and blood products are likely to be required.
We designate a nursing leader to monitor the patient and another to keep the staff and unit on alert for potential surgical intervention. If uterine rupture or an invasive placental abnormality is suspected, we assemble the surgical team, including any potential consultant surgeon. We also notify the best available surgeons so that they can be ready to perform the necessary techniques. In addition, we notify the OR and surgical intensive care unit, in case they are needed.
OBG Management: How can obstetricians and obstetric units practice the response to OB hemorrhage so that, when a hemorrhage occurs, they are at the top of their game?
Dr. Brown: Obstetric units prepare by performing drills and simulations. These drills are now considered part of most units’ quality and safety programs.
Because obstetric hemorrhage can occur on any unit at any time, the team must be prepared to respond around the clock promptly and effectively to reduce the risk of morbidity and death.
After emergent surgical management of obstetric hemorrhage, the team should be assembled again to discuss what occurred and how they performed or could have performed more effectively as a team.
OBG Management: Should all obstetricians who perform repeat cesarean delivery be able to perform a cesarean hysterectomy in the event that uncontrollable hemorrhage is encountered?
Dr. Brown: It is an absolute must that any clinician who allows VBAC be capable of performing peripartum cesarean hysterectomy and know the indications for hysterectomy, as we have discussed. In fact, any obstetrician who performs cesarean delivery should be capable of performing a cesarean hysterectomy.
11. What do you recommend for practice?
OBG Management: How would you summarize the main points of management of postpartum hemorrhage?
Dr. Brown: I would suggest that the first step is organizing the team (obstetricians, nurses, anesthesiologist), followed by:
- resuscitation of the mother with oxygen and fluids through large-bore intravenous access sites
- notification of the blood bank (with typing and cross-matching) of the possible need for 4 to 6 U of blood for trans-fusion
- liberal assessment of laboratory values, especially coagulation status (International Normalized Ratio [INR], prothrombin time, and partial thromboplastin time) and blood counts (hemoglobin and hematocrit). Values may be lower if there has been significant blood loss and aggressive fluid resuscitation. Blood products such as fresh frozen plasma and cryoprecipitate are indicated, in addition to packed RBCs, if the patient has or is developing a coagulopathy. Also give platelets if the count is low. Once it becomes apparent that surgical intervention will be necessary, begin transfusion and replace clotting factors before beginning the procedure
- monitoring of vital signs and urine output throughout resuscitation and medical and surgical intervention
- elimination of the cause of bleeding as soon as possible by whatever means necessary to prevent maternal death, beginning with conservative medical management and, if necessary, followed by surgical intervention.
Tell us about a challenging case of postpartum hemorrhage and how you managed it.
Go to Send Us Your Letters. Please include your name, city, and state. We’ll publish intriguing “pearls” in an upcoming issue.
We know the potentially tragic outcome of postpartum hemorrhage (PPH): Worldwide, more than 140,000 women die every year as a result of PPH—one death every 4 minutes! Lest you dismiss PPH as a concern largely for developing countries, where it accounts for 25% of maternal deaths, consider this: In our highly developed nation, it accounts for nearly 8% of maternal deaths—a troubling statistic, to say the least.
The significant maternal death rate associated with PPH, and questions about how to reduce it, prompted the editors of OBG Management to talk with Haywood L. Brown, MD. Dr. Brown is Roy T. Parker Professor and chair of obstetrics and gynecology at Duke University Medical Center in Durham, NC. He is also a nationally recognized specialist in maternal-fetal medicine. In this interview, he discusses the full spectrum of management of PPH, from proactive assessment of a woman’s risk to determination of the cause to the tactic of last resort, emergent hysterectomy.
Uterine atony is the leading cause of postpartum hemorrhage. When medical management fails to stanch the bleeding, bilateral uterine artery ligation is one surgical option.
1. What is PPH?
OBG Management: Dr. Brown, let’s start with a simple but important aspect of PPH—how do you define it?
Dr. Brown: Obstetric hemorrhage is excessive bleeding that occurs during the intrapartum or postpartum period—specifically, estimated blood loss of 500 mL or more after vaginal delivery or 1,000 mL or more after cesarean delivery.
PPH is characterized as early or late, depending on whether the bleeding occurs within 24 hours of delivery (early, or primary) or between 24 hours and 6 to 12 weeks postpartum (late, or secondary). Primary PPH occurs in 4% to 6% of pregnancies.
Another way to define PPH: a decline of 10% or more in the baseline hematocrit level.
OBG Management: How do you measure blood loss?
Dr. Brown: The estimation of blood loss after delivery is an inexact science and typically yields an underestimation. Most clinicians rely on visual inspection to estimate the amount of blood collected in the drapes after vaginal delivery and in the suction bottles after cesarean delivery. Some facilities weigh lap pads or drapes to get a more accurate assessment of blood loss. In a routine delivery, no specific calorimetric measuring devices are used to estimate blood loss.
At my institution, we make an attempt to estimate blood loss at every delivery—vaginal or cesarean—and record the estimate. By doing this routinely, the clinician improves in accuracy and becomes more adept at identifying excessive bleeding.
OBG Management: Is blood loss the only variable that arouses concern about possible hemorrhage?
Dr. Brown: Because pregnant women experience an increase in blood volume and physiologic cardiovascular changes, the usual sign of significant bleeding can sometimes be masked. Therefore, any changes in maternal vital signs, such as a drop in blood pressure, tachycardia, or sensorial changes, may suggest that more blood has been lost than has been estimated.
Hypotension, dizziness, tachycardia or palpitations, and decreasing urine output will typically occur when more than 10% of maternal blood volume has been lost. In this situation, the patient should be given additional fluids, and a second intravenous line should be started using large-bore, 14-gauge access. In addition, the patient’s hemoglobin and hematocrit levels should be measured. All these actions constitute a first-line strategy to prevent shock and potential irreversible renal failure and cardiovascular collapse.
Low: 500 to 1,000 mL
This level of hemorrhage should be anticipated and can usually be managed with uterine massage and administration of a uterotonic agent, such as oxytocin. Intravenous fluids and careful monitoring of maternal vital signs are also warranted.
Active management of the third stage of labor has been shown to reduce the risk of significant postpartum hemorrhage (PPH). Active management includes:
- administration of a uterotonic agent immediately after delivery of the infant
- early cord clamping and cutting
- gentle cord traction with uterine counter-traction when the uterus is well contracted
- uterine massage.2
If these methods are unsuccessful in correcting the atony, uterotonics such as a prostaglandin (rectally administered misoprostol [800 mg] or intramuscular carboprost tromethamine [Hemabate; 250 μg/mL]) will usually succeed.
Medium: 1,000 to 1,500 mL
Blood loss of this volume is usually accompanied by cardiovascular signs, such as a fall in blood pressure, diaphoresis, and tachycardia. Women with this level of hemorrhage exhibit mild signs of shock.
It is important to correct maternal hypotension with fluids, restabilize vital signs, and resolve the bleeding expeditiously. If uterotonics and massage fail to stanch the bleeding, consider placing a balloon (e.g., Bakri balloon). Once the balloon is placed and inflated, it can be left for as long as 24 hours or until the uterus regains its tone.
Be sure to check hemoglobin and hematocrit levels and transfuse the patient, if necessary, especially if vital signs have not stabilized.
High: 1,500 to 2,000 mL, or greater
This is a medical emergency that must be managed aggressively to prevent morbidity and death. Blood loss of this volume will usually bring significant cardiovascular changes, such as hypotension, tachycardia, restlessness, pallor, oliguria, and cardiovascular collapse from hemorrhagic shock. this degree of blood loss means that the patient has lost 25% to 35% of her blood volume and will need blood-product replacement to prevent coagulation and the cascade of hemorrhage.
If conservative measures are unsuccessful, timely surgical intervention with B-Lynch suture, uterine vessel ligation, or hysterectomy is lifesaving.—HAYWOOD L. BROWN, MD
2. What causes PPH?
OBG Management: Why does PPH occur?
Dr. Brown: The leading cause is uterine atony, a failure of the uterus to contract and undergo resolution following delivery of an infant. Approximately 80% of cases of early PPH are related to uterine atony.
There are other causes of PPH:
- lacerations of the genital tract (perineum, vagina, cervix, or uterus)
- retained fragments of placental tissue
- uterine rupture
- blood clotting abnormalities
- uterine inversion.
3. Is it possible to prepare for PPH?
OBG Management: What is the starting point for management of PPH?
Dr. Brown: Prevention of, and preparation for, hemorrhage begin well before delivery. During the prenatal period, for example, it is important to assess the woman’s level of risk for PPH. Among the variables that increase her risk:
- any situation that leads to overstretching of the uterus, including multiple gestation, whether delivery is vaginal or cesarean
- a history of PPH.
It is important that women with these characteristics maintain adequate hemoglobin and hematocrit levels by taking vitamin and iron supplements in the antepartum period.
In addition, women who have abnormal placental implantation, such as placenta previa, are at risk for bleeding during the antepartum period and during cesarean delivery. They should maintain a hematocrit in the mid-30s because of expected blood loss during delivery.
OBG Management: What preparatory steps should be taken at the time of hospital admission if a woman has an elevated risk of bleeding?
Dr. Brown: When the patient is hospitalized in anticipation of delivery—whether vaginal or cesarean—the team should assess her hemoglobin and hematocrit levels and type and screen for possible transfusion. The patient should also be apprised of her risk and the potential for transfusion.
Last, the anesthesia team should be alerted to her risk factors for postpartum bleeding.
4. What intrapartum variables signal an increased risk of PPH?
OBG Management: During labor and delivery, what variables signal an elevated risk of bleeding?
Dr. Brown: Risk factors for hemorrhage become more apparent during this period. They include prolonged or rapid labor, prolonged use of oxytocin, operative delivery, infections such as chorioamnionitis, and vaginal birth after cesarean delivery (VBAC).
Bleeding with VBAC merits special attention because it could signal uterine rupture. Women who have a low transverse uterine scar and who undergo VBAC have a risk of uterine scar separation during labor of 0.5% to 1%.
OBG Management: What about retained placenta or a placenta that requires manual removal?
Dr. Brown: These intrapartum variables are not as easy to anticipate. They may suggest a condition such as placenta accreta, especially if the patient is undergoing VBAC.
Uterine inversion can also lead to hemorrhage and is a medical emergency.
OBG Management: What steps should be taken at the time of labor to ensure a safe outcome?
Dr. Brown: A type and screen should be available for all women on labor and delivery, and the team should anticipate the need to cross-match for blood if there is a high potential for transfusion. For example, a woman known to have anemia (hematocrit <30%) should have a cross-match performed so that blood can be prepared for transfusion.
In addition, women who are undergoing planned delivery for placental implantation disorders should have blood in the operating room ready for transfusion when cesarean is performed. These women are at great risk of hemorrhage and peripartum hysterectomy.
5. What first-line strategies do you recommend?
OBG Management: Do you recommend oxytocin administration and fundal massage for every patient after delivery of the infant?
Dr. Brown: Yes. These strategies lessen the risk of uterine atony and excessive bleeding after vaginal delivery. At the time of cesarean delivery, expression of the placenta and uterine massage, along with oxytocin administration, reduce the risk of excessive blood loss.
If bleeding continues even after the uterus begins to contract, look for other causes of the bleeding, such as uterine laceration or retained placental fragments.
OBG Management: What uterotonic agents do you use besides oxytocin, and when?
Dr. Brown: Oxytocin is the first-line agent for control of hemorrhage. I give a dosage of 10 to 40 U/L of normal saline or lactated Ringer solution, infused continuously. Alternatively, 10 U can be given intramuscularly (IM). Second-line drugs and their dosages are listed in the TABLE.
Uterotonic agents and how to administer them
| Drug | Dosage and route | Considerations |
|---|---|---|
| FIRST-LINE | ||
| Oxytocin | 10–40 U/L of saline or lactated ringer solution, infused continuously, Or 10 U IM | The preferred drug—often the only one needed |
| SECOND-LINE | ||
| Misoprostol (Cytotec, Prostaglandin e1) | 800–1,000 μg can be given rectally | Often, the second-line drug that is given just after oxytocin because it is easy to administer |
| Methylergonovine (Methergine) | 0.2 mg IM every 2–4 hr | Contraindicated in hypertension |
| Carboprost tromethamine (Hemabate) | 0.25 mg IM every 15–90 minutes (maximum of 8 doses) | Avoid in patients who have asthma. Contra-indicated in hepatic, renal, and cardiac disease |
| Dinoprostone (Prostin e2) | 20 mg suppository can be given vaginally or rectally every 2 hours | Avoid in hypotension |
6. How do you assess the patient once PPH is identified?
OBG Management: How do you assess the patient after hemorrhage begins?
Dr. Brown: We recheck the hemoglobin and hematocrit levels and monitor vital signs for hypotension and tachycardia. We also begin fluid resuscitation and type and cross-match blood and blood products.
A delayed response to hemorrhage raises the risk of maternal morbidity and death.
We notify the anesthesia team when it seems likely that a surgical approach to the hemorrhage will be needed. And we notify interventional radiology if the bleeding may respond to uterine artery embolization.
7. Why is it important to replace blood products?
OBG Management: You’ve been known to say, “The more blood a patient loses, the more blood she loses.” What do you mean by that?
Dr. Brown: Excessive bleeding leads to a loss of critical clotting factors that are made in the liver. Once the clotting factors are depleted, the woman is at risk of coagulopathy or disseminated intravascular coagulation. This depletion potentiates the cycle of hemorrhage. When that occurs, the hemorrhage can be controlled only with transfusion of red blood cells (RBCs) and replacement of clotting factors with fresh frozen plasma, platelets, and cryoprecipitate, along with prompt correction of the process that is causing the bleeding.
OBG Management: What blood products do you administer to a patient with hemorrhage, and when?
Dr. Brown: The first line of defense for blood loss requiring transfusion is packed RBCs. Each unit of packed cells increases the hematocrit by 3% and hemoglobin by 1 g/dL, assuming bleeding is under control. After that, consider:
- Platelets. Depending on the severity of the hemorrhage and the level of platelets once the coagulation status is checked, platelets can be given. A 50-mL unit can raise the platelet count 5,000–10,000/mm3. Platelets should be considered if the count is below 50,000/mm3.
- Fresh frozen plasma should be given to replace clotting factors. Fresh frozen plasma contains fibrinogen, antithrombin III, factor V, and factor VIII. Each unit of fresh frozen plasma increases the fibrinogen level by 10 mg/dL.
- Cryoprecipitate contains fibrinogen, factors VIII and XIII, and von Willebrand factor. Each unit of cryoprecipitate increases fibrinogen by 10 mg/dL.
- Factor VII can be given if the hemorrhage is still active, but it should only be given after fresh frozen plasma and cryo-precipitate have been given to replace clotting factors. Factor VII is ineffective without clotting factor replacement prior to its administration. This medication is associated with a high risk of thromboembolism. It is also expensive.
- Synthetic fibrinogen (RiaSTAP) is available for use in the United States, but it has FDA approval only for the treatment of acute bleeding in patients who have congenital fibrinogen deficiency. It may have potential for use during PPH when essential clotting factors have been depleted.
A woman who is obese has additional risk factors for hemorrhage. Obesity itself is associated with prolonged labor and large-for-gestational-age infants, which, in turn, lead to poor contractility of the uterus and the potential for early postpartum hemorrhage.
Begin by ensuring that the obese or morbidly obese woman has appropriate intravenous access at the time of labor and receives early regional anesthesia (epidural). also alert anesthesia to the risk and assess baseline hemoglobin and hematocrit levels, including a type and screen.
An obese woman undergoing cesarean delivery has a heightened risk of uterine laceration, difficult extraction of the fetus, and uterine atony, especially if prolonged labor preceded the cesarean. Second-stage arrest and prolonged pushing before the cesarean may make extraction of the infant difficult and lead to poor uterine contractility once the placenta is removed.
All obese women, as well as other women at risk of postpartum uterine atony, should have oxytocin infused before the placenta is removed, especially at the time of cesarean delivery. Expressing the placenta at the time of cesarean delivery—as opposed to manual removal—is associated with lower blood loss and allows the uterus to begin contracting before the placenta is removed.—HAYWOOD L. BROWN, MD
8. When do you use the intrauterine balloon?
OBG Management: When is the intrauterine balloon a management option?
Dr. Brown: The balloon offers a way to actively manage hemorrhage and has been associated with decreasing morbidity and a reduced need for surgical intervention, including hysterectomy. It works through a tamponade effect. Once the balloon is inflated with 300 to 500 mL of saline, it compresses the uterine cavity until the uterus develops predelivery tone. It can be left in place as long as 24 hours, need be.
Several balloons are available for use, with the Bakri balloon being the prototype. The balloon may cut off uterine blood flow as a mechanism of action.
Before the advent of manufactured balloons, uterine tamponade was attempted using packing with gauze and a large-bore Foley catheter.
9. How do you proceed when surgery is necessary?
OBG Management: What surgical techniques—aside from hysterectomy—may be useful in stanching hemorrhage?
Dr. Brown: The first-line surgical approach after vaginal delivery is uterine exploration to evacuate uterine clots and check for retained placental fragments. This act alone may impart improved uterine contractility. If retained placental fragments are suspected, a gentle curettage of the uterine cavity, using a large curette, is appropriate.
When it is obvious that atony is the cause of the hemorrhage, and medical management has failed, these surgical steps are appropriate:
- Uterine artery ligation, using the “O’Leary” technique, can be performed bilaterally. The utero-ovarian vessels can also be ligated (but not cut!)
- B-Lynch suture as a technique to compress the uterus. This strategy uses outside, draping, absorbable suture to collapse the uterine cavity. It can be quite successful when combined with the use of uterotonics. One study reported more than 1,000 B-Lynch procedures, with only seven failures.1 Hemostatic multiple-square compression is a surgical technique that works according to a similar principle
- Hypogastric artery ligation can be performed by an experienced surgeon but is rarely employed in severe hemorrhage owing to the risk of complications and lengthy procedure time.
OBG Management: When does hysterectomy become an option?
Dr. Brown: Hysterectomy is the last defense against morbidity and maternal death from hemorrhage due to atony.
Clearly, when hysterectomy is performed, sooner is better than later, especially if uterine artery ligation and B-Lynch suture do not appear to be controlling the hemorrhage and the patient is hemodynamically unstable.
If the patient is a young woman with low parity, the uterus should be preserved, if at all possible, unless the hemorrhage cannot be controlled and the woman’s life is jeopardized.
When a uterine rupture has occurred, usually after a VBAC attempt, it may be prudent to proceed to hysterectomy, especially if the uterus appears to be difficult to repair.
10. When do you call for help?
OBG Management: When do you call in extra help?
Dr. Brown: As soon as hemorrhage occurs, the team should be assembled. It is critical that anesthesia be notified immediately, in the event that the patient requires surgical management. The blood bank should be notified that blood and blood products are likely to be required.
We designate a nursing leader to monitor the patient and another to keep the staff and unit on alert for potential surgical intervention. If uterine rupture or an invasive placental abnormality is suspected, we assemble the surgical team, including any potential consultant surgeon. We also notify the best available surgeons so that they can be ready to perform the necessary techniques. In addition, we notify the OR and surgical intensive care unit, in case they are needed.
OBG Management: How can obstetricians and obstetric units practice the response to OB hemorrhage so that, when a hemorrhage occurs, they are at the top of their game?
Dr. Brown: Obstetric units prepare by performing drills and simulations. These drills are now considered part of most units’ quality and safety programs.
Because obstetric hemorrhage can occur on any unit at any time, the team must be prepared to respond around the clock promptly and effectively to reduce the risk of morbidity and death.
After emergent surgical management of obstetric hemorrhage, the team should be assembled again to discuss what occurred and how they performed or could have performed more effectively as a team.
OBG Management: Should all obstetricians who perform repeat cesarean delivery be able to perform a cesarean hysterectomy in the event that uncontrollable hemorrhage is encountered?
Dr. Brown: It is an absolute must that any clinician who allows VBAC be capable of performing peripartum cesarean hysterectomy and know the indications for hysterectomy, as we have discussed. In fact, any obstetrician who performs cesarean delivery should be capable of performing a cesarean hysterectomy.
11. What do you recommend for practice?
OBG Management: How would you summarize the main points of management of postpartum hemorrhage?
Dr. Brown: I would suggest that the first step is organizing the team (obstetricians, nurses, anesthesiologist), followed by:
- resuscitation of the mother with oxygen and fluids through large-bore intravenous access sites
- notification of the blood bank (with typing and cross-matching) of the possible need for 4 to 6 U of blood for trans-fusion
- liberal assessment of laboratory values, especially coagulation status (International Normalized Ratio [INR], prothrombin time, and partial thromboplastin time) and blood counts (hemoglobin and hematocrit). Values may be lower if there has been significant blood loss and aggressive fluid resuscitation. Blood products such as fresh frozen plasma and cryoprecipitate are indicated, in addition to packed RBCs, if the patient has or is developing a coagulopathy. Also give platelets if the count is low. Once it becomes apparent that surgical intervention will be necessary, begin transfusion and replace clotting factors before beginning the procedure
- monitoring of vital signs and urine output throughout resuscitation and medical and surgical intervention
- elimination of the cause of bleeding as soon as possible by whatever means necessary to prevent maternal death, beginning with conservative medical management and, if necessary, followed by surgical intervention.
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1. Allam MS, B-Lynch C. The B-Lynch and other uterine compression techniques. Int J Gynaecol Obstet. 2005;89(3):236-241.
2. Prendiville WJ, Elbourne D, McDonald S. Active versus expectant management in the third stage of labour. Cochrane Database Syst Rev. 2000;(3):CD000007.-
- Activated factor VII proves to be a lifesaver in postpartum hemorrhage
Robert L. Barbieri, MD (February 2007) - Postpartum hemorrhage: Solutions to 2 intractable cases
Michael L. Stitely, MD, and Robert B. Gherman, MD (April 2007) - Give a uterotonic routinely during the third stage of labor
Robert L. Barbieri, MD (May 2007) - Consider retroperitoneal packing for postpartum hemorrhage
Maj. William R. Fulton, DO (July 2008) - You should add the Bakri balloon to your treatments for OB bleeds
Robert L. Barbieri, MD (February 2009) - Planning reduces the risk of maternal death. This tool helps.
Robert L. Barbieri, MD (August 2009) - What you can do to optimize blood conservation in ObGyn practice
Eric J. Bieber, MD, Linda Scott, RN, Corinna Muller, DO, Nancy Nuss, RN, and Edie L. Derian, MD (February 2010)
1. Allam MS, B-Lynch C. The B-Lynch and other uterine compression techniques. Int J Gynaecol Obstet. 2005;89(3):236-241.
2. Prendiville WJ, Elbourne D, McDonald S. Active versus expectant management in the third stage of labour. Cochrane Database Syst Rev. 2000;(3):CD000007.-
- Activated factor VII proves to be a lifesaver in postpartum hemorrhage
Robert L. Barbieri, MD (February 2007) - Postpartum hemorrhage: Solutions to 2 intractable cases
Michael L. Stitely, MD, and Robert B. Gherman, MD (April 2007) - Give a uterotonic routinely during the third stage of labor
Robert L. Barbieri, MD (May 2007) - Consider retroperitoneal packing for postpartum hemorrhage
Maj. William R. Fulton, DO (July 2008) - You should add the Bakri balloon to your treatments for OB bleeds
Robert L. Barbieri, MD (February 2009) - Planning reduces the risk of maternal death. This tool helps.
Robert L. Barbieri, MD (August 2009) - What you can do to optimize blood conservation in ObGyn practice
Eric J. Bieber, MD, Linda Scott, RN, Corinna Muller, DO, Nancy Nuss, RN, and Edie L. Derian, MD (February 2010)