Rhinophymatous Amelanotic Melanoma

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Unilateral Volar Annular Syringomata

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Turning the Tide [editorial]

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Are any alternative therapies effective in treating asthma?

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EVIDENCE-BASED ANSWER

Yes, some are. Acupuncture relieves subjective symptoms of asthma and reduces medication use in mild to moderate asthma (strength of recommendation [SOR]: A, based on systematic review of randomized controlled trials [RCTs] of variable quality). Herbal medications, such as Ginkgo biloba, appear to improve lung function, while herbs such as Tylophora indica and Tsumura saiboku-to may decrease asthma symptoms (SOR: B, based on systematic review of RCTs with poor methodology). No evidence, however, supports the use of room air ionizers, manual therapy, homeopathy, or mind-body therapy for treatment of asthma (SOR: A, based on systematic reviews and meta-analyses of RCTs and individual RCTs).

Clinical commentary

Though this research is interesting, we should adhere to current guidelines
Vincent Lo, MD
San Joaquin General Hospital, French Camp, Calif

Guidelines for the diagnosis and management of asthma are widely disseminated by the National Asthma Education and Prevention Program through its Expert Panel Reports (updated in 2002).1 Nevertheless, nearly 500,000 hospitalizations, 2 million emergency department visits, and 5000 deaths were reported annually in the US among those who have asthma.2 Furthermore, a significant difference in asthma prevalence, health care use, and mortality was found among different ethnic groups.1

Poor patient understanding of asthma control, nonadherence to medication regimens, cultural beliefs, and disparity of access to the health care system, together with physicians’ lack of close monitoring and inadequate compliance with national asthma guidelines, contribute to suboptimal control of chronic asthma. Family physicians must guide and empower their patients with the knowledge and responsibility of how to manage their asthma. For now, we should adhere to current national guidelines of management of asthma and avoid routine recommendation of any complimentary alternative treatments.

Evidence summary

Although complementary and alternative medicine (CAM) therapies are widely used, the overall body of research into CAM for asthma is still small and of limited quality. Interpreting the research is hampered by lack of standardized therapeutic approaches, lack of accepted methods for appropriate trials, and the fact that many CAM treatments are used as part of a multi-pronged, individualized approach to treatment in actual practice. Our search found 4 good-quality systematic reviews of RCTs, 1 good-quality systematic review of randomized trials, and 1 small additional pilot RCT of various CAM treatments for asthma.

 

Acupuncture and herbals provide some benefit

While a Cochrane review of 11 RCTs with variable trial quality and a total of 324 participants found that acupuncture had no significant effect on pulmonary function or global assessment of well-being, the review noted that some studies reported significant positive changes in daily symptoms, reductions in medication use, and improved quality of life. This suggests that some patients with mild to moderate asthma may benefit from acupuncture.3 In 1 RCT, improvement in general well-being was reported by 79% of 38 patients receiving acupuncture compared with 47% of 18 patients in the control group.4

 

 

When it comes to herbal remedies, a good-quality systematic review5 of 17 trials, with overall poor methodological quality and a total of 1445 participants, reported significant improvements in clinically relevant measures with 6 different herbal medicines.

  • Ginkgo biloba liquor increased forced expiratory volume in 1 second (FEV1) by 10% at 4 weeks and by a more clinically relevant 15% at 8 weeks (significantly greater than placebo, P<.05).
  • Invigorating Kidney for Preventing Asthma (IKPA) tablets increased FEV1 by 30% at 3 months compared with 17% in controls (P<.05).
  • Wenyang Tonglulo Mixture (WTM) improved FEV1 by 30% at 8 weeks compared with a 16% increase in the control group using oral salbutamol and inhaled beclomethasone (P<.05).
  • Dried ivy extract, thought to work as both a secretolytic and bronchospasmolytic, reduced airway resistance in children by 23.6% compared with placebo (P=.036).
  • Tylophora indica (a rare herb also known as Indian ipecac) provided significant improvement in nocturnal dyspnea when compared with controls (P<.01) in a study that relied on patients’ symptom diaries.
  • Tsumura saiboku-to (TJ-96) provided patients in one RCT with significant, but unspecified, asthma symptom relief when compared with those in a control group (P<.01).5

Other therapies didn’t quite make the grade

Homeopathy. A Cochrane review of 6 RCTs of mixed quality, with a total of 556 patients, concluded the evidence is insufficient to evaluate the possible role of homeopathy for the treatment of asthma, due to heterogeneity of interventions, patient populations, and outcome assessments. Each study evaluated a different homeopathic remedy, making any overall assessment difficult.

The review notes there have been only limited attempts to study a complete “package of care,” which includes the in-depth, one-on-one consultation, treatment, and follow-up that characterizes most homeopathic treatment in practice.6

 

Room air ionizers. A Cochrane review of 6 good-quality trials with a total of 106 participants reported no significant effect of room air ionizers on pulmonary function measures, symptoms, or medication use.7

Manual therapy. A Cochrane review8 of 3 moderate- to poor-quality RCTs with 156 participants reported no significant effect of chiropractic spinal manipulation (2 trials) or massage therapy (1 trial) on lung function, asthma symptoms, or medication use.

Mind-body therapy. A pilot RCT9 with 33 adults found a nonsignificant reduction in medication use among the subjects practicing mental imagery, but no overall effect on lung function or quality-of-life measures.

Recommendations from others

The New Zealand Guideline Group (NZGG)10 gives a Grade B recommendation for Buteyko Breathing Techniques as an intervention that may be helpful in reducing acute exacerbation medication use and improving patient quality of life. However, the NZGG did not find other benefits to this intervention and noted that it might be costly for the patient to obtain training in these techniques. The NZGG further recommends as a good practice point that healthcare professionals be open to the use of CAM therapies and that such therapies be tried by patients who are interested in them, with monitoring and self-assessment to assist patients in determining which therapies are of value.

References

1. Guidelines for the diagnosis and management of asthma. Update on selected topics 2002. Available at: www.nhlbi.nih.gov/guidelines/asthma/index.htm. Accessed on March 30, 2007.

2. Mannino DM, Home DW, Akinbami LJ, Morrman JE, Guynn C, Redd SC. Surveillance of Asthma—1980–1999. MMWR Surveill Summ 2002;51:1-13.

3. McCarney RW, Brinkhaus B, Lasserson TJ, Linde K. Acupuncture for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000008.-

4. Joos S, Schott C, Zou H, Daniel V, Martin E. Immunomodulatory effects of acupuncture in the treatment of allergic asthma: a randomized controlled study. J Altern Complementary Med 2000;6:519-525.

5. Huntley A, Ernst E. Herbal medicines for asthma: a systemic review. Thorax 2000;55:925-929.

6. McCarney RW, Linde K, Lasserson TJ. Homeopathy for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000353.-

7. Blackhall K, Appleton S, Cates FJ. Ionisers for chronic asthma. Cochrane Database Syst Rev 2003;(3):CD002986.-

8. Hondras MA, Jones LK, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev 2005;(2):CD001002.-

9. Epstein GN, Halper JP, Barrett EA, et al. A pilot study of mind-body changes in adults with asthma who practice mental imagery. Alternative Therapies 2004;10:66-71.

10. New Zealand Guidelines Group (NZGG) The diagnosis and treatment of adult asthma. Best Practice Evidence-Based Guideline. Wellington, NZ: NZGG; 2007. Available at: www.nzgg.org.nz/guidelines/0003/Full_text_Guideline.pdf. Accessed on March 30, 2007.

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Dolores Zegar Judkins, MLS
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EVIDENCE-BASED ANSWER

Yes, some are. Acupuncture relieves subjective symptoms of asthma and reduces medication use in mild to moderate asthma (strength of recommendation [SOR]: A, based on systematic review of randomized controlled trials [RCTs] of variable quality). Herbal medications, such as Ginkgo biloba, appear to improve lung function, while herbs such as Tylophora indica and Tsumura saiboku-to may decrease asthma symptoms (SOR: B, based on systematic review of RCTs with poor methodology). No evidence, however, supports the use of room air ionizers, manual therapy, homeopathy, or mind-body therapy for treatment of asthma (SOR: A, based on systematic reviews and meta-analyses of RCTs and individual RCTs).

Clinical commentary

Though this research is interesting, we should adhere to current guidelines
Vincent Lo, MD
San Joaquin General Hospital, French Camp, Calif

Guidelines for the diagnosis and management of asthma are widely disseminated by the National Asthma Education and Prevention Program through its Expert Panel Reports (updated in 2002).1 Nevertheless, nearly 500,000 hospitalizations, 2 million emergency department visits, and 5000 deaths were reported annually in the US among those who have asthma.2 Furthermore, a significant difference in asthma prevalence, health care use, and mortality was found among different ethnic groups.1

Poor patient understanding of asthma control, nonadherence to medication regimens, cultural beliefs, and disparity of access to the health care system, together with physicians’ lack of close monitoring and inadequate compliance with national asthma guidelines, contribute to suboptimal control of chronic asthma. Family physicians must guide and empower their patients with the knowledge and responsibility of how to manage their asthma. For now, we should adhere to current national guidelines of management of asthma and avoid routine recommendation of any complimentary alternative treatments.

Evidence summary

Although complementary and alternative medicine (CAM) therapies are widely used, the overall body of research into CAM for asthma is still small and of limited quality. Interpreting the research is hampered by lack of standardized therapeutic approaches, lack of accepted methods for appropriate trials, and the fact that many CAM treatments are used as part of a multi-pronged, individualized approach to treatment in actual practice. Our search found 4 good-quality systematic reviews of RCTs, 1 good-quality systematic review of randomized trials, and 1 small additional pilot RCT of various CAM treatments for asthma.

 

Acupuncture and herbals provide some benefit

While a Cochrane review of 11 RCTs with variable trial quality and a total of 324 participants found that acupuncture had no significant effect on pulmonary function or global assessment of well-being, the review noted that some studies reported significant positive changes in daily symptoms, reductions in medication use, and improved quality of life. This suggests that some patients with mild to moderate asthma may benefit from acupuncture.3 In 1 RCT, improvement in general well-being was reported by 79% of 38 patients receiving acupuncture compared with 47% of 18 patients in the control group.4

 

 

When it comes to herbal remedies, a good-quality systematic review5 of 17 trials, with overall poor methodological quality and a total of 1445 participants, reported significant improvements in clinically relevant measures with 6 different herbal medicines.

  • Ginkgo biloba liquor increased forced expiratory volume in 1 second (FEV1) by 10% at 4 weeks and by a more clinically relevant 15% at 8 weeks (significantly greater than placebo, P<.05).
  • Invigorating Kidney for Preventing Asthma (IKPA) tablets increased FEV1 by 30% at 3 months compared with 17% in controls (P<.05).
  • Wenyang Tonglulo Mixture (WTM) improved FEV1 by 30% at 8 weeks compared with a 16% increase in the control group using oral salbutamol and inhaled beclomethasone (P<.05).
  • Dried ivy extract, thought to work as both a secretolytic and bronchospasmolytic, reduced airway resistance in children by 23.6% compared with placebo (P=.036).
  • Tylophora indica (a rare herb also known as Indian ipecac) provided significant improvement in nocturnal dyspnea when compared with controls (P<.01) in a study that relied on patients’ symptom diaries.
  • Tsumura saiboku-to (TJ-96) provided patients in one RCT with significant, but unspecified, asthma symptom relief when compared with those in a control group (P<.01).5

Other therapies didn’t quite make the grade

Homeopathy. A Cochrane review of 6 RCTs of mixed quality, with a total of 556 patients, concluded the evidence is insufficient to evaluate the possible role of homeopathy for the treatment of asthma, due to heterogeneity of interventions, patient populations, and outcome assessments. Each study evaluated a different homeopathic remedy, making any overall assessment difficult.

The review notes there have been only limited attempts to study a complete “package of care,” which includes the in-depth, one-on-one consultation, treatment, and follow-up that characterizes most homeopathic treatment in practice.6

 

Room air ionizers. A Cochrane review of 6 good-quality trials with a total of 106 participants reported no significant effect of room air ionizers on pulmonary function measures, symptoms, or medication use.7

Manual therapy. A Cochrane review8 of 3 moderate- to poor-quality RCTs with 156 participants reported no significant effect of chiropractic spinal manipulation (2 trials) or massage therapy (1 trial) on lung function, asthma symptoms, or medication use.

Mind-body therapy. A pilot RCT9 with 33 adults found a nonsignificant reduction in medication use among the subjects practicing mental imagery, but no overall effect on lung function or quality-of-life measures.

Recommendations from others

The New Zealand Guideline Group (NZGG)10 gives a Grade B recommendation for Buteyko Breathing Techniques as an intervention that may be helpful in reducing acute exacerbation medication use and improving patient quality of life. However, the NZGG did not find other benefits to this intervention and noted that it might be costly for the patient to obtain training in these techniques. The NZGG further recommends as a good practice point that healthcare professionals be open to the use of CAM therapies and that such therapies be tried by patients who are interested in them, with monitoring and self-assessment to assist patients in determining which therapies are of value.

EVIDENCE-BASED ANSWER

Yes, some are. Acupuncture relieves subjective symptoms of asthma and reduces medication use in mild to moderate asthma (strength of recommendation [SOR]: A, based on systematic review of randomized controlled trials [RCTs] of variable quality). Herbal medications, such as Ginkgo biloba, appear to improve lung function, while herbs such as Tylophora indica and Tsumura saiboku-to may decrease asthma symptoms (SOR: B, based on systematic review of RCTs with poor methodology). No evidence, however, supports the use of room air ionizers, manual therapy, homeopathy, or mind-body therapy for treatment of asthma (SOR: A, based on systematic reviews and meta-analyses of RCTs and individual RCTs).

Clinical commentary

Though this research is interesting, we should adhere to current guidelines
Vincent Lo, MD
San Joaquin General Hospital, French Camp, Calif

Guidelines for the diagnosis and management of asthma are widely disseminated by the National Asthma Education and Prevention Program through its Expert Panel Reports (updated in 2002).1 Nevertheless, nearly 500,000 hospitalizations, 2 million emergency department visits, and 5000 deaths were reported annually in the US among those who have asthma.2 Furthermore, a significant difference in asthma prevalence, health care use, and mortality was found among different ethnic groups.1

Poor patient understanding of asthma control, nonadherence to medication regimens, cultural beliefs, and disparity of access to the health care system, together with physicians’ lack of close monitoring and inadequate compliance with national asthma guidelines, contribute to suboptimal control of chronic asthma. Family physicians must guide and empower their patients with the knowledge and responsibility of how to manage their asthma. For now, we should adhere to current national guidelines of management of asthma and avoid routine recommendation of any complimentary alternative treatments.

Evidence summary

Although complementary and alternative medicine (CAM) therapies are widely used, the overall body of research into CAM for asthma is still small and of limited quality. Interpreting the research is hampered by lack of standardized therapeutic approaches, lack of accepted methods for appropriate trials, and the fact that many CAM treatments are used as part of a multi-pronged, individualized approach to treatment in actual practice. Our search found 4 good-quality systematic reviews of RCTs, 1 good-quality systematic review of randomized trials, and 1 small additional pilot RCT of various CAM treatments for asthma.

 

Acupuncture and herbals provide some benefit

While a Cochrane review of 11 RCTs with variable trial quality and a total of 324 participants found that acupuncture had no significant effect on pulmonary function or global assessment of well-being, the review noted that some studies reported significant positive changes in daily symptoms, reductions in medication use, and improved quality of life. This suggests that some patients with mild to moderate asthma may benefit from acupuncture.3 In 1 RCT, improvement in general well-being was reported by 79% of 38 patients receiving acupuncture compared with 47% of 18 patients in the control group.4

 

 

When it comes to herbal remedies, a good-quality systematic review5 of 17 trials, with overall poor methodological quality and a total of 1445 participants, reported significant improvements in clinically relevant measures with 6 different herbal medicines.

  • Ginkgo biloba liquor increased forced expiratory volume in 1 second (FEV1) by 10% at 4 weeks and by a more clinically relevant 15% at 8 weeks (significantly greater than placebo, P<.05).
  • Invigorating Kidney for Preventing Asthma (IKPA) tablets increased FEV1 by 30% at 3 months compared with 17% in controls (P<.05).
  • Wenyang Tonglulo Mixture (WTM) improved FEV1 by 30% at 8 weeks compared with a 16% increase in the control group using oral salbutamol and inhaled beclomethasone (P<.05).
  • Dried ivy extract, thought to work as both a secretolytic and bronchospasmolytic, reduced airway resistance in children by 23.6% compared with placebo (P=.036).
  • Tylophora indica (a rare herb also known as Indian ipecac) provided significant improvement in nocturnal dyspnea when compared with controls (P<.01) in a study that relied on patients’ symptom diaries.
  • Tsumura saiboku-to (TJ-96) provided patients in one RCT with significant, but unspecified, asthma symptom relief when compared with those in a control group (P<.01).5

Other therapies didn’t quite make the grade

Homeopathy. A Cochrane review of 6 RCTs of mixed quality, with a total of 556 patients, concluded the evidence is insufficient to evaluate the possible role of homeopathy for the treatment of asthma, due to heterogeneity of interventions, patient populations, and outcome assessments. Each study evaluated a different homeopathic remedy, making any overall assessment difficult.

The review notes there have been only limited attempts to study a complete “package of care,” which includes the in-depth, one-on-one consultation, treatment, and follow-up that characterizes most homeopathic treatment in practice.6

 

Room air ionizers. A Cochrane review of 6 good-quality trials with a total of 106 participants reported no significant effect of room air ionizers on pulmonary function measures, symptoms, or medication use.7

Manual therapy. A Cochrane review8 of 3 moderate- to poor-quality RCTs with 156 participants reported no significant effect of chiropractic spinal manipulation (2 trials) or massage therapy (1 trial) on lung function, asthma symptoms, or medication use.

Mind-body therapy. A pilot RCT9 with 33 adults found a nonsignificant reduction in medication use among the subjects practicing mental imagery, but no overall effect on lung function or quality-of-life measures.

Recommendations from others

The New Zealand Guideline Group (NZGG)10 gives a Grade B recommendation for Buteyko Breathing Techniques as an intervention that may be helpful in reducing acute exacerbation medication use and improving patient quality of life. However, the NZGG did not find other benefits to this intervention and noted that it might be costly for the patient to obtain training in these techniques. The NZGG further recommends as a good practice point that healthcare professionals be open to the use of CAM therapies and that such therapies be tried by patients who are interested in them, with monitoring and self-assessment to assist patients in determining which therapies are of value.

References

1. Guidelines for the diagnosis and management of asthma. Update on selected topics 2002. Available at: www.nhlbi.nih.gov/guidelines/asthma/index.htm. Accessed on March 30, 2007.

2. Mannino DM, Home DW, Akinbami LJ, Morrman JE, Guynn C, Redd SC. Surveillance of Asthma—1980–1999. MMWR Surveill Summ 2002;51:1-13.

3. McCarney RW, Brinkhaus B, Lasserson TJ, Linde K. Acupuncture for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000008.-

4. Joos S, Schott C, Zou H, Daniel V, Martin E. Immunomodulatory effects of acupuncture in the treatment of allergic asthma: a randomized controlled study. J Altern Complementary Med 2000;6:519-525.

5. Huntley A, Ernst E. Herbal medicines for asthma: a systemic review. Thorax 2000;55:925-929.

6. McCarney RW, Linde K, Lasserson TJ. Homeopathy for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000353.-

7. Blackhall K, Appleton S, Cates FJ. Ionisers for chronic asthma. Cochrane Database Syst Rev 2003;(3):CD002986.-

8. Hondras MA, Jones LK, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev 2005;(2):CD001002.-

9. Epstein GN, Halper JP, Barrett EA, et al. A pilot study of mind-body changes in adults with asthma who practice mental imagery. Alternative Therapies 2004;10:66-71.

10. New Zealand Guidelines Group (NZGG) The diagnosis and treatment of adult asthma. Best Practice Evidence-Based Guideline. Wellington, NZ: NZGG; 2007. Available at: www.nzgg.org.nz/guidelines/0003/Full_text_Guideline.pdf. Accessed on March 30, 2007.

References

1. Guidelines for the diagnosis and management of asthma. Update on selected topics 2002. Available at: www.nhlbi.nih.gov/guidelines/asthma/index.htm. Accessed on March 30, 2007.

2. Mannino DM, Home DW, Akinbami LJ, Morrman JE, Guynn C, Redd SC. Surveillance of Asthma—1980–1999. MMWR Surveill Summ 2002;51:1-13.

3. McCarney RW, Brinkhaus B, Lasserson TJ, Linde K. Acupuncture for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000008.-

4. Joos S, Schott C, Zou H, Daniel V, Martin E. Immunomodulatory effects of acupuncture in the treatment of allergic asthma: a randomized controlled study. J Altern Complementary Med 2000;6:519-525.

5. Huntley A, Ernst E. Herbal medicines for asthma: a systemic review. Thorax 2000;55:925-929.

6. McCarney RW, Linde K, Lasserson TJ. Homeopathy for chronic asthma. Cochrane Database Syst Rev 2004;(1):CD000353.-

7. Blackhall K, Appleton S, Cates FJ. Ionisers for chronic asthma. Cochrane Database Syst Rev 2003;(3):CD002986.-

8. Hondras MA, Jones LK, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev 2005;(2):CD001002.-

9. Epstein GN, Halper JP, Barrett EA, et al. A pilot study of mind-body changes in adults with asthma who practice mental imagery. Alternative Therapies 2004;10:66-71.

10. New Zealand Guidelines Group (NZGG) The diagnosis and treatment of adult asthma. Best Practice Evidence-Based Guideline. Wellington, NZ: NZGG; 2007. Available at: www.nzgg.org.nz/guidelines/0003/Full_text_Guideline.pdf. Accessed on March 30, 2007.

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Treating posttraumatic stress in motor vehicle accident survivors

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Treating posttraumatic stress in motor vehicle accident survivors

Stopped at a red light, Mr. O glances in the rearview mirror and sees headlights coming up fast. The sport utility vehicle behind him is not slowing down. He braces himself as the SUV plows into the back of his car, snapping his head back and forth violently.

As white smoke fills his eyes and lungs. Mr. O realizes he has been pushed into the intersection, and for a moment thinks about never seeing his wife and children again. As he hears tires screeching, his car is struck by a truck.

Mr. O does not die, as he feared, but 6 months later he is “just not ready” to return to work. The doctor who is treating his whiplash injury refers him for evaluation of lingering anxiety.

Posttraumatic stress disorder (PTSD) resulting from a motor vehicle accident (MVA) can have a persistent disabling effect. To help you effectively treat patients such as Mr. O, this article examines:

  • common PTSD symptoms in accident survivors
  • recommended diagnostic interviews and assessment tools
  • techniques for using psychotherapy to overcome residual PTSD symptoms.

CASE CONTINUED: Lingering impairment

In the 6 months since the accident, Mr. O’s sleep is disrupted by pain and worry; when he can sleep, he frequently has nightmares about the accident. Mr. O feels anxious and irritable, and thoughts of that evening play over and over in his mind.

Mr. O doesn’t like to talk about the accident and has not resumed driving. He avoids all but required trips, such as to doctors’ appointments, which he endures with extreme anxiety. Whenever his wife drives without him, he insists that she immediately call him when she reaches her destination. At the same time, he feels emotionally distant from her and the children. He shows little interest in hobbies he’d previously enjoyed.

3 symptom clusters of PTSD

To meet DSM-IV-TR criteria for PTSD, a person must have experienced, witnessed, or been confronted by an event that involved actual or threatened death or serious injury, to which he responded with intense fear, helplessness, or horror.1 PTSD’s 3 symptom clusters—reexperiencing, avoidance/numbing, and hyperarousal—encompass 17 core symptoms, and a patient must exhibit at least the minimum number of symptoms from each cluster (Table 1).

MVA survivors with PTSD often have intrusive memories and nightmares. They might avoid talking about the accident and resist or abstain from driving or traveling by car. They often fear and avoid people, places, activities, and reminders of the MVA that can trigger upsetting reactions, such as anxiety, tachycardia, and panic. They may be irritable, detached, or estranged from loved ones, or have difficulty sleeping or concentrating. These symptoms must persist for ≥30 days and cause clinically significant distress and impaired functioning for a person to meet the criteria for chronic PTSD.

Table 1

Patients experience 3 ‘clusters’ of PTSD symptoms

Symptom clusterSymptoms
Reexperiencing
(≥1 required)
  • Distressing recollections of the trauma
  • Distressing dreams of the trauma
  • Acting/feeling as if the trauma were recurring
  • Psychological distress upon confronting trauma cues
  • Physiologic reactivity upon confronting trauma cues
Avoidance/numbing
(≥3 required)
  • Avoiding trauma-related thoughts, feelings, or conversations
  • Avoiding activities, places, or people reminiscent of the trauma
  • Inability to recall an important aspect of the trauma
  • Diminished interest or participation in significant activities
  • Feeling of detachment or estrangement from others
  • Restricted range of affect
  • Sense of foreshortened future
Hyperarousal
(≥2 required)
  • Sleep difficulties
  • Irritability or outbursts of anger
  • Difficulty concentrating
  • Hypervigilance
  • Exaggerated startle response
Note: In addition to having the minimum number of symptoms from each cluster as indicated above, for a patient to meet PTSD criteria, symptoms must cause clinically significant distress and impairment in functioning.
PTSD: posttraumatic stress disorder
Source: DSM-IV-TR

CASE CONTINUED: Reaching a diagnosis

Using a combination of interviews and self-report measures, the psychiatrist diagnoses Mr. O with chronic PTSD. Since the MVA, Mr. O has developed the required number of reexperiencing, avoidance/numbing, and hyperarousal symptoms. These symptoms have persisted for >30 days and significantly impair his functioning.

Use multiple assessment tools

To assess an MVA survivor for PTSD and related problems, we advocate using a combination of:

  • unstructured clinical interviews
  • structured clinical interviews
  • self-report measures.

Also collect information from collateral sources, such as patients’ spouses or significant others, when appropriate and available.

In an unstructured interview, obtain:

  • a thorough, detailed description of the MVA, including what occurred and the patient’s thoughts and feelings during and since the accident
  • a description of physical injuries, medical treatments, and medication use.

This information can rule out physical causes of PTSD-like symptoms, such as a traumatic brain injury that results in concentration difficulties and irritability. Also assess the MVA’s effect on travel behavior because this information will help inform treatment.

 

 

Structured diagnostic interviews are straightforward and easy to administer with minimal training. We prefer the 30-question Clinician Administered PTSD Scale (CAPS) because evidence supports its reliability and validity.2,3 Use the CAPS to rate intensity and frequency of the 17 core PTSD symptoms over the past week, month, or lifetime. The CAPS can be scored for a PTSD diagnosis and for symptom severity. This tool’s drawback is that it takes 30 to 60 minutes to administer and a few more minutes to score.

Self-report measures are quick to administer and score and provide valuable information about symptom presence and severity.4 We recommend the PTSD Checklist (PCL), a widely used measure that has been shown to reliably and validly assess MVA-related PTSD.5,6 Consisting of 17 items corresponding to the DSM-IV-TR PTSD symptoms, the PCL takes about 5 minutes to complete and 1 or 2 minutes to score. A score ≥44 is a highly accurate indication of PTSD.6

Patients with MVA-related PTSD often have psychiatric comorbidities.7 The most frequently diagnosed are:

  • major depressive disorder (in about one-half of persons with MVA-related PTSD)
  • anxiety disorders, such as generalized anxiety disorder (in about one-third)
  • chronic pain
  • alcohol or other substance abuse.

We use the Structured Clinical Interview for DSM-IV (SCID) to diagnose comorbid conditions.8 If you do not have time to administer a structured clinical interview, we recommend using psychometrically sound self-report measures, such as the Beck Depression Inventory9 and the State Trait Anxiety Inventory.10

Length of time since the MVA gives a good indication of how likely PTSD is to remit without intervention. Longitudinal studies have found that within 1 year, PTSD will remit without intervention in nearly two-thirds of those diagnosed within 1 to 4 months of the MVA. PTSD that persists after 1 year is much less likely to resolve without treatment.11 Other predictors of PTSD persistence include:

  • lack of physical recovery
  • major depression within the first 2 months of the MVA
  • current major depression
  • alcohol abuse before the MVA
  • perceived vulnerability during the MVA
  • poor family relationships after the MVA.11

PTSD symptoms that initially do not meet diagnostic criteria (subsyndromal PTSD) can worsen in the first year postMVA and lead to a diagnosis of delayed-onset PTSD.12 Having less social support and experiencing additional life stressors—such as another accident, worsening physical health, or change in job—can contribute to delayed-onset PTSD.

CASE CONTINUED: Overcoming fears with psychotherapy

As part of cognitive-behavioral therapy (CBT), the therapist teaches Mr. O a simple breathing exercise to reduce anxiety. He also leads Mr. O through a progression of imaginal and in vivo exposure exercises. The former involves having the patient think about provocative situations in a graded fashion, from easiest to most difficult, while in the psychiatrist’s office. The latter involves having Mr. O seek out red lights—first as a passenger in a vehicle, then as a driver with a passenger, and then while driving alone—until they no longer cause distress.

The American Psychiatric Association,13 Veterans Affairs/Department of Defense,14 International Society of Traumatic Stress Studies,15 and other organizations recommend CBT to treat PTSD.16 Randomized, controlled trials and other evidence support CBT’s efficacy for MVA-related PTSD.11,17

Before implementing CBT, cultivate a strong therapeutic relationship with MVA survivors. The exercises may be acutely distressing, and you will be asking them to complete between-session practice tasks.

CBT for MVA-related PTSD can be delivered to individuals or groups,18 typically in 8 to 16 weekly or semi-weekly, 60- to 90-minute sessions. (Table 2) explains which elements of CBT address specific PTSD symptoms.11

Therapy usually begins with psychoeducation about PTSD symptoms and expected reactions to trauma (the “flight, fight, or freeze” response) to normalize these reactions and place them within the cognitive-behavioral conceptualization. Teach your patients that avoiding memories and reminders of the trauma maintains PTSD and that they must overcome avoidance for treatment to be successful. Note that avoidance can be subtle, such as a patient going to a feared place but distracting himself while there.

CBT for PTSD often includes teaching an anxiety management skill (Box). Imaginal and in vivo exercises also are usually part of treatment.

In imaginal exposure, patients repeatedly and fully confront their frightening memories within session by recounting as much detail about the MVA as possible, including what they were sensing, feeling, and thinking. This description of the MVA can be recorded during the session or written outside of therapy and read aloud by the patient during sessions.

 

 

Either way, assign your patients to review the written or recorded account 2 to 3 times per day between sessions. Repeating this exercise results in habituation to these memories, and the thoughts will evoke progressively less distress.

In vivo exposure is designed to extinguish the conditioned associations patients formed during the MVA. Travel-related anxiety is the primary focus of in vivo exposure because almost all patients experience it.11

This type of exposure therapy uses a fear hierarchy—a list of feared MVA reminders. Patients rate each reminder using a distress scale, such as the Subjective Units of Discomfort Scale (SUDS). Together the therapist and patient agree on a situation in the fear hierarchy that the patient feels able to confront in person without escaping. Patients confront the situation until their distress scale score declines by at least half, repeatedly addressing each item on the hierarchy until they have overcome the most frightening reminders. Consider recruiting patients’ family or friends to help complete these homework exercises.

Box

Manage anxiety with easy-to-use skills

Typically taught early in the course of cognitive-behavioral therapy, an anxiety management skill gives the patient an easy-to-use, effective way to reduce hyperarousal symptoms.

Anxiety management skills range from simple paced diaphragmatic breathing—where the patient learns to breathe from the abdomen, inhaling and exhaling to a count of 3—to more involved techniques, such as progressive muscle relaxation, when patients systemically tense and relax designated muscle groups in a sequential, articulated fashion.

The patient can use an anxiety management skill to lower basal physical arousal and acute arousal brought on by a stressful experience, such as confronting a reminder of the motor vehicle accident.

Cognitive therapy typically is conducted simultaneously with the other therapeutic components. Early in therapy, the clinician assesses patients’ beliefs related to the accident (such as “The world is very dangerous” or “I have no control over what happens on the road”) and their psychological experiences (“I will lose control of my emotions if I think about it”) and challenges the veracity of these assumptions by bringing up these distortions and statements as they occur within the treatment session. By using forms designed to identify thoughts and beliefs that produce anxiety, patients learn to monitor and challenge their maladaptive thoughts, in essence becoming their own cognitive therapists.

Scheduling pleasant events—assigning patients to participate in activities they previously enjoyed but have discontinued—has been used effectively to treat depression.19 For MVA survivors, this therapy is designed to target PTSD’s numbing symptoms by increasing patients’ social support and resilience.

Patients initially may need some cajoling, but once they begin pleasant activities they often find the experience reinforcing and mood-enhancing, which increases their future participation.

Although pharmacologic therapy for PTSD is beyond the scope of this article, antidepressants—including selective serotonin reuptake inhibitors (such as paroxetine and sertraline), tricyclics, and monoamine oxidase inhibitors—have been shown to effectively treat PTSD.20 For some patients, a combination of medication and psychotherapy may be best.

Patients with MVA-related PTSD often present other problems, including chronic pain, sleep problems, and generalized anxiety. How—and even if—to address these problems in therapy for PTSD is a matter of clinical judgment. Some evidence suggests that CBT can help improve comorbid conditions.7,21

Table 2

Cognitive-behavioral therapy: What’s effective for MVA-related PTSD

Symptom clusterCBT component that targets it
ReexperiencingIn vivo and imaginal exposure
AvoidanceIn vivo exposure (for MVA reminders) Imaginal exposure (for MVA memories and related affect)
NumbingPleasant events scheduling
HyperarousalAnxiety management skills training
All symptom clustersPsychoeducation about PTSD
All symptom clustersCognitive therapy
Note: Although listed as targeting specific symptom clusters, CBT components have an effect across all clusters.
CBT: cognitive-behavior therapy; MVA: motor vehicle accident; PTSD: posttraumatic stress disorder
Source: Reference 11

CASE CONTINUED: Getting back on the road

After 4 months of CBT, Mr. O’s symptoms have resolved to the point where he is able to drive and return to work. When confronted with situations that had been problematic, Mr. O uses the CBT tools he learned to monitor thoughts and reactions that previously led to distress. With each change and improvement he feels a growing sense of confidence.

Related resources

  • National Center for Posttraumatic Stress Disorder. U.S. Department of Veterans Affairs. www.ncptsd.va.gov.
  • Hickling EJ, Blanchard EB. Overcoming the trauma of your motor vehicle accident: a cognitive behavioral treatment program, therapist guide. New York: Oxford University Press; 2006.
  • Follette VM, Ruzek JI, Abueg FR. Cognitive-behavioral therapies for trauma, 2nd ed. New York: Guilford Press; 1998.

Drug brand names

  • Paroxetine • Paxil
  • Sertraline • Zoloft
 

 

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

References

1. Diagnostic and statistical manual of mental disorders. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000.

2. Blake AT, Weathers F, Nagy L, et al. Clinician administered PTSD scale for DSM-IV (CAPS). Boston, MA: National Center for Post-traumatic Stress Disorder, Behavioral Science Division; 1998.

3. Weathers FW, Keane TM, Davidson JRT. Clinician-administered PTSD scale: a review of the first ten years of research. Depress Anxiety 2001;13(3):132-56.

4. Shear MK, Feske U, Brown C, et al. Anxiety disorders measures. In: Rush AJ Jr, Pincus HA, First MB, et al, eds. Handbook of psychiatric measures. Washington, DC: American Psychiatric Press; 2000:549-89.

5. Weathers FW, Litz BT, Herman DS, et al. The PTSD checklist: reliability, validity&diagnostic utility. Paper presented at: annual meeting of the International Society for Traumatic Stress Studies; October 1993; San Antonio, TX.

6. Blanchard EB, Jones-Alexander J, Buckley TC, Forneris CA. Psychometric properties of the PTSD Checklist (PCL). Behav Res Ther 1996;34:669-73.

7. Blanchard EB, Hickling EJ, Freidenberg BM, et al. Two studies of the psychiatric morbidity among motor vehicle accident survivors 1 year after the crash. Behav Res Ther 2004;42:569-83.

8. Spitzer RL, Williams JBW, Gibbon M, First MB. Structured clinical interview for DSM-IV—non-patient version. New York: Biometrics Research Department, New York State Psychiatric Institute; 1996.

9. Beck AT, Ward CH, Mendelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry 1961;5:561-71.

10. Spielberger CD, Gorsuch RL, Lushune RE. Manual for the state-trait anxiety inventory. Palo Alto, CA: Consulting Psychologists Press; 1970.

11. Blanchard EB, Hickling EJ. After the crash: assessment and treatment of motor vehicle accident survivors. Washington, D.C.: American Psychological Association; 2004.

12. Buckley T, Blanchard EB, Hickling EJ. A prospective examination of delayed onset PTSD secondary to motor vehicle accidents. J Abnorm Psychol 1998;107:508-19.

13. Ursano RJ, Bell C, Eth S, et al. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:3-31.

14. Veterans Health Administration. Management of posttraumatic stress (Office of Quality and Performance Publication #10Q-CPG/PTSD-04). Washington, DC: Veterans Administration, Department of Defense Clinical Practice Guideline Working Group; 2003. Available at: http://www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm. Accessed March 21, 2007.

15. Foa EB, Keane TJ, Friedman MJ. Effective treatments for PTSD: practice guidelines from the International Society for Traumatic Stress Studies. New York: Guilford Press; 2000.

16. Bradley R, Greene J, Russ E, et al. A multidimensional meta-analysis of psychotherapy for PTSD. Am J Psychiatry 2005;162:214-27.

17. Ehlers A, Clark DM. Early psychological interventions for adult survivors of trauma: a review. Biol Psychiatry 2003;53:817-26.

18. Beck GJ, Coffey SF. Group cognitive behavioral treatment for PTSD: treatment of motor vehicle accident survivors. Cogn Behav Pract 2004;12:267-77.

19. Jacobson NS, Dobson KS, Truax PA, et al. A component analysis of cognitive-behavioral treatment for depression. J Consult Clin Psychol 1996;64:295-304.

20. Davidson J, Bernik M, Connor K, et al. A new treatment algorithm for posttraumatic stress disorder. Psychiatr Ann 2005;35:887-900.

21. Shipherd JC, Beck JG, Hamblen JL, et al. A preliminary examination of treatment for posttraumatic stress disorder in chronic pain patients: a case study. J Trauma Stress 2003;16(5):451-7.

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Eric Kuhn, PhD
PTSD education coordinator, Sierra-Pacific Mental Illness Research, Education, and Clinical Center, VA Palo Alto Health Care System, Palo Alto, CA

Edward J. Hickling, PsyD
Center for Stress and Anxiety Disorders, University at Albany, State University of New York, Capital Psychological Associates, Albany, NY

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Edward J. Hickling, PsyD
Center for Stress and Anxiety Disorders, University at Albany, State University of New York, Capital Psychological Associates, Albany, NY

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PTSD education coordinator, Sierra-Pacific Mental Illness Research, Education, and Clinical Center, VA Palo Alto Health Care System, Palo Alto, CA

Edward J. Hickling, PsyD
Center for Stress and Anxiety Disorders, University at Albany, State University of New York, Capital Psychological Associates, Albany, NY

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Stopped at a red light, Mr. O glances in the rearview mirror and sees headlights coming up fast. The sport utility vehicle behind him is not slowing down. He braces himself as the SUV plows into the back of his car, snapping his head back and forth violently.

As white smoke fills his eyes and lungs. Mr. O realizes he has been pushed into the intersection, and for a moment thinks about never seeing his wife and children again. As he hears tires screeching, his car is struck by a truck.

Mr. O does not die, as he feared, but 6 months later he is “just not ready” to return to work. The doctor who is treating his whiplash injury refers him for evaluation of lingering anxiety.

Posttraumatic stress disorder (PTSD) resulting from a motor vehicle accident (MVA) can have a persistent disabling effect. To help you effectively treat patients such as Mr. O, this article examines:

  • common PTSD symptoms in accident survivors
  • recommended diagnostic interviews and assessment tools
  • techniques for using psychotherapy to overcome residual PTSD symptoms.

CASE CONTINUED: Lingering impairment

In the 6 months since the accident, Mr. O’s sleep is disrupted by pain and worry; when he can sleep, he frequently has nightmares about the accident. Mr. O feels anxious and irritable, and thoughts of that evening play over and over in his mind.

Mr. O doesn’t like to talk about the accident and has not resumed driving. He avoids all but required trips, such as to doctors’ appointments, which he endures with extreme anxiety. Whenever his wife drives without him, he insists that she immediately call him when she reaches her destination. At the same time, he feels emotionally distant from her and the children. He shows little interest in hobbies he’d previously enjoyed.

3 symptom clusters of PTSD

To meet DSM-IV-TR criteria for PTSD, a person must have experienced, witnessed, or been confronted by an event that involved actual or threatened death or serious injury, to which he responded with intense fear, helplessness, or horror.1 PTSD’s 3 symptom clusters—reexperiencing, avoidance/numbing, and hyperarousal—encompass 17 core symptoms, and a patient must exhibit at least the minimum number of symptoms from each cluster (Table 1).

MVA survivors with PTSD often have intrusive memories and nightmares. They might avoid talking about the accident and resist or abstain from driving or traveling by car. They often fear and avoid people, places, activities, and reminders of the MVA that can trigger upsetting reactions, such as anxiety, tachycardia, and panic. They may be irritable, detached, or estranged from loved ones, or have difficulty sleeping or concentrating. These symptoms must persist for ≥30 days and cause clinically significant distress and impaired functioning for a person to meet the criteria for chronic PTSD.

Table 1

Patients experience 3 ‘clusters’ of PTSD symptoms

Symptom clusterSymptoms
Reexperiencing
(≥1 required)
  • Distressing recollections of the trauma
  • Distressing dreams of the trauma
  • Acting/feeling as if the trauma were recurring
  • Psychological distress upon confronting trauma cues
  • Physiologic reactivity upon confronting trauma cues
Avoidance/numbing
(≥3 required)
  • Avoiding trauma-related thoughts, feelings, or conversations
  • Avoiding activities, places, or people reminiscent of the trauma
  • Inability to recall an important aspect of the trauma
  • Diminished interest or participation in significant activities
  • Feeling of detachment or estrangement from others
  • Restricted range of affect
  • Sense of foreshortened future
Hyperarousal
(≥2 required)
  • Sleep difficulties
  • Irritability or outbursts of anger
  • Difficulty concentrating
  • Hypervigilance
  • Exaggerated startle response
Note: In addition to having the minimum number of symptoms from each cluster as indicated above, for a patient to meet PTSD criteria, symptoms must cause clinically significant distress and impairment in functioning.
PTSD: posttraumatic stress disorder
Source: DSM-IV-TR

CASE CONTINUED: Reaching a diagnosis

Using a combination of interviews and self-report measures, the psychiatrist diagnoses Mr. O with chronic PTSD. Since the MVA, Mr. O has developed the required number of reexperiencing, avoidance/numbing, and hyperarousal symptoms. These symptoms have persisted for >30 days and significantly impair his functioning.

Use multiple assessment tools

To assess an MVA survivor for PTSD and related problems, we advocate using a combination of:

  • unstructured clinical interviews
  • structured clinical interviews
  • self-report measures.

Also collect information from collateral sources, such as patients’ spouses or significant others, when appropriate and available.

In an unstructured interview, obtain:

  • a thorough, detailed description of the MVA, including what occurred and the patient’s thoughts and feelings during and since the accident
  • a description of physical injuries, medical treatments, and medication use.

This information can rule out physical causes of PTSD-like symptoms, such as a traumatic brain injury that results in concentration difficulties and irritability. Also assess the MVA’s effect on travel behavior because this information will help inform treatment.

 

 

Structured diagnostic interviews are straightforward and easy to administer with minimal training. We prefer the 30-question Clinician Administered PTSD Scale (CAPS) because evidence supports its reliability and validity.2,3 Use the CAPS to rate intensity and frequency of the 17 core PTSD symptoms over the past week, month, or lifetime. The CAPS can be scored for a PTSD diagnosis and for symptom severity. This tool’s drawback is that it takes 30 to 60 minutes to administer and a few more minutes to score.

Self-report measures are quick to administer and score and provide valuable information about symptom presence and severity.4 We recommend the PTSD Checklist (PCL), a widely used measure that has been shown to reliably and validly assess MVA-related PTSD.5,6 Consisting of 17 items corresponding to the DSM-IV-TR PTSD symptoms, the PCL takes about 5 minutes to complete and 1 or 2 minutes to score. A score ≥44 is a highly accurate indication of PTSD.6

Patients with MVA-related PTSD often have psychiatric comorbidities.7 The most frequently diagnosed are:

  • major depressive disorder (in about one-half of persons with MVA-related PTSD)
  • anxiety disorders, such as generalized anxiety disorder (in about one-third)
  • chronic pain
  • alcohol or other substance abuse.

We use the Structured Clinical Interview for DSM-IV (SCID) to diagnose comorbid conditions.8 If you do not have time to administer a structured clinical interview, we recommend using psychometrically sound self-report measures, such as the Beck Depression Inventory9 and the State Trait Anxiety Inventory.10

Length of time since the MVA gives a good indication of how likely PTSD is to remit without intervention. Longitudinal studies have found that within 1 year, PTSD will remit without intervention in nearly two-thirds of those diagnosed within 1 to 4 months of the MVA. PTSD that persists after 1 year is much less likely to resolve without treatment.11 Other predictors of PTSD persistence include:

  • lack of physical recovery
  • major depression within the first 2 months of the MVA
  • current major depression
  • alcohol abuse before the MVA
  • perceived vulnerability during the MVA
  • poor family relationships after the MVA.11

PTSD symptoms that initially do not meet diagnostic criteria (subsyndromal PTSD) can worsen in the first year postMVA and lead to a diagnosis of delayed-onset PTSD.12 Having less social support and experiencing additional life stressors—such as another accident, worsening physical health, or change in job—can contribute to delayed-onset PTSD.

CASE CONTINUED: Overcoming fears with psychotherapy

As part of cognitive-behavioral therapy (CBT), the therapist teaches Mr. O a simple breathing exercise to reduce anxiety. He also leads Mr. O through a progression of imaginal and in vivo exposure exercises. The former involves having the patient think about provocative situations in a graded fashion, from easiest to most difficult, while in the psychiatrist’s office. The latter involves having Mr. O seek out red lights—first as a passenger in a vehicle, then as a driver with a passenger, and then while driving alone—until they no longer cause distress.

The American Psychiatric Association,13 Veterans Affairs/Department of Defense,14 International Society of Traumatic Stress Studies,15 and other organizations recommend CBT to treat PTSD.16 Randomized, controlled trials and other evidence support CBT’s efficacy for MVA-related PTSD.11,17

Before implementing CBT, cultivate a strong therapeutic relationship with MVA survivors. The exercises may be acutely distressing, and you will be asking them to complete between-session practice tasks.

CBT for MVA-related PTSD can be delivered to individuals or groups,18 typically in 8 to 16 weekly or semi-weekly, 60- to 90-minute sessions. (Table 2) explains which elements of CBT address specific PTSD symptoms.11

Therapy usually begins with psychoeducation about PTSD symptoms and expected reactions to trauma (the “flight, fight, or freeze” response) to normalize these reactions and place them within the cognitive-behavioral conceptualization. Teach your patients that avoiding memories and reminders of the trauma maintains PTSD and that they must overcome avoidance for treatment to be successful. Note that avoidance can be subtle, such as a patient going to a feared place but distracting himself while there.

CBT for PTSD often includes teaching an anxiety management skill (Box). Imaginal and in vivo exercises also are usually part of treatment.

In imaginal exposure, patients repeatedly and fully confront their frightening memories within session by recounting as much detail about the MVA as possible, including what they were sensing, feeling, and thinking. This description of the MVA can be recorded during the session or written outside of therapy and read aloud by the patient during sessions.

 

 

Either way, assign your patients to review the written or recorded account 2 to 3 times per day between sessions. Repeating this exercise results in habituation to these memories, and the thoughts will evoke progressively less distress.

In vivo exposure is designed to extinguish the conditioned associations patients formed during the MVA. Travel-related anxiety is the primary focus of in vivo exposure because almost all patients experience it.11

This type of exposure therapy uses a fear hierarchy—a list of feared MVA reminders. Patients rate each reminder using a distress scale, such as the Subjective Units of Discomfort Scale (SUDS). Together the therapist and patient agree on a situation in the fear hierarchy that the patient feels able to confront in person without escaping. Patients confront the situation until their distress scale score declines by at least half, repeatedly addressing each item on the hierarchy until they have overcome the most frightening reminders. Consider recruiting patients’ family or friends to help complete these homework exercises.

Box

Manage anxiety with easy-to-use skills

Typically taught early in the course of cognitive-behavioral therapy, an anxiety management skill gives the patient an easy-to-use, effective way to reduce hyperarousal symptoms.

Anxiety management skills range from simple paced diaphragmatic breathing—where the patient learns to breathe from the abdomen, inhaling and exhaling to a count of 3—to more involved techniques, such as progressive muscle relaxation, when patients systemically tense and relax designated muscle groups in a sequential, articulated fashion.

The patient can use an anxiety management skill to lower basal physical arousal and acute arousal brought on by a stressful experience, such as confronting a reminder of the motor vehicle accident.

Cognitive therapy typically is conducted simultaneously with the other therapeutic components. Early in therapy, the clinician assesses patients’ beliefs related to the accident (such as “The world is very dangerous” or “I have no control over what happens on the road”) and their psychological experiences (“I will lose control of my emotions if I think about it”) and challenges the veracity of these assumptions by bringing up these distortions and statements as they occur within the treatment session. By using forms designed to identify thoughts and beliefs that produce anxiety, patients learn to monitor and challenge their maladaptive thoughts, in essence becoming their own cognitive therapists.

Scheduling pleasant events—assigning patients to participate in activities they previously enjoyed but have discontinued—has been used effectively to treat depression.19 For MVA survivors, this therapy is designed to target PTSD’s numbing symptoms by increasing patients’ social support and resilience.

Patients initially may need some cajoling, but once they begin pleasant activities they often find the experience reinforcing and mood-enhancing, which increases their future participation.

Although pharmacologic therapy for PTSD is beyond the scope of this article, antidepressants—including selective serotonin reuptake inhibitors (such as paroxetine and sertraline), tricyclics, and monoamine oxidase inhibitors—have been shown to effectively treat PTSD.20 For some patients, a combination of medication and psychotherapy may be best.

Patients with MVA-related PTSD often present other problems, including chronic pain, sleep problems, and generalized anxiety. How—and even if—to address these problems in therapy for PTSD is a matter of clinical judgment. Some evidence suggests that CBT can help improve comorbid conditions.7,21

Table 2

Cognitive-behavioral therapy: What’s effective for MVA-related PTSD

Symptom clusterCBT component that targets it
ReexperiencingIn vivo and imaginal exposure
AvoidanceIn vivo exposure (for MVA reminders) Imaginal exposure (for MVA memories and related affect)
NumbingPleasant events scheduling
HyperarousalAnxiety management skills training
All symptom clustersPsychoeducation about PTSD
All symptom clustersCognitive therapy
Note: Although listed as targeting specific symptom clusters, CBT components have an effect across all clusters.
CBT: cognitive-behavior therapy; MVA: motor vehicle accident; PTSD: posttraumatic stress disorder
Source: Reference 11

CASE CONTINUED: Getting back on the road

After 4 months of CBT, Mr. O’s symptoms have resolved to the point where he is able to drive and return to work. When confronted with situations that had been problematic, Mr. O uses the CBT tools he learned to monitor thoughts and reactions that previously led to distress. With each change and improvement he feels a growing sense of confidence.

Related resources

  • National Center for Posttraumatic Stress Disorder. U.S. Department of Veterans Affairs. www.ncptsd.va.gov.
  • Hickling EJ, Blanchard EB. Overcoming the trauma of your motor vehicle accident: a cognitive behavioral treatment program, therapist guide. New York: Oxford University Press; 2006.
  • Follette VM, Ruzek JI, Abueg FR. Cognitive-behavioral therapies for trauma, 2nd ed. New York: Guilford Press; 1998.

Drug brand names

  • Paroxetine • Paxil
  • Sertraline • Zoloft
 

 

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

Stopped at a red light, Mr. O glances in the rearview mirror and sees headlights coming up fast. The sport utility vehicle behind him is not slowing down. He braces himself as the SUV plows into the back of his car, snapping his head back and forth violently.

As white smoke fills his eyes and lungs. Mr. O realizes he has been pushed into the intersection, and for a moment thinks about never seeing his wife and children again. As he hears tires screeching, his car is struck by a truck.

Mr. O does not die, as he feared, but 6 months later he is “just not ready” to return to work. The doctor who is treating his whiplash injury refers him for evaluation of lingering anxiety.

Posttraumatic stress disorder (PTSD) resulting from a motor vehicle accident (MVA) can have a persistent disabling effect. To help you effectively treat patients such as Mr. O, this article examines:

  • common PTSD symptoms in accident survivors
  • recommended diagnostic interviews and assessment tools
  • techniques for using psychotherapy to overcome residual PTSD symptoms.

CASE CONTINUED: Lingering impairment

In the 6 months since the accident, Mr. O’s sleep is disrupted by pain and worry; when he can sleep, he frequently has nightmares about the accident. Mr. O feels anxious and irritable, and thoughts of that evening play over and over in his mind.

Mr. O doesn’t like to talk about the accident and has not resumed driving. He avoids all but required trips, such as to doctors’ appointments, which he endures with extreme anxiety. Whenever his wife drives without him, he insists that she immediately call him when she reaches her destination. At the same time, he feels emotionally distant from her and the children. He shows little interest in hobbies he’d previously enjoyed.

3 symptom clusters of PTSD

To meet DSM-IV-TR criteria for PTSD, a person must have experienced, witnessed, or been confronted by an event that involved actual or threatened death or serious injury, to which he responded with intense fear, helplessness, or horror.1 PTSD’s 3 symptom clusters—reexperiencing, avoidance/numbing, and hyperarousal—encompass 17 core symptoms, and a patient must exhibit at least the minimum number of symptoms from each cluster (Table 1).

MVA survivors with PTSD often have intrusive memories and nightmares. They might avoid talking about the accident and resist or abstain from driving or traveling by car. They often fear and avoid people, places, activities, and reminders of the MVA that can trigger upsetting reactions, such as anxiety, tachycardia, and panic. They may be irritable, detached, or estranged from loved ones, or have difficulty sleeping or concentrating. These symptoms must persist for ≥30 days and cause clinically significant distress and impaired functioning for a person to meet the criteria for chronic PTSD.

Table 1

Patients experience 3 ‘clusters’ of PTSD symptoms

Symptom clusterSymptoms
Reexperiencing
(≥1 required)
  • Distressing recollections of the trauma
  • Distressing dreams of the trauma
  • Acting/feeling as if the trauma were recurring
  • Psychological distress upon confronting trauma cues
  • Physiologic reactivity upon confronting trauma cues
Avoidance/numbing
(≥3 required)
  • Avoiding trauma-related thoughts, feelings, or conversations
  • Avoiding activities, places, or people reminiscent of the trauma
  • Inability to recall an important aspect of the trauma
  • Diminished interest or participation in significant activities
  • Feeling of detachment or estrangement from others
  • Restricted range of affect
  • Sense of foreshortened future
Hyperarousal
(≥2 required)
  • Sleep difficulties
  • Irritability or outbursts of anger
  • Difficulty concentrating
  • Hypervigilance
  • Exaggerated startle response
Note: In addition to having the minimum number of symptoms from each cluster as indicated above, for a patient to meet PTSD criteria, symptoms must cause clinically significant distress and impairment in functioning.
PTSD: posttraumatic stress disorder
Source: DSM-IV-TR

CASE CONTINUED: Reaching a diagnosis

Using a combination of interviews and self-report measures, the psychiatrist diagnoses Mr. O with chronic PTSD. Since the MVA, Mr. O has developed the required number of reexperiencing, avoidance/numbing, and hyperarousal symptoms. These symptoms have persisted for >30 days and significantly impair his functioning.

Use multiple assessment tools

To assess an MVA survivor for PTSD and related problems, we advocate using a combination of:

  • unstructured clinical interviews
  • structured clinical interviews
  • self-report measures.

Also collect information from collateral sources, such as patients’ spouses or significant others, when appropriate and available.

In an unstructured interview, obtain:

  • a thorough, detailed description of the MVA, including what occurred and the patient’s thoughts and feelings during and since the accident
  • a description of physical injuries, medical treatments, and medication use.

This information can rule out physical causes of PTSD-like symptoms, such as a traumatic brain injury that results in concentration difficulties and irritability. Also assess the MVA’s effect on travel behavior because this information will help inform treatment.

 

 

Structured diagnostic interviews are straightforward and easy to administer with minimal training. We prefer the 30-question Clinician Administered PTSD Scale (CAPS) because evidence supports its reliability and validity.2,3 Use the CAPS to rate intensity and frequency of the 17 core PTSD symptoms over the past week, month, or lifetime. The CAPS can be scored for a PTSD diagnosis and for symptom severity. This tool’s drawback is that it takes 30 to 60 minutes to administer and a few more minutes to score.

Self-report measures are quick to administer and score and provide valuable information about symptom presence and severity.4 We recommend the PTSD Checklist (PCL), a widely used measure that has been shown to reliably and validly assess MVA-related PTSD.5,6 Consisting of 17 items corresponding to the DSM-IV-TR PTSD symptoms, the PCL takes about 5 minutes to complete and 1 or 2 minutes to score. A score ≥44 is a highly accurate indication of PTSD.6

Patients with MVA-related PTSD often have psychiatric comorbidities.7 The most frequently diagnosed are:

  • major depressive disorder (in about one-half of persons with MVA-related PTSD)
  • anxiety disorders, such as generalized anxiety disorder (in about one-third)
  • chronic pain
  • alcohol or other substance abuse.

We use the Structured Clinical Interview for DSM-IV (SCID) to diagnose comorbid conditions.8 If you do not have time to administer a structured clinical interview, we recommend using psychometrically sound self-report measures, such as the Beck Depression Inventory9 and the State Trait Anxiety Inventory.10

Length of time since the MVA gives a good indication of how likely PTSD is to remit without intervention. Longitudinal studies have found that within 1 year, PTSD will remit without intervention in nearly two-thirds of those diagnosed within 1 to 4 months of the MVA. PTSD that persists after 1 year is much less likely to resolve without treatment.11 Other predictors of PTSD persistence include:

  • lack of physical recovery
  • major depression within the first 2 months of the MVA
  • current major depression
  • alcohol abuse before the MVA
  • perceived vulnerability during the MVA
  • poor family relationships after the MVA.11

PTSD symptoms that initially do not meet diagnostic criteria (subsyndromal PTSD) can worsen in the first year postMVA and lead to a diagnosis of delayed-onset PTSD.12 Having less social support and experiencing additional life stressors—such as another accident, worsening physical health, or change in job—can contribute to delayed-onset PTSD.

CASE CONTINUED: Overcoming fears with psychotherapy

As part of cognitive-behavioral therapy (CBT), the therapist teaches Mr. O a simple breathing exercise to reduce anxiety. He also leads Mr. O through a progression of imaginal and in vivo exposure exercises. The former involves having the patient think about provocative situations in a graded fashion, from easiest to most difficult, while in the psychiatrist’s office. The latter involves having Mr. O seek out red lights—first as a passenger in a vehicle, then as a driver with a passenger, and then while driving alone—until they no longer cause distress.

The American Psychiatric Association,13 Veterans Affairs/Department of Defense,14 International Society of Traumatic Stress Studies,15 and other organizations recommend CBT to treat PTSD.16 Randomized, controlled trials and other evidence support CBT’s efficacy for MVA-related PTSD.11,17

Before implementing CBT, cultivate a strong therapeutic relationship with MVA survivors. The exercises may be acutely distressing, and you will be asking them to complete between-session practice tasks.

CBT for MVA-related PTSD can be delivered to individuals or groups,18 typically in 8 to 16 weekly or semi-weekly, 60- to 90-minute sessions. (Table 2) explains which elements of CBT address specific PTSD symptoms.11

Therapy usually begins with psychoeducation about PTSD symptoms and expected reactions to trauma (the “flight, fight, or freeze” response) to normalize these reactions and place them within the cognitive-behavioral conceptualization. Teach your patients that avoiding memories and reminders of the trauma maintains PTSD and that they must overcome avoidance for treatment to be successful. Note that avoidance can be subtle, such as a patient going to a feared place but distracting himself while there.

CBT for PTSD often includes teaching an anxiety management skill (Box). Imaginal and in vivo exercises also are usually part of treatment.

In imaginal exposure, patients repeatedly and fully confront their frightening memories within session by recounting as much detail about the MVA as possible, including what they were sensing, feeling, and thinking. This description of the MVA can be recorded during the session or written outside of therapy and read aloud by the patient during sessions.

 

 

Either way, assign your patients to review the written or recorded account 2 to 3 times per day between sessions. Repeating this exercise results in habituation to these memories, and the thoughts will evoke progressively less distress.

In vivo exposure is designed to extinguish the conditioned associations patients formed during the MVA. Travel-related anxiety is the primary focus of in vivo exposure because almost all patients experience it.11

This type of exposure therapy uses a fear hierarchy—a list of feared MVA reminders. Patients rate each reminder using a distress scale, such as the Subjective Units of Discomfort Scale (SUDS). Together the therapist and patient agree on a situation in the fear hierarchy that the patient feels able to confront in person without escaping. Patients confront the situation until their distress scale score declines by at least half, repeatedly addressing each item on the hierarchy until they have overcome the most frightening reminders. Consider recruiting patients’ family or friends to help complete these homework exercises.

Box

Manage anxiety with easy-to-use skills

Typically taught early in the course of cognitive-behavioral therapy, an anxiety management skill gives the patient an easy-to-use, effective way to reduce hyperarousal symptoms.

Anxiety management skills range from simple paced diaphragmatic breathing—where the patient learns to breathe from the abdomen, inhaling and exhaling to a count of 3—to more involved techniques, such as progressive muscle relaxation, when patients systemically tense and relax designated muscle groups in a sequential, articulated fashion.

The patient can use an anxiety management skill to lower basal physical arousal and acute arousal brought on by a stressful experience, such as confronting a reminder of the motor vehicle accident.

Cognitive therapy typically is conducted simultaneously with the other therapeutic components. Early in therapy, the clinician assesses patients’ beliefs related to the accident (such as “The world is very dangerous” or “I have no control over what happens on the road”) and their psychological experiences (“I will lose control of my emotions if I think about it”) and challenges the veracity of these assumptions by bringing up these distortions and statements as they occur within the treatment session. By using forms designed to identify thoughts and beliefs that produce anxiety, patients learn to monitor and challenge their maladaptive thoughts, in essence becoming their own cognitive therapists.

Scheduling pleasant events—assigning patients to participate in activities they previously enjoyed but have discontinued—has been used effectively to treat depression.19 For MVA survivors, this therapy is designed to target PTSD’s numbing symptoms by increasing patients’ social support and resilience.

Patients initially may need some cajoling, but once they begin pleasant activities they often find the experience reinforcing and mood-enhancing, which increases their future participation.

Although pharmacologic therapy for PTSD is beyond the scope of this article, antidepressants—including selective serotonin reuptake inhibitors (such as paroxetine and sertraline), tricyclics, and monoamine oxidase inhibitors—have been shown to effectively treat PTSD.20 For some patients, a combination of medication and psychotherapy may be best.

Patients with MVA-related PTSD often present other problems, including chronic pain, sleep problems, and generalized anxiety. How—and even if—to address these problems in therapy for PTSD is a matter of clinical judgment. Some evidence suggests that CBT can help improve comorbid conditions.7,21

Table 2

Cognitive-behavioral therapy: What’s effective for MVA-related PTSD

Symptom clusterCBT component that targets it
ReexperiencingIn vivo and imaginal exposure
AvoidanceIn vivo exposure (for MVA reminders) Imaginal exposure (for MVA memories and related affect)
NumbingPleasant events scheduling
HyperarousalAnxiety management skills training
All symptom clustersPsychoeducation about PTSD
All symptom clustersCognitive therapy
Note: Although listed as targeting specific symptom clusters, CBT components have an effect across all clusters.
CBT: cognitive-behavior therapy; MVA: motor vehicle accident; PTSD: posttraumatic stress disorder
Source: Reference 11

CASE CONTINUED: Getting back on the road

After 4 months of CBT, Mr. O’s symptoms have resolved to the point where he is able to drive and return to work. When confronted with situations that had been problematic, Mr. O uses the CBT tools he learned to monitor thoughts and reactions that previously led to distress. With each change and improvement he feels a growing sense of confidence.

Related resources

  • National Center for Posttraumatic Stress Disorder. U.S. Department of Veterans Affairs. www.ncptsd.va.gov.
  • Hickling EJ, Blanchard EB. Overcoming the trauma of your motor vehicle accident: a cognitive behavioral treatment program, therapist guide. New York: Oxford University Press; 2006.
  • Follette VM, Ruzek JI, Abueg FR. Cognitive-behavioral therapies for trauma, 2nd ed. New York: Guilford Press; 1998.

Drug brand names

  • Paroxetine • Paxil
  • Sertraline • Zoloft
 

 

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

References

1. Diagnostic and statistical manual of mental disorders. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000.

2. Blake AT, Weathers F, Nagy L, et al. Clinician administered PTSD scale for DSM-IV (CAPS). Boston, MA: National Center for Post-traumatic Stress Disorder, Behavioral Science Division; 1998.

3. Weathers FW, Keane TM, Davidson JRT. Clinician-administered PTSD scale: a review of the first ten years of research. Depress Anxiety 2001;13(3):132-56.

4. Shear MK, Feske U, Brown C, et al. Anxiety disorders measures. In: Rush AJ Jr, Pincus HA, First MB, et al, eds. Handbook of psychiatric measures. Washington, DC: American Psychiatric Press; 2000:549-89.

5. Weathers FW, Litz BT, Herman DS, et al. The PTSD checklist: reliability, validity&diagnostic utility. Paper presented at: annual meeting of the International Society for Traumatic Stress Studies; October 1993; San Antonio, TX.

6. Blanchard EB, Jones-Alexander J, Buckley TC, Forneris CA. Psychometric properties of the PTSD Checklist (PCL). Behav Res Ther 1996;34:669-73.

7. Blanchard EB, Hickling EJ, Freidenberg BM, et al. Two studies of the psychiatric morbidity among motor vehicle accident survivors 1 year after the crash. Behav Res Ther 2004;42:569-83.

8. Spitzer RL, Williams JBW, Gibbon M, First MB. Structured clinical interview for DSM-IV—non-patient version. New York: Biometrics Research Department, New York State Psychiatric Institute; 1996.

9. Beck AT, Ward CH, Mendelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry 1961;5:561-71.

10. Spielberger CD, Gorsuch RL, Lushune RE. Manual for the state-trait anxiety inventory. Palo Alto, CA: Consulting Psychologists Press; 1970.

11. Blanchard EB, Hickling EJ. After the crash: assessment and treatment of motor vehicle accident survivors. Washington, D.C.: American Psychological Association; 2004.

12. Buckley T, Blanchard EB, Hickling EJ. A prospective examination of delayed onset PTSD secondary to motor vehicle accidents. J Abnorm Psychol 1998;107:508-19.

13. Ursano RJ, Bell C, Eth S, et al. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:3-31.

14. Veterans Health Administration. Management of posttraumatic stress (Office of Quality and Performance Publication #10Q-CPG/PTSD-04). Washington, DC: Veterans Administration, Department of Defense Clinical Practice Guideline Working Group; 2003. Available at: http://www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm. Accessed March 21, 2007.

15. Foa EB, Keane TJ, Friedman MJ. Effective treatments for PTSD: practice guidelines from the International Society for Traumatic Stress Studies. New York: Guilford Press; 2000.

16. Bradley R, Greene J, Russ E, et al. A multidimensional meta-analysis of psychotherapy for PTSD. Am J Psychiatry 2005;162:214-27.

17. Ehlers A, Clark DM. Early psychological interventions for adult survivors of trauma: a review. Biol Psychiatry 2003;53:817-26.

18. Beck GJ, Coffey SF. Group cognitive behavioral treatment for PTSD: treatment of motor vehicle accident survivors. Cogn Behav Pract 2004;12:267-77.

19. Jacobson NS, Dobson KS, Truax PA, et al. A component analysis of cognitive-behavioral treatment for depression. J Consult Clin Psychol 1996;64:295-304.

20. Davidson J, Bernik M, Connor K, et al. A new treatment algorithm for posttraumatic stress disorder. Psychiatr Ann 2005;35:887-900.

21. Shipherd JC, Beck JG, Hamblen JL, et al. A preliminary examination of treatment for posttraumatic stress disorder in chronic pain patients: a case study. J Trauma Stress 2003;16(5):451-7.

References

1. Diagnostic and statistical manual of mental disorders. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000.

2. Blake AT, Weathers F, Nagy L, et al. Clinician administered PTSD scale for DSM-IV (CAPS). Boston, MA: National Center for Post-traumatic Stress Disorder, Behavioral Science Division; 1998.

3. Weathers FW, Keane TM, Davidson JRT. Clinician-administered PTSD scale: a review of the first ten years of research. Depress Anxiety 2001;13(3):132-56.

4. Shear MK, Feske U, Brown C, et al. Anxiety disorders measures. In: Rush AJ Jr, Pincus HA, First MB, et al, eds. Handbook of psychiatric measures. Washington, DC: American Psychiatric Press; 2000:549-89.

5. Weathers FW, Litz BT, Herman DS, et al. The PTSD checklist: reliability, validity&diagnostic utility. Paper presented at: annual meeting of the International Society for Traumatic Stress Studies; October 1993; San Antonio, TX.

6. Blanchard EB, Jones-Alexander J, Buckley TC, Forneris CA. Psychometric properties of the PTSD Checklist (PCL). Behav Res Ther 1996;34:669-73.

7. Blanchard EB, Hickling EJ, Freidenberg BM, et al. Two studies of the psychiatric morbidity among motor vehicle accident survivors 1 year after the crash. Behav Res Ther 2004;42:569-83.

8. Spitzer RL, Williams JBW, Gibbon M, First MB. Structured clinical interview for DSM-IV—non-patient version. New York: Biometrics Research Department, New York State Psychiatric Institute; 1996.

9. Beck AT, Ward CH, Mendelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry 1961;5:561-71.

10. Spielberger CD, Gorsuch RL, Lushune RE. Manual for the state-trait anxiety inventory. Palo Alto, CA: Consulting Psychologists Press; 1970.

11. Blanchard EB, Hickling EJ. After the crash: assessment and treatment of motor vehicle accident survivors. Washington, D.C.: American Psychological Association; 2004.

12. Buckley T, Blanchard EB, Hickling EJ. A prospective examination of delayed onset PTSD secondary to motor vehicle accidents. J Abnorm Psychol 1998;107:508-19.

13. Ursano RJ, Bell C, Eth S, et al. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:3-31.

14. Veterans Health Administration. Management of posttraumatic stress (Office of Quality and Performance Publication #10Q-CPG/PTSD-04). Washington, DC: Veterans Administration, Department of Defense Clinical Practice Guideline Working Group; 2003. Available at: http://www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm. Accessed March 21, 2007.

15. Foa EB, Keane TJ, Friedman MJ. Effective treatments for PTSD: practice guidelines from the International Society for Traumatic Stress Studies. New York: Guilford Press; 2000.

16. Bradley R, Greene J, Russ E, et al. A multidimensional meta-analysis of psychotherapy for PTSD. Am J Psychiatry 2005;162:214-27.

17. Ehlers A, Clark DM. Early psychological interventions for adult survivors of trauma: a review. Biol Psychiatry 2003;53:817-26.

18. Beck GJ, Coffey SF. Group cognitive behavioral treatment for PTSD: treatment of motor vehicle accident survivors. Cogn Behav Pract 2004;12:267-77.

19. Jacobson NS, Dobson KS, Truax PA, et al. A component analysis of cognitive-behavioral treatment for depression. J Consult Clin Psychol 1996;64:295-304.

20. Davidson J, Bernik M, Connor K, et al. A new treatment algorithm for posttraumatic stress disorder. Psychiatr Ann 2005;35:887-900.

21. Shipherd JC, Beck JG, Hamblen JL, et al. A preliminary examination of treatment for posttraumatic stress disorder in chronic pain patients: a case study. J Trauma Stress 2003;16(5):451-7.

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Does breast exam only qualify as screening visit?

Q. I recently saw a 62-year-old Medicare patient for a breast examination only. Here is my documentation of the visit:

  • Patient is a virgin, takes no hormones, and refuses a pelvic exam and Pap smear. Blood pressure is in the normal range. Body mass index is 21. She reports no problems and has no questions.
  • Examination of breasts reveals normal skin and nipples, no masses or tenderness, and no lymph-node swelling.
  • Patient is given a slip for a routine mammogram and instructions on performing breast self-exam, and is instructed to return in 1 year, barring problems or concerns.
My question is: Does this visit qualify for billing Medicare with code G0101 (cervical or vaginal cancer screening; pelvic and clinical breast examination) or should it be billed a low-level problem E/M service instead? We would use the diagnosis code V76.19 (other screening breast examination).

A. You face an interesting situation. This is a preventive service, but a diagnosis of V76.19, although accurate here, will cause code G0101, which requires that a pelvic exam have been performed, to be denied.

If you report this visit as a problem E/M service using only this diagnosis, on the other hand, you are more than likely to be denied by Medicare.

For Medicare to consider this a covered service billed as a problem E/M service, you would also have to list diagnostic codes that indicate a complaint, a history of a breast condition, or a strong family history of breast cancer. Medicare will pay for the screening mammogram, but the screening breast exam by itself may not be considered a covered service.

You have a few options:

  • Contact the Medicare carrier and explain the situation. See if they propose a coding solution that they will accept. Get their answer in writing!
  • Bill Medicare using a low-level E/M code (eg, 99212, problem focused exam with straightforward medical decision making) linked to the diagnosis code V76.19. If you choose this option, have the patient sign a waiver that she is responsible for payment should Medicare deny the service. Add the modifier –GA (waiver of liability statement on file) to the problem E/M code. This will allow you to collect payment from the patient.
  • Submit the unlisted code or preventive services 99429 because you performed an exam—although not one that meets the criteria of age-specific preventive codes. This code is never reimbursed by Medicare, but once you get a denial, you either can collect from the patient or are able to submit the charge to any secondary insurance she might have. A modifier –GY (item or service statutorily excluded or does not meet the definition of any Medicare benefit) would also need to be added to the preventive medicine code.

Fern testing: CLIA-waived but payer might not cover

Q. What is the correct code for fern testing? The codes recommended to us are 89060 or 87210, not Q0114, which isn’t recognized by some of our payers. Can you give us advice?

A. The fern test should never be coded 87210 because that code does not represent how the test is performed. (Fern testing is simply applying vaginal fluid to a slide, which is left to dry, and observing whether a ferning develops when the residue is viewed under a microscope.) The test is performed by the provider, not the laboratory; as such, Q0114 is the correct code.

Code 87210, in addition to requiring addition of saline or potassium chloride, is not a CLIA-waived test. You would not be able to bill for it unless you have an advanced lab certificate.

Code 89060 is assigned when looking for crystals in synovial fluid. It is also not a CLIA-waived or physician-performed microscopy test, so billing using this code would require an advanced lab certificate as well.

The advent of the national code set has meant that your payers are required to recognize all codes, although they can determine whether to cover a service or not. It may be that this test isn’t covered by your payer, rather than the code not being recognized as correct.

Two voiding studies: Bill together but specify parts

Q. Can both the 51795 voiding pressure study and 51797 intra-abdominal voiding pressure study be billed together? When I checked the bundling software, it lists these codes as mutually exclusive, with 51795 having an indicator of “1” and 51797 a “9.” If the codes can be billed together, should I use a modifier -59 (distinct service)?

 

 

A. Voiding pressure studies (51795) measure urinary flow rate and pressure during bladder emptying; intra-abdominal voiding pressure studies (51797) measure how the patient must strain to void. These codes can be billed together because they measure different events. More important, they are not bundled.

The “9” indicator used by Medicare for bundled codes means that the edit was deleted. In this case, it was deleted on the same date it was added. For some reason, Medicare elects not to remove deleted code pairs from the master database. Although you will get paid for both of these codes, the code order is different depending on whether you are using your own equipment (because of differences in relative value units).

If you bill each test with a modifier -26 (professional component only), you do not own the equipment and the place of service is a facility. In that case, list 51797-26 first and 51795-26-51 second. The modifier -51 is used on the second code because this is a multiple procedure. If you are billing both professional and technical components (ie, you are using your equipment, in the office), billing order is reversed: List 51797 first and 51795-51 second. Do not use a modifier -59 with this code combination.

Fetal genetic abnormality inferred from US; code for further study

Q. What diagnosis code should we use for a bilateral choroid plexus cyst found on ultrasonography?

A. Choroid plexus cysts (CPCs) are considered a “soft marker” for a gene abnormality called Edward’s syndrome. Although these markers, taken alone, do the baby no harm, they may be associated with an increased risk of another abnormality, including cardiac defects. The presence of a soft marker is not diagnostic of this other abnormality; it is just a noted association.

At the time of the sonogram, therefore, you can only suspect a problem with the fetal genes; further testing is required. In that case, report 655.13 (known or suspected chromosomal abnormality of the fetus affecting management of mother; antepartum condition or complication) with a secondary diagnosis of 793.99 (other nonspecific abnormal findings on radiological and other examinations of body structure).

Positive ANA—don’t leap to “autoimmune disorder”

Q. One of our obstetric patients had a positive antinuclear antibody (ANA) test. We‘ll follow her with biophysical profiles and non-stress testing, and track amniotic fluid volume. Because we have not yet diagnosed systemic lupus erythematosus (SLE) or other specific condition, is it appropriate to use a diagnosis of unspecified autoimmune disorder (279.4) in addition to a pregnancy complication code?

A. Many illnesses and conditions are associated with a positive ANA, including rheumatoid arthritis, Sjögren syndrome, scleroderma, and SLE; infectious diseases such as mononucleosis; and autoimmune thyroid and liver disease. Some medications can cause a positive ANA, and many healthy people have a positive ANA.

Because you have not eliminated the other possibilities for the positive ANA, it is premature to assign the code for an autoimmune condition. Instead, report 648.93 as your primary code (Other current conditions in the mother classifiable elsewhere, complicating pregnancy, childbirth, or the puerperium; antepartum condition or complication), with the secondary diagnosis code 795.79 (Other and unspecified nonspecific immunological findings).

Coding Zoladex depends on the patient’s condition

Q. We have begun using Zoladex for our patients. How do we best code for administering this agent? We have been told to use chemotherapy codes, but this is not a chemotherapeutic agent.

A. Zoladex (goserelin acetate) is classified as a hormonal antineoplastic. It is used to treat endometriosis before surgery because it thins the lining of the uterus, and to treat breast cancer by inhibiting production of estrogen.

The drug is supplied as tiny pellets, which are injected under the skin of the abdomen using a small, “trocar-like” needle and syringe. The procedure constitutes an injection. If you are treating breast cancer with this drug, the correct code would be 96402 (Chemotherapy administration, subcutaneous or intramuscular; hormonal antineoplastic). The code for the pellets is J9202 (Goserelin acetate implant, per 3.6 mg). If you administer more than 3.6 mg at a time, remember to adjust the quantity you bill for. If you are using this drug to treat endometriosis or fibroids, CPT directs you to report 90772 for the injection because it is then considered a nonantineoplastic hormone injection.

Call a contraceptive a contraceptive when coding

Q. How should we code for Implanon insertions?

A. Code this S0180 (Etonogestrel [contraceptive] implant system, including implants and supplies). For the procedure, I recommend code 11975 (insertion, implantable contraceptive capsules).

Implanon’s manufacturer thinks the correct code is 11981 (Insertion, nonbiodegradable drug delivery implant), but I disagree: This is a contraceptive that is implanted under the skin and, under CPT rules, you must use the code that most closely describes the procedure.

 

 

Note also that, although Implanon involves insertion of one rod (other systems require insertion of several), the code 11981 has greater relative value units than 11975. This payment difference will not be lost on most payers because the diagnostic link for the procedure, whichever code is reported, is V25.5 (insertion of implantable subdermal contraceptive).

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Does breast exam only qualify as screening visit?

Q. I recently saw a 62-year-old Medicare patient for a breast examination only. Here is my documentation of the visit:

  • Patient is a virgin, takes no hormones, and refuses a pelvic exam and Pap smear. Blood pressure is in the normal range. Body mass index is 21. She reports no problems and has no questions.
  • Examination of breasts reveals normal skin and nipples, no masses or tenderness, and no lymph-node swelling.
  • Patient is given a slip for a routine mammogram and instructions on performing breast self-exam, and is instructed to return in 1 year, barring problems or concerns.
My question is: Does this visit qualify for billing Medicare with code G0101 (cervical or vaginal cancer screening; pelvic and clinical breast examination) or should it be billed a low-level problem E/M service instead? We would use the diagnosis code V76.19 (other screening breast examination).

A. You face an interesting situation. This is a preventive service, but a diagnosis of V76.19, although accurate here, will cause code G0101, which requires that a pelvic exam have been performed, to be denied.

If you report this visit as a problem E/M service using only this diagnosis, on the other hand, you are more than likely to be denied by Medicare.

For Medicare to consider this a covered service billed as a problem E/M service, you would also have to list diagnostic codes that indicate a complaint, a history of a breast condition, or a strong family history of breast cancer. Medicare will pay for the screening mammogram, but the screening breast exam by itself may not be considered a covered service.

You have a few options:

  • Contact the Medicare carrier and explain the situation. See if they propose a coding solution that they will accept. Get their answer in writing!
  • Bill Medicare using a low-level E/M code (eg, 99212, problem focused exam with straightforward medical decision making) linked to the diagnosis code V76.19. If you choose this option, have the patient sign a waiver that she is responsible for payment should Medicare deny the service. Add the modifier –GA (waiver of liability statement on file) to the problem E/M code. This will allow you to collect payment from the patient.
  • Submit the unlisted code or preventive services 99429 because you performed an exam—although not one that meets the criteria of age-specific preventive codes. This code is never reimbursed by Medicare, but once you get a denial, you either can collect from the patient or are able to submit the charge to any secondary insurance she might have. A modifier –GY (item or service statutorily excluded or does not meet the definition of any Medicare benefit) would also need to be added to the preventive medicine code.

Fern testing: CLIA-waived but payer might not cover

Q. What is the correct code for fern testing? The codes recommended to us are 89060 or 87210, not Q0114, which isn’t recognized by some of our payers. Can you give us advice?

A. The fern test should never be coded 87210 because that code does not represent how the test is performed. (Fern testing is simply applying vaginal fluid to a slide, which is left to dry, and observing whether a ferning develops when the residue is viewed under a microscope.) The test is performed by the provider, not the laboratory; as such, Q0114 is the correct code.

Code 87210, in addition to requiring addition of saline or potassium chloride, is not a CLIA-waived test. You would not be able to bill for it unless you have an advanced lab certificate.

Code 89060 is assigned when looking for crystals in synovial fluid. It is also not a CLIA-waived or physician-performed microscopy test, so billing using this code would require an advanced lab certificate as well.

The advent of the national code set has meant that your payers are required to recognize all codes, although they can determine whether to cover a service or not. It may be that this test isn’t covered by your payer, rather than the code not being recognized as correct.

Two voiding studies: Bill together but specify parts

Q. Can both the 51795 voiding pressure study and 51797 intra-abdominal voiding pressure study be billed together? When I checked the bundling software, it lists these codes as mutually exclusive, with 51795 having an indicator of “1” and 51797 a “9.” If the codes can be billed together, should I use a modifier -59 (distinct service)?

 

 

A. Voiding pressure studies (51795) measure urinary flow rate and pressure during bladder emptying; intra-abdominal voiding pressure studies (51797) measure how the patient must strain to void. These codes can be billed together because they measure different events. More important, they are not bundled.

The “9” indicator used by Medicare for bundled codes means that the edit was deleted. In this case, it was deleted on the same date it was added. For some reason, Medicare elects not to remove deleted code pairs from the master database. Although you will get paid for both of these codes, the code order is different depending on whether you are using your own equipment (because of differences in relative value units).

If you bill each test with a modifier -26 (professional component only), you do not own the equipment and the place of service is a facility. In that case, list 51797-26 first and 51795-26-51 second. The modifier -51 is used on the second code because this is a multiple procedure. If you are billing both professional and technical components (ie, you are using your equipment, in the office), billing order is reversed: List 51797 first and 51795-51 second. Do not use a modifier -59 with this code combination.

Fetal genetic abnormality inferred from US; code for further study

Q. What diagnosis code should we use for a bilateral choroid plexus cyst found on ultrasonography?

A. Choroid plexus cysts (CPCs) are considered a “soft marker” for a gene abnormality called Edward’s syndrome. Although these markers, taken alone, do the baby no harm, they may be associated with an increased risk of another abnormality, including cardiac defects. The presence of a soft marker is not diagnostic of this other abnormality; it is just a noted association.

At the time of the sonogram, therefore, you can only suspect a problem with the fetal genes; further testing is required. In that case, report 655.13 (known or suspected chromosomal abnormality of the fetus affecting management of mother; antepartum condition or complication) with a secondary diagnosis of 793.99 (other nonspecific abnormal findings on radiological and other examinations of body structure).

Positive ANA—don’t leap to “autoimmune disorder”

Q. One of our obstetric patients had a positive antinuclear antibody (ANA) test. We‘ll follow her with biophysical profiles and non-stress testing, and track amniotic fluid volume. Because we have not yet diagnosed systemic lupus erythematosus (SLE) or other specific condition, is it appropriate to use a diagnosis of unspecified autoimmune disorder (279.4) in addition to a pregnancy complication code?

A. Many illnesses and conditions are associated with a positive ANA, including rheumatoid arthritis, Sjögren syndrome, scleroderma, and SLE; infectious diseases such as mononucleosis; and autoimmune thyroid and liver disease. Some medications can cause a positive ANA, and many healthy people have a positive ANA.

Because you have not eliminated the other possibilities for the positive ANA, it is premature to assign the code for an autoimmune condition. Instead, report 648.93 as your primary code (Other current conditions in the mother classifiable elsewhere, complicating pregnancy, childbirth, or the puerperium; antepartum condition or complication), with the secondary diagnosis code 795.79 (Other and unspecified nonspecific immunological findings).

Coding Zoladex depends on the patient’s condition

Q. We have begun using Zoladex for our patients. How do we best code for administering this agent? We have been told to use chemotherapy codes, but this is not a chemotherapeutic agent.

A. Zoladex (goserelin acetate) is classified as a hormonal antineoplastic. It is used to treat endometriosis before surgery because it thins the lining of the uterus, and to treat breast cancer by inhibiting production of estrogen.

The drug is supplied as tiny pellets, which are injected under the skin of the abdomen using a small, “trocar-like” needle and syringe. The procedure constitutes an injection. If you are treating breast cancer with this drug, the correct code would be 96402 (Chemotherapy administration, subcutaneous or intramuscular; hormonal antineoplastic). The code for the pellets is J9202 (Goserelin acetate implant, per 3.6 mg). If you administer more than 3.6 mg at a time, remember to adjust the quantity you bill for. If you are using this drug to treat endometriosis or fibroids, CPT directs you to report 90772 for the injection because it is then considered a nonantineoplastic hormone injection.

Call a contraceptive a contraceptive when coding

Q. How should we code for Implanon insertions?

A. Code this S0180 (Etonogestrel [contraceptive] implant system, including implants and supplies). For the procedure, I recommend code 11975 (insertion, implantable contraceptive capsules).

Implanon’s manufacturer thinks the correct code is 11981 (Insertion, nonbiodegradable drug delivery implant), but I disagree: This is a contraceptive that is implanted under the skin and, under CPT rules, you must use the code that most closely describes the procedure.

 

 

Note also that, although Implanon involves insertion of one rod (other systems require insertion of several), the code 11981 has greater relative value units than 11975. This payment difference will not be lost on most payers because the diagnostic link for the procedure, whichever code is reported, is V25.5 (insertion of implantable subdermal contraceptive).

Does breast exam only qualify as screening visit?

Q. I recently saw a 62-year-old Medicare patient for a breast examination only. Here is my documentation of the visit:

  • Patient is a virgin, takes no hormones, and refuses a pelvic exam and Pap smear. Blood pressure is in the normal range. Body mass index is 21. She reports no problems and has no questions.
  • Examination of breasts reveals normal skin and nipples, no masses or tenderness, and no lymph-node swelling.
  • Patient is given a slip for a routine mammogram and instructions on performing breast self-exam, and is instructed to return in 1 year, barring problems or concerns.
My question is: Does this visit qualify for billing Medicare with code G0101 (cervical or vaginal cancer screening; pelvic and clinical breast examination) or should it be billed a low-level problem E/M service instead? We would use the diagnosis code V76.19 (other screening breast examination).

A. You face an interesting situation. This is a preventive service, but a diagnosis of V76.19, although accurate here, will cause code G0101, which requires that a pelvic exam have been performed, to be denied.

If you report this visit as a problem E/M service using only this diagnosis, on the other hand, you are more than likely to be denied by Medicare.

For Medicare to consider this a covered service billed as a problem E/M service, you would also have to list diagnostic codes that indicate a complaint, a history of a breast condition, or a strong family history of breast cancer. Medicare will pay for the screening mammogram, but the screening breast exam by itself may not be considered a covered service.

You have a few options:

  • Contact the Medicare carrier and explain the situation. See if they propose a coding solution that they will accept. Get their answer in writing!
  • Bill Medicare using a low-level E/M code (eg, 99212, problem focused exam with straightforward medical decision making) linked to the diagnosis code V76.19. If you choose this option, have the patient sign a waiver that she is responsible for payment should Medicare deny the service. Add the modifier –GA (waiver of liability statement on file) to the problem E/M code. This will allow you to collect payment from the patient.
  • Submit the unlisted code or preventive services 99429 because you performed an exam—although not one that meets the criteria of age-specific preventive codes. This code is never reimbursed by Medicare, but once you get a denial, you either can collect from the patient or are able to submit the charge to any secondary insurance she might have. A modifier –GY (item or service statutorily excluded or does not meet the definition of any Medicare benefit) would also need to be added to the preventive medicine code.

Fern testing: CLIA-waived but payer might not cover

Q. What is the correct code for fern testing? The codes recommended to us are 89060 or 87210, not Q0114, which isn’t recognized by some of our payers. Can you give us advice?

A. The fern test should never be coded 87210 because that code does not represent how the test is performed. (Fern testing is simply applying vaginal fluid to a slide, which is left to dry, and observing whether a ferning develops when the residue is viewed under a microscope.) The test is performed by the provider, not the laboratory; as such, Q0114 is the correct code.

Code 87210, in addition to requiring addition of saline or potassium chloride, is not a CLIA-waived test. You would not be able to bill for it unless you have an advanced lab certificate.

Code 89060 is assigned when looking for crystals in synovial fluid. It is also not a CLIA-waived or physician-performed microscopy test, so billing using this code would require an advanced lab certificate as well.

The advent of the national code set has meant that your payers are required to recognize all codes, although they can determine whether to cover a service or not. It may be that this test isn’t covered by your payer, rather than the code not being recognized as correct.

Two voiding studies: Bill together but specify parts

Q. Can both the 51795 voiding pressure study and 51797 intra-abdominal voiding pressure study be billed together? When I checked the bundling software, it lists these codes as mutually exclusive, with 51795 having an indicator of “1” and 51797 a “9.” If the codes can be billed together, should I use a modifier -59 (distinct service)?

 

 

A. Voiding pressure studies (51795) measure urinary flow rate and pressure during bladder emptying; intra-abdominal voiding pressure studies (51797) measure how the patient must strain to void. These codes can be billed together because they measure different events. More important, they are not bundled.

The “9” indicator used by Medicare for bundled codes means that the edit was deleted. In this case, it was deleted on the same date it was added. For some reason, Medicare elects not to remove deleted code pairs from the master database. Although you will get paid for both of these codes, the code order is different depending on whether you are using your own equipment (because of differences in relative value units).

If you bill each test with a modifier -26 (professional component only), you do not own the equipment and the place of service is a facility. In that case, list 51797-26 first and 51795-26-51 second. The modifier -51 is used on the second code because this is a multiple procedure. If you are billing both professional and technical components (ie, you are using your equipment, in the office), billing order is reversed: List 51797 first and 51795-51 second. Do not use a modifier -59 with this code combination.

Fetal genetic abnormality inferred from US; code for further study

Q. What diagnosis code should we use for a bilateral choroid plexus cyst found on ultrasonography?

A. Choroid plexus cysts (CPCs) are considered a “soft marker” for a gene abnormality called Edward’s syndrome. Although these markers, taken alone, do the baby no harm, they may be associated with an increased risk of another abnormality, including cardiac defects. The presence of a soft marker is not diagnostic of this other abnormality; it is just a noted association.

At the time of the sonogram, therefore, you can only suspect a problem with the fetal genes; further testing is required. In that case, report 655.13 (known or suspected chromosomal abnormality of the fetus affecting management of mother; antepartum condition or complication) with a secondary diagnosis of 793.99 (other nonspecific abnormal findings on radiological and other examinations of body structure).

Positive ANA—don’t leap to “autoimmune disorder”

Q. One of our obstetric patients had a positive antinuclear antibody (ANA) test. We‘ll follow her with biophysical profiles and non-stress testing, and track amniotic fluid volume. Because we have not yet diagnosed systemic lupus erythematosus (SLE) or other specific condition, is it appropriate to use a diagnosis of unspecified autoimmune disorder (279.4) in addition to a pregnancy complication code?

A. Many illnesses and conditions are associated with a positive ANA, including rheumatoid arthritis, Sjögren syndrome, scleroderma, and SLE; infectious diseases such as mononucleosis; and autoimmune thyroid and liver disease. Some medications can cause a positive ANA, and many healthy people have a positive ANA.

Because you have not eliminated the other possibilities for the positive ANA, it is premature to assign the code for an autoimmune condition. Instead, report 648.93 as your primary code (Other current conditions in the mother classifiable elsewhere, complicating pregnancy, childbirth, or the puerperium; antepartum condition or complication), with the secondary diagnosis code 795.79 (Other and unspecified nonspecific immunological findings).

Coding Zoladex depends on the patient’s condition

Q. We have begun using Zoladex for our patients. How do we best code for administering this agent? We have been told to use chemotherapy codes, but this is not a chemotherapeutic agent.

A. Zoladex (goserelin acetate) is classified as a hormonal antineoplastic. It is used to treat endometriosis before surgery because it thins the lining of the uterus, and to treat breast cancer by inhibiting production of estrogen.

The drug is supplied as tiny pellets, which are injected under the skin of the abdomen using a small, “trocar-like” needle and syringe. The procedure constitutes an injection. If you are treating breast cancer with this drug, the correct code would be 96402 (Chemotherapy administration, subcutaneous or intramuscular; hormonal antineoplastic). The code for the pellets is J9202 (Goserelin acetate implant, per 3.6 mg). If you administer more than 3.6 mg at a time, remember to adjust the quantity you bill for. If you are using this drug to treat endometriosis or fibroids, CPT directs you to report 90772 for the injection because it is then considered a nonantineoplastic hormone injection.

Call a contraceptive a contraceptive when coding

Q. How should we code for Implanon insertions?

A. Code this S0180 (Etonogestrel [contraceptive] implant system, including implants and supplies). For the procedure, I recommend code 11975 (insertion, implantable contraceptive capsules).

Implanon’s manufacturer thinks the correct code is 11981 (Insertion, nonbiodegradable drug delivery implant), but I disagree: This is a contraceptive that is implanted under the skin and, under CPT rules, you must use the code that most closely describes the procedure.

 

 

Note also that, although Implanon involves insertion of one rod (other systems require insertion of several), the code 11981 has greater relative value units than 11975. This payment difference will not be lost on most payers because the diagnostic link for the procedure, whichever code is reported, is V25.5 (insertion of implantable subdermal contraceptive).

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Symptoms Postdischarge

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Frequency of new or worsening symptoms in the posthospitalization period

The Institute of Medicine reports To Err is Human and Crossing the Quality Chasm have drawn great attention to quality improvement and patient safety in the hospital setting.13 With the growth of the hospitalist field over the past several years,4 there has been increasing discussion about the importance of assuring quality of care, and some have argued that improving health care quality and reducing avoidable errors may be among the hospitalist's most important functions.5 Most discussions about the quality of hospital care have concerned the inpatient stay itself. However, the growth of hospital medicine, with its inherent discontinuity between inpatient and outpatient physicians, has intensified interest in the transition period from hospital discharge until first outpatient appointment.

At discharge, physicians may prescribe medications, order home health services, and arrange follow‐up appointments. It is often assumed a patient will remain stable after discharge and will follow up at the outpatient physician's office. Previous research has shown there may be problems with these assumptions. A patient may not understand the postdischarge treatment plan as well as the physician thinks.6 A recent study found that adverse events after discharge were common and often preventable.7 A follow‐up study confirmed that approximately 25% of patients had an adverse event after hospital discharge and that most adverse events caused symptoms but did not result in an emergency department visit, hospitalization, or death.8 Another study also found the prevalence of medical errors following hospitalization was high because of the discontinuity of care from the inpatient to the outpatient setting.9 These errors resulted in an increased rate of rehospitalization.

Telephone follow‐up may be a useful method of bridging the gap in care between discharge and the first outpatient appointment.10, 11 In most previous studies it was 2 or 3 weeks after discharge before patients were contacted or their records studied. By this point, patients who had done poorly may already have been readmitted or sought care at alternative locations. In one small study, pharmacists found that 12 of 79 patients (15%) contacted by telephone within 2 days of discharge12 had symptoms there were new or had worsened since discharge. The purpose of the present investigation was to extend these previous findings through a large multicenter study of how frequently patients had new or worsened symptoms within several days of discharge.

METHODS

Settings and Participants

IPCThe Hospitalist Company has hospitalist practices at more than 150 health care facilities in 10 health care markets. At the time of the study, IPC employed more than 300 internal medicine and family practice physicians and discharged approximately 11,000 adult patients per month. The study is a retrospective analysis of data collected from May 1, 2003, to October 31, 2003.

Data Acquisition

Physicians entered clinical and financial information on all hospitalized patients into a handheld personal digital assistant (PDA) utilizing functions of IPC‐LINK software. At the time of discharge, a physician completed a discharge summary on the PDA that was transmitted electronically to a centralized data center. Copies of the discharge summary were also faxed to the outpatient physician's office. Patients were first interviewed by call‐center patient representatives, unlicensed staff with medical backgrounds. Call‐center representatives made several attempts by telephone to reach all patients discharged home within several days of discharge. Using a scripted survey instrument (Appendix A), they asked patients or family members a series of questions about clinical status, new or worsening symptoms, problems with medications or prescribed home health care services, follow‐up appointments with their outpatient physician, and satisfaction with the care received. Call‐center nurses, licensed personnel with extensive medical/surgical and case management experience, contacted patients whose answers to questions on the scripted survey instrument (see last section of Appendix A) indicated a high risk of postdischarge problems, intervening as necessary to resolve the health care issues.

Health status was self rated on a 5‐point Likert scale from excellent to poor in response to the health status question on the SF‐12.13, 14 Patient age was calculated using birth date and admit date from the IPC‐Link discharge summary. With clinical data from the IPC‐Link discharge summary, the 3M DRG Grouper was used to assign each patient a DRG and severity of illness (SOI) score.15 Reported symptoms were grouped in clinically meaningful categories by the lead author.

Statistical Analysis

Logistic regression analysis was performed to analyze the effects of sex, health insurance, inpatient severity of illness, and self‐reported health status on the proportion of patients with symptoms. Sex, health status, and severity of illness were treated as ordered variables. Because insurance type is a nominal variable, HMO was used as the reference category, and the other categories were converted to indicator variables. Pearson chi‐square testing was used for all other analyses. The large number of planned analyses necessitated adjustment of the P values computed for the tests to maintain the type I error rate at 0.05. Therefore, a step‐down Bonferroni procedure was used.16

Role of the Funding Source

Data collection, analysis, and interpretation were funded by IPC and performed by employees of IPC.

RESULTS

During the study period, 48,236 patients were discharged to their homes from an acute care hospital. The IPC call center successfully contacted 16,135 patients after discharge, of whom 368 patients (2.3%) were excluded because of incomplete answers, leaving 15,767 as the valid study population (effective response rate = 32.4%). Of these, 98.9% were contacted within the first 5 days. The primary reasons for nonresponse or noninclusion in the present analysis were no answer after 2 attempts (52%) and missing or incorrect phone numbers (16%). If there was an answering machine, a message was left for the patient to call back. Those who called back accounted for fewer than 1% of all the patients.

A comparison of participants versus nonparticipants is shown in Table 1. The mean age of surveyed patients was 60.1 years, and 57% were female. The most common categories of insurance coverage were Medicare and HMO. The inpatient severity of illness of most patients was minor to moderate. Self‐reported health status was normally distributed, with the greatest percentage of patients rating their health as fair or good. On average, nonparticipants were younger than participants, more likely to be male, had a different pattern of health insurance, and a slightly lower severity of illness. The top 10 DRGs were the same for the respondents and nonrespondents, and the order of these 10 diagnoses was very similar.

Characteristics of Patients in Study
CharacteristicPatients in StudyPatients Not in StudyP Value*
Number of PatientsPercentage of All PatientsNumber of PatientsPercentage of All Patients
  • P value obtained from Pearson chi‐square testing of the difference in rates for each variable between patients in study versus patients not in study.

  • Patients not in study were not able to complete the survey; therefore health status could not be determined.

All patients15,767 32,101  
Mean age (years)60.1 54.1 <.0001
Sex     
Female898557.0%1722053.7%<.0001
Male651541.3%1433744.7%<.0001
Unknown2671.7%5441.7%.897
Insurance type     
HMO639140.5%1254039.1%<.001
Medicaid10666.8%28158.8%<.0001
Medicare605538.4%977730.4%<.0001
Commercial and other13708.7%349010.9%<.0001
Self‐pay8855.6%347910.9%<.0001
Severity of illness     
Minor674042.7%1467945.7%<.0001
Moderate685443.5%1319741.1%
Major168810.7%30919.6%<.0001
Extreme1180.7%2190.7%.571
Unknown3672.3%9152.9%.001
Health status     
Excellent3432.2%N/A
Very good13928.8%N/A
Good550534.9%N/A
Fair590137.4%N/A
Poor14689.3%N/A
Unknown11587.3%N/A

Of the 15,767 patients contacted, 11.9% (N = 1876) reported symptoms that were new or had worsened since leaving the hospital. Sixty‐four percent of these patients had new symptoms, and 36% had worsening symptoms. These two groups were combined for analysis in this study because for both groups, identification and action are important. Of the patients with new or worse symptoms, 37% required no assistance from the nurse because they had already notified a doctor and/or were doing something about it. The other 63% either had not notified their doctor or had concerns about their signs and symptoms. The most common action taken by the nurse was patient education regarding the symptoms. Of those requiring nurse intervention in addition to education, the most common intervention was to contact the patient's primary care provider or specialist about the patient's symptoms, followed by contacting the hospitalist. In 72% of nurse interventions, the patient's primary care physician or a specialist was contacted about the new or worsened symptoms. Other interventions included contacting the physician's office to obtain a prescription for a medication for the symptom, to get an appointment for the patient, or to reschedule an appointment to be earlier. A referral to an emergency room or urgent care center was given to 4% of patients.

Mean age of the patients with new or worsened symptoms was 60.5 years. The age distribution of symptomatic and asymptomatic patients was not significantly different, whether comparing by mean, median, or decades. Table 2 illustrates factors associated with the increased rate of new or worsened symptoms. Women were more likely than men to report symptoms (13.0% vs. 10.3%, P < .0001). As health status worsened, the percentage of patients with new or worsened symptoms increased (P < .0001), as it did with increased inpatient SOI (P < .0001). There was no correlation between self‐rated health status and SOI score based on DRG score, suggesting they measured different parameters. Table 3 lists the percentages of patients reporting new or worsened symptoms for the most common DRGs. The only significant distinction was that patients discharged with a DRG of chest pain were less likely to report symptoms than were all patients.

Characteristics of Patients with New or Worsening Symptoms
CharacteristicNumber of Patients with New or Worsening SymptomsPercentage of All Patients with New or Worsening SymptomsP Value for Difference or Trend*
All Patients187611.9% 
Sex  <.0001
Female117013.0% 
Male67210.3% 
Insurance Type   
HMO72211.3%.89
Medicare74812.4%.21
Commercial and other16512.0%.53
Medicaid12812.0%.27
Self‐pay11312.8% 
Severity of illness  .17
Minor74811.1% 
Moderate81411.9% 
Major24714.6% 
Extreme1916.1% 
Health Status  <.0001
Excellent226.4%
Very good856.1% 
Good4297.8% 
Fair72512.3% 
Poor38426.2% 
Prevalence of New Symptoms for the Top 10 DRGs*
DRGDescriptionNumber of PatientsPercentage of PatientsPatients with New or Worsening SymptomsRate of New or Worsening SymptomsP value
  • Results for patients in study only.

  • Obtained from Pearson chi‐square testing for rate of new/worsening symptoms for each DRG versus the mean.

Total patients in Study 15,767 187611.9% 
143Chest pain13068.3%1289.8%0.027
182Digest disorders with complications8015.1%9211.5%0.767
183Digest disorders without complications6324.0%7812.3%0.783
127Heart failure and shock5443.5%5510.1%0.230
89Pneumonia with complications4262.7%399.2%0.098
88COPD3802.4%4411.6%0.913
278Cellulitis3232.0%329.9%0.313
174GI hemorrhage with complications3202.0%4012.5%0.809
15CVA3021.9%258.3%0.066
175GI hemorrhage without complications2871.8%3411.8%0.948

The symptoms the patients reported are categorized in Table 4 without distinction as to whether they are primary or secondary. Gastrointestinal symptoms were the most common category of symptoms, followed by general symptoms, cardiovascular symptoms, and pain. The most common symptoms reported were fatigue/weakness, nausea/vomiting, and edema.

Major Symptoms Reported By Patients Post‐Discharge*
CategorySpecific SymptomNumber% 0f Total
  • Only symptoms with greater than 2% prevalence are listed, although symptoms with lower prevalence are included in the category subtotals. Therefore, category subtotals may be greater than the sum of the symptoms listed.

  • Patients complaining of reactions to their medications. Medication issues described in the text refer to problems obtaining or understanding how to take medications (see Appendix).

Gastrointestinal 77124.1%
 Nausea/vomiting2457.7%
 Abdominal pain1625.1%
 Diarrhea1464.6%
 Eating problems1073.3%
 Constipation712.2%
General 52716.5%
 Fatigue or weakness36011.3%
 Dizziness1675.2%
Cardiovascular 38812.1%
 Edema2196.8%
 Chest pain1013.2%
Pain 38211.9%
 Back and neck1183.7%
 Lower exttremity (including hip)1153.6%
 Generalized762.4%
Psychological 2096.5%
 Sleeping problems1253.9%
 Change in mental status/psychiatric symptoms842.6%
Pulmonary 38211.9%
 Dyspnea1344.2%
Neurological 1996.2%
 Headache1183.7%
Infectious 1926.0%
 Fever822.6%
Dermatological 652.0%
Urological 621.9%
ENT 501.6%
Diabetic (problems with blood sugar) 451.4%
Postoperative wound problems 391.2%
Problems with intravenous sites 170.5%
Medication Reaction 140.4%
Bleeding (other than above locations) 140.4%
Gynecological 90.3%
Others 892.8%

The call center assessed whether the patient had difficulty making a follow‐up appointment and whether an appointment was scheduled within 2 weeks of discharge. Patients with new or worsening symptoms were only minimally more likely to have scheduled follow‐up (61.0% vs. 58.4% for patients not reporting new or worsening symptoms, P < .05). Symptomatic patients had a higher prevalence of medication issues, defined as not picking up their prescriptions or not understanding how to take their medication (22.2% vs. 6.8% for asymptomatic patients; P < .0001). Likewise, the prevalence of symptomatic patients having problems receiving scheduled home health care services was 5.8%, compared with a prevalence of 3.6% for asymptomatic patients (P < .0001).

DISCUSSION

Enhancing the quality of care provided by hospitalists means not only improving care during hospitalization but also assuring patient stability between discharge and outpatient follow‐up. As part of efforts to improve transition management, the call center at IPC attempted to contact all patients discharged home within several days of discharge. Of 15,767 patients surveyed between May 1, 2003, and October 31, 2003, 11.9% (N = 1876) had new or worsening symptoms since leaving the hospital only 2 or 3 days earlier. We had hypothesized that older patients might be more symptomatic than younger ones, but found no difference in the prevalence of new or worsening symptoms based on age. Women were more likely to be symptomatic than men.

We defined appropriate postdischarge follow‐up as having an appointment with an outpatient physician within 2 weeks. A previous study of psychiatric patients documented that keeping a follow‐up appointment significantly reduces the risk of rehospitalization.17 Similar data do not exist for medical patients. Our data demonstrated that symptomatic patients were only minimally more likely to have made a follow‐up appointment with their outpatient physician within the first 2 weeks than were those patients who were not symptomatic. As part of patient education at discharge, clinicians routinely counsel patients to call their outpatient physician should they experience new or worsening symptoms once at home. Inpatient physicians may assume this recommendation provides a safety net for the patients should they develop problems after discharge. However, our finding that almost 40% of patients with new or worsening symptoms within 2‐3 days of discharge had not made a follow‐up appointment with their physician suggests many patients fall through this safety net. Although there was a slight statistically significant difference between the groups, this difference was not clinically significant. One potential limitation of our data is that we did not examine whether there was a correlation between the day of the week that a patient was discharged and inability to make a follow‐up appointment.

As part of the survey script (see Appendix), we inquired whether patients were able to pick up their prescriptions and whether they understood how to take their medication. A high percentage of patients in our study reported having one of these medication issues in the first several days following hospital discharge, providing an opportunity for early intervention and prevention of medical error. Forster and others have demonstrated that adverse events and medical errors are common in the postdischarge period, affecting 23%‐49% of patients.79 Errors in the transition from inpatient to outpatient care increased the 3‐month rate of rehospitalization.9 New or worsening symptoms represented the most common adverse event.8 Noting that many of these postdischarge complications could be preventable if detected early, Forster suggested system changes such as earlier follow‐up with the outpatient physician or a postdischarge telephone call to check on the patient's status.7, 18 Future studies are planned to further analyze our data on medication issues and to determine if these problems are more prevalent for certain medications or diagnoses.

Comprehensive discharge planning remains an essential step in the discharge process. This may involve prescribing medications, arranging home health care services, and arranging outpatient follow‐up. The traditional hospital discharge process does not adequately ensure that patients understand their discharge plan and are able to comply with it. Calkins et al. compared physicians' perceptions of patients' understanding of medication side effects and activity restrictions with patients' actual understanding.6 They found that, compared with what was reported by patients, physicians overestimated the time spent discussing discharge plans and how well patients understood medication side effects and activity restrictions.

An important method for reducing patient problems is to contact patients by telephone after discharge in order to identify any health care issues. Previous research has confirmed that follow‐up telephone calls improve health outcomes and decrease resource utilization of patients, mainly those discharged from the emergency department.10, 11, 1923 A study of telephone follow‐up after ambulatory care visits did not find significant benefits of this procedure.24 In one of the few studies of telephone calls after hospitalization, pharmacists contacted patients 2 days after discharge and were able to detect and resolve medication‐related problems in 19% of patients and learned of new or worsening symptoms in 15%. Patient satisfaction was improved, and the intervention resulted in a lower rate of repeat visits to the emergency room within 30 days of discharge.12 Another study of telephone follow‐up following hospital discharge compared proactively calling all patients with providing a phone number that patients can call if they have questions. The study demonstrated that very few patients called the number provided, but of those patients called by the nursing service, more than 90% had questions about self‐care and recovery.25 These findings demonstrate the value of proactively contacting patients in the first several days after discharge, when problems can be detected and interventions initiated earlier.

One potential concern with this study was the low response rate. This was a retrospective analysis of an existing discharge management call‐center system, not a prospective study. We were not able to reach 52% of the patients discharged after 2 attempts by telephone. To have our call center make additional attempts to reach each patient by telephone would require a significant increase in the size of the call center, because at the time of the study, the staff was handling more than 370 patients discharged home a day. The telephone number of 16% of patients was missing or incorrect. We have since developed internal quality improvement mechanisms to decrease this percentage. After subtracting the patients we were unable to reach and those whose phone number was missing or incorrect, we were able to contact 32.4% of all the patients discharged home.

Several reasons explain the response rate found by many prospective research studies. In most studies of telephone follow‐up, patients must be able to consent to participate in order to be considered eligible inclusion. This raises the response rate because patients who do not consent to participate, have language barriers, or have no telephone are excluded from the study. In our study none of these types of patients were excluded. There are 2 additional differences between our study and many published studies that involve telephone surveys. Ours was not a prospective research study, and we contacted many more patients than did other studies. For example, a study by Forster et al. involved only 581 patients, and the research staff was diligent in its efforts to reach the patients,7 making up to 20 attempts for each patient. They reported a response rate of 69%. If they had included patients who were non‐English speakers or had no phone in their study, the response rate would have been 59%. Shesser et al. were able to reach 144 of 297 patients in their study of emergency room follow‐up, for a 48.4% response rate.25 The response rate in a study of telephone consultation with asthma patients was quite similar to ours. They enrolled 932 eligible patients, of whom they were able to reach 278, for a response rate of 30%.

It is possible that the rate of symptoms and the other variables we measured relative to this would have been different if we had been able to reach 100% of patients. There were some demographic differences between the patients we were able to reach and those we were not (Table 1). The nonresponders were slightly younger and slightly more likely to be female. Nonresponders were more likely to have Medicaid or commercial insurance or be self‐pay and were less likely to have Medicare. In addition, nonresponders had less severe illness. Although this scenario is highly unlikely, if none of the nonresponders had new or worsening symptoms, the rate of symptoms would only have been 3.86%. Conversely, it is possible but also very unlikely that a greater percentage of the nonresponders had new or worsening symptoms. Given the demographics of our study participants, we would expect a potentially slightly lower rate of signs and symptoms.

The present study had several other limitations. First, all patients surveyed were cared for by IPC‐employed physicians. It is possible that reported rates of symptoms and other postdischarge issues are not generalizable to other hospitalist practices. However, the present data were collected at more than 100 health care facilities in 10 health care markets, and the patients were cared for by more than 200 physicians. Therefore, it is unlikely these results would have been significantly influenced by a particular physician's or institution's practice patterns.

Second, because of the large number of facilities involved and that we could only track readmissions to facilities where our own hospitalists practice, we were not able to report 30‐ or 90‐day readmission rates or emergency room visit rates. In a prospective study, these would be important variables to track in order to assess the clinical relevance of the symptoms. We could track this data for some institutions, but for most of them, the quality of data was not sufficient to be meaningful or to make conclusions.

An additional limitation is that the call center did not differentiate between clinically minor and major symptoms. The inclusion of symptoms perhaps considered minor might have elevated the reported symptom frequency. However, the definitions of minor and major symptoms are very subjective, and a clinician's definitions might differ from those of a patient who is at home and uncomfortable. For example, nausea or loss of appetite related to new medications may be considered minor clinically but could be devastating to the patient experiencing them, leading the patient to stop taking the medication. Conversely, symptoms that may be considered nonsignificant by the patient may be interpreted as indicating clinically significant disease by a physician. Therefore, we would argue that, regardless of the severity of the symptom, follow‐up with a clinician is important.

Another limitation is based on our definition of an adequate follow‐up appointment as one scheduled within 2 weeks of discharge. It might be argued that if a patient's new symptoms were considered minor clinically, then a follow‐up interval greater than 2 weeks might be considered adequate. However, as already noted, a patient's criteria for considering a symptom minor and not requiring follow‐up may differ from a clinician's criteria. Also, the standardized discharge process requires that the hospitalist identify a physician for outpatient follow‐up and specify the period when the patient is to see the physician. Because of the inherent variability in having a many hospitalists practicing in many hospitals, not all patients had a scheduled appointment at discharge. We were not able to determine whether patients had an appointment date and time for follow‐up before discharge or had only received instructions to call the office for an appointment.

The Institute of Medicine, in its report Crossing the Quality Chasm, identified the coordination of care across services and sites of care as one of the health care system's redesign imperatives.2 Hospitalists are in a unique position to address transition care issues. Managing the transition from inpatient to outpatient care is vitally important, and hospitalists should play an essential role in designing a transition management system for discharged patients. Although individual efforts by hospitalists are essential to assuring postdischarge contact with patients, there is increasing agreement that system solutions are needed to improve the quality of care in the transition period following hospitalization. Improving a health care process involves more than working harder; it involves working differently.3 It is therefore imperative that hospitalist programs develop effective systems to manage the transition period until safe arrival by the patient in the outpatient physician's office.

In summary, 11.9% of patients contacted by a telephone call center within several days of discharge had new or worsening symptoms since discharge. There was no difference by age in the prevalence of symptoms. Patients who rated their health status as fair to poor were more likely to be symptomatic. Symptomatic patients were also more likely to have difficulty obtaining or understanding how to take their medications and receiving home health services. Patients who felt poorly were only minimally more likely to have made an appointment for follow‐up with their outpatient physician. It is hoped that by identifying patients who are doing poorly after discharge and intervening as necessary, we can improve the health outcome of our patients, as well as reduce the number of emergency room visits and readmission rates. Although actions by individual physicians are important, a system to manage the postdischarge transition period is essential for improving posthospitalization outcomes.

Acknowledgements

The authors thank Rahul M. Dodhia for his assistance in the statistical analysis of the data and Sunil Kripalani for his thoughtful review of the manuscript.

APPENDIX

0

Survey Questions
References
  1. Kohn LT,Corrigan J,Donaldson M, editors. To Err Is Human: Building a Safer Health System.Washington, DC:National Academy Press;2000:xxi,287.
  2. Institute of Medicine (U.S.).Committee on Quality of Health Care in America. Crossing the Quality Chasm: a New Health System for the 21st Century.Washington, DC:National Academy Press;2001:xx,337.
  3. Lurie JD,Merrens EJ,Lee Splaine ME.An approach to hospital quality improvement.Med Clin North Am.2002;86:825845.
  4. Wachter RM,Goldman L.The hospitalist movement 5 years later.JAMA.2002;287:487494.
  5. Leape L.Making health care safe. Supplement on hospital medicine and patient safety.The Hospitalist.2004:34.
  6. Calkins DR,Davis RB,Reiley P, et al.Patient‐physician communication at hospital discharge and patients' understanding of the postdischarge treatment plan.Arch Intern Med.1997;157:10261030.
  7. Forster AJ,Murff HJ,Peterson JF,Gandhi TK,Bates DW.The incidence and severity of adverse events affecting patients after discharge from the hospital.Ann Intern Med.2003;138:161167.
  8. Forster AJ,Clark HD,Menard A, et al.Adverse events among medical patients after discharge from the hospital.CMAJ.2004;170:345349.
  9. Moore C,Wisnievsky J,Williams S,McGinn T.Medical errors related to discontinuity of care from an inpatient to an outpatient setting.J Gen Intern Med.2003;18:646651.
  10. Wasson J,Gaudette C,Whaley F,Sauvigne A,Baribeau P,Welch HG.Telephone care as a substitute for routine clinic follow‐up.JAMA.1992;267:17881793.
  11. Riegel B,Carlson B,Koop Z,LePetri B,Glasser D,Unger A.Effect of a standardized nurse case‐management telephone intervention on resource use in patients with chronic heart failure.Arch Intern Med.2002;162:705712.
  12. Dudas V,Bookwalter T,Kerr KM,Pantilat SZ.The impact of follow‐up telephone calls to patients after hospitalization.Am J Med.2001;111(9B):26S30S.
  13. Medical Outcomes Trust.How to Score the SF‐12 Short Form Health Survey.Boston:The Medical Outcomes Trust;1992.
  14. Ratner P,Johnson J,Jeffery B.Examining emotional, physical, social, and spiritual health as determinants of self‐rated health status.Am J Health Promot.1998;12:275282.
  15. 3M Health Information Systems, 3M All Patient Refined DRG Software. Available at: http://3m.com/market/healthcare/his/us/products/apr_drg/brochure.html.
  16. Holm S.A simple sequentially rejective Bonferroni test procedure.Scand J Stat.1979;6:6570.
  17. Nelson EA,Maruish ME,Axler JL.Effects of discharge planning and compliance with outpatient appointments on readmission rates.Psychiatr Serv.2000;51:885889.
  18. Forster A.J. Can you prevent adverse drug events after hospital discharge?CMAJ.2006;174:921922.
  19. Chande VT,Exum V.Follow‐up phone calls after an emergency department visit.Pediatrics.1994;93:513514.
  20. Jones J,Clark W,Bradford J,Dougherty J.Efficacy of a telephone follow‐up system in the emergency department.J Emerg Med.1988;6:249254.
  21. Jones PK,Jones SL,Katz J.A randomized trial to improve compliance in urinary tract infection patients in the emergency department.Ann Emerg Med.1990;19:1620.
  22. Shesser, R.,Smith M,Adams S,Walls R,Paxton M.The effectiveness of an organized emergency department follow‐up system.Ann Emerg Med.1986;15:911915.
  23. Nelson JR.The importance of postdischarge telephone follow‐up for hospitalists: a view from the trenches.Am J Med.2001;111(9B):43S44S.
  24. Welch HG,Johnson DJ,Edson R.Telephone care as an adjunct to routine medical follow‐up. A negative randomized trial.Eff Clin Pract.2000;3:123130.
  25. Bostrom JCaldwell J,McGuire K,Everson D.Telephone follow‐up after discharge from the hospital: does it make a difference?Appl Nurs Res.1996;9:4752.
Article PDF
Issue
Journal of Hospital Medicine - 2(2)
Page Number
58-68
Legacy Keywords
quality improvement, hospitalist medicine, transition of care, discharge management
Sections
Article PDF
Article PDF

The Institute of Medicine reports To Err is Human and Crossing the Quality Chasm have drawn great attention to quality improvement and patient safety in the hospital setting.13 With the growth of the hospitalist field over the past several years,4 there has been increasing discussion about the importance of assuring quality of care, and some have argued that improving health care quality and reducing avoidable errors may be among the hospitalist's most important functions.5 Most discussions about the quality of hospital care have concerned the inpatient stay itself. However, the growth of hospital medicine, with its inherent discontinuity between inpatient and outpatient physicians, has intensified interest in the transition period from hospital discharge until first outpatient appointment.

At discharge, physicians may prescribe medications, order home health services, and arrange follow‐up appointments. It is often assumed a patient will remain stable after discharge and will follow up at the outpatient physician's office. Previous research has shown there may be problems with these assumptions. A patient may not understand the postdischarge treatment plan as well as the physician thinks.6 A recent study found that adverse events after discharge were common and often preventable.7 A follow‐up study confirmed that approximately 25% of patients had an adverse event after hospital discharge and that most adverse events caused symptoms but did not result in an emergency department visit, hospitalization, or death.8 Another study also found the prevalence of medical errors following hospitalization was high because of the discontinuity of care from the inpatient to the outpatient setting.9 These errors resulted in an increased rate of rehospitalization.

Telephone follow‐up may be a useful method of bridging the gap in care between discharge and the first outpatient appointment.10, 11 In most previous studies it was 2 or 3 weeks after discharge before patients were contacted or their records studied. By this point, patients who had done poorly may already have been readmitted or sought care at alternative locations. In one small study, pharmacists found that 12 of 79 patients (15%) contacted by telephone within 2 days of discharge12 had symptoms there were new or had worsened since discharge. The purpose of the present investigation was to extend these previous findings through a large multicenter study of how frequently patients had new or worsened symptoms within several days of discharge.

METHODS

Settings and Participants

IPCThe Hospitalist Company has hospitalist practices at more than 150 health care facilities in 10 health care markets. At the time of the study, IPC employed more than 300 internal medicine and family practice physicians and discharged approximately 11,000 adult patients per month. The study is a retrospective analysis of data collected from May 1, 2003, to October 31, 2003.

Data Acquisition

Physicians entered clinical and financial information on all hospitalized patients into a handheld personal digital assistant (PDA) utilizing functions of IPC‐LINK software. At the time of discharge, a physician completed a discharge summary on the PDA that was transmitted electronically to a centralized data center. Copies of the discharge summary were also faxed to the outpatient physician's office. Patients were first interviewed by call‐center patient representatives, unlicensed staff with medical backgrounds. Call‐center representatives made several attempts by telephone to reach all patients discharged home within several days of discharge. Using a scripted survey instrument (Appendix A), they asked patients or family members a series of questions about clinical status, new or worsening symptoms, problems with medications or prescribed home health care services, follow‐up appointments with their outpatient physician, and satisfaction with the care received. Call‐center nurses, licensed personnel with extensive medical/surgical and case management experience, contacted patients whose answers to questions on the scripted survey instrument (see last section of Appendix A) indicated a high risk of postdischarge problems, intervening as necessary to resolve the health care issues.

Health status was self rated on a 5‐point Likert scale from excellent to poor in response to the health status question on the SF‐12.13, 14 Patient age was calculated using birth date and admit date from the IPC‐Link discharge summary. With clinical data from the IPC‐Link discharge summary, the 3M DRG Grouper was used to assign each patient a DRG and severity of illness (SOI) score.15 Reported symptoms were grouped in clinically meaningful categories by the lead author.

Statistical Analysis

Logistic regression analysis was performed to analyze the effects of sex, health insurance, inpatient severity of illness, and self‐reported health status on the proportion of patients with symptoms. Sex, health status, and severity of illness were treated as ordered variables. Because insurance type is a nominal variable, HMO was used as the reference category, and the other categories were converted to indicator variables. Pearson chi‐square testing was used for all other analyses. The large number of planned analyses necessitated adjustment of the P values computed for the tests to maintain the type I error rate at 0.05. Therefore, a step‐down Bonferroni procedure was used.16

Role of the Funding Source

Data collection, analysis, and interpretation were funded by IPC and performed by employees of IPC.

RESULTS

During the study period, 48,236 patients were discharged to their homes from an acute care hospital. The IPC call center successfully contacted 16,135 patients after discharge, of whom 368 patients (2.3%) were excluded because of incomplete answers, leaving 15,767 as the valid study population (effective response rate = 32.4%). Of these, 98.9% were contacted within the first 5 days. The primary reasons for nonresponse or noninclusion in the present analysis were no answer after 2 attempts (52%) and missing or incorrect phone numbers (16%). If there was an answering machine, a message was left for the patient to call back. Those who called back accounted for fewer than 1% of all the patients.

A comparison of participants versus nonparticipants is shown in Table 1. The mean age of surveyed patients was 60.1 years, and 57% were female. The most common categories of insurance coverage were Medicare and HMO. The inpatient severity of illness of most patients was minor to moderate. Self‐reported health status was normally distributed, with the greatest percentage of patients rating their health as fair or good. On average, nonparticipants were younger than participants, more likely to be male, had a different pattern of health insurance, and a slightly lower severity of illness. The top 10 DRGs were the same for the respondents and nonrespondents, and the order of these 10 diagnoses was very similar.

Characteristics of Patients in Study
CharacteristicPatients in StudyPatients Not in StudyP Value*
Number of PatientsPercentage of All PatientsNumber of PatientsPercentage of All Patients
  • P value obtained from Pearson chi‐square testing of the difference in rates for each variable between patients in study versus patients not in study.

  • Patients not in study were not able to complete the survey; therefore health status could not be determined.

All patients15,767 32,101  
Mean age (years)60.1 54.1 <.0001
Sex     
Female898557.0%1722053.7%<.0001
Male651541.3%1433744.7%<.0001
Unknown2671.7%5441.7%.897
Insurance type     
HMO639140.5%1254039.1%<.001
Medicaid10666.8%28158.8%<.0001
Medicare605538.4%977730.4%<.0001
Commercial and other13708.7%349010.9%<.0001
Self‐pay8855.6%347910.9%<.0001
Severity of illness     
Minor674042.7%1467945.7%<.0001
Moderate685443.5%1319741.1%
Major168810.7%30919.6%<.0001
Extreme1180.7%2190.7%.571
Unknown3672.3%9152.9%.001
Health status     
Excellent3432.2%N/A
Very good13928.8%N/A
Good550534.9%N/A
Fair590137.4%N/A
Poor14689.3%N/A
Unknown11587.3%N/A

Of the 15,767 patients contacted, 11.9% (N = 1876) reported symptoms that were new or had worsened since leaving the hospital. Sixty‐four percent of these patients had new symptoms, and 36% had worsening symptoms. These two groups were combined for analysis in this study because for both groups, identification and action are important. Of the patients with new or worse symptoms, 37% required no assistance from the nurse because they had already notified a doctor and/or were doing something about it. The other 63% either had not notified their doctor or had concerns about their signs and symptoms. The most common action taken by the nurse was patient education regarding the symptoms. Of those requiring nurse intervention in addition to education, the most common intervention was to contact the patient's primary care provider or specialist about the patient's symptoms, followed by contacting the hospitalist. In 72% of nurse interventions, the patient's primary care physician or a specialist was contacted about the new or worsened symptoms. Other interventions included contacting the physician's office to obtain a prescription for a medication for the symptom, to get an appointment for the patient, or to reschedule an appointment to be earlier. A referral to an emergency room or urgent care center was given to 4% of patients.

Mean age of the patients with new or worsened symptoms was 60.5 years. The age distribution of symptomatic and asymptomatic patients was not significantly different, whether comparing by mean, median, or decades. Table 2 illustrates factors associated with the increased rate of new or worsened symptoms. Women were more likely than men to report symptoms (13.0% vs. 10.3%, P < .0001). As health status worsened, the percentage of patients with new or worsened symptoms increased (P < .0001), as it did with increased inpatient SOI (P < .0001). There was no correlation between self‐rated health status and SOI score based on DRG score, suggesting they measured different parameters. Table 3 lists the percentages of patients reporting new or worsened symptoms for the most common DRGs. The only significant distinction was that patients discharged with a DRG of chest pain were less likely to report symptoms than were all patients.

Characteristics of Patients with New or Worsening Symptoms
CharacteristicNumber of Patients with New or Worsening SymptomsPercentage of All Patients with New or Worsening SymptomsP Value for Difference or Trend*
All Patients187611.9% 
Sex  <.0001
Female117013.0% 
Male67210.3% 
Insurance Type   
HMO72211.3%.89
Medicare74812.4%.21
Commercial and other16512.0%.53
Medicaid12812.0%.27
Self‐pay11312.8% 
Severity of illness  .17
Minor74811.1% 
Moderate81411.9% 
Major24714.6% 
Extreme1916.1% 
Health Status  <.0001
Excellent226.4%
Very good856.1% 
Good4297.8% 
Fair72512.3% 
Poor38426.2% 
Prevalence of New Symptoms for the Top 10 DRGs*
DRGDescriptionNumber of PatientsPercentage of PatientsPatients with New or Worsening SymptomsRate of New or Worsening SymptomsP value
  • Results for patients in study only.

  • Obtained from Pearson chi‐square testing for rate of new/worsening symptoms for each DRG versus the mean.

Total patients in Study 15,767 187611.9% 
143Chest pain13068.3%1289.8%0.027
182Digest disorders with complications8015.1%9211.5%0.767
183Digest disorders without complications6324.0%7812.3%0.783
127Heart failure and shock5443.5%5510.1%0.230
89Pneumonia with complications4262.7%399.2%0.098
88COPD3802.4%4411.6%0.913
278Cellulitis3232.0%329.9%0.313
174GI hemorrhage with complications3202.0%4012.5%0.809
15CVA3021.9%258.3%0.066
175GI hemorrhage without complications2871.8%3411.8%0.948

The symptoms the patients reported are categorized in Table 4 without distinction as to whether they are primary or secondary. Gastrointestinal symptoms were the most common category of symptoms, followed by general symptoms, cardiovascular symptoms, and pain. The most common symptoms reported were fatigue/weakness, nausea/vomiting, and edema.

Major Symptoms Reported By Patients Post‐Discharge*
CategorySpecific SymptomNumber% 0f Total
  • Only symptoms with greater than 2% prevalence are listed, although symptoms with lower prevalence are included in the category subtotals. Therefore, category subtotals may be greater than the sum of the symptoms listed.

  • Patients complaining of reactions to their medications. Medication issues described in the text refer to problems obtaining or understanding how to take medications (see Appendix).

Gastrointestinal 77124.1%
 Nausea/vomiting2457.7%
 Abdominal pain1625.1%
 Diarrhea1464.6%
 Eating problems1073.3%
 Constipation712.2%
General 52716.5%
 Fatigue or weakness36011.3%
 Dizziness1675.2%
Cardiovascular 38812.1%
 Edema2196.8%
 Chest pain1013.2%
Pain 38211.9%
 Back and neck1183.7%
 Lower exttremity (including hip)1153.6%
 Generalized762.4%
Psychological 2096.5%
 Sleeping problems1253.9%
 Change in mental status/psychiatric symptoms842.6%
Pulmonary 38211.9%
 Dyspnea1344.2%
Neurological 1996.2%
 Headache1183.7%
Infectious 1926.0%
 Fever822.6%
Dermatological 652.0%
Urological 621.9%
ENT 501.6%
Diabetic (problems with blood sugar) 451.4%
Postoperative wound problems 391.2%
Problems with intravenous sites 170.5%
Medication Reaction 140.4%
Bleeding (other than above locations) 140.4%
Gynecological 90.3%
Others 892.8%

The call center assessed whether the patient had difficulty making a follow‐up appointment and whether an appointment was scheduled within 2 weeks of discharge. Patients with new or worsening symptoms were only minimally more likely to have scheduled follow‐up (61.0% vs. 58.4% for patients not reporting new or worsening symptoms, P < .05). Symptomatic patients had a higher prevalence of medication issues, defined as not picking up their prescriptions or not understanding how to take their medication (22.2% vs. 6.8% for asymptomatic patients; P < .0001). Likewise, the prevalence of symptomatic patients having problems receiving scheduled home health care services was 5.8%, compared with a prevalence of 3.6% for asymptomatic patients (P < .0001).

DISCUSSION

Enhancing the quality of care provided by hospitalists means not only improving care during hospitalization but also assuring patient stability between discharge and outpatient follow‐up. As part of efforts to improve transition management, the call center at IPC attempted to contact all patients discharged home within several days of discharge. Of 15,767 patients surveyed between May 1, 2003, and October 31, 2003, 11.9% (N = 1876) had new or worsening symptoms since leaving the hospital only 2 or 3 days earlier. We had hypothesized that older patients might be more symptomatic than younger ones, but found no difference in the prevalence of new or worsening symptoms based on age. Women were more likely to be symptomatic than men.

We defined appropriate postdischarge follow‐up as having an appointment with an outpatient physician within 2 weeks. A previous study of psychiatric patients documented that keeping a follow‐up appointment significantly reduces the risk of rehospitalization.17 Similar data do not exist for medical patients. Our data demonstrated that symptomatic patients were only minimally more likely to have made a follow‐up appointment with their outpatient physician within the first 2 weeks than were those patients who were not symptomatic. As part of patient education at discharge, clinicians routinely counsel patients to call their outpatient physician should they experience new or worsening symptoms once at home. Inpatient physicians may assume this recommendation provides a safety net for the patients should they develop problems after discharge. However, our finding that almost 40% of patients with new or worsening symptoms within 2‐3 days of discharge had not made a follow‐up appointment with their physician suggests many patients fall through this safety net. Although there was a slight statistically significant difference between the groups, this difference was not clinically significant. One potential limitation of our data is that we did not examine whether there was a correlation between the day of the week that a patient was discharged and inability to make a follow‐up appointment.

As part of the survey script (see Appendix), we inquired whether patients were able to pick up their prescriptions and whether they understood how to take their medication. A high percentage of patients in our study reported having one of these medication issues in the first several days following hospital discharge, providing an opportunity for early intervention and prevention of medical error. Forster and others have demonstrated that adverse events and medical errors are common in the postdischarge period, affecting 23%‐49% of patients.79 Errors in the transition from inpatient to outpatient care increased the 3‐month rate of rehospitalization.9 New or worsening symptoms represented the most common adverse event.8 Noting that many of these postdischarge complications could be preventable if detected early, Forster suggested system changes such as earlier follow‐up with the outpatient physician or a postdischarge telephone call to check on the patient's status.7, 18 Future studies are planned to further analyze our data on medication issues and to determine if these problems are more prevalent for certain medications or diagnoses.

Comprehensive discharge planning remains an essential step in the discharge process. This may involve prescribing medications, arranging home health care services, and arranging outpatient follow‐up. The traditional hospital discharge process does not adequately ensure that patients understand their discharge plan and are able to comply with it. Calkins et al. compared physicians' perceptions of patients' understanding of medication side effects and activity restrictions with patients' actual understanding.6 They found that, compared with what was reported by patients, physicians overestimated the time spent discussing discharge plans and how well patients understood medication side effects and activity restrictions.

An important method for reducing patient problems is to contact patients by telephone after discharge in order to identify any health care issues. Previous research has confirmed that follow‐up telephone calls improve health outcomes and decrease resource utilization of patients, mainly those discharged from the emergency department.10, 11, 1923 A study of telephone follow‐up after ambulatory care visits did not find significant benefits of this procedure.24 In one of the few studies of telephone calls after hospitalization, pharmacists contacted patients 2 days after discharge and were able to detect and resolve medication‐related problems in 19% of patients and learned of new or worsening symptoms in 15%. Patient satisfaction was improved, and the intervention resulted in a lower rate of repeat visits to the emergency room within 30 days of discharge.12 Another study of telephone follow‐up following hospital discharge compared proactively calling all patients with providing a phone number that patients can call if they have questions. The study demonstrated that very few patients called the number provided, but of those patients called by the nursing service, more than 90% had questions about self‐care and recovery.25 These findings demonstrate the value of proactively contacting patients in the first several days after discharge, when problems can be detected and interventions initiated earlier.

One potential concern with this study was the low response rate. This was a retrospective analysis of an existing discharge management call‐center system, not a prospective study. We were not able to reach 52% of the patients discharged after 2 attempts by telephone. To have our call center make additional attempts to reach each patient by telephone would require a significant increase in the size of the call center, because at the time of the study, the staff was handling more than 370 patients discharged home a day. The telephone number of 16% of patients was missing or incorrect. We have since developed internal quality improvement mechanisms to decrease this percentage. After subtracting the patients we were unable to reach and those whose phone number was missing or incorrect, we were able to contact 32.4% of all the patients discharged home.

Several reasons explain the response rate found by many prospective research studies. In most studies of telephone follow‐up, patients must be able to consent to participate in order to be considered eligible inclusion. This raises the response rate because patients who do not consent to participate, have language barriers, or have no telephone are excluded from the study. In our study none of these types of patients were excluded. There are 2 additional differences between our study and many published studies that involve telephone surveys. Ours was not a prospective research study, and we contacted many more patients than did other studies. For example, a study by Forster et al. involved only 581 patients, and the research staff was diligent in its efforts to reach the patients,7 making up to 20 attempts for each patient. They reported a response rate of 69%. If they had included patients who were non‐English speakers or had no phone in their study, the response rate would have been 59%. Shesser et al. were able to reach 144 of 297 patients in their study of emergency room follow‐up, for a 48.4% response rate.25 The response rate in a study of telephone consultation with asthma patients was quite similar to ours. They enrolled 932 eligible patients, of whom they were able to reach 278, for a response rate of 30%.

It is possible that the rate of symptoms and the other variables we measured relative to this would have been different if we had been able to reach 100% of patients. There were some demographic differences between the patients we were able to reach and those we were not (Table 1). The nonresponders were slightly younger and slightly more likely to be female. Nonresponders were more likely to have Medicaid or commercial insurance or be self‐pay and were less likely to have Medicare. In addition, nonresponders had less severe illness. Although this scenario is highly unlikely, if none of the nonresponders had new or worsening symptoms, the rate of symptoms would only have been 3.86%. Conversely, it is possible but also very unlikely that a greater percentage of the nonresponders had new or worsening symptoms. Given the demographics of our study participants, we would expect a potentially slightly lower rate of signs and symptoms.

The present study had several other limitations. First, all patients surveyed were cared for by IPC‐employed physicians. It is possible that reported rates of symptoms and other postdischarge issues are not generalizable to other hospitalist practices. However, the present data were collected at more than 100 health care facilities in 10 health care markets, and the patients were cared for by more than 200 physicians. Therefore, it is unlikely these results would have been significantly influenced by a particular physician's or institution's practice patterns.

Second, because of the large number of facilities involved and that we could only track readmissions to facilities where our own hospitalists practice, we were not able to report 30‐ or 90‐day readmission rates or emergency room visit rates. In a prospective study, these would be important variables to track in order to assess the clinical relevance of the symptoms. We could track this data for some institutions, but for most of them, the quality of data was not sufficient to be meaningful or to make conclusions.

An additional limitation is that the call center did not differentiate between clinically minor and major symptoms. The inclusion of symptoms perhaps considered minor might have elevated the reported symptom frequency. However, the definitions of minor and major symptoms are very subjective, and a clinician's definitions might differ from those of a patient who is at home and uncomfortable. For example, nausea or loss of appetite related to new medications may be considered minor clinically but could be devastating to the patient experiencing them, leading the patient to stop taking the medication. Conversely, symptoms that may be considered nonsignificant by the patient may be interpreted as indicating clinically significant disease by a physician. Therefore, we would argue that, regardless of the severity of the symptom, follow‐up with a clinician is important.

Another limitation is based on our definition of an adequate follow‐up appointment as one scheduled within 2 weeks of discharge. It might be argued that if a patient's new symptoms were considered minor clinically, then a follow‐up interval greater than 2 weeks might be considered adequate. However, as already noted, a patient's criteria for considering a symptom minor and not requiring follow‐up may differ from a clinician's criteria. Also, the standardized discharge process requires that the hospitalist identify a physician for outpatient follow‐up and specify the period when the patient is to see the physician. Because of the inherent variability in having a many hospitalists practicing in many hospitals, not all patients had a scheduled appointment at discharge. We were not able to determine whether patients had an appointment date and time for follow‐up before discharge or had only received instructions to call the office for an appointment.

The Institute of Medicine, in its report Crossing the Quality Chasm, identified the coordination of care across services and sites of care as one of the health care system's redesign imperatives.2 Hospitalists are in a unique position to address transition care issues. Managing the transition from inpatient to outpatient care is vitally important, and hospitalists should play an essential role in designing a transition management system for discharged patients. Although individual efforts by hospitalists are essential to assuring postdischarge contact with patients, there is increasing agreement that system solutions are needed to improve the quality of care in the transition period following hospitalization. Improving a health care process involves more than working harder; it involves working differently.3 It is therefore imperative that hospitalist programs develop effective systems to manage the transition period until safe arrival by the patient in the outpatient physician's office.

In summary, 11.9% of patients contacted by a telephone call center within several days of discharge had new or worsening symptoms since discharge. There was no difference by age in the prevalence of symptoms. Patients who rated their health status as fair to poor were more likely to be symptomatic. Symptomatic patients were also more likely to have difficulty obtaining or understanding how to take their medications and receiving home health services. Patients who felt poorly were only minimally more likely to have made an appointment for follow‐up with their outpatient physician. It is hoped that by identifying patients who are doing poorly after discharge and intervening as necessary, we can improve the health outcome of our patients, as well as reduce the number of emergency room visits and readmission rates. Although actions by individual physicians are important, a system to manage the postdischarge transition period is essential for improving posthospitalization outcomes.

Acknowledgements

The authors thank Rahul M. Dodhia for his assistance in the statistical analysis of the data and Sunil Kripalani for his thoughtful review of the manuscript.

APPENDIX

0

Survey Questions

The Institute of Medicine reports To Err is Human and Crossing the Quality Chasm have drawn great attention to quality improvement and patient safety in the hospital setting.13 With the growth of the hospitalist field over the past several years,4 there has been increasing discussion about the importance of assuring quality of care, and some have argued that improving health care quality and reducing avoidable errors may be among the hospitalist's most important functions.5 Most discussions about the quality of hospital care have concerned the inpatient stay itself. However, the growth of hospital medicine, with its inherent discontinuity between inpatient and outpatient physicians, has intensified interest in the transition period from hospital discharge until first outpatient appointment.

At discharge, physicians may prescribe medications, order home health services, and arrange follow‐up appointments. It is often assumed a patient will remain stable after discharge and will follow up at the outpatient physician's office. Previous research has shown there may be problems with these assumptions. A patient may not understand the postdischarge treatment plan as well as the physician thinks.6 A recent study found that adverse events after discharge were common and often preventable.7 A follow‐up study confirmed that approximately 25% of patients had an adverse event after hospital discharge and that most adverse events caused symptoms but did not result in an emergency department visit, hospitalization, or death.8 Another study also found the prevalence of medical errors following hospitalization was high because of the discontinuity of care from the inpatient to the outpatient setting.9 These errors resulted in an increased rate of rehospitalization.

Telephone follow‐up may be a useful method of bridging the gap in care between discharge and the first outpatient appointment.10, 11 In most previous studies it was 2 or 3 weeks after discharge before patients were contacted or their records studied. By this point, patients who had done poorly may already have been readmitted or sought care at alternative locations. In one small study, pharmacists found that 12 of 79 patients (15%) contacted by telephone within 2 days of discharge12 had symptoms there were new or had worsened since discharge. The purpose of the present investigation was to extend these previous findings through a large multicenter study of how frequently patients had new or worsened symptoms within several days of discharge.

METHODS

Settings and Participants

IPCThe Hospitalist Company has hospitalist practices at more than 150 health care facilities in 10 health care markets. At the time of the study, IPC employed more than 300 internal medicine and family practice physicians and discharged approximately 11,000 adult patients per month. The study is a retrospective analysis of data collected from May 1, 2003, to October 31, 2003.

Data Acquisition

Physicians entered clinical and financial information on all hospitalized patients into a handheld personal digital assistant (PDA) utilizing functions of IPC‐LINK software. At the time of discharge, a physician completed a discharge summary on the PDA that was transmitted electronically to a centralized data center. Copies of the discharge summary were also faxed to the outpatient physician's office. Patients were first interviewed by call‐center patient representatives, unlicensed staff with medical backgrounds. Call‐center representatives made several attempts by telephone to reach all patients discharged home within several days of discharge. Using a scripted survey instrument (Appendix A), they asked patients or family members a series of questions about clinical status, new or worsening symptoms, problems with medications or prescribed home health care services, follow‐up appointments with their outpatient physician, and satisfaction with the care received. Call‐center nurses, licensed personnel with extensive medical/surgical and case management experience, contacted patients whose answers to questions on the scripted survey instrument (see last section of Appendix A) indicated a high risk of postdischarge problems, intervening as necessary to resolve the health care issues.

Health status was self rated on a 5‐point Likert scale from excellent to poor in response to the health status question on the SF‐12.13, 14 Patient age was calculated using birth date and admit date from the IPC‐Link discharge summary. With clinical data from the IPC‐Link discharge summary, the 3M DRG Grouper was used to assign each patient a DRG and severity of illness (SOI) score.15 Reported symptoms were grouped in clinically meaningful categories by the lead author.

Statistical Analysis

Logistic regression analysis was performed to analyze the effects of sex, health insurance, inpatient severity of illness, and self‐reported health status on the proportion of patients with symptoms. Sex, health status, and severity of illness were treated as ordered variables. Because insurance type is a nominal variable, HMO was used as the reference category, and the other categories were converted to indicator variables. Pearson chi‐square testing was used for all other analyses. The large number of planned analyses necessitated adjustment of the P values computed for the tests to maintain the type I error rate at 0.05. Therefore, a step‐down Bonferroni procedure was used.16

Role of the Funding Source

Data collection, analysis, and interpretation were funded by IPC and performed by employees of IPC.

RESULTS

During the study period, 48,236 patients were discharged to their homes from an acute care hospital. The IPC call center successfully contacted 16,135 patients after discharge, of whom 368 patients (2.3%) were excluded because of incomplete answers, leaving 15,767 as the valid study population (effective response rate = 32.4%). Of these, 98.9% were contacted within the first 5 days. The primary reasons for nonresponse or noninclusion in the present analysis were no answer after 2 attempts (52%) and missing or incorrect phone numbers (16%). If there was an answering machine, a message was left for the patient to call back. Those who called back accounted for fewer than 1% of all the patients.

A comparison of participants versus nonparticipants is shown in Table 1. The mean age of surveyed patients was 60.1 years, and 57% were female. The most common categories of insurance coverage were Medicare and HMO. The inpatient severity of illness of most patients was minor to moderate. Self‐reported health status was normally distributed, with the greatest percentage of patients rating their health as fair or good. On average, nonparticipants were younger than participants, more likely to be male, had a different pattern of health insurance, and a slightly lower severity of illness. The top 10 DRGs were the same for the respondents and nonrespondents, and the order of these 10 diagnoses was very similar.

Characteristics of Patients in Study
CharacteristicPatients in StudyPatients Not in StudyP Value*
Number of PatientsPercentage of All PatientsNumber of PatientsPercentage of All Patients
  • P value obtained from Pearson chi‐square testing of the difference in rates for each variable between patients in study versus patients not in study.

  • Patients not in study were not able to complete the survey; therefore health status could not be determined.

All patients15,767 32,101  
Mean age (years)60.1 54.1 <.0001
Sex     
Female898557.0%1722053.7%<.0001
Male651541.3%1433744.7%<.0001
Unknown2671.7%5441.7%.897
Insurance type     
HMO639140.5%1254039.1%<.001
Medicaid10666.8%28158.8%<.0001
Medicare605538.4%977730.4%<.0001
Commercial and other13708.7%349010.9%<.0001
Self‐pay8855.6%347910.9%<.0001
Severity of illness     
Minor674042.7%1467945.7%<.0001
Moderate685443.5%1319741.1%
Major168810.7%30919.6%<.0001
Extreme1180.7%2190.7%.571
Unknown3672.3%9152.9%.001
Health status     
Excellent3432.2%N/A
Very good13928.8%N/A
Good550534.9%N/A
Fair590137.4%N/A
Poor14689.3%N/A
Unknown11587.3%N/A

Of the 15,767 patients contacted, 11.9% (N = 1876) reported symptoms that were new or had worsened since leaving the hospital. Sixty‐four percent of these patients had new symptoms, and 36% had worsening symptoms. These two groups were combined for analysis in this study because for both groups, identification and action are important. Of the patients with new or worse symptoms, 37% required no assistance from the nurse because they had already notified a doctor and/or were doing something about it. The other 63% either had not notified their doctor or had concerns about their signs and symptoms. The most common action taken by the nurse was patient education regarding the symptoms. Of those requiring nurse intervention in addition to education, the most common intervention was to contact the patient's primary care provider or specialist about the patient's symptoms, followed by contacting the hospitalist. In 72% of nurse interventions, the patient's primary care physician or a specialist was contacted about the new or worsened symptoms. Other interventions included contacting the physician's office to obtain a prescription for a medication for the symptom, to get an appointment for the patient, or to reschedule an appointment to be earlier. A referral to an emergency room or urgent care center was given to 4% of patients.

Mean age of the patients with new or worsened symptoms was 60.5 years. The age distribution of symptomatic and asymptomatic patients was not significantly different, whether comparing by mean, median, or decades. Table 2 illustrates factors associated with the increased rate of new or worsened symptoms. Women were more likely than men to report symptoms (13.0% vs. 10.3%, P < .0001). As health status worsened, the percentage of patients with new or worsened symptoms increased (P < .0001), as it did with increased inpatient SOI (P < .0001). There was no correlation between self‐rated health status and SOI score based on DRG score, suggesting they measured different parameters. Table 3 lists the percentages of patients reporting new or worsened symptoms for the most common DRGs. The only significant distinction was that patients discharged with a DRG of chest pain were less likely to report symptoms than were all patients.

Characteristics of Patients with New or Worsening Symptoms
CharacteristicNumber of Patients with New or Worsening SymptomsPercentage of All Patients with New or Worsening SymptomsP Value for Difference or Trend*
All Patients187611.9% 
Sex  <.0001
Female117013.0% 
Male67210.3% 
Insurance Type   
HMO72211.3%.89
Medicare74812.4%.21
Commercial and other16512.0%.53
Medicaid12812.0%.27
Self‐pay11312.8% 
Severity of illness  .17
Minor74811.1% 
Moderate81411.9% 
Major24714.6% 
Extreme1916.1% 
Health Status  <.0001
Excellent226.4%
Very good856.1% 
Good4297.8% 
Fair72512.3% 
Poor38426.2% 
Prevalence of New Symptoms for the Top 10 DRGs*
DRGDescriptionNumber of PatientsPercentage of PatientsPatients with New or Worsening SymptomsRate of New or Worsening SymptomsP value
  • Results for patients in study only.

  • Obtained from Pearson chi‐square testing for rate of new/worsening symptoms for each DRG versus the mean.

Total patients in Study 15,767 187611.9% 
143Chest pain13068.3%1289.8%0.027
182Digest disorders with complications8015.1%9211.5%0.767
183Digest disorders without complications6324.0%7812.3%0.783
127Heart failure and shock5443.5%5510.1%0.230
89Pneumonia with complications4262.7%399.2%0.098
88COPD3802.4%4411.6%0.913
278Cellulitis3232.0%329.9%0.313
174GI hemorrhage with complications3202.0%4012.5%0.809
15CVA3021.9%258.3%0.066
175GI hemorrhage without complications2871.8%3411.8%0.948

The symptoms the patients reported are categorized in Table 4 without distinction as to whether they are primary or secondary. Gastrointestinal symptoms were the most common category of symptoms, followed by general symptoms, cardiovascular symptoms, and pain. The most common symptoms reported were fatigue/weakness, nausea/vomiting, and edema.

Major Symptoms Reported By Patients Post‐Discharge*
CategorySpecific SymptomNumber% 0f Total
  • Only symptoms with greater than 2% prevalence are listed, although symptoms with lower prevalence are included in the category subtotals. Therefore, category subtotals may be greater than the sum of the symptoms listed.

  • Patients complaining of reactions to their medications. Medication issues described in the text refer to problems obtaining or understanding how to take medications (see Appendix).

Gastrointestinal 77124.1%
 Nausea/vomiting2457.7%
 Abdominal pain1625.1%
 Diarrhea1464.6%
 Eating problems1073.3%
 Constipation712.2%
General 52716.5%
 Fatigue or weakness36011.3%
 Dizziness1675.2%
Cardiovascular 38812.1%
 Edema2196.8%
 Chest pain1013.2%
Pain 38211.9%
 Back and neck1183.7%
 Lower exttremity (including hip)1153.6%
 Generalized762.4%
Psychological 2096.5%
 Sleeping problems1253.9%
 Change in mental status/psychiatric symptoms842.6%
Pulmonary 38211.9%
 Dyspnea1344.2%
Neurological 1996.2%
 Headache1183.7%
Infectious 1926.0%
 Fever822.6%
Dermatological 652.0%
Urological 621.9%
ENT 501.6%
Diabetic (problems with blood sugar) 451.4%
Postoperative wound problems 391.2%
Problems with intravenous sites 170.5%
Medication Reaction 140.4%
Bleeding (other than above locations) 140.4%
Gynecological 90.3%
Others 892.8%

The call center assessed whether the patient had difficulty making a follow‐up appointment and whether an appointment was scheduled within 2 weeks of discharge. Patients with new or worsening symptoms were only minimally more likely to have scheduled follow‐up (61.0% vs. 58.4% for patients not reporting new or worsening symptoms, P < .05). Symptomatic patients had a higher prevalence of medication issues, defined as not picking up their prescriptions or not understanding how to take their medication (22.2% vs. 6.8% for asymptomatic patients; P < .0001). Likewise, the prevalence of symptomatic patients having problems receiving scheduled home health care services was 5.8%, compared with a prevalence of 3.6% for asymptomatic patients (P < .0001).

DISCUSSION

Enhancing the quality of care provided by hospitalists means not only improving care during hospitalization but also assuring patient stability between discharge and outpatient follow‐up. As part of efforts to improve transition management, the call center at IPC attempted to contact all patients discharged home within several days of discharge. Of 15,767 patients surveyed between May 1, 2003, and October 31, 2003, 11.9% (N = 1876) had new or worsening symptoms since leaving the hospital only 2 or 3 days earlier. We had hypothesized that older patients might be more symptomatic than younger ones, but found no difference in the prevalence of new or worsening symptoms based on age. Women were more likely to be symptomatic than men.

We defined appropriate postdischarge follow‐up as having an appointment with an outpatient physician within 2 weeks. A previous study of psychiatric patients documented that keeping a follow‐up appointment significantly reduces the risk of rehospitalization.17 Similar data do not exist for medical patients. Our data demonstrated that symptomatic patients were only minimally more likely to have made a follow‐up appointment with their outpatient physician within the first 2 weeks than were those patients who were not symptomatic. As part of patient education at discharge, clinicians routinely counsel patients to call their outpatient physician should they experience new or worsening symptoms once at home. Inpatient physicians may assume this recommendation provides a safety net for the patients should they develop problems after discharge. However, our finding that almost 40% of patients with new or worsening symptoms within 2‐3 days of discharge had not made a follow‐up appointment with their physician suggests many patients fall through this safety net. Although there was a slight statistically significant difference between the groups, this difference was not clinically significant. One potential limitation of our data is that we did not examine whether there was a correlation between the day of the week that a patient was discharged and inability to make a follow‐up appointment.

As part of the survey script (see Appendix), we inquired whether patients were able to pick up their prescriptions and whether they understood how to take their medication. A high percentage of patients in our study reported having one of these medication issues in the first several days following hospital discharge, providing an opportunity for early intervention and prevention of medical error. Forster and others have demonstrated that adverse events and medical errors are common in the postdischarge period, affecting 23%‐49% of patients.79 Errors in the transition from inpatient to outpatient care increased the 3‐month rate of rehospitalization.9 New or worsening symptoms represented the most common adverse event.8 Noting that many of these postdischarge complications could be preventable if detected early, Forster suggested system changes such as earlier follow‐up with the outpatient physician or a postdischarge telephone call to check on the patient's status.7, 18 Future studies are planned to further analyze our data on medication issues and to determine if these problems are more prevalent for certain medications or diagnoses.

Comprehensive discharge planning remains an essential step in the discharge process. This may involve prescribing medications, arranging home health care services, and arranging outpatient follow‐up. The traditional hospital discharge process does not adequately ensure that patients understand their discharge plan and are able to comply with it. Calkins et al. compared physicians' perceptions of patients' understanding of medication side effects and activity restrictions with patients' actual understanding.6 They found that, compared with what was reported by patients, physicians overestimated the time spent discussing discharge plans and how well patients understood medication side effects and activity restrictions.

An important method for reducing patient problems is to contact patients by telephone after discharge in order to identify any health care issues. Previous research has confirmed that follow‐up telephone calls improve health outcomes and decrease resource utilization of patients, mainly those discharged from the emergency department.10, 11, 1923 A study of telephone follow‐up after ambulatory care visits did not find significant benefits of this procedure.24 In one of the few studies of telephone calls after hospitalization, pharmacists contacted patients 2 days after discharge and were able to detect and resolve medication‐related problems in 19% of patients and learned of new or worsening symptoms in 15%. Patient satisfaction was improved, and the intervention resulted in a lower rate of repeat visits to the emergency room within 30 days of discharge.12 Another study of telephone follow‐up following hospital discharge compared proactively calling all patients with providing a phone number that patients can call if they have questions. The study demonstrated that very few patients called the number provided, but of those patients called by the nursing service, more than 90% had questions about self‐care and recovery.25 These findings demonstrate the value of proactively contacting patients in the first several days after discharge, when problems can be detected and interventions initiated earlier.

One potential concern with this study was the low response rate. This was a retrospective analysis of an existing discharge management call‐center system, not a prospective study. We were not able to reach 52% of the patients discharged after 2 attempts by telephone. To have our call center make additional attempts to reach each patient by telephone would require a significant increase in the size of the call center, because at the time of the study, the staff was handling more than 370 patients discharged home a day. The telephone number of 16% of patients was missing or incorrect. We have since developed internal quality improvement mechanisms to decrease this percentage. After subtracting the patients we were unable to reach and those whose phone number was missing or incorrect, we were able to contact 32.4% of all the patients discharged home.

Several reasons explain the response rate found by many prospective research studies. In most studies of telephone follow‐up, patients must be able to consent to participate in order to be considered eligible inclusion. This raises the response rate because patients who do not consent to participate, have language barriers, or have no telephone are excluded from the study. In our study none of these types of patients were excluded. There are 2 additional differences between our study and many published studies that involve telephone surveys. Ours was not a prospective research study, and we contacted many more patients than did other studies. For example, a study by Forster et al. involved only 581 patients, and the research staff was diligent in its efforts to reach the patients,7 making up to 20 attempts for each patient. They reported a response rate of 69%. If they had included patients who were non‐English speakers or had no phone in their study, the response rate would have been 59%. Shesser et al. were able to reach 144 of 297 patients in their study of emergency room follow‐up, for a 48.4% response rate.25 The response rate in a study of telephone consultation with asthma patients was quite similar to ours. They enrolled 932 eligible patients, of whom they were able to reach 278, for a response rate of 30%.

It is possible that the rate of symptoms and the other variables we measured relative to this would have been different if we had been able to reach 100% of patients. There were some demographic differences between the patients we were able to reach and those we were not (Table 1). The nonresponders were slightly younger and slightly more likely to be female. Nonresponders were more likely to have Medicaid or commercial insurance or be self‐pay and were less likely to have Medicare. In addition, nonresponders had less severe illness. Although this scenario is highly unlikely, if none of the nonresponders had new or worsening symptoms, the rate of symptoms would only have been 3.86%. Conversely, it is possible but also very unlikely that a greater percentage of the nonresponders had new or worsening symptoms. Given the demographics of our study participants, we would expect a potentially slightly lower rate of signs and symptoms.

The present study had several other limitations. First, all patients surveyed were cared for by IPC‐employed physicians. It is possible that reported rates of symptoms and other postdischarge issues are not generalizable to other hospitalist practices. However, the present data were collected at more than 100 health care facilities in 10 health care markets, and the patients were cared for by more than 200 physicians. Therefore, it is unlikely these results would have been significantly influenced by a particular physician's or institution's practice patterns.

Second, because of the large number of facilities involved and that we could only track readmissions to facilities where our own hospitalists practice, we were not able to report 30‐ or 90‐day readmission rates or emergency room visit rates. In a prospective study, these would be important variables to track in order to assess the clinical relevance of the symptoms. We could track this data for some institutions, but for most of them, the quality of data was not sufficient to be meaningful or to make conclusions.

An additional limitation is that the call center did not differentiate between clinically minor and major symptoms. The inclusion of symptoms perhaps considered minor might have elevated the reported symptom frequency. However, the definitions of minor and major symptoms are very subjective, and a clinician's definitions might differ from those of a patient who is at home and uncomfortable. For example, nausea or loss of appetite related to new medications may be considered minor clinically but could be devastating to the patient experiencing them, leading the patient to stop taking the medication. Conversely, symptoms that may be considered nonsignificant by the patient may be interpreted as indicating clinically significant disease by a physician. Therefore, we would argue that, regardless of the severity of the symptom, follow‐up with a clinician is important.

Another limitation is based on our definition of an adequate follow‐up appointment as one scheduled within 2 weeks of discharge. It might be argued that if a patient's new symptoms were considered minor clinically, then a follow‐up interval greater than 2 weeks might be considered adequate. However, as already noted, a patient's criteria for considering a symptom minor and not requiring follow‐up may differ from a clinician's criteria. Also, the standardized discharge process requires that the hospitalist identify a physician for outpatient follow‐up and specify the period when the patient is to see the physician. Because of the inherent variability in having a many hospitalists practicing in many hospitals, not all patients had a scheduled appointment at discharge. We were not able to determine whether patients had an appointment date and time for follow‐up before discharge or had only received instructions to call the office for an appointment.

The Institute of Medicine, in its report Crossing the Quality Chasm, identified the coordination of care across services and sites of care as one of the health care system's redesign imperatives.2 Hospitalists are in a unique position to address transition care issues. Managing the transition from inpatient to outpatient care is vitally important, and hospitalists should play an essential role in designing a transition management system for discharged patients. Although individual efforts by hospitalists are essential to assuring postdischarge contact with patients, there is increasing agreement that system solutions are needed to improve the quality of care in the transition period following hospitalization. Improving a health care process involves more than working harder; it involves working differently.3 It is therefore imperative that hospitalist programs develop effective systems to manage the transition period until safe arrival by the patient in the outpatient physician's office.

In summary, 11.9% of patients contacted by a telephone call center within several days of discharge had new or worsening symptoms since discharge. There was no difference by age in the prevalence of symptoms. Patients who rated their health status as fair to poor were more likely to be symptomatic. Symptomatic patients were also more likely to have difficulty obtaining or understanding how to take their medications and receiving home health services. Patients who felt poorly were only minimally more likely to have made an appointment for follow‐up with their outpatient physician. It is hoped that by identifying patients who are doing poorly after discharge and intervening as necessary, we can improve the health outcome of our patients, as well as reduce the number of emergency room visits and readmission rates. Although actions by individual physicians are important, a system to manage the postdischarge transition period is essential for improving posthospitalization outcomes.

Acknowledgements

The authors thank Rahul M. Dodhia for his assistance in the statistical analysis of the data and Sunil Kripalani for his thoughtful review of the manuscript.

APPENDIX

0

Survey Questions
References
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  12. Dudas V,Bookwalter T,Kerr KM,Pantilat SZ.The impact of follow‐up telephone calls to patients after hospitalization.Am J Med.2001;111(9B):26S30S.
  13. Medical Outcomes Trust.How to Score the SF‐12 Short Form Health Survey.Boston:The Medical Outcomes Trust;1992.
  14. Ratner P,Johnson J,Jeffery B.Examining emotional, physical, social, and spiritual health as determinants of self‐rated health status.Am J Health Promot.1998;12:275282.
  15. 3M Health Information Systems, 3M All Patient Refined DRG Software. Available at: http://3m.com/market/healthcare/his/us/products/apr_drg/brochure.html.
  16. Holm S.A simple sequentially rejective Bonferroni test procedure.Scand J Stat.1979;6:6570.
  17. Nelson EA,Maruish ME,Axler JL.Effects of discharge planning and compliance with outpatient appointments on readmission rates.Psychiatr Serv.2000;51:885889.
  18. Forster A.J. Can you prevent adverse drug events after hospital discharge?CMAJ.2006;174:921922.
  19. Chande VT,Exum V.Follow‐up phone calls after an emergency department visit.Pediatrics.1994;93:513514.
  20. Jones J,Clark W,Bradford J,Dougherty J.Efficacy of a telephone follow‐up system in the emergency department.J Emerg Med.1988;6:249254.
  21. Jones PK,Jones SL,Katz J.A randomized trial to improve compliance in urinary tract infection patients in the emergency department.Ann Emerg Med.1990;19:1620.
  22. Shesser, R.,Smith M,Adams S,Walls R,Paxton M.The effectiveness of an organized emergency department follow‐up system.Ann Emerg Med.1986;15:911915.
  23. Nelson JR.The importance of postdischarge telephone follow‐up for hospitalists: a view from the trenches.Am J Med.2001;111(9B):43S44S.
  24. Welch HG,Johnson DJ,Edson R.Telephone care as an adjunct to routine medical follow‐up. A negative randomized trial.Eff Clin Pract.2000;3:123130.
  25. Bostrom JCaldwell J,McGuire K,Everson D.Telephone follow‐up after discharge from the hospital: does it make a difference?Appl Nurs Res.1996;9:4752.
References
  1. Kohn LT,Corrigan J,Donaldson M, editors. To Err Is Human: Building a Safer Health System.Washington, DC:National Academy Press;2000:xxi,287.
  2. Institute of Medicine (U.S.).Committee on Quality of Health Care in America. Crossing the Quality Chasm: a New Health System for the 21st Century.Washington, DC:National Academy Press;2001:xx,337.
  3. Lurie JD,Merrens EJ,Lee Splaine ME.An approach to hospital quality improvement.Med Clin North Am.2002;86:825845.
  4. Wachter RM,Goldman L.The hospitalist movement 5 years later.JAMA.2002;287:487494.
  5. Leape L.Making health care safe. Supplement on hospital medicine and patient safety.The Hospitalist.2004:34.
  6. Calkins DR,Davis RB,Reiley P, et al.Patient‐physician communication at hospital discharge and patients' understanding of the postdischarge treatment plan.Arch Intern Med.1997;157:10261030.
  7. Forster AJ,Murff HJ,Peterson JF,Gandhi TK,Bates DW.The incidence and severity of adverse events affecting patients after discharge from the hospital.Ann Intern Med.2003;138:161167.
  8. Forster AJ,Clark HD,Menard A, et al.Adverse events among medical patients after discharge from the hospital.CMAJ.2004;170:345349.
  9. Moore C,Wisnievsky J,Williams S,McGinn T.Medical errors related to discontinuity of care from an inpatient to an outpatient setting.J Gen Intern Med.2003;18:646651.
  10. Wasson J,Gaudette C,Whaley F,Sauvigne A,Baribeau P,Welch HG.Telephone care as a substitute for routine clinic follow‐up.JAMA.1992;267:17881793.
  11. Riegel B,Carlson B,Koop Z,LePetri B,Glasser D,Unger A.Effect of a standardized nurse case‐management telephone intervention on resource use in patients with chronic heart failure.Arch Intern Med.2002;162:705712.
  12. Dudas V,Bookwalter T,Kerr KM,Pantilat SZ.The impact of follow‐up telephone calls to patients after hospitalization.Am J Med.2001;111(9B):26S30S.
  13. Medical Outcomes Trust.How to Score the SF‐12 Short Form Health Survey.Boston:The Medical Outcomes Trust;1992.
  14. Ratner P,Johnson J,Jeffery B.Examining emotional, physical, social, and spiritual health as determinants of self‐rated health status.Am J Health Promot.1998;12:275282.
  15. 3M Health Information Systems, 3M All Patient Refined DRG Software. Available at: http://3m.com/market/healthcare/his/us/products/apr_drg/brochure.html.
  16. Holm S.A simple sequentially rejective Bonferroni test procedure.Scand J Stat.1979;6:6570.
  17. Nelson EA,Maruish ME,Axler JL.Effects of discharge planning and compliance with outpatient appointments on readmission rates.Psychiatr Serv.2000;51:885889.
  18. Forster A.J. Can you prevent adverse drug events after hospital discharge?CMAJ.2006;174:921922.
  19. Chande VT,Exum V.Follow‐up phone calls after an emergency department visit.Pediatrics.1994;93:513514.
  20. Jones J,Clark W,Bradford J,Dougherty J.Efficacy of a telephone follow‐up system in the emergency department.J Emerg Med.1988;6:249254.
  21. Jones PK,Jones SL,Katz J.A randomized trial to improve compliance in urinary tract infection patients in the emergency department.Ann Emerg Med.1990;19:1620.
  22. Shesser, R.,Smith M,Adams S,Walls R,Paxton M.The effectiveness of an organized emergency department follow‐up system.Ann Emerg Med.1986;15:911915.
  23. Nelson JR.The importance of postdischarge telephone follow‐up for hospitalists: a view from the trenches.Am J Med.2001;111(9B):43S44S.
  24. Welch HG,Johnson DJ,Edson R.Telephone care as an adjunct to routine medical follow‐up. A negative randomized trial.Eff Clin Pract.2000;3:123130.
  25. Bostrom JCaldwell J,McGuire K,Everson D.Telephone follow‐up after discharge from the hospital: does it make a difference?Appl Nurs Res.1996;9:4752.
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What will board certification be—and mean—for hospitalists?

Soon after they form, most new medical fields begin agitating for a special certification, something that says, We're here, and we're different. As I've noted previously in the Journal of Hospital Medicine, the field of hospital medicine resisted this impulse in its early years, fearing that any special designation or certification would actually harm the field's growth and status.1 The concern was that managed‐care organizationsconvinced by the evidence that hospitalists improve efficiency and might improve quality2would react to any new hospitalist sheepskin by mandating that anyone providing hospital care to its covered patients have one. The backlash from primary care physicians locked out of the hospital by such a mandate would have been swift and ultimately damaging to hospitalists. In addition to these political considerations, the early field of hospital medicine lacked the academic credibility and scientific underpinning needed for specialty designation.3

Times have changed. There are now more than 15,000 hospitalists in the United States, and nearly half of American hospitals have hospitalists on their medical staffs. In many markets, including my own, hospitalists care for most internal medicine inpatients, as well as significant numbers of pediatric and surgical patients. The field has achieved academic legitimacy, with this journal, several textbooks, large and flourishing groups in every academic medical center, and several residency tracks and fellowship programs.4, 5 The Society of Hospital Medicine (SHM) has grown to more than 6000 members, become a widely respected and dynamic member of the community of professional societies, and published its core competencies.6

With this as a background, in 2004 SHM asked the American Board of Internal Medicine (ABIM) to consider a program of certification for hospitalists. As a past SHM president and now a member of the ABIM Board of Directors, I am privileged to have a bird's‐eye view of the process. In this article, I reflect on some of the key issues it raises.

THE NUTS AND BOLTS OF BOARD CERTIFICATION

Since the first board (ophthalmology) was formed in 1917, 24 specialty boards have emerged, all under the umbrella of the American Board of Medical Specialties (ABMS).7 Because no one type of physician can do it all, certifying boards have had to struggle not only with how to assess competency in existing disciplines, but with the dynamic and often controversial questions raised when new fields emerge. In the past few decades, certifying boards have grappled with specialties formed around new procedures (such as cardiac electrophysiology), discrete populations (geriatrics, palliative care), complex diseases (HIV medicine), and sites of care (intensive care medicine, emergency medicine). It is this latter category that now includes hospital medicine.

In the past, it was relatively simple for a physician to obtain board certification. Residency or fellowship training was believed to confer on its graduates the presumption of competence and professionalismthe program director's attestation served as the graduate's Good Housekeeping seal of approval. Passing the board exam was the final step, ensuring that newly minted graduates had the requisite knowledge and judgment to practice in their fields.

Remarkably, for the first half century of the specialty boards, all certifications lasted for a physician's professional lifetime. Beginning with the 1969 decision of the American Board of Family Practice to limit the validity of its certificates to 7 years, all ABMS member boards now time limit their certifications, usually to 7‐10 years.7 Of course, in an environment of rapidly changing medical knowledge and new procedures, periodiceven continuousdemonstration of competence is increasingly expected by the public.

For ABIM, the mechanism to promote lifelong learning and demonstrate ongoing competence in the face of a rapidly changing environment is known as maintenance of certification (MOC).8 Through MOC, board‐certified internists demonstrate their ongoing clinical expertise and judgment, their involvement in lifelong learning and quality improvement activities, and their professionalism. Because MOC involves no new training requirements and includes an assessment of a physician's actual practice, it provides a potential mechanism, heretofore untapped, of demonstrating a unique professional focus that emerges after the completion of formal training.

HOSPITALIST CERTIFICATION AND THE MOC PROCESS

As ABIM considered a separate certification pathway for hospital medicine, it faced a conundrum. The vast majority of hospitalists are general internists (most of the rest are generalists in family medicine or pediatrics) who entered hospital medicine at the completion of their internal medicine training or after a period of primary care practice. Job opportunities for hospitalists are plentiful, andexcept for additional training in quality improvement, systems leadership, care transitions, palliative care, and communication9there is little clinical rationale to prolong internal medicine training for hospitalists (some individuals may opt for fellowships to enhance their leadership skills or to launch a research career,5 but few would argue for mandatory additional clinical training in hospital medicine at this time).

So, in the absence of formal training, how could the ABIM (or other boards) recognize the focused practice of hospitalists? This question must be framed within a broader challenge: Is it possible and appropriate for certifying boards to recognize expertise and focus that is accrued not through formal training, but through actual practice experience and accompanying self‐directed learning?

In 2006, the ABIM took up this question, producing a report (New and Emerging Disciplines in Internal Medicine II [NEDIM II]) that delineated several criteria to guide whether a new field merited focused recognition through MOC (Table 1). Judging by these criteria, hospital medicine appears to be a suitable first candidate for recognition of focused practice through MOC.

The American Board of Internal Medicine's Criteria for Determining Whether a New Field Merits Focused Recognition through Its Maintenance of Certification Program (from the New and Emerging Disciplines in Internal Medicine II [NEDIM II] Report, American Board of Internal Medicine, 2006)

  • Large numbers of internists must focus their practice only in the discipline, while others in the parent discipline do not focus their practice in the area of focused recognition.

  • There must be an important social need for the discipline and evidence that focusing practice in the discipline improves patient care.

  • Proficiency or expertise can be gained through rigorous demonstration of self‐directed, continuous learning and self‐evaluation of practice over time, and does not require direct observation of technical procedures or skills that can only be achieved through formal residency or fellowship training.

  • To become proficient in the discipline requires a volume of experience (focus) that defines the discipline; specific thresholds of experience volume will be established and must be exceeded for recognition in an area of focus.

  • The positive value of certification in the focused area must outweigh any negative impact on the practice of, or education in, general internal medicine or an existing subspecialty of internal medicine.

PRELIMINARY THOUGHTS ON FOCUSED RECOGNITION IN HOSPITAL MEDICINE

The ABIM has endorsed the concept of recognition of focused practice in hospital medicine and charged a subcommittee (that I chair) with working out the details. It would be premature to describe the committee's deliberations in detail (particularly because the final plan needs to be approved by both the ABIM and the ABMS), but the following are some key issues being discussed.

First, demonstration of focused practice requires some minimum volume of hospitalized patients. In the absence of hard data defining a threshold number of cases for hospitalists, we are likely to endorse a number that has face validity and that reliably separates self‐identified hospitalists from nonhospitalist generalists. As with all volume requirements, we will struggle over how to handle academic physicians, physician‐administrators, and physician‐researchers who limit their overall clinical practice but who spend most of their clinical time in hospital medicine and the bulk of their nonclinical time trying to improve hospital care.

The requirements to demonstrate performance in practice and lifelong learning may be more straightforward. As with all such MOC requirements, the ABIM is increasingly looking to use real practice data, trying to harmonize its data requirements with those of other organizations such as insurers, Medicare, the Joint Commission, or for pay‐for‐performance initiatives. Despite the operational challenges, this effort is vital: for MOC (including focused recognition) to be highly valued by patients, purchasers, and diplomates, it will increasingly need to measure not only what physicians know, but also what they do.

Finally, there is the test. It is likely that a secure exam for MOC with Recognition of Focused Practice in Hospital Medicine will involve core content in internal medicine (information that every internist should know), augmented by substantial and challenging content in hospital medicine. Because it will be vital that a competent hospitalist understand key elements of outpatient practice, the exam will not be stripped of ambulatory content but will likely have fewer questions on topics that hospitalists are unlikely to confront (osteoporosis, cancer screening).

ONGOING ISSUES

As hospital medicine continues its explosive growth, it is important to develop ways to make board certification relevant to hospitalists. The ABIM believes that modifying the MOC process to recognize physicians who have focused their practice and achieved special expertise in hospital medicine is a good way to launch this effort. Ultimately, this process is likely to evolve, particularly if separate training pathways for hospital medicine emerge. For now, the development of Recognition of Focused Practice in Hospital Medicine will further legitimize the new field, provide ABIM with insights into how to recognize physicians who have advanced through practice‐based learning rather than through training, and help to guide other certifying boards (particularly family medicine and pediatrics) considering hospitalist certification. In the end, the process will need to be user‐friendly for and satisfying to diplomates, flexible enough to allow for career transitions (both toward and away from hospital medicine), and sufficiently rigorous to be credible to all stakeholders, particularly patients.

References
  1. Wachter RM.Reflections: the hospitalist movement a decade later.J Hosp Med.2006;1:248252.
  2. Wachter RM,Goldman L.The hospitalist movement 5 years later.JAMA2002;287:48794.
  3. Kelley MA.The hospitalist: a new medical specialty?Ann Intern Med.1999;130:373375.
  4. Wachter RM,Goldman L.Implications of the hospitalist movement for academic departments of medicine: lessons from the UCSF experience.Am J Med.1999;106:127133.
  5. Ranji SR,Rosenman DJ,Amin AN,Kripalani S.Hospital medicine fellowships: works in progress.Am J Med.2006;119:72.e1e7.
  6. Dressler DD,Pistoria MJ,Budnitz TL,McKean SC,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1:4856.
  7. Norcini JJ.Recertification in the United States.BMJ.1999;319:11831185.
  8. Cassel C,Holmboe ES.Professional standards in the USA: overview and new developments.Clin Med.2006;6:363367.
  9. Plauth WH,Pantilat SZ,Wachter RM,Fenton CL.Hospitalists' perceptions of their residency training needs: results of a national survey.Am J Med.2001;111:247254.
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Soon after they form, most new medical fields begin agitating for a special certification, something that says, We're here, and we're different. As I've noted previously in the Journal of Hospital Medicine, the field of hospital medicine resisted this impulse in its early years, fearing that any special designation or certification would actually harm the field's growth and status.1 The concern was that managed‐care organizationsconvinced by the evidence that hospitalists improve efficiency and might improve quality2would react to any new hospitalist sheepskin by mandating that anyone providing hospital care to its covered patients have one. The backlash from primary care physicians locked out of the hospital by such a mandate would have been swift and ultimately damaging to hospitalists. In addition to these political considerations, the early field of hospital medicine lacked the academic credibility and scientific underpinning needed for specialty designation.3

Times have changed. There are now more than 15,000 hospitalists in the United States, and nearly half of American hospitals have hospitalists on their medical staffs. In many markets, including my own, hospitalists care for most internal medicine inpatients, as well as significant numbers of pediatric and surgical patients. The field has achieved academic legitimacy, with this journal, several textbooks, large and flourishing groups in every academic medical center, and several residency tracks and fellowship programs.4, 5 The Society of Hospital Medicine (SHM) has grown to more than 6000 members, become a widely respected and dynamic member of the community of professional societies, and published its core competencies.6

With this as a background, in 2004 SHM asked the American Board of Internal Medicine (ABIM) to consider a program of certification for hospitalists. As a past SHM president and now a member of the ABIM Board of Directors, I am privileged to have a bird's‐eye view of the process. In this article, I reflect on some of the key issues it raises.

THE NUTS AND BOLTS OF BOARD CERTIFICATION

Since the first board (ophthalmology) was formed in 1917, 24 specialty boards have emerged, all under the umbrella of the American Board of Medical Specialties (ABMS).7 Because no one type of physician can do it all, certifying boards have had to struggle not only with how to assess competency in existing disciplines, but with the dynamic and often controversial questions raised when new fields emerge. In the past few decades, certifying boards have grappled with specialties formed around new procedures (such as cardiac electrophysiology), discrete populations (geriatrics, palliative care), complex diseases (HIV medicine), and sites of care (intensive care medicine, emergency medicine). It is this latter category that now includes hospital medicine.

In the past, it was relatively simple for a physician to obtain board certification. Residency or fellowship training was believed to confer on its graduates the presumption of competence and professionalismthe program director's attestation served as the graduate's Good Housekeeping seal of approval. Passing the board exam was the final step, ensuring that newly minted graduates had the requisite knowledge and judgment to practice in their fields.

Remarkably, for the first half century of the specialty boards, all certifications lasted for a physician's professional lifetime. Beginning with the 1969 decision of the American Board of Family Practice to limit the validity of its certificates to 7 years, all ABMS member boards now time limit their certifications, usually to 7‐10 years.7 Of course, in an environment of rapidly changing medical knowledge and new procedures, periodiceven continuousdemonstration of competence is increasingly expected by the public.

For ABIM, the mechanism to promote lifelong learning and demonstrate ongoing competence in the face of a rapidly changing environment is known as maintenance of certification (MOC).8 Through MOC, board‐certified internists demonstrate their ongoing clinical expertise and judgment, their involvement in lifelong learning and quality improvement activities, and their professionalism. Because MOC involves no new training requirements and includes an assessment of a physician's actual practice, it provides a potential mechanism, heretofore untapped, of demonstrating a unique professional focus that emerges after the completion of formal training.

HOSPITALIST CERTIFICATION AND THE MOC PROCESS

As ABIM considered a separate certification pathway for hospital medicine, it faced a conundrum. The vast majority of hospitalists are general internists (most of the rest are generalists in family medicine or pediatrics) who entered hospital medicine at the completion of their internal medicine training or after a period of primary care practice. Job opportunities for hospitalists are plentiful, andexcept for additional training in quality improvement, systems leadership, care transitions, palliative care, and communication9there is little clinical rationale to prolong internal medicine training for hospitalists (some individuals may opt for fellowships to enhance their leadership skills or to launch a research career,5 but few would argue for mandatory additional clinical training in hospital medicine at this time).

So, in the absence of formal training, how could the ABIM (or other boards) recognize the focused practice of hospitalists? This question must be framed within a broader challenge: Is it possible and appropriate for certifying boards to recognize expertise and focus that is accrued not through formal training, but through actual practice experience and accompanying self‐directed learning?

In 2006, the ABIM took up this question, producing a report (New and Emerging Disciplines in Internal Medicine II [NEDIM II]) that delineated several criteria to guide whether a new field merited focused recognition through MOC (Table 1). Judging by these criteria, hospital medicine appears to be a suitable first candidate for recognition of focused practice through MOC.

The American Board of Internal Medicine's Criteria for Determining Whether a New Field Merits Focused Recognition through Its Maintenance of Certification Program (from the New and Emerging Disciplines in Internal Medicine II [NEDIM II] Report, American Board of Internal Medicine, 2006)

  • Large numbers of internists must focus their practice only in the discipline, while others in the parent discipline do not focus their practice in the area of focused recognition.

  • There must be an important social need for the discipline and evidence that focusing practice in the discipline improves patient care.

  • Proficiency or expertise can be gained through rigorous demonstration of self‐directed, continuous learning and self‐evaluation of practice over time, and does not require direct observation of technical procedures or skills that can only be achieved through formal residency or fellowship training.

  • To become proficient in the discipline requires a volume of experience (focus) that defines the discipline; specific thresholds of experience volume will be established and must be exceeded for recognition in an area of focus.

  • The positive value of certification in the focused area must outweigh any negative impact on the practice of, or education in, general internal medicine or an existing subspecialty of internal medicine.

PRELIMINARY THOUGHTS ON FOCUSED RECOGNITION IN HOSPITAL MEDICINE

The ABIM has endorsed the concept of recognition of focused practice in hospital medicine and charged a subcommittee (that I chair) with working out the details. It would be premature to describe the committee's deliberations in detail (particularly because the final plan needs to be approved by both the ABIM and the ABMS), but the following are some key issues being discussed.

First, demonstration of focused practice requires some minimum volume of hospitalized patients. In the absence of hard data defining a threshold number of cases for hospitalists, we are likely to endorse a number that has face validity and that reliably separates self‐identified hospitalists from nonhospitalist generalists. As with all volume requirements, we will struggle over how to handle academic physicians, physician‐administrators, and physician‐researchers who limit their overall clinical practice but who spend most of their clinical time in hospital medicine and the bulk of their nonclinical time trying to improve hospital care.

The requirements to demonstrate performance in practice and lifelong learning may be more straightforward. As with all such MOC requirements, the ABIM is increasingly looking to use real practice data, trying to harmonize its data requirements with those of other organizations such as insurers, Medicare, the Joint Commission, or for pay‐for‐performance initiatives. Despite the operational challenges, this effort is vital: for MOC (including focused recognition) to be highly valued by patients, purchasers, and diplomates, it will increasingly need to measure not only what physicians know, but also what they do.

Finally, there is the test. It is likely that a secure exam for MOC with Recognition of Focused Practice in Hospital Medicine will involve core content in internal medicine (information that every internist should know), augmented by substantial and challenging content in hospital medicine. Because it will be vital that a competent hospitalist understand key elements of outpatient practice, the exam will not be stripped of ambulatory content but will likely have fewer questions on topics that hospitalists are unlikely to confront (osteoporosis, cancer screening).

ONGOING ISSUES

As hospital medicine continues its explosive growth, it is important to develop ways to make board certification relevant to hospitalists. The ABIM believes that modifying the MOC process to recognize physicians who have focused their practice and achieved special expertise in hospital medicine is a good way to launch this effort. Ultimately, this process is likely to evolve, particularly if separate training pathways for hospital medicine emerge. For now, the development of Recognition of Focused Practice in Hospital Medicine will further legitimize the new field, provide ABIM with insights into how to recognize physicians who have advanced through practice‐based learning rather than through training, and help to guide other certifying boards (particularly family medicine and pediatrics) considering hospitalist certification. In the end, the process will need to be user‐friendly for and satisfying to diplomates, flexible enough to allow for career transitions (both toward and away from hospital medicine), and sufficiently rigorous to be credible to all stakeholders, particularly patients.

Soon after they form, most new medical fields begin agitating for a special certification, something that says, We're here, and we're different. As I've noted previously in the Journal of Hospital Medicine, the field of hospital medicine resisted this impulse in its early years, fearing that any special designation or certification would actually harm the field's growth and status.1 The concern was that managed‐care organizationsconvinced by the evidence that hospitalists improve efficiency and might improve quality2would react to any new hospitalist sheepskin by mandating that anyone providing hospital care to its covered patients have one. The backlash from primary care physicians locked out of the hospital by such a mandate would have been swift and ultimately damaging to hospitalists. In addition to these political considerations, the early field of hospital medicine lacked the academic credibility and scientific underpinning needed for specialty designation.3

Times have changed. There are now more than 15,000 hospitalists in the United States, and nearly half of American hospitals have hospitalists on their medical staffs. In many markets, including my own, hospitalists care for most internal medicine inpatients, as well as significant numbers of pediatric and surgical patients. The field has achieved academic legitimacy, with this journal, several textbooks, large and flourishing groups in every academic medical center, and several residency tracks and fellowship programs.4, 5 The Society of Hospital Medicine (SHM) has grown to more than 6000 members, become a widely respected and dynamic member of the community of professional societies, and published its core competencies.6

With this as a background, in 2004 SHM asked the American Board of Internal Medicine (ABIM) to consider a program of certification for hospitalists. As a past SHM president and now a member of the ABIM Board of Directors, I am privileged to have a bird's‐eye view of the process. In this article, I reflect on some of the key issues it raises.

THE NUTS AND BOLTS OF BOARD CERTIFICATION

Since the first board (ophthalmology) was formed in 1917, 24 specialty boards have emerged, all under the umbrella of the American Board of Medical Specialties (ABMS).7 Because no one type of physician can do it all, certifying boards have had to struggle not only with how to assess competency in existing disciplines, but with the dynamic and often controversial questions raised when new fields emerge. In the past few decades, certifying boards have grappled with specialties formed around new procedures (such as cardiac electrophysiology), discrete populations (geriatrics, palliative care), complex diseases (HIV medicine), and sites of care (intensive care medicine, emergency medicine). It is this latter category that now includes hospital medicine.

In the past, it was relatively simple for a physician to obtain board certification. Residency or fellowship training was believed to confer on its graduates the presumption of competence and professionalismthe program director's attestation served as the graduate's Good Housekeeping seal of approval. Passing the board exam was the final step, ensuring that newly minted graduates had the requisite knowledge and judgment to practice in their fields.

Remarkably, for the first half century of the specialty boards, all certifications lasted for a physician's professional lifetime. Beginning with the 1969 decision of the American Board of Family Practice to limit the validity of its certificates to 7 years, all ABMS member boards now time limit their certifications, usually to 7‐10 years.7 Of course, in an environment of rapidly changing medical knowledge and new procedures, periodiceven continuousdemonstration of competence is increasingly expected by the public.

For ABIM, the mechanism to promote lifelong learning and demonstrate ongoing competence in the face of a rapidly changing environment is known as maintenance of certification (MOC).8 Through MOC, board‐certified internists demonstrate their ongoing clinical expertise and judgment, their involvement in lifelong learning and quality improvement activities, and their professionalism. Because MOC involves no new training requirements and includes an assessment of a physician's actual practice, it provides a potential mechanism, heretofore untapped, of demonstrating a unique professional focus that emerges after the completion of formal training.

HOSPITALIST CERTIFICATION AND THE MOC PROCESS

As ABIM considered a separate certification pathway for hospital medicine, it faced a conundrum. The vast majority of hospitalists are general internists (most of the rest are generalists in family medicine or pediatrics) who entered hospital medicine at the completion of their internal medicine training or after a period of primary care practice. Job opportunities for hospitalists are plentiful, andexcept for additional training in quality improvement, systems leadership, care transitions, palliative care, and communication9there is little clinical rationale to prolong internal medicine training for hospitalists (some individuals may opt for fellowships to enhance their leadership skills or to launch a research career,5 but few would argue for mandatory additional clinical training in hospital medicine at this time).

So, in the absence of formal training, how could the ABIM (or other boards) recognize the focused practice of hospitalists? This question must be framed within a broader challenge: Is it possible and appropriate for certifying boards to recognize expertise and focus that is accrued not through formal training, but through actual practice experience and accompanying self‐directed learning?

In 2006, the ABIM took up this question, producing a report (New and Emerging Disciplines in Internal Medicine II [NEDIM II]) that delineated several criteria to guide whether a new field merited focused recognition through MOC (Table 1). Judging by these criteria, hospital medicine appears to be a suitable first candidate for recognition of focused practice through MOC.

The American Board of Internal Medicine's Criteria for Determining Whether a New Field Merits Focused Recognition through Its Maintenance of Certification Program (from the New and Emerging Disciplines in Internal Medicine II [NEDIM II] Report, American Board of Internal Medicine, 2006)

  • Large numbers of internists must focus their practice only in the discipline, while others in the parent discipline do not focus their practice in the area of focused recognition.

  • There must be an important social need for the discipline and evidence that focusing practice in the discipline improves patient care.

  • Proficiency or expertise can be gained through rigorous demonstration of self‐directed, continuous learning and self‐evaluation of practice over time, and does not require direct observation of technical procedures or skills that can only be achieved through formal residency or fellowship training.

  • To become proficient in the discipline requires a volume of experience (focus) that defines the discipline; specific thresholds of experience volume will be established and must be exceeded for recognition in an area of focus.

  • The positive value of certification in the focused area must outweigh any negative impact on the practice of, or education in, general internal medicine or an existing subspecialty of internal medicine.

PRELIMINARY THOUGHTS ON FOCUSED RECOGNITION IN HOSPITAL MEDICINE

The ABIM has endorsed the concept of recognition of focused practice in hospital medicine and charged a subcommittee (that I chair) with working out the details. It would be premature to describe the committee's deliberations in detail (particularly because the final plan needs to be approved by both the ABIM and the ABMS), but the following are some key issues being discussed.

First, demonstration of focused practice requires some minimum volume of hospitalized patients. In the absence of hard data defining a threshold number of cases for hospitalists, we are likely to endorse a number that has face validity and that reliably separates self‐identified hospitalists from nonhospitalist generalists. As with all volume requirements, we will struggle over how to handle academic physicians, physician‐administrators, and physician‐researchers who limit their overall clinical practice but who spend most of their clinical time in hospital medicine and the bulk of their nonclinical time trying to improve hospital care.

The requirements to demonstrate performance in practice and lifelong learning may be more straightforward. As with all such MOC requirements, the ABIM is increasingly looking to use real practice data, trying to harmonize its data requirements with those of other organizations such as insurers, Medicare, the Joint Commission, or for pay‐for‐performance initiatives. Despite the operational challenges, this effort is vital: for MOC (including focused recognition) to be highly valued by patients, purchasers, and diplomates, it will increasingly need to measure not only what physicians know, but also what they do.

Finally, there is the test. It is likely that a secure exam for MOC with Recognition of Focused Practice in Hospital Medicine will involve core content in internal medicine (information that every internist should know), augmented by substantial and challenging content in hospital medicine. Because it will be vital that a competent hospitalist understand key elements of outpatient practice, the exam will not be stripped of ambulatory content but will likely have fewer questions on topics that hospitalists are unlikely to confront (osteoporosis, cancer screening).

ONGOING ISSUES

As hospital medicine continues its explosive growth, it is important to develop ways to make board certification relevant to hospitalists. The ABIM believes that modifying the MOC process to recognize physicians who have focused their practice and achieved special expertise in hospital medicine is a good way to launch this effort. Ultimately, this process is likely to evolve, particularly if separate training pathways for hospital medicine emerge. For now, the development of Recognition of Focused Practice in Hospital Medicine will further legitimize the new field, provide ABIM with insights into how to recognize physicians who have advanced through practice‐based learning rather than through training, and help to guide other certifying boards (particularly family medicine and pediatrics) considering hospitalist certification. In the end, the process will need to be user‐friendly for and satisfying to diplomates, flexible enough to allow for career transitions (both toward and away from hospital medicine), and sufficiently rigorous to be credible to all stakeholders, particularly patients.

References
  1. Wachter RM.Reflections: the hospitalist movement a decade later.J Hosp Med.2006;1:248252.
  2. Wachter RM,Goldman L.The hospitalist movement 5 years later.JAMA2002;287:48794.
  3. Kelley MA.The hospitalist: a new medical specialty?Ann Intern Med.1999;130:373375.
  4. Wachter RM,Goldman L.Implications of the hospitalist movement for academic departments of medicine: lessons from the UCSF experience.Am J Med.1999;106:127133.
  5. Ranji SR,Rosenman DJ,Amin AN,Kripalani S.Hospital medicine fellowships: works in progress.Am J Med.2006;119:72.e1e7.
  6. Dressler DD,Pistoria MJ,Budnitz TL,McKean SC,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1:4856.
  7. Norcini JJ.Recertification in the United States.BMJ.1999;319:11831185.
  8. Cassel C,Holmboe ES.Professional standards in the USA: overview and new developments.Clin Med.2006;6:363367.
  9. Plauth WH,Pantilat SZ,Wachter RM,Fenton CL.Hospitalists' perceptions of their residency training needs: results of a national survey.Am J Med.2001;111:247254.
References
  1. Wachter RM.Reflections: the hospitalist movement a decade later.J Hosp Med.2006;1:248252.
  2. Wachter RM,Goldman L.The hospitalist movement 5 years later.JAMA2002;287:48794.
  3. Kelley MA.The hospitalist: a new medical specialty?Ann Intern Med.1999;130:373375.
  4. Wachter RM,Goldman L.Implications of the hospitalist movement for academic departments of medicine: lessons from the UCSF experience.Am J Med.1999;106:127133.
  5. Ranji SR,Rosenman DJ,Amin AN,Kripalani S.Hospital medicine fellowships: works in progress.Am J Med.2006;119:72.e1e7.
  6. Dressler DD,Pistoria MJ,Budnitz TL,McKean SC,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1:4856.
  7. Norcini JJ.Recertification in the United States.BMJ.1999;319:11831185.
  8. Cassel C,Holmboe ES.Professional standards in the USA: overview and new developments.Clin Med.2006;6:363367.
  9. Plauth WH,Pantilat SZ,Wachter RM,Fenton CL.Hospitalists' perceptions of their residency training needs: results of a national survey.Am J Med.2001;111:247254.
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Perspectives from the other side of the ocean: A Croatian hospital experience

When I went back to Croatia this summer to visit family and friends, little did I think I would find myself standing in the hospital where I trained as an intern. At 1:00 AM I took my father to the ER for an acute episode of nausea, vomiting, dizziness, chest tightness, and dyspnea. Earlier that day, he had been watching the World Cup, not moving from his chair for several hours. The ER saw him promptly and transferred him to the main hospital in town.

Hours later, I was alone in the middle of a wide, marble corridor. Memories flowed back to when I was a young nursing student and later an intern, full of life, energy, and dreams. Now the walls were yellow and darker than I remembered. They were barren, almost sad: no pictures, no art, no life. On my left, patients were taken to a room for procedures such as thoracentesis and lumbar puncture. The next door led to a balcony where cigarettes glowed like orange fireflies. Dark shapes murmured to one another as they nursed their habit. At least smoking wasn't allowed in the patient rooms.

On my right were alternating male and female patient rooms: up to 7 beds per room. They would add an eighth and potentially squeeze in a ninth bed when needed. There were no private rooms, even if you had money or status. There were no dividers or curtains between patients. With no privacy and nothing else to do, patients entertained each other. Some were young, others older. Some had fought in the last war; others were tourists who were visiting. They shared their stories. They overheard each other's plans of care during morning rounds conducted by physicians and nurses.

Each hospital bed had a little nightstand, but that was about it. If you were lucky, you got pajamas. My dad got warm flannel pajamas in the middle of the summer, but at least he got something. We left the house in a hurry and didn't bring anything. No towels? You had to bring your own. No toothpaste or a toothbrush? There was running water but no cup to drink it in. There was not even toilet paper. You had to bring your own.

Everything was nice and clean but something was missing in this former military hospital, as if the life had been drained out of it. It was once a premier facility. Maybe it was getting older or worn out by the war, or lack of maintenance. The best equipment (including new ventilators) were reportedly stolen and sent to another city.

There was no army of people serving you. No medical assistants, physicians assistants, nurse‐practitioners, or technicians. No physical therapists or occupational therapists or even a front desk where people were greeted. No case managers. The hospital population was so much younger than in the United States. There was only 1 patient on the ward who was 90 years old, as opposed to the usual 10 patients on my service in their 80s and 90s. Most patients were discharged home with their families; very few were sent to nursing homes. There was no length of stay to worry about. There were no insurance hassles, preapproval for a test or for an additional day of hospitalization.

There were no daily blood draws. They are not watching him closely enough, I worried. The ER physician apparently ruled out cardiac causes before admitting my father to the neurology service for presumed vertebrobasilar insufficiency. Was the ER physician's history, cardiac bedside exam, 2 normal EKGs an hour apart, and CXR enough to assure him there was no need for a CPK or a troponin? I was told the CPK was normal but never saw the result. They used to do troponin but had stopped because it was too expensive. I cannot imagine admitting a patient in the United States with chest tightness without ordering cardiac enzymes. Are we scared we'll miss something or afraid of litigation? There was no such fear that I could detect in Croatia.

The inpatient workup was otherwise thorough, and everyone was courteous. Nonetheless, the money was tight. If a patient needed over the‐counter medications, a family member would be asked to buy it, sometimes at significant cost. Almost every patient had a peripheral IV but there were no unnecessary IV infusions, unlike the occasional TKO IVs we see here to justify hospitalization for a little old lady who didn't have a place to go or whose insurance would otherwise refuse to pay.

My father seemed dehydrated.

Could you put some normal saline in? I asked.

He already got some, the charge nurse replied.

What did he get?

Metoclopramide infusion in 500 cc of normal saline. He is not vomiting any longer, he can eat and drink, and he doesn't need any more IVs. It is expensive. Go buy some water and juices for him, the charge nurse said.

The meals were served 3 times a day. No snacks in‐between unless friends and family brought something.

Visiting hours were 2‐4 PM daily. Information time for families took place on Tuesday and Friday afternoons. I arrived 30 minutes early to speak with the neurologist. In less than 20 minutes the room was filled. Everyone patiently waited their turn. The time spent with the doctor was brief but was better than nothing. As hospitalists, we spend a significant amount of time on the telephone tracking down family members, talking to them, or arranging a meeting to accommodate their schedule. On the other hand, there are family members who become frustrated because they have difficulty catching the doctor. I wonder if it would be helpful for us to have a dedicated information time. It could prevent frustration, unnecessary phone calls and pages, and perhaps save us time. Given our shorter length of stay, information time only twice a week probably wouldn't be enough.

What are you doing here? Dr. T., a friend of mine, exclaimed. Come on, a doctor from America waiting for the information! Come here, you don't need to wait! Your father is already better. We did a head CT, and we'll do a cervical spine x‐ray and carotid ultrasound tomorrow. Although I was hesitant, my brother, a medical student, tried to question the current treatment.

Why are you giving him diazepam and diclofenac intramuscularly? he asked.

What do you mean why? Because this is how we do it, Dr. T. said.

You already have an IV access. Couldn't you give it to him IV? my brother persisted. Dr. T. looked at him like he had fallen off the apple cart.

I had never seen it done this way in Austria or Germany, my brother continued. Why cause unnecessary pain and complications?

What complications? said Dr. T., now impatient. We use it intramuscularly. This is how it is done. It is only 10 injections. That's nothing.

Ten injections? You can injure a nerve! my brother exclaimed.

What nerve? Not if you do it right. We've been doing it this way forever. Your dad had dizziness and vomiting, and now he is better.

My father was better. Something had worked. Was it the medications or that he had slept and was rested?

The night had sneaked up on us again. The ward was quiet. No call lights. No patient telephones. No TVs. No IV machines and their beeping. No vital signs were taken in the middle of the night. No early‐morning blood draws. No pagers. The hospital was a place to get some rest.

The following day I spoke to the on‐call physician. The head CT and labs were normal. After 4 days in the hospital, I needed to know what the weekend plans would be.

How much longer will he need to be in the hospital? I asked.

Oh, about 10 to 14 days.

Ten to 14 days? I couldn't hide my surprise. What for? I might have as well asked if pigs were falling from the sky. This is how it was done.

Documentation was scanty. No worries of audits to justify the work done. How much time was saved this way? No wonder each physician saw 20 to 30 patients or more. There were 2 forms at discharge typed into a computer by the physician: a short one containing discharge medications and follow‐up plans and a long one to be completed later. We got the short one immediately and made follow‐up appointments. But many weeks later, we are still waiting for the long one. Apparently not all the lab tests are back.

Looking back, I see that when I tried to push for more information, I was viewed as pushy. So I stopped pushing. When I asked some logical questions, I felt like I was showing off. So I stopped asking too many questions. When I asked dad to tell me what happened during the day, he did not know. He did not remember the name of the consultants or what they said. When I asked him to try harder, he refused. When I asked him to write things down, he hesitated. It would mark him as a troublemaker. He was concerned that he would be labeled as an outsider, despite having lived in Croatia his whole life. Years after the war, a person's last name could still conjure up barely concealed hatred or suspicion. My father wanted to be seen as a good and compliant patient. He felt too vulnerable to be pushing for answers. Somehow, against my better judgment, I fell into the same mode.

Coming back to my hometown curiously hampered me. I still don't understand why. Was it sadness in my heart and nostalgia? Or emotional remnants of the recent war lingering in the air? Or a more patriarchal mentality and the unwritten rules of thinking and behaving that I had forgotten about? I was both a daughter and a visitor. I grew up in Croatia, but I left 2 weeks before the fighting broke out, and my prewar memories were still pristine. I was both a native and an American physician with all the expectations of stateside care. When I was a student there, physicians were authoritative and almost never questioned.

In the end, my father received care that was professional and thorough. The hospital lacked some basic necessities. They were on a strict budget for medicines including IV solutions. On the other hand, they kept my father in for 9 days, consulted an internist, an ENT. and a urologist. They also did numerous studies, including a head CT, cervical spine x‐ray, carotid ultrasound, hearing test and vestibulogram, CXR, and abdominal ultrasound. He had only 2 blood draws: CBC and Chem 7 (one time, one stick) and thyroid tests and PSA (one time, second stick). If he had been my patient, I would have probably tried to discharge him within 2 days and have him complete the evaluation as an outpatient. They gave him 9 days of diclofenac and diazepam intramuscularly and 7 days of 500 cc of normal saline and metoclopramide IV. My father was released from the hospital several days early at his insistence and mine. He had no more nausea or vomiting, no chest pain or shortness of breath. He was calm and relaxed. He was well rested. He felt better. And he is fine today.

Acknowledgements

The author is grateful for S.R.C. and his support in writing this manuscript.

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When I went back to Croatia this summer to visit family and friends, little did I think I would find myself standing in the hospital where I trained as an intern. At 1:00 AM I took my father to the ER for an acute episode of nausea, vomiting, dizziness, chest tightness, and dyspnea. Earlier that day, he had been watching the World Cup, not moving from his chair for several hours. The ER saw him promptly and transferred him to the main hospital in town.

Hours later, I was alone in the middle of a wide, marble corridor. Memories flowed back to when I was a young nursing student and later an intern, full of life, energy, and dreams. Now the walls were yellow and darker than I remembered. They were barren, almost sad: no pictures, no art, no life. On my left, patients were taken to a room for procedures such as thoracentesis and lumbar puncture. The next door led to a balcony where cigarettes glowed like orange fireflies. Dark shapes murmured to one another as they nursed their habit. At least smoking wasn't allowed in the patient rooms.

On my right were alternating male and female patient rooms: up to 7 beds per room. They would add an eighth and potentially squeeze in a ninth bed when needed. There were no private rooms, even if you had money or status. There were no dividers or curtains between patients. With no privacy and nothing else to do, patients entertained each other. Some were young, others older. Some had fought in the last war; others were tourists who were visiting. They shared their stories. They overheard each other's plans of care during morning rounds conducted by physicians and nurses.

Each hospital bed had a little nightstand, but that was about it. If you were lucky, you got pajamas. My dad got warm flannel pajamas in the middle of the summer, but at least he got something. We left the house in a hurry and didn't bring anything. No towels? You had to bring your own. No toothpaste or a toothbrush? There was running water but no cup to drink it in. There was not even toilet paper. You had to bring your own.

Everything was nice and clean but something was missing in this former military hospital, as if the life had been drained out of it. It was once a premier facility. Maybe it was getting older or worn out by the war, or lack of maintenance. The best equipment (including new ventilators) were reportedly stolen and sent to another city.

There was no army of people serving you. No medical assistants, physicians assistants, nurse‐practitioners, or technicians. No physical therapists or occupational therapists or even a front desk where people were greeted. No case managers. The hospital population was so much younger than in the United States. There was only 1 patient on the ward who was 90 years old, as opposed to the usual 10 patients on my service in their 80s and 90s. Most patients were discharged home with their families; very few were sent to nursing homes. There was no length of stay to worry about. There were no insurance hassles, preapproval for a test or for an additional day of hospitalization.

There were no daily blood draws. They are not watching him closely enough, I worried. The ER physician apparently ruled out cardiac causes before admitting my father to the neurology service for presumed vertebrobasilar insufficiency. Was the ER physician's history, cardiac bedside exam, 2 normal EKGs an hour apart, and CXR enough to assure him there was no need for a CPK or a troponin? I was told the CPK was normal but never saw the result. They used to do troponin but had stopped because it was too expensive. I cannot imagine admitting a patient in the United States with chest tightness without ordering cardiac enzymes. Are we scared we'll miss something or afraid of litigation? There was no such fear that I could detect in Croatia.

The inpatient workup was otherwise thorough, and everyone was courteous. Nonetheless, the money was tight. If a patient needed over the‐counter medications, a family member would be asked to buy it, sometimes at significant cost. Almost every patient had a peripheral IV but there were no unnecessary IV infusions, unlike the occasional TKO IVs we see here to justify hospitalization for a little old lady who didn't have a place to go or whose insurance would otherwise refuse to pay.

My father seemed dehydrated.

Could you put some normal saline in? I asked.

He already got some, the charge nurse replied.

What did he get?

Metoclopramide infusion in 500 cc of normal saline. He is not vomiting any longer, he can eat and drink, and he doesn't need any more IVs. It is expensive. Go buy some water and juices for him, the charge nurse said.

The meals were served 3 times a day. No snacks in‐between unless friends and family brought something.

Visiting hours were 2‐4 PM daily. Information time for families took place on Tuesday and Friday afternoons. I arrived 30 minutes early to speak with the neurologist. In less than 20 minutes the room was filled. Everyone patiently waited their turn. The time spent with the doctor was brief but was better than nothing. As hospitalists, we spend a significant amount of time on the telephone tracking down family members, talking to them, or arranging a meeting to accommodate their schedule. On the other hand, there are family members who become frustrated because they have difficulty catching the doctor. I wonder if it would be helpful for us to have a dedicated information time. It could prevent frustration, unnecessary phone calls and pages, and perhaps save us time. Given our shorter length of stay, information time only twice a week probably wouldn't be enough.

What are you doing here? Dr. T., a friend of mine, exclaimed. Come on, a doctor from America waiting for the information! Come here, you don't need to wait! Your father is already better. We did a head CT, and we'll do a cervical spine x‐ray and carotid ultrasound tomorrow. Although I was hesitant, my brother, a medical student, tried to question the current treatment.

Why are you giving him diazepam and diclofenac intramuscularly? he asked.

What do you mean why? Because this is how we do it, Dr. T. said.

You already have an IV access. Couldn't you give it to him IV? my brother persisted. Dr. T. looked at him like he had fallen off the apple cart.

I had never seen it done this way in Austria or Germany, my brother continued. Why cause unnecessary pain and complications?

What complications? said Dr. T., now impatient. We use it intramuscularly. This is how it is done. It is only 10 injections. That's nothing.

Ten injections? You can injure a nerve! my brother exclaimed.

What nerve? Not if you do it right. We've been doing it this way forever. Your dad had dizziness and vomiting, and now he is better.

My father was better. Something had worked. Was it the medications or that he had slept and was rested?

The night had sneaked up on us again. The ward was quiet. No call lights. No patient telephones. No TVs. No IV machines and their beeping. No vital signs were taken in the middle of the night. No early‐morning blood draws. No pagers. The hospital was a place to get some rest.

The following day I spoke to the on‐call physician. The head CT and labs were normal. After 4 days in the hospital, I needed to know what the weekend plans would be.

How much longer will he need to be in the hospital? I asked.

Oh, about 10 to 14 days.

Ten to 14 days? I couldn't hide my surprise. What for? I might have as well asked if pigs were falling from the sky. This is how it was done.

Documentation was scanty. No worries of audits to justify the work done. How much time was saved this way? No wonder each physician saw 20 to 30 patients or more. There were 2 forms at discharge typed into a computer by the physician: a short one containing discharge medications and follow‐up plans and a long one to be completed later. We got the short one immediately and made follow‐up appointments. But many weeks later, we are still waiting for the long one. Apparently not all the lab tests are back.

Looking back, I see that when I tried to push for more information, I was viewed as pushy. So I stopped pushing. When I asked some logical questions, I felt like I was showing off. So I stopped asking too many questions. When I asked dad to tell me what happened during the day, he did not know. He did not remember the name of the consultants or what they said. When I asked him to try harder, he refused. When I asked him to write things down, he hesitated. It would mark him as a troublemaker. He was concerned that he would be labeled as an outsider, despite having lived in Croatia his whole life. Years after the war, a person's last name could still conjure up barely concealed hatred or suspicion. My father wanted to be seen as a good and compliant patient. He felt too vulnerable to be pushing for answers. Somehow, against my better judgment, I fell into the same mode.

Coming back to my hometown curiously hampered me. I still don't understand why. Was it sadness in my heart and nostalgia? Or emotional remnants of the recent war lingering in the air? Or a more patriarchal mentality and the unwritten rules of thinking and behaving that I had forgotten about? I was both a daughter and a visitor. I grew up in Croatia, but I left 2 weeks before the fighting broke out, and my prewar memories were still pristine. I was both a native and an American physician with all the expectations of stateside care. When I was a student there, physicians were authoritative and almost never questioned.

In the end, my father received care that was professional and thorough. The hospital lacked some basic necessities. They were on a strict budget for medicines including IV solutions. On the other hand, they kept my father in for 9 days, consulted an internist, an ENT. and a urologist. They also did numerous studies, including a head CT, cervical spine x‐ray, carotid ultrasound, hearing test and vestibulogram, CXR, and abdominal ultrasound. He had only 2 blood draws: CBC and Chem 7 (one time, one stick) and thyroid tests and PSA (one time, second stick). If he had been my patient, I would have probably tried to discharge him within 2 days and have him complete the evaluation as an outpatient. They gave him 9 days of diclofenac and diazepam intramuscularly and 7 days of 500 cc of normal saline and metoclopramide IV. My father was released from the hospital several days early at his insistence and mine. He had no more nausea or vomiting, no chest pain or shortness of breath. He was calm and relaxed. He was well rested. He felt better. And he is fine today.

Acknowledgements

The author is grateful for S.R.C. and his support in writing this manuscript.

When I went back to Croatia this summer to visit family and friends, little did I think I would find myself standing in the hospital where I trained as an intern. At 1:00 AM I took my father to the ER for an acute episode of nausea, vomiting, dizziness, chest tightness, and dyspnea. Earlier that day, he had been watching the World Cup, not moving from his chair for several hours. The ER saw him promptly and transferred him to the main hospital in town.

Hours later, I was alone in the middle of a wide, marble corridor. Memories flowed back to when I was a young nursing student and later an intern, full of life, energy, and dreams. Now the walls were yellow and darker than I remembered. They were barren, almost sad: no pictures, no art, no life. On my left, patients were taken to a room for procedures such as thoracentesis and lumbar puncture. The next door led to a balcony where cigarettes glowed like orange fireflies. Dark shapes murmured to one another as they nursed their habit. At least smoking wasn't allowed in the patient rooms.

On my right were alternating male and female patient rooms: up to 7 beds per room. They would add an eighth and potentially squeeze in a ninth bed when needed. There were no private rooms, even if you had money or status. There were no dividers or curtains between patients. With no privacy and nothing else to do, patients entertained each other. Some were young, others older. Some had fought in the last war; others were tourists who were visiting. They shared their stories. They overheard each other's plans of care during morning rounds conducted by physicians and nurses.

Each hospital bed had a little nightstand, but that was about it. If you were lucky, you got pajamas. My dad got warm flannel pajamas in the middle of the summer, but at least he got something. We left the house in a hurry and didn't bring anything. No towels? You had to bring your own. No toothpaste or a toothbrush? There was running water but no cup to drink it in. There was not even toilet paper. You had to bring your own.

Everything was nice and clean but something was missing in this former military hospital, as if the life had been drained out of it. It was once a premier facility. Maybe it was getting older or worn out by the war, or lack of maintenance. The best equipment (including new ventilators) were reportedly stolen and sent to another city.

There was no army of people serving you. No medical assistants, physicians assistants, nurse‐practitioners, or technicians. No physical therapists or occupational therapists or even a front desk where people were greeted. No case managers. The hospital population was so much younger than in the United States. There was only 1 patient on the ward who was 90 years old, as opposed to the usual 10 patients on my service in their 80s and 90s. Most patients were discharged home with their families; very few were sent to nursing homes. There was no length of stay to worry about. There were no insurance hassles, preapproval for a test or for an additional day of hospitalization.

There were no daily blood draws. They are not watching him closely enough, I worried. The ER physician apparently ruled out cardiac causes before admitting my father to the neurology service for presumed vertebrobasilar insufficiency. Was the ER physician's history, cardiac bedside exam, 2 normal EKGs an hour apart, and CXR enough to assure him there was no need for a CPK or a troponin? I was told the CPK was normal but never saw the result. They used to do troponin but had stopped because it was too expensive. I cannot imagine admitting a patient in the United States with chest tightness without ordering cardiac enzymes. Are we scared we'll miss something or afraid of litigation? There was no such fear that I could detect in Croatia.

The inpatient workup was otherwise thorough, and everyone was courteous. Nonetheless, the money was tight. If a patient needed over the‐counter medications, a family member would be asked to buy it, sometimes at significant cost. Almost every patient had a peripheral IV but there were no unnecessary IV infusions, unlike the occasional TKO IVs we see here to justify hospitalization for a little old lady who didn't have a place to go or whose insurance would otherwise refuse to pay.

My father seemed dehydrated.

Could you put some normal saline in? I asked.

He already got some, the charge nurse replied.

What did he get?

Metoclopramide infusion in 500 cc of normal saline. He is not vomiting any longer, he can eat and drink, and he doesn't need any more IVs. It is expensive. Go buy some water and juices for him, the charge nurse said.

The meals were served 3 times a day. No snacks in‐between unless friends and family brought something.

Visiting hours were 2‐4 PM daily. Information time for families took place on Tuesday and Friday afternoons. I arrived 30 minutes early to speak with the neurologist. In less than 20 minutes the room was filled. Everyone patiently waited their turn. The time spent with the doctor was brief but was better than nothing. As hospitalists, we spend a significant amount of time on the telephone tracking down family members, talking to them, or arranging a meeting to accommodate their schedule. On the other hand, there are family members who become frustrated because they have difficulty catching the doctor. I wonder if it would be helpful for us to have a dedicated information time. It could prevent frustration, unnecessary phone calls and pages, and perhaps save us time. Given our shorter length of stay, information time only twice a week probably wouldn't be enough.

What are you doing here? Dr. T., a friend of mine, exclaimed. Come on, a doctor from America waiting for the information! Come here, you don't need to wait! Your father is already better. We did a head CT, and we'll do a cervical spine x‐ray and carotid ultrasound tomorrow. Although I was hesitant, my brother, a medical student, tried to question the current treatment.

Why are you giving him diazepam and diclofenac intramuscularly? he asked.

What do you mean why? Because this is how we do it, Dr. T. said.

You already have an IV access. Couldn't you give it to him IV? my brother persisted. Dr. T. looked at him like he had fallen off the apple cart.

I had never seen it done this way in Austria or Germany, my brother continued. Why cause unnecessary pain and complications?

What complications? said Dr. T., now impatient. We use it intramuscularly. This is how it is done. It is only 10 injections. That's nothing.

Ten injections? You can injure a nerve! my brother exclaimed.

What nerve? Not if you do it right. We've been doing it this way forever. Your dad had dizziness and vomiting, and now he is better.

My father was better. Something had worked. Was it the medications or that he had slept and was rested?

The night had sneaked up on us again. The ward was quiet. No call lights. No patient telephones. No TVs. No IV machines and their beeping. No vital signs were taken in the middle of the night. No early‐morning blood draws. No pagers. The hospital was a place to get some rest.

The following day I spoke to the on‐call physician. The head CT and labs were normal. After 4 days in the hospital, I needed to know what the weekend plans would be.

How much longer will he need to be in the hospital? I asked.

Oh, about 10 to 14 days.

Ten to 14 days? I couldn't hide my surprise. What for? I might have as well asked if pigs were falling from the sky. This is how it was done.

Documentation was scanty. No worries of audits to justify the work done. How much time was saved this way? No wonder each physician saw 20 to 30 patients or more. There were 2 forms at discharge typed into a computer by the physician: a short one containing discharge medications and follow‐up plans and a long one to be completed later. We got the short one immediately and made follow‐up appointments. But many weeks later, we are still waiting for the long one. Apparently not all the lab tests are back.

Looking back, I see that when I tried to push for more information, I was viewed as pushy. So I stopped pushing. When I asked some logical questions, I felt like I was showing off. So I stopped asking too many questions. When I asked dad to tell me what happened during the day, he did not know. He did not remember the name of the consultants or what they said. When I asked him to try harder, he refused. When I asked him to write things down, he hesitated. It would mark him as a troublemaker. He was concerned that he would be labeled as an outsider, despite having lived in Croatia his whole life. Years after the war, a person's last name could still conjure up barely concealed hatred or suspicion. My father wanted to be seen as a good and compliant patient. He felt too vulnerable to be pushing for answers. Somehow, against my better judgment, I fell into the same mode.

Coming back to my hometown curiously hampered me. I still don't understand why. Was it sadness in my heart and nostalgia? Or emotional remnants of the recent war lingering in the air? Or a more patriarchal mentality and the unwritten rules of thinking and behaving that I had forgotten about? I was both a daughter and a visitor. I grew up in Croatia, but I left 2 weeks before the fighting broke out, and my prewar memories were still pristine. I was both a native and an American physician with all the expectations of stateside care. When I was a student there, physicians were authoritative and almost never questioned.

In the end, my father received care that was professional and thorough. The hospital lacked some basic necessities. They were on a strict budget for medicines including IV solutions. On the other hand, they kept my father in for 9 days, consulted an internist, an ENT. and a urologist. They also did numerous studies, including a head CT, cervical spine x‐ray, carotid ultrasound, hearing test and vestibulogram, CXR, and abdominal ultrasound. He had only 2 blood draws: CBC and Chem 7 (one time, one stick) and thyroid tests and PSA (one time, second stick). If he had been my patient, I would have probably tried to discharge him within 2 days and have him complete the evaluation as an outpatient. They gave him 9 days of diclofenac and diazepam intramuscularly and 7 days of 500 cc of normal saline and metoclopramide IV. My father was released from the hospital several days early at his insistence and mine. He had no more nausea or vomiting, no chest pain or shortness of breath. He was calm and relaxed. He was well rested. He felt better. And he is fine today.

Acknowledgements

The author is grateful for S.R.C. and his support in writing this manuscript.

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Missing the forest for the trees

A 56‐year‐old woman from Colombia presented to the emergency department after 24 hours of abdominal pain. One week before, she had experienced similar pain that lasted for 4 hours and spontaneously resolved. She was nauseated but had no vomiting. She reported an unintentional 14‐pound weight loss over the preceding 3 weeks. She denied fever, chills, night sweats, diarrhea, constipation, dysuria, or jaundice.

In a middle‐aged woman with abdominal pain and nausea, diagnostic considerations include gallbladder disease, diseases of the bowel (such as a partial small‐bowel obstruction or inflammatory conditions), hepatic or pancreatic conditions, and nongastrointestinal ailments such as cardiac ischemia. Knowing the specific location of pain, its quality, precipitating factors, and accompanying systemic symptoms may help to narrow the diagnosis. The unintentional weight loss preceding the onset of pain may be an important clue because it suggests a systemic condition, and in a South American immigrantparticularly if she has traveled recentlyit is important to consider parasitic illnesses. The absence of fever makes some infections such as tuberculosis and malaria less likely. At this point, in addition to a thorough history and physical, laboratory tests should include a complete blood count (with quantification of eosinophils) and a metabolic panel with liver enzymes and albumin.

The patient described pain in the midline, just inferior to the umbilicus. The pain was constant, developed without any particular provocation, and was not related to meals or exertion. There were no constitutional symptoms aside from weight loss. She had a history of bipolar disorder, hypothyroidism, osteoarthritis, and chronic sinusitis and had previously undergone cholecystectomy and abdominal hysterectomy. She was taking levothyroxine, montelukast, bupropion, oxcarbazepine, fexofenadine, meloxicam, zolpidem, and, as needed, acetaminophen. She had recently completed a 10‐day course of levofloxacin for acute sinusitis. She had immigrated to the United States 10 years earlier and lived with her husband and daughter. She denied the use of tobacco, alcohol or illicit drugs. She had visited Colombia 6 months earlier but had no other recent travel history.

The history of cholecystectomy makes a biliary tract process unlikely. Its location reduces the likelihood of a hepatic or pancreatic process, but I would like to see the liver enzymes, especially given her recent acetaminophen use. The comorbid illnessesparticularly her bipolar disordermay be relevant because psychiatric illness might be associated with medication overuse or undisclosed toxic ingestions. For example, excess thyroxine might lead to weight loss while overuse of nonsteroidal anti‐inflammatory drugs such as meloxicam can cause intestinal ulceration, not only in the upper tract, but also in the colon. Undisclosed ingestions may also be associated with abdominal symptoms. Her surgical history makes adhesions with a secondary partial bowel obstruction possible. With no travel outside this country in the last 6 months, exotic infections are less likely. Finally, the recent course of levofloxacin may be relevant because many antibiotics are associated with nonspecific abdominal symptoms, and Clostridium difficile colitis occasionally presents without diarrhea.

The patient reported taking her medications as prescribed and denied ingesting other medications. On physical examination, she had a temperature of 98.9F, a pulse of 81 beats per minute, a blood pressure of 110/80 mm Hg, and a respiratory rate of 16 respirations per minute. She had a normal oxygen saturation while breathing ambient air. Her weight was 58 kg. There was no scleral icterus or jugular venous distension. She had a small painless ulcer involving the hard palate. Her lungs were clear to auscultation, and cardiac examination was normal. The abdomen was soft, bowel sounds were present, and there was moderate tenderness to palpation inferior to the umbilicus. There was no rebound or guarding, hepatosplenomegaly or other masses. There was no peripheral edema and no lymphadenopathy. Neurological examination was normal.

The oral ulcer may or may not be related to the clinical presentation because oral ulcers, whether painful or painless, are ubiquitous and may be isolated or may be associated with a wide range of infectious and noninfectious systemic diseases. Although some systemic causes of mucocutaneous ulcers are associated with weight loss (including Crohn's disease, Behcet's disease, celiac sprue, human immunodeficiency virus [HIV], herpesviruses, syphilis, and systemic lupus erythematosus [SLE], among others), the lack of specificity of this finding limits its diagnostic utility. However, it is reasonable to ask whether the patient has noted frequent ulceration in the mouth or genitalia, as recurrent or severe ulcerations may narrow the diagnostic considerations. On the other hand, the focal nature of the pain inferior to the umbilicus suggests a discrete process in the abdomen or pelvis, such as an abscess, mass, or localized area of bowel inflammation. A plain abdominal film is likely to be low yield in this situation, so pursuing computed tomography is appropriate. Not all patients with focal abdominal pain require abdominal imaging, but in the context of weight loss and persistent symptoms for more than a week, imaging is prudent in this case.

The patient denied genital ulceration but did report painless oral ulcers over the preceding months. Laboratory evaluation revealed a white‐cell count of 1000/mm3, of which 6% were neutrophils, 5% were band forms, 36% were lymphocytes, and 47% were monocytes. The absolute neutrophil count was 110/mm3. Hemoglobin level was 10.2 g/dL with a mean corpuscular volume of 90 m3, and the platelet count was 151,000/mm3. Other results of laboratory studies were: sodium, 140 mmol/L; potassium, 3.8 mmol/L; chloride, 96 mmol/L; bicarbonate, 23 mmol/L; blood urea nitrogen, 13 mg/dL; creatinine, 0.4 mg/dL; lipase, 32 U/L (normal range, 13‐60); amylase, 73 U/L (normal range, 30‐110); albumin, 4.0 g/dL; aspartate aminotransferase, 779 U/L (normal range, 13‐35); alanine aminotransferase, 330 U/L (normal range, 7‐35); alkaline phosphatase, 510 U/L (normal range, 35‐104); and total bilirubin, 0.9 mg/dL (normal range, 0.1‐1.2). The lactate dehydrogenase level was 200 U/L (normal range, 135‐214). The corrected reticulocyte count was 1.6% (normal range, 0.3‐2.3), and haptoglobin was 190 mg/dL (normal range, 43‐212). A direct Coomb's test was positive. The erythrocyte sedimentation rate was 113 mm/hour (normal range, 1‐25). Urinalysis was normal without evidence of protein or blood.

Laboratory abnormalities include elevated transaminases and alkaline phosphatase, a markedly elevated erythrocyte sedimentation rate, and profound leukopenia with neutropenia. The patient is anemic, which may elevate the sedimentation rate but not typically to this degree. The patient is not febrile, but if she were to develop a fever, empiric antibiotics would be prudent. The normal albumin and bilirubin suggest that hepatic synthetic and excretory functions remain intact. Although the direct Coombs test is positive, the reticulocyte and lactate dehydrogenase levels argue against brisk hemolysis; this abnormality may simply be a marker of nonspecific immune activation. A variety of infections can cause neutropenia and liver enzyme abnormalities including parasites (malaria or leishmaniasis), viruses (cytomegalovirus or Epstein‐Barr virus [EBV]), tick‐borne bacterial infections (ehrlichiosis or rickettsial infection), and granulomatous infections (tuberculosis). Malignant infiltration of the reticuloendothelial system can also lead to cytopenias and liver enzyme abnormalities. Autoimmunity remains a consideration, as SLE may lead to cytopenias, oral ulcers, and nonspecific immune phenomena. Rather than ordering a large number of blood tests, I favor a targeted approach with abdominal computed tomography followed by biopsy of either the liver or bone marrow.

Chest radiography revealed no abnormalities. Computed tomography of the chest, abdomen, and pelvis with intravenous and oral contrast demonstrated concentric wall thickening of the transverse colon, but no evidence of obstruction or free air. The patient was treated with intravenous fluids, morphine, and cefepime. Bone marrow biopsy was performed, which demonstrated a hypercellular marrow with increased myeloid precursors and a left shift and megakaryocytic hyperplasia. Flow cytometry revealed no abnormally restricted clonal populations. A concerted search for an infectious etiology of the patient's neutropenia was unrevealing, including tests for HIV, cytomegalovirus, hepatitis A, hepatitis B, hepatitis C, Mycoplasma pneumoniae, EBV, and parvovirus B19.

I hope blood cultures were drawn prior to the initiation of antibiotics. Hypercellularity of the bone marrow in the context of leukopenia raises concern that white blood cells are being destroyed peripherally. Autoimmunity against neutrophils can be transiently induced by viruses such as HIV, hepatitis B, and EBV, but these infections have been excluded. Testing for antinuclear antibodies is reasonable. A normal‐sized spleen on the abdominal CT excludes hypersplenism. Colonic thickening can be associated with infection, ischemia, inflammatory bowel disease, and malignancy. The question is whether the colonic thickening is part of the same disease process causing the leukopenia and liver enzyme elevation or whether it represents a secondary infectious process in the setting of neutropenia (such as Clostridium difficile infection or typhlitis). Testing for stool pathogens (including ova and parasites) is certainly appropriate, and consideration of a colonoscopy with biopsy is reasonable, provided that appropriate antimicrobial coverage remains in place.

Blood cultures obtained prior to starting antibiotics were negative. The patient's abdominal pain improved, and she was discharged home to have close follow‐up with a hematologist. The results of her liver function tests improved, and her absolute neutrophil count was 230/mm3 at the time of discharge. Her neutropenia was believed to be secondary to peripheral destruction from a viral, drug‐mediated, or autoimmune process. Oxcarbazepine (Trileptal) was discontinued, as it was believed to be the medication most likely to be responsible. She returned to the hospital 3 days later with recurrence of her abdominal pain and diarrhea. She remained afebrile. Additional history revealed arthralgias over the previous 2 months, mild alopecia, and prior symptoms suggestive of Raynaud's phenomenon. Stool studies failed to establish an infectious etiology for the diarrhea, and her continued neutropenia responded appropriately to treatment with subcutaneous filgrastim. Colonoscopy could be performed only to the hepatic flexure and revealed no abnormalities. A serologic test for antinuclear antibodies was positive at a titer of 1:640 in a homogenous pattern, and a test for antineutrophil cytoplasmic antibodies was negative. Complement levels were normal, and tests for cryoglobulins, rapid plasma reagin, anticardiolipin antibody, lupus anticoagulant, rheumatoid factor, and antibodies to extractable nuclear antigens were all negative.

Raynaud's phenomenon is consistent with lupus. Double‐stranded DNA antibodies should be sent, although the urine did not demonstrate protein or an active sediment. Systemic sclerosis and the CREST syndrome is strongly associated with Raynaud's phenomenon and high‐titer ANA, but the patient does not have sclerodactyly, which is generally the earliest skin involvement. Autoimmune hepatitis is often associated with high‐titer ANA but does not fit this clinical picture. Given that the patient's presentation included segmental bowel wall thickening and a transient but marked liver enzyme elevation with AST predominance, I am concerned about vasculitis of the abdominal vasculature and would strongly consider a mesenteric angiogram.

To exclude mesenteric vasculitis, the patient underwent magnetic resonance angiography of the abdomen, the results of which were normal. A repeat test for antinuclear antibodies was positive at a titer of 1:2560 in a uniform pattern. A test for anti‐double‐stranded DNA was positive at 1370 U/mL. The patient was diagnosed with systemic lupus and probable lupus enteritis, and therapy with oral prednisone (10 mg daily) and hydroxychloroquine was initiated. She had prompt improvement in her abdominal pain, and was discharged home. Five months later she developed proteinuria and underwent a renal biopsy, which showed minor, nonspecific glomerular abnormalities, suggesting possible mild lupus nephritis. Eight months after her initial presentation, she remains free of abdominal pain and has regained the weight she had initially lost. Her oral ulcers have resolved, and her blood counts have normalized. Her serum creatinine has remained normal. She is now maintained on prednisone (15 mg daily), hydroxychloroquine, and mycophenolate mofetil.

COMMENTARY

A diagnosis of systemic lupus erythematosus (SLE) provided a unifying explanation for the patient's findings. Indeed, she manifested 4 of the 11 American College of Rheumatology criteria for systemic lupus (oral ulcers, leukopenia, positive anti‐DNA, and positive ANA), meeting criteria for a definite diagnosis of SLE. She additionally had multiple other features suggestive of lupus including Raynaud's phenomenon, arthralgias, alopecia, mild thrombocytopenia, and a positive Coombs' test (although the normal reticulocyte count, lactate dehydrogenase, and haptoglobin were most consistent with anemia of a chronic disease).

The protean manifestations of SLE can present significant diagnostic challenges. In this case, physicians were immediately drawn to the patient's acute abdominal pain and severe neutropenia and failed to recognize more subtle disease manifestations that may have aided in establishing a unifying diagnosis sooner. The initial history and review of systems did not disclose arthralgias, alopecia, or Raynaud's phenomenon. In an era of increasing use of hospitalists, which creates potential discontinuity between inpatient and outpatient physicians, a thorough history and review of systems may be particularly important in diagnosing acute manifestations of chronic systemic disease. Inpatient physicians may be overly focused on the small subset of acute complaints leading to hospitalization, without considering the larger constellation of symptoms that may facilitate accurate diagnosis. Our discussant quickly recognized the multisystem nature of the patient's illness and appropriately focused on infectious, neoplastic, and autoimmune categories of disease as being most likely. When infectious and neoplastic conditions were excluded with reasonable certainty, a directed serologic investigation for autoimmune disease was requested, culminating in a diagnosis of SLE.

Involvement of the skin as well as hematologic, renal, and musculoskeletal systems in SLE is commonly recognized, whereas gastrointestinal involvement is perceived to occur much less frequently. However, abdominal pain occurs in up to 40% of patients with lupus.14 Abdominal pain in lupus patients can arise from non‐lupus‐related conditions as well as lupus‐related entities, including serositis, mesenteric vasculitis with or without infarction, mesenteric thrombosis, pancreatitis, inflammatory bowel disease, and adverse medication effects including peptic ulcer disease. Abnormal liver chemistries, as seen in our patient, occur in 20%‐50% of patients with lupus and may be due to lupus hepatitis, concomitant autoimmune hepatitis, or medications including NSAIDs.5, 6 Oral ulcers and leukopenia are likewise common in SLE, with each seen in up to half of patients.4, 7, 8 Leukopenia in SLE may a result of neutropenia, lymphocytopenia, or both. However, severe neutropenia (ie, absolute count less than 500/L), as seen in our case, is more often a result of myelotoxicity from immunosuppressive therapy, rather than SLE itself.9

Lupus enteritis represents bowel microischemia from small‐vessel arteritis or venulitis that often is not evident on conventional mesenteric angiography.4, 10, 11 The reported prevalence of intestinal vasculitis in patients with SLE varies widely, depending on the characteristics of lupus patients sampled in individual studies. Intestinal vasculitis affects 0.2%‐0.5% of SLE patients in general,4, 12 whereas among SLE patients with active disease and an acute abdomen, vasculitis has been reported in up to 53% of patients.10 Antiphospholipid antibodies, antibodies to extractable nuclear antigens, the SLE Disease Activity Index, complement levels, erythrocyte sedimentation rate, C‐reactive protein, and anti‐double‐stranded DNA do not reliably differentiate lupus enteritis from acute abdominal pain due to other etiologies in patients with SLE.11 However, a concomitant drop in the white blood cell count at the onset of symptoms may be useful in distinguishing lupus enteritis from other causes of acute abdominal pain among lupus patients.11 Computed tomography findings consistent with lupus enteritis are nonspecific and include bowel‐wall thickening, submucosal edema (eg, target sign), dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat.13 Colonoscopy may reveal areas of ischemia and ulceration, and biopsy can confirm intestinal vasculitis. However, intestinal involvement may be segmental, and pathologic confirmation may be difficult. Contrast enema, gallium scanning, and indium‐labeled white cell scanning may be useful, but lack specificity. No controlled trials to date have evaluated the optimal therapy for lupus enteritis, but pulsed methylprednisolone is often recommended.4 Cyclophosphamide, azathioprine, methotrexate, and cyclosporine have also been used as adjunctive agents. Patients may progress to intestinal infarction and perforation, which augurs a poor prognosis, and early surgical exploration should be considered in severely ill patients.10 Death may occur in more than two‐thirds of patients whose disease progresses to intestinal perforation.1

In summary, a multisystem disease such as SLE requires a comprehensive history, physical exam, and review of systems to establish a correct diagnosis. In our case, an extensive evaluation was necessary to exclude other etiologies of abdominal pain and systemic illness, particularly as infectious and neoplastic conditions occur far more often than lupus enteritis in the general population. However, profound laboratory abnormalities may have preoccupied the attention of treating physicians, leading them to overlook less obvious but important historical and physical findings suggestive of SLE. The cohesively abnormal forest may thus have been obscured by erratically abnormal individual trees. Gastrointestinal symptoms may be underrecognized in SLE. When these result for lupus enteritis, timely recognition may be lifesaving.

References
  1. Hoffman BI,Katz WA.The gastrointestinal manifestations of systemic lupus erythematosus: a review of the literature.Semin Arthritis Rheum.1980;9:237.
  2. Zizic TM,Classen JN,Stevens MB.Acute abdominal complications of systemic lupus erythematosus and polyarteritis nodosa.Am J Med.1982;73:525531.
  3. Jovaisas A,Kraag G.Acute gastrointestinal manifestations of systemic lupus erythematosus.Can J Surg.1987;30:185188.
  4. Sultan SM,Ioannou Y,Isenberg DA.A review of gastrointestinal manifestations of systemic lupus erythematosus.Rheumatology.1999;38:917932.
  5. Youssef WI,Tavill AS.Connective tissue disease and the liver.J Clin Gastroenterol.2002;35:345349.
  6. Runyon BA,LaBrecque DR,Anuras S.The spectrum of liver disease in systemic lupus erythematosus: report of 33 histologically‐proved cases and review of the literature.Am J Med.1980;69:187194.
  7. Budman DR,Stein berg AD.Hematologic aspects of systemic lupus erythematosus: current concepts.Ann Intern Med.1977;86:220229.
  8. Nossent JC,Swaak AJ.Prevalence and significance of hematological abnormalities in patients with systemic lupus erythematosus.Q J Med1991;80:60512.
  9. Martinez‐Banos D,Crispin JC,Lazo‐Langner A, et al.Moderate and severe neutropenia in patients with systemic lupus erythematosus.Rheumatology.2006;45:994998.
  10. Medina F,Ayala A,Lara LJ, et al.Acute abdomen in systemic lupus erythematosus: the importance of early laparotomy.Am J Med.1997;103:100105.
  11. Lee C,Ahn MS,Lee EY, et al.Acute abdominal pain in systemic lupus erythematosus: focus on lupus enteritis (gastrointestinal vasculitis).Ann Rheum Dis,2002;61:547550.
  12. Drenkard C,Villa AR,Reyes E, et al.Vasculitis in systemic lupus erythematosus.Lupus.1997;6:235242.
  13. Byun JY,Ha HK,Yu SY, et al.CT features of systemic lupus erythematosus in patients with acute abdominal pain: emphasis on ischemic bowel disease.Radiology.1999;211:203209.
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A 56‐year‐old woman from Colombia presented to the emergency department after 24 hours of abdominal pain. One week before, she had experienced similar pain that lasted for 4 hours and spontaneously resolved. She was nauseated but had no vomiting. She reported an unintentional 14‐pound weight loss over the preceding 3 weeks. She denied fever, chills, night sweats, diarrhea, constipation, dysuria, or jaundice.

In a middle‐aged woman with abdominal pain and nausea, diagnostic considerations include gallbladder disease, diseases of the bowel (such as a partial small‐bowel obstruction or inflammatory conditions), hepatic or pancreatic conditions, and nongastrointestinal ailments such as cardiac ischemia. Knowing the specific location of pain, its quality, precipitating factors, and accompanying systemic symptoms may help to narrow the diagnosis. The unintentional weight loss preceding the onset of pain may be an important clue because it suggests a systemic condition, and in a South American immigrantparticularly if she has traveled recentlyit is important to consider parasitic illnesses. The absence of fever makes some infections such as tuberculosis and malaria less likely. At this point, in addition to a thorough history and physical, laboratory tests should include a complete blood count (with quantification of eosinophils) and a metabolic panel with liver enzymes and albumin.

The patient described pain in the midline, just inferior to the umbilicus. The pain was constant, developed without any particular provocation, and was not related to meals or exertion. There were no constitutional symptoms aside from weight loss. She had a history of bipolar disorder, hypothyroidism, osteoarthritis, and chronic sinusitis and had previously undergone cholecystectomy and abdominal hysterectomy. She was taking levothyroxine, montelukast, bupropion, oxcarbazepine, fexofenadine, meloxicam, zolpidem, and, as needed, acetaminophen. She had recently completed a 10‐day course of levofloxacin for acute sinusitis. She had immigrated to the United States 10 years earlier and lived with her husband and daughter. She denied the use of tobacco, alcohol or illicit drugs. She had visited Colombia 6 months earlier but had no other recent travel history.

The history of cholecystectomy makes a biliary tract process unlikely. Its location reduces the likelihood of a hepatic or pancreatic process, but I would like to see the liver enzymes, especially given her recent acetaminophen use. The comorbid illnessesparticularly her bipolar disordermay be relevant because psychiatric illness might be associated with medication overuse or undisclosed toxic ingestions. For example, excess thyroxine might lead to weight loss while overuse of nonsteroidal anti‐inflammatory drugs such as meloxicam can cause intestinal ulceration, not only in the upper tract, but also in the colon. Undisclosed ingestions may also be associated with abdominal symptoms. Her surgical history makes adhesions with a secondary partial bowel obstruction possible. With no travel outside this country in the last 6 months, exotic infections are less likely. Finally, the recent course of levofloxacin may be relevant because many antibiotics are associated with nonspecific abdominal symptoms, and Clostridium difficile colitis occasionally presents without diarrhea.

The patient reported taking her medications as prescribed and denied ingesting other medications. On physical examination, she had a temperature of 98.9F, a pulse of 81 beats per minute, a blood pressure of 110/80 mm Hg, and a respiratory rate of 16 respirations per minute. She had a normal oxygen saturation while breathing ambient air. Her weight was 58 kg. There was no scleral icterus or jugular venous distension. She had a small painless ulcer involving the hard palate. Her lungs were clear to auscultation, and cardiac examination was normal. The abdomen was soft, bowel sounds were present, and there was moderate tenderness to palpation inferior to the umbilicus. There was no rebound or guarding, hepatosplenomegaly or other masses. There was no peripheral edema and no lymphadenopathy. Neurological examination was normal.

The oral ulcer may or may not be related to the clinical presentation because oral ulcers, whether painful or painless, are ubiquitous and may be isolated or may be associated with a wide range of infectious and noninfectious systemic diseases. Although some systemic causes of mucocutaneous ulcers are associated with weight loss (including Crohn's disease, Behcet's disease, celiac sprue, human immunodeficiency virus [HIV], herpesviruses, syphilis, and systemic lupus erythematosus [SLE], among others), the lack of specificity of this finding limits its diagnostic utility. However, it is reasonable to ask whether the patient has noted frequent ulceration in the mouth or genitalia, as recurrent or severe ulcerations may narrow the diagnostic considerations. On the other hand, the focal nature of the pain inferior to the umbilicus suggests a discrete process in the abdomen or pelvis, such as an abscess, mass, or localized area of bowel inflammation. A plain abdominal film is likely to be low yield in this situation, so pursuing computed tomography is appropriate. Not all patients with focal abdominal pain require abdominal imaging, but in the context of weight loss and persistent symptoms for more than a week, imaging is prudent in this case.

The patient denied genital ulceration but did report painless oral ulcers over the preceding months. Laboratory evaluation revealed a white‐cell count of 1000/mm3, of which 6% were neutrophils, 5% were band forms, 36% were lymphocytes, and 47% were monocytes. The absolute neutrophil count was 110/mm3. Hemoglobin level was 10.2 g/dL with a mean corpuscular volume of 90 m3, and the platelet count was 151,000/mm3. Other results of laboratory studies were: sodium, 140 mmol/L; potassium, 3.8 mmol/L; chloride, 96 mmol/L; bicarbonate, 23 mmol/L; blood urea nitrogen, 13 mg/dL; creatinine, 0.4 mg/dL; lipase, 32 U/L (normal range, 13‐60); amylase, 73 U/L (normal range, 30‐110); albumin, 4.0 g/dL; aspartate aminotransferase, 779 U/L (normal range, 13‐35); alanine aminotransferase, 330 U/L (normal range, 7‐35); alkaline phosphatase, 510 U/L (normal range, 35‐104); and total bilirubin, 0.9 mg/dL (normal range, 0.1‐1.2). The lactate dehydrogenase level was 200 U/L (normal range, 135‐214). The corrected reticulocyte count was 1.6% (normal range, 0.3‐2.3), and haptoglobin was 190 mg/dL (normal range, 43‐212). A direct Coomb's test was positive. The erythrocyte sedimentation rate was 113 mm/hour (normal range, 1‐25). Urinalysis was normal without evidence of protein or blood.

Laboratory abnormalities include elevated transaminases and alkaline phosphatase, a markedly elevated erythrocyte sedimentation rate, and profound leukopenia with neutropenia. The patient is anemic, which may elevate the sedimentation rate but not typically to this degree. The patient is not febrile, but if she were to develop a fever, empiric antibiotics would be prudent. The normal albumin and bilirubin suggest that hepatic synthetic and excretory functions remain intact. Although the direct Coombs test is positive, the reticulocyte and lactate dehydrogenase levels argue against brisk hemolysis; this abnormality may simply be a marker of nonspecific immune activation. A variety of infections can cause neutropenia and liver enzyme abnormalities including parasites (malaria or leishmaniasis), viruses (cytomegalovirus or Epstein‐Barr virus [EBV]), tick‐borne bacterial infections (ehrlichiosis or rickettsial infection), and granulomatous infections (tuberculosis). Malignant infiltration of the reticuloendothelial system can also lead to cytopenias and liver enzyme abnormalities. Autoimmunity remains a consideration, as SLE may lead to cytopenias, oral ulcers, and nonspecific immune phenomena. Rather than ordering a large number of blood tests, I favor a targeted approach with abdominal computed tomography followed by biopsy of either the liver or bone marrow.

Chest radiography revealed no abnormalities. Computed tomography of the chest, abdomen, and pelvis with intravenous and oral contrast demonstrated concentric wall thickening of the transverse colon, but no evidence of obstruction or free air. The patient was treated with intravenous fluids, morphine, and cefepime. Bone marrow biopsy was performed, which demonstrated a hypercellular marrow with increased myeloid precursors and a left shift and megakaryocytic hyperplasia. Flow cytometry revealed no abnormally restricted clonal populations. A concerted search for an infectious etiology of the patient's neutropenia was unrevealing, including tests for HIV, cytomegalovirus, hepatitis A, hepatitis B, hepatitis C, Mycoplasma pneumoniae, EBV, and parvovirus B19.

I hope blood cultures were drawn prior to the initiation of antibiotics. Hypercellularity of the bone marrow in the context of leukopenia raises concern that white blood cells are being destroyed peripherally. Autoimmunity against neutrophils can be transiently induced by viruses such as HIV, hepatitis B, and EBV, but these infections have been excluded. Testing for antinuclear antibodies is reasonable. A normal‐sized spleen on the abdominal CT excludes hypersplenism. Colonic thickening can be associated with infection, ischemia, inflammatory bowel disease, and malignancy. The question is whether the colonic thickening is part of the same disease process causing the leukopenia and liver enzyme elevation or whether it represents a secondary infectious process in the setting of neutropenia (such as Clostridium difficile infection or typhlitis). Testing for stool pathogens (including ova and parasites) is certainly appropriate, and consideration of a colonoscopy with biopsy is reasonable, provided that appropriate antimicrobial coverage remains in place.

Blood cultures obtained prior to starting antibiotics were negative. The patient's abdominal pain improved, and she was discharged home to have close follow‐up with a hematologist. The results of her liver function tests improved, and her absolute neutrophil count was 230/mm3 at the time of discharge. Her neutropenia was believed to be secondary to peripheral destruction from a viral, drug‐mediated, or autoimmune process. Oxcarbazepine (Trileptal) was discontinued, as it was believed to be the medication most likely to be responsible. She returned to the hospital 3 days later with recurrence of her abdominal pain and diarrhea. She remained afebrile. Additional history revealed arthralgias over the previous 2 months, mild alopecia, and prior symptoms suggestive of Raynaud's phenomenon. Stool studies failed to establish an infectious etiology for the diarrhea, and her continued neutropenia responded appropriately to treatment with subcutaneous filgrastim. Colonoscopy could be performed only to the hepatic flexure and revealed no abnormalities. A serologic test for antinuclear antibodies was positive at a titer of 1:640 in a homogenous pattern, and a test for antineutrophil cytoplasmic antibodies was negative. Complement levels were normal, and tests for cryoglobulins, rapid plasma reagin, anticardiolipin antibody, lupus anticoagulant, rheumatoid factor, and antibodies to extractable nuclear antigens were all negative.

Raynaud's phenomenon is consistent with lupus. Double‐stranded DNA antibodies should be sent, although the urine did not demonstrate protein or an active sediment. Systemic sclerosis and the CREST syndrome is strongly associated with Raynaud's phenomenon and high‐titer ANA, but the patient does not have sclerodactyly, which is generally the earliest skin involvement. Autoimmune hepatitis is often associated with high‐titer ANA but does not fit this clinical picture. Given that the patient's presentation included segmental bowel wall thickening and a transient but marked liver enzyme elevation with AST predominance, I am concerned about vasculitis of the abdominal vasculature and would strongly consider a mesenteric angiogram.

To exclude mesenteric vasculitis, the patient underwent magnetic resonance angiography of the abdomen, the results of which were normal. A repeat test for antinuclear antibodies was positive at a titer of 1:2560 in a uniform pattern. A test for anti‐double‐stranded DNA was positive at 1370 U/mL. The patient was diagnosed with systemic lupus and probable lupus enteritis, and therapy with oral prednisone (10 mg daily) and hydroxychloroquine was initiated. She had prompt improvement in her abdominal pain, and was discharged home. Five months later she developed proteinuria and underwent a renal biopsy, which showed minor, nonspecific glomerular abnormalities, suggesting possible mild lupus nephritis. Eight months after her initial presentation, she remains free of abdominal pain and has regained the weight she had initially lost. Her oral ulcers have resolved, and her blood counts have normalized. Her serum creatinine has remained normal. She is now maintained on prednisone (15 mg daily), hydroxychloroquine, and mycophenolate mofetil.

COMMENTARY

A diagnosis of systemic lupus erythematosus (SLE) provided a unifying explanation for the patient's findings. Indeed, she manifested 4 of the 11 American College of Rheumatology criteria for systemic lupus (oral ulcers, leukopenia, positive anti‐DNA, and positive ANA), meeting criteria for a definite diagnosis of SLE. She additionally had multiple other features suggestive of lupus including Raynaud's phenomenon, arthralgias, alopecia, mild thrombocytopenia, and a positive Coombs' test (although the normal reticulocyte count, lactate dehydrogenase, and haptoglobin were most consistent with anemia of a chronic disease).

The protean manifestations of SLE can present significant diagnostic challenges. In this case, physicians were immediately drawn to the patient's acute abdominal pain and severe neutropenia and failed to recognize more subtle disease manifestations that may have aided in establishing a unifying diagnosis sooner. The initial history and review of systems did not disclose arthralgias, alopecia, or Raynaud's phenomenon. In an era of increasing use of hospitalists, which creates potential discontinuity between inpatient and outpatient physicians, a thorough history and review of systems may be particularly important in diagnosing acute manifestations of chronic systemic disease. Inpatient physicians may be overly focused on the small subset of acute complaints leading to hospitalization, without considering the larger constellation of symptoms that may facilitate accurate diagnosis. Our discussant quickly recognized the multisystem nature of the patient's illness and appropriately focused on infectious, neoplastic, and autoimmune categories of disease as being most likely. When infectious and neoplastic conditions were excluded with reasonable certainty, a directed serologic investigation for autoimmune disease was requested, culminating in a diagnosis of SLE.

Involvement of the skin as well as hematologic, renal, and musculoskeletal systems in SLE is commonly recognized, whereas gastrointestinal involvement is perceived to occur much less frequently. However, abdominal pain occurs in up to 40% of patients with lupus.14 Abdominal pain in lupus patients can arise from non‐lupus‐related conditions as well as lupus‐related entities, including serositis, mesenteric vasculitis with or without infarction, mesenteric thrombosis, pancreatitis, inflammatory bowel disease, and adverse medication effects including peptic ulcer disease. Abnormal liver chemistries, as seen in our patient, occur in 20%‐50% of patients with lupus and may be due to lupus hepatitis, concomitant autoimmune hepatitis, or medications including NSAIDs.5, 6 Oral ulcers and leukopenia are likewise common in SLE, with each seen in up to half of patients.4, 7, 8 Leukopenia in SLE may a result of neutropenia, lymphocytopenia, or both. However, severe neutropenia (ie, absolute count less than 500/L), as seen in our case, is more often a result of myelotoxicity from immunosuppressive therapy, rather than SLE itself.9

Lupus enteritis represents bowel microischemia from small‐vessel arteritis or venulitis that often is not evident on conventional mesenteric angiography.4, 10, 11 The reported prevalence of intestinal vasculitis in patients with SLE varies widely, depending on the characteristics of lupus patients sampled in individual studies. Intestinal vasculitis affects 0.2%‐0.5% of SLE patients in general,4, 12 whereas among SLE patients with active disease and an acute abdomen, vasculitis has been reported in up to 53% of patients.10 Antiphospholipid antibodies, antibodies to extractable nuclear antigens, the SLE Disease Activity Index, complement levels, erythrocyte sedimentation rate, C‐reactive protein, and anti‐double‐stranded DNA do not reliably differentiate lupus enteritis from acute abdominal pain due to other etiologies in patients with SLE.11 However, a concomitant drop in the white blood cell count at the onset of symptoms may be useful in distinguishing lupus enteritis from other causes of acute abdominal pain among lupus patients.11 Computed tomography findings consistent with lupus enteritis are nonspecific and include bowel‐wall thickening, submucosal edema (eg, target sign), dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat.13 Colonoscopy may reveal areas of ischemia and ulceration, and biopsy can confirm intestinal vasculitis. However, intestinal involvement may be segmental, and pathologic confirmation may be difficult. Contrast enema, gallium scanning, and indium‐labeled white cell scanning may be useful, but lack specificity. No controlled trials to date have evaluated the optimal therapy for lupus enteritis, but pulsed methylprednisolone is often recommended.4 Cyclophosphamide, azathioprine, methotrexate, and cyclosporine have also been used as adjunctive agents. Patients may progress to intestinal infarction and perforation, which augurs a poor prognosis, and early surgical exploration should be considered in severely ill patients.10 Death may occur in more than two‐thirds of patients whose disease progresses to intestinal perforation.1

In summary, a multisystem disease such as SLE requires a comprehensive history, physical exam, and review of systems to establish a correct diagnosis. In our case, an extensive evaluation was necessary to exclude other etiologies of abdominal pain and systemic illness, particularly as infectious and neoplastic conditions occur far more often than lupus enteritis in the general population. However, profound laboratory abnormalities may have preoccupied the attention of treating physicians, leading them to overlook less obvious but important historical and physical findings suggestive of SLE. The cohesively abnormal forest may thus have been obscured by erratically abnormal individual trees. Gastrointestinal symptoms may be underrecognized in SLE. When these result for lupus enteritis, timely recognition may be lifesaving.

A 56‐year‐old woman from Colombia presented to the emergency department after 24 hours of abdominal pain. One week before, she had experienced similar pain that lasted for 4 hours and spontaneously resolved. She was nauseated but had no vomiting. She reported an unintentional 14‐pound weight loss over the preceding 3 weeks. She denied fever, chills, night sweats, diarrhea, constipation, dysuria, or jaundice.

In a middle‐aged woman with abdominal pain and nausea, diagnostic considerations include gallbladder disease, diseases of the bowel (such as a partial small‐bowel obstruction or inflammatory conditions), hepatic or pancreatic conditions, and nongastrointestinal ailments such as cardiac ischemia. Knowing the specific location of pain, its quality, precipitating factors, and accompanying systemic symptoms may help to narrow the diagnosis. The unintentional weight loss preceding the onset of pain may be an important clue because it suggests a systemic condition, and in a South American immigrantparticularly if she has traveled recentlyit is important to consider parasitic illnesses. The absence of fever makes some infections such as tuberculosis and malaria less likely. At this point, in addition to a thorough history and physical, laboratory tests should include a complete blood count (with quantification of eosinophils) and a metabolic panel with liver enzymes and albumin.

The patient described pain in the midline, just inferior to the umbilicus. The pain was constant, developed without any particular provocation, and was not related to meals or exertion. There were no constitutional symptoms aside from weight loss. She had a history of bipolar disorder, hypothyroidism, osteoarthritis, and chronic sinusitis and had previously undergone cholecystectomy and abdominal hysterectomy. She was taking levothyroxine, montelukast, bupropion, oxcarbazepine, fexofenadine, meloxicam, zolpidem, and, as needed, acetaminophen. She had recently completed a 10‐day course of levofloxacin for acute sinusitis. She had immigrated to the United States 10 years earlier and lived with her husband and daughter. She denied the use of tobacco, alcohol or illicit drugs. She had visited Colombia 6 months earlier but had no other recent travel history.

The history of cholecystectomy makes a biliary tract process unlikely. Its location reduces the likelihood of a hepatic or pancreatic process, but I would like to see the liver enzymes, especially given her recent acetaminophen use. The comorbid illnessesparticularly her bipolar disordermay be relevant because psychiatric illness might be associated with medication overuse or undisclosed toxic ingestions. For example, excess thyroxine might lead to weight loss while overuse of nonsteroidal anti‐inflammatory drugs such as meloxicam can cause intestinal ulceration, not only in the upper tract, but also in the colon. Undisclosed ingestions may also be associated with abdominal symptoms. Her surgical history makes adhesions with a secondary partial bowel obstruction possible. With no travel outside this country in the last 6 months, exotic infections are less likely. Finally, the recent course of levofloxacin may be relevant because many antibiotics are associated with nonspecific abdominal symptoms, and Clostridium difficile colitis occasionally presents without diarrhea.

The patient reported taking her medications as prescribed and denied ingesting other medications. On physical examination, she had a temperature of 98.9F, a pulse of 81 beats per minute, a blood pressure of 110/80 mm Hg, and a respiratory rate of 16 respirations per minute. She had a normal oxygen saturation while breathing ambient air. Her weight was 58 kg. There was no scleral icterus or jugular venous distension. She had a small painless ulcer involving the hard palate. Her lungs were clear to auscultation, and cardiac examination was normal. The abdomen was soft, bowel sounds were present, and there was moderate tenderness to palpation inferior to the umbilicus. There was no rebound or guarding, hepatosplenomegaly or other masses. There was no peripheral edema and no lymphadenopathy. Neurological examination was normal.

The oral ulcer may or may not be related to the clinical presentation because oral ulcers, whether painful or painless, are ubiquitous and may be isolated or may be associated with a wide range of infectious and noninfectious systemic diseases. Although some systemic causes of mucocutaneous ulcers are associated with weight loss (including Crohn's disease, Behcet's disease, celiac sprue, human immunodeficiency virus [HIV], herpesviruses, syphilis, and systemic lupus erythematosus [SLE], among others), the lack of specificity of this finding limits its diagnostic utility. However, it is reasonable to ask whether the patient has noted frequent ulceration in the mouth or genitalia, as recurrent or severe ulcerations may narrow the diagnostic considerations. On the other hand, the focal nature of the pain inferior to the umbilicus suggests a discrete process in the abdomen or pelvis, such as an abscess, mass, or localized area of bowel inflammation. A plain abdominal film is likely to be low yield in this situation, so pursuing computed tomography is appropriate. Not all patients with focal abdominal pain require abdominal imaging, but in the context of weight loss and persistent symptoms for more than a week, imaging is prudent in this case.

The patient denied genital ulceration but did report painless oral ulcers over the preceding months. Laboratory evaluation revealed a white‐cell count of 1000/mm3, of which 6% were neutrophils, 5% were band forms, 36% were lymphocytes, and 47% were monocytes. The absolute neutrophil count was 110/mm3. Hemoglobin level was 10.2 g/dL with a mean corpuscular volume of 90 m3, and the platelet count was 151,000/mm3. Other results of laboratory studies were: sodium, 140 mmol/L; potassium, 3.8 mmol/L; chloride, 96 mmol/L; bicarbonate, 23 mmol/L; blood urea nitrogen, 13 mg/dL; creatinine, 0.4 mg/dL; lipase, 32 U/L (normal range, 13‐60); amylase, 73 U/L (normal range, 30‐110); albumin, 4.0 g/dL; aspartate aminotransferase, 779 U/L (normal range, 13‐35); alanine aminotransferase, 330 U/L (normal range, 7‐35); alkaline phosphatase, 510 U/L (normal range, 35‐104); and total bilirubin, 0.9 mg/dL (normal range, 0.1‐1.2). The lactate dehydrogenase level was 200 U/L (normal range, 135‐214). The corrected reticulocyte count was 1.6% (normal range, 0.3‐2.3), and haptoglobin was 190 mg/dL (normal range, 43‐212). A direct Coomb's test was positive. The erythrocyte sedimentation rate was 113 mm/hour (normal range, 1‐25). Urinalysis was normal without evidence of protein or blood.

Laboratory abnormalities include elevated transaminases and alkaline phosphatase, a markedly elevated erythrocyte sedimentation rate, and profound leukopenia with neutropenia. The patient is anemic, which may elevate the sedimentation rate but not typically to this degree. The patient is not febrile, but if she were to develop a fever, empiric antibiotics would be prudent. The normal albumin and bilirubin suggest that hepatic synthetic and excretory functions remain intact. Although the direct Coombs test is positive, the reticulocyte and lactate dehydrogenase levels argue against brisk hemolysis; this abnormality may simply be a marker of nonspecific immune activation. A variety of infections can cause neutropenia and liver enzyme abnormalities including parasites (malaria or leishmaniasis), viruses (cytomegalovirus or Epstein‐Barr virus [EBV]), tick‐borne bacterial infections (ehrlichiosis or rickettsial infection), and granulomatous infections (tuberculosis). Malignant infiltration of the reticuloendothelial system can also lead to cytopenias and liver enzyme abnormalities. Autoimmunity remains a consideration, as SLE may lead to cytopenias, oral ulcers, and nonspecific immune phenomena. Rather than ordering a large number of blood tests, I favor a targeted approach with abdominal computed tomography followed by biopsy of either the liver or bone marrow.

Chest radiography revealed no abnormalities. Computed tomography of the chest, abdomen, and pelvis with intravenous and oral contrast demonstrated concentric wall thickening of the transverse colon, but no evidence of obstruction or free air. The patient was treated with intravenous fluids, morphine, and cefepime. Bone marrow biopsy was performed, which demonstrated a hypercellular marrow with increased myeloid precursors and a left shift and megakaryocytic hyperplasia. Flow cytometry revealed no abnormally restricted clonal populations. A concerted search for an infectious etiology of the patient's neutropenia was unrevealing, including tests for HIV, cytomegalovirus, hepatitis A, hepatitis B, hepatitis C, Mycoplasma pneumoniae, EBV, and parvovirus B19.

I hope blood cultures were drawn prior to the initiation of antibiotics. Hypercellularity of the bone marrow in the context of leukopenia raises concern that white blood cells are being destroyed peripherally. Autoimmunity against neutrophils can be transiently induced by viruses such as HIV, hepatitis B, and EBV, but these infections have been excluded. Testing for antinuclear antibodies is reasonable. A normal‐sized spleen on the abdominal CT excludes hypersplenism. Colonic thickening can be associated with infection, ischemia, inflammatory bowel disease, and malignancy. The question is whether the colonic thickening is part of the same disease process causing the leukopenia and liver enzyme elevation or whether it represents a secondary infectious process in the setting of neutropenia (such as Clostridium difficile infection or typhlitis). Testing for stool pathogens (including ova and parasites) is certainly appropriate, and consideration of a colonoscopy with biopsy is reasonable, provided that appropriate antimicrobial coverage remains in place.

Blood cultures obtained prior to starting antibiotics were negative. The patient's abdominal pain improved, and she was discharged home to have close follow‐up with a hematologist. The results of her liver function tests improved, and her absolute neutrophil count was 230/mm3 at the time of discharge. Her neutropenia was believed to be secondary to peripheral destruction from a viral, drug‐mediated, or autoimmune process. Oxcarbazepine (Trileptal) was discontinued, as it was believed to be the medication most likely to be responsible. She returned to the hospital 3 days later with recurrence of her abdominal pain and diarrhea. She remained afebrile. Additional history revealed arthralgias over the previous 2 months, mild alopecia, and prior symptoms suggestive of Raynaud's phenomenon. Stool studies failed to establish an infectious etiology for the diarrhea, and her continued neutropenia responded appropriately to treatment with subcutaneous filgrastim. Colonoscopy could be performed only to the hepatic flexure and revealed no abnormalities. A serologic test for antinuclear antibodies was positive at a titer of 1:640 in a homogenous pattern, and a test for antineutrophil cytoplasmic antibodies was negative. Complement levels were normal, and tests for cryoglobulins, rapid plasma reagin, anticardiolipin antibody, lupus anticoagulant, rheumatoid factor, and antibodies to extractable nuclear antigens were all negative.

Raynaud's phenomenon is consistent with lupus. Double‐stranded DNA antibodies should be sent, although the urine did not demonstrate protein or an active sediment. Systemic sclerosis and the CREST syndrome is strongly associated with Raynaud's phenomenon and high‐titer ANA, but the patient does not have sclerodactyly, which is generally the earliest skin involvement. Autoimmune hepatitis is often associated with high‐titer ANA but does not fit this clinical picture. Given that the patient's presentation included segmental bowel wall thickening and a transient but marked liver enzyme elevation with AST predominance, I am concerned about vasculitis of the abdominal vasculature and would strongly consider a mesenteric angiogram.

To exclude mesenteric vasculitis, the patient underwent magnetic resonance angiography of the abdomen, the results of which were normal. A repeat test for antinuclear antibodies was positive at a titer of 1:2560 in a uniform pattern. A test for anti‐double‐stranded DNA was positive at 1370 U/mL. The patient was diagnosed with systemic lupus and probable lupus enteritis, and therapy with oral prednisone (10 mg daily) and hydroxychloroquine was initiated. She had prompt improvement in her abdominal pain, and was discharged home. Five months later she developed proteinuria and underwent a renal biopsy, which showed minor, nonspecific glomerular abnormalities, suggesting possible mild lupus nephritis. Eight months after her initial presentation, she remains free of abdominal pain and has regained the weight she had initially lost. Her oral ulcers have resolved, and her blood counts have normalized. Her serum creatinine has remained normal. She is now maintained on prednisone (15 mg daily), hydroxychloroquine, and mycophenolate mofetil.

COMMENTARY

A diagnosis of systemic lupus erythematosus (SLE) provided a unifying explanation for the patient's findings. Indeed, she manifested 4 of the 11 American College of Rheumatology criteria for systemic lupus (oral ulcers, leukopenia, positive anti‐DNA, and positive ANA), meeting criteria for a definite diagnosis of SLE. She additionally had multiple other features suggestive of lupus including Raynaud's phenomenon, arthralgias, alopecia, mild thrombocytopenia, and a positive Coombs' test (although the normal reticulocyte count, lactate dehydrogenase, and haptoglobin were most consistent with anemia of a chronic disease).

The protean manifestations of SLE can present significant diagnostic challenges. In this case, physicians were immediately drawn to the patient's acute abdominal pain and severe neutropenia and failed to recognize more subtle disease manifestations that may have aided in establishing a unifying diagnosis sooner. The initial history and review of systems did not disclose arthralgias, alopecia, or Raynaud's phenomenon. In an era of increasing use of hospitalists, which creates potential discontinuity between inpatient and outpatient physicians, a thorough history and review of systems may be particularly important in diagnosing acute manifestations of chronic systemic disease. Inpatient physicians may be overly focused on the small subset of acute complaints leading to hospitalization, without considering the larger constellation of symptoms that may facilitate accurate diagnosis. Our discussant quickly recognized the multisystem nature of the patient's illness and appropriately focused on infectious, neoplastic, and autoimmune categories of disease as being most likely. When infectious and neoplastic conditions were excluded with reasonable certainty, a directed serologic investigation for autoimmune disease was requested, culminating in a diagnosis of SLE.

Involvement of the skin as well as hematologic, renal, and musculoskeletal systems in SLE is commonly recognized, whereas gastrointestinal involvement is perceived to occur much less frequently. However, abdominal pain occurs in up to 40% of patients with lupus.14 Abdominal pain in lupus patients can arise from non‐lupus‐related conditions as well as lupus‐related entities, including serositis, mesenteric vasculitis with or without infarction, mesenteric thrombosis, pancreatitis, inflammatory bowel disease, and adverse medication effects including peptic ulcer disease. Abnormal liver chemistries, as seen in our patient, occur in 20%‐50% of patients with lupus and may be due to lupus hepatitis, concomitant autoimmune hepatitis, or medications including NSAIDs.5, 6 Oral ulcers and leukopenia are likewise common in SLE, with each seen in up to half of patients.4, 7, 8 Leukopenia in SLE may a result of neutropenia, lymphocytopenia, or both. However, severe neutropenia (ie, absolute count less than 500/L), as seen in our case, is more often a result of myelotoxicity from immunosuppressive therapy, rather than SLE itself.9

Lupus enteritis represents bowel microischemia from small‐vessel arteritis or venulitis that often is not evident on conventional mesenteric angiography.4, 10, 11 The reported prevalence of intestinal vasculitis in patients with SLE varies widely, depending on the characteristics of lupus patients sampled in individual studies. Intestinal vasculitis affects 0.2%‐0.5% of SLE patients in general,4, 12 whereas among SLE patients with active disease and an acute abdomen, vasculitis has been reported in up to 53% of patients.10 Antiphospholipid antibodies, antibodies to extractable nuclear antigens, the SLE Disease Activity Index, complement levels, erythrocyte sedimentation rate, C‐reactive protein, and anti‐double‐stranded DNA do not reliably differentiate lupus enteritis from acute abdominal pain due to other etiologies in patients with SLE.11 However, a concomitant drop in the white blood cell count at the onset of symptoms may be useful in distinguishing lupus enteritis from other causes of acute abdominal pain among lupus patients.11 Computed tomography findings consistent with lupus enteritis are nonspecific and include bowel‐wall thickening, submucosal edema (eg, target sign), dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat.13 Colonoscopy may reveal areas of ischemia and ulceration, and biopsy can confirm intestinal vasculitis. However, intestinal involvement may be segmental, and pathologic confirmation may be difficult. Contrast enema, gallium scanning, and indium‐labeled white cell scanning may be useful, but lack specificity. No controlled trials to date have evaluated the optimal therapy for lupus enteritis, but pulsed methylprednisolone is often recommended.4 Cyclophosphamide, azathioprine, methotrexate, and cyclosporine have also been used as adjunctive agents. Patients may progress to intestinal infarction and perforation, which augurs a poor prognosis, and early surgical exploration should be considered in severely ill patients.10 Death may occur in more than two‐thirds of patients whose disease progresses to intestinal perforation.1

In summary, a multisystem disease such as SLE requires a comprehensive history, physical exam, and review of systems to establish a correct diagnosis. In our case, an extensive evaluation was necessary to exclude other etiologies of abdominal pain and systemic illness, particularly as infectious and neoplastic conditions occur far more often than lupus enteritis in the general population. However, profound laboratory abnormalities may have preoccupied the attention of treating physicians, leading them to overlook less obvious but important historical and physical findings suggestive of SLE. The cohesively abnormal forest may thus have been obscured by erratically abnormal individual trees. Gastrointestinal symptoms may be underrecognized in SLE. When these result for lupus enteritis, timely recognition may be lifesaving.

References
  1. Hoffman BI,Katz WA.The gastrointestinal manifestations of systemic lupus erythematosus: a review of the literature.Semin Arthritis Rheum.1980;9:237.
  2. Zizic TM,Classen JN,Stevens MB.Acute abdominal complications of systemic lupus erythematosus and polyarteritis nodosa.Am J Med.1982;73:525531.
  3. Jovaisas A,Kraag G.Acute gastrointestinal manifestations of systemic lupus erythematosus.Can J Surg.1987;30:185188.
  4. Sultan SM,Ioannou Y,Isenberg DA.A review of gastrointestinal manifestations of systemic lupus erythematosus.Rheumatology.1999;38:917932.
  5. Youssef WI,Tavill AS.Connective tissue disease and the liver.J Clin Gastroenterol.2002;35:345349.
  6. Runyon BA,LaBrecque DR,Anuras S.The spectrum of liver disease in systemic lupus erythematosus: report of 33 histologically‐proved cases and review of the literature.Am J Med.1980;69:187194.
  7. Budman DR,Stein berg AD.Hematologic aspects of systemic lupus erythematosus: current concepts.Ann Intern Med.1977;86:220229.
  8. Nossent JC,Swaak AJ.Prevalence and significance of hematological abnormalities in patients with systemic lupus erythematosus.Q J Med1991;80:60512.
  9. Martinez‐Banos D,Crispin JC,Lazo‐Langner A, et al.Moderate and severe neutropenia in patients with systemic lupus erythematosus.Rheumatology.2006;45:994998.
  10. Medina F,Ayala A,Lara LJ, et al.Acute abdomen in systemic lupus erythematosus: the importance of early laparotomy.Am J Med.1997;103:100105.
  11. Lee C,Ahn MS,Lee EY, et al.Acute abdominal pain in systemic lupus erythematosus: focus on lupus enteritis (gastrointestinal vasculitis).Ann Rheum Dis,2002;61:547550.
  12. Drenkard C,Villa AR,Reyes E, et al.Vasculitis in systemic lupus erythematosus.Lupus.1997;6:235242.
  13. Byun JY,Ha HK,Yu SY, et al.CT features of systemic lupus erythematosus in patients with acute abdominal pain: emphasis on ischemic bowel disease.Radiology.1999;211:203209.
References
  1. Hoffman BI,Katz WA.The gastrointestinal manifestations of systemic lupus erythematosus: a review of the literature.Semin Arthritis Rheum.1980;9:237.
  2. Zizic TM,Classen JN,Stevens MB.Acute abdominal complications of systemic lupus erythematosus and polyarteritis nodosa.Am J Med.1982;73:525531.
  3. Jovaisas A,Kraag G.Acute gastrointestinal manifestations of systemic lupus erythematosus.Can J Surg.1987;30:185188.
  4. Sultan SM,Ioannou Y,Isenberg DA.A review of gastrointestinal manifestations of systemic lupus erythematosus.Rheumatology.1999;38:917932.
  5. Youssef WI,Tavill AS.Connective tissue disease and the liver.J Clin Gastroenterol.2002;35:345349.
  6. Runyon BA,LaBrecque DR,Anuras S.The spectrum of liver disease in systemic lupus erythematosus: report of 33 histologically‐proved cases and review of the literature.Am J Med.1980;69:187194.
  7. Budman DR,Stein berg AD.Hematologic aspects of systemic lupus erythematosus: current concepts.Ann Intern Med.1977;86:220229.
  8. Nossent JC,Swaak AJ.Prevalence and significance of hematological abnormalities in patients with systemic lupus erythematosus.Q J Med1991;80:60512.
  9. Martinez‐Banos D,Crispin JC,Lazo‐Langner A, et al.Moderate and severe neutropenia in patients with systemic lupus erythematosus.Rheumatology.2006;45:994998.
  10. Medina F,Ayala A,Lara LJ, et al.Acute abdomen in systemic lupus erythematosus: the importance of early laparotomy.Am J Med.1997;103:100105.
  11. Lee C,Ahn MS,Lee EY, et al.Acute abdominal pain in systemic lupus erythematosus: focus on lupus enteritis (gastrointestinal vasculitis).Ann Rheum Dis,2002;61:547550.
  12. Drenkard C,Villa AR,Reyes E, et al.Vasculitis in systemic lupus erythematosus.Lupus.1997;6:235242.
  13. Byun JY,Ha HK,Yu SY, et al.CT features of systemic lupus erythematosus in patients with acute abdominal pain: emphasis on ischemic bowel disease.Radiology.1999;211:203209.
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Journal of Hospital Medicine - 2(2)
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Journal of Hospital Medicine - 2(2)
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