Psychosomatics 48:446-447, September-October
doi: 10.1176/appi.psy.48.5.446
© 2007 Academy of Psychosomatic Medicine
Acute Endocarditis in a Patient With Severe Anorexia Nervosa and Autoaggressive Behavior
Frank Zimmermann-Viehoff, M.D.,
Cora Weber, M.D.,
Werner Köpp, M.D.,
Marcus Mannel, M.D., and
Hans-Christian Deter, M.D.
Received October 13, 2006; revised November 15, 2006; accepted November 28, 2006. From the Dept. of Psychosomatic Medicine and Psychotherapy, Charité Universitätsmedizin, Campus Benjamin Franklin, Berlin, Germany. Send correspondence and reprint requests to Frank Zimmermann, M.D., Charité Universitätsmedizin, Berlin, Psychosomatic Medicine, Hindenburgdamm 30 Berlin, Germany 14050. e-mail: frank.zimmermann{at}charite.de
© 2007 The Academy of Psychosomatic Medicine
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INTRODUCTION
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We present below the case of an anorexia nervosa (AN) patient in whom autoaggressive behavior, as well as decreased functioning of the immune system, contributed to the development of acute endocarditis of the mitral valve.
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Case Report
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The 33-year-old female patient was admitted to the Charité Campus Benjamin Franklin Hospital in August 2005 with severe malnutrition and electrolyte disturbances. AN, purging subtype, had been diagnosed when she was 20 years old on the basis of the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition.1 Her initial weight was 26.5 kg (58.4 lbs.) at a height of 168 cm (66.1 in.), the corresponding body mass index being 9.4 kg/m2. Laboratory results revealed decreased levels of potassium (2.7 mmol/liter [normal range: 3.4–5.2 mmol/liter]), sodium (126 mmol/L [normal range: 134–145 mmol/L]), and chloride (93 mmol/L [normal range: 95–112 mmol/L]), as well as an elevation of creatinine (1.12 mg/dL [normal: <1.0 mg/dL]). A slight increase in leukocyte count (11.2/nl [normal range: 4.5–11.0/nl]) and erythrocyte count (5.61/pl [normal range: 3.9–5.4/pl]) was probably due to dehydration. All other routine laboratory parameters, including cortisol levels, were in the normal range.
The physical examination showed extreme underweight, with discrete edema of the calves. Her abdomen was covered with multiple scars resulting from burns by hot-water bottles she had used to "relieve abdominal pain." Autodestructive behavior also comprised a massive abuse of laxatives (up to several hundred Bisacodyl tablets per day) and occasional self-induced vomiting.
The patient had been hospitalized six times between 1999 and 2002; these hospitalizations had included the delivery of nutrition via nasogastric tube.
Because the patient at this time refused to have a gastric tube or a percutaneous endoscopic gastrostomy because of a "bad experience" in the past, there was an indication for additional parenteral nutrition via central venous line. Five days after admission, the staff reported that the patient had been manipulating the infusion systems, which she retrospectively confirmed. Two days later, she displayed a single rise of temperature to 39.8°C (103.6°F). Laboratory results then showed an elevation of leukocytes (17.9/nl [normal range: 4.5–11.0/nl) and C-reactive protein (19.32 mg/dL [normal: <0.5 mg/dL). At the same time, a systolic cardiac murmur appeared. Staphylococcus aureus was later isolated from the blood cultures. The diagnosis of acute endocarditis was confirmed by transesophageal cardiac ultrasound, which also revealed a massive mitral regurgitation. The patient was immediately transferred to the Department of Cardiovascular Surgery, where an emergency reconstruction of the valve was performed. There were no postoperative complications. The patient was then transferred to our Psychosomatic Clinic, where she received combined somatic and psychotherapy. Antibiotic treatment was continued for 6 weeks. At discharge, 7 weeks after the intervention, the patient weighed 32.7 kg (72.1 lbs.; BMI: 11.6 kg/m2), and the cardiac ultrasound showed regular functioning of the reconstructed valve.
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Discussion
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AN is associated with the high mortality rate of 11%,2 with severe infections among the major causes of death.3,4 AN can be associated with relevant changes in immune functioning, such as elevation of cortisol levels5 and neutropenia.6,7 In the present case, blood count as well as cortisol levels were not significantly altered at the time of admission. However, a reduced granulocyte killing rate of Staphylococcus aureus, as previously reported,8 might have been present.
A rise in temperature initiated the investigations leading to the diagnosis of endocarditis. In this context, it must be kept in mind that fever may be absent in AN patients despite severe infection.9,10
Autodestructive tendencies in AN patients have been described previously.11,12 In a long-term follow-up of AN patients, lower self-destructive tendencies predicted good somatic outcome after 8 years.13 From all available data, the complication of endocarditis in our patient was very likely the result of the self-imposed trauma.
In conclusion, AN patients must be considered to be at increased risk for potentially fatal infections when undergoing infusion therapy because of possible immune suppression and/or self-manipulating tendencies. Furthermore, the diagnosis may be delayed because of the lack of a febrile response. We therefore suggest close monitoring of autoaggressive behavior and clinical signs of infection.
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REFERENCES
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- American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994
- Deter HC, Herzog W: Anorexia nervosa in a long-term perspective: results of The Heidelberg-Mannheim Study. Psychosom Med 1994; 56:20–27[Abstract/Free Full Text]
- Birmingham CL, Su J, Hlynski JA, et al: The mortality rate from anorexia nervosa. Int J Eat Disord 2005; 38:143–146[CrossRef][Medline]
- Zipfel S, Löwe B, Reas DL, et al: Long-term prognosis in anorexia nervosa: lessons from a 21-year follow-up study. Lancet 2000; 355:721–722[CrossRef][Medline]
- Limone P, Biglino A, Bottino F, et al: Evidence for a positive correlation between serum cortisol levels and IL-1 beta production by peripheral mononuclear cells in anorexia nervosa. J Endocrinol Invest 2000; 23:422–427[Medline]
- Lambert M, Hubert C, Depresseux G, et al: Hematological changes in anorexia nervosa are correlated with total body fat mass depletion. Int J Eat Disord 1997; 21:329–334[CrossRef][Medline]
- Devuyst O, Lambert M, Rodhain J, et al: Hematological changes and infectious complications in anorexia nervosa: a case-control study. Q J Med 1993; 86:791–799[Medline]
- Gotch FM, Spry CJ, Mowat AG, et al: Reversible granulocyte-killing defect in anorexia nervosa. Clin Exp Immunol 1975; 21:244–249[Medline]
- Brown RF, Bartrop R, Beaumont P, et al: Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord 2005; 37:261–265[CrossRef][Medline]
- Birmingham CL, Hodgson DM, Fung J, et al: Reduced febrile response to bacterial infection in anorexia nervosa patients. Int J Eat Disord 2003; 34:269–272[CrossRef][Medline]
- Fliege H, Burkert U, Danzer G, et al: Self-destructive behaviour: occurrence and typological classification in a university psychosomatic unit. Z Psychosom Med Psychother 2000; 46:286–303[Medline]
- Danzer G, Mulzer J, Weber G, et al: Advanced anorexia nervosa associated with pneumomediastinum, pneumothorax, and soft-tissue emphysema without esophageal lesion. Int J Eat Disord 2005; 38:281–284[CrossRef][Medline]
- Deter HC, Schellberg D, Kopp W, et al: Predictability of a favourable outcome in anorexia nervosa. Eur Psychiatry 2005; 20:165–172[CrossRef][Medline]
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INTRODUCTION
Case Report
