Psychosomatics 45:364-365, August 2004
© 2004 The Academy of Psychosomatic Medicine
Severe Depression, Obsessive-Compulsive Disorder, and Pulmonary Embolism
Daniel A. Llano, M.D., Ph.D., and
Robert S. Abernethy, III, M.D., Boston, Mass.
Key Words: OCD • depression • other personality disorder
TO THE EDITOR: The relationship between depression and coronary artery disease has been well described.1,2 Data suggest that this may be due, in part, to disordered platelet biology in depressed patients.3,4 However, to our knowledge, a database describing the incidence of pulmonary emboli in depressed patients, although case reports do exist.5 Depressed, inactive patients would appear to be at significant risk for pulmonary embolism, given their lack of activity and putative platelet pathology. We report the case of a patient with longstanding severe depression who presented with bilateral pulmonary emboli without risk factors other than his depression and inactivity.
Case Report
Mr. A was a 52-year-old man with a longstanding history of major depressive disorder, obsessive-compulsive disorder, and obsessive-compulsive personality disorder. His psychiatric history included one hospitalization 2 years before for treatment of a profound amotivational state with ECT. His response to ECT was initially positive, and he was able to obtain and hold a desk job thereafter. However, while not at work, he reported that he spent almost all of his time in bed, sleeping and watching television. Weekends were spent completely in bed, without exception for personal hygiene. This behavioral pattern had existed for approximately 1 year. Mr. A had no history of psychosis or mutism. His current medication regimen consisted of oral citalopram, 60 mg/day, oral risperidone, 2 mg at bedtime, and oral clonazepam, 1 mg b.i.d. as needed. Mr. A had no history of nonpsychiatric disease and had no family history of hypercoagulopathy. He had no history of smoking.
Mr. A came to our medical service with a history of sudden onset of severe shortness of breath and right-sided pleuritic pain. A physical examination revealed a nonobese man with bibasilar rales but no other evidence of heart failure. An early workup revealed low arterial oxygen saturation, a D-dimer of greater than 1000 ng/ml (reference range <500 ng/ml) and bilateral pulmonary emboli by both a computerized tomography (CT) angiogram and a ventilation/perfusion scan. An ultrasound investigation did not reveal thrombi in the lower extremities. Because Mr. A had no apparent risk factors for pulmonary emboli, a workup for potential causes was performed. A series of biochemical markers for hypercoagulable states, including homocysteine, antithrombin III, protein C, protein S, anticardiolipin antibody, lupus anticoagulant, factor V Leiden mutation, and prothrombin gene mutation G20210A, were obtained. All values were found to be normal, with the exception of a slightly decreased protein S value (66%; reference range=70%–140%). The possibility of colonic malignancy was investigated by means of a colonoscopy, which revealed a single benign polyp. A CT of the abdomen and pelvis revealed two small hypodense areas in the liver, which were subsequently found to be consistent with benign hemangiomata per ultrasound; no other abnormalities were found. Prostate-specific antigen was found to be 1.6 ng/ml (normal=0–4.0 ng/ml). Blood and urine cultures were negative. Mr. A was treated with intravenous heparin and supportive oxygen therapy. His oxygenation status improved over the next 5–7 days, and he was transitioned from heparin-based anticoagulation to coumadin and discharged to the psychiatric service for treatment of his behavioral decompensation.
Discussion
This scenario illustrates the case of a patient with multiple pulmonary emboli without any recognized risk factors other than the patient's profound inactivity and subsequent venous stasis. His hypercoagulability panel did reveal a slightly decreased protein S value, which is often seen as an artifact of elevated factor VIII. (In this patient, the value was 225% [reference range=50%–200%], which is an acute phase reactant and was likely elevated secondary to this patient's multiple pulmonary emboli.6) This is supported by the patient's elevated fibrinogen (812 mg/dl; reference range=150–400 mg/dl), another acute phase reactant. A convalescent serum level was not available for comparison since the patient was placed on long-term coumadin therapy. No malignancy was found with either age-appropriate testing or with additional examination of the abdomen and pelvis with a CT scan. We submit that the patient's severely maladaptive behavioral pattern was the principal factor predisposing him to the formation of a deep-venous thrombus and ultimately to a pulmonary embolus.
There is increasing epidemiological evidence that depressive disorder is an independent risk factor for coronary artery disease,1,2 and recent studies have demonstrated that platelets in depressed patients are hyperaggregable.3,4 In addition, it has been shown that catatonia is a risk factor the development of pulmonary emboli.7,8 However, to our knowledge, there have been no large-scale reports describing the development of pulmonary emboli in noncatatonic but severely anhedonic patients. This case, combined with the evolving view of depression as a systemic illness involving hematological pathology3,4 and the high prevalence of this disease, suggests that a systematic study of the incidence of pulmonary emboli in depressed patients would have clinical impact. Furthermore, for patients such as the one described here, aggressive intervention to reverse the anhedonic state should be implemented to prevent life-threatening complications. In refractory cases, prophylactic use of heparin or heparinoids may be useful.
REFERENCES
- Musselman D, Evans D, Nemeroff C: The relationship of depression to cardiovascular disease: epidemiology, biology and treatment. Arch Gen Psychiatry 1998; 55:580–592[Abstract/Free Full Text]
- Glassman A, Shapiro P: Depression and the course of coronary artery disease. Am J Psychiatry 1998; 155:4–11[Abstract/Free Full Text]
- Lederbogen F, Gilles M, Maras A, Hamann B, Colla M, Heuser I, Dueschle M: Increased platelet aggregability in major depression? Psychiatry Res 2001; 102:255–261[CrossRef][Medline]
- Musselman DL, Tomer A, Manatunga AK, Knight BT, Porter MR, Kasey S, Marzee U, Harker LA, Nemeroff CB: Exaggerated platelet reactivity in major depression. Am J Psychiatry 1996; 153:1313–1317[Abstract/Free Full Text]
- Arnone D, Hansen L, Davies G: Pulmonary embolism and severe depression. Am J Psychiatry 2002; 159:873–874[Free Full Text]
- Van Cott EM, Laposata M: Laboratory evaluation of hypercoagulable states. Hematology/Oncology Clin North Am 1998; 12:1141–1166
- McCall WV, Mann SC, Shelp FE, Caroff SN: Fatal pulmonary embolism in the catatonic syndrome: two case reports and a literature review. J Clin Psychiatry 1995; 56:21–25[Medline]
- Regestein QR, Alpert JS, Reich P: Sudden catatonic stupor with disastrous outcome. JAMA 1977; 238:618–620[Abstract]
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