Chronic thromboembolic disease in a 43-year-old man.

Case Report A 43-year-old man was admitted to the hospital complaining of nonproductive cough, progressive shortness of breath, increasing dyspnea on exertion, and fatigue of approximately 3 months’ duration. The patient stated he could no longer walk without shortness of breath. He denied syncope, lightheadedness, palpitations, chest pain, wheezing, hemoptysis, fever, weight change, or night sweats. Other than having the sickle cell trait, the patient related no additional medical or surgical history. He had never smoked tobacco and denied use of alcohol. One month earlier he returned from reserve military duty, where he had served for 8 months as an F-14 naval flight officer. While flying, the patient was exposed to immobility and excess gravitational forces. At the time of admission he was a full-time student. His family history was notable for hypertension. He had no known drug or food allergies and was not taking any medications, herbal supplements, or vitamins. The patient was visibly short of breath walking into the Emergency Department. His temperature was 99.1°F, heart rate 93 beats per minute, respiratory rate 20/min, blood pressure 130/92 mm Hg, and oxygen saturation 89% on room air. His oxygen saturation increased to 98% on 4 L of oxygen while using a nasal cannula. Findings during the patient’s physical examination were normal, except during the cardiac examination. He had a regular rate and rhythm, with a fixed, split S2, and a prominent pulmonary component (P2). There was no murmur or gallop. Stool was negative for occult blood. There were no palpable cords in the lower extremities, and there was no lower extremity edema. Arterial blood gas on room air was pH 7.441, PaCO2 32 mm Hg, PaO2 67 mm Hg, bicarbonate 21.3 mEq/L, and a base excess of 1.7, findings consistent with chronic respiratory alkalosis and metabolic compensation. The alveolar-arterial gradient was 42 mm Hg. His chest radiograph showed prominent right central pulmonary arteries, but was otherwise unremarkable, and there was no evidence of effusion, infiltrate, or pneumothorax. An electrocardiogram showed a normal sinus rhythm at 79 beats per minute, and there were inverted T waves in leads II, III, aVF, and V1 through V5, consistent with right heart strain. A ventilation-perfusion scan showed multiple, bilateral, moderate-to-large, segmental, mismatched perfusion defects and was read as high probability for pulmonary embolus. A sonogram of the lower extremities showed extensive chronic intraluminal thrombi in the left superficial femoral and proximal popliteal veins and collateralization by the left superficial vein. The right lower extremity had no thrombi. An echocardiogram showed severe pulmonary hypertension with right ventricular pressure overload findings and right ventricular hypokinesis. The estimated systolic pulmonary artery pressure was 92 mm Hg (normal 14–30 mm Hg). The right atrium and right ventricle were enlarged, and the intraatrial septum was bulging into the left atrium. Severe pulmonary arterial hypertension was evident on a pulmonary angiogram, with pulmonary arterial pressures reaching 87/33 mm Hg (mean of 52 mm Hg) at their highest levels. There were Submitted, revised, 26 December 2001. From the Family Practice Residency Training Program (LASM) and Department of Pulmonary Medicine (RDM), Naval Hospital Pensacola, Pensacola, Fla. Address reprint requests to Commanding Officer, Code 55, Lee A. SavoiaMcHugh, MD, Family Practice Residency Training Program, Naval Hospital Pensacola, 6000 Highway 98 West, Pensacola, FL 32512. The opinions presented in this article represent those of the authors and do not represent the opinions of the United States Navy.