Hemothorax

D. S. Green, MD and D. K. Payne, MD, FCCP--Division of Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, Shreveport, LA

Introduction: Hemothorax is most commonly caused by trauma or iatrogenic causes. Nontraumatic spontaneous etiologies include pulmonary embolus, thoracic aorta aneurysm rupture, bleeding disorders, and pulmonary arteriovenous malformations (AVMs). We describe the occurrence of a spontaneous hemothorax in an obstetric patient due to ruptured pulmonary AVMs.

Case Presentation: A nineteen year-old gravid female in her 3rd trimester presented to an outlying hospital with the acute onset of shortness of breath and left-sided pleuritic chest pain. She denied hemoptysis, fever, trauma, or history of blood clots in her or her family. Her past obstetrical history was unremarkable except for one spontaneous abortion. She had one episode of vaginal bleeding which resolved spontaneously and had been placed on bed rest for the past 4 weeks for premature labor. Physical exam at the outlying hospital was remarkable for tachypnea and absent breath sounds in her left lung field. Pertinent labs included a leukocyte count of 23,000, hematocrit of 27%, hemoglobin of 11 gm/dl, platelet count of 140,000, and a prothrombin time of 11.8 seconds. A room-air arterial blood gas showed a pH of 7.43, pCO2 of 31 mm Hg, and a pO2 of 71 mm Hg. A chest x-ray revealed a moderate-sized left pleural effusion, a normal heart size, and no other significant abnormalities. A perfusion scan obtained at the outlying hospital was interpreted as high-probability for a pulmonary embolus. The patient was placed on intravenous heparin for a presumptive pulmonary embolus and transferred to Louisiana State University Hospital in Shreveport for further management. On arrival, a lower extremity doppler ultrasound was performed and revealed no evidence of deep venous thrombosis. A spiral computed tomography of her chest demonstrated a large left pleural effusion with compression atelectasis of her left lower lobe, but no obvious pulmonary embolus. A family history revealed that her mother and maternal relatives had the diagnosis of Osler-Weber-Rendu syndrome. Her mother reported episodes of hemoptysis and epistaxis. Because of the pertinent family history, heparin was stopped and the pulmonary service was consulted. The patient's vital signs included a respiratory rate of 20/minute, blood pressure of 123/72, pulse of 100/minute, and a temperature of 99 [degrees] F. Fetal heart tones were 120/minute. Her cardiac exam revealed tachycardia without murmurs or gallops. Her lung exam revealed absent breath sounds in her left posterior lung fields with dullness to percussion. Her extremities revealed no clubbing, cyanosis, edema, and no calf or thigh tenderness. Her skin was remarkable for the presence of telangiectasias on both upper extremities and her lower lip. A thoracentesis was performed and revealed a grossly bloody effusion that had a total nucleated cell count of 7700/cc and a red blood cell count of 3.7 million/cc. Cultures and smears for bacteria, tuberculosis, and fungi were negative. A hematocrit obtained on the pleural fluid was 35%, consistent with a hemothorax. A total of 1 liter of bloody fluid was removed. Approximately 6 hours after the thoracentesis, the patient became extremely dyspneic. A chest x-ray revealed opacification of her entire left lung. A chest tube was placed and immediately drained 1.5 liters of bloody fluid. A C-section was performed with the delivery of a 6-pound boy. Following delivery, a pulmonary arteriogram was obtained and revealed the presence of multiple large pulmonary parenchymal arteriovenous malformations in the left lung. They were not felt to be amenable to embolization because of their large size. Her right lung revealed no vascular malformations. Subsequently, the patient underwent a left lower-lobe lobectomy and lingular segmentectomy.

Discussion: Osler-Weber-Rendu syndrome is an autosomal dominant syndrome characterized by mucocutaneous telangiectasias, central nervous system vascular malformations, and pulmonary AVMs. The incidence is approximately 1 to 2 per 100,000 people. Pulmonary AVMs can increase in size during pregnancy due to increased blood volume. Rupture into the pleural space may result in a spontaneous hemothorax, such as occurred in this patient.

Conclusion: Pulmonary AVMs are a rare cause of hemothorax. Although rare, a spontaneous hemothorax in an obstetric patient may be due to a ruptured pulmonary AVM, especially in a patient with Osler-Weber-Rendu syndrome.

COPYRIGHT 2000 American College of Chest Physicians
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