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(Chest. 1999;116:1478-1480.)
© 1999 American College of Chest Physicians

Painless Left Hemorrhagic Pleural Effusion*

An Unusual Presentation of Dissecting Ascending Aortic Aneurysm

Stephen Little, MD; John Johnson, MD, FCCP; Be-Yung Moon, MD and Sanjay Mehta, MD

* From the Division of Respirology, Department of Medicine (Drs. Little, Johnson, and Mehta), and the Department of Cardiovascular Surgery (Dr. Moon), London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada.

Correspondence to: Sanjay Mehta, MD, Division of Respirology, London Health Sciences Centre, Victoria South St Campus, 375 South St, London, Ontario, Canada, N6A 4G5, e-mail: sanjay.mehta{at}lhsc.on.ca


   Abstract
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 Abstract
Introduction
 Case Report
 Discussion
 References
 
Aortic dissection is a catastrophic event that is commonly associated with severe pain, massive hemorrhage, and high mortality. In this report, we present the case of a 31-year-old man who presented with painless, hemorrhagic left pleural effusion. Further investigation revealed a 9-cm dissecting ascending aortic aneurysm that was thought to be due to a congenitally bicuspid aortic valve. We suggest that ascending aortic aneurysm be included in the differential diagnosis of hemorrhagic pleural effusion, even in the absence of the classic features of aortic dissection, such as chest pain, advanced age, or history of hypertension.

Key Words: aortic aneurysm • aortic dissection • bicuspid aortic valve • hemorrhagic effusion • pleural effusion


   Introduction
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 Abstract
 Introduction
Case Report
 Discussion
 References
 
A hemorrhagic pleural effusion is an important but uncommon clinical problem that is often due to a serious underlying illness. The differential diagnosis includes traumatic injury to the heart, great vessels, or chest wall; pleuropulmonary malignancy; tuberculosis; pulmonary thromboembolic disease; subphrenic disease, such as splenic injury; a hemorrhagic diathesis; and a dissecting aneurysm of the descending aorta. Aortic dissection is an uncommon, catastrophic event that is characterized by dissection of blood along the laminar planes of the aortic media, with the formation of a blood-filled channel within the aortic wall. Rupture of this channel typically causes massive hemorrhage and has been associated with a mortality rate > 50%.1 2 A complete breach of the arterial wall may lead to formation of a contained, perivascular hematoma, termed a pseudoaneurysm.


   Case Report
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 Abstract
 Introduction
 Case Report
Discussion
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A 31-year-old white man was referred to the Division of Respirology admitting service with a presumptive diagnosis of aspiration pneumonia and a parapneumonic effusion. He had been well until 5 weeks previously, when he experienced a single, witnessed, generalized seizure. Over the past 3 weeks, he had developed fatigue, intermittent chills, and new onset dyspnea on moderate exertion. The patient denied any cough, sputum, hemoptysis, chest pain, abdominal discomfort, fevers, weight loss, IV drug use, high-risk sexual activity, travel, trauma, or risk factors for pulmonary thromboembolism. He had a 15-pack-year smoking history and consumed 1 to 2 oz of alcohol per week.

On physical examination, the patient appeared pale. Vital signs were as follows: BP, 120/80 mm Hg in both arms, with no postural change; heart rate, 90 beats/min and regular; respiratory rate, 18 breaths/min; and temperature, 36.5°C. In the chest, there was dullness to percussion and diminished breath sounds at the left base. The patient had a normal apex beat and heart sounds, with no murmurs or pericardial rub detected. Jugular venous pressure was 4 cm above the sternal angle, and no peripheral edema was noted. Peripheral pulses were symmetrical. Abdominal, musculoskeletal, and neurologic examination findings were unremarkable.

Initial laboratory investigations revealed a normochromic and normocytic anemia with a hemoglobin content of 10.8 g/100 mL; WBC count, 7,700/µL (7.7 x 109/L); platelets, 566,000/µL (566 x 109/L); international normalized ratio, 1.3; and partial thromboplastin time, 33 s (control, 30 s). Electrolytes and renal function were normal. An arterialized capillary blood gas sample while breathing ambient air revealed pH of 7.47; PaO2, 67 mm Hg; PaCO2, 33 mm Hg; and HCO3, 24 mEq/L. An ECG was normal. Chest radiograph revealed a moderate-sized left pleural effusion and a prominent convexity along the right mediastinal border (Fig 1 ). A left thoracentesis revealed thin, grossly hemorrhagic, reddish-brown pleural fluid that did not clot, did not clear on sequential samples, and had no obvious odor. Fluid chemistry findings included the following: lactate dehydrogenase, 187 U/L (serum lactate dehydrogenase, 130 U/L); protein, 4.5 g/100 mL (serum protein, 7.1 g/100 mL); and pH, 7.44. A manual cell count revealed the following: nucleated cells, 2,700/µL; and RBC count, "too many to count" (> 1.5 to 2.0 x 106/µL [RBC count normal range, 4.5 to 6.0 x 106/µL]). No organisms were identified on Gram’s stain or culture, nor were malignant cells identified by cytology.



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  		Figure 1. Posteroanterior radiograph of the chest revealed a moderate-sized left pleural effusion and a prominent convexity along the right mediastinal border.

 
The patient was admitted for monitoring and further imaging of the prominent right mediastinal border using CT while IV antibiotics were continued. The next day, the patient’s symptoms were unchanged; however, hemoglobin content had decreased to 8.5 g/100 mL. On physical examination, a new, grade 4/6 diastolic decrescendo murmur was noted at the left sternal border. An urgent thoracic aortogram revealed a 9-cm-diameter ascending aortic aneurysm that extended to the origin of the right brachiocephalic artery and was associated with moderate aortic regurgitation due to dilation of the aortic annulus (Fig 2 ). There was also a 3 x 8-cm ovoid collection at the anteromedial border of the ascending aorta that communicated freely with the aortic lumen, consistent with a pseudoaneurysm. Transesophageal echocardiography demonstrated dissection of the ascending aorta with a tented intimal flap, confirmed the aortic regurgitation, and also demonstrated a moderate-sized pericardial collection and a congenitally bicuspid aortic valve.



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  		Figure 2. Thoracic aortogram showed a large (9 cm) ascending aortic aneurysm tapering at the level of the right brachiocephalic artery. Anteromedially to the left of the ascending aorta, a 3 x 8-cm ovoid density that communicated freely with the aortic lumen was noted, consistent with a pseudoaneurysm or localized mediastinal collection (arrow). There was moderate aortic regurgitation with filling of the left ventricle.

 
The patient underwent an urgent modified Bentol procedure involving prosthetic replacement of both the bicuspid aortic valve and the ascending aorta. The patient’s postoperative course was unremarkable, and he remains well 18 months later. Histopathologic examination of the ascending aortic aneurysm showed degenerative changes, complicated atherosclerosis, and superimposed blood clot. There was no evidence of mural inflammation, granulomas, or cystic medial necrosis. The venereal disease research laboratory serology finding was subsequently negative.


   Discussion
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 Abstract
 Introduction
 Case Report
 Discussion
References
 
In patients who survive the initial tear, the typical presentation of aortic dissection is that of severe, "tearing"-type pain, either in the anterior chest, which is suggestive of an ascending aortic dissection, or in the posterior chest or back, which is suggestive of a descending aortic dissection. The pain may radiate anywhere in the thorax or abdomen, and the initial differential diagnosis is often extensive. In one large series of 236 cases of aortic dissection, the most common symptom for all types of dissection was pain, most often severe. Of the 33 patients (15%) who presented with painless aortic dissection, congestive heart failure, stroke, and syncope were the next most common presentations.3

Aortic dissection commonly occurs in two groups of patients. The first group consists principally of older hypertensive men, in whom painful dissection of the descending aorta is by far the most common presentation.1 3 The second major subgroup consists of patients with a systemic or localized abnormality of aortic connective tissue. In these typically younger patients, predisposing factors include aortic coarctation, a bicuspid aortic valve, and disorders of collagen, including Marfan’s syndrome, Ehlers-Danlos syndrome, and degeneration of the aortic media.4 In the aforementioned case series, bicuspid aortic valve was uncommon, being diagnosed in 7% by echocardiography, intraoperatively or by postmortem examination, but was the second most common predisposing factor after hypertension (78%).3

A hemorrhagic left pleural effusion as the presenting feature of aortic dissection has been reported, but only in the context of descending aortic dissection.5 A review of the English language literature using MEDLINE and manual journal searches did not uncover any similar reports of an association of a left hemorrhagic pleural effusion with painless ascending aortic dissecting aneurysm. The presence of a left hemorrhagic effusion in the present report is most likely related to the localized para-aortic, anterior mediastinal pseudoaneurysmal collection and resulting leak into the adjacent left pleural space. Although this type of presentation of ascending aortic dissection is decidedly rare, the risk factor of a bicuspid aortic valve is not rare. Bicuspid aortic valve is the most frequent congenital cardiac malformation and is present in approximately 1 to 2% of the North-American population.6

Although it is not possible to definitively link the history of the recent seizure to the evolving aortic dissection, the association is highly probable, given previous reports of syncope and stroke with aortic dissection.3 Furthermore, the advanced degree of aortic atherosclerosis and mural thrombosis noted on histologic examination suggests that the seizure was likely due to a cerebral embolic event.

In summary, this case highlights the notoriously variable clinical presentation of a potentially disastrous condition, dissecting aortic aneurysm. We suggest that aortic dissection be included in the differential diagnosis of painless, hemorrhagic pleural effusion, even in the absence of hypertension and advanced age.

Received for publication March 22, 1999. Accepted for publication June 10, 1999.


   References
TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Hirst, AE, Jr, Johns, VJ, Kime, SW, Jr (1958) Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 37,217-279[Medline]
  2. McCloy, RM, Spittell, JA, Jr, McGoon, DC (1965) The prognosis in aortic dissection (dissecting aortic hematoma or aneurysm). Circulation 31,665-669[Abstract/Free Full Text]
  3. Spittell, PC, Spittell, JA, Jr, Joyce, JW, et al (1993) Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990). Mayo Clin Proc 68,642-651[ISI][Medline]
  4. Larson, EM, Edwards, WD (1984) Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 53,849-855[CrossRef][ISI][Medline]
  5. Gandelman, G, Barzilay, N, Krupsky, M, et al (1994) Left pleural hemorrhagic effusion: a presenting sign of thoracic aortic dissecting aneurysm. Chest 106,636-638[Abstract/Free Full Text]
  6. Nugent, EW, Plauth, WH, Edwards, JE, et al (1990) Congenital heart disease. Hurst, JW Schlant, RC Rackley, CEet al eds. The heart 7th ed. ,655-794 McGraw-Hill New York, NY.



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