Unilateral Pulmonary Edema

Unilateral Pulmonary Edema

7 Rochester DF, Braun NMT, Laine S. Diaphra~atic ener~ expenditure in chronic respiratory. failure: the effect of assisted ventilation with body venti...

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7 Rochester DF, Braun NMT, Laine S. Diaphra~atic ener~ expenditure in chronic respiratory. failure: the effect of assisted ventilation with body ventilators. Am J Med 1977; 63:223-32 8 Delaubier A. Traitement de l'insuffisance respiratoire chronique dans les dystrophies musculaires. In: Memoires de certficat d'etudes superieures de reeducation et readaptation fonctionelles. Paris: Universite R. Descartes, 1984:1-124 9 Kerby GR, Mayer LS, Pingleton SK. Nocturnal positive pressure ventilation via nasal mask. Am Rev Respir Dis 1987; 135:738-40 10 Bach JR, Alba A, Mosher R, Delaubier A. Intermittent positive pressure ventilation via nasal access in the management of respiratory insufficiency. Chest 1987; 92:168-70 II Carrey Z, Gottfried SB, Levy RD. Ventilatory muscle support in respiratory failure with nasal positive pressure ventilation. Chest 1990; 97:150-58 12 Gay P, Viggiano R, Edell E, Staats B. Treatment ofcomplications from intermittent nasal ventilation for neuromuscular disease and hypercarbic respiratory failure. Chest 1989; 96: 173S 13 Bach JR, Alba AS. Management of chronic alveolar hypoventilation by nasal ventilation. Chest 1990; 97:52-7 14 Bach JR, Alba AS, Shin D. Management alternatives for postpolio respiratory insufficiency: assisted ventilation by nasal or oral-nasal interface. Am J Phys Med Rehab 1989; 68:264-71 15 Bach JR, Alba AS. Noninvasive options for ventilatory support of the traumatic high level quadriplewc patient. Chest 1990; 98:613-19

Unilateral Pulmonary Edema* An Unusual Cause Steven E Kagele, M.D.; and Nirmal B. Charan, M.D., EC.C.P.

A patient presented with shortness of breath without fever, cough or sputum production. The patient was hypoxic without leukocytosis and a chest x-ray 6lm demonstrated a right unilateral pulmonary in6ltrate. A chest CT showed a large ascending thoracic aortic aneurysm with dissection. During surgical repair, the aneurysm was noted to be compressing the single right pulmonary vein. The in6ltrate resolved postoperatively, and the patient has remained symptom-free for one year. (Chellt 1992; 102:1279-80)



FICURE 1. Cbest x-ray film demonstmting sternal wires fnlm previous (.'()ronary surgery and a diffuse right-sided interstitial infiltrate. cough. He denied orthopnea, paroxysmal nocturnal dyspnea, chest pain, leg swelling, fever, chills, hemoptysis, rash and night sweats. He was retired and traveled extensively in his motor home throughout the Southwest, Northwest and Central United States. Symptoms were more pnmounced the weekend before admission while tbe patient was camping at 8,000 feet elevation. He had a history of myocardial infarction with congestive heart failure and had a threevessel coronary artery bypass in 1971. Initial vital signs showed temperature of 37°C, respiratory rate of 35 breaths per minute, blood pressure of 120160 mm Hg and a regular heart rate of 65 beats per minute. Oral mucosa was moist and there was no jugular venous distention. Lung fields were clear. Heart examination revealed a grade 216 systolic ejection murmur at the upper left sternal border without any gallop. A chest x-ray film showed a diffuse right-sided pulmonary infiltrate without cardiomegaly, masses or pleural effusions (Fig I). Laboratory examination showed a white blood cell count of 9,500 cells/dl, with a normal differential <:ell count, a bematocrit value of 39 and a normal platelet count. A room air arterial blood gas value analysis showed pH to be 7.46; PaCO" 33 mm Hg; PaO" 56 mm Hg; SaO" 90 percent. Prior to admission, his room air PaO, was 75 mm Hg. Cold agglutinins and

=direct fluorescent antibody

presentation ofpulmonary edema, though well U nilateral known to occur, is an uncommon entity. While it most

commonly occurs in patients with cardiac decompensation who are in a dependent position, it is also recognized in those who have either a unilateral perfusion defect or in conditions affecting the vascular permeability of one lung only. We present here an unusual case of unilateral pulmonary edema via a mechanism that has not been described previously. CASE REPORT

A 76-year-old man presented with a two-week history of progressive shortness of breath, dyspnea on exertion, and a nonproductive *From the Division of Pulmonary and Critical Care Medicine, Department of Medicine, Division of Pulmonary and Critical Care Medicine, VA Medical Center, Boise, Idaho, and University of Washington, Seattle.

FICURE 2. Patient's chest CT scan demonstrating the large ascending aortic aneurysm adjacent to the right pulmonary artery with ('~lmpression of the superior vena cava. CHEST I 102 I 4 I OCTOBER, 1992


Legionella DFA were negative. A ventilation-perfusion scan was low probability for pulmonary embolus, and Dco performed within 48 h of admission was within the normal ran~e and unchanged from the patient's previous values. An echocardiogram showed normal left ventricular function. Results ofbronchos<..'Opy and transbronchial biopsies were normal. The patient be~an receiving intravenously administered erythromycin initially, but this was stopped after 24 h. He then be~an re<..-eiving oxygen by nasal cannula and activity was restricted to bed rest. The chest x-ray film partially resolved over one week and the patient was discharged with a room air Pa0 2 level of 62 mm Hg. Fhllow-up two days later showed continued resolution of the infiltrate. He returned two weeks later with similar complaints, except this time he also <..'omplained of constant substernal chest pain not related to exercise. Vital signs were normal. He had 8 cm jugular venous distension without distinct venous pulsation, and chest examination revealed rales half way up the right side only. No gallop was detected. The chest x-ray film showed the return of the diffuse ri~ht-sided infiltrate. A chest CT showed an ascending thoracic aneurysm with dissection (Fi~ 2) and compression of the superior vena cava. An angio~ram confirmed dissection and a thora<..'Otomy was performed, where a lar~e ascending thoracic aortic aneurysm was noted to be severely compressing the patient's single right pulmonary vein. The aneurysm was repaired, and the patient's subsequent chest x-ray film showed complete clearin~ of the right-sided infiltrate. He has been asymptomatic for one year postoperatively and chest x-ray films have remained normal. DISCUSSION

Unilateral pulmonary edema often is confused with other unilateral alveolar or interstitial infiltrates. Calenoff et all divided the known causes of unilateral pulmonary edema into two groups: those associated with ipsilateral edema and those associated with contralateral edema. The ipsilateral conditions usually are due to acute alterations in components of the alveolar-capillary membrane in one lung only. These include congenital heart disease with systemic-to-pulmonary artery shunts~ bronchial obstructions, unilateral venoocclusive disease, prolonged lateral decubitus position~ unilateral aspiration, pulmonary contusion, unilateral infusion of hypotonic saline solution via a catheter misplaced in the pulmonary artery, and rapid thoracentesis of pleural fluid or air. The patient described here had no hydrothorax or pneumothorax, no invasive catheters and no clinical history consistent with the other disorders just mentioned. Contralateral pulmonary edema refers to edema occurrin~ on the side opposite a lun~ with a perfusion defect; the lung that is not perfused adequately does not become edematous. These disorders include cardiac decompensation in the face of a large unilateral pulmonary embolism, congenital absence or hypoplasia of the pulmonary artery, Swyer-James syndrome, localized emphysema and previous lobectomy (where the remaining lun~ becomes emphysematous in compensation). Pulmonary edema after reexpansion of a pneumothorax can occur on the ipsilateral side as mentioned previously, but can also occur on the contralateral side in patients with left heart failure, presumably secondary to temporary compromise of perfusion of the collapsed lun~ from increased pulmonary vascular resistance. 2 Preexisting pleural fluid also may cause unilateral edema, since lung compression by fluid has decreased perfusion, and when left heart failure occurs the poorly perfused lung remains unaffected. 1280

Position may lead to unilateral pulmonary edema in left heart failure since the dependent portion of the lung receives most of the blood flow and increase in the hydrostatic pressures..1 Unilateral pulmonary edema of neurogenic origin also has been described, and also \\'as thought to he secondary to prolonged lateral decubitus position. ~ Other causes of unilateral pulmonary edema include ruptured aneurysm of the sinus of Valsalva5 and from an expanding aneurysm of the pulmonary artery that unilaterally cornpressed the pulmonary veins. fi The patient described here had a history of coronary artery disease and con~estive heart failure at the time of his previous myocardial infarction, but had no history of a prolonged lateral decubitus position. He had no history of paroxysmal nocturnal dyspnea or orthopnea suggestive of significant left ventricular dysfunction. We postulate that the most probable mechanism of his unilateral pulmonary edema was increased right-sided pulmonary venous pressures caused hy the aneurysm ~ resulting in high intravascular hydrostatic pressures. The resolution during the first hospitalization was not entirely clear~ hut may he related to oxygen therapy and bed rest. We postulate that the aneurysm expanded between the first and second admission. This expansion resulted in compression of the superior vena cava, as seen on CT scan, leading to the jugular venous distention noted during the second adrnission. llis chest pain during this admission also is consistent \\'ith aneurysrnal expansion. The worsening of his symptorns \vhile campin~ at 8,000 feet may be related to hypoxia from high altitude. It is surprising that the patient did not have more hypoxia at presentation in vie\\' of the extensive unilateral nature of the infiltrate. This may have been due to the some\\rhat long-standing nature of the unilateral edenla which rnay have allowed for improved ventilation-perfusion Inatching and decreased shunt. This may b{~ a clinical feature \\rhich could be utilized to differentiate this cause of pulmonary edema from some of the other more acute causes discussed hefi)re. We believe this is the first reported case of unilateral pulmonary edema due to pulmonary venous conlpression by a thoracic aortic aneurysrn. REFERENCES 1 Calenoff L, Kruglik GO, \Voodruff A. Unilateral pulrnonary edema. Radiology 1978: 126: 19-24 2 Steckel RJ. Unilateral pulmonary eclenla after pneumothorax. N Engl J Med 1973; 289:621-22 3 ~1eerhaeghe A van. Unilateral pulrnonary ederna seeondary to left heart failure. Respiration 1981; 42:67-70 4 Goff N\V Jr, \Veese \VC. A ease of unilateral neurogenic pulmonary edema. Ariz Med 1981: 3R:8.12-33 .5 Harari A, Hazan E, (;eshwind II, de Langenhagt»n B. Acute unilateral pulnlonary edema as the first sign of a nlptured aneurysm of the sinus of Valsalva. NOHV Presse ~1ed 1973; 2:1773-


6 Dremser C, Cajulis R, Glagov S. Pulrnonary vein and superior vena eava ohstruetion due to expanding aneurysnl of the pulmonary artery. Chest 1988; 93:206-07 Unilateral Pulmonary Edema (Kagele. Charan)