Acute localised pulmonary oedema

Abstract

Foucart ( 1875) and Ortncr (1899) were the first to describe pulmonary ocdcina as a complication of drainage of hydrothoraces. Subsequently. others reported a similar complication after the treatment of pneumothoraces.' , L Acute unilateral pulmonary oedema was also described in a case which occurred in the operating room at the end of thoracotomy and pleurodesis for recurrent pneumothorax from a lung cyst..' Our case is the l i n t report in the literature of localised pulmonary oedema which developed immediately after the surgical repair of a ruptured hemidiaphrapi. Case historyA 23-year-old man was admitted to hospital after a road traffic accident. He had multiple bilateral rib fractures with ;I right haemothorax, and a traumatic rupture of the right hcinidiaphragm with herniation of the liver into the pleural caviry which resulted in right lung collapse (Fig. 1). He also sustained fracturcs of the 12th thoracic, Ist, 4th and 5th lumbar vertebrae. which were associated with paraplegia. There was no evidence of head injury.He was resuscitated successfully and the haeniothorax \ q x cv;icuated by B right thoracostomy. Six days later he wiis transferred to our hospital for thoracotorny and rcpair of thc ruptured right hemidiaphragm: these procedures wcre performed 14 days after the iii.jury. The right lung tlui-ing the operation wits found to be about 609' " compressed by thc liver and transverse colon, and requircd manual re-infation with positive pressure ventilation after thc surgical repair of the ruptured diaphragm. The lung looked normal after complete re-expansion with no evidence of contusion. An underwater seal chest drain was inserted postoperatively and w a s allowed to drain passively.The patient's lungs were ventilated electively in the intensive care unit after the operation. His condition deteriorated suddenly less than one hour after operation. He became sweaty, restless. tachypnoeic and hypotcnsive. and copious amounts of slightly blood-stained frothy sputum were aspirated from thc trachea. A chcst X ray (Fig. 3 ) showed pulmonary ocdcnia in the right lowcr and middle lobes. Blood gas analysis showed a pH of 7.2. arterial carbon dioxide tcnsion of 8.3 kPa and arterial oxygen tension of 6.5 kPa with an inspircd oxygen concentralion of 60%. Ventilation improved with positivc end-expiratory pressure (PEEP) of + 1 kPa and muscle paralysis. Central vcnous pressure was 10 cmH20.Fluids were transfused and inotropic support started. Thc ocdcma fluid from the tracheal tube iinmediatel!. turned yellow. the colour of tlic infusatc when 20% albumin was given. Llnfortunately no specimen was obtained for protein analysis. Eight hours later his condition improved markedly; a repeat chest X ray (Fig. 3) showed complete resolution of the pulmonary ocdcnia. Hc continued to make good progress and was subsequently discharged to thc general ward and thence to a rehabilitation unit. DiscussionI'ulmonary oedeina is an abnormal collcction o f fluid in the extravascular tissucs and r p x x s of the lung.4 Fluid exchang...

Unilateral pulmonary oedema following the removal of a giant pleural tumour.

“…It has also been reported after unilateral bronchial obstruction2 and lung compression by a ruptured hemidiaphragm. 3 The protein content of the oedema fluid is high and increased pulmonary capillary permeability is thought to be the major underlying cause.4 Hypoxic damage to the pulmonary microvasculature results from the reduced blood flow in a lung that has usually been collapsed for several days.5 This damage is compounded by the rapid increase in blood flow, and consequently in capillary pressure, on re-expansion, and the capillaries may also suffer mechanical stress as they become overdilated.6 Pulmonary oedema results from transudation across the leaky alveolar capillary membrane, almost exclusively on the side of previous collapse, although re-expansion oedema has been reported in the contralateral lung; the cause in this case was thought to be capillary damage secondary to systemic hypotension and hypoxaemia compounded by acute pulmonary hypertension.! Precautions should therefore be taken to retard re-expansion to prevent a sudden drop in pressure across the alveolarcapillary membrane.…”