Actn Anaesthesia1 Scnnd 1994: 38: 518-520 Printed zn Denmark - all righis reserved

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Acta Anaesthesiologica Scandinavica ISSN 0001-5l72

Case Report

Re-expansion pulmonary oedema following removal of intrathoracic haernatoma H. MORIKAWA', K. HIROTA,, K. KITO~, H. FUJITA' and S. MISHIMA' 'Department of Anaesthesia, Ohtsu Municipal Hospital, Shiga and 'Department of Anaesthesiology, Kyoto University School of Medicine, Kyoto, Japan

Acute ipsilateral pulmonary oedema is a well documented complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion and atelectasis. We present a case of bilateral re-expansion pulmonary oedema following removal of an intrathoracic haematoma. High protein concentration of the oedema fluid suggests increased pulmonary vascular permeability as a cause of this pulmonary oedema.

Received 4 April, accepted for publication 26 Augwt 1993

Key words: Intrathoracic hematoma; pulmonary edema; re-expansion.

A 43-year-old man was referred for surgical repair of Budd-Chiari syndrome. Preoperative laboratory tests were unremarkable, except for a mild elevation of biliary enzymes. Bypass surgery was performed be- tween the right atrium and the inferior vena cava. The intraoperative course was uneventful. Total estimated blood loss amounted to 2000 ml or more. Three thou- sand ml of blood products were needed to maintain haematocrit (Ht) above 30%.

The patient was transferred to the intensive care unit (ICU) after operation with his trachea intubated. Blood gas analysis was Pao, 35.8 kPa, Paco, 5.6 kPa with Fio, 0.6. Bleeding in the right thoracic cavity was evident in the immediate postoperative period. Chest tube output was more than 100 ml h- ' . Chest X-ray revealed atelectasis of the entire right lung as a result of haematoma and leftward deviation of the medias- tinum, which further compressed the left lung (Fig. 1) . Re-operation was withheld because the patient's family rejected it for religious reasons and it took an extra day to persuade them to accept it. Thirty-five hours after transfer to ICU, central venous pressure (CVP) reached 25 cmH,O and pulmonary capillary wedge pressure (PCWP) rose to 20 mmHg. Laboratory data revealed slight anaemia (Ht 28%) and impaired coagulation (prothrombin time 30%). The ventilatory condition was such that peak inspiratory pressure IWXhed 50 cmH,O. Blood gases were Pa% 10.8 kPa and Paco, 7 .7 kPa with Fio, 1.0.

0 Acta Anaesthesiologica Scandinauica 38 (1994)

Fig. I . Massive right intrathoracic haematoma has completely col- lapsed the right lung. The left lung is also severely compressed by the markedty deviated mediastinum.

RE-EXPANSION PULMONARY OEDEMA AFTER REMOV'4L OF lNTRATHORACIC HAEMATOMA 519

The patient was re-operated 40 h after the bypass surgery. Removal of some 3000 ml of intrathoracic haematoma led to an improvement of haemodynamic status. Systolic arterial pressure increased from 60 mmHg to 100 mmHg and both CVP and PCWP decreased (1 1 cmH,O and 12 mmHg, respectively). Airway pressure decreased and blood gas analysis im- proved as well; Pao., 34.3 kPa, Paco, 3.4 kPa with Fio, 0.8. Forty minutes later, however, airway pressure began to increase again in association with decreased oxygen saturation and increased end-tidal carbon dioxide tension. Over the next hour, more than 500 ml of blood-stained, frothy secretions spouted out of the endotracheal tube. Protein concentration of the secretory fluid was 7.0 g dl-', whereas that of serum was 4.2 g dl-I. At the end of operation, CVP was 15 cmH,O and PCWP was 18 mmHg. Blood gases were Pao, 10.6 kPa and Paco, 7.1 kPa with Fio, 0.8. Chest X-ray taken after the operation demonstrated extensive bilateral pulmonary oedema (Fig. 2 ) .

During the stay in ICU and re-operation, total esti- mated blood loss was 5800 ml, while 4900 ml of blood products and 6600 ml of fluids were transfused.

A number of therapeutic modalities were tried post- operatively, including application of PEEP, adminis-

Fig. 2. Extensive bilateral pulmonary oedema immediately after the wcond operation.

tration of steroid, transfusion of fresh frozen plasma and institution of high frequency ventilation. In spite of all these interventions, evacuation of frothy secre- tions persisted for one and a half days. Complete resol- ution of pulmonary oedema on chest X-ray took an- other five days.

Ten months later, the patient returned to his pre- vious occupation (constructor) in a reasonably good state of health. There was no evidence of occlusion of the graft, which was confirmed by vascular endo- scopy.

DISCUSSION Ipsilateral re-expansion pulmonary oedema after treat- ment of collapsed lung secondary to pneumothorax, pleural effusion or atelectasis is a well-known, although rare, clinical entity. However, we could find only four reported cases of bilateral or contralateral re-expansion pulmonary oedema; three of which were related to pneumothorax (1, 2) and one was related to drainage of pleural effusion (3). Incidentally, a case of re-expan- sion pulmonary oedema after surgical extirpation of a mediastinal tumour was reported recently (4).

There are several possible mechanisms involved in this case. A large volume of blood and fluids were administered before re-operation to deal with the un- stable haemodynamic status. However, PCWP and CVP just prior to the development of pulmonary oede- ma (1 1 c m H 2 0 and 12 mmHg, respectively) were lower than the preoperative values (25 cmH,O and 20 mmHg, respectively) because of diminished intrathor- acic pressure following removal of massive haematoma. This excludes elevated pulmonary capillary hydro- static pressure as the causative factor of pulmopary oedema. On the other hand, the secretory fluid had a high protein concentration, even higher than serum (7.0 g dl-' compared with 4.2 g dl-I) . This apparent paradox is difficult to explain. In one paper, this is attributed either to haemodilution with large volumes of fluids infused after the oedema fluid has already formed or to water resorption in the airway, with consequent increase in protein concentration of the secretory fluid (5). Anyway, this strongly suggests that an increase in pulmonary vascular permeability was involved in the pathogenesis of pulmonary oedema.

Most of the reported cases of re-expansion pulmon- ary oedema are associated with expansion of a col- lapsed lung by application of negative intrapleural pressure. Thus, it is quite natural that it should have been attributed to decreased lung interstitial pressure. Recent evidence, however, strongly supports increased pulmonary vascular permeability to be the major aeti- ologic factor in its development (6-8). One of the

520 H. MORIKAWA ET AL.

proposed mechanisms that causes increased microvas- cular permeability is as follows (9). A collapsed lung i s relatively hypoxic due to the absence of alveolar ventilation and reduced pulmonary blood flow as a result of hypoxic pulmonary vasoconstriction. It is noteworthy that hypoxia per se has no direct effect on pulmonary vascular permeability (10) and there is no oedema formation in the collapsed, hypoxic, lung. The restoration of ventilation and perfusion caused by ex- pansion of the collapsed lung seems to play a key role. This reintroduces oxygen into previously hypoxic areas of the lung and leads to the generation of oxygen free radicals which may damage the pulmonary microvas- cular endothelium. The rate of re-expansion is believed to be critical in the development of re-expansion pul- monary oedema (1 2 ) . Stretching of pulmonary micro- vessels during re-expansion could also contribute to increased vascular permeability ( 1 1, 13).

Re-expansion pulmonary oedema is generally re- ported to occur in the ipsilateral lung, whereas both lungs were affected in the present case. There is evi- dence that a large number of neutrophils are present in the re-expanded lung (9) and various mediators could be released and affect the microvasculature of the contralateral lung (14). In our case, however, hae- matoma in the right thoracic cavity was so massive that not only the right lung but the left lung was also compressed by the deviated mediastinum. Removal of haematoma led to rapid re-expansion of both lungs followed by the development of bilateral pulmonary oedema. Thus, same mechanism could have operated in both lungs.

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Address: Hitoshi Morikawa Department of Anaesthesia Ohtsu Municipal Hospital 2-9-9 Motomiya Ohtsu Shiga 520 Japan