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Pulmonary oedema after venous air embolism during craniotomy

El Kettani, C.; Badaoui, R.; Fikri, M.; Jeanjean, P.; Montpellier, D.; Tchaoussoff, J.

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European Journal of Anaesthesiology (EJA): November 2002 - Volume 19 - Issue 11 - p 846-848
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Venous air embolism during general anaesthesia is a well-documented complication and the risk is not confined to neurosurgical procedures performed in the sitting position [1,2]. Venous air embolism is known to cause acute pulmonary oedema in animal experiments. This syndrome has been said to be due to a rupture of capillary integrity [3].

A 66-yr-old male was admitted for a craniotomy to excise a parasaggital tumour. He presented with a 6 month history of a focal convulsion and was treated with carbamazepine. In the past, he had had peritonitis but no respiratory or cardiovascular problems. Heart rate was 80 beats min−1, arterial pressure 135/80 mmHg and respiratory rate 14 breaths min−1. Examination of heart and lungs was normal as were haematological and biochemical investigations, the electrocardiogram (ECG), echocardiogram and chest radiograph. Computed tomography (CT) scan showed a left parasaggital meningioma without signs of raised intracranial pressure. Hydroxyzine premedication, 100 mg by mouth, was given 1 h before surgery. Anaesthesia was induced with thiopental 5 mg kg−1, sufentanil 0.3 μg kg−1; rocuronium 0.3 mg kg−1 was also given and a size 7.5 tube used to intubate the trachea. Patient monitoring consisted of continuous ECG with automatic ST segment analysis, intraarterial pressure and central venous pressure (CVP), pulse oximetry, capnography, airway pressure and urine output. Controlled ventilation of the lungs was by a Dräger ventilator (CATO M33285®; Dräger, Lübeck, Germany), without any end-expired positive pressure, using a 50% oxygen in air mixture (VT = 8 mL kg−1, frequency 12 breaths min−1). Anaesthesia was maintained with an infusion of sufentanil 0.3 μg kg−1 h−1 and 1-MAC sevoflurane. The operative procedure was performed in the supine position with a 20° head-up tilt and slight neck flexion.

The procedure progressed uneventfully until the bone flap had been raised when a sudden fall in PETCO2 from 4.4 to 1.9 kPa was noticed. Also oxygen saturation (SPO2) decreased from 99 to 85% with a fall in systolic arterial pressure from 120 to 90 mmHg and a rise in CVP from 4 to 8 mmHg, but without changes in heart rate or ST-segment. Because venous air embolism was suspected, surgery was stopped immediately, the operation site flooded with saline and wet packs applied. Breath sounds were normal but although no heart murmur was detected, air was successfully aspirated via the CVP cannula (40 mL air with 85 mL blood). The jugular veins were compressed by squeezing both sides of the neck, manual ventilation with 100% oxygen was instituted and an end-inspiratory 'hold' helped to localize the site of air entry. After the surgeon had achieved haemostasis, SpO2 recovered to 97%, PETCO2 increased to 4.0 kPa within 5 min and cardiovascular variables rapidly returned to normal. Further surgery was uneventful with stable SPO2, PETCO2 and cardiovascular variables. At the end of surgery, the patient was extubated and transferred to the intensive care unit (ICU).

Three hours after extubation, the patient became hypoxaemic with a respiratory frequency of 22 breaths min−1, SPO2 decreased (from 97 to 90%) but without significant changes of heart rate, arterial pressure or CVP. Examination of the lungs revealed inspiratory crackles at the lung bases. Arterial blood-gas status (FiO2 0.45 by facemask) was: pH 7.40; PO2 10.1 kPa; PCO2 5.3 kPa. Chest radiography showed developing oedema with a moderate bilateral pleural effusion (Fig. 1); an echocardiograph performed immediately was unchanged. The ECG, serial cardiac enzyme concentrations and osmolality were normal for the next 48 h. The patient required supplemental oxygen by facemask (FiO2 0.7) to maintain adequate oxygenation (SPO2 > 94%) and was managed successfully with diuretics. By the second postoperative day, the hypoxaemia had resolved and the chest radiograph was normal. The patient was discharged from the ICU the next day: his respiratory, cardiac and neurological status were normal and he was discharged home 7 days after operation.

Figure 1
Figure 1:
Chest X-ray; pulmonary oedema with a moderate bilateral pleural effusion.

The cause of pulmonary oedema after venous air embolization is likely to be due to leaky capillaries in the pulmonary microvasculature; structural damage to pulmonary capillaries is caused by increased wall stress following mechanical obstruction of the pulmonary outflow tract of the right ventricle [4]. Microscopically, the damage seen in animal models of venous air embolism is identical to that seen in animal models of oedema induced by supraphysiological intravascular pressures [3]. Endothelial damage is caused by the production and release of toxic oxygen metabolites from leukocytes, and the vascular permeability caused by i.v. air emboli is dramatically reduced by superoxide dismutase, a free radical-scavenger enzyme. Recent studies favour the theory of toxicity of air bubbles on pulmonary endothelial cells. In animal lungs, neutrophils aggregate around the air bubbles in the small pulmonary arteries and arterioles [5]. Protein-rich lung lymph flow is increased after venous air embolism signifying an increase in microvascular permeability. Pulmonary oedema may occur immediately after a large bolus of venous air, or may develop several hours later after multiple episodes of air trapping [4]. It can result from small air emboli and may go unrecognized intraoperatively, but can cause the same significant postoperative morbidity as large air emboli. Pulmonary oedema after venous air embolism is characterized by its rapid development, diffuse involvement and rapid resolution. Clinical symptoms include coughing, tachypnoea, pink bubbly secretions, cyanosis or respiratory failure. The protein content of tracheal aspirates is high. Confirmation of the diagnosis requires chest radiography: the distribution of the pulmonary oedema can be diffuse, unilateral or localized within a single lobe of lung, there is always an associated pleural effusion [6].

Pulmonary oedema can cause secondary deterioration of neurological function and severe cardiovascular changes necessitating inotropic support and large volumes of plasma to replace the fluid lost as pulmonary oedema [5]. In our patient, the pulmonary oedema occurred 3 h after the end of surgery and was manifested by hypoxaemia without change in cardiovascular variables. Pulmonary disturbances occurring after neurosurgical operations may have multiple causes including cardiogenic or non-cardiogenic oedema, pulmonary aspiration or infection. The incidence of postoperative pulmonary dysfunction is not related to the operative sitting position [7]. Black and colleagues noted a similar incidence of respiratory complications in patients in whom surgery was performed in the sitting and supine positions (2 and 3% respectively) [1]. Moreover, the occurrence of venous air embolism was not associated with an increased incidence of pulmonary dysfunction. Our patient showed no significant cardiovascular changes and there was no alteration of the ECG or elevation of cardiac enzymes in the 48 h after surgery. An echocardiogram performed 24 h postoperatively showed no abnormality. In view of the low CVP (4 mmHg), the possibility of fluid overload was unlikely. There was no evidence of pulmonary aspiration during induction, maintenance of anaesthesia and extubation. Postoperatively the patient showed leukocytosis without fever and infection was unlikely in view of the rapid development and resolution of the pulmonary changes, and the diagnosis of pulmonary oedema secondary to the venous air embolism was supported by the occurrence of an atypical episode of venous air embolism during the operation. This case shows that pulmonary oedema secondary to a venous air embolism should always be considered in the differential diagnosis of pulmonary changes after a neurosurgical operation.

C. El Kettani

R. Badaoui

M. Fikri

P. Jeanjean

D. Montpellier

J. Tchaoussoff

Department of Anesthesiology and Intensive Care; Amiens University Hospital; Amiens, France


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© 2002 European Academy of Anaesthesiology