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Case Report

Fatal air embolism: a complication of manipulation of a cavitating metastatic lesion of the liver

Saad, R. S. G.

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European Journal of Anaesthesiology: May 1998 - Volume 15 - Issue 3 - p 372-375



Air embolism is not an uncommon complication of surgery and may be fatal. It was first recorded by Magendie in 1821, and by Barlow in 1830 [1]. It can result from a wide variety of causes including diagnostic and therapeutic manoeuvers. It can also complicate trauma and medical conditions e.g. Crohn's disease [2].

Case report

A 65-year-old Caucasian female was admitted with a history of abdominal pain, weight loss and polyuria during the previous 3 months. Her medical history was unremarkable apart from hypertension treated with atenolol, 25 mg b.d. orally. On examination her temperature was 38.2 °C, her blood pressure was 170/90 and a small mobile swelling was noted in the front of her neck and assumed to be a thyroid swelling.

Abdominal examination revealed a tender epigastric swelling but there was no guarding or rebound tenderness. Intestinal sounds were present.

Laboratory investigations showed microcytic normochromic anaemia (HB 9.8), elevated white cell count (17.7 × 109) and raised blood glucose of 21.8 mmol−1. Urea and electrolytes, serum amylase and thyroid function tests were within normal limits. Liver function tests revealed a low serum albumin, high levels of serum lactate dehydrogenase (681 U litre−1) and γ-glutamyl transpeptidase (289 U litre−1), but a coagulation screen was normal. An abdominal ultrasound scan was reported to show a multiloculated gas-containing space around and partially within the liver. A radiological diagnosis of rupture of a gascontaining liver abscess into the subhepatic and subphrenic spaces was made.

Initial resuscitation was started with intravenous (i.v.) fluids (1.5 litre of compound sodium lactate) and insulin by sliding scale. An emergency laparotomy was performed by a consultant surgeon within 48 h of her admission. Anaesthesia was induced using sodium thiopentone (250 mg), and suxamethonium, (75 mg), as part of a rapid sequence technique. Following tracheal intubation, anaesthesia was maintained with enflurane in O2/N2O. Muscle relaxation was maintained with vecuronium and ventilation was controlled to maintain normocapnia. Increments of morphine were given as required for analgesia throughout the procedure. Laparotomy revealed an inoperable metastatic liver tumour with its primary in the transverse colon. Multiple cavitating secondaries were noted in the liver, as well as para-aortic lymph node involvement. After omental biopsies the abdomen was closed after about 20 min. After reversal of the non-depolarizing muscle relaxant with neostigmine 2.5 mg and atropine 1.2 mg, the patient developed pulsus bigeminy but she remained haemodynamically stable. In spite of the onset of spontaneous respiratory effort, the patient did not regain full consciousness. In the recovery area, the patient was given doxapram hydrochloride, 80 mg i.v. and naloxone hydrochloride increments up to 400 μg. Incomplete reversal of vecuronium was excluded by the absence of fade when using a nerve stimulator. A trial of extubation was unsuccessful, as the patient failed to maintain oxygen saturation. The patient was reintubated, but in view of the poor prognosis, it was decided that no further resuscitation be attempted. The patient was kept comfortable until she died in recovery without regaining consciousness within 30 min. (Figure 1)

Fig. 1
Fig. 1:
Abdominal CT showing gas-filled cavities in the liver.

Postmortem examination revealed that the cause of death was massive air embolism, which was likely to have been caused either by infiltration of the hepatic veins by the cavitating tumour, or air entry via hepatic veins during surgical manipulation of the liver.


Air embolism has been reported following a wide variety of surgical diagnostic and therapeutic procedures. Many examples of air embolism have a medicolegal significance, as the entry into the circulation often comes about as a result of trauma, barotrauma, or from criminal intervention. It can also occur as a result of accidental ingress of air into an open vein. Gaseous microemboli also occur during the use of bubble oxygenators for cardiopulmonary bypass [3].

The variable recorded incidence of air embolism during similar procedures is mainly caused by differences in the method used to detect the occurrence of air embolism, with Doppler ultrasound being the most sensitive. In a study of the incidence of venous air embolism during total hip arthoplasty, Spiess and coworkers [4] reported that changes in the monitored variables consistent with venous air embolism were noted in 57% by Doppler ultrasound, 9% by mass spectrometry, 4% by central venous catheter and 3% of cases by arterial blood gases.

The physiological changes of gas emboli will depend on the speed by which the gas enters the venous system and its volume. The posture of the individual, the size and pressure within the venous system, as well as the general condition of the patient will also affect the outcome of gas embolism. The pathological changes of gas embolism are caused by obstruction of the apical part of the right ventricle thus preventing pulmonary blood flow [5] and platelet damage which will lead to the formation of microemboli. There is also polymorphonuclear leucocyte infiltration, increased capillary permeability and pulmonary oedema, which can be reduced by scavenging O2 free radicals [6].

To reduce the incidence of the severity of air embolism under certain circumstances, the following measures have been suggested: head-up tilt of 5° [7], the use of arterial filters [8], moderate hypoventilation [9] and the use of central venous catheters to retrieve air once it has gained access to the circulation. Monitoring patients at risk is extremely important as clinical symptoms and signs are unreliable.

When venous air embolism is suspected, certain specific therapies should be instituted promptly: placing the patient in the left lateral decubitus position, administration of 100% O2 and aspiration of air from the right atrium, ventricle or pulmonary artery with a central venous or pulmonary artery catheter. During general anaesthesia, N2O should be discontinued as it increases the size of air bubbles in the pulmonary vasculature. Closed chest compression has been reported to be helpful and anticoagulation has been suggested in the treatment of fibrin microemboli [10]. High dose steroids have been shown to decrease pulmonary oedema in sheep [6] and hyperbaric oxygen therapy, if readily available has also been proposed [11]. Hepatic surgery, both open and laparoscopic, has been associated with air embolism. Fatal air embolism has been reported following laparoscopic cholecystectomy [12], laparoscopic liver tumour resection with argon beam [13], pancreaticoduodenectomy [14], hepatic resection [15], orthotopic liver transplantation [16], and hepatic artery ligation [17].

In the patient described here, the most likely cause of gas embolism was the ingress of atmospheric air, and/or intrahepatic gas from the large gas-filled metastatic liver deposits into the circulation via the hepatic veins and sinusoids during surgical manipulation. The only possible intra-operative manifestation of air embolism was the change in the patient's heart rhythm, and there were no alterations in haemodynamic variables or end-tidal CO2. It is possible that the embolism did not occur until the early post-operative period; however, capnography had unfortunately not been continued in the recovery room.

In patients at higher risk of gas embolism e.g. where there is gas in an abnormal location within the body, more sensitive diagnostic tools (e.g. pericordial Doppler) may be justified. Although in the above case, early detection of air embolism would not have altered the patient management, in others it might be the difference between life and death.


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© 1998 European Society of Anaesthesiology