1 Department of Anaesthesia and Intensive Care Medicine, S. Anna Hospital, I-44100 Ferrara, Italy. 2 Department of Nuclear Medicine, University of Ferrara, Ferrara, Italy*Corresponding author
Accepted for publication: July 4, 2002
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Abstract |
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Br J Anaesth 2002; 89: 7758
Keywords: anaesthesia, urology; complications, air embolism; therapy, hyperbaric oxygen
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Introduction |
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Case report |
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Seven hours after the presumed venous air embolism, the patient complained of nausea and retching. Metoclopramide 10 mg was administered i.m., with benefit. At that time, arterial blood gas analysis revealed mild hypoxaemia (PaO2 9 kPa). Two hours later the patient suddenly complained of complete blindness, while his tendon reflexes were increased on the left side and a tremor was evident in the left arm. Ophthalmological examination revealed bilateral amaurosis without funduscopic abnormalities; the retinal vessels and the optic disc were normal. The patient underwent magnetic resonance imaging (MRI) including diffusion-weighted imaging (DW-MRI), which showed only a mild hyperintense area in the left cerebellar hemisphere with corticalsubcortical extension. Nevertheless, despite the negative MRI data, on the basis of a strong clinical suspicion of paradoxical air embolism the patient was transferred as rapidly as possible to a hyperbaric centre. It took 5 h from the onset of blindness to instigate hyperbaric therapy. During the first hyperbaric session (Table 1) the patients sight started to recover (he could see shadows).
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Discussion |
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Air bubbles, the surfaces of which are covered by a network of fibrin, platelets and fat globules, induce neutrophil-mediated microvascular damage, activate the intrinsic coagulation cascade and obstruct lung capillaries. This will cause an increased physiological dead space,13 14 disordered ventilationperfusion matching15 and reduced cardiac output as a result of right ventricular outflow obstruction, leading to decreased PE'CO2, SpO2 and systolic arterial pressure, together with an increased end-tidal arterial carbon dioxide gradient. In our case, we assumed venous air embolism rather than pulmonary thromboembolism, because coagulation was normal and there was a rapid improvement after ventilation with oxygen 100%. The oxygen concentration gradient could have facilitated the release from the air embolus of both nitrogen and nitrous oxide.
Eight hours after the venous air embolism, the patient displayed the features of the air having moved to the arterial side of the circulation, a phenomenon described most frequently in acute decompression illness after diving.
We used PE'CO2 to detect air embolism.16 Doppler transthoracic ultrasound is more sensitive, but only early transoesophageal echocardiography might have demonstrated the presence of air which could progress through either a patent foramen ovale or through pulmonary shunts16 to cause paradoxical air embolism. In our case, transoesophageal echocardiography did not demonstrate right-to-left interatrial shunting. However, the delay between venous and arterial embolic episodes suggests transpulmonary passage, which has been described in dogs17 and humans18 and has also been demonstrated by transoesophageal echocardiography.19 20 Pathways involved in transatrial or transpulmonary air transport become functionally open only during episodes of venous air embolism in which significant elevation of pulmonary artery pressure occurs.19 In our case, such an increase in pulmonary artery pressure could have been induced during the retching episodes. While the patient was in the head-up position, air crossing to the systemic arterial circulation could have migrated up to the carotid and cerebellar arteries and then to the cerebral and cerebellar hemispheres.18
Although DW-MRI is widely recognized to be the earliest imaging technique that detects brain ischaemia, in our case the early MRI scan (performed immediately after the onset of symptoms) did not show abnormalities consistent with ischaemic tissue, as described in a similar case report.21 These findings could be related to the small dimensions of the injured areas21 at the time of the first MRI scan. The later DW-MRI scan demonstrated abnormalities consistent with ischaemic brain damage in the occipital and cerebellar cortex. The SPET study of the brain confirmed these findings with enhanced sensitivity in indicating the extent and localization of the brain damage, even though the total number of counts recorded was only 9 000 000, with a reduced acquisition time (Fig. 1). The second SPET study (Fig. 2), which recorded a total of 13 000 000 counts with a standard acquisition time, provided definitive evidence of recovery.
In neurosurgical procedures in which the patient is in the sitting position, invasive monitoring to detect venous air embolism and the insertion of a catheter in the right atrium to aspirate air are used routinely. In other surgical procedures,10 such as nephrolithotripsy, these precautionary measures may not be so easily justified. However, our case suggests that transoesophageal echocardiography can demonstrate the presence of air in the right heart or pulmonary veins, and this should be removed from the venous circulation through a right atrial catheter. In the case of persistent air trapping, prophylactic hyperbaric oxygen therapy should be performed. Until prospective studies provide an estimate of the true incidence of venous air embolism and paradoxical air embolism, it is difficult to decide whether transoesophageal echocardiography and central venous catheterization should be used routinely during percutaneous lithotripsy.
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References |
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