Air embolism: diagnosis with single-photon emission tomography and successful hyperbaric oxygen therapy

L. Droghetti*,1, M. Giganti2, A. Memmo1 and R. Zatelli1

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


    Abstract
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
Venous air embolism may occur when the surgical field is above the level of the heart. We present a case of venous air embolism in a patient undergoing percutaneous nephrolithotripsy in the prone position and presenting with blindness and neurological deficits 8 h later. The clinical diagnosis of paradoxical air embolism was confirmed by early single-photon emission tomography (SPET), whereas magnetic resonance imaging including diffusion-weighted imaging (DW-MRI) was diagnostic only 30 h later. Hyperbaric oxygen therapy was successful. In this case, early DW-MRI scan was inconclusive, but a SPET study of the brain appeared to be useful in confirming the clinical diagnosis. Early hyperbaric oxygen was demonstrated to be a successful therapy.

Br J Anaesth 2002; 89: 775–8

Keywords: anaesthesia, urology; complications, air embolism; therapy, hyperbaric oxygen


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
During surgical procedures in which the surgical field is positioned above the level of the heart, venous air embolism may occur. When the air passes through to the arterial system, causing paradoxical air embolism, the consequences can be devastating. We present a case of venous air embolism occurring in percutaneous nephrolithotripsy in the prone position, with features of paradoxical air embolism appearing 8 h later.


    Case report
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A previously healthy 36-yr-old male, height 175 cm, weight 84 kg, was scheduled for nephrolithotripsy for an upper pole staghorn calculus. Anaesthesia was induced with alfentanil 7 µg kg–1 and propofol 2 mg kg–1 i.v., and neuromuscular block was achieved with vecuronium bromide 0.1 mg kg–1. After tracheal intubation with a cuffed tube, artificial ventilation was started and anaesthesia maintained with 60% nitrous oxide in oxygen and sevoflurane at an end-expiratory concentration of 1.5 vol%. Continuous intra operative monitoring included an electrocardiogram (ECG), pulse oximetry (SpO2), end-tidal carbon dioxide concentration (PE'CO2), end-tidal volatile anaesthetic agent concentration, and ventilation volumes and pressures, while non-invasive blood pressure was measured at 3-min intervals. Cystoscopy was performed and a catheter was inserted into the right ureter. The patient was then placed in the prone position with his head and legs down. A nephroscope connected to an ultrasound generator (Calculson-Storz, Tuttlingen, Germany) at 26 000 Hz was inserted into the renal pelvis, which was perfused constantly with saline solution flowing from an irrigating bag placed 40 cm above the surgical field and drained by an aspirating pump. About 10 min after the beginning of ultrasound lithotripsy, the PE'CO2decreased abruptly from 4 to 2.9 then to 1.8 kPa. The SpO2 decreased from 100 to 86% and the systolic arterial pressure from 120 to 96 mm Hg. The heart rate decreased from 75 to 60 beats min–1. As the airway pressures and tidal volume were unchanged, airway obstruction was excluded and, with the strong suspicion of air embolism, the nitrous oxide was discontinued and manual ventilation of the lungs was performed with oxygen 100%. Within 2–3 min, the patient was placed supine. The PE'CO2 increased to 4 kPa and the SpO2 increased to 100%. A catheter was inserted into the left radial artery and arterial blood gas analysis showed a PaCO2 of 5.4 kPa, while the PE'CO2 was still 3.8 kPa. The surgery was stopped and the patient was awakened and his trachea extubated. He was conscious, haemodynamically stable and his SpO2 was 100% while breathing air. Neurological examination, biochemical and haematological profiles, coagulation indices (indexed normalized ratio 1.12, thromboplastin time 30.12 s, D dimers 269 ng ml–1 and fibrinogen 412 mg ml–1) and blood gas analysis were normal.

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 cortical–subcortical 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 patient’s sight started to recover (he could see shadows).


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Table 1 Scheme of the early hyperbaric treatment
 
Thirty hours later, a new MRI showed two hyperintense areas in the left cerebellar hemisphere with cortical–subcortical extension and bilateral hyperintensity in the cortical occipital gyrus, more evident on the right side than the left. A single-photon emission tomography (SPET) study of the brain was performed (Fig. 1), and this demonstrated a reduced uptake of isotopic tracer (99mTc-HMPAO, 740 MBq) in the right cerebellar hemisphere (Fig. 1A) and bilateral cerebral occipital (Fig. 1B) and left frontal (Fig. 1C) defects. Immediately after the SPET study, contrast transthoracic echocardiography was performed. No evidence of air in the right side of the heart or of interatrial or interventricular shunt was found, even after a Valsalva manoeuvre. Hyperbaric therapy was scheduled daily for 9 days (1.8 bar for 80 min), even though the patient recovered completely about 48 h after the paradoxical air embolism. Thirteen days after surgery, a further SPET study provided evidence of complete recovery of the occipital (Fig. 2B) and frontal (Fig. 2C) defects, only a mild interhemispheric cerebellar asymmetry persisting (Fig. 2A).



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Fig 1 Three representative transverse slices of the SPET study of the brain with 99mTc-HMPAO, performed 31 h after paradoxical air embolism. (A) The arrow indicates a right cerebellar hemisphere uptake defect with interhemispheric asymmetry. (B) The arrow indicates bilateral occipital defects. (C) The arrow indicates a left frontal defect.

 


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Fig 2 SPET study of the brain performed 13 days after injury. Mild interhemispheric cerebellar asymmetry (A) and completely normal tracer uptake in the occipital (B) and frontal (C) cerebral regions.

 

    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
The phenomenon of pyelovenous backflow was first described in 1856 by Gigon, who noted the passage of fluids from the calyces into the renal veins.1 Later, pyelovenous2 3 and tubulovenous4 backflow was described. Air embolism as a complication of retrograde pyelography5 and air entering the hepatic veins after nephrolithotripsy have been reported.6 Saline solution flowing from a bag placed 40 cm above the surgical field applies a pressure of about 4 kPa to the pelvocaliceal space. This pressure is reduced by an unknown amount by the aspirating pump. Because of the high rate of saline flow, accidental injection of small amounts of air, in the form of microbubbles, cannot be excluded. In addition, the high power of therapeutic shock waves could induce cavitation,7 an ultrasound-related mechanical effect. The prone position8 of the patient in this case produced a significant gravitational gradient between the right side of the heart and the renal pelvis, and air could thus have been drawn into open veins by negative pressure. This case demonstrates the problems associated with the combination of a gravitational gradient,9 decreased caval pressure due to the position of the lower limbs, a likely high pressure5 of irrigating fluid, possibly containing air bubbles,10 11 and ultrasound shock waves.12

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 ventilation–perfusion 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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 Discussion
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