Therapeutic hypothermia in cerebral air embolism: a case report
© Bäuerle et al.; licensee Springer. 2013
Received: 16 March 2013
Accepted: 27 August 2013
Published: 28 August 2013
Cerebral air embolism is a life-threatening complication of various diagnostic and therapeutic procedures. Hyperbaric oxygenation is considered to be the cornerstone of its treatment.
We report a patient with cerebral air embolism after endoscopy of a perineal abscess. Immediate CT imaging confirmed the diagnosis and MRI showed cortically localized areas of restricted diffusion along the gyri. Since hyperbaric oxygenation was not available, moderate hypothermia was applied for neuroprotection.
This case illustrates a rare complication of endoscopic interventions, and imaging characteristics of cerebral air embolism were described. Furthermore, we discuss the potential utility of therapeutic hypothermia in cerebral air embolism.
Cerebral air embolism (CAE) is a life-threatening complication of various diagnostic and therapeutic procedures. Diagnosis is difficult to establish and depends primarily on clinical experience. We report a patient with CAE after endoscopic bouginage of a perineal abscess treated with hypothermia immediately after diagnosis.
A 59-year-old man developed sudden respiratory distress, tachycardia, hypotonia, and coma about one minute after flexible endoscopy with dilatation and irrigation of a perineal abscess under sedation with propofol. Two years ago he had undergone pelvic exenteration because of advanced prostate cancer with intraoperative (15 Gy) and adjuvant radiotherapy (63 Gy). Wound healing was complicated by a perineal wound infection and development of a perineal abscess. Afterwards, periodical bouginage by flexible endoscopy (Hegar bouginage) of the abscess fistula had been necessary in order to drain pus and to keep the fistula open.
Discussion and conclusion
This case illustrates that systemic air embolism should be considered as cause of neurological and cardiopulmonary deterioration during pelvic interventions (Mirski et al. 2007).
In our patient we assume that insufflated air entered the venous circulation via a disruption of the endothelial surface of the abscess and passed perineal venous vessels which drain into the inferior vena cava. The initial head CT of our patient showed air in both the arterial and the venous system. Arterial air entrapment is suggestive for a patent foramen ovale as cause for paradoxical air embolism. Additionally, intrapulmonary shunts and transcapillary passage of air have been proposed as alternative mechanisms, especially in cases with large venous air volumes (Mirski et al. 2007). We did not perform a transesophageal echocardiography for detection of an intra cardiac shunt, since this would not have implied any therapeutic consequences for our patient. Furthermore, air accumulation in the cavernous sinus may be explained by jugular valve insufficiency and retrograde air passage through the internal jugular veins (Nedelmann et al. 2007).
Our report emphasizes that unenhanced CT of the head is capable to detect CAE if performed directly after symptom onset. Immediate brain imaging is thus required to verify the diagnosis. However, the absence of intracerebral air on CT does not exclude the diagnosis (Muth and Shank 2000). MRI demonstrated cortical ischemia predominately in the territory of the right middle cerebral artery. The gyriform pattern of restricted diffusion has been observed in several cases of CAE previously (Caulfield et al. 2006; Verro 2010; Koster et al. 2012) and may be the result of end-arterial occlusion and endothelial damage by air bubbles (Sobolewski et al. 2012). Interestingly, these cortical DWI changes resemble laminar necrosis on MRI in patients with hypoxic brain injury. If this finding exhibits a diagnostic value of CAE in cases without detection of intracerebral air on CT remains unclear and should be evaluated in prospective studies.
At present, hyperbaric oxygenation is considered to be the cornerstone of CAE treatment (Muth and Shank 2000; Mirski et al. 2007). However, prospective trails demonstrating its efficacy are lacking. In our case hyperbaric oxygenation was not available. Since induced hypothermia after cardiac arrest provides substantial neuroprotective effects (Hypothermia after Cardiac Arrest Study Group 2002), and CAE may induce pathophysiological changes similar to hypoxic brain injury, we decided to apply moderate hypothermia for neuroprotection. We are aware of the limited significance of this case report since we are not able to estimate the effect of hypothermia on the course of our patient. Otherwise, the initial neurologic status heralded a poor outcome of our patient and he retained a moderately severe disability after 3 months. Similarly, Inoue et al. reported a favorable outcome of a patient with CAE after pleural lavage treated with therapeutic hypothermia (Inoue et al. 2013). Therefore, we conclude that hypothermia is feasible in CAE and may have a neuroprotective effect in this disorder. In contrast to hyperbaric oxygenation, permanent availability makes hypothermia highly beneficial. Thus, as potential neuroprotective approach in CAE therapeutic hypothermia should be further investigated.
Written informed consent was obtained from the patient for publication of this case report.
The article processing charge was funded by the German Research Foundation (DFG) and the Albert-Ludwigs-University Freiburg in the funding program Open Access Publishing.
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