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Neurology India, Vol. 59, No. 4, July-August, 2011, pp. 641-642 Letter to Editor Non-awakening from anesthesia following posterior fossa surgery due to skull pin-induced tension pneumocephalus Smita Vimala, Madhusudan K. R Reddy, Umamaheswara G Rao PMID: 21891959 DOI: 10.4103/0028-3886.84363 Non-awakening after intracranial surgery though described, is rare. [1] We describe non-awakening after anesthesia following posterior fossa surgery due to tension pneumocephalus (TP) and discuss the possible mechanism. A 2-year-boy presented with difficulty in walking and irritability. Neurological examination revealed bilateral sixth nerve palsy and ataxic gait. Computerized tomography (CT) scan showed an infratentorial mass lesion and venticulomegaly. He was scheduled for excision of lesion. After anesthetic induction, patient's head was fixed with pediatric Mayfield clamp. Tumor was excised uneventfully. Despite neuromuscular blockade reversal, normothermia and anesthetic gas clearance, the child did not wake up even after 30 minutes and there was no motor response. Postoperative CT scan revealed TP and depressed fracture at pin site [Figure - 1]a. He was shifted to ICU for ventilation and TP decompressed with bifrontal twist-drill. There was immediate improvement in the neurological status. He had slight elevation of blood pressure (138/90) and slow heart rate (68/min) the next day. Repeat CT scan showed persistence of pneumocephalus, which was aspirated [Figure - 1]b. The child improved thereafter and at discharge, he was conscious, with no motor deficits. TP after craniotomy results because air cannot escape or be absorbed quickly, resulting in mass effect and intracranial hypertension. [2] This can result in progressive brain compression and neurological deterioration. Pressure exerted by pediatric Mayfield skull pins varies between 10 and 40 pounds. [3] In our patient pin application resulted in depressed fracture through the thin temporal bone weakened by intracranial hypertension. This might have acted as conduit for rapid entry of air through the breach after pins were removed. The pins prevented air entrainment intraoperatively and thus did not manifest with brain bulge or hemodynamic changes. However, bradycardia, hypertension and irregular respiration were observed immediately after the pin removal. Displacement of brain posteriorly due to change in the position from prone to supine and loss of cerebrospinal fluid via negative-pressure drain might have facilitated air entry from the fracture site. [4] In our patient absence of intraventricular air suggests that the air probably had not entered from the operative site. For TP, immediate aspiration of air is required to prevent rapid and irreversible neurological deterioration. In our patient partial removal of air in the first instance might have resulted in secondary neurological deterioration. Upright position, avoidance of valsalva manoeuvre, analgesia and high concentration oxygen are recommended for less severe cases. In conclusion, non-awakening from anesthesia can result from TP and high index of suspicion is required to prevent irreversible neurological sequelae and hemodynamic disturbances. Depressed fracture at the pin site as possible source of pneumocephalus should be considered in such situation. References
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