OBJECTIVEAfter craniectomy, although intracranial pressure (ICP) is controlled, episodes of brain hypoxia might still occur. Cerebral hypoxia is an indicator of poor outcome independently of ICP and cerebral perfusion pressure. No study has systematically evaluated the incidence and characteristics of brain hypoxia after craniectomy. The authors’ objective was to describe the incidence and characteristics of brain hypoxia after craniectomy.METHODSThe authors included 25 consecutive patients who underwent a craniectomy after traumatic brain injury or intracerebral hemorrhage and who were monitored afterward with a brain tissue oxygen pressure monitor.RESULTSThe frequency of hypoxic values after surgery was 14.6% despite ICP being controlled. Patients had a mean of 18 ± 23 hypoxic episodes. Endotracheal (ET) secretions (17.4%), low cerebral perfusion pressure (10.3%), and mobilizing the patient (8.6%) were the most common causes identified. Elevated ICP was rarely identified as the cause of hypoxia (4%). No cause of cerebral hypoxia could be determined 31.2% of the time. Effective treatments that were mainly used included sedation/analgesia (20.8%), ET secretion suctioning (15.4%), and increase in fraction of inspired oxygen or positive end-expiratory pressure (14.1%).CONCLUSIONSCerebral hypoxia is common after craniectomy, despite ICP being controlled. ET secretion and patient mobilization are common causes that are easily treatable and often not identified by standard monitoring. These results suggest that monitoring should be pursued even if ICP is controlled. The authors’ findings might provide a hypothesis to explain the poor functional outcome in the recent randomized controlled trials on craniectomy after traumatic brain injury where in which brain tissue oxygen pressure was not measured.
Transsphenoidal surgery (TSS) is a frequently used technique to remove pituitary adenomas. Rare complications of TSS include development of postoperative pneumocephalus. Many patients undergoing TSS also suffer from obstructive sleep apnea (OSA) and thus require positive pressure ventilation. The exact timing of when to safely reintroduce the CPAP machine in this subset of patients is presently not exactly known but is most often cited as being two to four weeks postoperatively. In this case, we describe the story of a 69-year-old female who underwent TSS for a nonsecreting pituitary adenoma in April 2012 and went on to develop pneumocephalus five weeks postoperatively after reintroduction of her CPAP machine. This is the latest presentation of pneumocephalus after reintroduction of CPAP documented in present literature. The case reopens the debate as to how many weeks postoperatively positive pressure ventilation should be withheld to prevent the development of pneumocephalus in patients having undergone TSS with simultaneous OSA.
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