Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jan 2008
Case ReportsEpidural blood patch for severe postoperative intracranial hypotension.
Brain sag is a rare but serious postoperative complication after craniotomy. It is a clinical entity that refers to severe cerebrospinal fluid hypovolemia causing acute neurologic decompensation and obtundation. The established treatment is trendelenberg positioning. ⋯ The administration of epidural blood patch resulted in immediate and dramatic reversal of obtundation in each of these patients. Epidural blood patch may be a life-saving intervention in postcraniotomy patients presenting with refractory brain sag. It should be offered in patients who meet the criteria for brain sag and are unresponsive to conventional treatment modalities, despite the clinical presentation of herniation and coma.
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Disseminated intravascular coagulation (DIC) is reported in neurosurgical patients; however, the incidence of DIC after craniotomy procedures is unknown. Using a surgical database, we identified 3164 patients who underwent primary craniotomy at Mayo Clinic Rochester between January 1, 2000 and December 31, 2004. Potential cases of DIC in this population were identified using 3 search triggers, patients: (1) in whom the diagnosis of DIC was noted on their hospital discharge summary, (2) who received red blood cell-free blood products, or (3) in whom a blood fibrinogen or d-dimer concentration was assessed. ⋯ Although this small sample of patients receiving salvaged blood requires caution in interpreting the results, the risk of DIC seemed to be greater with salvaged blood than without [odds ratio 24 (CI=2.5-237)]. In children, 2 of 3 patients who developed DIC had congenital malformations of the brain. Findings from this study suggest that DIC is rare after craniotomy, but is often associated with mortality.
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J Neurosurg Anesthesiol · Jan 2008
Randomized Controlled TrialStewart's physicochemical approach in neurosurgical patients with hyperchloremic metabolic acidosis during propofol anesthesia.
There is both in vitro and clinical evidence that high-dose propofol can inhibit mitochondrial respiration, resulting in metabolic acidosis. The purpose of this study was to evaluate the effects of propofol anesthesia on the acid-base status in neurosurgical patients with large amount of normal saline administration. Thirty patients undergoing clipping of cerebral aneurysm were randomly assigned to receive propofol (n=15) or isoflurane (n=15). ⋯ SIDa and SIDe significantly decreased in both groups, and lactate and strong ion gap significantly increased after surgery in propofol group, but there were no significant differences between 2 groups. Both propofol and isoflurane were associated with hyperchloremic metabolic acidosis in neurosurgical patients with large amount of normal saline administration. The acid-base balance between the 2 anesthetics was similar using Stewart's physicochemical approach.
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J Neurosurg Anesthesiol · Jan 2008
Isoflurane-induced neuroapoptosis in the developing brain of nonhypoglycemic mice.
Drugs that suppress neuronal activity, including general anesthetics used in pediatric and obstetric medicine, trigger neuroapoptosis in the developing rodent brain. Exposure of infant rats for 6 hours to a combination of anesthetic drugs (midazolam, nitrous oxide, isoflurane) reportedly causes widespread apoptotic neurodegeneration, followed by lifelong cognitive deficits. Isoflurane, the dominant ingredient in this triple cocktail, has not been evaluated individually for apoptogenic potential. ⋯ Blood glucose determinations ruled out hypoglycemia as a potential cause of the brain damage. It is concluded that exposure to sub-MAC concentrations of isoflurane for one or more hours triggers neuroapoptosis in the infant mouse brain. These findings are consistent with other recent evidence demonstrating that brief exposure to ethanol, ketamine, or midazolam triggers neuroapoptosis in the developing mouse brain.