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Recent animal and human studies have raised concern that exposure to anesthetic agents in children may cause neuronal damage and be associated with adverse neurodevelopmental outcomes. Exposure of young animals to anesthetic agents above threshold doses and durations during a critical neurodevelopmental window in the absence of concomitant painful stimuli causes widespread neuronal apoptosis and subsequent abnormal behaviors. The relevance of such animal data to humans is unknown. Untreated neonatal pain and stress also are associated with enhanced neuronal death and subsequent maladaptive behaviors, which can be prevented by exposure to these same anesthetic agents. Retrospective observational human studies have suggested a dose-dependent association between multiple anesthetic exposures in early childhood and subsequent learning disability, the causality of which is unknown. Ongoing prospective investigations are underway, the results of which may clarify if and what neurodevelopmental risks are associated with pediatric anesthesia. No change in current practice is yet indicated.

Surgical removal of a cerebral hemisphere may be undertaken in patients with intractable seizure disorders. Anesthetic management of such patients has not been reviewed in detail before. This study retrospectively analyzed hospital records of ten patients undergoing cerebral hemispherectomy at the Johns Hopkins Hospital between July 1983 and February 1988. Patient records were reviewed for diagnosis, physical characteristics, preoperative medications, anesthetic management, and postoperative course in the intensive care unit (ICU). Massive and sudden blood loss was a common finding in these patients, and during the intraoperative and postoperative periods, fluid resuscitation frequently was an ongoing process. In some patients, the blood loss exceeded one blood volume and was associated with coagulopathy, hypokalemia, and hypothermia. Urine output was elevated by a glucose-induced diuresis in some patients, giving misleading information as to intravascular volume status. Seizures and hemorrhage into the hemispherectomy cavity were management problems in the ICU. From this review, the authors conclude that blood loss may be marked and precipitous during surgical removal of a cerebral hemisphere. Monitoring of intra-arterial pressure and central venous pressure (CVP) is necessary for patient management during the intraoperative and postoperative periods. Intravenous (IV) access should allow rapid intravascular volume administration as it becomes necessary. Patients should remain intubated and observed closely during the immediate postoperative period due to difficulties with hemodynamic stability, seizures, and hemorrhage.

Hypoglycemia of sufficient severity to cause cessation of EEG activity (coma) is accompanied by energy failure and by loss of ion homeostasis, the latter encompassing a marked rise in extracellular fluid (ECF) K+ concentration and a fall in ECF Ca2+ concentration. Presumably, ECF Na+ concentration decreases as well. In the present study, the extent that the altered ECF-plasma gradients give rise to net ion fluxes between plasma and tissue is explored. Accordingly, whole tissue contents of Ca2+, Mg2+, K+, and Na+ were measured. The experiments were carried out in anaesthetized and artificially ventilated rats given insulin i.p.; cerebral cortical tissue was sampled at the stage of slow-wave EEG activity, after 10, 30, and 60 min of coma (defined as isoelectric EEG), as well as after 1.5, 6, and 24 h of recovery. In the precomatose animals (with a slow-wave EEG pattern), no changes in electrolyte contents were observed. During coma, tissue Na+ content increased progressively and the K+ content fell (each by 20 mumol g-1 during 60 min). During recovery, these alterations were reversed within the first 6 h. The Mg2+ content remained unchanged. In spite of the appreciable plasma to ECF Ca2+ gradient, no significant calcium accumulation was observed. It is concluded significant calcium accumulation was observed. It is concluded that hypoglycemia leads to irreversible neuronal necrosis in the absence of gross accumulation of calcium in the tissue.