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Craniopharyngioma surgery is frequently associated with the occurrence of central diabetes insipidus, and oral rehydration therapy is reliable for postoperative management if the patient’s thirst is normal. A 61-year-old Japanese male patient underwent extended endoscopic transsphenoidal surgery for craniopharyngioma. He was undergoing acute treatment for postoperative central diabetes insipidus and hypopituitarism in the intensive care unit. Two days after the surgery, he started to vomit occasionally, despite receiving oral rehydration therapy for central diabetes insipidus. Despite increasing the dose of parenteral hydrocortisone, the periodic vomiting persisted during fasting periods and progressed to aspiration pneumonia and severe sepsis. Abdominal computed tomography was performed to identify the cause of persistent vomiting and revealed the presence of a pseudo-intestinal obstruction extending from the small to large intestine. When oral rehydration therapy for central diabetes insipidus is accompanied by vomiting symptoms suggestive of hypopituitarism, a holistic evaluation of the gastrointestinal system is advisable.

unlikely that the modest IABP-induced pulse pressure of only 24 ± 8 mm Hg would generate a dp/dt of 645 ± 64 mm Hg/s, particularly at the level of small cerebral arteries, and thus be enough to produce sufficient stretch to induce significant production of L-arginine in the small cerebral arteries. If the pulse pressure was not sufficient, then significant cerebral vasodilation would not be obtained to affect the SjvO 2 , and hence the IABP-induced pulsatility would be unable to ameliorate the impaired SjvO 2 . A similar study using a pulsatile system capable of producing a pulse pressure of 50 to 60 mm Hg 6 to mimic that produced by the natural heart would be needed to be able to definitely exclude or include the role played by pulsatility. The study only demonstrates that the modest IABP-induced pulsatility was not effective but by no means excludes the role pulsatility may have.3. It is widely known that during CPB the levels of circulating endogenous catecholamines including norepinephrine are increased. During systemic infusion of norepinephrine, increased electrical brain activity (consisting of increased low-voltage high-frequency waves and decreased high-voltage slow-frequency waves) suggestive of promotion of excitatory (N-methyl-D-aspartate?) receptor activation has been noted in nonischemic rabbits (unpublished observations of electroencephalograms concurrent to brain microdialysis studies), which may lead to Na + and Ca ++ influx. To maintain the normal Na + and Ca ++ transmembrane gradient, the demand for mechanisms to extrude them, which are highly oxygen consuming, will be increased. Therefore during late CPB the decreased SjvO 2 might be a manifestation of that increased oxygen extraction not counteracted by the anesthetics, pressures, or pulsatility used by the authors. The exact effect of increased circulating catecholamines during CPB on the cerebral vasculature is not known, but if it was equivalent to increased sympathetic activity, then vasoconstriction of small cerebral vessels would result with consequent decreased flow. 7 If both effects are operating, the development of decreased SjvO 2 over the first 20 minutes of perfusion and the return to normal after CPB, also in 20 or 30 minutes, are easily explainable.Norepinephrine determination with and without blockade in conjunction with metabolic studies across the brain in both groups might shed some light.

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