Abstract

BackgroundAbdominal compartment syndrome has been linked to detrimental hemodynamic side effects that include increased intracranial pressure and diminished renal function, but the mechanisms behind this continue to be elucidated. In this study, we sought to investigate any direct association between acute elevations in intra-abdominal pressure and intracranial hypertension during experimentally induced abdominal compartment syndrome and between acutely elevated intracranial pressure and the hemodynamic response that might be elicited by a vasopressin-induced Cushing reflex affecting urine osmolality and urine output. The aim of this study is to explain the Cushing reflex and the vasopressin-mediated hemodynamic response to intracranial pressure during acute elevations in intra-abdominal pressure. MethodsWe measured intra-abdominal pressure, intrathoracic pressure, optic nerve sheath diameter as an indirect sign of intracranial pressure, vasopressin levels in blood, urine osmolality, and urine output at 4 time points during surgery in 16 patients undergoing sleeve gastrectomy for morbid obesity. Values for the 4 time points were compared by repeated-measures analysis of variance. ResultsMore than 50-fold elevations in serum vasopressin paralleled increases in optic nerve sheath diameter, rising throughout prepneumoperitoneum and tapering off afterward, in conjunction with a marked decrease in urine but not serum osmolality. Mean arterial pressure rose transiently during pneumoperitoneum without elevated positive end-expiratory pressure but was not significantly elevated thereafter. ConclusionsThese findings support our hypothesis that the oliguric response observed in abdominal compartment syndrome might be the result of the acutely elevated intra-abdominal pressure triggering increased intrathoracic pressure, decreased venous outflow from the central nervous system, increased intracranial pressure, and resultant vasopressin release via a Cushing reflex.

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