The Cushing reflex and the vasopressin-mediated hemodynamic response to increased intracranial pressure during acute elevations in intraabdominal pressure

Abstract

Background: Abdominal 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 intraabdominal pressure. Methods: We 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. Results: More 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. Conclusions: These 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.

Postoperative protocols following endoscopic skull base surgery: An evidence‐based review with recommendations

“…Literature review did not yield any studies that were pertinent to postoperative effects of urinary catheter placement following ESBS. Previous studies have found that increased intra‐abdominal pressure, which can be directly affected by bladder volume, can result in increased ICP and vasopressin release via the Cushing reflex 60–62 . This reasoning can be used to postulate that urinary catheters may be used during the postoperative period to prevent ICP shifts by preventing urinary retention.…”

“…Previous studies have found that increased intra-abdominal pressure, which can be directly affected by bladder volume, can result in increased ICP and vasopressin release via the Cushing reflex. [60][61][62] This reasoning can be used to postulate that urinary catheters may be used during the postoperative period to prevent ICP shifts by preventing urinary retention. Aggregate grade of evidence: D (no dedicated studies)…”

Medical Comorbidities Associated With Outcomes in Patients With Traumatic Epidural Hematomas

“…We additionally found that patients with gastrointestinal diseases were more likely to require a neurosurgical procedure. Gastrointestinal processes that increase intraabdominal pressure have long been associated with increased intracranial pressure, especially as noted in severe disease processes such as abdominal compartment syndrome [ 13 ]. Although gastrointestinal processes were not stratified by specific disease in our cohort, the underlying principle of increased intra-abdominal pressure, either due to pain from the underlying disease or the disease itself, may biologically be related to increased intracranial pressure leading to additional neurosurgical procedures.…”

Abdominal compartment syndrome in critically ill patients

“…An increase in intrathoracic pressure elevates the central venous pressure, leading to diminished venous circulation through the jugular vein. This increases intracranial pressure [ 46 , 47 ].…”