The hallmark of acute liver failure is hepatic encephalopathy, which often presents with the devastating complication of cerebral edema. Given the extremely high mortality rate associated with the development of cerebral edema, it is prudent to aggressively manage this pathology. One tool that is used to guide treatment of cerebral edema is an intracranial pressure monitor. This article will review the literature regarding the use of intracranial pressure monitors in acute liver failure in an effort to elucidate their utility in this setting.
Some patients with severe acute respiratory distress syndrome (ARDS) experience hypoxemia during lung-protective ventilation, refractory to a fraction of inspired oxygen of 1.0 and high levels of positive end-expiratory pressure. Management options for refractory ARDS are discussed, including neuromuscular blocking agents (NMBA), prone positioning, inhaled pulmonary vasodilators, high-frequency oscillatory ventilation (HFOV), and extracorporeal membrane oxygenation (ECMO).
Impairments in function after resolution of critical illness are common and may be under-recognized. Cognitive dysfunction, mood disorders, respiratory impairment, physical debility and reduced quality of life, occur at high rates among survivors of critical illness, with important clinical and public health implications. The elderly, patients with preexisting comorbidities, and those experiencing delirium during hospitalization are at elevated risk for impairment after critical illness resolves. Predicting impairment after critical illness and developing interventions to prevent impairment are areas of ongoing research.
Intravenous fluid administration is a cornerstone of intensive care resuscitation. When considering fluid therapy, clinicians must attempt to answer two fundamental questions: (1) Is an increase in cardiac output likely to reverse or improve a hypoperfusion state? and (2) Is a fluid bolus likely to increase the cardiac output? Recent data on the potentially harmful effect of fluid overload in ICU patients have led intensivists to reconsider the sacrosanct practice of the “fluid challenge”. As such, various predictors of fluid responsiveness have been proposed as potential alternatives to inform clinicians on the best course of action. A better understanding of the largely ignored basic physiologic mechanisms that determine fluid responsiveness can inform the choice of available bedside maneuvers, interpretation of data, and use of available technologies in hypoperfused patients.
The physiological changes induced by liberation from mechanical ventilation are usually well tolerated by patients deemed to have passed a “spontaneous” breathing trial. However, a subset of patients with acceptable indices of respiratory load while on very low ventilator support will subsequently experience cardiopulmonary collapse following removal of the endotracheal tube. These patients typically have underlying co-morbid cardiopulmonary disease whereby poor physiological reserve in either organ system induces and perpetuates pathophysiology in the other. Knowledge of these deleterious interactions may help the clinician anticipate abnormal cardio-respiratory load and hemodynamic embarrassment after extubation.