A comatose 23-year-old woman with acute liver failure due to an overdose of acetaminophen had indications of intracranial hypertension and underwent liver transplantation. Her level of arousal did not improve, and on postoperative day 1, clinical signs of cerebral herniation became apparent. An intracranial pressure monitor was placed, and intracranial hypertension was documented. Elevations in intracranial pressure persisted despite maximal osmotherapy, and therapeutic hypothermia was started. Normalization of intracranial pressure was rapid. Findings on neurological examination improved and the patient was discharged from the hospital with no neurological impairment. (American Journal of Critical Care. 2012;21:75,72-74) A 23-year-old woman was admitted to our medical intensive care unit from an outside hospital. She had acute liver failure after ingesting approximately 90 tablets of oxycodone/acetaminophen and an unknown quantity of benzodiazepines. She arrived comatose at the outside hospital and was promptly intubated for airway protection. On initial examination, heart rate was 93/min, and blood pressure was 130/90 mm Hg. Her score on the Glasgow Coma Scale was 3T; her pupils were constricted but equal and reactive to light. The patient was given intravenous N-acetylcysteine for an initial acetaminophen level of 212 µg/mL (to convert to micromoles per liter, multiply by 6.614). During the next 48 hours, fulminant hepatic failure developed. Laboratory findings were as follows: Continued on page 72Cases of Note features peer-reviewed case reports and case series that document clinically relevant findings from critical and high acuity care environments. Cases that illuminate a clinical diagnosis or a management issue in the treatment of critically and acutely ill patients and include discussion of the patient's experience with the illness or intervention are encouraged.
Background In the critically ill, mineralocorticoid deficiency (MD) is associated with greater disease severity, the development of acute renal insufficiency, and increased mortality. We hypothesized that severely injured trauma patients presenting with hemorrhagic shock would demonstrate a high degree of MD. We also hypothesized that MD in these patients would be associated with increased length of stay, hypotension, fluid requirements, and acute kidney injury (AKI). Materials and methods Thirty-two trauma patients in hemorrhagic shock on admission to the trauma bay (SBP <90 mm Hg × 2) were enrolled. Blood samples were obtained on ICU admission and 8, 16, 24, and 48 hours later. Plasma aldosterone (PA) and renin (PR) were assayed by radioimmunoassay. MD was defined as a ratio of PA/PR ≤2. Demographic data, injury severity score, ICU and hospital length of stay, fluid requirements, mean arterial pressure, serum sodium, hypotension, and risk for AKI were compared for patients with and without MD. Results At ICU admission, 48% of patients met criteria for MD. Patients with MD were significantly more likely to experience hypotension (MAP ≤60 mm Hg) during the study period. MD patients required significantly more units of blood in 48 h than non-MD patients (13 [7–22] versus 5 [2–7], P = 0.015) and had increased crystalloid requirements (18L [14–23] versus 9L [6–10], P < 0.001). MD patients were at higher risk for AKI according to RIFLE and AKIN criteria. Conclusions MD is a common entity in trauma patients presenting in hemorrhagic shock. Patients with MD required a more aggressive resuscitative effort, were more likely to experience hypotension, and had a higher risk of AKI than non-MD patients. Future studies are needed to fully understand the impact of MD following trauma and the potential role for hormonal replacement therapy.
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