Mild hypothermia, as compared with normothermia, in organ donors after declaration of death according to neurologic criteria significantly reduced the rate of delayed graft function among recipients. (Funded by the Health Resources and Services Administration; ClinicalTrials.gov number, NCT01680744.).
This document was developed through the collaborative efforts of the Society of Critical Care Medicine, the American College of Chest Physicians, and the Association of Organ Procurement Organizations. Under the auspices of these societies, a multidisciplinary, multi-institutional task force was convened, incorporating expertise in critical care medicine, organ donor management, and transplantation. Members of the task force were divided into 13 subcommittees, each focused on one of the following general or organ-specific areas: death determination using neurologic criteria, donation after circulatory death determination, authorization process, general contraindications to donation, hemodynamic management, endocrine dysfunction and hormone replacement therapy, pediatric donor management, cardiac donation, lung donation, liver donation, kidney donation, small bowel donation, and pancreas donation. Subcommittees were charged with generating a series of management-related questions related to their topic. For each question, subcommittees provided a summary of relevant literature and specific recommendations. The specific recommendations were approved by all members of the task force and then assembled into a complete document. Because the available literature was overwhelmingly comprised of observational studies and case series, representing low-quality evidence, a decision was made that the document would assume the form of a consensus statement rather than a formally graded guideline. The goal of this document is to provide critical care practitioners with essential information and practical recommendations related to management of the potential organ donor, based on the available literature and expert consensus.
Standard dosing of enoxaparin leads to low anti-Xa levels in half of surgical ICU patients. Low levels are associated with a significant increase in the risk of DVT. These data support future studies using adjusted-dose enoxaparin.
Although clinical syndromes consistent with rhabdomyolysis were recognized in the late 19th and early 20th centuries, the modern history of the crush syndrome begins with Bywaters' and Beal's classic description of the entrapped bombing victims of London during World War II [1 -4]. They reported five cases of crush injury, in which victims had one or more of their extremities trapped under debris for prolonged periods of time. All five patients presented in shock, had swollen extremities, developed dark urine, progressed to renal failure, and eventually died. Histologic examination of the kidney revealed tubular necrosis and pigmented casts. In 1944, Bywaters and Stead identified myoglobin as the urinary pigment and proposed its role in the development of renal failure [5].Large numbers of patients with crush injuries and rhabdomyolysis have been reported after the collapse of mines [6,7], severe beatings [8], and earthquakes [9 -15]. In the United States, alcohol intoxication associated with prolonged muscle compression and seizures is the most common etiology of rhabdomyolysis [16]. Serum creatine kinase (CK) levels correlate with the degree of muscle injury [14] and can be used to assess the severity of rhabdomyolysis. Acute renal failure (ARF) is one of the most serious consequences of rhabdomyolysis and occurs in 4% to 33% of cases, carrying with it a mortality rate of 3% to 50% [17]. Rhabdomyolysis accounts for 5% to 7% of all cases of ARF in the United States [18].This article focuses on the pathophysiology and treatment of myoglobinuric renal failure caused by traumatic rhabdomyolysis and crush injuries.
Hypothesis: Central venous blood gas (VBG) measurements of pH, PCO 2 , and base excess can be substituted for the same values obtained from an arterial blood gas (ABG) analysis in mechanically ventilated trauma patients, obviating the need for arterial puncture. Design and Setting: Prospective comparison of 99 sets of VBGs and ABGs at a level 1 academic trauma center. Patients: A consecutive sample of 25 trauma patients admitted to the intensive care unit who required mechanical ventilation and had both central venous and arterial catheters. Main Outcome Measures: Pearson correlations and Bland-Altman limits of agreement (LOAs) for pH, PCO 2 , and base excess values from each set of VBGs and ABGs. Results: When VBG and ABG values were compared, pH had R=0.92, PϽ.001, and 95% LOAs of −0.09 to 0.03; PCO 2 , R=0.88, PϽ.001, and 95% LOAs of −2.2 to 10.9; and base excess, R=0.96, PϽ.001, and 95% LOAs of −2.2 to 1.8. A receiver operating characteristic curve showed that a central venous PCO 2 of 50 mm Hg had 100% sensitivity and 84% specificity for determining significant hypercarbia (arterial PCO 2 Ͼ 50 mm Hg). Conclusions: Central venous and arterial PCO 2 , pH, and base excess values correlate well, but their LOAs represent clinically significant ranges that could affect management. Although VBGs cannot be substituted for ABGs in mechanically ventilated trauma patients during the initial phases of resuscitation, clinically reliable conclusions can be reached with VBG analysis.
HVI occurred in less than 1% of all blunt trauma admissions. Delays in operative intervention are associated with an increased mortality. A high index of suspicion is needed to make a timely diagnosis and minimize risk.
Resuscitation of uncontrolled hemorrhagic shock with NS requires significantly greater volume and is associated with greater urine output, hyperchloremic acidosis, and dilutional coagulopathy as compared with LR. Resuscitation with LR results in an elevation of the lactate level that is not associated with acidosis. Lactated Ringer's solution is superior to NS for the resuscitation of uncontrolled hemorrhagic shock in swine.
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