Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.

Rhabdomyolysis is a clinical syndrome that comprises destruction of skeletal muscle with outflow of intracellular muscle content into the bloodstream. There is a great heterogeneity in the literature regarding definition, epidemiology, and treatment. The aim of this systematic literature review was to summarize the current state of knowledge regarding the epidemiologic data, definition, and management of rhabdomyolysis. A systematic search was conducted using the keywords “rhabdomyolysis” and “crush syndrome” covering all articles from January 2006 to December 2015 in three databases (MEDLINE, SCOPUS, and ScienceDirect). The search was divided into two steps: first, all articles that included data regarding definition, pathophysiology, and diagnosis were identified, excluding only case reports; then articles of original research with humans that reported epidemiological data (e.g., risk factors, common etiologies, and mortality) or treatment of rhabdomyolysis were identified. Information was summarized and organized based on these topics. The search generated 5632 articles. After screening titles and abstracts, 164 articles were retrieved and read: 56 articles met the final inclusion criteria; 23 were reviews (narrative or systematic); 16 were original articles containing epidemiological data; and six contained treatment specifications for patients with rhabdomyolysis. Most studies defined rhabdomyolysis based on creatine kinase values five times above the upper limit of normal. Etiologies differ among the adult and pediatric populations and no randomized controlled trials have been done to compare intravenous fluid therapy alone versus intravenous fluid therapy with bicarbonate and/or mannitol.

In critically ill patients who are receiving mechanical ventilation, the factors associated with physicians' decisions to withdraw ventilation in anticipation of death are unclear. The objective of this study was to examine the clinical determinants that were associated with the withdrawal of mechanical ventilation. We studied adults who were receiving mechanical ventilation in 15 intensive care units, recording base-line physiological characteristics, daily Multiple Organ Dysfunction Scores, the patient's decision-making ability, the type of life support administered, the use of do-not-resuscitate orders, the physician's prediction of the patient's status, and the physician's perceptions of the patient's preferences about the use of life support. We examined the relation between these factors and withdrawal of mechanical ventilation, using Cox proportional-hazards regression analysis. Of 851 patients who were receiving mechanical ventilation, 539 (63.3 percent) were successfully weaned, 146 (17.2 percent) died while receiving mechanical ventilation, and 166 (19.5 percent) had mechanical ventilation withdrawn. The need for inotropes or vasopressors was associated with withdrawal of the ventilator (hazard ratio, 1.78; 95 percent confidence interval, 1.20 to 2.66; P=0.004), as were the physician's prediction that the patient's likelihood of survival in the intensive care unit was less than 10 percent (hazard ratio, 3.49; 95 percent confidence interval, 1.39 to 8.79; P=0.002), the physician's prediction that future cognitive function would be severely impaired (hazard ratio, 2.51; 95 percent confidence interval, 1.28 to 4.94; P=0.04), and the physician's perception that the patient did not want life support used (hazard ratio, 4.19; 95 percent confidence interval, 2.57 to 6.81; P<0.001). Rather than age or the severity of the illness and organ dysfunction, the strongest determinants of the withdrawal of ventilation in critically ill patients were the physician's perception that the patient preferred not to use life support, the physician's predictions of a low likelihood of survival in the intensive care unit and a high likelihood of poor cognitive function, and the use of inotropes or vasopressors.

Noncardiogenic pulmonary edema is often associated with increased intracranial pressure and can be the initial manifestation of hyponatremic encephalopathy. Marathon runners tend to develop conditions that lead to hyponatremia. To describe the development and treatment of noncardiogenic pulmonary edema in marathon runners that was associated with hyponatremic encephalopathy. Case series. One university hospital and two community hospitals. Seven healthy marathon runners who had a history of nonsteroidal anti-inflammatory drug use. The runners collapsed after competing in a marathon and were hospitalized with pulmonary edema. Plasma sodium levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or computed tomographic scans of the brain. Patients had nausea, emesis, and obtundation. The mean (±SD) plasma sodium level was 121 ± 3 mmol/L, and oxygen saturation was less than 70%. Electrocardiograms and echocardiograms were normal. Chest radiographs showed pulmonary edema with a normal heart. Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated. Scanning of the brain showed cerebral edema. All patients were intubated and mechanically ventilated. Treatment with intravenous NaCl, 514 mmol/L, increased plasma sodium levels by 10 mmol/L in 12 hours. Pulmonary and cerebral edema resolved as the sodium level increased. One patient had unsuspected hyponatremic encephalopathy and died of cardiopulmonary arrest caused by brainstem herniation. All six treated patients recovered and were well after 1 year of follow-up. In healthy marathon runners, noncardiogenic pulmonary edema can be associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed and can be successfully treated with hypertonic NaCl.