25 Aug 06
Posted in Head injury, Propofol at 9:24 by Laci
By SM Corbett,J Moore, JA Rebuck, FB Rogers, CM Greene
Case report
Critical Care Medicine 2006;34:2479-2483
Patient
A 21-yr-old male with traumatic brain injury was administered high doses of propofol for sedation and intracranial pressure control combined with vasopressor therapy to maintain cerebral perfusion pressure >60 mmHg. He developed a significant metabolic acidosis with a lactic acid level of 10.9 mmol/L.
Measurements and Main Results
An exploratory abdominal laparotomy was negative for traumatic injury. During the procedure, the propofol infusion was considered a possible cause and was discontinued. On review, it became apparent that a combination of high-dose propofol and catecholamines were responsible for the lactic acidosis. An echocardiogram revealed severe left ventricular dysfunction and cardiomyopathy, which resolved within 19 days.
Conclusions
High-dose propofol should be avoided and alternative agents should be instituted for sedation and intracranial pressure management. The use of catecholamine infusions to maintain cerebral perfusion pressure in the setting of a high-dose propofol infusion may be pharmacologically unsound and may be a triggering factor for propofol infusion syndrome. Identification of the syndrome and discontinuation of propofol resulted in complete reversal of symptoms in the case described.
Permalink
Posted in Sepsis, Troponin at 9:15 by Laci
By R Favory and R Neviere
Critical Care 2006, 10:224
Because no bedside method is currently available to evaluate myocardial contractility independent of loading conditions, a biological marker that could detect myocardial dysfunction in the early stage of severe sepsis would be a helpful tool in the management of septic patients. Clinical and experimental studies have reported that plasma cardiac troponin levels are increased in sepsis and could indicate myocardial dysfunction and poor outcome. The high prevalence of elevated levels of cardiac troponins in sepsis raises the question of what mechanism results in their release into the circulation. Apart from focal ischemia, several factors may contribute to the microinjury and minimal myocardial cell damage in the setting of septic shock. A possible direct cardiac myocytotoxic effect of endotoxins, cytokines or reactive oxygen radicals induced by the infectious process and produced by activated neutrophils, macrophages and endothelial cells has been postulated. The presence of microvascular failure and regional wall motion abnormalities, which are frequently observed in positive-troponin patients, also suggest ventricular wall strain and cardiac cell necrosis. Altogether, the available studies support the contention that cardiac troponin release is a valuable marker of myocardial injury in patients with septic shock.
Permalink
Posted in Anticoagulation at 9:14 by Laci
By M Levi and S M Opal
Critical Care 2006, 10:222
Many critically ill patients develop hemostatic abnormalities, ranging from isolated thrombocytopenia or prolonged global clotting tests to complex defects, such as disseminated intravascular coagulation. There are many causes for a deranged coagulation in critically ill patients and each of these underlying disorders may require specific therapeutic or supportive management. In recent years, new insights into the pathogenesis and clinical management of many coagulation defects in critically ill patients have been accumulated and this knowledge is helpful in determining the optimal diagnostic and therapeutic strategy.
Permalink
Posted in Critical Care, General at 9:13 by Laci
By LG Forni, W McKinnon and PJ Hilton
Critical Care 2006, 10:220
In the critically ill, metabolic acidosis is a common observation and, in clinical practice, the cause of this derangement is often multi-factorial. Various measures are often employed to try and characterise the aetiology of metabolic acidosis, the most popular of which is the anion gap. The purpose of the anion gap can be perceived as a means by which the physician is alerted to the presence of unmeasured anions in plasma that contribute to the observed acidosis. In many cases, the causative ion may be easily identified, such as lactate, but often the causative ion(s) remain unidentified, even after exclusion of the ‘classic’ causes. We describe here the various attempts in the literature that have been made to address this observation and highlight recent studies that reveal potential sources of such hitherto unmeasured anions.
Permalink