European journal of anaesthesiology. Supplement
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Animal and human studies suggest that hypertonic saline is a potential therapeutic agent to assist with the medical treatment of patients with traumatic brain injury. It may have a place as osmotherapy to decrease brain size, predominantly of uninjured brain and has several potential advantages over mannitol. ⋯ Animal studies support its use, but definitive human trials using mortality end-points in brain trauma are lacking. Hypertonic saline may be considered a therapeutic adjunct to the medical management of traumatic brain injury, awaiting definitive evidence to support routine use.
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Eur J Anaesthesiol Suppl · Jan 2008
ReviewEffects of catecholamines on cerebral blood vessels in patients with traumatic brain injury.
Data on the cerebrovascular effects of catecholamines after head injury are difficult both to interpret and to compare. Diverse parameters with regard to brain trauma animal models, methods of determining the effects on the cerebral blood flow and metabolism and choice of end-points have been used. Many studies investigate the cerebrovascular effects of catecholamines over a range of cerebral perfusion pressures above the range recommended by current guidelines. ⋯ For all other catecholamines and related substances there are insufficient data on the cerebrovascular effects after head injury. This suggests that norepinephrine may be the catecholamine that is the most suitable substance to maintain or restore adequate cerebral perfusion. The data, however, are insufficient to formulate a guideline.
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Postanoxic coma is a state of unconsciousness caused by global anoxia of the brain, most commonly due to cardiac arrest. Outcome after postanoxic coma lasting more than several hours is generally, but not invariably, poor. Recovery of consciousness reported in the literature varies from 8% to 72% of patients, but is mostly thought to be around 20-30% in patients surviving in coma for at least 24 h. ⋯ Poor outcome was defined as death, coma or severe disability after 6 months. The following factors were found to reliably predict this outcome: myoclonic status epilepticus within the first 24 h, absent pupillary responses after 24 h, absent corneal reflexes after 48 h, motor response to pain absent or extensor after 72 h and absent somatosensory evoked potentials (as defined above) after 1-3 days. Results for biochemical parameters (such as neuron-specific enolase) and neuroimaging are inconclusive.
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Eur J Anaesthesiol Suppl · Jan 2008
ReviewHypothermia and neurological outcome after cardiac arrest: state of the art.
Multi-centred studies in patients who remain comatose after cardiac arrest and also in newborn babies with perinatal asphyxia have clearly demonstrated that mild hypothermia (32-34 degrees C) can improve neurological outcome after post-anoxic injury. This represents a highly promising development in the field of neurocritical care. This review discusses the place of mild therapeutic hypothermia in the overall therapeutic strategy for cardiac arrest patients. ⋯ Regarding the use of hypothermia, early induction and proper management of side-effects are the key elements of successful implementation. Treatment should include the rapid infusion of 1500-3000 mL of cold fluids to induce hypothermia and prevent hypovolaemia and hypotension. Educational activities to increase awareness and acceptance of new therapeutic options and European Resuscitation Council guidelines are urgently required.
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Eur J Anaesthesiol Suppl · Jan 2008
ReviewCritical illness myopathy: sepsis-mediated failure of the peripheral nervous system.
With better survival of critically ill patients, 'de novo' arising neuromuscular complications like critical illness myopathy or polyneuropathy have been increasingly observed. Prolonged hospitalization not only imposes risks like pneumonia or thrombosis on patients but also represents a real budget threat to modern intensive-care medicine. Clinical symptoms like muscle weakness and weaning failure are common to critical illness myopathy and critical illness polyneuropathy and do not allow for distinction. ⋯ For (ii), both protein proteolysis and protein build up at the transcriptional level seem to be involved. Findings from different studies are put into a common context to propose a model for cytokine-mediated failure of muscle in severe sepsis. This can open a series of new possible trials to test specific therapeutic strategies in the future.