European journal of anaesthesiology. Supplement最新文献

Since shunting is almost a purely mechanical treatment that radically affects pressure-volume compensation, patients' cerebrospinal fluid hydrodynamics compensation should be examined before a shunt is implanted. Apart from an opening pressure and a resistance to cerebrospinal fluid outflow, pulse amplitude of intracranial pressure and the content of vasogenic waves are useful to gauge cerebrospinal fluid dynamics. Infusion studies, although invasive, may help with the decision about surgery. They also provide basic information for further management of shunted patients, when complications, such as shunt blockage, under- and over-drainage, arise.

Managing end-of-life care can be difficult because of the particular nature of intensive care support, which can separate the biological and the biographical aspects of life. Artificial organ support can temporarily delay death but, at the same time, may fail to restore a quality of life that the patient judges acceptable. For this reason, two concepts must be considered: that the mission of the healthcare system should be to care for patients according to their interests and wishes and that quality of care is related above all to the careful commitment of healthcare workers to the patient's best interests. Keeping these concepts in mind, the rule of the five Cs (competence, collegiality, communication, continuity of care and compassion) might be helpful in the management of end-of-life care. Unfortunately, neither the rule of the five Cs nor the careful use of moral principles in order to promote the patients' dignity can assure a universally acceptable decision. A reasonable level of 'moral certainty', however, might be achieved using a deliberative approach, which provides for the inclusion of all the different subjects involved in the decision-making process (patient, family, doctors, nurses and other carers), in order to reach the best possible decision in a specific situation.

In the long term after traumatic brain injury, the most disabling problems are generally related to neuropsychiatric sequelae, including personality change and cognitive impairment, rather than neurophysical sequelae. Cognitive impairment after severe injury is likely to include impaired speed of information processing, poor memory and executive problems. Personality change may include poor motivation, and a tendency to be self-centred and less aware of the needs of others. Patients may be described as lazy and thoughtless. Some become disinhibited and rude. Agitation and aggression can be very difficult to manage. Anxiety and depression symptoms are quite frequent and play a role in the development of persistent post-concussion syndrome after milder injury. Depression may be associated with a deterioration in disability over time after injury. Psychosis is not unusual though it has been difficult to confirm that traumatic brain injury is a cause of schizophrenia. Head injury may, many years later, increase the risk of Alzheimer's disease. Good rehabilitation probably minimizes the risk of psychiatric sequelae, but specific psychological and pharmacological treatments may be needed.

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. Hypertonic saline has clinically desirable physiological effects on cerebral blood flow, intracranial pressure and inflammatory responses in models of neurotrauma. 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.

Routine motor nerve conduction studies measure latencies, conduction velocities and amplitudes of compound action potentials. These measurements can be very useful in defining the pathology, while they provide little insight into the underlying disease mechanisms. Increasingly, the technique of 'threshold tracking' is being used in research and clinical studies on large myelinated axons. Nerve excitability testing is a non-invasive approach in investigating the pathophysiology of peripheral nerve disorders, which determines the electrical properties of the nerve membrane at the site of stimulation. We have found evidence that in patients with critical illness polyneuropathy peripheral nerves are depolarized. The correlations with serum factors suggest that this membrane depolarization is related to endoneurial hyperkalemia and/or hypoxia. While other mechanisms of depolarization may well be involved, the degree to which potential-sensitive nerve excitability indices are related to serum potassium and bicarbonate suggests that other factors, independent of potassium and acid-base balance, are likely to be of relatively minor significance.

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. Specific therapies are not yet available, and the quest for the pathomechanisms has proved more complicated than anticipated. Especially for critical illness myopathy, multiple sites of disturbances to the excitation-contraction coupling cascade are possible causes of muscle weakness. The present review summarizes the epidemiological, clinical and diagnostic features of critical illness myopathy and then focuses on current concepts of the presumed pathomechanisms of critical illness myopathy. Sepsis was shown to be a major cause of critical illness myopathy and special emphasis will be placed on how sepsis and inflammatory mediators influence (i) the membrane excitability at the level of voltage-gated ion channels and (ii) the intracellular protein signalling that results in selective loss of myosin protein content and muscle wasting. For (i), critical illness myopathy represents a new type of acquired channelopathy affecting the inactivation properties of Na+ channels. 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.

Drugs that inhibit platelet function are widely used to decrease the risk of occlusive arterial events in patients with atherosclerosis. There are three families of anti-platelet agents with proven clinical efficacy: (1) cyclo-oxygenase inhibitors, such as aspirin; (2) adenosine diphosphate receptor antagonists, such as the thienopyridine compounds ticlopidine and clopidogrel; and (3) glycoprotein IIb/IIIa antagonists. All these drugs are used during coronary interventions and in the medical management of acute coronary syndromes, while only aspirin and thienopyridine compounds are used in the long-term prevention of cardiovascular and cerebrovascular events in patients at risk. Despite the good risk-to-benefit ratio of anti-platelet agents, the risk of severe bleeding complications, including cerebral haemorrhage, is slightly increased, albeit to a much lesser extent than that associated with the use of other antithrombotic drugs, such as anticoagulants or thromobolytic agents. In addition, it must be noted that the increased incidence of haemorrhagic stroke is usually outweighed by a significant decrease in the incidence of ischaemic strokes. The combination of aspirin and vitamin K antagonists may be associated with the heightened risk of cerebral haemorrhage, compared to treatment with either drug alone.

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. The relationship between patient outcome and the use of a specific substance to improve cerebral perfusion has not been investigated. Dopamine, norepinephrine and phenylephrine all seem to increase cerebral blood flow in various animal models and in patients. The data suggest that norepinephrine may be the most predictable. It is associated with an improved restoration of global and regional oxygenation when compared to dopamine. Dopamine has been associated with an increase in brain oedema. There is further evidence that dopamine has many disadvantages in critically ill patients due to its ability to suppress circulating concentrations of most anterior pituitary-dependent hormones. Both aspects would further discourage its use. Data on phenylephrine are scarce. It has been associated with increased intracranial pressure and a failure to improve cerebral oxygenation despite markedly improved cerebral perfusion pressure. 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.

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. Research is directed at defining factors that reliably predict poor outcome in these patients. Favourable outcome proves impossible to predict. Studies on outcome prediction have focussed mostly on neurological examination, clinical neurophysiological tests and biochemical parameters. The most recent and extensive study in this respect was the PROPAC study in The Netherlands (407 patients). This study confirmed earlier findings that bilaterally absent early cortical response after median nerve somatosensory potentials (absent somatosensory evoked potentials) is the most reliable predictor of poor outcome (no recovery of consciousness). A serum neuron-specific-enolase level >33 microg L(-1) seemed equally reliable. In 2006, the American Practice Parameter on anoxic-ischaemic coma was published, summarizing the findings from the different studies. 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.