European journal of anaesthesiology. Supplement最新文献

Transcranial Doppler is an innovative, flexible, accessible tool for the bedside monitoring of static and dynamic cerebral flow and treatment response. Introduced by Rune Aaslid in 1982, it has become indispensable in clinical practice. The main obstacle to ultrasound penetration of the skull is bone. Low frequencies, 1-2 MHz, reduce the attenuation of the ultrasound wave caused by bone. Transcranial Doppler also provides the advantage of acoustic windows representing specific points of the skull where the bone is thin enough to allow ultrasounds to penetrate. There are four acoustic windows: transtemporal, transorbital, suboccipital and retromandibular. The identification of each intracranial vessel is based on the following elements: (a) velocity and direction; (b) depth of signal capture; (c) possibility of following the vessel its whole length; (d) spatial relationship with other vessels; and (e) response to homolateral and contralateral carotid compression. The main fields of clinical application of transcranial Doppler are assessment of vasospasm, detection of stenosis of the intracranial arteries, evaluation of cerebrovascular autoregulation, non-invasive estimation of intracranial pressure, measure of effective downstream pressure and assessment of brain death. Mean flow velocity is directly proportional to flow and inversely proportional to the section of the vessel. Any circumstance that leads to a variation of one of these factors can thus affect mean velocity. The main pathological condition affecting flow velocity is the vasospasm. Vasospasm is a frequent complication of subarachnoid haemorrhage, it often remains clinically silent and the factors that make it symptomatic are largely unknown. Threshold velocities above which vasospasm comes into place are well defined as regards the median cerebral artery, while there is no consensus for the other vessels. Nevertheless, an increase in velocity alone is not sufficient to arrive at a diagnosis of vasospasm; a condition of hyperaemia also presents with an increase in flow velocity. The Lindegaard Index has therefore been introduced, which is defined by the ratio between the mean flow velocity in the median cerebral artery and the mean flow velocity in the internal carotid artery. Criteria for diagnosis of a stenosis >50% of an intracranial vessel with transcranial Doppler include: (a) segmentary acceleration of flow velocity; (b) drop in velocity below the stenotic segment; (c) asymmetry; and (d) circumscribed flow disturbances (turbulence and musical murmur). The transcranial Doppler enables us to assess both components of self-regulation. The static component is measured by observing changes in flow velocity caused by pharmacologically induced episodes of hypertension and hypotension. The dynamic component of autoregulation can be measured using a method devised by Aaslid known as the 'cuff test'. A very effective and safe device for measuring cerebral autoregulation is the trans

Recent studies have demonstrated that bedside cranial burr hole and insertion of intraparenchymal catheters for intracranial pressure monitoring performed by intensive care physicians is a safe procedure, with a complication rate comparable to other series published by neurosurgeons. The overall morbidity rate is comparable to, or even lower than, that caused by central vein catheterization. The procedure is also quite simple and modern disposable intracranial procedural kits are available. After the skin is prepped the landmark for skin incision, called the 'Kocher's point', located about 2-4 cm lateral to the midline (mid-pupillary line) and 2-3 cm anterior to the coronal suture, is found. Then the surgical field is prepared with the sterile drapes and the skin infiltrated with local anaesthetic (0.5% lidocaine with 1 : 200000 epinephrine). After skin incision and retraction of the skin and subcutaneous tissue, the periosteum should be scraped off in order expose the skull. The skin is then divaricated, exposing the underlying bone. The hole is drilled with either an electric drill or a twist drill (the drilling procedure must be performed with the drill held within 10 degrees of the perpendicular position to the incision site). The hole is then irrigated with sterile saline and an 18-G spinal needle may be used to open the dura (exercise caution when perforating the dura so as to avoid damage to the underlying structures). Following opening of the dura, the Bolt, containing a stylet, is screwed manually into the skull at approximately 5 mm to 1 cm for adults. The stylet is then removed after the bolt has been screwed in, after which the bolt should be filled with saline. Finally, the zeroing of the transducer is performed by simply holding the tip in air while zeroing on the monitor. The transducer is inserted inside the bolt and the screw tightened. The intracranial pressure value can then be read.

The most informative neurophysiological techniques available in the neurosurgical intensive care unit are electroencephalograph and somatosensory evoked potentials. Such tools, which give an evaluation of cerebral function in comatose patients, support clinical evaluation and are complementary to neuroimaging. They serve both diagnostic/prognostic and monitoring purposes. While for the former, discontinuous monitoring is sufficient, for the latter, to obtain increased clinical impact, continuous monitoring is necessary. To perform and interpret these examinations in the neurosurgical intensive care unit, both the technician and the neurophysiologist need specific training in the intensive care field. There is sufficient evidence to show that somatosensory evoked potentials are the best single indicator of early prognosis in traumatic and hypoxic-ischaemic coma compared to the Glasgow Coma Score, computed tomography scan and electroencephalograph. Indeed, somatosensory evoked potentials should always be combined with clinical examination to determine the prognosis of coma. Despite widespread use of somatosensory evoked potentials and their prognostic utility in acute brain injury, few studies exist on continuous somatosensory evoked potential monitoring in the intensive care unit. We carried out a pilot study of continuous electroencephalograph-somatosensory evoked potential monitoring in the neurosurgical intensive care unit (traumatic brain injury and intracranial haemorrhage, Glasgow Coma Score <9, intracranial pressure monitoring). All patients stable from a clinical and computed tomography scan point of view showed no significant somatosensory evoked potential modifications, while in the case of clinical deterioration (23%), somatosensory evoked potentials always showed significant modifications. While somatosensory evoked potentials correlated with short-term outcome, intracranial pressure showed a poor correlation. We believe neurophysiological monitoring is an ideal complement to the other parameters monitored in the neurosurgical intensive care unit. Whereas intracranial pressure is simply a pressure index, electroencephalograph-somatosensory evoked potential monitoring reflects to what extent cerebral parenchyma still remains metabolically active during acute brain injury.

Neurobehavioural sequelae of traumatic brain injuries require an appropriate/effective pharmacological response in that they represent an important cause of disability. In this field, there is no evidence that reaches the level of a standard: there are guidelines on the use of methylphenidate, donepezil and bromocriptine for the treatment of cognitive disturbances, for the non-use of phenytoin and for the use of beta-blockers for controlling aggressiveness. Resolving a single symptom is not relevant in a rehabilitation project if it is not in the context of a more complex picture of neurobehavioural recovery, in which the positive and negative effects of every therapeutic choice are considered. For example, phenytoin could be used for the positive control of epileptic crises but is not advised since it impedes the recovery of cognitive functions in general. Analogous effects not yet identified may concern benzodiazepine, neuroleptics and other sedatives usually prescribed in cases of cranial trauma. Psychotropic drugs are considered to be able to influence the neuronal plasticity processes. Studies on animals have shown that the administration of D-amphetamine combined with sensorial-motor exercise produces the steady acceleration of motor recovery, which acts as a catalyst to the neurological recovery process. On the other hand, alpha1-NA receptor antagonist drugs produce negative effects; these include clonidine (antihypertension) and haloperidol (neuroleptic). Studies need to be carried out to evaluate the effectiveness of particular drugs. These studies need to focus not only on the disappearance of symptoms but also on the positive and negative effects on overall rehabilitation and on the neurobiological recovery of the patient.

In spite of the many tools available for monitoring the central nervous system, there are no clinical trials which prove that continuous monitoring of any single variable in the intensive care unit has had any significant impact on the outcome of patients. Even in the absence of robust evidence proving the efficacy of neuromonitoring tools, we believe it is time to re-examine the basic objectives of neuromonitoring. The main reasons for monitoring neurocritical patients could be summarized as follows: (1) to detect early neurological worsening before irreversible brain damage occurs; (2) to individualize patient care decisions; (3) to guide patient management; (4) to monitor therapeutic response of some interventions and to avoid any consequent adverse effects; (5) to allow clinicians to be able to understand the pathophysiology of complex disorders; (6) to design and implement management protocols; and (7) to improve neurological outcome and quality of life in survivors of severe brain injuries. To reach these goals, there is a need to overcome some obstacles, such as the learning curve needed for any monitor and establishing consensus among experts on how to interpret monitor readings. In this review, the obstacles confronted in running randomized clinical trials in this field are discussed. The lack of equipoise and the ethical concerns in conducting such trials are discussed. In addition, the reasons for failure to improve outcome through the use of some monitoring devices are discussed and potential solutions proposed.

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. Cooling should not be viewed in isolation but in the context of a 'treatment bundle,' which together can significantly improve outcome after cardiac arrest. Favourable outcomes of 50-60% are now routinely achieved in many centres in patients with witnessed arrest and an initial rhythm of ventricular fibrillation or ventricular tachycardia. These results have been achieved by combining a number of therapeutic strategies, including early and effective resuscitation with greater emphasis on continuing chest compressions throughout various procedures (including resumption of compressions immediately after defibrillation even if rhythm has been restored) as well as prevention of hypoxia and hypotension in all stages following restoration of spontaneous circulation. 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.

In industrial countries it is estimated that the incidence of out-of-hospital sudden cardiac arrest lies between 36 and 128 per 100,000 inhabitants per year. Almost 80% of patients who initially survive a cardiac arrest present with coma lasting more than 1 h. Current therapy during cardiac arrest concentrates on the external support of circulation and respiration with additional drug and electrical therapy. Therapeutic hypothermia provides a new and very effective therapy for neuroprotection in patients after cardiac arrest. It is critical that mild hypothermia has to be applied very early after the ischaemic insult to be effective, otherwise the beneficial effects would be diminished or even abrogated. There are numerous methods available for cooling patients after ischaemic states. Surface cooling devices are non-invasive and range from simple ice packs to sophisticated machines with automatic feedback control. Other non-invasive methods include drugs and cold liquid ventilation. The newer devices have cooling rates comparable to invasive catheter techniques. Invasive cooling methods include the administration of ice-cold fluids intravenously, the use of intravascular cooling catheters, body cavity lavage, extra-corporeal circuits and selective brain cooling. Most of these methods are quite invasive and are still in an experimental stage. The optimal timing and technique for the induction of hypothermia after cardiac arrest have not yet been defined, and it is currently a major topic of ongoing research. The induction of hypothermia after cardiac arrest needs to be an integral component of the initial evaluation and stabilization of the patient.

Sepsis, a systemic inflammatory response to infection, is a leading cause of death in intensive care units. Recent investigations into the pathogenesis of sepsis reveal a biphasic inflammatory process. An early phase is characterized by pro-inflammatory cytokines (e.g. tumour necrosis factor-alpha), whereas a late phase is mediated by an inflammatory high-mobility group box 1 and an anti-inflammatory interleukin-10. Inflammation aberrantly activates coagulation cascades as sepsis progresses. This dual inflammatory response concomitant with dysregulated coagulation partially accounts for unsuccessful anti-cytokine therapies that have solely targeted early pro-inflammatory mediators (e.g. tumour necrosis factor-alpha). In contrast, activated protein C, which modifies both inflammatory and coagulatory pathways, has improved survival in patients in severe sepsis. Inhibition of the late mediator high-mobility group box 1 improves survival in established sepsis in pre-clinical studies. In addition, recent advances in molecular medicine have shed light on two novel experimental interventions against sepsis. Accelerated apoptosis of lymphocytes has been shown to play an important role in organ dysfunction in sepsis and techniques to suppress apoptosis have improved survival rate in sepsis models. The vagus nerve system has also been shown to suppress innate immune response through endogenous release and exogenous administration of cholinergic agonists, ameliorating inflammation and lethality in sepsis models.

Direct muscular stimulation is quick, simple, non-invasive and can be carried out at the patient's bedside. More importantly, it is reliable even when the patients cannot cooperate or are comatose. From the small amount of data available, it seems to be as accurate as neuromuscular biopsy in diagnosing critical illness myopathy. It would therefore be advisable to use it in everyday clinical practice.