Neurocritical care
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Cerebral perfusion pressure (CPP) is one aspect of an all-encompassing approach in the management of traumatic brain injury (TBI). The clinical use of CPP is based on theoretical considerations that optimal cerebral blood flow is necessary to meet the metabolic needs of the injured brain. The goal is to preserve the ischemic penumbra and avoid secondary insults. ⋯ Recently, the Brain Trauma Foundation updated their Web-based recommendation of a lower CPP goal of 60 mmHg. However, the lack of definitive data, such as from a randomized prospective intention-to-treat clinical trials, leaves this goal open to controversy. Therefore, for a variety of reasons, the physician may be most prudent to use the published CPP guideline of 70 mmHg until a consensus statement is published advocating a different value.
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Review Case Reports
Medical futility: definition, determination, and disputes in critical care.
Physicians may employ the concept of medical futility to justify a decision not to pursue certain treatments that may be requested or demanded by patients or surrogates. Medical futility means that the proposed therapy should not be performed because available data show that it will not improve the patient's medical condition. Medical futility remains ethically controversial for several reasons. ⋯ Medical futility has been conceptualized as a power struggle for decisional authority between physicians and patients/surrogates. Medical futility disputes are best avoided by strategies that optimize communication between physicians and surrogates; encourage physicians to provide families with accurate, current, and frequent prognostic estimates; assure that physicians address the emotional needs of the family and try to understand the problem from the family's perspective; and facilitate excellent palliative care through the course of the illness. Critical care physicians should support the drafting of state laws embracing futility considerations and should assist hospital policymakers in drafting hospital futility policies that both provide a fair process to settle disputes and embrace an ethic of care.
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Neuromuscular disorders increasingly are recognized as a complication in patients in the intensive care unit (ICU) and represent a common cause of prolonged ventilator dependency. The distinct syndromes of critical illness myopathy, prolonged neuromuscular blockade, and critical illness polyneuropathy (CIP) may arise as a consequence of sepsis, multi-organ failure, and exposure to various medications--notably, intravenous corticosteroids and neuromuscular blocking agents--but the pathophysiology of these disorders remains poorly understood. More than one syndrome may occur simultaneously, and the distinctions may be difficult in a particular patient, but a specific diagnosis usually can be established after careful clinical, electrodiagnostic, and, when necessary, histological evaluation. ⋯ Repetitive nerve stimulation shows a decrement of the compound muscle action potential and, in most cases, establishes a disorder of neuromuscular transmission. With the recent epidemic of West Nile virus infection, a clinical syndrome of acute flaccid paralysis with several features indistinguishable from poliomyelitis has emerged. This article critically examines the clinical, electrophysiological, and pathological features of these and other acute neuromuscular syndromes that arise in the context of ICU care and summarizes the current understanding of the pathophysiology and treatment of these disorders.
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Tuberculous meningitis (TBM) remains a common serious neurological emergency especially in the developing world. Elevated intracranial pressure (ICP) is often a feature of severe TBM and is associated with high morbidity and mortality. The pathology associated with TBM, such as cerebral edema, hydrocephalus, tuberculoma(s), and infarcts related to arthritis, contribute to increase in intracranial volume and, therefore, elevated ICP. ⋯ Use of steroids reduces not only cerebral edema but also the production of cytokines and other chemicals involved in the immunopathogenesis of TBM. Fever associated with TBM should be aggressively treated, because fever can worsen the impact of elevated ICP. Hyponatremia may complicate TBM and requires appropriate correction because it can aggravate cerebral edema.
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The ideal therapy and neurocritical care for patients with aneurysmal subarachnoid hemorrhage (SAH) follows from an early and accurate diagnosis. However, approximately 30% of patients with SAH are misdiagnosed at their initial visit to a physician. ⋯ I suggest a strategy for selecting which patients with headache require evaluation beyond history and physical examination and how that evaluation should proceed. Other diagnostic issues are also discussed, such as use of magnetic resonance scanning and angiography for diagnosis, distinguishing the traumatic LP from true SAH, the concept of warning bleeds, and the LP-first diagnostic strategy.