Neurocritical care
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Review Case Reports
Spontaneous spinal epidural hematoma of unknown etiology: case report and literature review.
Our objective is to emphasize the importance of recognizing and rapidly treating spontaneous spinal epidural hematoma (SSEH). SSEH is a pathologic entity traditionally thought to be exceptionally rare but which, in the era of MR imaging, is becoming increasingly prevalent, and which if treated with sufficient rapidity can be completely curable. ⋯ As evidenced in the literature, outcome depends on time to operation and prognosis is impacted by age and preoperative deficit. Because of the high risk of poor outcome without treatment, SSEH should always be a diagnostic consideration in patients whose presentation is even slightly suggestive. Rapid, appropriate treatment of these patients can often lead to complete recovery of function, whereas any delay in appropriate treatment can be catastrophic.
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Thrombolysis heralded a new era of acute intervention for ischemic stroke, accompanied by an increasing need for comprehensive acute critical care support. There remains the prospect of novel cerebral protection strategies. Cerebral ischemia initiates a complex cascade of events at genomic, molecular, and cellular levels, and inflammation is important in this cascade, both in the CNS and in the periphery. ⋯ A promising novel therapeutic approach is the interleukin-1 receptor antagonist (IL-1ra), which limits the action of the cytokine IL-1, a pivotal mediator in the pathophysiology of acute neurodegeneration. Critical care has much to offer some patients after acute ischemic stroke, including the delivery of acute interventions, often with very short therapeutic time windows, physiological support, and the management of complications. We discuss inflammation and its mediators in acute ischemic stroke, the systemic stress, and acute phase protein responses to acute ischemic stroke, how inflammation is relevant in deteriorating ischemic stroke, the impact of physiological variables, and both current and emerging interventions for acute ischemic stroke.
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The management of Dysautonomia following severe traumatic brain injury (TBI) remains problematic, primarily due to an inadequate understanding of the pathophysiology of the condition. While the original theories inferred an epileptogenic source, there is greater support for disconnection theories in the literature. Disconnection theories suggest that Dysautonomia follows the release of one or more excitatory centres from higher centre control. ⋯ This article presents a critical review of the competing theories against the available observational, clinical and neurotransmitter evidence. Following this process, it is suggested that the EIR Model more readily explains pathophysiological and treatment data compared to conventional disconnection models. In particular, the EIR Model provides an explanatory model that encompasses other acute autonomic emergency syndromes, accommodates 'triggering' of paroxysms and provides a rationale for all known medication effects.
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Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. ⋯ Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited.
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In the current era of early surgery, there has been little interest in the use of antifibrinolytic therapy to prevent rebleeding after aneurysmal subarachnoid hemorrhage (aSAH). Older studies demonstrated that antifibrinolytics can reduce rebleeding, but long-term therapy results in increased cerebral ischemia from vasospasm, leading to no appreciable effect on mortality. While early surgery would seem to obviate the need for long-term antifibrinolytic use, a subgroup of patients may benefit from early therapy. ⋯ In this review, we examine the clinical pharmacology, dosing, monitoring, complications, and side effects of antifibrinolytic treatment. We conclude that early short-term antifibrinolytic therapy might be a reasonable strategy to prevent acute rebleeding and improve long-term outcome in aSAH patients. Additional randomized clinical trials are necessary to determine whether this management strategy is effective.