Neurocritical care
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We describe institutional vasopressor usage, and examine the effect of vasopressors on hemodynamics: heart rate (HR), mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygenation (PbtO(2)), and jugular venous oximetry (SjVO(2)) in adults with severe traumatic brain injury (TBI). ⋯ Most severe TBI patients received phenylephrine. Patients who received phenylephrine had higher MAP and CPP than patients who received dopamine and norepinephrine, respectively.
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Cerebral fat embolism is a well-described complication associated with long-bone fracture. However, with contemporary imaging, there is a distinct magnetic resonance imaging (MRI) pattern emerging. ⋯ This case highlights the MRI findings associated with fat embolism, their reversibility, and offers insight into the significant clinical improvement that may occur in such patients.
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Patients with acute brain injury but normal lung function are often intubated for airway protection, but extubation often fails. Currently, no clinical data exist that describe the events leading to extubation failure in this population. We examined the extubation failure rate, reintubation rate, and clinical characteristics of patients whose reason for intubation was a primary neurological injury. We then identified the clinical characteristics of those patients with primary brain injury who were reintubated. ⋯ The extubation failure rate in our neurocritical care unit is low. In patients with encephalopathy and primary brain injury who were reintubated, respiratory distress caused by altered mental status was the most common cause of reintubation. These patients demonstrated signs disrupted ventilation usually with periods of prolonged hypoventilation. Increased work of breathing from lung injury due to pneumonia or aspiration was not the most common cause of reintubation in this population.
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We report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution's standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient's mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient's entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injury. ⋯ Given the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.
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Case Reports
Lactate-to-pyruvate ratio as a marker of propofol infusion syndrome after subarachnoid hemorrhage.
Propofol infusion syndrome (PRIS) is a rare but frequently fatal condition. It is characterized by cardiovascular collapse and metabolic derangement due to propofol exposure. The pathophysiology of PRIS is poorly understood, and its study has previously been limited to animal models and clinical observations. We present the first in vivo brain biochemical data in a patient with PRIS. ⋯ Cerebral LPR may be a sensitive marker of PRIS. Increases in LPR following propofol exposure should alert clinicians to the possibility of PRIS and might prompt early discontinuation of propofol thereby avoiding fatal complications.