Citations

AbstractMetabolic derangements, when acute and severe, affect brain function. This presents mostly with a marked decline in the level of consciousness, resulting in impaired responsiveness, abnormal receptivity, impaired content, and loss of memory retention. The term metabolic encephalopathy has been used but is conjecture that can be challenged in the age of modern neuroimaging. We now recognize that many metabolic encephalopathies may involve structural lesions and at an early stage. Common clinical conundrums are the evaluation of the degree of brain injury and its recoverability. This review discusses the appropriate terminology for these conditions, the diagnostic approach, therapy recommendations, and prediction of recovery potential. In evaluating a presumed metabolic cause for encephalopathy, we must (1) search for and rule out structural injury to the brain despite an obvious explanatory metabolic derangement, (2) recognize that several confounding conditions often co‐exist, and (3) acknowledge that resolution of brain dysfunction may be protracted despite normalization of laboratory values.

Angioinvasive fungal infections of the cerebral vasculature often lead to significant morbidity and mortality. High clinical suspicion and early antifungal therapy could improve outcomes. We describe the fatal case of a patient with a rapidly enlarging cavernous carotid aneurysm due to angioinvasive fungus. This case highlights the challenges in diagnosis and management of this condition.

Introduction: Timing of clinical grading has not been fully studied in patients with aneurysmal subarachnoid hemorrhage (aSAH). Our primary objective was to identify at which time point the clinical assessment using the World Federation of Neurological Surgeons Scale (WFNS) and the Glasgow Coma Scale (GCS) is most predictive of poor functional outcome. Methods: Retrospective cohort study on the association of clinical grading determined at presentation, nadir and post-resuscitation, and poor outcome. Poor functional outcome was defined as Glasgow Outcome Scale score of 1-3 at 6 months. The study was approved by our Institutional Review Board. Results: We identified 186 consecutive patients admitted to a teaching hospital between January 2002 and June 2008. Patients’ mean age was 56.9±13.7 years and 63% of the patients were women. Twenty-four percent had poor functional outcome (mortality was 17%). On univariable logistic regression analyses, GCS determined at presentation (OR=0.80; p<0.0001), nadir (OR=0.73; p<0.0001) and post-resuscitation (OR=0.53; p<0.0001), modified Fisher Scale (OR=2.21;p=0.0013), WFNS assessed at presentation (OR=1.92;p<0.0001), nadir (OR=3.51; <0.0001) and post-resuscitation (OR=3.91; <0.0001), intracerebral hematoma on initial CT (OR=4.55;p<0.0002), acute hydrocephalus (OR=2.29;p=0.0375), and cerebral infarction (OR=4.84; <0.0001) were associated with poor outcome. On multivariable logistic regression analysis, only cerebral infarction (OR=5.80; 0.0013) and WFNS grade post-resuscitation (OR=3.43;<0.0001) were associated with poor outcome. Receiving operating characteristics/area under the curve (AUC) analysis demonstrated that WFNS determined post-resuscitation had a stronger association with poor outcome (AUC=0.90) than WFNS assessed upon admission or at nadir. Conclusions: Timing of WFNS assessment affects its prognostic value. Outcome after aSAH is best predicted by rating WFNS after neurological resuscitation.

Propofol “frenzy” is considered a severe propofol-induced neuroexcitatory reaction involving nonepileptic spells of extremity thrashing, marked agitation, irregular eye movements, and impaired consciousness. Patients with propofol neuroexcitation present unique challenges for anesthesia providers due to underrecognition, lack of diagnostic tests, and differentiating from other comparable disorders that require medications that can exacerbate symptoms. We present a case of a healthy young patient whose postoperative course was complicated by propofol frenzy and functional limb paralysis following hip surgery with a spinal anesthetic and propofol sedation. This case highlights anesthesia considerations for propofol frenzy and discusses dexmedetomidine as a promising modality for prompt management.

Heparin-induced thrombocytopenia (HIT) is a prothrombotic state caused by autoantibodies against platelet factor 4 (PF4)-heparin complexes. Although HIT typically presents 5-10 days after the initiation of heparin, thrombosis and thrombocytopenia may occur up to several weeks following heparin withdrawal, so-called delayed-onset HIT. Although rare, there have been isolated reports of HIT-induced cerebral venous sinus thrombosis (CVST), which carry high rates of morbidity and mortality. There is a need to further characterize the etiology, clinical presentation, treatment paradigms, and outcomes of patients with HIT-induced CVST. Here, we present the case of a 57-year old female who presented to the emergency department with a headache and seizure 11 days following a right total knee arthroplasty for which she received 3 post-operative doses of enoxaparin. Work-up demonstrated acute intracerebral hemorrhage (ICH), CVST, and thrombocytopenia. Intravenous heparin resulted in rapidly deteriorating platelet count and subsequent serologic testing confirmed the diagnosis of HIT. Treatment with bivalirudin was initiated, the HIT resolved, and the patient was discharged home on hospital day 19 with long-term anticoagulation mediated by warfarin. At 3-month follow up, the patient had mild upper motor neuron pattern weakness and was living independently. This case depicts a rare case of delayed-onset HIT and CVST, highlights the importance of establishing a fluid treatment plan for managing HIT-induced CVST, and illustrates the importance of employing rapid anticoagulation despite acute ICH to achieve a desirable clinical outcome.