Wijdicks, Eelco F.

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.

Abstract BACKGROUND AND IMPORTANCE Progressive episodic spells of altered levels of consciousness, often advancing to include paroxysmal autonomic instability, may be indicative of a diencephalic dysfunction underlying spontaneous intracranial hypotension (SIH). A rare, and often indolent, etiology may be spinal cerebrospinal fluid (CSF) leak—an elusive diagnosis, especially in cases of CSF-venous fistula (CVF) that are often missed on routine computed tomography (CT) myelography and magnetic resonance imaging (MRI). CLINICAL PRESENTATION We report an unusual case of a 50-yr-old woman who presented with rapidly progressive cyclical, self-resolving episodes of altered mentation and decreased arousal later in the day. Scrutiny of serial brain MRIs led to a diagnosis of SIH, with severe downward diencephalic and brain stem displacement—resulting in cerebral aqueduct occlusion with obstructive hydrocephalus. Initial clinical improvement occurred with CSF diversion, but the patient quickly deteriorated—developing diencephalic spells, including extensor posturing and severely depressed levels of consciousness. Clinical improvement was seen with stopping CSF diversion and Trendelenburg-positioning. After intensive spinal imaging, dynamic CT myelography identified a left T10 nerve root diverticula and CSF-venous fistula. Surgical obliteration resulted in rapid, profound neurological improvement, and ultimately full neurological recovery by 1 yr. CONCLUSION In our patient, worsening episodes of confusion, postural headaches, and autonomic instability developed due to SIH, which induced profound downward displacement and compression of the diencephalon and brain stem, and accompanied by subsequent obstructive hydrocephalus. Diagnostic persistence identified the CVF, which had caused the complex multifold pathophysiology and clinical presentation. If suspicion remains high for CVF, persistent spinal imaging, particularly with dynamic myelography, may be crucial.

Objectives: Spontaneous intracranial hemorrhage, including subarachnoid hemorrhage and intracerebral hemorrhage, is associated with significant morbidity and mortality. Although many of these patients will require ICU admission, little is known regarding their outcomes and the costs incurred. We evaluated this population in order to identify outcomes and cost patterns. Design: Retrospective cohort analysis of a health administrative database. Setting: Two ICUs within a single hospital system. Patients: Eight-thousand four-hundred forty-seven patients admitted to ICU from 2011 to 2014, of whom 332 had a diagnosis of spontaneous intracranial hemorrhage. Control patients were defined as randomly selected age, sex, and comorbidity index–matched nonintracranial hemorrhage ICU patients (1:4 matching ratio). Interventions: None. Measurements and Main Results: Mean age of ICU intracranial hemorrhage patients was 60.1 years, and 120 (36.1%) died prior to discharge. Intracranial hemorrhage was associated with a mean total cost of $75,869, compared with $52,471 in control patients (p < 0.01). Mean cost per survivor of intracranial hemorrhage patients was $118,813. Subarachnoid hemorrhage was associated with significantly higher mean total costs than intracerebral hemorrhage ($92,794 vs $53,491; p < 0.01) and higher mean cost per day ($4,377 vs $3,604; p < 0.01). Patients with intracranial hemorrhage who survived to hospital discharge were significantly costlier than decedents ($100,979 vs $30,872; p < 0.01). Intracranial hemorrhage associated with oral anticoagulant use had a mean total cost of $152,373, compared with $66,548 in nonoral anticoagulant intracranial hemorrhage (p < 0.01). Conclusions: Patients admitted to ICU with intracranial hemorrhage have high costs and high mortality, leading to elevated cost per survivor. Subarachnoid hemorrhage patients incur greater costs than intracerebral hemorrhage patients, and oral anticoagulant–associated intracerebral hemorrhage is particularly costly. Our findings provide novel information regarding financial impact of this common ICU population.