Acute atraumatic subdural hematoma is a rare occurrence and there exist few case studies which describe suspected cases and causes for this condition. We present a case of a 36-year-old female at 32-week gestation who initially presented to the emergency department for evaluation of lower extremity cellulitis but had acute neurologic change while being in the ED. Computed tomography revealed a right subdural hematoma with midline shift and mass effect. The primary cause for the patient's subdural hematoma is unknown; however, this patient had several risk factors for developing an atraumatic subdural hematoma.

BackgroundIntracranial abscesses are rare and life-threatening conditions that typically originate from direct extension from nearby structures, hematogenous dissemination or following penetrating cerebral trauma or neurosurgery.FindingsA 36-year-old male presented to our emergency department with complaints of left eye swelling, headache and drowsiness. On physical exam, the patient was febrile and his left upper eyelid was markedly swollen with fluctuance and drainage. Maxillofacial computed tomography was obtained to evaluate for orbital pathology but revealed bifrontal brain abscesses.ConclusionsBrain abscesses should be considered in the differential diagnosis for patients who present with the classic triad of headache, fever and neurological deficit.

Alveolar hemorrhage is a rare yet devastating clinical entity if not identified and treated aggressively. Exceedingly rare are the cases of anticoagulant-induced alveolar hemorrhage with very few cases described in the current literature. The nonspecific presentation of an alveolar hemorrhage makes its diagnosis and appropriate treatment difficult in the emergency department. We report a case of a patient on warfarin for atrial fibrillation who was initially misdiagnosed as having community-acquired pneumonia, but subsequently was identified to have a fatal alveolar hemorrhage.

Background: Hypertonic saline (HTS) is an effective treatment for patients with increased intracranial pressure (ICP) secondary to traumatic brain injury (TBI). The ideal concentration for use in these patients is not well defined. The aim of our study was to compare Glasgow coma scale (GCS) and mortality of patients after administration of 3% vs. 23.4% HTS in the initial resuscitation. Methods: We performed a retrospective analysis of patients admitted to the surgical intensive care unit (ICU) under the trauma service with a diagnosis of TBI who received HTS during initial resuscitation. Patient medical records were reviewed to collect data including in-hospital mortality, ICU length of stay, hospital length of stay, GCS at the time of admission and discharge, serum sodium and serum osmolality values at 24, 48 and 72 h after arrival, acute kidney injury and severe hypernatremia. Results: Patients ≥ 18 years of age admitted to trauma ICU with a diagnosis of TBI. Pregnant, incarcerated, or non-traumatic intracranial hemorrhage patients were excluded. Thirty-one patients were included in the study. The 3% arm included 21 patients, and 23.4% arm had 10 patients. All patients received 3% HTS continuous infusion following initial bolus. Median injury severity scores (ISS) were 22 vs. 25 in the 3% vs. 23.4% HTS groups, respectively (P = 0.37). There was no difference in in-hospital mortality between the two groups (52.4% vs. 50.0%, P = 0.45). There was a significant improvement in GCS at discharge, 8.3% vs. 44.4% in 3% HTS vs. 23.4% HTS arms, respectively (P = 0.029). Patients reaching goal serum sodium and serum osmolality at 24 h was significantly higher in the 23.4% group (33.3% vs. 70.0%; P = 0.028 and 35.7% vs. 77.8%; P = 0.026, respectively). Significant increase in incidence of severe hypernatremia in the 23.4% arm was noted (0.0% vs. 40.0%, P = 0.009). Conclusion: This study demonstrates no significant difference in inhospital mortality for patients who received 3% vs. 23.4% HTS. Significantly higher percentage of patients receiving 23.4% HTS reached goal serum sodium and osmolality levels at 24 h with a concomitant significantly increased rate of severe hypernatremia.

The authors herein present the case of a 53-year-old female who was being treated as an outpatient for seizure disorder but was also receiving high-dose methadone therapy. She presented to the emergency department (ED) for what appeared to be a seizure and was found to have a prolonged QT interval, as well as runs of paroxysmal polymorphic ventricular tachycardia with seizure-like activity occurring during the arrhythmia. The markedly prolonged QT interval corrected after treatment with intravenous magnesium; subsequent electroencephalogram, neurology and cardiology consultations confirmed the cause of the recurrent seizure-like episodes to be secondary to the cardiotoxic effects of methadone.