Administration of anticoagulation for elderly patients with a CHADS2 score at 2 or more in the setting of sepsis can be associated with an increased risk of anticoagulation-related complications (eg, bleeding, heparin-induced thrombocytopenia). Managing and targeting a therapeutic goal with warfarin therapy in critically ill patients with sepsis is challenging. Further studies are necessary to provide appropriate recommendations in this setting.

A 70-year-old previously independent man developed progressive proximal leg weakness resulting in a fall at home suffering traumatic brain injury. He was prescribed a statin medication two years prior, but this was discontinued on admission to the hospital due to concern for statin myopathy. His weakness continued to progress while in acute rehabilitation, along with the development of dysphagia requiring placement of gastrostomy tube and respiratory failure requiring tracheostomy. Corticosteroids and intravenous immunoglobulin were administered without response. Nerve conduction study demonstrated no evidence of neuropathy; electromyography revealed spontaneous activity suggestive of myopathy. A muscle biopsy was performed and demonstrated myonecrosis. Serology was positive for autoantibodies to 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), verifying our diagnosis of statin-associated autoimmune myopathy (SAM). The patient was subsequently treated with rituximab and methotrexate and demonstrated mild clinical improvement. He was eventually liberated from the ventilator. However, later in the course of treatment, he developed respiratory distress and required ventilator support. The patient was discharged to long-term acute care two months after his initial presentation and died due to ventilator-acquired pneumonia three months later. Since their introduction 30 years ago, statin medications have been widely prescribed to prevent cardiovascular diseases. Myalgias and/or myopathic symptoms are among the most recognized side effects of the medication. Statin-associated autoimmune myopathy is a very rare complication of statin use and estimated to affect two to three for every 100,000 patients treated. Clinically, the condition presents as progressive symmetric weakness, muscle enzyme elevations, necrotizing myopathy on muscle biopsy, and the presence of autoantibodies to HMGCR. These findings will often persist and even progress despite discontinuation of the statin. Very few cases of SAM have been described in the literature. Describing this rare condition and the ultimately fatal outcome of our patient, we aim to further understanding of SAM, its presentation and clinical course to promote earlier diagnosis and prompt management.

Neuromyelitis optica spectrum disorders (NMOSDs) are a set of demyelinating disorders that primarily target the optic nerves and the spinal cord. Previously thought to be a subset of multiple sclerosis (MS), now is recognized as a distinct entity. We present a 59-year-old female patient who was admitted for acute upper and lower extremity weakness. The patient had woken up from sleep with sudden onset of weakness. Patient was initially diagnosed with a right hemispheric stroke; however, magnetic resonance imaging of the cervical spine later performed showed abnormal enhancement from C2-C4, representing transverse myelitis. Cerebrospinal fluid was negative for organisms and inflammatory biomarkers. An anti-aquaporin-4 receptor antibody titer was found to be elevated with titers >80 units/mL. The patient was treated with high-dose steroids and plasmapheresis. The NMOSD is a rare entity and, here, we present a rare presentation of the disease. Since its description in 1870, it was confused with MS for years. The advent of anti-aquaporin-4 antibody has been instrumental in differentiating the disease process from MS. This distinction is important, in terms of agents used for treatment and prognostication. The NMOSD is a set of debilitating disease, which requires prompt recognition and appropriate treatment, to avoid the disabling sequelae. Future prospects of the disease include development of novel biological treatment modalities which focus on restoring the loss of immune tolerance which is key to the pathogenesis of the disease.

Facial palsy is a neurological disorder triggered by dysfunction of the seventh cranial nerve, categorized as either central, between the cerebral cortex and brainstem nuclei, or peripheral, between the brainstem nuclei and peripheral organs. Central lesions cause impairment of the contralateral lower facial musculature with associated sparing of the forehead and ocular muscles. Conversely, peripheral lesions produce ipsilateral whole-sided facial hemiplegia including both forehead and ocular muscles. Facial palsy is diagnosed clinically, while imaging studies and additional subsidiary testing (e.g. electromyography, nerve conduction studies), serologies, and rarely biopsy can assist in confirming or refuting the working diagnosis. The differential diagnosis comprises Bell's palsy (idiopathic), HIV infection, Ramsey Hunt syndrome, Lyme, sarcoidosis, amyloidosis, acoustic neuroma, parotid gland tumor, temporal bone biopsy, otitis media, Guillain-Barre syndrome, and brainstem infarct. Facial palsy is branded as Bell's palsy if one of the aforementioned etiologies is not identified as the root cause. Herein, we report the case of a 58-year-old male, who presented with left facial weakness involving both the upper and lower face, posterior circulation symptoms in the setting of hypertensive emergency. Initial magnetic resonance imaging (MRI) was unrevealing for any acute process, however given lack of improvement repeat imaging was ordered. The patient was ultimately confirmed to have an acute versus subacute pontine infarct where the seventh and eighth cranial nerve exits at the cerebellopontine angle. Ancillary laboratory studies were non-contributory. Subsequently, the patient's symptoms continued to improve, blood pressure control was achieved, and was consequently discharged on goal-directed medical therapy.