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.
Introduction: Atrial fibrillation is a common comorbid condition in patients with severe sepsis admitted to the medical intensive care unit (ICU). While anticoagulation is indicated for moderate to high-risk patients with non-valvular atrial fibrillation (AF) to reduce risk of thromboembolic complications, its benefit in critically ill patients has not been determined. We conducted a study to assess the safety and efficacy of anticoagulation in AF patients with severe sepsis. Methods: A retrospective chart review of 115 patients with AF admitted from February 2004 to February 2009 with a primary diagnosis of sepsis to a teaching community-based hospital was conducted. Medical records were reviewed to confirm AF, determine stroke risk factors (CHAD2) and documented contraindications for anticoagulation. The primary endpoints included stroke and anticoagulation-related bleeding complications before hospital discharge. Results: Amongst 115 patients (mean age 81yrs ± 9.5 and CHAD2 3.17 ± 1.20), the majority of patients 71.3% (82/115) did not receive anticoagulation with a supratherapeutic admission INR>3 being the most common reason for withholding anticoagulation. None of the patients in the non-anticoagulated group developed any embolic events. There was no difference between the anticoagulated and the non-anticoagulated groups in the ICU and hospital length of stay 8.6 days ± 9.1 and 13.6 ± 11.3 vs 7.0 ± 6.7 and 15.6 ± 10.6. Anticoagulation-related complications occurred more often in the anticoagulation group (9.1% [3/33] vs 0%, p = 0.006): these included a nonfatal gastrointestinal bleed (1/33), fatal CNS hemorrhage (1/33), and heparin-induced thrombocytopenia (1/33). In addition, a majority of the patients who received anticoagulation had a therapeutic range achieved in less than 50% of their ICU stay. The two groups had similar hospital survival (64.6% [53/82] for the non-anticoagulated group vs 78.8% [26/33] in the anticoagulated group, p= 0.14). Conclusion: The risk of thromboembolic complications from AF in patients with severe sepsis is exceedingly low and prophylaxis anticoagulation is not warranted. Moreover, a safe anticoagulation range in septic patients is difficult to achieve and is associated with increased risk of bleeding.
Spontaneous coronary artery dissection (SCAD) is a variant of acute coronary syndrome (ACS) that is poorly understood. SCAD has been linked to fibromuscular dysplasia (FMD), connective tissue disease (CTD), pregnancy and hormonal imbalance, systemic inflammatory conditions (e.g. IBD, vasculitis), and coronary artery vasospasm rather than traditional cardiac risk factors. Symptomology generally accompanying SCAD is indistinguishable from ACS making the timely recognition and diagnosis vital for prompt treatment. Management of SCAD is not well defined given the absence of guidelines; conservative therapy with or without invasive intervention is assessed on a case-by-case basis. In this article, we report the case of a 62-year-old male, who presented with chest pain and dyspnea on exertion and was found to have an elevated troponin-I level and corresponding electrocardiogram (EKG) findings, subsequently diagnosed with a non-ST elevation myocardial infarction (NSTEMI). Coronary angiography revealed a distal right coronary artery (RCA) dissection, which was confirmed later with intravascular ultrasound (IVUS). The patient then underwent percutaneous coronary intervention (PCI) followed by stenting of the distal RCA and was discharged on optimal medical therapy. Herein, we report a case of SCAD in an otherwise healthy male with chest pain at rest and with mild exertion without conventional cardiac risk factors.
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