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Introduction: Severe acute respiratory syndrome from COVID 19 typically presents with cough, fever, myalgias and progresses to respiratory and multi-organ failure. However, neurological manifestations of COVID 19, namely Guillain-Barre syndrome are rare. We present a case of acute inflammatory demyelinating polyneuropathy (AIDP), a form of GBS in a patient with recent COVID infection. Case: 66 year old man with no significant medical history presented to the emergency department for progressive weakness of all extremities for 2 days. Patient was diagnosed with COVID 19 three weeks prior to onset of weakness. As per patient, he only had mild respiratory illness with cough, general weakness without respiratory symptoms. Two days prior to presentation, he felt weakness in his lower extremities, which then progressed to involve the upper extremities. On initial evaluation the patient's pupils were symmetric and 3mm, reactive to light, visual field were full to confrontation, cranial nerves intact, shoulder shrug symmetric with full strength. He had decreased motor tone with 2/5 strength in both upper and lower extremities and depressed or absent reflexes in all extremities. His labs were significant for positive COVID 19 PCR and antibodies. CT head was negative for acute stroke or intracranial pathology. The patient was admitted to MICU where he developed respiratory muscle weakness with diminished vital capacity of 12ml/kg and negative inspiratory force of 12mmHg and he was intubated. Cerebral spinal fluid showed elevated protein to 145mg/dL, WBC of 4/UL with 50% lymphocytes and glucose of 67. Other CSF studies were negative for oligoclonal bands, EBV, CMV, cryptococcus, syphilis, and sarcoidosis. Electromyography was consistent with moderate AIDP. He received 5 doses of IVIG with no significant improvement so he underwent tracheostomy and was initiated on plasmapheresis for AIDP. Discussion: GBS is an immune-mediated disease that typically affects the peripheral neurons and nerve roots after respiratory or gastrointestinal illness. Typical infections are Campylobacter jejuni, Zika virus, Influenza, and there are even reports of GBS after MERS and SARS COV-1. However, there has been increasing evidence of COVID 19 causing neurologic manifestations such as encephalitis, meningitis, stroke, and GBS [1]. Patients, such as the one presented in this report with GBS, usually have a long and protracted disease despite aggressive treatments with IVIG and plasmapheresis with reliance on mechanical ventilator. Understanding the full spectrum of diseases and systems affected by COVID 19 can help clinicians provide better care.
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INTRODUCTION: We present a rare case of severe COVID-19 infection developing desmopressin resistant polyuria with mixed central diabetes insipidus (DI) and osmotic diuresis. METHODS: 53-year man presented with cough, dyspnea and fever was confirmed to be COVID-19 positive. He was intubated and was treated with standard ARDS management in ICU. On day 10, he began to have sudden onset polyuria, fluctuating vitals with maximum temperature of 105 F and acute encephalopathy. Brain MRI, CSF analysis, cortisol/ TSH/free T4 were unremarkable. Desmopressin was started along with aggressive fluid. Despite 7 days of high dose IV desmopressin and vasopressin infusion, patient's urine output was not suppressed. Laboratory findings revealed serum osmolality <270 mOsm/kg, urine osmolality 300-500 mOsm/ kg and urine sodium 138 mmol/L. Blood glucose was normal. Intravenous fluids were discontinued. Urine output decreased slowly and normalized after 17 days. RESULTS: SARS-CoV-2 virus is hypothesized to enter via ACE2 receptor distributed widely including pituitary gland. This may lead to hypothalamic-pituitary-adrenal (HPA) dysfunction causing polyuria. Polyuria is classified as osmotic and water diuresis. Osmotic diuresis (Uosmolality >600 mOsm/kg) is seen due to glycosuria in uncontrolled DM or use of SGLT2 inhibitor, urea diuresis after acute kidney injury and sodium diuresis after use of large volume of normal saline. Water diuresis results in large volumes of hypotonic urine (Uosmolality <300 mOsm/kg). Causes include primary polydipsia and DI. Central DI is commonly seen in intracranial trauma, stroke, meningoencephalitis or idiopathic. Types of water diuresis can be distinguished by water restriction test, desmopressin/DDAVP or hypertonic saline. Central DI responds to water deprivation followed by desmopressin use with an increase in both plasma and urine osmolality. In our case, urine osmolality stayed in range of 300-500 mOsm/kg. The sudden onset of polyuria, high fever, and acute encephalopathy with pertinent lab was highly suggestive of HPA malfunction. Most likely cause of polyuria was mixed central DI and osmotic diuresis. To our knowledge there is no reported case that establishes polyuria or DI with COVID-19. A high degree of suspicion of DI should be made in COVID-19 patients developing polyuria.
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: SARS-CoV-2 is a respiratory virus causing mostly pulmonary manifestations. It has been associated with intracerebral pathology including stroke encephalitis and encephalopathy. Intraventricular hemorrhage may be an unknown fatal extrapulmonary presentation in patients with COVID-19 or a coincidental finding. CASE PRESENTATION: We report a case of a 32-year-old man with asthma not on any home medications particularly antiplatelet and anti-coagulation medications who presented to the hospital after cardiac arrest at home. He reported blurry vision that morning and collapsed soon after. As per family patient is not on any medications or drug abuse. He was resuscitated and mechanically ventilated in the field and arrived in the emergency department in an irreversible coma. On arrival, his vitals are recorded as tachycardia to 120, and blood pressure is 136/80. Initial labs showed anion gap metabolic acidosis with lactic acidosis and respiratory acidosis, leukocytosis, elevated ferritin, elevated AST, and ALT and in acute kidney injury, urine toxicology is negative. Computed tomographic imaging of the brain revealed diffuse intraventricular hemorrhage with associated hydrocephalus with no obvious parenchymal source of bleeding. Computed tomographic imaging of the chest showed bilateral pneumonia highly suspicious of COVID-19. DISCUSSION: Recent evidence shows that SARS-CoV-2 (COVID-19) can be complicated by coagulopathy, which may lead to prothrombotic events including venous thromboembolism, pulmonary embolism, and stroke;however, hemorrhagic manifestations are rare in patients with COVID-19. It has been hypothesized that dysfunction of brain ACE II receptors due to COVID-19 could lead to disruption of autoregulation in the cerebral vessel leading to rupture of the arterial wall causing hemorrhage. CONCLUSIONS: Intracerebral hemorrhage as extrapulmonary manifestations of SARS-CoV-2 is rare and can be fatal. Current literature lacks evidence to support the pathophysiology of hemorrhagic and extrapulmonary manifestations except for entry through the ACE II receptors. More studies should be done in the future to determine possible mechanisms for extrapulmonary manifestations of COVID 19. Reference #1: Deliwala S, Abdulhamid S, Abusalih MF, Al-Qasmi MM, Bachuwa G. Encephalopathy as the Sentinel Sign of a Cortical Stroke in a Patient Infected With Coronavirus Disease-19 (COVID-19). Cureus. 2020;12(5):e8121. Published 2020 May 14. DOI:10.7759/cureus.8121. Reference #2: Sharifi-Razavi A, Karimi N, Rouhani N. COVID-19, and intracerebral hemorrhage: causative or coincidental?. New Microbes New Infect. 2020;35:100669. Published 2020 Mar 27. DOI:10.1016/j.nmni.2020.100669. Reference #3: Kollias A, Kyriakoulis KG, Dimakakos E, Poulakou G, Stergiou GS, Syrigos K. Thromboembolic risk and anticoagulant therapy in COVID-19 patients: emerging evidence and call for action [published online ahead of print, 2020 Apr 18]. Br J Haematol. 2020;10.1111/bjh.16727. DOI:10.1111/bjh.16727 DISCLOSURES: Speaker/Speaker's Bureau relationship with pfizer Please note: $1001 - $5000 Added 06/11/2020 by Yizhak Kupfer, source=Web Response, value=Consulting fee No relevant relationships by kiran para, source=Web Response No relevant relationships by Elizabeth Weiner, source=Web Response