Compartment syndrome: An unsuspected consequence of hypercoagulable state in a patient with severe covid-19 illness

Introduction Coronavirus 19 (COVID-19) is a viral illness that is caused by SARS-CoV-2. It has a surface spike protein that binds to human angiotensin-converting enzyme 2 receptors expressed in the kidneys, lung, and vascular endothelium. Here we present a case of a 73-year-old critically ill male with COVID pneumonia and acute respiratory distress syndrome (ARDS), who developed compartment syndrome and rhabdomyolysis as a consequence of extensive right lower extremity arterial thrombosis related to a COVID induced hypercoagulable state. Case A 73-year-old COVID positive male with past medical history of coronary artery disease status-post triple coronary artery bypass 10 years ago and type 2 diabetes mellitus presented to the emergency department with progressively worsening dyspnea for one week. His initial oxygen saturation on room air measured 85%, so he was placed on 3 liters per minute supplementation via nasal cannula. CXR showed bilateral diffuse alveolar infiltrates and he was admitted for observation. He developed worsening respiratory failure five days into hospitalization, placed on maximum supplementation via high flow nasal cannula (HFNC), and transferred to the medical ICU. Ultimately, he was intubated and mechanically ventilated for the remainder of his hospitalization due to severe ARDS. After three days in the ICU, his right lower extremity was cold, without palpable nor detectable pulses via bedside Doppler from the femoral to pedal landmarks. Formal ultrasound Doppler that morning confirmed arterial clot extending from the right external iliac to posterior tibial arteries. The patient received embolectomy, stenting, and therapeutic heparin. Within 24 hours, though his creatinine kinase was normal, he developed significantly elevated myoglobin, lactate and worsening acidosis. The patient had a fasciotomy to the right lower extremity at bedside. The next day, he was anuric, with severe acidosis, hyperkalemia, and hypotension, requiring continuous renal replacement therapy (CRRT) and vasopressor support. Discussion Compartment syndrome is characterized by increased pressure within fascial compartments, leading to circulatory compromise, cellular necrosis, and rhabdomyolysis. In this case, the COVID-19 viral effect on coagulation led to extensive arterial thrombosis, complicated by compartment syndrome and renal failure necessitating CRRT. While the exact pathophysiology of the hypercoagulable state in COVID-19 illness is debated, we have observed its manifestations ranging from deep venous thrombosis (DVT), pulmonary embolism (PE), to stroke. Conclusion COVID-19 is known to be a virulent, multifactorial, intelligent virus with myriad end-organ and vascular consequences. When attending to the most critically ill patients with COVID-19, it is wise to consider all forms of vascular thromboembolism.

ACUTE ONSET ACUTE DISSEMINATED ENCEPHALOMYELITIS IN AN ADULT HEALTHY FEMALE: A RARE AUTOIMMUNE CONDITION

TOPIC: Imaging TYPE: Medical Student/Resident Case Reports INTRODUCTION: Acute disseminated encephalomyelitis (ADEM), is an autoimmune demyelinating disease of the central nervous system, with acute onset of encephalopathy and rapidly progressive multifocal neurologic deficits. ADEM is an uncommon illness in adults, thus the precise incidence is unknown. CASE PRESENTATION: 38 year old female with no prior history besides prior COVID infection 6 months ago, presented with 2 day history of nausea, intractable vomiting, ataxia, confusion, and generalized weakness.Initial MRI brain reported numerous white matter lesions supratentorially and infratentorially. LP demonstrated oligoclonal bands, WBC 14, no xanthochromia. She was diagnosed with multiple sclerosis (MS) and received 5 day course of Solumedrol, with no improvement. Her mental status worsened, and she required mechanical ventilation. She later developed rigidity of the neck and lower extremities, with meningeal signs and dystonia. EEG was done for dystonia but no epileptiform activity was captured. The HIV, syphilis Ig G antibody, ANA Ab, HSV and enterovirus PCR were negative. A continuous EEG for 48 hours did not capture any seizure activity.A repeat MRI Brain demonstrted worsening white matter lesions with symmetrical distribution through thalamus, basal ganglia, internal capsule, and brainstem (Figure 1). Spinal MRI revealed no abnormal enhancement. Given the large monophasic infratentorial and supratentorial lesions ADEM was suspected. Patient received IVIG treatment and plasmapheresis, with mild clinical improvement to date. DISCUSSION: ADEM is theorized to be an immunologically mediated demyelinating disease triggered by a febrile illness or recent vaccination, eliciting an inflammatory response affecting the central nervous system. Possible mechanisms may include either molecular mimicry or direct inflammatory damage to myelinated neurons. Radiographically, the T2/FLAIR (MRI) lesions of ADEM are diffuse, asymmetric, often irregular, patchy areas of homogeneous signal hyperintensities often involving both gray and white matter with over half of the cases involving infratentorial structures. ADEM diagnosis remains a challenge and is particularly difficult to differentiate from MS. In contrast to MS, ADEM should be suspected whenever a patient presents with a prodromal viral illness, fever, neck stiffness, ataxia and encephalopathy. Unlike MS, ADEM does not follow a relapsing-remitting course. Treatment involves high dose corticosteroids, intravenous immunoglobulin (IVIG), and plasmapheresis. CONCLUSIONS: The diagnosis of ADEM entails careful clinical assessment and characteristic imaging findings, as no clear criteria exist. It should be highly suspected in patients with atypical MS. REFERENCE #1: Nicole Mahdi, Peter A. Abdelmalik, Mark Curtis, Barak Bar, "A Case of Acute Disseminated Encephalomyelitis in a Middle-Aged Adult", Case Reports in Neurological Medicine, vol. 2015. REFERENCE #2: De Seze J, Debouverie M, Zephir H, et al. Acute fulminant demyelinating disease: a descriptive study of 60 patients. Arch Neurol 2007;64:1426. REFERENCE #3: Ceronie B, Cockerell OC. Acute disseminated encephalomyelitis in an older adult following prostate resection. eNeurologicalSci. 2018;14:40-42 DISCLOSURES: No relevant relationships by Jeannie Lee, source=Web Response No relevant relationships by Barbara Mantilla, source=Web Response No relevant relationships by Arunee Motes, source=Web Response No relevant relationships by Victor Test, source=Web Response No relevant relationships by Myrian Vinan Vega, source=Web Response

COVID-19 INFECTION COMPLICATED BY GUILLAIN-BARRÉ SYNDROME: A CASE REPORT

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 (SARS-CoV-2) is causing a current pandemic. It commonly manifests with fever, dyspnea, and cough. Few COVID-19 patients with Guillain-Barré Syndrome (GBS) have been reported. The severe inflammatory response and the critically-ill nature of many COVID-19 patients is a challenge to distinguish GBS from critical illness polyneuropathy and myopathy. We present a COVID-19 patient complicated by GBS. CASE PRESENTATION: A 60-year-old woman presented with fever, cough, myalgia, and dyspnea for 10 days. A swab for SARS-CoV-2 RT-PCR was positive. CT chest revealed bilateral “ground-glass” opacities. She was started on oxygen, azithromycin, and hydroxychloroquine. Three weeks later, she developed bilateral symmetrical LE numbness and weakness that progressed to UE. Respiratory status worsened with increasing O2 requirements. Neuro exam showed weakness (2/5) in LE and (3/5) in UE. Respiratory muscle testing demonstrated a NIF of -35 cm H2O and an FVC of 1.7 L. MRI spine showed contrast enhancement of cauda equina nerve roots (Fig 1). CSF analysis revealed cytoalbuminologic dissociation (CAD) with 197 mg/dL of proteins and 0 WBC. She was diagnosed with GBS and started on intravenous immunoglobulin (IVIG) 0.4g/Kg/day for 5 days. After a week of therapy, the patient improved, recovered from COVID-19, and was discharged home. DISCUSSION: GBS is a disorder in which the immune system attacks gangliosides on the peripheral nervous system. It presents with ascending weakness and can cause total body paralysis and respiratory failure in severe cases. It is associated with a variety of viral and bacterial infections. 12 cases of GBS have been reported in COVID-19 infection. GBS developed within 10 days of COVID diagnosis and presented with ascending progressive, flaccid quadriparesis. All except 2 patients underwent CSF analysis and 91% showed CAD. IVIG was used for all the patients, and one was started on plasmapheresis. The involvement of the PNS supports the coronavirus neurotropic invasion pathway. It is still unclear if SARS-CoV-2 can directly invade neurons and cause neuropathy. We could not test for SARS-CoV-2 in CSF in our case, but the absence of WBC in the CSF indicated an immune response typically seen in GBS rather than direct neuronal invasion, in which pleocytosis is expected. MRI usually showed contrast enhancement of cauda-equina nerve roots due to radicular irritation. CSF showing CAD is usually observed in the second week after symptom onset. IVIG is preferred over plasmapheresis for treating GBS due to fewer side effects. However, thrombotic events occur in 1–16.9%. All of the reported COVID-19 cases with GBS, including our case, received IVIG, and none of them reported thrombotic events. CONCLUSIONS: Our case emphasizes that GBS should be considered as one of the differentials in patients with COVID-19 patients with ARDS, polyneuropathy, and difficulty weaning off ventilator. Reference #1: 1. Sedaghat, Z. and N. Karimi, Guillain Barre syndrome associated with COVID-19 infection: A case report. J Clin Neurosci, 2020. Reference #2: 2. Zhao, H., et al., Guillain-Barre syndrome associated with SARS-CoV-2 infection: causality or coincidence? Lancet Neurol, 2020. 19(5): p. 383-384. Reference #3: 3. El Otmani, H., et al., Covid-19 and Guillain-Barre syndrome: More than a coincidence! Rev Neurol (Paris), 2020. DISCLOSURES: No relevant relationships by Somedeb Ball, source=Web Response No relevant relationships by Tulio Bueso, source=Web Response No relevant relationships by Saif El Naser El Nawaa, source=Web Response No relevant relationships by Mohamed Elmassry, source=Web Response No relevant relationships by Ximena Solis, source=Web Response No relevant relationships by Victor Test, source=Web Response