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Background: The presence of an elevated international normalized ratio (INR) is common in patients in the intensive care unit (ICU), but the cause rarely determined. These patients are at risk to receive prophylactic plasma prior to invasive procedures.Study design and methods: Samples from patients with an INR of 1.5 or greater were frozen and subsequently thawed and assayed for procoagulant and anticoagulant clotting factors and anti-Xa to determine the likely cause of the INR. Samples showing a low FVII, FX, PC, and PS were categorized as a vitamin K deficiency pattern. Samples showing a low FV, low or normal fibrinogen, and high FVIII were categorized as a liver disease pattern. Samples showing an anti-Xa >0.01 IU/ml were assayed for anti-Xa DOACs. Samples which could not be categorized were grouped as equivocal. Results: A total of 48 samples were obtained over a 6-month period. Nineteen showed a Vitamin K deficiency pattern, 17 a liver disease pattern, 7 showed an anti-Xa DOAC and 5 were equivocal. High FVIII and D-dimers and reduced levels of the anticoagulant proteins were present in the majority of the samples. FVII levels correlated inversely with the INR (r = À0. 81), as did FX (r = À0.67) but not FV (r = À0.04) nor fibrinogen (r = À0.15). Conclusion:Transfusion of plasma to reverse an elevated INR in the ICU should be discouraged since such a practice is either avoidable by the use of vitamin K or inappropriate in the case of liver disease or an anti-Xa DOAC.

New clinical manifestations of coronavirus disease 2019 (COVID-19) have been emerging throughout the pandemic and are being reported to the medical community. There have been limited reports that the virus can cause acute airway compromise. Here, we describe a young patient with a recent COVID-19 infection now presenting with acute airway compromise, presumed to be pharyngitis, and their clinical course during their hospitalization. The purpose of this case presentation was to shed light on a newly reported, presumed, presentation of COVID-19 that can be life-threatening in people of all ages. Though there have been limited reported cases, it is important to include this virus in the differential diagnosis of virus-induced airway compromise.

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Patient is a seventy year old Egyptian female with past medical history of coronary artery disease, systolic heart failure, chronic kidney disease stage 3, hiatal hernia, and a benign pheochromocytoma previously worked up at a neighboring hospital, who was admitted for dyspnea and subjective fever intermittently for the past two weeks. Vitals on admission were normal except for a pulse oximetry of 93% and heart rate of 110. Chest x-ray revealed bilateral pulmonary infiltrates. She was treated for community acquired pneumonia with ceftriaxone and azithromycin. Four days after admission patient had a rapid response for respiratory distress and code sepsis called for fever of 102 degrees, leukocytosis of 23 (from 11.3 on admission), respiratory rate of 30, heart rate of 131, with blood pressure of 183/56 and pulse oximetry of 84%. Patient was intubated and transferred to ICU, where antibiotic coverage was broadened with vancomycin and piperacillin-tazobactam. Pan cultures obtained on admission returned negative and her symptoms resolved two days later. Patient's antibiotics were deescalated and patient was then discharged home. It was thought that her sepsis was likely secondary to pneumonia resulting in acute hypercapnic hypoxic respiratory failure. Patient returned four days later and was readmitted directly to the ICU for worsening dyspnea with a temperature of 102.0, leukocytosis of 27.4, heart rate of 149, respiratory rate of 30, with a blood pressure of 172/90 and pulse oximetry of 83%. Chest x-ray revealed new bilateral infiltrates from previous admission. Patient was intubated and treated with piperacillin-tazobactam, vancomycin, and gentamycin. Cultures again were obtained and again returned negative. At this point it was thought patient's hiatal hernia was leading to cough and aspiration during sleep causing recurrent pneumonia, but this did not explain the negative cultures. It was then thought after researching similar cases that the patient's pheochromocytoma could be leading to a "pseudo" septic picture. Records were obtained from a neighboring hospital that were significant for a PET scan revealing a 2.6x1.9cm left adrenal nodule with increased FDG avidity, elevated serum total metanephrines (676 mcg), urine total metanephrines (2021 mcg), urine normetanephrines (173 mcg). The pathology from biopsy study results were most consistent with pheochromocytoma with neoplastic cells, reactive for chromogranin, synaptophysin and vimentin. It was then determined that patient's septic symptoms were likely due to pheochromocytoma as patient's blood pressure would coincide with febrile episodes and dyspnea. Patient was placed on prazosin and blood pressure normalized during admission without return of fever. Pheochromocytoma should be considered as part of the differential diagnosis in the setting of recurrent dyspnea and sepsis when more common causes have been ruled out. It is also important to do this early as to prevent unnecessary antibiotic use and to prevent antibiotic resistance.