INTRODUCTION: COVID-19 infection has varied presentations and complications inclusive of pneumonia(PNA),gastroenteritis(GE) and Acute kidney injury(AKI).Prompt identification with aggressive therapy is needed to reduce morbidity and mortality.We present a case of COVID-19 infection with septic shock and severe AKI,successfully treated CASE PRESENTATION: A 65-year-old female presented with 7-days of vomiting,diarrhea,fever,dry cough,fatigue & confusion.Multiple household members had recently tested positive for SARS CoV-19.She had a history of localized breast cancer on tamoxifen,HTN and CKD3a.Baseline creatinine(Cr) 3 months prior was 1.2.On exam,BP was 86/48mm/hg, T 95F,RR 27 breaths/ min.She had dry mucous membranes, coarse breath sounds & rales bilaterally on auscultation,confusion & flapping wrist tremor.Significant labs were a Cr of 21.5,BUN 162, CO2 9,D-dimer >20,CRP 55 & random urine protein on 19 (<12mg/dl).ABG on 3L nasal cannula showed PH 7.21, PO2 104, PCO2 30.CXR noted right upper lobe infiltrate.CT head and EEG were unremarkable.SARS-CoV-2 PCR was positive.She was transferred to ICU for management of septic shock from COVID-19 PNA & GE with severe AKI.Despite aggressive IV fluids,she remained hypotensive requiring phenylephrine for pressor support.She received IV D5
INTRODUCTION: Since the emergence of highly active antiretroviral therapy (HAART), incidence cryptococcosis has fallen. We discuss a rare presentation of disseminated cryptococcosis.CASE PRESENTATION: A previously well 31 year old woman presented with 3 weeks of nausea, vomiting & headache. She was sent to hospital when she developed dizziness & palpitations after a positive HIV test was found on an outpatient visit. Examination revealed diffuse adenopathy. Urine was positive for opiates, cannabinoids & barbiturates. Non-contrast computed tomography head revealed no acute abnormalities, but abdomen/pelvis found abdominal & retroperitoneal lymphadenopathy. On day 2, she developed diaphoresis, cold extremities with HR160bpm, BP89/53mmhg, RR44bpm, SpO289% & T100F. She was intubated & put on vasopressors. She subsequently had 3 PEA cardiac arrests with return of spontaneous circulation after several minutes. Bedside transthoracic echocardiogram (TTE) revealed a severely hypokinetic dilated right ventricle (RV) & underfilled left ventricle (LV). Bedside transesophageal echocardiogram noted hyperdynamic apex, akinetic base & echogenic material within the right pulmonary artery, concerning for a pulmonary embolism. Hemodynamic instability was refractory to thrombolytics & she was placed on veno-arterial ECMO. She was empirically given vancomycin, piperacillin-tazobactam & clindamycin/ primaquine. Blood cultures were later positive for yeast, so caspofungin & fluconazole added. Follow-up TTE showed minimal improvement in RV or LV function. On day 3, after 24 hours off sedation, pupils were dilated & brainstem reflexes absent. Apnea test confirmed brain death. After expiration, HIV viral load was found to be 528,000 copies/ml (reference range: not detected), CD4 was <20 cells/mcl (490-1740cells/mcl), & Cryptococcus neoformans was isolated, with titer $1:2560 (normal: negative).DISCUSSION: Cryptococcosis is the most common fungal disease in HIV, but its incidence has decreased in the US. Earlier HIV diagnosis & HAART explain this. It most commonly affects the nervous system. Occasionally, blood cultures are positive indicating disseminated disease. We postulate that pulmonary vascular occlusion can occur due to disseminated cryptococcal infection. Cryptococcomas are extremely rare solid tumor-like masses which have been reported to invade the central nervous system & the skin. Our suspicion for this is high given her poor response to TPA & significant fungemia which likely led to right heart failure & cardiovascular collapse. Literature review identified one other such case. More common sequelae include meningitis or pulmonary involvement. Amphotericin B & Flucytosine represent the most potent therapy for severe disease.CONCLUSIONS: Cardiopulmonary collapse from right heart failure with disseminated cryptococcus is extremely rare. Early diagnosis & treatment of HIV remains the most important tool.
The coronavirus disease 2019 (COVID-19) is characterized by flu-like symptoms or complications related to pneumonia and acute respiratory distress syndrome. Later in the disease course, clinically significant thrombotic events, both venous and arterial, are being recognized. Our case describes ST elevation myocardial infarction (STEMI) as a complication of COVID-19. CASE PRESENTATION: A 38-year-old male with no medical history and non-smoker presented with 10 days of fever, cough, malaise, myalgia, and exertional dyspnea. He denied chest pain. He had completed a five-day course of azithromycin and steroids. No personal or family history of clotting disorders or heart disease. Exam revealed oxygen saturation of 89% on room air with bilateral crepitations. Chest x-ray showed bilateral patchy parenchymal airspace disease. Electrocardiogram (EKG) showed sinus tachycardia without ischemic changes. Labs showed C-reactive protein 179 mg/L and D-dimer 0.64 ug/mL. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by polymerase chain reaction assay was positive. He was started on ceftriaxone, doxycycline, hydroxychloroquine, enoxaparin, and methylprednisolone. After 5 days, he was discharged on prophylactic apixaban. He returned 1 day later with substernal chest pain. EKG showed ST elevation in the inferior leads. Troponin T was 3.74 ng/mL, D-dimer 0.75 ug/mL, and coagulation profile was normal. Emergent coronary angiography revealed 100% occlusion of mid-right coronary artery and right posterolateral branch requiring extensive thrombectomy and placement of drug eluting stents. He was started on aspirin, ticagrelor, eptifibatide, high intensity statin, and metoprolol. Echocardiography revealed severe basal to mid-inferior and posterior wall hypokinesis with left ventricular ejection fraction of 40%. He was discharged on ticagrelor, apixaban, atorvastatin and metoprolol. Antiphospholipid antibody panel testing results returned normal.
INTRODUCTION: Corona Virus Disease (COVID-19) main presenting feature is hypoxia which coincidentally is a feature of Pulmonary Embolism (PE) that can be life-threatening if not diagnosed early. COVID-19 causes excessive inflammation that can induce expression tissue factors, which is a major coagulation activator1,2. Therefore, PE should also be a consideration for those presenting with COVID-19 with worsening hypoxia. CASE PRESENTATION: 79-year-old a man with non-ischemic cardiomyopathy with Ejection Fraction (EF) 45-50% presented with worsening shortness of breath, dry cough, and bilateral lower limb edema for 2 weeks. On presentation, he was afebrile normotensive with tachypnea, tachycardia, and hypoxia. On physical examination, he was in respiratory distress with faint bilateral crackles and bilateral lower limb edema. Lab Investigations showed elevated Brain Natriuretic Peptide to 1830 pg/ml (normal range 0-100 PG/ml), troponin level to 6.89 ng/ml (normal range 0.00-0.03 ng/ml) and the D-dimer level was >20.00 UG/ ml FEU (normal range 0.00-0.40 UG/ml FEU). Viral PCR confirmed COVID-19. No ischemic changes noted in EKG. Echocardiography (Echo) revealed EF (Ejection Fraction) at 10-15%, dilated right ventricle with reduced function, and left ventricular thrombus. In CT chest with contrast noted to have acute segmental right middle lobe pulmonary arterial embolus. He was therapeutically anti-coagulated with enoxaparin. He received antibiotics, systemic steroids, and diuresis On day 3 of admission, he had worsening hypoxia and dyspnea while on 100% oxygen therapy. The patient opted for no escalation in care with ventilation or resuscitation. As he had no clinical improvement, the family agreed on comfort care. He died on day 5 of admission. No relevant relationships by Fausto Lisung, source¼Web Response No relevant relationships by Rani Sittol, source¼Web Response
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