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1.
Neuroendocrinology Letters ; 42(8):508-511, 2021.
Article in English | EMBASE | ID: covidwho-2303830

ABSTRACT

COVID-19 disease is caused by the new coronavirus SARS-CoV-2. The disease first appeared in China in 2019 and quickly spread throughout the world. It primarily affects the respiratory tract, manifested by fever, cough and the devel-opment of dyspnoea, but the symptoms and complications can affect any organ system. Neurological symptoms include headaches, muscle and joint pain, taste and smell disorders. Complications include inflammatory diseases of the central nervous system, ataxia, peripheral nerve and muscle diseases, worsening of extra-pyramidal diseases, and neuropsychiatric disorders. This paper presents a case report of a 62-year-old man with cere bellar syndrome, ataxia, intentional tremor and hypermetria when dealing with COVID-19 disease.Copyright © 2021 Neuroendocrinology Letters.

2.
American Journal of the Medical Sciences ; 365(Supplement 1):S11, 2023.
Article in English | EMBASE | ID: covidwho-2229465

ABSTRACT

Case Report: Most common causes of shortness of breath are asthma, COPD, CHF, pulmonary embolism, diffuse lung parenchymal diseases and obesity hypoventilation syndrome. Rare conditions can be bronchiectasis, constrictive pericarditis, kyphoscoliosis, tracheomalacia, cardiomyopathies and so on. We present a rare case of tracheal stenosis presenting with repeated hospital admissions followed by intubations and resolution after spontaneous expectoration. A 52-year-old female with a history of end stage renal disease on hemodialysis, resistant hypertension, and COVID pneumonia on supplemental oxygen, presented with dyspnea associated with yellowish productive sputum for one day. She was admitted one week prior due to the same complaint associated with encephalopathy due to hypercapnia, required endotracheal intubation, got extubated four days later, was provisionally diagnosed with asthma and volume overload, and discharged home. During the admission of interest, the patient's examwas normal except severe hypertension with BP of 192/101, bilateral crackles and rhonchi. Arterial blood gasses (ABGs) again showed hypercapnia. CT thorax showed evidence of left lower lobe pulmonary infiltrate and ground-glass opacities. Due to repeated admissions for hypercapnic respiratory failure, suspicion for persistent anatomic or pathologic abnormality was high. Reexamination of CT thorax suggested subglottic stenosis and she underwent fiberoptic laryngoscopy which revealed grade 3 subglottic stenosis. On day three, she became hypoxic and unresponsive, ABGs revealed PCO2 of 150, and got intubated again. Soon after intubation, the patient had spontaneous expectoration of a large piece of firm, fleshy, blood-tinged, thick, luminal tissue. On the histologic examination, the material was found to be a plug of fibrin with small to moderate numbers of inflammatory cells embedded in the matrix. Follow-up CT neck and chest revealed resolution of previously visualized tracheal stenosis. She underwent repeat direct laryngoscopy and flexible bronchoscopy which did not show any tracheal stenosis. The patient remained hemodynamically stable and was discharged home. Tracheal stenosis is challenging to diagnose. Examples of tracheal stenosis due to pseudomembrane formation are rare in medical literature, and the expectoration of fibrin material after intubation in a person with this condition is even rarer. A similar case has been described before with an identical situation of coughing up soft tissue and comparable histopathology report. Our case highlights the importance of critical analysis for broad differentials, adding up pieces of the puzzle to explain the missing link. This patient came with recurrent episodes of dyspnea that were misdiagnosed as volume overload, pneumonia, and asthma exacerbations. CT chest findings of possible subglottic stenosis were the missing link in this case which steered further work-up and led to the final diagnosis. Copyright © 2023 Southern Society for Clinical Investigation.

3.
Chest ; 162(4):A2478, 2022.
Article in English | EMBASE | ID: covidwho-2060950

ABSTRACT

SESSION TITLE: COVID-19 Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pneumomediastinum is the presence of air or other gas in the mediastinum which can be due to trauma related to mechanical ventilation or spontaneous in preexisting lung diseases. Here, we present the case of Covid-19 pneumonia, who developed pneumomediastinum without any trauma or other risk factors. CASE PRESENTATION: A 56-year-old male COVID unvaccinated with a history of essential hypertension presented to the ED with shortness of breath and worsening cough for one week. He was living with his father, who was admitted to the ICU and receiving treatment for COVID pneumonia. The patient appeared to be in respiratory distress. His initial vital signs were temperature of 99.6 F, respiratory rate of 26 breaths per minute, blood pressure 125/71 mm Hg, heart rate 109 beats per minute with a regular rhythm, and oxygen saturation of 50% while he was breathing ambient air. Pulmonary examination revealed use of respiratory accessory muscle and widespread bilateral coarse rhonchi on auscultation. The rest of the physical examination was within normal limits. RT- PCR COVID -19 test was positive. The blood gas analysis reported respiratory alkalosis. Inflammatory markers were elevated: erythrocyte sedimentation rate (35.2 mg/L), C-Reactive Protein (17.70 mg/dL), Ferritin (1108.1 ng/mL), Lactate Dehydrogenase (813 U/L), Lactate (2.4 mg/dL), D-Dimer (35.20 mg/L) and Troponin High Sensitivity-236.6 ng/L. His CBC, electrolytes, and kidney function were normal. Chest X-ray showed Pneumomediastinum with dense basilar predominant consolidation. CT Angio Chest with contrast reported Pneumomediastinum likely from the left central airway source and bilateral dense ground glass consolidation. An echocardiogram showed an ejection fraction of 60-65%, no valvular abnormalities. He was placed on vapotherm(Oxygen 40L/min) with 100% FiO2. He was given Dexamethasone 6mg for ten days, Remdesivir, Barcitinib, and a 7-day course of Azithromycin and Ceftriaxone for community-acquired pneumonia. He was advised to practice prone positioning for 12 hours or more per day. Pulmonology, Infectious Disease, and Cardiology were consulted. Gradually, his oxygen requirement was weaned down and Pneumomediastinum resolved on serial chest x rays. He was discharged on home oxygen in a clinically stable condition. DISCUSSION: Pneumomediastinum in viral pneumonia is rare. The exact mechanism is unknown. Covid-19 pneumonia causes diffuse alveolar wall damage, which might cause air leakage into the mediastinum. The development of pneumomediastinum is an ominous sign in these patients. Fortunately, our patient did not worsen and was weaned off high flow oxygenation requirement. CONCLUSIONS: Few isolated reported cases of pneumomediastinum in a COVID-19 patient have been associated with life-threatening complications. It should be used as a prognostic marker, and close monitoring of these patients is advisable. Reference #1: Damous, S.H.B., dos Santos Junior, J.P., Pezzano, Á.V.A. et al. Pneumomediastinum complicating COVID-19: a case series. Eur J Med Res 26, 114 (2021) DISCLOSURES: No relevant relationships by Saad Ansari No relevant relationships by Akshit Chitkara No relevant relationships by Sudeshna Ghosh No relevant relationships by Femina Patel

4.
Chest ; 162(4):A877, 2022.
Article in English | EMBASE | ID: covidwho-2060716

ABSTRACT

SESSION TITLE: Critical Care Infections SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Francisella tularensis is a zoonotic disease by an aerobic, gram negative coccobacillus. It is transmitted by exposure to infected animal or vectors in individuals who landscape or camp. Common symptoms are fever, chills, anorexia, and headache. Abdominal tularemia can present with abdominal pain, emesis, diarrhea, and rarely intestinal ulceration and hemorrhage. It is treated with aminoglycosides, fluoroquinolones and tetracycline. CASE PRESENTATION: 38-year-old male presented with fever, cough, anorexia, and black stool for 5 days. Patient worked as a landscaper. He has no pets, travel history or sick contacts. He does not take any medications at home. Physical exam was significant for sinus tachycardia and rhonchi of right upper lobe. Significant labs include WBC of 9.8 with 41% bands, hemoglobin 15.5, sodium 125, procalcitonin 27.3, and lactic acid 1.8. COVID-19, MRSA, Legionella and Pneumococcal urine antigen were negative. CTA chest revealed mass-like opacity in right upper lobe with multiple bilateral pulmonary nodules. Lower respiratory culture showed Candida albicans. Patient was empirically started on ceftriaxone and azithromycin. He was transferred to intensive care for worsening respiratory status and was placed on non-invasive ventilation on hospital day 1. Antibiotics were broadened to ceftaroline and levofloxacin due to suspicion of tularemia. Amphotericin B was added. Labs for Histoplasma, Blastomyces, TB, Leptospira, and HIV were negative. Patient then suffered a cardiac arrest on hospital day 2 after having large brown secretions pouring from his mouth. Cardiopulmonary resuscitation was initiated and patient was intubated and started on vasopressors with return of spontaneous circulation. Massive blood transfusion protocol was initiated. Emergent bedside upper endoscopy showed large blood clot adherent to duodenal ulcer. Interventional radiology planned on performing gastric duodenal artery embolization. However, patient suffered two more cardiac arrest with resuscitation efforts terminated per family request. Karius Digital Culture later was positive for Francisella tularensis. Autopsy revealed diffuse alveolar hemorrhage, hilar lymphadenopathy, and perforated duodenal ulceration with large adherent clot. DISCUSSION: Gastrointestinal tularemia is rare and usually from drinking contaminated water or oral inoculation of bacteria. Intestinal tract involvement can present with mesenteric lymphadenopathy and ulcerative lesions resulting in gastrointestinal bleeding with case fatality rate of 50%. Even though this is noted in the literature, to our knowledge no case reports have been published. CONCLUSIONS: Careful history taking and early identification of risk factors are important when severe tularemia infection is suspected such as in individuals with extensive outdoor activities. Treatment should be empirically initiated in high risk patients. Reference #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585636/ Reference #2: https://casereports.bmj.com/content/2017/bcr-2017-22125. Reference #3: Altman GB, Wachs JE. Tularemia: A pathogen in nature and a biological weapon. Aaohn Journal. 2002 Aug;50(8):373-9. DISCLOSURES: No relevant relationships by Maria Haider Baig

5.
Chest ; 162(4):A585, 2022.
Article in English | EMBASE | ID: covidwho-2060637

ABSTRACT

SESSION TITLE: COVID-19 Case Report Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Acute eosinophilic pneumonia (AEP) is a rare cause of acute respiratory failure. AEP has been reported in association with smoking, drugs, and infections. Very few reports of AEP accompanied by Coronavirus disease 2019 (COVID-19) exist in current literature. Here we describe a case of AEP in association with COVID-19. CASE PRESENTATION: A 58-year-old female, non-smoker, with no medical history presented to the emergency room with fever, cough, and shortness of breath for 10 days. She received two doses of vaccine against COVID-19. Her vital signs were notable for oxygen saturation of 56% on room air and respiratory rate of 35 breaths per minute. Her physical exam was notable for distress, tachypnea, and diffuse rhonchi on lung auscultation. Her chest x-ray showed multifocal bilateral peripheral and basilar airspace opacities. A respiratory pathogen panel detected SARS-CoV-2. She was admitted to the medical intensive care unit and suffered worsening acute hypoxemic respiratory failure requiring intubation. She was treated with dexamethasone 6mg for a 10-day course with gradually decreasing oxygen requirements, and she underwent tracheostomy on hospital day 11. Despite this, she continued to deteriorate clinically. Review of laboratory results showed significant eosinophilia of 15.6% on her complete blood count upon withdrawal of steroids. A CTA scan of the chest showed no evidence of pulmonary embolic disease and demonstrated bilateral extensive dense consolidations. A diagnosis of acute eosinophilic pneumonia was suspected. Fungal cultures and stool ova and parasites were negative. She was started on methylprednisolone 1mg/kg and a bronchoscopy was performed with bronchioalveolar lavage (BAL) samples showing 4% eosinophils despite high dose steroid therapy. She was continued on high dose steroids with rapid improvement in her oxygen requirements. DISCUSSION: AEP is an acute febrile illness that can lead to acute respiratory failure. The presence of dense infiltrates in the early stages of COVID-19 and elevated inflammatory markers and reticence to perform bronchoscopy can delay making a diagnosis of AEP in a patient diagnosed with COVID19. The diagnostic hallmark of AEP is the detection of > 25% eosinophils in BAL samples. While this patient did not meet that criterion, she received high dose corticosteroids which may have suppressed pulmonary eosinophilia. A high index of suspicion for AEP should be maintained in patients with COVID-19 with evidence of eosinophilia and clinical deterioration, given that AEP improves rapidly with the appropriate treatment. CONCLUSIONS: AEP is an uncommon cause of respiratory failure that should be considered in patients with unexplained worsening respiratory status and evidence of eosinophilia. Bronchoscopy with bronchoalveolar lavage should be considered early, even in the setting of COVID-19 in patients without risk factors who develop severe disease. Reference #1: De Giacomi F, Vassallo R, Yi ES, Ryu JH. Acute Eosinophilic Pneumonia. Causes, Diagnosis, and Management. Am J Respir Crit Care Med. 2018;197(6):728-736. doi:10.1164/rccm.201710-1967CI Reference #2: Murao K, Saito A, Kuronuma K, Fujiya Y, Takahashi S, Chiba H. Acute eosinophilic pneumonia accompanied with COVID-19: a case report. Respirol Case Rep. 2020;8(9): e00683. Published 2020 Nov 16. doi:10.1002/rcr2.683 DISCLOSURES: No relevant relationships by Hadya Elshakh No relevant relationships by Christina Jee Ah Rhee no disclosure on file for Lourdes Sanso;

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