Acute or chronic? Failing left ventricle in a 34 year old

Submission content Introduction: An unusual case of a very young patient without previously known cardiac disease presenting with severe left ventricular failure, detected by a point of care echocardiogram. Main Body: A 34 year old previously well man was brought to hospital after seeing his general practitioner with one month of progressive shortness of breath on exertion. This began around the time the patient received his second covid-19 vaccination. He was sleeping in a chair as he was unable to lie flat. Abnormal observations led the GP to call an ambulance. In the emergency department, the patient required oxygen 5L/min to maintain SpO2 >94%, but he was not in respiratory distress at rest. Blood pressure was 92/53mmHg, mean 67mmHg. Point of care testing for COVID-19 was negative. He was alert, with warm peripheries. Lactate was 1.0mmol/L and he was producing more than 0.5ml/kg/hr of urine. There was no ankle swelling. ECG showed sinus tachycardia. He underwent CT pulmonary angiography which demonstrated no pulmonary embolus, but there was bilateral pulmonary edema. Troponin was 17ng/l, BNP was 2700pg/ml. Furosemide 40mg was given intravenously by the general medical team. Critical care outreach asked for an urgent intensivist review given the highly unusual diagnosis of pulmonary edema in a man of this age. An immediate FUSIC Heart scan identified a dilated left ventricle with end diastolic diameter 7cm and severe global systolic impairment. The right ventricle was not severely impaired, with TAPSE 18mm. There was no significant pericardial effusion. Multiple B lines and trace pulmonary effusions were identified at the lung bases. The patient was urgently discussed with the regional cardiac unit in case of further deterioration, basic images were shared via a cloud system. A potential diagnosis of vaccination-associated myocarditis was considered,1 but in view of the low troponin, the presentation was felt most likely to represent decompensated chronic dilated cardiomyopathy. The patient disclosed a family history of early cardiac death in males. Aggressive diuresis was commenced. The patient was admitted to a monitored bed given the potential risk of arrhythmia or further haemodynamic deterioration. Advice was given that in the event of worsening hypotension, fluids should not be administered but the cardiac centre should be contacted immediately. Formal echocardiography confirmed the POCUS findings, with ejection fraction <35%. He was initiated on ACE inhibitors and beta adrenergic blockade. His symptoms improved and he was able to return home and to work, and is currently undergoing further investigations to establish the etiology of his condition. Conclusion(s): Early echocardiography provided early evidence of a cardiac cause for the patient's presentation and highlighted the severity of the underlying pathology. This directed early aggressive diuresis and safety-netting by virtue of discussion with a tertiary cardiac centre whilst it was established whether this was an acute or decompensated chronic pathology. Ultrasound findings: PLAX, PSAX and A4Ch views demonstrating a severely dilated (7cm end diastolic diameter) left ventricle with global severe systolic impairment.

Use of metolazone as an adjunct therapy to loop diuretics in diuretic resistant acute decompensation of heart failure: A systematic review and meta-analysis: Metolazone in diuretic resistant AHF: A Meta-Analysis

Introduction: Loop diuretics are the first-line treatment for volume overload in acute decompensation of congestive heart failure (AHF). Loop diuretic resistance is common due to pharmacologic tachyphylaxis. Therefore, thiazide and thiazide-like diuretics are often used as add-on therapy to combine two different pharmacologic mechanisms. This systemic review and meta-analysis aimed to synthesize the current evidence on the efficacy and safety of metolazone and other thiazide-like diuretics in AHF. Method(s): PRISMA guidelines were followed in conducting this systematic review. PubMed, Scopus, PubMed Central, and Embase databases were searched using relevant keywords for studies published before 5 Jan 2022. and title screening was performed, followed by full-text screening using the Covidence software. Data were extracted, and analysis was done using Cochrane Review Manager (RevMan v5.1). The results were reported in odds ratio and mean difference with 95% confidence intervals. Result(s): Out of 2999 studies identified by database search, eight studies met the inclusion criteria (2 RCTs and 6 cohort studies). Pooled analysis using a random-effects model showed no difference in mean difference among the metolazone group and control group for 24 hours total urine output (MD 69.32, 95% CI -638.29 to 776.94;n = 551;I2 = 84%), change in urine output in 24 hours (MD -284.09, 95% CI -583.99 to 15.81;n = 345;I2 = 0%), 48 hours total urine output (MD -465.62, 95% CI -1302.22 to 370.99;n = 242;I2 = 0%) and urine output at 72 hours (MD -13.24, 95% CI -90.88 to 64.40;n = 205;I2 = 0%). However, studies with furosemide only in the comparator arm, 24 hours of total urine outcome favored metolazone (MD 692.70, 95% CI 386.59 to 998.82;n = 334;I2 = 0%). There was no difference between the two groups in the rate of adverse events, loss of weight, mortality, or readmission rates. Conclusion(s): Metolazone therapy in diuretic resistant AHF may improves urine output and facilitates achieving a net negative balance. Thus, metolazone and thiazide-like diuretics can be used as add-on therapy in acute decompensation of heart failure, especially in diuretic resistance.Copyright © 2023 The Author(s)

Bilateral Spontaneous Pneumothorax in a Child with Multisystem Inflammatory Syndrome Associated with COVID-19

Introduction: Spontaneous pneumothorax is a rare complication of coronavirus disease 2019 (COVID-19), primarily reported in adults. Pediatric cases with bilateral pneumothorax are much less reported. Case Presentation: We presented the case of a five-year-old previously healthy boy who developed persistent fever, abdominal pain, generalized maculopapular rash, and dyspnea before admission. His chest computed tomography (CT) showed a viral involvement pattern of pneumonia suggestive of COVID-19. Subsequently, he was confirmed with multisystem inflammatory syndrome in children (MIS-C). While he responded well to the therapies, on the fifth day of admission, he developed respiratory distress again. A chest roentgenogram showed bilateral spontaneous pneumothorax. Bilateral chest tubes were inserted, and his condition improved sig-nificantly after five days of admission to the intensive care unit. Two weeks later, he was discharged in good condition. Conclusion(s): Children with MIS-C associated with COVID-19 may develop primary spontaneous pneumothorax. Owing to the clinical picture overlapping with MIS-C associated with COVID-19, the timely diagnosis of pneumothorax may be challenging in such patients.Copyright © 2022, Author(s).

Report of the Association Between Multisystem Inflammatory Syndrome and Severe Myocarditis

Introduction: The people worldwide have been affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection since its appearance in December, 2019. Kawasaki disease-like hyperinflammatory shock associated with SARS-CoV-2 infection in previously healthy children has been reported in the literature, which is now referred to as a multisystem inflammatory syndrome in children (MIS-C). Some aspects of MIS-C are similar to those of Kawasaki disease, toxic shock syndrome, secondary hemophagocytic syndrome, and macrophage activation syndrome. Case Presentation: This study reported an 11-year-old boy with MIS-C presented with periorbital and peripheral edema, abdominal pain, elevated liver enzymes, severe right pleural effusion, moderate ascites, and severe failure of right and left ventricles. Conclusion(s): Due to the increasing number of reported cases of critically ill patients afflicted with MIS-C and its life-threatening complications, it was recommended that further studies should be carried out in order to provide screening tests for myocardial dysfunction. Adopting a multidisciplinary approach was found inevitable.Copyright © 2023, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

Angioedema induced by angiotensin-converting enzyme inhibitors: An analysis of hospitalizations during the covid-19 pandemic.

BACKGROUND: The pathogenesis of angioedema induced by angiotensin-converting enzyme inhibitors is based on the accumulation of bradykinin as a result of angiotensin-converting enzyme blockade. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the angiotensin-converting enzyme 2 receptor, which may inhibit its production and thereby lead to an increase in bradykinin levels. Thus, SARS-CoV-2 infection may be a likely trigger for the development of angioedema. AIMS: This study aimed to analyze cases of hospitalizations of patients with angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers during the coronavirus disease 2019 (COVID-19) pandemic. MATERIALS AND METHODS: This study retrospectively analyzed medical records of patients admitted to the Vitebsk Regional Clinical Hospital between May 2020 and December 2020 with isolated (without urticaria) angioedema while receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. In all patients, smears from the naso and oropharynx for COVID-19 were analyzed by polymerase chain reaction. RESULT(S): Fifteen inpatients (9 men and 6 women) aged 44-72 years were admitted because of emergent events, of which 53.6% had isolated angioedema. In two cases, a concomitant diagnosis of mild COVID-19 infection was established with predominant symptoms of angioedema, including edema localized in the face, tongue, sublingual area, and soft palate. All patients had favorable disease outcomes. CONCLUSION(S): Patients with angiotensin-converting enzyme inhibitor-induced angioedema may require hospitalization to monitor upper respiratory tract patency. There were cases of a combination of angiotensin-converting enzyme inhibitor-induced angioedema and mild COVID-19. Issues requiring additional research include the effect of SARS- CoV-2 infection on the levels of bradykinin and its metabolites, the triggering role of COVID-19 in the development of angioedema in patients receiving angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, recommendations for the management of patients with angiotensin-converting enzyme inhibitor-induced angioedema, and a positive result for COVID-19.Copyright © 2020 Pharmarus Print Media All rights reserved.

Prevalence of adverse drug reactions associated with emergency department visits and risk factors for hospitalization

Objective: Adverse drug reactions increase morbidity and mortality, prolong hospital stay and increase healthcare costs. The primary objective of this study was to determine the prevalence of emergency department visits for adverse drug reactions and to describe their characteristics. The secondary objective was to determine the predictor variables of hospitalization for adverse drug reactions associated with emergency department visits. Method(s): Observational and retrospective study of adverse drug reactions registered in an emergency department, carried out from November 15th to December 15th, 2021. The demographic and clinical characteristics of the patients, the drugs involved and the adverse drug reactions were described. Logistic regression was performed to identify factors related to hospitalization for adverse drug reactions. Result(s): 10,799 patients visited the emergency department and 216 (2%) patients with adverse drug reactions were included. The mean age was 70 +/- 17.5 (18-98) years and 47.7% of the patients were male. A total of 54.6% of patients required hospitalization and 1.6% died from adverse drug reactions. The total number of drugs involved was 315 with 149 different drugs. The pharmacological group corresponding to the nervous system constituted the most representative group (n = 81). High-risk medications, such as antithrombotic agents (n = 53), were the subgroup of medications that caused the most emergency department visits and hospitalization. Acenocumarol (n = 20) was the main drug involved. Gastrointestinal (n = 62) disorders were the most common. Diarrhea (n = 16) was the most frequent adverse drug reaction, while gastrointestinal bleeding (n = 13) caused the highest number of hospitalizations. Charlson comorbidity index behaved as an independent risk factor for hospitalization (aOR 3.24, 95% CI: 1.47-7.13, p = 0.003, in Charlson comorbidity index 4-6;and aOR 20.07, 95% CI: 6.87-58.64, p = 0.000, in Charlson comorbidity index >= 10). Conclusion(s): The prevalence of emergency department visits for adverse drug reactions continues to be a non-negligible health problem. High-risk drugs such as antithrombotic agents were the main therapeutic subgroup involved. Charlson comorbidity index was an independent factor in hospitalization, while gastrointestinal bleeding was the adverse drug reaction with the highest number of hospital admissions.Copyright © 2022 Sociedad Espanola de Farmacia Hospitalaria (S.E.F.H)

Acute exantematic pustulosis generalized by meropenem, differential diagnosis with COVID

Case report We present the case of a 63-year- old man with two consecutive admissions, due to COVID19 infection and subsequent bacterial superinfection. Three days after the second admission (04/28), and 43 days from the beginning of the infection an assessment by dermatology and allergology is then requested. The patient had generalized erythematous maculopapular rash in the trunk, back, groin and limbs. On the left side and back, pustular lesions not focused on follicles were also added, with a fever of 37.7degreeC. There were no oral and genital lesions. No psoriasis. The drugs used during the present and previous admissions were reviewed. Previous admission (04/04-22/ 20): Linezolid, ciprofloxacin, meropenem 04/13-22, piperacillin/tazobactam, hydroxychloroquine, azithromycin, ceftriaxone. Upon discharge amoxicillin/acid clavulanic. Present admission (04/25) Cutaneous reaction 04/28. 04/25: meropenem, paracetamol, enoxaparin, insulin, omeprazole, venlafaxine. 04/26: Darbepoetin, furosemide, mycophenolate in single dose. 04/27: Linezolid, macrogol, Clopidogrel, Magnesium, Calcitriol. Medical records: DM type 2, liver transplantation due to HCV cirrhosis, HCV recurrence, uninodular hepatocarcinoma, advanced CKD, secondary hyperparathyroidism, multiple neurological antecedents. We performed a detailed study. We hypothesized with a pharmagological/ drug reaction with several drugs possibly involved and our main suspicion was an allergic reaction to beta-lactams. Biopsy: Subcorneal pustules, basal spongiosis and presence in the superficial dermis of edema and an inflammatory infiltrate with abundant neutrophils. No fungi. Findings compatible with clinical diagnosis of generalized acute exanthematic pustulosis (PEGA). Immunohistochemical study Covid19. (Jimenez Diaz Foundation) Finely granular positivity in endothelium and more coarse in sweaty epithelium. Neutrophilic superficial inflammatory component with presumably spure staining. ACe-2 (positive external control) is not detected. The patient presents a EuroSCAR score of 9, sum of the clinic and the pathological anatomy, and therefore defined diagnosis. Clinical diagnosis: PEGA secondary to meropenem. Conclusion(s): We present the case of a PEGA by meropenem, not very often described in the literature. We highlight the importance of differential diagnosis with viral infections. Skin tests, especially epicutaneous tests, are key to the diagnosis. (Figure Presented).

A contrasting diagnosis: iododerma

An 86-year-old woman presented to the emergency department with acute shortness of breath. She was treated with intravenous furosemide for acute-on-chronic heart failure. Her past medical history included atrial fibrillation, hypertension, diverticulosis and hypothyroidism. Rivaroxaban and levothyroxine were her only long-term medications. On day 5 of hospital admission, she developed painful haemorrhagic and purulent bullae on her dorsal hands, head and neck. These evolved to large suppurative, vegetative plaques over a 72 h period and she developed additional lesions on her trunk, upper back and thighs. The patient had routine blood tests, which showed a raised C-reactive protein at 260 mg L-1, and an acute kidney injury with a glomerular filtration rate of 54 mL-1 min-1. She had a negative COVID-19 swab, and swabs from the lesions for bacterial culture and viral polymerase chain reaction were negative. She had a normal serum protein electrophoresis, immunoglobulin, antinuclear antibody and antineutrophil cytoplasmic antibody. She had computed tomography of her chest 24 h prior to the onset of her lesions, which showed mild bilateral pleural effusions in keeping with fluid overload secondary to heart failure. A biopsy taken from her hand showed orthokeratosis and parakeratosis, and there was bulla formation subepidermally. There was a dense neutrophilic infiltrate with microabscess formation with scattered eosinophils and lymphocytes. There was no evidence of vasculitis. Direct immunofluorescence was negative and a tissue culture for atypical mycobacteria was negative. The patient was commenced on high-dose intravenous methylprednisolone at 500 mg for 3 days followed by 40 mg prednisolone orally for 1 week, but there was a limited response. Our initial differential was Sweet syndrome or pyoderma vegetans;however, the patient had no fevers and no risk factors (malignancy, inflammatory disease, infection, etc.). She also had no response to high-dose oral prednisolone. Given the timing of her CT examination in relation to her acute dermatosis and the use of radioiodine for contrast, we assessed the patient's serum iodine and urine iodine. These were both high at 1.02 mmol L-1 (reference interval 0.32- 0.63) and 3.46 mmol L-1 (reference interval 0.0-2.43), respectively. A diagnosis of iododerma was made. The patient's eruption slowly resolved and at 12 weeks there was evidence of postinflammatory skin changes only. Her urine and serum iodine were rechecked, and both had normalized. In the last 20 years there have been approximately 20 case reports of iododerma. Most have been following iodine contrast use in patients with abnormal kidney function, like our patient. Most describe an acneiform eruption that subsequently evolves to vegetative plaques (Chalela JG, Aguilar L. Iododerma from contrast material. N Engl J Med 2016;374: 2477). Iododerma is largely a diagnosis of exclusion, but histopathology and urine and serum iodine levels can help support diagnosis.

Case report of congenital disorder of glycosylation type Ia combined with dilated cardiomyopathy.

Clinical data and follow-up of a case of congenital disorder of glycosylation type Ia (CDG-Ia) combined with dilated cardiomyopathy admitted to the Department of Cardiology, Children's Hospital of Nanjing Medical University were analyzed retrospectively.The 5-year-old female patient was admitted in December 2016 due to recu-rrent shortness of breath for 2 months.Clinical symptoms and signs included repeated attacks of shortness of breath, physical retardation, malnutrition, binocular esotropia, multiple episodes of hypoglycemia, hepatosplenomegaly, hypotonia and other multi-system damages.Cardiac echocardiography suggested the feature of dilated cardiomyopathy, including the significant enlargement of the left ventricle, and decreased systolic function.Genetic testing revealed a compound heterozygous mutation in the PMM2 gene, and as a result, the patient was diagnosed as CDG-Ia.The patient's condition improved after symptomatic treatments such as Cedilanid, Dopamine, Dobutamine, Furosemide, as well as support treatments like myocardium nutrition, blood sugar maintenance, liver protection, etc.After discharge, the patient was given oral Digoxin, Betaloc, Captopril and diuretics, and hypoglycemia-controlling agents.The patient was followed up every 3-6 months.After more than 2 years of follow-up, the heart function and heart enlargement gradually returned to normal.During the Corona Virus Disease 2019 outbreak, self-withdrawal continued for 2 months.Re-examinations showed decreased cardiac function and enlarged left ventricle again.Medications were resumed again, and the patient was followed up closely.This case report suggested that CDG-Ia may be associated with dilated cardiomyopathy, and the cardiac phenotype may be improved by symptomatic supportive treatment.Copyright © 2021 by the Chinese Medical Association.

Acute Mesenteric Thrombosis, Small Intestine Necrosis and Peritonitis as a Complication of Covid-19 - a Case Report

Introduction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) belongs to a family of ribonucleic acid (RNA) viruses, causing novel coronavirus disease 2019 (COVID-19). Because of a global inflammatory response and endothelial damage, COVID-19 may predispose to coagulation disorders and severe thrombotic events. Case presentation. A 62-year-old man patient was admitted for COVID-19 pneumonia and abdominal pain for 10 days. Because of the rapid deterioration of the clinical status, shock and evidence of peritoneal irritation, the patient was consulted by a surgeon. The native spiral computed tomography (CT) of the abdomen detected enlarged colon filled with air collections and hydro-aeric levels. The surgical intervention revealed diffuse peritonitis with necrosis of the distal ileum secondary to mesenteric thrombosis. A partial resection of the ileum was done. The histological examination showed an infarcted small bowel, with hemorrhage, vascular thrombosis, and signs of necrotizing endovasculitis. Conclusions. SARS-CoV-2 binds to ACE2 receptor, which results in increased signalling by thrombin receptors on platelet and endothelial cells, leading to coagulopathy. In older patients presenting with abdominal pain, shock and peritonitis, the most common underlying cause is mesenteric thrombosis which could be a complication of COVID-19.Copyright © 2022 Balkan Medical Union.

Furosemide-induced haemolytic anaemia in an extreme elderly patient.

Furosemide, a loop diuretic, is commonly used to treat fluid overload symptoms and heart failure. Drug-induced immune haemolytic anaemia is an unusual drug-adverse event. Furosemide-induced haemolysis is even rarer. This case report presents a 91-year-old male who developed acute haemolytic anaemia 3 days after initiating furosemide to treat myocardial infarction complicated with acute decompensated heart failure. He had increased lactate dehydrogenase and unconjugated bilirubin with undetectable haptoglobin, which indicated the destruction of red blood cells. Other causes for haemolytic anaemia, including hereditary, microangiopathic haemolytic anaemia, and paroxysmal nocturnal haemoglobinuria, were also excluded. He improved with drug cessation and a short course of glucocorticoids. This report aims to raise awareness of this rare complication caused by commonly prescribed drugs. Despite a negative result of a direct antiglobulin test, physicians must remain suspicious of drug-induced immune haemolytic anaemia in unclear cases of haemolysis.

Pneumopericardium in COVID-19 Infection

Pneumopericardium is a rare medical condition that occurs following trauma, surgery, or other medical interventions. The presence of pneumopericardium after COVID-19 pneumonia has been reported in some cases, and it has been explained that most cases could be self-limited. Here, we describe a 51-year-old man afflicted by pneumopericardium with COVID-19 infection. The patient had pneumopericardium and massive pericardial effusions, necessitating surgical strategies such as pericardial windows. This case highlights the potential severity of COVID-19. We also suggest that cardiologists pay attention to the possibility of pneumopericardium in cases with COVID-19 infection. © 2023, Iranian Heart Association. All rights reserved.

Lung Injury in COVID-19 Has Pulmonary Edema as an Important Component and Treatment with Furosemide and Negative Fluid Balance (NEGBAL) Decreases Mortality.

The SARS-CoV2 promotes dysregulation of Renin-Angiotensin-Aldosterone. The result is excessive retention of water, producing a state of noxious hypervolemia. Consequently, in COVID-19 injury lung is pulmonary edema. Our report is a case-control study, retrospective. We included 116 patients with moderate-severe COVID-19 lung injury. A total of 58 patients received standard care (Control group). A total of 58 patients received a standard treatment with a more negative fluid balance (NEGBAL group), consisting of hydric restriction and diuretics. Analyzing the mortality of the population studied, it was observed that the NEGBAL group had lower mortality than the Control group, p = 0.001. Compared with Controls, the NEGBAL group had significantly fewer days of hospital stay (p < 0.001), fewer days of ICU stay (p < 0.001), and fewer days of IMV (p < 0.001). The regressive analysis between PaO2/FiO2BAL and NEGBAL demonstrated correlation (p = 0.04). Compared with Controls, the NEGBAL group showed significant progressive improvement in PaO2/FiO2 (p < 0.001), CT score (p < 0.001). The multivariate model, the vaccination variables, and linear trends resulted in p = 0.671 and quadratic trends p = 0.723, whilst the accumulated fluid balance is p < 0.001. Although the study has limitations, the promising results encourage more research on this different therapeutic approach, since in our research it decreases mortality.

Severe progression of autoimmune hepatitis in a young COVID-19 adult patient: A case report

Rationale: The impact of COVID-19 in patients with autoimmune liver disease treated with immunosuppressive therapy has not been described so far. This case report describes the clinical course of a patient with autoimmune hepatitis (AIH) who developed COVID-19 and the features of cytokine syndrome leading to its deterioration in our intensive care unit. Patient's Concern: A 28-year-old male presented with generalized anasarca for two weeks and chronic liver disease for 8 months. Diagnosis: AIH and Covid-19 with features of cytokine storm syndrome. Interventions: Intravenous furosemide, mannitol, syrup lactulose, steroids (prednisolone 40 mg), azathioprine 1 mg/kg body weight, rifaximin, vitamin K, and blood products. Outcomes: The patient had hepatic encephalopathy and AIH and died on the 10th day after admission despite ventilatory support, sustained low-efficiency hemodialysis, and resuscition. Lessons: The dramatic release of cytokines and the inflammatory-immune responses not only alter the pathophysiology but also affects the onset and severity of disease progression in patients with AIH.

Severe Pulmonary Hemorrhage in a 3 Weeks Old Neonate with Covid-19 Infection

Aims To describe a case of 3 weeks old neonate presenting with severe pulmonary hemorrhage due to COVID-19 infection and its outcome. Methods We report an interesting case of pulmonary hemorrhage presenting at a young age of 3 weeks, in a previously healthy neonate who was infected with COVID-19 virus;Literature review and investigation results are included. This is a 3-week-old female, a product of full-term pregnancy and an uneventful perinatal course. She was admitted from the emergency department initially as a case of late neonatal sepsis, where a full septic workup was done. Her presenting complaints were low-grade fever and a blocked nose for one day. She was hemodynamically stable in the emergency department except for tachycardia secondary to fever, which improved once the fever was controlled. Her initial blood workup, including blood gas and CSF study, was reassuring (table 1a). Her COVID PCR was positive with a CT value of 17.77. She was treated with IV antibiotics and supportive management. Later that day, the patient developed cardiopulmonary arrest, CPR was initiated, and the patient was intubated. The patient was found to have pulmonary hemorrhage as evident by the fresh blood coming out of the endotracheal tube and the chest X-Ray findings of ground-glass opacities and dense consolidation (figure 1). After initial brief stabilization, the patient started deteriorating requiring escalation of respiratory support to HFOV. The patient continued to deteriorate and developed bilateral pneumothorax requiring bilateral chest tube insertion. After chest tube insertion, there was a mild transient improvement in oxygenation. The patient was put on the maximum ventilatory settings, but she kept having frequent desaturation, requiring frequent manual bag to tube ventilation. Later, she started developing progressive hypotension, that required support with maximum doses of inotropes. Her urine output started decreasing, for which frusemide were started with no response. Blood investigations showed severe DIC picture (table 1b and 1c). She was empirically covered with Meropenem and Vancomycin along with Remdesivir and Dexamethasone for COVID 19 pneumonia. Eventually, the child developed progressive desaturation, hypotension, and poor perfusion. Shortly after that, she developed cardiac arrest and was declared dead. Results The clinical picture of COVID 19 infection is more indistinct in children than in adults, with the most common symptoms being fever, cough, dyspnea, and malaise. In the few published cases of COVID-19 in the neonate, the presentation was that of late neonatal sepsis;interestingly, the lung involvement was not described as frequently as in older age groups. Pulmonary hemorrhage has been reported in adults but rarely in children. Some reports in adults suggested that patients with COVID infection had an increased inflammatory state that led to the development of vasculitis and pulmonary hemorrhage. Up to our knowledge, this is the youngest age at which a patient with COVID-19 infection developed pulmonary hemorrhage with no other underlying cause of it. Conclusion While many of the cases of COVID infection in children are mild, fatal complications like pulmonary hemorrhage can be present. Adding new challenges to the management of this viral infection.

Minimal recovery of drug from extracorporeal treatment in a case of phenytoin toxicity associated with coma and hypothermia

Background: The Extracorporeal Treatments in Poisoning (EXTRIP) workgroup provides a weak conditional recommendation in support of hemodialysis (HD) for select patients with severe phenytoin poisoning. Despite this recommendation, the HD clearance of phenytoin is poorly studied. We present a patient who developed phenytoin toxicity that was treated with hemodialysis and report on the efficacy of phenytoin removal during HD. Case report: An 87-year-old man with epilepsy who was maintained on a stable dose of 300mg phenytoin extended-release daily was admitted to the hospital for treatment of Coronavirus Disease 2019 and congestive heart failure. On hospital day 14, the patient had a gradual onset of depressed mental status with hypothermia (nadir 35 degrees Celsius). At this time, he had a rising total blood phenytoin concentration (peak 49.3 mcg/mL [therapeutic 10-20mcg/mL] with an albumin of 3.8 g/dL [normal 3.4-5.4 g/dL]). The patient's other medications included furosemide, aspirin, atorvastatin, digoxin, doxycycline, metoprolol tartrate, and warfarin;he was also receiving albumin and crystalloid for hypovolemia (albumin nadir on hospital day 14: 2.5 g/dL). Free phenytoin concentrations were not available. Alternate etiologies of hypothermia (endocrine, infectious) were excluded. The Poison Control Center was consulted and recommended HD because of the concern for prolonged coma, as per EXTRIP guidelines. The patient received three sessions of HD over a period of 6 days at 2.5-3 h per session using an F160 Optiflux membrane filter (Fresenius Medical Care, Waltham, MA, USA), with a blood flow rate of 350mL/min and a dialysate flow rate of 700mL/min. After the first session of HD (2.5 h) on hospital day 21, his hypothermia resolved and his phenytoin concentration fell from 39.2mcg/mL to 34.2 mcg/mL with only mild improvement in his mental status. After 6 days (hospital day 27), his phenytoin concentration decreased to 19.5 mcg/mL and his mental status normalized. Effluent from the first HD session had phenytoin concentrations below the limit of detection (0.50mcg/mL). Thus, no greater than 52mg of phenytoin was removed during a 2.5-h session of hemodialysis. Discussion(s): The reason for the sudden increase in blood phenytoin concentrations in this patient is unclear in the absence of drug-drug interactions or dosing changes to the phenytoin. Although uncommonly reported, patients with phenytoin toxicity can experience hypothermia. In this case, the patient's hypothermia resolved during HD, although it is unclear if this was related to changes in phenytoin concentration or (more likely) direct extracorporeal warming via the HD machine. If the patient's phenytoin clearance from the first session were extrapolated to subsequent sessions an estimated maximum of 166.4mg of phenytoin would be removed in 8 total hours of HD, which is far less than previously reported phenytoin clearances on the order of grams. This difference may be related to the use of high cutoff dialysis membranes in prior studies, which are not routinely used. Conclusion(s): Although HD rapidly resolved this patient's hypothermia, a minimal amount of phenytoin was recovered in the patient's dialysate. Prior studies suggesting consequential clearance and efficacy of phenytoin removal by extracorporeal treatment may not apply to routine HD methods. Further studies on the utility of extracorporeal treatment for phenytoin toxicity are needed.

Early experience with myocarditis and pericarditis in adolescents following vaccination against COVID-19 in latvia

Background and Aim: The European Medicines Agency has approved mRNA vaccines developed by Pfizer/BioNTech and Moderna for the vaccination of adolescents against the SARS-CoV-2 infection. Cases of myocarditis and pericarditis have been described as rare postvaccination complications. We describe the Latvian experience with adolescents suffering from myocarditis following COVID-19 vaccination. Method(s): From June to December 2021 four cases consistent with postvaccination myocarditis were admitted to the Children's Clinical University Hospital, which is the only centre with special-ized paediatric cardiology care in Latvia. The Pfizer/BioNTech vaccine had been used in all. An ECG, Holter monitoring and ECHO was done, HS Troponin I levels checked, the most common infectious causes of myocarditis were excluded, and a cardiac MRI was performed in all cases. Result(s): Case 1: 12-year-old girl, developed chest pain on postvac-cination day Nr 4 (PVD4) after the 1st dose. Holter monitoring revealed rare non-sustained ventricular tachycardia (NSVT), ECHO showed moderate mitral insufficiency, and a hyperecho-genic papillary muscle, troponin level peaked at 5339 pg/ml (PVD6), MRI (PVD 7) showed widespread myocardial oedema, transmural fibrosis. Symptoms resolved in 1 day, metoprolol suc-cinate and lisinopril were prescribed. Mitral insufficiency persists 5 months later. Case 2: 15-year-old boy, developed chest pain after the 2nd dose on PVD2 and lasted for 7 days, he was admitted on PVD11 with a peak troponin level of 19pg/ml. MRI (PVD15) showed widespread myocardial oedema. Metoprolol succinate was prescribed. Case 3: 15-year-old boy, developed chest pains on the day of the 1st dose and persisted for 35 days, he was admitted on PVD24 with peak troponin level 15ng/ml. MRI (PVD29) showed mild myocardial oedema, myocardial and pericardial fib-rosis. Case 4: 13-year-old boy, developed chest pain on PVD2, which lasted for 65 days, he had an episode of syncope. Holter monitoring showed frequent PVCs, and NSVT, on PVD34 tro-ponin level was 2,5pg/ml. The child received a course of NSAIDs and was referred to us on PVD68. MRI (PVD69) revealed wide-spread myocardial oedema, fibrosis, and pericarditis. Methylprednisolone was given, and betaxolol was prescribed. Conclusion(s): Our case series show that some cases of postvaccination myocarditis develop complications requiring long-term treatment.

POST-COVID-19 EOSINOPHILIC PNEUMONIA

SESSION TITLE: Post-COVID-19 Infection Complications SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: We present two cases of symptomatic post-COVID eosinophilic pneumonia responsive to steroids. CASE PRESENTATION: Case 1: A 73-year-old gentleman with underlying asymptomatic rheumatoid arthritis (RA), was admitted with COVID pneumonia for which he received tocilizumab, remdesivir, and 12 days of dexamethasone. His course was complicated by MRSA pneumonia and bacteremia, so was discharged on IV Vancomycin. Six days post discharge, he redeveloped respiratory distress. Labs showed a WBC 18,000 and proBNP 2828. A chest CT revealed bilateral ground-glass opacities, worsening right upper lung airspace disease and bilateral pleural effusions. Despite receiving Furosemide, Vancomycin, and Ceftazidime, he required high-flow nasal cannula oxygenation (HFNC). Bronchoscopy demonstrated thick right bronchial secretions. BAL fluid revealed 7% eosinophils and grew MRSA. Case 2: A 70-year-old gentleman with extensive smoking history, emphysema, psoriasis, Guillain-Barré syndrome and a recent hospitalization for COVID pneumonia was discharged on a steroid taper. He returned 23 days post discharge in respiratory distress requiring HFNC, 5 days after discontinuing steroids. The chest CT revealed worsening fibrosis and bronchiectasis. Intravenous Levofloxacin and Vancomycin resulted in no clinical improvement. Bronchoscopy showed inflamed bronchi with secretions and BAL analysis revealed 6% eosinophils. For both patients, BAL was negative for fungi and PJP and CTA ruled out PE. Both patients were started on Prednisone with a prolonged taper. They improved clinically with decreased oxygen requirements to 4L nasal cannula and dramatic decrease in subjective dyspnea within 48 hours of starting steroids. DISCUSSION: The differential diagnosis for the clinical deterioration and worsening radiographs in both patients includes bacterial/fungal superinfection, PE, post-COVID-ILD and eosinophilic pneumonia. For the first patient, his RA was inactive. His BAL was positive for MRSA but did not improve until steroids were initiated. Neither of the patients were stable for VATS biopsy. Eosinophilic pneumonia is defined as pulmonary infiltrates with peripheral blood eosinophilia =500/ml, BAL eosinophils > 5% or eosinophilic infiltration on lung biopsy [1]. Both of our patients had >5% BAL eosinophils. Potentially, prolonged COVID-ILD stimulates T-Helper-2 cells, causing the release of IL-4/5/13 with recruitment of eosinophils. Studies report post-COVID-ILD biopsies show organizing pneumonia and fibrosis but have not yet been associated with eosinophilia. In both patients, we observed eosinophilia on BAL. It can be hypothesized that a delayed inflammatory response mediated by eosinophils play a role. CONCLUSIONS: Pulmonary eosinophilic pneumonia is a complication of post-COVID-ILD and can be successfully managed with steroids. 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 Mar 15;197(6):728-736. doi: 10.1164/rccm.201710-1967CI. PMID: 29206477. DISCLOSURES: No relevant relationships by farrukh ahmad No relevant relationships by Deborah Markowitz No relevant relationships by Dhiraj Shah No relevant relationships by Garima Singh No relevant relationships by Aakriti Soni

REACTIVATION MILIARY TB IN THE SETTING OF POSTINFECTIOUS COVID-19 LUNGS

SESSION TITLE: Pathologies of the Post-COVID-19 World SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Tuberculosis, caused from infection by M. tuberculosis, affects 2.7 per 100,000 people in the United States. 1 Miliary, or disseminated, TB is a progressive disease characterized by lymphohematogenous dissemination of TB infection that occurs in only 1-2% of TB cases. Little research has gone into pulmonary complications post recovery from COVID-19 infection, especially reactivation of latent TB. Here we present a case of reactivation of latent TB and progression to miliary TB in the setting of post COVID infection. CASE PRESENTATION: A 49-year-old male presented to the ER with fever, shortness of breath, and chest pain. His CXR showed diffuse bilateral, multifocal infiltrates and laboratory testing later came back positive for COVID-19. Two days later, he came back to the ED with acute respiratory failure with 87% oxygen saturation with ambulation. A CT chest done that showed diffuse lung disease consistent with COVID-19 infection, and a right upper lobe lesion likely a granuloma (image 1). He was treated for COVID pneumonia for ten days in the hospital with Decadron, Lasix, and tocilizumab. He required high flow nasal canula during the hospitalization and was discharged when his respiratory status had improved. One year later, he returns with few days of hemoptysis, fever, and chills. He had a progressive cough and 19 pound weight loss overt the last month. Clinically, he appeared mildly diaphoretic without acute distress. He had a room-air oxygen saturation of 95% without labored respiration and did not have increased oxygen demand. CT of the showed diffuse pulmonary parenchymal abnormalities and uniform nodular consolidative changes in the upper lobes bilaterally with areas of cavitation and multiple areas of lung parenchymal changes consistent with miliary TB (image 2). Sputum culture was positive for acid-fast bacilli, and he was started on RIPE therapy with rifampin, isoniazid, pyrazinamide, and ethambutol. He was symptomatically improved within one week of admission and was hospitalized until three negative sputum cultures were drawn. DISCUSSION: This case report gives us novel understanding of the extent of possible complications post recovery from COVID-19 infection. We have already started to see many patients who have recovered from an initial COVID infection, but progressed to secondary lung disease due to this. In our patient particularly, during his initial presentation he was seen to have upper lobe granulomatous disease with concern for latent TB. It is likely that due to the extent of damage done to his lung parenchyma over time it led to reactivation of his latent TB. As we see more patients recovering from COVID infections, we are likely to see more of similar cases of latent infection reactivation. CONCLUSIONS: Patients with latent TB are likely at a high risk of reactivation post recovering from COVID-19 infection, due to immunosuppression and lung parenchymal damage Reference #1: Trends 2019 ;Data & Statistics ;TB ;CDC. Cdc.gov. https://www.cdc.gov/tb/publications/factsheets/statistics/tbtrends.htm. Published 2021. Accessed September 25, 2021. Reference #2: Rodriquez-Morales AJ et al. Clinical, laboratory, and imaging features of COVID-19: a systemic review and meta-analysis. Travel Med Infect Dis. 34: 101623 Reference #3: Colditz GA, Brewer TF, Berkey CS, et al. Efficacy of BCG vaccine in the prevention of tuberculosis. Meta-analysis of the published literature. JAMA. 1994;271(9):698-702 DISCLOSURES: No relevant relationships by Sharmin Asha No relevant relationships by Heather Bernstein no disclosure on file for zachary brittingham;no disclosure on file for Vedee Ramdass;