Risk of Aki in Covid-19 Patients: Clinical Course and Outcomes

Introduction: Acute kidney injury (AKI) occurs in 0.5 to 25% of hospitalized COVID-19 patients. Clinical severity and renal involvement are due to inflammation, immune and endothelial dysfunction. On the other hand, risk factors such as age, comorbidities, mechanical ventilation requirement, hypovolemia and MAP <65 mm Hg are associated with AKI development. This study aim to evaluate the development of AKI and determine the relationship between serum creatinine and inflammatory. Method(s): A single center, retrospective study involving 166 patients under the diagnosis of moderate to severe COVID-19 infection in Hospital General Regional 110 Oblatos, Guadalajara, Mexico. A consecutive sample was approached. AKI was determined and classify when changes in serum creatinine met KDIGO definition. Demographics, clinical and biochemical data, risk factors for AKI and RRT prescription were assessed and reported during diagnosis and discharge. Outcome measures were renal recovery, mortality and causes of death. Differences were compared using 2-sample t test for continuous variables and chi-square for categorical variables. Relationship between creatinine changes and inflammation markers were assessed using Pearson correlation coefficients. All statistical tests were performed using SPSS 28.0 and a P < 0.05 level of significance. Result(s): Mean age 59 +/- 18.38 years. 60 cases (36%) were diagnose as AKI. 41% were in stage 1, whereas 35% and 24% made up stage 2 and 3, respectively. Changes in serum creatinine (SCr) correlated with gender (r=0.155, p 0.48), changes in hemoglobin (r= -0.384, p < 0.01), neutrophil/ lymphocyte ratio (NLR) (r= 0.229;p 0.003), serum phosphate (r= 0.555, p < 0.01), serum calcium (r= -0.210, p < 0.011), serum potassium (r= 0.555, p < 0.01), serum magnesium (r= 0.212, p < 0.012), D-dimer (r= 0.246, p 0.02) and (r= -0.322, p < 0.01). After adjusting model for cofounders, hospitalization length and age (OR: 3.03, CI 0.39, 11.56, p=0.033) trend to be a significant data, other cofounders in relation to the presence of AKI o changes in SCr were no significant with other potential outcomes. [Formula presented] Conclusion(s): The present study highlighted that the presence of AKI is associated the increased of inflammation, but the current evidence limits the outcomes in already none predictive factors. Further studies are needed to establish early strategies aimed to prevent AKI and its evolution in COVID-19 patients and pandemics ahead. No conflict of interestCopyright © 2023

Association of Dysnatremia with Morbidity and Mortality of Covid-19 Patients Admitted in the Intensive Care Units of a Tertiary Care Hospital: A Retrospective Cohort Study

Introduction: The coronavirus disease 2019 (COVID-19) has rapidly spread globally and infected millions, with increasing infection rates and mortality. In our institution, there have been several cases of COVID-19 patients who, in the initial laboratory exam at the ED (Emergency Department), turned out to be dysnatremic. On admission, most patients with normal serum Na+ developed dysnatremia during their ICU (Intensive Care Unit) stay. This study aimed to determine the relationship between serum Na+ levels on presentation and any point during hospitalization with morbidity and mortality in critically ill COVID-19 subjects. Method(s): This retrospective cohort study included 261 patients aged 18 years and above diagnosed with COVID-19 infection confirmed by positive real-time RT PCR test, who were admitted from January 2020 to December 2021 in the critical care units of a tertiary care hospital. The outcomes were evaluated after 8 weeks of hospitalization as to AKI (Acute Kidney Injury), length of hospital stay, length of ICU stay, need for ventilator support, vasopressor support, COVID recovery, and mortality. Subjects' serum Na+ levels were obtained on admission, day 3, day 7, day 14, and the last serum Na+ before death or discharge. Result(s): Among the 261 COVID-19 cases analyzed, the number of patients with either hyponatremia or hypernatremia on presentation and anytime during hospitalization was 67.05%. The predominant disorder was hyponatremia, seen in 51.34% of patients (95% CI 45.10% to 57.55%). Hypernatremia was seen in 36 patients, or 13.79%. The most common etiology of both disorders was hypovolemia, mostly from poor oral intake, followed by insensible losses from fever and tachypnea, and GI losses. Mortality rates were higher in hypovolemic patients compared to euvolemic patients (86.21% vs. 42.86% in hypernatremic patients;62.77% vs. 53.85% in hyponatremic patients). Patients with dysnatremia had a significantly higher proportion of AKI (80% vs. 31.4%, p < 0.001), a longer length of ICU stay (19 vs. 12 days, p < 0.001), a higher proportion that required ventilator support (80% vs. 28%, p < 0.001) or vasopressor support (73.71% vs. 20.93%, p < 0.001), and death (64% vs. 2.33%, p < 0.001) after 8 weeks of hospitalization. In a subgroup analysis of hypernatremic and hyponatremic patients, it appeared that hypernatremia had worse outcomes in terms of AKI (94.44% vs. 75.37%), length of ICU stay (IQR 16-35 vs. 14-25), need for ventilator support (91.67% vs. 77.61%), vasopressor support (86.11% vs. 70.9%), and death (77.78% vs. 60.45%). [Formula presented] Conclusion(s): Dysnatremia at any time point during the ICU stay is related to excess mortality. Hypernatremia was a significant risk factor for mortality, especially for the subgroup of hypovolemic patients. Dysnatremia was found to be more frequent on the day of presentation in the ED, making it a potential risk stratification tool for determining COVID-19 severity and poor outcomes. Clinicians managing COVID-19 patients should know that dysnatremia anytime during hospitalization confers a higher risk for death than those presenting with normal Na+ levels, and early nephrology referral may provide benefit. No conflict of interestCopyright © 2023

Not all shortness of breath and throat pain is COVID

Case Report: A previously, healthy 18-year-old female presents to a Pediatric Emergency Medicine Department with shortness of breath, fever, and worsening throat and abdominal pain for 3 days. She had a sick contact, a teacher that tested positive for COVID-19 2 weeks prior to presentation. She denies runny/stuffy nose, cough, loss of taste/smell, or rashes/lesions. She denies any significant past medical history including allergies, as well as any history of smoking or any illicit drug use. Upon arrival to the ED, the patient was noted to be tachycardic, hypotensive and febrile. There were no desaturations. Initial physical examination revealed a generally uncomfortable female that was alert and oriented, with noted tenderness over the right anterior neck region, diffuse cervical lymphadenopathy, and painful neck range of motion. Her pharynx was noted to be erythematous without exudates or any unilateral tonsillar swelling. In the ED patient received IV fluid resuscitation and was started on norepinephrine drip, broad spectrum antibiotics. Initial lab workup revealed an anion gap metabolic acidosis, likely secondary to uremia or lactic acidosis from poor perfusion in setting of sepsis and hypovolemia. BUN and creatinine were elevated, likely due to an acute kidney injury (AKI) secondary to hypovolemia. The patient was also found to have an elevated LDH, fibrinogen, and mild elevation of AST. D-Dimer was elevated at 29 000. Covid PCR, Rapid Strep, and respiratory PCR panel were negative. Her chest X-ray (CXR) was negative and ECG showed sinus tachycardia. Given the patient's history of throat and neck pain with shortness of breath, in the setting of a septic picture, a CT scan of neck, chest, abdomen was ordered prior to transferring the patient to the PICU. CT scan of the chest revealed small patches of consolidation with ground glass opacities in the right lung apex, as well as an nearly occlusive, acute thrombosis of the anterior right facial vein. The patient's initial blood cultures grew gram negative bacilli which later were revealed to be Fusobacterium necrophorum. These findings are consistent with Lemierre's syndrome. The patient was treated in the PICU on vasopressors, heparin anticoagulation, and antibiotics for 6 days and discharged with a course of Augmentin. Lemierre's syndrome is an infectious thrombophlebitis of the internal jugular vein. First described by Andre Lemierre in 1936, it begins as a bacterial pharyngitis, generally developing into a peritonsillar abscess or other deep space neck infection with progressive erosion into the internal jugular vein. Diagnostic criteria for Lemierre's syndrome includes radiographically evidence of thrombophlebitis of the internal vein and positive blood cultures. CT and MRI can help make the diagnosis, but are not always required. Treatment is prompt intravenous antibiotics with beta-lactamase penicillins, metronidazole, clindamycin, and third generation cephalosporins. [Figure presented] Copyright © 2023 Southern Society for Clinical Investigation.

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.

A CASE OF ANTISYNTHETASE SYNDROME: THE IMPORTANCE OF HISTORY IN DISTINGUISHING ETIOLOGY OF INTERSTITIAL LUNG DISEASE IN A COVID-19 WORLD

SESSION TITLE: Systemic Diseases Causing Pulmonary Havoc SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: In the coronavirus disease 2019 (COVID-19) era, the etiology of interstitial lung disease (ILD) should remain broad to ensure accurate diagnosis and the proper treatment of patients. Vital to the art of medicine is taking a comprehensive history, and anchoring on a common diagnosis such as COVID-19 can result in early dismissal of alternate etiologies that physicians have an obligation to explore. CASE PRESENTATION: A 58-year-old male with a history of diabetes, hypothyroidism, and hypertension presented to the emergency department (ED) with dyspnea and fever. Initial CT chest imaging was significant for reticular and fibrotic changes with peripheral ground-glass and solid nodular opacities, some with areas of central clearing. Despite negative PCR testing, he was diagnosed with COVID-19 and discharged on oxygen with pulmonary follow-up. He continued to have arthralgias, proximal muscle weakness, low-grade fevers, and weight loss. He re-presented to the ED and was admitted for hypovolemia and further exploration into a potential autoimmune etiology of his symptoms. Labs were significant for a creatine kinase of 3,381 U/L, positive autoimmune antibodies [ANA (1:320), Jo-1 (>8.0 U), and SS-A/Ro (1.4 U)], and elevated ESR and CRP (30 mm/hr and 81 mg/L). Repeat CT revealed persistent parenchymal changes. Bronchoscopy was performed without anatomical abnormalities, and bronchoalveolar lavage (BAL) fluid was normal in appearance and negative for infectious etiologies. Though the patient was a farmer and possessed risk factors for hypersensitivity pneumonitis, lack of lymphocytic predominance on BAL, negative hypersensitivity panel, and uncharacteristic CT findings helped exclude this diagnosis. The patient was diagnosed with antisynthetase syndrome and treated with pulse dose intravenous solumedrol before transitioning to prednisone with resolution of muscle weakness and radiographic improvement in lung infiltrates. Muscle biopsy was deferred given the rapid clinical response and serum markers consistent with the diagnosis. DISCUSSION: Antisynthetase syndrome is a rare cause of ILD and often presents with myositis, arthritis, skin changes, Raynaud's phenomenon, and fever [1]. These symptoms, combined with the aminoacyl-tRNA synthetase antibody—most commonly the Jo-1 antibody—help confirm the diagnosis [2]. Due to a lack of established diagnostic criteria, muscle biopsy is often used to exclude other causes of myositis [3]. The ILD associated with antisynthetase syndrome is a significant cause of morbidity and mortality, and delay in diagnosis can lead to progression of lung injury. CONCLUSIONS: Chest imaging findings in COVID-19 are nonspecific, and post-COVID lung disease often presents similarly to other ILDs [1]. Because of this, history and physical exam remain crucial tools to reflect on alternate diagnoses for ILD and will continue to be necessary as we evolve through this COVID-19 era. Reference #1: Devi HG, Pasha MM, Padmaja MS, Halappa S. Antisynthetase Syndrome: A Rare Cause for ILD. Journal of Clinical and Diagnostic Research : JCDR. 2016;10(3):OD08. doi:10.7860/JCDR/2016/16872.7361 Reference #2: Cavagna L, Trallero-Araguás E, Meloni F, et al. Influence of Antisynthetase Antibodies Specificities on Antisynthetase Syndrome Clinical Spectrum Time Course. Journal of Clinical Medicine. 2019;8(11). doi:10.3390/jcm8112013 Reference #3: Schmidt J. Current Classification and Management of Inflammatory Myopathies. J Neuromuscul Dis. 2018;5(2):109-129. doi: 10.3233/JND-180308. PMID: 29865091;PMCID: PMC6004913. DISCLOSURES: No relevant relationships by Dustin Norton No relevant relationships by Alyssa Simon No relevant relationships by Kang Rui Xiang

COVID-19-INDUCED POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Postural orthostatic tachycardia syndrome (POTS) is one of the most common autonomic disorders (1). POTS is diagnosed by increasing heart rate by 30 bpm on more, within the first 10 minutes of standing, without orthostatic hypotension (2). Associated debilitating symptoms are lightheadedness, fainting, tremor, orthostatic intolerance, and tachycardia (2). Viral infections such as HIV, hepatitis C, mumps, Epstein bar virus, and influenza have been commonly reported with POTS syndrome (3 ). We are presenting a rare case of COVID-19 induced POTS. CASE PRESENTATION: 38-year-old presented to the hospital with the chief complaint of shortness of breath chest tightness. Her past medical history was significant for COVID-19 infection two weeks before presentation. On arrival patient's vitals were within normal limits. Her physical examination was unremarkable. Laboratory investigations, including complete blood count, thyroid function test, and comprehensive metabolic profile, were unremarkable. Chest x-ray, CT angiogram, and echocardiogram were unremarkable for any consolidation, pulmonary embolism, and congestive heart failure. Orthostatic vitals were obtained, showing that the patient's heart rate increased from 90 beats/minute to 140 beats/minute, from supine to standing. This patient was diagnosed with COVID-19 induced POTS, given she was meeting the criteria of POTS and no other reason was found for postural orthostatic tachycardia. She was managed conservatively with hydration, and the patient was also instructed about yoga therapy. She was discharged home with a cardiology follow-up. DISCUSSION: COVID-19 induced POTS is a relatively new entity that most commonly affect female, and the estimated prevalence is around is 17 per 100,000 patients (3). It has been reported that 10% of the patient who tests positive for COVID-19 infection remains unwell beyond three weeks after recovery from the infection (2). For some of those patients, POTS may be the cause of their symptoms. The exact pathophysiology for COVID-19 induced POTS is poorly understood and may includes peripheral neuropathy, baroreceptor dysfunction, hypovolemia, and increased serum norepinephrine (2). Nonpharmacological treatment includes increasing fluid consumption of 2 to 3 L of water per day, lower limb compression stockings, and regular exercise (2). The commonly off-label pharmacological treatment include ivabradine, fludrocortisone, midodrine, and beta-blockers (2). CONCLUSIONS: POTS is a new and under-recognized entity. The clinician should have a high suspicion of POTS syndrome in a patient with a history of recent or remote COVID-19 infection presenting with orthostatic symptoms. Timely diagnosis is essential to prevent the morbidity associated with debilitating symptoms. Reference #1: Blitshteyn S & Whitelaw S. Postural Orthostatic Tachycardia Syndrome (POTS) and Other Autonomic Disorders After COVID-19 Infection: A Case Series of 20 Patients. Immunol Res. 2021;69(2):205-11. Reference #2: Jenna Stephanie O'Sullivan, Andrew Lyne, Carl J Vaughan. COVID-19-Induced Postural Orthostatic Tachycardia Syndrome Treated with Ivabradine. BMJ Case Reports CP. 2021;14(6):e243585. Reference #3: Sujana Reddy, Satvik Reddy, Manish Arora. A Case of Postural Orthostatic Tachycardia Syndrome Secondary to the Messenger RNA COVID-19 Vaccine. Cureus. 2021;13(5). DISCLOSURES: No relevant relationships by Arshan Khan

A CASE OF POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME AFTER MRNA COVID-19 VACCINE

CASE: Ms.X is a 31-year-old female with an unremarkable medical history who presented to the general medicine clinic with palpitations that started 3 days after taking her second dose of Pfizer Covid vaccine. The palpitations ocurred exclusively when standing, with no associated chest pain, dizziness, or presyncope. History is negative for tobacco smoking, drug or alcohol use, and consumption of energy or caffeinated beverages. The physical examination was notable for moist mucous membranes and normal volume examination. Orthostatic vitals were remarkable for an increase in HR by 30 beats with minimal change in BP. EKG showed a normal sinus rhythm, and lab workup inclusive of a CBC, CMP, and TSH was unremarkable. As such, the patient was referred for tilt-table testing. Within 8 minutes of upright tilting, HR was137 from a baseline of 77, and BP was 144/108 from 125/71. A looprecorder was inserted which revealed presence of patient triggered episodes of sinus tachycardia upon standing. The patient was started on propranolol 10 mg every 4-6 hours while awake with almost complete resolution of palpitations. IMPACT/DISCUSSION: The incidence of POTS is 0.2-1% in developed countries, with a 5:1 female-male ratio. It presents with orthostatic symptoms like light-headedness, presyncope, and palpitations. It can occasionally present with non-orthostatic symptoms like nausea, bloating, and diarrhea. The pathophysiology is not well-understood but is postulated to be due to an autoimmune disorder, abnormally increased sympathetic activity, and/or sympathetic denervation leading to central hypovolemia and reflex tachycardia. It is a diagnosis of exclusion, but table-tilt test is used to help confirm it. The onset is typically precipitated by immunological stressors like viral infections, vaccination, and pregnancy. Recently, several case reports have been published describing POTS following infection with COVID-19 infection. This was described as long-COVID postural tachycardia syndrome by the American Autonomic Society. However, the association of POTS with COVID-19 vaccine is unclear. Only one case report was published describing the development of POTS after COVID-19 mRNA vaccine. Information relating to this remain limited, and approach to diagnosis and treatment is variable. Our understanding of this condition in relation to vaccination is mostly extrapolated from previously published reports describing it in relation to HPV vaccine. As more people continue to take the vaccine, physicians should be alert to the diagnosis. CONCLUSION: POTS is a frequently underdiagnosed or misdiagnosed disorder. It is characterized by an increase in HR by 30 within 10 minutes of standing . In rare instances, it has been described as a postvaccination adverse immune phenomena, and more recently related to mRNA COVID-19 vaccination. Increased recognition, diagnosis, and reporting will contribute to better understanding and treatment.

Undifferentiated Shock: A Case of Idiopathic Capillary Leak Syndrome

Systemic capillary leak syndrome (SCLS or Clarkson's disease) is a rare condition characterized by episodes of vascular hyperpermeability. The extravasation of plasma to the interstitial space results in hemoconcentration, hypoalbuminemia, hypovolemia and compartment syndrome of the extremities. The disease can be idiopathic or secondary to causes including viral infections or chemotherapeutic toxicity. We present a fatal case of idiopathic SCLS which rapidly deteriorated to multiple organ failure despite initial improvement with methylene blue. A 57-year-old male presented for worsening back pain over one month. He described a flulike illness 2 weeks prior. Testing for respiratory viruses including SARS-CoV-2 was negative. He received intravenous crystalloid fluids acutely developed respiratory distress and hypotension requiring emergent intubation and initiation of norepinephrine infusion. CT angiography of the chest demonstrated pulmonary edema. Early during his hospitalization urine output ceased and body weight increased by 10 kg, developing tense anasarca. Hematocrit concentrated from 42.7 to 54.4%. Serum albumin dropped from 4.6 to 2.5 g/dL. C1 esterase inhibitor level and IgM were normal. Ferritin was elevated at 2515 ng/ml. He received cefepime and vancomycin, though infectious workup returned unremarkable. Continuous renal replacement therapy and stress dose steroids were initiated. Vasopressor requirement worsened until he was on three vasopressors at one point. Given the constellation of hemoconcentration, hypoalbuminemia, and shock a diagnosis was made of idiopathic SCLS. Treatment was started with methylene blue, montelukast, and the β-adrenergic agonist terbutaline. Blood pressure improved and patient came off pressors and lactate improved from 13 to 4. However, he later developed rising creatine kinase continued to climb to >40,000 U/L. He developed rhabdomyolysis with concern for compartment syndrome of the extremities due to third spacing of fluids. Orthopedic surgery was consulted;but did not believe a fasciotomy was indicated due to rapid decline. Lactic acidosis rose to 18 mmol/L. His family decided to transition to comfort measures. He passed with family at bedside on Day 4 of hospitalization. There are fewer than 500 cases of SCLS reported since initial discovery in 1960. Given the overlap in presentation with common causes of plasma leakage such as sepsis, it is likely that many cases are unrecognized. Patients are often mismanaged;development of severe hypovolemia despite fluids and compartment syndrome is overlooked. This case builds on our evolving recognition of this disease, and the potential for the use of methylene blue to help acute exacerbations of the disease.

ACUTE RENAL FAILURE IN COVID-19 PATIENTS IN A LATIN AMERICAN HEALTH INSTITUTION

BACKGROUND AND AIMS: Acute renal failure in hospitalized patients for COVID- 19 occurs in 3%-28% and is a poor prognostic factor. The mechanisms of renal involvement are not completely clarified. However, it has been evaluated that the presentation of renal failure increases adverse outcomes. METHOD: Prospective observational study of all the cases that were admitted for COVID-19 between January and December 2021. Clinical and analytical data of kidney complications in patients with COVID-19 were collected. RESULTS: A total of 306 patients with a mean age of 70.2 years, 75.1% men and with previous chronic kidney disease in 29.7% were analyzed. A total of 50.8% had severe pneumonia or acute respiratory distress syndrome and 22.9% required admission to the ICU. Proteinuria was registered in 77.6% and hematuria in 67.6%. A total of 20.9% of the patients required renal replacement therapy. Renal failure was of prerenal etiology in 59.2%, acute tubular necrosis in the context of sepsis in 23.5%, glomerular in 8.1% and due to tubular toxicity in 9.2%. The median stay was 15 days, and 31.7% died. Patients who developed kidney failure during admission had higher C-reactive protein, LDH, and D-dimer values, more severe lung involvement, more need for ICU admission, and greater need for renal replacement therapy. CONCLUSION: Hypovolemia and dehydration are common causes of acute kidney injury in COVID-19 patients. Those who develop renal complications have a worse pulmonary, renal and systemic prognosis profile. We point out that monitoring an individualized management of blood volume can be decisive in preventing worse outcomes.

ACUTE KIDNEY INJURY AMONG COVID-19 POSITIVE PATIENTS IS ASSOCIATED WITH HIGHER MORTALITY: SINGLE CENTER EXPERIENCE

BACKGROUND AND AIMS: Despite the lungs are the major targets of COVID-19, other organs such as the kidneys are also affected. Renal complications of COVID-19 are not yet well studied. We aimed to study the prevalence of acute kidney injury (AKI) among positive COVID-19 cases that were managed in the intensive care unit (ICU) in a single isolation hospital during the pandemic, and to explore its impact on patient outcome. METHOD: This retrospective study included 616 patients with COVID-19 who were managed in the ICU in a single isolation hospital in Kuwait during the pandemic, from February to December 2020. AKI was defined according to the serum creatinine criteria in the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. Of the 616 patients, 40.2% developed AKI (group 1, n = 248) and were compared with the patients without AKI (group 2, n = 368). RESULTS: Most of cases in the two groups were males (73% versus 70.7%), aged (60.8 ± 14 versus 51.7 ± 16 years), respectively. The two groups were comparable regarding chronic kidney disease (2% versus 0.8%) and chronic pulmonary disease. Other factors were significantly predominating among group 1 as diabetes mellitus (63.7 versus 40.5%), hypertension (74.2% versus 40.5%) and ischemic heart disease (26.2% versus 12.5%) (P < .05). Fever, cough, shortness of breath and dehydration were significantly more frequent presentations among patients of group 1, and had radiological findings that were synchronized with COVID-19 (89.5% versus 50.8%) (P < .05). Moreover, sepsis, volume depletion, shock, arrhythmias and ARDS predominated among the AKI group (P < .05). The number of cases who were managed by therapeutic anticoagulation was significantly higher in AKI patients (89.9% versus 51.9%);also, cases who received supportive vasopressors and convalescent plasma transfusion as well as steroid were significantly higher in the same group (P < .05). Other therapeutic modalities such as antivirals, tocilizumab and hydroxychloroquine were comparable in both groups. We found that acute respiratory failure requiring mechanical ventilation was significant among the AKI group (66.8% versus 29.4%), and the overall mortality rate was significantly higher in the same group (62.5% versus 32.8%). CONCLUSION: The prevalence of AKI in patients with COVID-19 was 40.2%, and it was associated with poor prognosis among ICU COVID-19 positive cases.

AVP-eGFP was significantly upregulated by hypovolemia in the parvocellular division of the paraventricular nucleus in the transgenic rats.

Arginine vasopressin (AVP) is produced in the paraventricular (PVN) and supraoptic nuclei (SON). Peripheral AVP, which is secreted from the posterior pituitary, is produced in the magnocellular division of the PVN (mPVN) and SON. In addition, AVP is produced in the parvocellular division of the PVN (pPVN), where corticotrophin-releasing factor (CRF) is synthesized. These peptides synergistically modulate the hypothalamic-pituitary-adrenal (HPA) axis. Previous studies have revealed that the HPA axis was activated by hypovolemia. However, the detailed dynamics of AVP in the pPVN under hypovolemic state has not been elucidated. Here, we evaluated the effects of hypovolemia and hyperosmolality on the hypothalamus, using AVP-enhanced green fluorescent protein (eGFP) transgenic rats. Polyethylene glycol (PEG) or 3% hypertonic saline (HTN) was intraperitoneally administered to develop hypovolemia or hyperosmolality. AVP-eGFP intensity was robustly upregulated at 3 and 6 h after intraperitoneal administration of PEG or HTN in the mPVN. While in the pPVN, eGFP intensity was significantly increased at 6 h after intraperitoneal administration of PEG with significant induction of Fos-immunoreactive (-ir) neurons. Consistently, eGFP mRNA, AVP hnRNA, and CRF mRNA in the pPVN and plasma AVP and corticosterone were significantly increased at 6 h after intraperitoneal administration of PEG. The results suggest that AVP and CRF syntheses in the pPVN were activated by hypovolemia, resulting in the activation of the HPA axis.

POS-008 USE OF POINT OF CARE CREATININE IN THE EMERGENCY DEPARTMENT AND COVID-19 ISOLATION CENTRES IN NIGERIA

Introduction: Early detection and management of community acquired Acute Kidney Injury (AKI) can reduce associated morbidity and mortality particularly in low and low middle-income countries where infrastructure for laboratory tests is limited and renal replacement therapy is largely unavailable. We have established a collaborative project between the Renal Unit of the University of Port Harcourt Teaching Hospital and the Renal Department of Salford Royal NHS Foundation Trust, supported by the International Society of Nephrology aiming at investigating the use of point of care (POC) Creatinine (Cr) for early identification and management of community acquired AKI. The first part of the study evaluated the accuracy of POC Cr technology by comparison with the central laboratory standard Cr assay used at the University of Port Harcourt Teaching Hospital and showed good overall correlation with mean bias of 27.2 umol/L concluding that POC Cr > 150 umol/L reflects AKI in the absence of known chronic kidney disease (CKD). Here we present the second part of the study investigating the use of POC Cr in the Emergency Department (ED) and the third part, that was formulated with the emergence of the COVID-19 pandemic, assessing the POC Cr technology in the COVID-19 isolation centres. Methods: The second part of this study was conducted at the ED of University of Port Harcourt Teaching Hospital (UPTH) between January and December 2020. Adult patients were screened by Nephrology residents with POC Cr using a capillary sample (fingerstick) with the NOVA Stasensor Xpress Cr analyser if there was clinical suspicion of community acquired AKI. The third part of this study was that of the use of POC Cr as screening tool to evaluate AKI in COVID-19 patients at 2 COVID-19 isolation centres in Rivers state. Data were extracted from the case notes of the patients and a proforma designed for the study. Results: In the second stage, between January and December 2020, 53 patients aged 48±19 with clinical suspicion of community acquired AKI were screened with POC Cr in the ED;45.3% were females, 5.7% had known chronic kidney disease and 75.5% had suspected infection and/or hypovolaemia. 21 out of 53 patients (39.6%) had POC Cr > 150 umol/L and 18 out 50 (36%) were attributed to AKI. In the third stage, 69 patients aged 38±14 diagnosed with COVID-19 were screened irrespective of symptoms. 21.7% were females and 1.4% had known CKD. 8 out of 61 (11.6%) had POC Cr > 150 umol/L attributed to AKI. COVID-19 associated AKI was associated with older age, higher respiratory rate, lower oxygen saturations and higher systolic blood pressure (55±11 vs 35±12 p <.001, 26±7 vs 21±2 p <.001, 88%±7 vs 97±3 p <.001 and 141±12 vs 124±15 p 0.002 respectively). Conclusions: POC Cr technology detected AKI in one third of patients with high-risk clinical presentation and can be a valuable and possibly cost-effective tool to assist clinical decision making regarding early interventions and triage decisions in the ED and in the community setting. In patients diagnosed with COVID-19, AKI was present in 1 out of 10 of patients irrespective of symptoms and was associated with clinical observations indicating disease severity. Conflict of interest Potential conflict of interest: I declare that the point of care creatinine device was provided by Nova in support of early detection and management of AKI.

POS-009 CAPTOPRIL-INDUCED ACUTE INTERSTITIAL NEPHRITIS: A RARE ASSOCIATION

Introduction: Acute interstitial nephritis (AIN) is an important reversible cause of acute kidney injury (AKI). Its prevalence is about 6-8% in histologically proven AKI.Early diagnosis of drug-induced AKI is vital because the discontinuation of the causal treatment facilitates recovery of the renal function. Methods: We report a case of captopril-induced AIN. Results: We report the case of a 82-year-old woman with a history of untreated hypertension. She was admittedin our department for AKI. Two days before admission, Captopril was initiated for high blood pressure (BP) as well as vitamin therapy for suspicion of a sars covid 19 infection, which was ruled out by a negative pcr covid test and a normal thoracic scan. The initial physical examination showed asthenia and a BP of 160/90 mmHg. Urinary labstix was negative. The biological analysis showed AKI: creatinine rose from 80 to 230 and then to 530 µmol/l, anemia at 7 g/dl and moderate hyper eosinophilia at 700 elements/ml. A renal biopsy was not performed because of the presence of cysts, and the diagnosis of interstitial nephritis was suspected. The drug-induced origin was confirmed after having eliminated infectious and tumoral origin. The pharmacovigilance investigation incriminated captopril. Captopril was stopped and the patient was put on corticosteroids 0.5 mg/kg/d. The evolution was favorable with an improvement of the renal function (creatinine at 120 µmol/l one month later). Conclusions: Angiotensin-converting enzyme (ACE) inhibitors can cause an increase in serum creatinine or potassium levels in patients with renal failure, renal artery stenosis, heart failure, or hypovolemia, but are rarely reported to be involved as an etiology of AIN. We report one of the rare cases of captopril-induced AIN. No conflict of interest

POS-092 SGLT2 INHIBITOR – INDUCED EUGLYCEMIC DIABETIC KETOACIDOSIS IN GUILLAIN-BARRE SYNDROME: A CASE REPORT

Introduction: Introduction: Euglycemic diabetic ketoacidosis (EuDKA) is a rare but increasingly reported serious adverse effect of SGLT2 inhibitors. There is not much published literature on the incidence of EuDKA and the factors associated with it. Though SGLT2 inhibitors were introduced as glucose lowering agents, recent trials have demonstrated their favourable cardiovascular outcome in heart failure and ability to retard progression of proteinuric kidney disease, including in non-diabetics. Hence use of this class of drugs is anticipated to increase exponentially, given the combined high global burden of diabetes, coronary artery disease and chronic kidney disease. As we embark to use the SGLT2 inhibitors in different clinical scenarios, it becomes imperative to report their adverse effects encountered in uncommon clinical conditions as well. Methods: Case history: A 42-year-old gentleman with history of type 2 diabetes mellitus for 15 years and coronary artery disease, presented with difficulty in climbing stairs and walking for 5 days with progressive difficulty in getting up from bed. He did not have past history of covid infection and had been immunised with 1 dose of covid vaccine. On examination, patient had normal hemodynamics. There was flaccid quadriparesis with areflexia and truncal muscle weakness. Nerve conduction study confirmed acute demyelinating polyradiculoneuropathy. His baseline laboratory investigations revealed normal renal parameters but metabolic acidosis was noted at the time of admission. Patient was started on iv immunoglobulin 2mg/kg and the motor weakness improved from grade 2/5 to 4/5. However, the high anion gap metabolic acidosis worsened over the next 4 days and patient developed acidotic breathing. His sugars were within normal limits and the patient was on metformin, glimeperide, vildagliptin, voglibose and dapagliflozin. As blood lactate levels were normal with urine acetone positivity, euglycemic diabetic ketoacidosis secondary to SGLT2 inhibitor was suspected and all the oral hypoglycemic agents were stopped. He was started on hydration and insulin infusion. After 48 hours of stopping dapagliflozin, acidosis resolved completely and the patient was reintroduced back on the other 4 class drugs. At follow-up, there was no recurrence of acidosis and patient was able to walk with support and physiotherapy. [Formula presented] Results: Discussion: SGLT2 inhibitors cause glycosuria and directly induce glucagon release from pancreas. Combined with insulin deficiency, this results in lipolysis, fatty acid oxidation and ketogenesis. They also cause increased renal reabsorption of ketone bodies. The precipitating factors for EuDKA identified so far include abrupt reduction in insulin dosage, reduced oral intake, infections, surgery, excess alcohol use, volume depletion, type 1 diabetes and heavy physical exercise. This is the first reported case of SGLT2 inhibitor-induced EuDKA in a patient with Guillain-Barre syndrome. As symptoms of dehydration may not be significant due to lack of hyperglycemia in EuDKA, there may be a delay in the diagnosis of this complication. Conclusions: Conclusion: The possibility of EuDKA to be kept in mind while evaluating metabolic acidosis in a diabetic patient on SGLT2 inhibitors. Temporarily withholding the SGLT2 inhibitors during an intercurrent illness will prevent the occurrence of the above serious adverse effect. No conflict of interest

Mysterious cause of hypotension in MIS-C

Case Report Multisystem inflammatory syndrome (MIS-C) involves severe multi-organ inflammatory injury 2-6 weeks after COVID-19 infection. Seventy to 85% of patients have cardiovascular involvement, including diminished left ventricular ejection fraction (EF), coronary aneurysm, arrhythmias, valvular dysfunction, and pericardial effusion. Here we present a patient who arrived to the pediatric emergency department (ED) with MIS-C and suspected cardiogenic shock, though without the echocardiogram abnormalities commonly associated with MIS-C. A 7 year old African American male presented for a third time to our ED over the course of 4 days of febrile illness and was found to have MIS-C. During this time, he had no chest pain, palpitations, shortness of breath, or abnormal cardiopulmonary exam. At the first 2 ED visits, he was generally well appearing and after treating fever, had vital signs normal for his age. At his third visit, his vital signs were notable for borderline hypotension 86/48 (threshold 83/39 for his height of 1.25 meters). Troponins, chest X-ray, and EKG were normal. Bedside ultrasound was normal, with EF 55-60% so the hypotension was presumed to be secondary to hypovolemia and sepsis. However, despite 40 mL/kg of fluid boluses and maintenance fluid x1.5, his blood pressure continued to downtrend to a nadir of 79/39. He soon developed an S3 gallop and facial edema indicating fluid overload. His proBNP 4986 pg/mL also resulted at this time, suggesting cardiac injury was present. A formal cardiology echocardiogram confirmed the bedside ultrasound findings, noting normal ventricular size and motion, trivial pericardial effusion, and normal coronary artery size. However, it also detected diastolic dysfunction evident in mildly elevated E/e' of 10.86 of lateral mitral annulus, and 12.7 at medial mitral annulus. Three hours after starting solumedrol for treatment of MIS-C, his blood pressure improved to 110/52. The patient had no further episodes of hypotension, though it is unclear if steroids had resolved this by alleviating the underlying inflammation or as a secondary effect. We present a case of MIS-C that led to diastolic heart failure detected by mild hypotension, elevated proBNP, and subtle findings on formal echocardiogram. Although less common than systolic dysfunction in MIS-C, early recognition of diastolic heart failure is important for effective fluid management and initiation of vasoactive agents in criticallly 'ill patients. Diastolic heart failure with preserved systolic function has been seen on echo of MIS-C patients, and is hypothesized to be the subacute period after recovery of systolic function. However, we did not find clinical symptoms of systolic heart failure prior to the patient's development of diastolic heart failure. It is therefore essential to recognize that a patient with MIS-C may present with diastolic heart failure without preceding symptoms or echo findings of other cardiac anomalies.

Preintubation echocardiographic assessment using subcostal-only view (easy) exam: A case series

INTRODUCTION/HYPOTHESIS: Induction and intubation can cause cardiovascular instability, hypoxemia, and cardiac arrest. The EASy exam is a subcostal four-chamber view (SC4C), followed by inferior vena cava (IVC) and upper lung field views performed in quick succession. The goal of this study was to evaluate the impact of single-day EASy training on management prior to induction and intubation. METHODS: EASy training consists of a combination of a web-based curriculum, live lecture, and 10 exams performed under direct supervision. The EASy protocol was performed before emergency intubation on five critically ill patients. In this case series, we describe findings and management based on the EASy phenotypes (pattern recognition). RESULTS: Five resident-obtained EASy studies were performed in the ICU for emergency intubation. Two patients had COVID-19. Three had hyperdynamic ventricles with a small left ventricular (LV) cavity size with a < 1.5cm fully collapsible IVC consistent with hypovolemia (two of which had thickened LV walls indicating likely diastolic dysfunction). These three patients received a 10 mL/kg IV fluid bolus to counteract vasodilation and decreased venous return, and were started on phenylephrine. The fourth had normal contractility and diastolic cavity size with a normal-sized collapsible IVC. The fifth patient had biventricular dilation with reduced systolic function and a plethoric IVC. For this patient, no fluid bolus was given, and a vasopressor with inotropic properties (norepinephrine) was started. Etomidate was used for induction and intubation. The mean time for completion was 3 minutes (range 2 to 4 minutes). Three studies were deemed “good” quality and two were deemed “adequate” by an attending physician proficient in critical care ultrasound. Vitals were monitored for 15 minutes post-intubation, and all patients maintained hemodynamic stability with MAP ≥ 65 mmHg. CONCLUSIONS: EASy exam aids clinical decision-making in the pre-induction and intubation period, where interventions can have deleterious and even fatal consequences.

Concomitant presence of COVID-19 infection and inaugural diabetic ketoacidosis in children and adolescents

Introduction: The COVID-19 pandemic, which has left its mark all over the world, has led to a decrease in the addressability to health care professionals, due to people's fear of becoming infected with COVID-19. This delays a correct diagnosis that can have lifethreatening consequences. Objectives: To establish if type 1 diabetes is triggered by COVID-19 Methods: We will present 3 cases pf type 1 diabetes at onset with ketoacidosis, triggered by the COVID-19 infection, diagnosed between December 2020 and April 2021. The diagnosis of SARSCoV2 infection was established based on RT-PCR (a reversetranscription polymerase-chain-reaction) positive for SARS-CoV2. Results: Case 1: 14 years old, boy, presented with Kussmaul breathing, abdominal pain, polyuria, polydipsia, weight loss (5 kg in 2 weeks), fever (38 C). The laboratory test showed a bicarbonate: 5 mEq/L, pH: 7.08, alkaline reserve: 6 mmol/l, glucose: 454 mg/dl, HbA1c: 14.5%. Case 2: 7 years old, boy presented with Kussmaul breathing, shock hypovolemic, hypotensive (Blood pressure 60/30 mmHg), fever, tachypnea, polyuria, polydipsia. The laboratory test showed a bicarbonate: 3 mEq/L, pH: 6,95, alkaline reserve: 2 mmol/l, glucose: 567 mg/dl, HbA1c: 12.6 %. Case 3: 10 years old, boy presented with similar clinical findings. The laboratory test showed a bicarbonate: 5 mEq/L, pH: 6,90, alkaline reserve: 3 mmol/l, glucose: 457 mg/dl, HbA1c: 16.6 %. All patients received treatment according to the diabetic ketoacidosis protocol treatment and switched to basal-bolus insulin treatment after an average of 48 hours. In all 3 cases the SARS-CoV2 infection was mild, with no changes in the lungs (lung x-rays being within normal limits). Conclusions: Due to the general fear of appearing in a hospital during the COVID-19 pandemic, there are delays in the diagnosis of lifethreatening conditions, such as ketoacidosis. The link between SARSCoV2 infection and type 1 diabetes in children and adolescents remains unknown and further studies are needed to gather more data.

Resuscitative Effect of Centhaquine (Lyfaquin®) in Hypovolemic Shock Patients: A Randomized, Multicentric, Controlled Trial.

INTRODUCTION: Centhaquine (Lyfaquin®) showed significant efficacy as a resuscitative agent in animal models of haemorrhagic shock. Its safety and tolerability were confirmed in healthy human volunteers. In this study, our primary objective was to determine the safety, and the secondary objective was to assess the efficacy of centhaquine in patients with hypovolemic shock. METHODS: A prospective, multicentre, randomized phase II study was conducted in male and female patients aged 18-70 years with hypovolemic shock having systolic BP ≤ 90 mmHg. Patients were randomized in a 1:1 ratio to either the control or centhaquine group. The control group received 100 ml of normal saline infusion over 1 h, while the centhaquine group received 0.01 mg/kg of centhaquine in 100 ml normal saline infusion over 1 h. Every patient received standard of care (SOC) and was followed for 28 days. RESULTS: Fifty patients were included, and 45 completed the trial: 22 in the control group and 23 in the centhaquine group. The demographics of patients in both groups were comparable. No adverse event related to centhaquine was recorded in the 28-day observation period. The baseline, Injury Scoring System score, haemoglobin, and haematocrit were similar in both groups. However, 91% of the patients in the centhaquine group needed major surgery, whereas only 68% in the control group (p = 0.0526). Twenty-eight-day all-cause mortality was 0/23 in the centhaquine group and 2/22 in the control group. The percent time in ICU and ventilator support was less in the centhaquine group than in the control group. The total amount of vasopressors needed in the first 48 h of resuscitation was lower in the centhaquine group than in the control group (3.12 ± 2.18 vs. 9.39 ± 4.28 mg). An increase in systolic and diastolic BP from baseline through 48 h was more marked in the centhaquine group than in the control group. Compared with the control group, blood lactate level was lower by 1.75 ± 1.07 mmol/l in the centhaquine group on day 3 of resuscitation. Improvements in base deficit, multiple organ dysfunction syndrome (MODS) score and adult respiratory distress syndrome (ARDS) were greater in the centhaquine group than in the control group. CONCLUSION: When added to SOC, centhaquine is a well-tolerated and effective resuscitative agent. It improves the clinical outcome of patients with hypovolemic shock. TRIAL REGISTRATION: ClinicalTrials.gov identifier number: NCT04056065.

Parallels in Sepsis and COVID-19 Conditions: Implications for Managing Severe COVID-19.

Sepsis is a life-threatening systemic illness attributed to a dysregulated host response to infection. Sepsis is a global burden killing ~11 million persons annually. In December 2019, a novel pneumonia condition termed coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged and has resulted in more than 1,535,982 deaths globally as of 8th December 2020. These two conditions share many pathophysiological and clinical features. Notably, both sepsis and COVID-19 patients experience consumptive thrombocytopenia, haemolytic anaemia, vascular microthrombosis, multi-organ dysfunction syndrome, coagulopathy, septic shock, respiratory failure, fever, leukopenia, hypotension, leukocytosis, high cytokine production and high predisposition to opportunistic infections. Considering the parallels in the immunopathogenesis and pathophysiological manifestations of sepsis and COVID-19, it is highly likely that sepsis care, which has a well-established history in most health systems, could inform on COVID-19 management. In view of this, the present perspective compares the immunopathogenesis and pathophysiology of COVID-19 and non-SARS-CoV-2 induced sepsis, and lessons from sepsis that can be applicable to COVID-19 management.

Fluid Replacement Versus Fluid Restriction in COVID-19 Associated Hyponatremia.

Hyponatremia is one of the most frequently observed electrolyte abnormalities in coronavirus disease 2019 (COVID-19). Literature describes syndrome of inappropriate anti diuretic hormone (SIADH) as the mechanism of hyponatremia in COVID-19 requiring fluid restriction for management. However, it is important to rule out other etiologies of hyponatremia in such cases keeping in mind the effect of an alternate etiology on patient management and outcome. We present a case of hypovolemic hyponatremia in a patient with COVID-19, which unlike SIADH, required fluid replacement early in the disease course for its correction. A 52-year-old Filipino gentleman presented with a three-week history of diarrhea and symptomatic hyponatremia. There was no history of fever or respiratory symptoms. Physical examination revealed a dehydrated and confused middle-aged gentleman. Labs revealed lymphopenia, thrombocytopenia, and severe hyponatremia (108 mmol/L). Blood cultures and stool workup were negative. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nasopharyngeal swab was positive. Hyponatremia workup excluded SIADH. The patient had hypovolemic hyponatremia due to gastrointestinal (GI) losses and was managed with saline infusion for correction of hyponatremia with improvement in his clinical status. Hyponatremia in COVID-19 is not only secondary to SIADH but can also be due to other etiologies. Hypovolemic hyponatremia should be distinguished from SIADH as these conditions employ different management strategies, and early diagnosis and management of hypovolemic hyponatremia affects morbidity and mortality.