Anti-SARS-CoV-2 antibodies important in diagnostics of acute hepatitis in children

The most common causes of acute hepatitis in children are hepatitis A and autoimmune hepatitis. Hepatitis in the course of Wilson's disease is sporadically registered in adolescents. An increase of activity of aminotransferases both in the course of multisystem inflammatory syndrome in children (MIS-C) and in the course of COVID-19 has been observed. Hepatitis is common in children with MIS-C and is associated with a more severe presentation and persistent elevation of liver function tests. To date, no cases of acute hepatitis in children due to COVID-19 have been reported. We present 2 cases of acute hepatitis in children where the only cause seems to be a previous asymptomatic SARS-CoV-2 infection.Copyright © 2023 Termedia Publishing House Ltd.. All rights reserved.

Acute Pancreatitis Following a Lower Extremity Angioplasty

Introduction: Acute pancreatitis affects a significant population globally. Usual etiologies are gallstones, alcohol, hypertriglyceridemia, medications;less frequent are trauma, hypercalcemia, infections, toxins, ischemia, anatomic anomalies, vasculitis, and idiopathic. Pancreatitis post coronary intervention is an uncommon cause with only 19 published cases in the last two decades. Being cognizant of this etiology is important given the increasing number of patients undergoing angiography. Case Description/Methods: An 81-year-old female with hypertension, diabetes, peripheral arterial disease, prior cholecystectomy underwent left lower extremity angioplasty at an outside center. Within a few hours, she started having severe epigastric pain radiating to her back, nausea, vomiting and loose bloody stool. She presented to the emergency department 24 hours after symptom onset. Epigastric tenderness was present on exam. Labs revealed leukocytosis (24,450/muL), elevated lipase (1410 U/L), elevated creatinine (1.3 mg/dL), lactate (3.1 mmol/L), calcium 9.4 mg/dL and triglycerides 161 mg/dL. Incidentally, found to be positive for COVID-19. Normal common bile duct diameter seen on sonogram. CT angiogram of the abdomen/pelvis showed acute pancreatitis, duodenal and central small bowel enteritis (Figure). She was not on any medications known to cause pancreatitis and denied alcohol use. Patient improved with analgesics and intravenous fluids. She had no recurrence of bloody stools and hemoglobin remained stable. On day 4, she was able to tolerate a regular diet, and leukocyte count and creatinine normalized. Patient did not have any COVID respiratory symptoms, and was discharged. Discussion(s): Given the temporal association to angioplasty and no other identifiable cause, acute pancreatitis was presumed to be due to the contrast used during angioplasty. Other possibilities included cholesterol embolism but no peripheral signs of cholesterol embolism were seen. Patient was an asymptomatic COVID-19 case. Although, there are case series of pancreatitis due to COVID, those were found in very sick symptomatic patients. On review of literature, cholesterol embolism was identified as a definite cause only on autopsy or laparotomy (Table). Other possible mechanisms are: high viscosity of the contrast media leading to ischemia and necrosis, contrast causing NF-kB activation followed by epithelial damage, and vasospasm. Pancreatitis after coronary angiography is rare, nonetheless, an important differential especially if there is a temporal relationship.

Neurogastroenterology & Motility Manifestations After COVID-19 Infection: A Case Series

Introduction: In a subset of Covid19-convalescent patients, a multitude of long-term sequelae are increasingly being reported. We report 4 cases with varying neuro-GI and motility manifestations after recent COVID-19 infection. Case Description/Methods: Case 1: A 23-year-old man contracted COVID-19 and had a protracted course of respiratory illness. Despite resolution of respiratory symptoms and dysgeusia, he continued to experience early satiety, postprandial nausea, vomiting and unintentional weight loss. Gastric Emptying Scan (GES) revealed gastroparesis (Figure A). Dietary modification and metoclopramide led to symptomatic improvement. Case 2: A 39-year-old woman with migraines, suffered from Covid-19 infection where anosmia and respiratory symptoms lasted for 2 weeks. Despite resolution of initial symptoms, she started experiencing nausea and vomiting, and reported stereotypical symptoms with complete absence of vomiting between episodes. Endoscopic examination, CT head and GES were normal. Urine tox screen was negative for cannabinoids. She responded favorably to amitriptyline and ondansetron. Case 3: A 47-year-old man started experiencing severe constipation associated with abdominal pain and bloating soon after being diagnosed with COVID-19. Three months after resolution of respiratory symptoms, in addition to constipation, he began reporting postprandial fullness, early satiation and epigastric pain. GES showed gastroparesis ( figure B) and a Sitzmarks Study revealed delayed colonic transit (Figure C). Prucalopride was started, leading to improvement in symptoms. Case 4: A 74-year-old woman with obesity and diabetes, was hospitalized and intubated for severe respiratory distress due to COVID-19. After discharge, she had persistent symptoms of brain fog, fatigue, dyspnea as well as diarrhea and abdominal cramping, persisting despite loperamide and dicyclomine. C. difficile toxin, random colonic biopsies and H2 breath test were unremarkable. Her symptoms eventually improved with rifaximin. Discussion(s): We report 4 cases with post-COVID gastroparesis, cyclical vomiting syndrome, pan-gut dysmotility, and post-infectious IBS phenotypes.The pathophysiology of post-infectious-gut-brain disorders is still obscure. The current conceptual framework implicates acquired neuropathy, altered motility, intestinal barrier disruption and persistent intestinal inflammation. Similar pathophysiology may be involved in COVID-19 infection leading to sustained neurogastroenterological dysfunction and gut dysmotility.

Holy Foley: Iatrogenic Duodenal Obstruction From a Make-Shift Gastrostomy Tube

Introduction: Enteral feeding is a physiologic process of providing adequate nutrition and has been shown to improve both mortality and quality of life in patients with inadequate oral intake. Improved critical care medicine and recent wave of Coronavirus Disease 2019 (COVID-19) has left us with a large proportion of patients needing alternative enteral nutrition. Although rare, intussusception is an important differential for patients presenting with acute abdominal pain post makeshift percutaneous endoscopic gastrostomy (PEG) tube placement. Case Description/Methods: A 58-year-old male was admitted to the hospital for coffee ground emesis over three days accompanied with epigastric pain. He had right sided hemiparesis secondary to cerebrovascular accident with PEG tube for enteral nutrition. Examination was significant for epigastric tenderness with normal bowel sounds. PEG tube aspiration revealed bile-tinged fluid. Significant labs included white blood cell count of 11,600 /mm3, hemoglobin 10.2 g/dL, and lactic acid of 2.3 mmol/L. A computerized tomography of the abdomen with IV contrast showed a small segment duodeno-duodenal intussusception at the horizontal segment around the distal end of the tube was noted (Figure A). An urgent esophagogastroduodenoscopy (EGD) revealed a Foley catheter acting as a makeshift PEG tube extending across the pylorus into the duodenum. The distal tip of the Foley catheter was visualized with an inflated balloon seen in the third portion of the duodenum (Figure B) The inflated catheter balloon acted as a lead point causing intussusception in a ball-valve effect. The balloon was deflated, and the catheter was replaced (Figure C) with a 20 Fr PEG tube. Discussion(s): Gastric outlet obstruction is an uncommon complication reported in few cases caused by migration of the gastrostomy tube. Rarely this migrating gastrostomy tube can invaginate the duodenum or the jejunum causing intussusception. Only handful of cases have been reported in the literature. Patients usually present with epigastric pain, vomiting or rarely hematemesis. CT scan of the abdomen is the investigation of choice. Amidst the pandemic and supply shortage, Foley catheters have been deemed as a viable alternative to gastrostomy tubes and are being used more often. It is important to recognize this rare complication and use of balloon catheter should raise further suspicion. Timely endoscopic intervention can help avoid bowel necrosis and surgical intervention.

Granulomatous Hepatitis as Primary Manifestation of Disseminated Histoplasmosis in an Immunocompetent Host Diagnosed on EUS FNA and Liver Biopsy

Introduction: Disseminated histoplasmosis (DH) presents as primarily lung manifestations with extrapulmonary involvement in immunocompromised hosts. Granulomatous hepatitis as first presentation of DH in an immunocompetent host is uncommon. Case Description/Methods: 25-year-old female presented with one month of fever, fatigue, myalgias, 30-pound weight loss, cough, nausea, vomiting, and epigastric pain. She has lived in the Midwest and southwestern US. Presenting labs: TB 1.9 mg/dL, AP 161 U/L, AST 172 U/L, ALT 463 U/L. Workup was negative for COVID, viral/autoimmune hepatitis, sarcoidosis, tuberculosis, and HIV. CT scan showed suspected gallstones and 9 mm left lower lobe noncalcified nodule. EUS showed a normal common bile duct, gallbladder sludge and enlarged porta hepatis lymph nodes which underwent fine needle aspiration (FNA). She was diagnosed with biliary colic and underwent cholecystectomy, with white plaques noted on the liver surface (A). Liver biopsy/FNA showed necrotizing granulomas (B) and fungal yeast on GMS stain (C). Although histoplasmosis urine and blood antigens were negative, histoplasmosis complement fixation was >1:256. She could not tolerate itraconazole for DH, requiring amphotericin B. She then transitioned to voriconazole, discontinued after 5 weeks due to increasing AP. However, her symptoms resolved with normal transaminases. At one year follow up, she is asymptomatic with normal liver function tests. Discussion(s): DH is a systemic granulomatous disease caused by Histoplasma capsulatum endemic to Ohio, Mississippi River Valley, and southeastern US. DH more commonly affects immunocompromised hosts with AIDS, immunosuppressants, and organ transplant. Gastrointestinal involvement is common in DH (70-90%) with liver involvement in 90%. However, granulomatous hepatitis as primary manifestation of DH is rare (4% of liver biopsies). Hepatic granulomas are seen in < 20%. Patients may present with nonspecific systemic symptoms. Serum/urine antigens may be negative. Gold standard for diagnosis is identifying yeast on tissue stains. Recommended treatment is amphotericin B followed by 1 year of itraconazole. However, shorter treatment duration may be effective in immunocompetent hosts. This case is unique in that granulomatous hepatitis was the first presentation of DH in our immunocompetent patient diagnosed on EUS FNA and liver biopsy. Clinicians must have a high degree of suspicion for DH in patients with fever of unknown origin especially in endemic areas regardless of immunologic status. (Table Presented).

Pancreatitis Secondary to Paxlovid-Induced Tacrolimus Toxicity

Introduction: Pancreatitis is a very common gastrointestinal disease that results in hospital admission. Early detection and treatment leads to better outcomes. This is the first reported case of pancreatitis secondary to elevated tacrolimus in a patient with prior renal transplantation after receiving Paxlovid for a COVID-19 infection. Case Description/Methods: A 57-year-old male with past medical history of 4 renal transplants secondary to posterior urethral valves who presented to the emergency room with acute onset epigastric pain for 24 hours. He was on tacrolimus 5 mg every 48 hours monotherapy for his immunosuppression. 10 days prior to his presentation he had developed chills and anxiety. He tested positive for COVID-19 at that time on a home rapid test. His symptoms had not significantly improved and given his immunosuppressed state he was given Paxlovid (Nirmatrelvir/ritonavir). He took 2 days of Paxlovid, however after his second day of treatment he developed severe epigastric pain requiring him to go to the emergency room. On admission his labs were notable for a lipase of 150 U/L (ULN 63 U/L). He underwent a CT scan was notable for an enlarged pancreatic head and neck with peripancreatic fat stranding (Figure). He also had a right upper quadrant ultrasound without any cholelithiasis and only trace sludge noted. His creatinine was noted to be 1.81 mg/dl which was above his baseline of 1.2 mg/dl. His tacrolimus trough level resulted at a level 45.6 ng/ml and later peaked at 82.2 ng/ml. His liver enzymes were normal. He was treated as acute pancreatitis with hydration and his tacrolimus was held with overall clinical improvement. Discussion(s): Tacrolimus is one of the most common medications used in solid organ transplantation. It is a calcineurin inhibitor that inhibits both T-lymphocyte signal transduction and IL-2 transcription. It is metabolized by the protein CYP3A and levels are monitored closely. Paxlovid is currently prescribed as an antiviral therapy for COVID-19 infection. The ritonavir compound in Paxlovid is potent inhibitor of CYP3A. Currently the guidelines do not recommend Paxlvoid as a therapeutic in patients taking tacrolimus as there is concern about increased drug levels. There have been several case reports of pancreatitis in setting of tacrolimus. This case report helps to demonstrate the need for close monitoring of therapeutics levels, especially in medications with high risk of drug to drug interaction to help prevent serious side effects such as tacrolimus induced pancreatitis.

Covid-19 Infection Presenting as Acute Pancreatitis

Purpose of study Introduction COVID-19 emerged at the end of 2019 as an epidemic of respiratory disease in Wuhan, China that later spread globally and was declared as pandemic. The common clinical manifestations of COVID-19 infection include fever, cough, myalgias, headache, sore throat, anosmia, nasal congestion, fatigue and chest pain. The most serious complications include bilateral multifocal pneumonia and acute respiratory distress syndrome. Acute pancreatitis is rarely reported in association with COVID-19 infection. We report a case of acute pancreatitis secondary to COVID-19 infection. Case Report: A 69-year-old man with past medical history of hyperlipidemia and seizure disorder presented with two days of epigastric pain radiating to back. The patient reported fever, malaise and dry cough for the last 3 days. Home medication included atorvastatin and carbamazepine for 10 and 15 years respectively. The patient denied smoking and alcohol use. COVID- 19 PCR was positive. Labs showed WBC of 3800/muL, hgb 11.8 g/dL, calcium 8.4 mg/dL , lipase 426 U/L, D-Dimer 179 ng/ml DDU, High sensitivity C-reactive protein 27.5 mg/L (normal <5 mg/L) ALT 26 U/L, AST 31 U/L, alkaline phosphatase 103 U/L and total bilirubin 0.3 mg/dL. Ultrasound of the right upper quadrant and CT abdomen showed normal pancreas, common bile duct and gallbladder with no evidence of gallstones. Triglyceride level was 70 mg/dL (<149 mg/dL) on the lipid panel. The patient was diagnosed with acute pancreatitis and received treatment with IV fluids and pain medication. The symptoms improved gradually and the patient was discharged home with resumption of home medications. Methods used Case Report Summary of results The common differentials for acute pancreatitis include alcohol use, gallstones, hypertriglyceridemia, viral infections like mumps and measles, hypercalcemia and medication-related, etc. Normal AST, ALT, alkaline phosphatase and total bilirubin along with absence of gallstones and normal common bile duct ruled out alcoholic and biliary pancreatitis. Normal calcium level and triglyceride level rule out hypercalcemia and hypertriglyceridemia as the cause of pancreatitis. Carbamazepine has rarely been reported to cause acute pancreatitis typically soon after the initiating the therapy or with increase in the dose. The use of carbamazepine for more than 15 years without any recent dose change makes this unlikely as the cause of pancreatitis. The onset of acute pancreatitis during the timeline of COVID-19 constitutional symptoms and absence of other risk factors suggests that COVID-19 infection is responsible for acute pancreatitis in our patient. Conclusions We report a case of acute pancreatitis secondary to COVID-19 infection. Further studies are warranted to better understand the etiology and the pathophysiology of acute pancreatitis secondary to COVID-19 infection.

Acute Pancreatitis as a Rare and Unusual Manifestation of COVID-19 in a Child with Acute Lymphoblastic Leukemia

Introduction: The coronavirus disease 2019 (COVID-19) mainly causes pulmonary disease. However, extrapulmonary manifesta-tions, which affect the gastrointestinal tract and hepatobiliary system, have been reported. Case Presentation: Here we reported a 4-year-old boy with acute lymphoblastic leukemia and abdominal pain who had acute necrotic pancreatitis secondary to COVID-19. Conclusion(s): According to the COVID-19 epidemic, if drug-induced pancreatitis is ruled out, viral causes, especially COVID-19, should be considered.Copyright © 2023, Author(s).

New Onset Diabetes and Acute Pancreatitis- A Sequela of Long COVID?

Introduction: The association between worse COVID-19 outcomes and diabetes has been well-established in the literature. However, with more cases of new-onset diabetes and pancreatitis being reported with or after COVID-19 infection, it poses the question if there is a causal relationship between them. Case Description: 31 y/o female with COVID-19 infection 4-6 weeks ago with moderate symptoms (not requiring hospital admission or monoclonal ab), presented to ED with bandlike epigastric pain radiating to back, which is worsened with food, associated with nausea, vomiting, polyuria, and fatigue. Workup showed lipase 232, AST 180, ALT 256. Blood glucose was 281 and HbA1c was 12. CT A/P showed post cholecystectomy status, normal pancreas with mesenteric adenitis. MRCP showed hepatic steatosis with trace fluid around the pancreas s/o inflammation, and no evidence of choledocholithiasis or biliary dilatation. She denied alcohol use and autoimmune workup for pancreatitis was unremarkable. Islet cell antibodies were negative. The patient improved with fluid resuscitation and was discharged home on insulin with plans to transition to oral agents outpatient. Discussion(s): Long COVID is defined as a range of conditions or symptoms in patients recovering from COVID-19, lasting beyond 4 weeks after infection. A retrospective cohort study showed increased new-onset diabetes incidence in patients after COVID-19. This was redemonstrated in a systematic review and meta-analysis that showed a 14.4% increased proportion of new diagnoses of diabetes in patients hospitalized with COVID-19. Possible pathophysiology that have been attributed to this include undiagnosed pre-existing diabetes, hyperglycemia secondary to acute illness and stress from increased inflammatory markers during the cytokine storm, the effect of viral infections on the pancreas, and concurrent steroid use in patients with severe respiratory disease. The binding of SARS-CoV-2 to ACE2 receptors is thought to the other mechanism by which COVID can cause pancreatitis and hyperglycemia. Study showed increased lipase and amylase levels in patients with COVID and the increase in serum levels was proportional to the severity of the disease. Patients who died due to COVID-19 were also found to have degeneration of the islet cells. While, several studies have showed new onset diabetes and pancreatitis during an active COVID infections, we need larger cohort studies to comment on its true association or causation, especially in patients with long COVID symptoms. As more cases of new onset diabetes and pancreatitis with COVID-19 are being reported, there may be a need for more frequent blood sugar monitoring during the recovery phase of COVID-19.Copyright © 2023

Another Cause of DKA in T2DM in COVID-19 Pandemic

Background: 47-year Emirati female, has history of T2DM since age of 39. Her overall diabetes poorly controlled with HbA1C of 8.6% (69 mmol/mol IFCC) on Empagliflozin 10 mg OD over the last 2 years well tolerated. NO micro- or macrovascular complications of her diabetes. No other significant medical history apart from hypertension she is taking Amlodipine 10 mg OD for it with good control. She has presented twice to the hospital 24 hours apart. 1st Visit to ER in our Hospital with fever epigastric pain discharged on Ciprofloxacin suspected gastroenteritis with PPI and sent home. Approximately, 24 hours later she presented again with same symptoms namely fever and epigastric pain but this time associated with diarrhea and nausea for last 20 hours. There was no shortness of Breath or cough. This time she has been admitted to isolating room giving suspicion of COVID-19. Vital signs as following: Temp 38.5 HR 105, BP 135/65 mmHg O2 Sats 96%. on RA. On examination, she was conscious, oriented to time place person. No signs of dehydration. abdomen soft non tender, Chest good air entry no added sound. Hear S1-S2 no murmurs. HRCT has been done at ER. HRCT shows wide spread area of multifocal ground glass opacification are seen in both lungs most of them shows peripheral sub-pleural distribution Around small size consolidation are seen within the ground glass opacification, CT findings are in favour of possibility of COVID-19. Result(s): Blood test as following On admission, FBC was normal, with Hb 13.2, WBC 8.0, Plt 388 cellX 10/ul, U/Es: S.NA 132, s.K 4.2 mmo/l, s. Creatinine normal (58 umol/L -NR 49-90 umol/L) LFTs, Amylase and lipase normal, LDH mild elevation 304 U/L (NR 81-234), Very low Phosphate 03 mmol/L (NR 0.87-1.45), D-Dimer 0.6 mg/L (NR 0.0- 0.5), Corrected Calcium normal, S. Ferritin was 242 ug/L (NR 8.00- 388.00 ug/L), Urinalysis Protein =1 and 4+ ketones, CRP was normal 1 mg/dl ( increased to 214 mg/ l 3rd day) before it goes done 41 mg/L on 7th day of admission. Giving the pandemic of COVID 19 and according to MOHAP Criteria for presenting symptoms. This lady underwent HRCT and COVID19 test by Nasal Swab. Meanwhile, Her Venous Blood gas shows sever metabolic acidosis pH 7.107, PCO2 12.90, PCO2 69.10 On RA, BC 8.9, BE -25.5. Blood sugar 13.2 mmol/L with Urinary Ketones of 4+. Patient has put on DKA Protocol according to our Hospital DKA protocol in addition Stopped her SGLT2 and start on Lantus as a basal. She has put on Scale C (which is the higher scale with infusion about 10 units per hour, for about 96 hours (i.e. 4 days till the blood sugar back to normal for Ketones to disappear, her acidosis didn't improve 1st 24 hours till we give her 1.26% of 500 ml of Sodium Bicarbonate over 6 hours. COVID 19 Test back after 72 hours with positive results. Once out of DKA Diabetes team has stopped her Lantus a stared-on Humalog mix 50% 25 unit TDS. Meanwhile, she has received the following medications waiting for COVID 19 test. Treated with Favipiravir 1600 mg BD for 1 day and 600 mg BD, Start Tazocin 4.5 (stopped after 3 days) Metronidazole, and with prophylactic dose of Clexane. The Hydroxychloroquine hasn't started as Prolong QTC has been notice). Discussion(s): This patient presentation with DKA is another example how COVID- 19 could be a reason for DKA, though SGLT2 could be another cause of her presentation, however the huge insulin requirement and unusual prolong DKA status even with sever acidosis is making COVID-19 more likely causing her presentation It. Conclusion(s): We report this case to highlight the fact DKA - and in fact sever resistant DKA need prolong treatment can happen to Patient with T2DM and COVID 19 positive, and special attention to be paid (with early referral to the diabetes team) if the patient already on SGLT2. And we recommend that to have low threshold to start investigation and treatment as early as possible, regardless the type of Diabetes these patient might have.

Multisystem inflammatory syndrome: A case report

Background: Multisystem inflammatory syndrome is a rare but severe complication of Coronavirus 19 infection (COVID-19) occurring about 2-12 weeks after the initial infection. It was initially reported in children (MIS-C) but later identified in adults (MIS-A). We report a case of MIS-A in a patient presenting with myocarditis.\ Method: Case report Results: A 36 years old female admitted due to 3 days history of fever and severe epigastric pain. She had exposure to a relative with COVID-19 3 weeks prior to symptoms and antigen test done was negative. On the day of admission, she started to experience shortness of breath and easy fatigability during activities of daily living. Upon examination, she was hypotensive requiring vasopressors. 12 lead ECG showed acute anteroseptal wall myocardial infarction and 2D echocardiography revealed hypokinesia of the entire interventricular septum and inferior left ventricular free wall, and reduced ejection fraction (EF) at 43.3%. Coronary angiogram showed normal findings. On work-up, she had mild normochromic, normocytic anemia, normal serum lipase, elevated AST 222 (<34 U/L), ALT 250 (<49 U/L), Troponin T > 2000 ng/L, CPK-Total 669 (<192 U/L), Ferritin 456.90 (<204 ng/ml), ESR 13 mm/hr, CRP 24 (<6 mg/L) and procalcitonin 0.35 (<0.5 ng/ml). Infectious workup revealed negative results and PCR for COVID-19 was negative. However, further workup revealed COVID-19 Enzyme Linked Fluorescent Assay (ELFA) IgG positive at 44.75 (>1.00) and IgM negative. The patient was managed as a case of MIS-A and was started on intravenous immunoglobulin (IVIg) and short course steroids with significant improvement in symptoms. On the 10th day of hospitalization, follow-up 2D echocardiography showed improvement in previously noted ventricular wall hypokinesia and normalization of EF to 55.8%. The patient was discharged well and improved. Conclusion(s): Diagnosis of MIS-A is challenging in patients without a previously known COVID-19. A positive serology result is required to fulfill the case definition of MIS-A. Determining a history of COVID-19 and its relationship to a patient's clinical course is important for making diagnosis and determining subsequent management.

Chilaiditi syndrome: The false pneumoperitoneum not to be ignored

The Chilaiditi syndrome is a set of clinical and radiological signs characterized by the interposition of the colon or the small intestine between the lower face of the diaphragm and the liver. It is a rare entity often fortuitously discovered. We report the case of two patients admitted to the emergency room, the first 74 years old for exploration of acute epigastric pain with dyspnea in a covid positive context while the second 66 years old for an occlusive syndrome with a history of chronic constipation. The scannographic exploration finds colonic anses in the interhepatodiaphragmatic space making evoke a Chilaiditi syndrome Chilaiditi syndrome represents the classic trap of false right pneumoperitoneum as it can mask a true pneumoperitoneum. The treatment is often conservative and surgery is reserved in case of complications.

Laparoscopic Roux-en-Y cysto-jejunostomy in a complicated Pancreatic Pseudocyst following SARS-CoV-2 virus pancreatitis in a child

Background: Pancreatic pseudocyst (PPC) is the rare complication of pancreatitis. Unlike to adults, it is ensued due to malunion of pancreatic ducts, autoimmune or frequently post-traumatic. During follow up although it might resolve by conservative treatment, may necessitate interventional approaches. Even endoscopic or percutaneous treatments have been the first line treatment, surgery is inevitably necessary in case of complicated or>6 cm diameter. In this study laparoscopic Roux-en-Y cysto-jejunostomy (LRYCJ), to complicated PPC that did not respond to percutaneous drainage, has been presented. Method(s): A 15-year-old boy had been admitted to state hospital with the complains of vomiting, epigastric pain two weeks after SARSCoV- 2 (SARSC2) virus infection. He has been following due to Autism. Initially he had been treated conservatively due to pancreatitis. One month after, PPC (20 mm) distal to pancreas had been specified. He was referred to our department as the cyst got bigger (75 mm) with recurrent complains. No ductal connection was identified however thrombosis of splenic vein, dilated collateral and distal esophageal variceal veins was detected. Ultrasound guided percutaneous drainage has been performed however two weeks after, 95175 mm PPC at the same location was detected. LRYCJ was performed with four ports via suspending stomach and transvers colon. While Roux-en-Y has been performed through expanded umbilical incision cysto-jejunostomy was intracorporeally performed. Penrose drain was left close to cysto-jejunostomy. Oral feeding has begun on postoperative day 2, drain was removed on day 3. Fullfed and discharged on postoperative day 4. Patient did well after a follow up of 3 months. Conclusion(s): Consequently, our case is the first reported PPC following pancreatitis owing to SARSC2 virus infection. Even endoscopic or percutaneous drainage is the most preferred approach for PPC, in case of large cyst or complicated ones, cysto-jejunostomy could be applied by minimally invasive approach in children also.

IgA Nephropathy as a Potential Complication of SARS-CoV-2 Vaccination

Introduction: Vaccination against COVID-19 is essential, however an immunological flare is a potential rare complication resulting in glomerulonephritis with IgA deposits in the mesangium. We present a case of a patient who developed IgA nephropathy postvaccination. Case Description: 48-year-old woman with a past medical history of Leukocytoclastic vasculitis and hypertension presented to the Emergency Department with fatigue, nausea, epigastric pain, foamy urine and a diffuse erythematous purpuric rash within days of receiving the SARS CoV-2 vaccination. Her creatinine was 1.92 mg/dL and urinalysis showed 3+blood and 30 mg/dL of protein. COVID-19 testing was negative. Protein/ creatinine ratio was 2.1 g/g and urine microscopy showed dysmorphic red blood cells. Serologies for HIV, Hepatitis B and C were negative. Further testing revealed negative ANA, normal ASO titer, absent cryoglobulins, rheumatoid factor < 20, C3 158 (nl) and C4 35 (nl). However, IgA level was elevated at 462 mg/dL (reference 70-312 mg/dL). Patient was started on prednisone at a dose of 1mg/kg with a presumptive diagnosis of IgA vasculitis/ HSP. Subsequent skin biopsy was consistent with leukocytoclastic vasculitis while kidney biopsy showed glomerular deposition of IgA and endocapillary hypercellularity. At one month follow-up with nephrology, prednisone taper was started because of good clinical response and partial remission with UPCR reduction to 1 g/g. Prednisone was gradually tapered over the next 2 months. At her 3 month follow-up she was found to be in complete remission with a UPCR 0.2 g/g and her creatinine was 0.83 mg/dL Discussion: We present a case of IgA nephropathy post-SARS CoV-2 mRNA vaccination. It has been speculated that the mRNA lipid nanoparticle-encapsulated platform contained within the mRNA vaccine produces such a robust CD4 and CD8 T-cell response that pro-inflammatory cytokines activate this immune complex associated glomerular disease. In conclusion, SARS CoV-2 vaccination may potentially trigger IgA nephropathy in predisposed patients. Steroid therapy may be efficacious in managing this rare complication.

TIGECYCLINE INDUCED ACUTE PANCREATITIS: A RARE CASE PRESENTATION

CASE: An 81-year-old female with multiple co-morbidities including recent covid-19, presented to the emergency room with shortness of breath. On arrival, she was febrile with a temperature of 101F, pulse 100 beats/min, respiratory rate 14, blood pressure 196/163 and saturating at 75% on 10 L non-rebreather mask. Initial blood work showed WBC 10.9, lactic acid 1.7, BUN/creatinine 27/1.7 (consistent with her baseline), ABG showed pH 7.37, PCO2 49, PO2 88, HCO3 27.9. Chest x-ray demonstrated volume loss in the left hemithorax, airspace disease in the left mid lung and lung base. Due to suspicion for superimposed bacterial pneumonia and positive blood cultures for staphylococcus haemolyticus, she was started on vancomycin and azithromycin. Choice of antibiotics was challenging as she was allergic to penicillin and cephalosporins. During hospitalization, her kidney function deteriorated, vancomycin was substituted with tigecycline on day 3. Day 5 of treatment, she developed multiple episodes of vomiting with epigastric pain, lipase was 4523. Acute pancreatitis was diagnosed with tigecycline presumed to be the inciting agent in the absence of other risk factors such as gall stones, chronic alcohol use, elevated triglycerides, previous known episodes of pancreatitis or any other causative medications. Tigecycline was switched back to vancomycin and she received aggressive IV fluid hydration which also improved her kidney function. Within 48 hours, the patient had improved oxygen saturation, resolution of her abdominal pain, and good oral intake marking significant overall clinical progress. She was discharged on home oxygen and few more days of IV vancomycin for bacteremia. IMPACT/DISCUSSION: Tigecycline is a broad-spectrum glycylcycline antimicrobial agent belonging to the tetracycline class of antibiotics. Tetracyclines have been associated with acute pancreatitis in literature, and concerns about tigecycline-induced acute pancreatitis have been raised over the past decade in post marketing surveys, we described one such case above. Using the Naranjo Adverse Drug reaction probability scale, a score of 6 was achieved, indicating that the patient's pancreatitis was probably related to tigecycline. CONCLUSION: We recommend physicians monitor patients for signs and symptoms of pancreatitis including abdominal pain after initiating treatment with tigecycline. There should be a low threshold for ordering lipase levels and abdominal CT imaging where indicated. If the patient has symptoms concerning for acute pancreatitis, consider stopping tigecycline and switching to a different class of antibiotics immediately.

A 51-YEAR-OLD MAN WITH WEIGHT LOSS AND CARDIOGENIC SHOCK

CASE: A 51-year-old man without significant past medical history presented to our hospital with dyspnea on exertion. SARS-CoV-2 was detected on routine occupational screening 2 months prior to admission. He subsequently reported a 100lb weight loss, during which time he experienced dysgeusia and ate primarily cereal, sandwiches, and potatoes and consumed nearly no fruits or vegetables. Three weeks prior to admission he developed postprandial nausea and vomiting and anorexia. A week later he developed progressive epigastric pain, lower extremity edema, and dyspnea while walking around the college campus where he worked as a security guard, and sought medical attention. He did not have fever, chills, night sweats, cough, orthopnea, paroxysmal nocturnal dyspnea, rash, or diarrhea. He had not seen a doctor in 20 years and took no medications. He did not drink alcohol, smoke cigarettes, or use illicit substances. Vital signs were T 36.6°F HR 104 BP 149/111 RR 20 and SpO2 97%. Physical examination revealed a cachectic man with bitemporal wasting, sunken orbits, poor dentition, and severe periodontal disease. JVP was 14cm of H2O at 45°. An S3 was present. The abdomen was tender to palpation in the mid epigastrium. The extremities were cool with 3+ pitting edema. Pancreatitis was diagnosed after discovery of markedly elevated lipase levels and peripancreatic fat stranding on abdominal CT. TTE showed biventricular systolic dysfunction with LVEF 15%. He developed cardiogenic shock complicated by oliguric renal failure, congestive hepatopathy and obtundation, requiring ICU transfer for diuresis and inotropic support. Further workup revealed deficiencies of thiamine, zinc, and vitamins A, C, and D. A regadenoson myocardial perfusion PET/CT showed no flow-limiting coronary artery disease, and workup for inflammatory, infectious, and toxic-metabolic causes of heart failure was unrevealing. While COVID myocarditis and multisystem inflammatory syndrome in adults (MIS-A) were considered, ultimately, a diagnosis of wet beriberi was made. After 5 months of aggressive nutritional supplementation via percutaneous gastrostomy tube and initiation of guideline-directed medical therapy, LVEF improved to 53% and weight increased by 35lbs. IMPACT/DISCUSSION: Wet beriberi is a potentially underrecognized cause of dilated cardiomyopathy in resource-rich areas. Within 3 months, thiamine deficiency can cause high-output heart failure due to impaired myocardial energy metabolism and dysautonomia. Risk factors include alcohol use disorder, prolonged vomiting, and history of bariatric surgery. CONCLUSION: The laboratory evaluation of non-ischemic dilated cardiomyopathy should include measurement of serum thiamine, carnitine, and selenium levels in select patients, alongside iron studies, ANA, screening for HIV, Chagas disease, and viral myocarditis, and genetic testing in patients with a suggestive family history. Empiric thiamine repletion should be considered in all critically ill patients with evidence of malnutrition.

POST-COVID-19 DISORDERS OF GUT-BRAIN INTERACTION (DGBI): AN INTERNET-BASED EPIDEMIOLOGICAL STUDY

Background: Post-COVID-19 conditions are defined as new, recurring, or ongoing health issues which present weeks after SARS-CoV-2 infection. The gastrointestinal (GI) involvement of COVID-19 suggests that a group of patients with lingering GI symptoms may develop Post-COVID-19 DGBI including irritable bowel syndrome (IBS) (Schmulson M et al. Am J Gastroenterol. 2021;116:4-7). In this study, we aimed to determine the epidemiological features of Post-COVID-19 DGBI. Methods: Subjects with confirmed COVID-19 at least 6 months before the study who had sustained GI symptoms were invited to complete an internet-based survey on Qualtrics, between March and August 2021. The survey included demographics, acute symptoms, comorbidities, as well as Rome IV questionnaire, Generalized Anxiety Disorder questionnaire (GAD-7) and Patient Health Questionnaire (PHQ)-9 for depression. Data was analyzed using ANOVA and multivariate analysis. Findings were reported as percentage or [p-value;(95% odds ratio CI)]. Results: Overall, 164 subjects (70% female, 14% male, and others unknown) with a positive COVID-19 test completed the survey. Among them, 4% were >65 years old and 24% reported hospitalization. Body mass index ³30 was present in 38%, diabetes in 6.7%, and vitamin D deficiency in 11% of the participants. In total, 108 (66%) subjects fulfilled Rome IV criteria for at least one DGBI. Of 108 with DGBI, only 27 (25%) had DGBI before COVID-19;DGBI developed in 81 subjects after COVID-19. The most common Post-COVID-19 DGBI were functional dyspepsia observed in 38 (postprandial distress syndrome n=31, epigastric pain syndrome n=22) followed by IBS in 26 subjects (IBS with Diarrhea n=7, IBS with Constipation n=4, Mixed-IBS n=14, Unsubtyped IBS n=1) (Table-1). The risk factors of severe COVID-19 including age >65, diabetes, and obesity were not associated with developing Post-COVID- 19 DGBI. Seventy (86%) of subjects with Post-COVID-19 DGBI had at least one GI symptom (abdominal pain, nausea/vomiting, and/or diarrhea) in the acute phase of COVID-19. Nausea/ vomiting during the acute illness increased [p-value of 0.02 with 95% OR CI (0.7-10.4)], and BMI less than 25 also increased the odds [p-value of 0.03 (95% OR CI: 0.26-8.4)] for Post-COVID-19 IBS. Anxiety was present in 48% and depression in 65% of subjects with Post-COVID-19 DGBI. Conclusions: Post-COVID-19 DGBI are new entities associated with a high rate of anxiety and depression. Although the majority of those with Post-COVID-19 DGBI reported having GI symptoms in the acute illness, some appeared in subjects without acute GI symptoms. (Table Presented)

COHORT STUDY IN PATIENTS WITH HYPERTENSIVE CRISIS: CHARACTERISTICS AND FOLLOW-UP AFTER 30 DAYS

Objective: Characterize patients with hypertensive crisis and evaluate occurrences 30 days after the hypertensive event. Design and method: Cohort study was performed with 583 patients treated between August 2020 and July 2021, from an Emergency Unit in a Hospital specializes in cardiology in São Paulo, Brazil. Inclusion criteria: 18 years old, systolic pressure > 180 mmHg and/or diastolic pressure > 120 mmHg, have telephone contact. A consulting on the electronic medical record was made to identify the elegible patients, whom after were included on the REDCap platform, and 30 days of the hypertensive event, an interview by telephone was made to investigate cardiovascular events. Results: The sample characteristics were: women (53%), 66.24(13.89) years, white ethnicity (78.7%), married (50.5%), high school (27.9%), retired people (77.5%), average [(mean(SD)] monthly income R$2384.6 (R$3438). The mean(SD) systolic/diastolic blood pressure, respectively, in emergency department was 189.74(17.46)/99.28(19.89) mmHg. Hypertensive emergencies were 63.8%, urgencies 27.4% and 8.7% were not possible to classify. The prevalent symptoms in the emergency department were: chest pain (41.2%), dyspnea (34.3%), nausea (11.7%), dizziness (10,4%), radiating pain (10.1%). The most used treatments were: anticoagulant (35.1%), diuretic (28.1%), analgesic (25.3%), ACE inhibitor (23.8.7%). Regarding the performance of tests: 85.6% underwent laboratory tests, 71% electrocardiogram, 36.3% echocardiogram and 30.5% computed tomography. After being treated at the emergency department, 60.1% of patients were discharged, 35.8% hospitalized, 3.8% transferred to other hospitals and 0,3% died. Regarding comorbidities, 97.7% had hypertension, 68.7% high cholesterol, 48.4% diabetes, 34.1% acute myocardial infarction, 25.1% heart failure, 19.6% kidney disease and 12% stroke. Regarding outcomes 30 days after the hypertensive event, 1.4% had some type of stroke, being 85.7% ischemic and 14.3% hemorrhagic, 2.3% had acute infarction of the myocardium, and 2% cardiorespiratory arrest. Also, 14.5% returned to a health service for high blood pressure, and 23.1% for others reasons like angina, bradycardia, aortic aneurysm, covid-19, acute pulmonary edema, epigastric pain, dyspnea. Besides we identify that 4.7% died within 30 days. Conclusions: The findings indicate the need for tertiary systematization, through outpatient follow-up programs for people with hypertensive crisis in emergencies units.

Longitudinal Myelitis as a COVID-19 Neurological Manifestation

Objective: To present a case of a longitudinal myelitis (LM) in the setting of SARS-CoV-2 infection. Background: While there is an established link between viral infections and new-onset demyelinating diseases [1, 2], data on the association between SARS-CoV-2 and myelitidies is lacking. Design/Methods: Consent obtained from patient. Results: A 53-year-old man presented with epigastric pain and urinary retention following ten days of fever, chills, headache, and cough. On presentation, he tested positive for SARS-CoV-2, prompting admission, then subsequently developed bilateral lower extremity weakness and numbness. MRI revealed T2 cord hyperintensity from C7 caudally to the conus. CSF revealed elevated total protein (67), WBC (16), IgG (11.1), and myelin-based protein (9). Testing for other demyelinating, infectious, and inflammatory conditions was negative. He had modest improvement in sensation following intravenous methylprednisolone and plasma exchange although remains paraplegic. Conclusions: This unique case of a longitudinal myelitis in the setting of SARS-CoV-2 infection adds to previously reported cases of acute disseminated encephalomyelitis, meningoencephalitis, and optic neuritis as neurological manifestations of SARS-CoV-2 infections [2].