Sick Contacts Research Articles

7241 Catamenial Diabetic Ketoacidosis

Abstract Disclosure: L. Javed: None. A. Rehan: None. L. Hashim: None. J. Lim: None. Introduction: Diabetic ketoacidosis (DKA) is a common cause of hospitalization and readmission in patients with diabetes mellitus. Etiologies are generally due to medication non-adherence, trauma, infection, or other precipitating illness. In approximately 10% of DKA cases, no discernible precipitating cause can be determined. The word catamenial is derived from a Greek word meaning monthly. It is used to describe the monthly occurrence of menstruation. Catamenial hyperglycemia is a phenomenon in which blood glucose levels change with the different phases in the menstrual cycle. This can precipitate recurrent, unexplained episodes of DKA. Here, we present a similar case. Case description:A 19-year-old woman with type 1 diabetes, gastroparesis, hypertension, dysmenorrhea and cyclical vomiting disorder presented with unrelenting nausea and vomiting for one day. Other symptoms included abdominal & chest pain that the patient attributed to premenstrual symptoms. She is afebrile, doesn’t have any other symptoms of infection and no recent sick contacts. She is compliant with her home insulin regimen of Insulin detemir 20 units BID and pre meal 8 units insulin aspart. Further interrogation reveals she has regular menstrual cycles and has been hospitalized three times in the last three months due to DKA coinciding with premenstrual symptoms, specifically severe abdominal pain and vomiting, typically starting five days before the onset of her menstrual cycle. She is hemodynamically stable and physical exam is significant for mid epigastric tenderness. Significant labs: WBC 16.52 (N<11 K/mm3), glucose 457 mg/dl, anion gap 23, K 4.1 (mmol/L), bicarbonate 18 (≥19 mmol/L), lactate 3.2 (N ≤ 1.9 mmol/L), beta hydroxybutyarate 4.0 (N ≤ 0.27 mmol/L), trop T 6 (N<10 ng/L), BHCG negative . Hba1c a month ago was 9.6%. Infectious work up was negative. EKG showed no signs of ischemia. She was treated per DKA protocol which results in resolution of symptoms and normalization of labs. Since no other precipitating factors for DKA are identified, and her symptoms corresponded with her menstrual periods, she is given a diagnosis of Catamenial DKA and scheduled for regular follow up in endocrinology clinic. Conclusion: This case highlights the importance of considering the association betweenmenstrual cycle phases and blood sugar levels as a possible trigger, underscoring the role of a thorough menstrual history in patients presenting with DKA. The impact of menstrual cycle fluctuations on glycemic control varies among patients however glucose profiles seem to be consistent across cycles for each individual woman. This highlights the need for personalized management strategies including patient education and adjustment of insulin during these periods. Addressing this adequately will improve overall glycemic control, reduce hospitalizations, and help improve the quality of life. Presentation: 6/1/2024

Postpartum Bilateral Nerve Palsy: A Harbinger for Preeclampsia?

Objective: To report a case of postpartum bilateral facial weakness that preceded the diagnosis of preeclampsia. Introduction: Bell’s palsy is a neuromuscular disorder that can cause paralysis or weakness of the face. It is the most common cause of unilateral facial weakness; however, bilateral weakness is rare. Bell’s palsy is one of the most common neuromuscular disorders observed in pregnancy, though the link between the two is not entirely clear. Proposed etiologies include reactivation of human herpes viruses, immune mediated inflammatory demyelination of the facial nerve, and microangiopathy as a result of systemic hypertension. There have been several case reports and studies suggesting a correlation between preeclampsia and Bell’s palsy. We present a rare case of postpartum bilateral Bell’s palsy in the setting of preeclampsia. Design: Case report. Results: Our patient is a 24 year-old G6P4116 Caucasian woman with no significant past medical history who presented with bilateral facial weakness and headache. She was postpartum day four from a spontaneous vaginal delivery of dichorionic diamniotic twins at 35 weeks at an outside hospital. She denied any elevated blood pressures during her pregnancy. Initially, on postpartum day two she had reported a severe headache that initially affected her occipital region bilaterally before migrating to her ears and forehead. At this time the patient was normotensive and was discharged home on analgesics. On postpartum day three, she returned to another emergency department with a worsening, severe headache. She was sent home with a diagnosis of anxiety. On postpartum day four, her symptoms persisted and she came to the emergency department at our facility. During our initial evaluation, her blood pressure was 170/98. She was admitted for severe preeclampsia and given IV magnesium and nifedipine. However, her headache persisted and she developed bilateral facial weakness, neck pain, and swelling. She reported that she was unable to move her face and had difficulty smiling. Her face was expressionless. She denied nausea, vomiting, dysphagia, double vision, gait disturbances, hearing loss, fever, shortness of breath, numbness, or tingling. She denied recent travel, sick contacts, or animal or tick bites. She was evaluated by neurology and her initial physical exam revealed intact cranial nerves, though the patient appeared to have difficulty squeezing her eyes shut and smiling. Periorbital edema was noted. Facial symmetry and sensation were intact bilaterally. She had difficulty saying the letter “P.” Her MRIs of both brain and cervical spine, chest x-ray, and lumbar puncture were all normal. Our working diagnoses included bilateral Bell’s palsy, Guillain-Barré and Miller-Fischer syndromes. The antibody panel drawn for Miller-Fischer syndrome subsequently resulted as negative. Our patient received three days of IVIG and was discharged on a week supply of prednisone 60mg with a taper thereafter. At discharge, she had severe bilateral facial droop. She was unable to puff out her cheeks or raise her eyebrows. Neurology recommended outpatient follow up. One month after discharge she had residual right sided facial droop, but the deficits of the left side of her face had mostly resolved. Discussion: Current literature suggests a correlation between preeclampsia and Bell’s palsy. There is some thought that elevated blood pressure leads to facial nerve compression secondary to edema or microemboli. One report suggested that the onset of Bell’s palsy antepartum or postpartum may be a predictor of preeclampsia. An English language PUBMED search revealed six case reports on bilateral Bell’s palsy in either the pregnant or postpartum state. Cases reported occurred in either the third trimester or within the first week postpartum. This was consistent with the onset of our patient’s symptoms during her first week postpartum. In one case, neurological symptoms preceded preeclampsia. Our patient complained of headaches and neck pain prior to having elevated blood pressures. Three of these cases included twin gestations, as did our case. Outcomes varied, with some patients seeing complete resolution of symptoms within weeks to others having recurring symptoms over a year. Providers should consider the relationship between preeclampsia and Bell’s palsy when treating pregnant or postpartum patients with new onset neurological symptoms. Pregnant and postpartum patients are at greater than three times increased risk for Bell’s palsy and have more severe symptoms and longer recovery times compared to the average population. It is important that obstetricians and gynecologists assess for signs of preeclampsia in pregnant or postpartum patients with concerns for Bell’s palsy, as well as refer patients for a complete neurological workup. Ultimately, more research is needed to further understand the relationship between preeclampsia and Bell’s palsy.

Postpartum Bilateral Nerve Palsy: A Harbinger for Preeclampsia?

Objective: To report a case of postpartum bilateral facial weakness that preceded the diagnosis of preeclampsia. Introduction: Bell’s palsy is a neuromuscular disorder that can cause paralysis or weakness of the face. It is the most common cause of unilateral facial weakness; however, bilateral weakness is rare. Bell’s palsy is one of the most common neuromuscular disorders observed in pregnancy, though the link between the two is not entirely clear. Proposed etiologies include reactivation of human herpes viruses, immune mediated inflammatory demyelination of the facial nerve, and microangiopathy as a result of systemic hypertension. There have been several case reports and studies suggesting a correlation between preeclampsia and Bell’s palsy. We present a rare case of postpartum bilateral Bell’s palsy in the setting of preeclampsia. Design: Case report. Results: Our patient is a 24 year-old G6P4116 Caucasian woman with no significant past medical history who presented with bilateral facial weakness and headache. She was postpartum day four from a spontaneous vaginal delivery of dichorionic diamniotic twins at 35 weeks at an outside hospital. She denied any elevated blood pressures during her pregnancy. Initially, on postpartum day two she had reported a severe headache that initially affected her occipital region bilaterally before migrating to her ears and forehead. At this time the patient was normotensive and was discharged home on analgesics. On postpartum day three, she returned to another emergency department with a worsening, severe headache. She was sent home with a diagnosis of anxiety. On postpartum day four, her symptoms persisted and she came to the emergency department at our facility. During our initial evaluation, her blood pressure was 170/98. She was admitted for severe preeclampsia and given IV magnesium and nifedipine. However, her headache persisted and she developed bilateral facial weakness, neck pain, and swelling. She reported that she was unable to move her face and had difficulty smiling. Her face was expressionless. She denied nausea, vomiting, dysphagia, double vision, gait disturbances, hearing loss, fever, shortness of breath, numbness, or tingling. She denied recent travel, sick contacts, or animal or tick bites. She was evaluated by neurology and her initial physical exam revealed intact cranial nerves, though the patient appeared to have difficulty squeezing her eyes shut and smiling. Periorbital edema was noted. Facial symmetry and sensation were intact bilaterally. She had difficulty saying the letter “P.” Her MRIs of both brain and cervical spine, chest x-ray, and lumbar puncture were all normal. Our working diagnoses included bilateral Bell’s palsy, Guillain-Barré and Miller-Fischer syndromes. The antibody panel drawn for Miller-Fischer syndrome subsequently resulted as negative. Our patient received three days of IVIG and was discharged on a week supply of prednisone 60mg with a taper thereafter. At discharge, she had severe bilateral facial droop. She was unable to puff out her cheeks or raise her eyebrows. Neurology recommended outpatient follow up. One month after discharge she had residual right sided facial droop, but the deficits of the left side of her face had mostly resolved. Discussion: Current literature suggests a correlation between preeclampsia and Bell’s palsy. There is some thought that elevated blood pressure leads to facial nerve compression secondary to edema or microemboli. One report suggested that the onset of Bell’s palsy antepartum or postpartum may be a predictor of preeclampsia. An English language PUBMED search revealed six case reports on bilateral Bell’s palsy in either the pregnant or postpartum state. Cases reported occurred in either the third trimester or within the first week postpartum. This was consistent with the onset of our patient’s symptoms during her first week postpartum. In one case, neurological symptoms preceded preeclampsia. Our patient complained of headaches and neck pain prior to having elevated blood pressures. Three of these cases included twin gestations, as did our case. Outcomes varied, with some patients seeing complete resolution of symptoms within weeks to others having recurring symptoms over a year. Providers should consider the relationship between preeclampsia and Bell’s palsy when treating pregnant or postpartum patients with new onset neurological symptoms. Pregnant and postpartum patients are at greater than three times increased risk for Bell’s palsy and have more severe symptoms and longer recovery times compared to the average population. It is important that obstetricians and gynecologists assess for signs of preeclampsia in pregnant or postpartum patients with concerns for Bell’s palsy, as well as refer patients for a complete neurological workup. Ultimately, more research is needed to further understand the relationship between preeclampsia and Bell’s palsy.

January 2024 Medical Image of the Month: Polyangiitis Overlap Syndrome (POS) Mimicking Fungal Pneumonia

No abstract available. Manuscript truncated after 150 words. A 32-year-old woman with a history including hypertension, end-stage renal disease requiring dialysis, asthma, nonischemic cardiomyopathy, and migraines, was directly transferred to our hospital in November 2023 for the evaluation of hemoptysis. The patient reported a two-week history of a nonproductive cough, runny nose, muscle aches, subjective fevers, chills, fatigue, nausea, and decreased appetite. Within the past 2 days the patient had also developed hemoptysis, with 5-6 episodes per day. Initial investigations, including chest X-ray and CT chest, revealed large biapical pulmonary consolidations with cavitation. Multiple nodular densities were observed throughout both lungs (Figures 1 and 2). The patient denied any recent sick contacts, travel history, and prior tuberculosis infection. She did, however, disclose a period of incarceration from 2011 to 2019. Upon arrival at our hospital, the patient recounted a relatively normal state of health until January 2023 when she underwent a two-month hospitalization, culminating in the diagnosis of …

Importance of History Taking and Physical Examination Before Rapid Laboratory Test for Seasonal Influenza Virus: A Single-Center Multiple Logistic Analysis.

Background Despite several rapid influenza diagnostic tests (RIDTs), they are predicting whether a patient has influenza before rapid testing is important. Here, we assessed factors predictive of a positive flu test via RIDTs by combining interviews and physical examination. Methods We analyzed the relationship between interviews and physical findings and results of RIDTs using multivariable logistic regression. Results Two hundred seventy-six children were enrolled throughout the 2018-2019 flu season. Accordingly, 115 patients (41.7%) were positive for flu A. Our logistic regression model identified age, body temperature, and the existence of upper respiratory symptoms as significant factors for predicting positive for RIDTs, with odds ratios (OR) of 1.17 [95% CI (confidence interval): 1.08-1.25]/+Δ1year old, 1.70 (95% CI: 1.27-2.27)/+Δ1 ℃, and 5.08 (95% CI: 2.57-10.00) for respiratory symptoms. In addition, the OR for sick contact was 7.67 (95% CI: 3.96-14.90). Our logistic regression model showed an area under the curve (AUC) of 0.84. History of vaccination was not identified as a significant factor in positive RIDTs. Conclusions The existence of sick contact was associated with a positive flu test via RIDTs. Although RIDTs are an easy and quick method for detecting the flu virus, we should perform the appropriate identification of cases for RIDTs by combining interviews and physical findings.

Abstract 16036: Concomitant Culture-Negative Left-Sided Native Valve Endocarditis With Splenic Emboli and Babesiosis: A Case Report

Description of Case: A 76-year-old man with type 2 diabetes and a previously drained hepatic abscess presented with 3 days of fevers and chills associated with dizziness, weakness, and fatigue after hiking at a New York State Park. He denied any shortness of breath, chest pain, abdominal pain, diarrhea, skin rashes, insect bites, IV drug use, recent travel or sick contacts but reported having dental work one month prior to admission. Initial vital signs were notable for a fever of 38.4°C with a blood pressure of 145/76, heart rate of 90, and physical examination was unremarkable. Extensive laboratory studies were drawn, which initially were notable for normocytic anemia, thrombocytopenia, low haptoglobin and elevated lactate dehydrogenase. Empiric antibiotics were initiated as the patient met criteria for systemic inflammatory response syndrome (SIRS). CT abdomen and pelvis was remarkable for right-sided spleen with polysplenia and multiple peripheral wedge-shaped splenic infarcts. A transthoracic echocardiogram (TTE) was inconclusive for infective endocarditis (IE). A subsequent transesophageal echocardiogram (TEE) showed vegetations on the aortic and mitral valves with mild regurgitation respectively. After cardiothoracic surgery evaluation, he was deemed not a surgical candidate. Blood and urine cultures remained negative, but the Babesia antibodies IgM and IgG antibodies, and Babesia microti PCR was detected. He was started on atovaquone 750 mg twice daily and azithromycin 250 mg once daily for 10 days for babesiosis. He was discharged on vancomycin 1g every 12 hours and ceftriaxone 2g every 24 hours for a total of 6 weeks for empiric IE treatment given splenic emboli. Discussion : We describe a rare case of fever caused by culture-negative mitral and aortic valvular endocarditis with splenic emboli and babesiosis. Recent dental work and hiking outdoors in the Northeast United States of America were the key predisposing factors. Given splenic infarcts, pursuing a TEE was pivotal in ascertaining the diagnosis. The patient received empiric IE treatment for gram-positive cocci, HACEK organisms and babesiosis with improvement of symptoms. Identifying and treating unusual causes of fever and SIRS are crucial in reducing mortality and morbidity.

Human Rhinovirus as a Cause of Fever in Neonates and Young Infants During the COVID-19 Pandemic, 2020-2022.

Human rhinovirus (HRV) was predominant and persistent during the coronavirus disease 2019 (COVID-19) pandemic despite nonpharmaceutical interventions. The data whether HRV persistence also occurred in neonates and young infants were very limited. This prospective observational study was conducted in Niigata, Japan, between January 2020 and September 2022. The participants were hospitalized neonates and infants less than 4 months of age with fever. We excluded patients with evidence of bacterial infection or obvious sick contact with influenza or respiratory syncytial virus infection, as confirmed by rapid antigen detection tests. COVID-19 diagnosed by polymerase chain reaction (PCR) or rapid antigen detection tests were also excluded. Parechovirus and enterovirus were examined by PCR using serum and/or cerebrospinal fluid. FilmArray Respiratory Panel v1.7 was conducted on nasopharyngeal swabs. If HRV was positive, the genotype was identified. We included 72 patients (median age, 54 days; interquartile range, 28.5-79 days), and sepsis was diagnosed in 31 (43.1%) patients. In total, 27 (37.5%) patients had had positive multiplex PCR tests. These patients were more likely to have rhinorrhea ( P = 0.004), cough ( P = 0.01), and sick contact ( P < 0.001) than those who with negative multiplex PCR. HRV was the most frequently detected virus (n = 23, 85.2%), and species A (n = 15, 71.4%) and C (n = 6, 28.6%) were genotyped. No seasonality or monthly predominance of the specific HRV types was observed. HRV was an important cause of fever in neonates and young infants during the COVID-19 pandemic, 2020 to 2022.

SAT680 Mounjaro: A Side Effect

Abstract Disclosure: K. Rao: None. E. Kyei Nimako: None. Mounjaro : A Side Effect Dr K Rao, Dr Evans-Nimako, Internal Medicine, North Alabama Medical Center Introduction: Mounjaro has been heralded as a new miracle drug both in the world of diabetes management and weight loss with its pending FDA approval in the latter category. Although common contraindications are known the wider spectrum and prevalence of side effects including diabetic retinopathy, acute kidney injury and gallbladder disease are still being identified. In this case we present a patient with Mounjaro induced AKI and ileus. Case Presentation: We present the case of a 64year-old diabetic, hypertensive male presenting with a 3-day history of nausea vomiting indigestion and excessive burping one day after taking his first dose of Mounjaro. The Patient was started at a walk-in clinic on 2.5 mg subcutaneously however on the very next day he noticed the onset of cramping abdominal pain with multiple episodes of vomiting and watery diarrhea. The patient has not had any other new foods, sick contacts or preceding illnesses. He had a history of previous hernia surgery, cholecystectomy and exploratory laparotomy some 18 years ago due to concerns for nonresolving small bowel obstruction. On examination he was afebrile but tachycardic and in mild distress. His abdomen was soft and nondistended. Bowel sounds were faint but present. He had generalized tenderness without evidence of rebound or guarding. Initial investigations demonstrated a white cell count of 14.7(10E3/ul), creatinine 1.7mg/dl, potassium 4.5mmol/L, blood glucose 176mg/dl and lactate of 2mmol/L. His urine analysis showed small volume ketones, glucosuria and trace leukocyte esterase with 3-5 white blood cells. CT of the abdomen and pelvis with contrast showed distended small and large bowel loops with fluid air levels but no transition point indicative of underlying ileus. The patient was hospitalized in total for approximately six days post the onset of his symptoms and treated with supportive measures including antiemetics, IV fluids and antacids. He never had any fevers or leukocytosis during his stay. His electrolytes remained within normal limits. Conclusion: Due to the impending widespread use and increasing popularity of Mounjaro this case presentation is aimed at raising awareness of potential side effects and their severity. We also hope to contribute towards further knowledge about specific subset of patients who may be more susceptible to the gastrointestinal side effects of Mounjaro. Particularly those patients who have had previous colonic or multiple abdominal surgeries or history of bowel obstruction. In this case the patient received the medication at a walk-in clinic this also highlights the dangers of lack of established care and monitoring of Mounjaro. Presentation: Saturday, June 17, 2023

FRI643 Tirzepatide Associated Partial Small Bowel Obstruction: A Case Report

Abstract Disclosure: A. Mathew: None. H. Hannoodee: None. Glucagon-like peptide-1 receptor agonists (GLP1 RA) are quickly becoming an adjunctive treatment modality for people with type-2 diabetes and is approved for chronic weight management. Tirzepatide has a dual GIP/GLP-1 RA action and has a synergistic effect when administered together. GLP-1 RA are associated with improved cardiovascular and all-cause mortality outcomes in patients with type-2 diabetes. Tirzepatide is associated with gastrointestinal (GI) side effects like nausea, diarrhea, abdominal pain, decreased appetite, and constipation. This case report discusses a case of small bowel obstruction (SBO) that was noted after patient was changed from dulaglutide to tirzepatide. Mr. X is a 61 y/o male with PMHx of type-2 DM, HTN, and HLD who presented to ER for severe epigastric pressure- like 7/10 abdominal pain. No association with food intake. He had 1 episode of semi-loose stools. Denied any abdomen cramping, sick contacts, nausea/vomiting, fever/chills, or constipation. His previous endoscopy was only relevant for benign colonic polyps, which were removed. He had been on GLP1 RA for more than a year, and previously on dulaglutide 3mg, which was switched to tirzepatide 2.5mg 5 weeks ago. He was able to tolerate the medication without significant side effects and was recently up-titrated to 5 mg. Labs showed WBC 7.2, Hb 13.6, Cr 1.45, BUN 12, lipase 25, and normal LFTs. Abdominal X-ray and CT abdomen were noted to be significant for a partial vs evolving SBO without any identifiable small bowel intrinsic pathology. Mr. X was managed conservatively with fluids, NPO diet, and pain medications. Serial abdominal images were obtained, and he was eventually advanced to soft diet. Tirzepatide was discontinued on discharge. As a response to enteral nutrition, distal small bowel and colon release GLP-1 hormone. Exogenous and endogenous GLP-1 are associated with reduced gastric motility. GLP 1 RA and dual GIP/GLP-1 RA are advised to be used with caution in patients with established gastroparesis, as they can worsen the symptoms. GLP-1 effect on small intestinal motility is not extensively studied, however, small bowel motility inhibition was noted in animal models. Some of these actions were dose-dependent. There are some case reports of SBO due to GLP-1 RA. An observational cohort study noted an increased incidence of SBO with GLP1 RA when compared to SGLT2i. They noted most incidents of SBO happened early within the initiation of therapy (within 3 months). At the time of writing this abstract, there are no published SBO case reports associated with tirzepatide. Further large-scale clinical trials need to be conducted to explore the association of SBO in patients with GIP/GLP-1 and GLP-1 RA. These studies will help guide if these drugs should be contraindicated or used with caution in people with a previous history of SBO or colonic obstruction. Presentation: Friday, June 16, 2023

FRI088 Vanishing Bile Duct Syndrome?

Abstract Disclosure: C.T. Malvar: None. D. Bleich: None. H. Moran: None. Background: Dyslipidemia is a common metabolic disorder in the US, but only a few conditions can cause a total cholesterol greater than 1000 mg/dl. We present a suspected case of vanishing bile duct syndrome in a patient referred to the emergency department due to transaminitis. Case Report: A 41-year-old female with type 2 diabetes mellitus and alcohol use disorder was found to have abnormal liver function tests. She had jaundice, pruritus, and bipedal edema for 2 weeks, but had quit drinking approximately 2 years ago. She denied any recent travel, sick contacts, prior history of hyperlipidemia, family history of premature CAD or lipid abnormalities. On chart review, she received Azithromycin 2 months before presentation for a presumed upper respiratory tract infection. On evaluation, she had scleral icterus and jaundice. Initial labs revealed Na 117 (133 - 145 meq/l), Cl 84 (97 - 110 meq/l), glucose of 542 (70 - 109 mg/dl), total bilirubin 20.9 (&amp;lt;=1.0 mg/dl), 218 (0 - 33 U/L), AST 133 (0 - 32 U/L), GGTP 778 (5 - 36 u/l), Alkaline phosphatase 2,327 (35 - 105 u/l), Lipase 252 (13 - 60 U/L), Total cholesterol 1329 (100 - 200 mg/dl), LDL 1282 (0 - 99 mg/dl), HDL 13, and Triglycerides 172 (0 - 200 mg/dL). Alpha 1 antitrypsin, Liver Kidney Microsomal (LKM-1) Antibody, ANA, Antimitochondrial antibody, Anti-smooth muscle antibody, Ceruloplasmin, CMV, EBV, HSV, and HIV were all within normal limits. An abdominal CT revealed a right pleural effusion and cholelithiasis without gallbladder wall thickening. A right upper quadrant ultrasound demonstrated hepatic steatosis. Magnetic resonance cholangiopancreatography (MRCP) showed no focal lesions, fatty infiltrations, or ductal dilatation. Ursodeoxycholic acid and cholestyramine were started for pruritus. Pseudohyponatremia was due to the increased lipid fraction in blood. Lipoprotein phenotyping revealed type IIb hypercholesterolemia with elevated triglycerides. An apo-lipoprotein B level was 147 mg/dl at the upper limit of normal (range 50-150 mg/dL). Cholestasis-induced hypercholesteremia was considered as a diagnosis. Endoscopy esophageal ultrasound with liver biopsy revealed a smooth liver with non-cirrhotic appearance, severe cholestatic pattern of injury, including bile duct infarcts, and marked bile ductular reaction. Ezetimibe was started instead of a statin due to elevated liver enzymes. Discussion: Vanishing bile duct syndrome is an extremely rare condition unknown to many clinicians. Patients present after drug-induced liver injury. Treatment focuses on symptomatic relief and supportive care. Hyperlipidemia in these patients minimally respond to statins and are thus avoided. The prognosis of these patients can vary from slow recovery to eventual cirrhosis with end-stage liver disease requiring transplant. Increasing awareness among physicians is essential to facilitate its diagnosis and management. Presentation: Friday, June 16, 2023

OA13 The skin as a snapshot of systemic inflammation

Abstract Introduction This case focuses on a polymorphic rash of multidisciplinary interest in the setting of seemingly disparate multi-organ inflammatory phenomena. The case highlights the use and shortcomings of skin histopathology in diagnosing systemic conditions, particularly when faced with the dilemma of ordering the differential diagnoses of infection, inflammation and autoimmunity, and the subsequent decision-making around antibiotics or immunosuppression. Case description A 71-year-old man was admitted to a tertiary referral hospital in Adelaide, Australia, with fever (39.4oC), malaise and vomiting following a brief fishing expedition. No sick contacts were noted, although six months prior he had hiked through mountainous Pennsylvania, USA. Shortly after admission, he developed an acute, widespread rash involving his arms, legs, chest and abdomen with relative sparing of the back and face. The rash was erythematous, non-pruritic and polymorphic with papulonodular areas, some coalescing into plaque-like lesions. In areas on the forearms, there were vesicular and pustular components to the rash. Multiple other inflammatory manifestations were subsequently determined: synovitis of the proximal interphalangeal joints, widespread lung nodulosis with associated ground-glass opacities, transverse colon colitis, bilateral epididymo-orchitis, vocal cord ulceration, and bilateral conjunctivitis. Blood tests showed a normocytic anaemia (haemoglobin 82g/L; mean cell volume, MCV 90fL), neutrophilia (11x10^9/L) and elevated C-reactive protein (CRP, 350mg/L). No serological, culture or imaging evidence of infection was found on extensive investigations, including bronchoscopy, colonoscopy and echocardiogram. PET scan revealed no FDG-avid malignancy, vasculitis or infection. A skin biopsy showed both medium vessel and leukocytoclastic vasculitis. Broad spectrum antibiotics appeared to result in partial improvement, with resolution of the rash, defervescence, improvement in ground-glass opacities on chest imaging and stabilisation of the CRP at 200mg/L. The anaemia, however, worsened (nadir haemoglobin 73g/L) and became symptomatic, requiring transfusion, and the patient developed marked hypoalbuminaemia (nadir 12g/L) with associated peripheral and pleural effusions. In the context of the skin biopsy results, a provisional diagnosis of systemic medium-vessel vasculitis was made, and steroid therapy commenced with significant subjective improvement, improvement in anaemia and hypoalbuminaemia, and normalisation of CRP. Two weeks after discharge, genetic testing returned with a somatic variant of the UBA1 gene (Met41Leu), revising the diagnosis to VEXAS (Vacuoles, E1 Enzyme, X-linked, Autoinflammatory, Somatic Syndrome). Discussion Since VEXAS was first described in 2020, there have been case reports of patients with this diagnosis, typically older males, who present with protean inflammatory manifestations. As a disease entity which exists on a novel continuum of autoinflammation and myelodysplasia, VEXAS can mimic other conditions including vasculitis, inflammatory arthritis, Sweet’s syndrome and relapsing polychondritis. Indeed, there exists a subset of patients previously labelled with these diagnoses who have subsequently been found to have mutation of the UBA1 gene. We report a case of VEXAS initially diagnosed as a medium-vessel vasculitis on the basis of the only definitive finding, namely the result of a skin biopsy, following extensive investigation for infection. Although biopsy remains an important investigation in diagnosing vasculitis, this case demonstrates that there are now instances where genetic testing supersedes histopathology in obtaining a diagnosis. In this case, testing for a UBA1 variant was prompted by widespread inflammatory phenomena and persistent anaemia. Notably, however, VEXAS has almost universally been reported with macrocytosis but the patient in this case had a persistent normocytic anaemia. This case features some distractors: the reported sudden onset of symptoms, recent travel overseas and a partial response to antibiotic therapy with resolution of the patient’s fevers and widespread skin rash. In retrospect, with the diagnosis of VEXAS in mind, it is likely that this improvement represented disease fluctuation rather than response to antibiotics. Outstanding questions from this case include which, if any, of the organs involved in this patient’s initial presentation most suggested VEXAS. Whether a bone marrow biopsy in the work-up of unexplained systemic inflammation would have obtained an earlier diagnosis with the finding of vacuoles (noting that these are not universally present in patients with VEXAS) is also uncertain. Finally, the lack of macrocytosis is unexplained and atypical for VEXAS. Key learning points VEXAS is thought to be underdiagnosed and should be considered as a differential diagnosis, particularly in an older male patient who presents with widespread inflammatory features and haematological abnormalities. VEXAS can cause a variety of rashes and skin histopathology demonstrating vasculitis may reflect systemic inflammation rather than systemic vasculitis. In the frequently encountered quandary of infection versus inflammation/autoimmunity, a seeming response to antibiotics does not necessarily confirm an infectious aetiology and may have other explanations such as the anti-inflammatory effects of antimicrobials (e.g. doxycycline) or natural fluctuations of inflammatory disease activity.

A Comparison of Pathogen Detection and Risk Factors among Symptomatic Children with Gastroenteritis Compared with Asymptomatic Children in the Post-rotavirus Vaccine Era

To describe demographics, pathogen distribution/seasonality, and risk factors in children seeking care for acute gastroenteritis (AGE) at a midwestern US emergency department during 5 postrotavirus vaccine years (2011-2016), and further, to compare the same data with matched healthy controls (HC). AGE and HC participants <11years old enrolled in the New Vaccine Surveillance Network study between December 2011 to June 2016 were included. AGE was defined as ≥3 diarrhea episodes or ≥1 vomiting episode. Each HC's age was similar to an AGE participant's age. Pathogens were analyzed for seasonality effects. Participant risk factors for AGE illness and pathogen detections were compared between HC and a matched subset of AGE cases. One or more organisms was detected in 1159 of 2503 children (46.3%) with AGE compared with 99 of 537 HC (17.3%). Norovirus was detected most frequently among AGE (n=568 [22.7%]) and second-most frequently in HC (n=39 [6.8%]). Rotavirus was the second most frequently detected pathogen among AGE (n=196 [7.8%]). Children with AGE were significantly more likely to have reported a sick contact compared with HC, both outside the home (15.6% vs 1.4%; P<.001) and inside the home (18.6% vs 2.1%; P<.001). Daycare attendance was higher among children with AGE (41.4%) compared with HC (29.5%; P<.001). The Clostridium difficile detection rate was slightly higher among HC (7.0%) than AGE (5.3%). Norovirus was the most prevalent pathogen among children with AGE. Norovirus was detected in some HC, suggesting potential asymptomatic shedding among HC. The proportion of AGE participants with a sick contact was approximately 10 times greater than that of HC.

Abstract #1405039: Melting Muscle: Rhabdomyolysis as a Rare Initial Presentation of Hashimoto’s Thyroiditis

Rhabdomyolysis is characterized by muscular necrosis and the release of intracellular muscle contents into circulation. The most common cause of primary hypothyroidism is Hashimoto’s thyroiditis (HT) in iodine-adequate areas. Although hypothyroid myopathy is commonly seen, rhabdomyolysis is a rare reported but serious complication in patients with HT. This case report aims to highlight this rare complication, so that diagnosticians will consider this in their differential diagnosis. A 44-year-old African American male with a history of asthma and hypertension presented to the emergency room due to mild generalized muscle cramps started several weeks ago. It worsened recently after he started a new job that required him to work in the yard for 3-6 hours daily. He denied any new medications, recent trauma, drug use, insect bites, sick contacts, recent travel, or strenuous exercise. His vital signs were stable. Initial laboratory workups were significant for elevated creatinine kinase at 4299 unit/L and creatinine of 1.57 mg/dl. Notably, his thyroid stimulating hormone was 42.94 uIU/mL, free thyroxine (T4) was 0.48 ng/mL, and his anti-microsomal antibody was >1300 units/mL. He was admitted to hospital for rhabdomyolysis secondary to Hashimoto’s thyroiditis. Levothyroxine therapy and intravenous fluid were given. His condition improved and was ultimately discharged with close primary and endocrinology follow-up. Hypothyroidism is well-associated with musculoskeletal problems, and it is estimated that around one-third of patients are accompanied with myopathy symptoms. Mechanism of hypothyroidism-induced myopathy is not fully understood. It is thought, however, to be linked to thyroxine’s role in glycogenolysis and mitochondrial oxidative processes. Thus, insufficiency of thyroxine may damage myocytes due to oxidative stress and may eventually lead to rhabdomyolysis. Although Hashimoto’s thyroiditis is recognized as one of the most common causes of hypothyroidism, as per our knowledge, this is the first case that a patient initially presenting with rhabdomyolysis was found out to have Hashimoto’s thyroiditis. Thus, hypothyroidism should be kept on the differential in patients with suspicion of rhabdomyolysis, and a thyroid panel should be considered as one of the initial workups.

Abstract #1408177: Spinal Muscle Atrophy Presenting with Non-Diabetic Ketoacidosis

Spinal muscle atrophy (SMA) is an untreatable neurodegenerative disease related to loss of survival motor neuron (SMN) 1 gene resulting in muscle atrophy leading to significant morbidity and mortality. Patients with SMA may present with metabolic disturbances including impaired glucose tolerance, fatty acid metabolism and hyperlipidemia. We present a case of SMA presenting with recurrent metabolic acidosis. 51-year-old female with hypertension, osteoporosis, and SMA (homozygous deletion of exon 7 in the SMN1 gene) with quadriplegia and chronic ventilator dependent respiratory failure was admitted with diarrhea, poor oral intake, nausea, and abdominal pain. She did not report sick contacts or fever and had no history of diabetes. She had similar past episodes of metabolic acidosis with acute illness. Vital signs were BP 135/74mmHg, HR 110/min, RR 20/min, afebrile, and SpO2 96% on room air. On exam she appeared ill and debilitated with dry oral mucosa, + abdominal distension and tenderness with no rebound. Labs showed anion gap metabolic acidosis, Na 136mEq/L, K 3.9mEq/L, Cl 102 mEq/L, CO2 12 mEq/L, Anion gap 22, pH 7.13, Creatinine <0.01mg/dl, glucose 110 mg/dl, 2+ urine ketones, beta hydroxybutyrate 7.39 mmol/L, WBC 23.97 K/ul and HbA1c 5.2%. She was treated for non-diabetic ketoacidosis with IV fluids and fixed dose IV insulin infusion with dextrose infusion in tandem. She had hypernatremia, hypocalcemia, hypophosphatemia and hypokalemia likely due to poor nutrition and dehydration, and with aggressive electrolyte replacement, she showed significant clinical improvement during hospitalisation. Patients with SMA are prone to metabolic derangements e.g. ketoacidosis. Several factors may contribute to ketoacidosis such as decreased muscle mass, defects in endocrine pancreatic function and abnormal fatty acid metabolism regardless of triggering factors. One study investigated glucose metabolism and pancreas development in the Smn (2B/-) intermediate SMA mouse model and type I SMA patients. In mice it demonstrated a dramatic cell fate imbalance within pancreatic islets, with a predominance of glucagon-producing α cells at the expense of insulin-producing β cells and mice displayed fasting hyperglycemia, hyperglucagonemia, and glucose resistance. Similar abnormalities in pancreatic islet cells were seen in deceased children with the severe infantile form of SMA indicating that defects in glucose metabolism may play an important contributory role in SMA pathogenesis. There are no present guidelines to manage this entity, but case reports indicated a role of volume resuscitation and electrolyte replacement for improvement and future prevention by avoiding fasting.

Transverse myelitis following bivalent COVID‐19 booster vaccine and quadrivalent seasonal influenza vaccine

Transverse myelitis following bivalent <scp>COVID</scp>‐19 booster vaccine and quadrivalent seasonal influenza vaccine

Refractory Pneumonia in a 12-year-old Girl with Hemoglobin SS Disease

Refractory Pneumonia in a 12-year-old Girl with Hemoglobin SS Disease

Clinical influence of multiplex polymerase chain reaction routine uses in urgent pediatric admissions.

The coronavirus disease 2019 outbreak has prompted some hospitals to implement screening tests upon admission since 2020. FilmArray® Respiratory 2.1 Panel (FilmArray) is a multiplex polymerase chain reaction (PCR) test with high sensitivity and specificity for detecting respiratory pathogens. We aimed to assess the clinical influence of the routine use of FilmArray for pediatric patients, including those without symptoms suggestive of an infection. We conducted a single-center retrospective observational study, which investigated patients aged ≤15 years who underwent FilmArray on admission in 2021. We collected the patients' epidemiological information, symptoms, and FilmArray results from their electronic health records. A positive result was observed in 58.6% of patients admitted to the general ward or intensive care unit (ICU) but only in 1.5% of patients in the neonatal ward. Among the patients admitted to the general ward or ICU who tested positive, 93.3% had symptoms suggestive of infections, 44.6% had a sick contact before admission, and 70.5% had siblings. However, 62 (28.2%) out of 220 patients without the four (fever, respiratory, gastrointestinal, and dermal) symptoms also had positive results. Among them, 18 patients with adenovirus and three with respiratory syncytial virus were isolated to private rooms. However, 12 (57.1%) patients were discharged without symptoms suggestive of viral infection. Multiplex PCR routine use for all inpatients may lead to excessive management of positive cases because FilmArray cannot quantify microorganisms. Thus, targets for testing should be considered carefully based on patients' symptoms and histories of sick contacts.

Acute management of pneumonia in adult patients.

Acute management of pneumonia in adult patients.

903: GRANULOMATOUS PLEURITIS IN A PREVIOUSLY COVID-19-INFECTED PATIENT

Introduction: The most common setting for granulomatous pleuritis is usually in the presence of Mycobacterium tuberculosis. This pathology draws interest due to its potential of long-term injury to lung pleura, as well as, the potential to harm the lung parenchyma by association. We present a rare presentation of granulomatous pleuritis following COVID19 infection. Description: The patient is a 28-year-old female who presents to the hospital with fever and malaise for one week. She reports having an outpatient CT which showed a large right pleural effusion so her pulmonologist instructed her to come in. She denies recent exposure to any sick contacts. She does note a history of COVID-19 a year ago which resulted in shortness of breath but did not require hospitalization. She has worked at a gun shooting range for the last two years, for which she assembles bullets. She notes that she is required to wear a particulate protection mask and has worn this consistently to limit exposure. Thoracic surgery was consulted and initially completed a thoracentesis with 500 mL of exudative fluid. Patient remained intermittently febrile with worsening right sided chest pain. Culture and gram stain were unremarkable. She subsequently underwent a bronchoscopy with bronchial washing, biopsy, and decortication. Pathology demonstrated non-necrotic granulomatous pleuritis with a small area of central fibrinoid necrosis. Repeat chest x-rays demonstrated a minimal pleural effusion, much improved from prior. Fevers had also subsided at this time. Patient was discharged home with instructions to follow-up with thoracic surgery regarding further management of steroids. Discussion: The findings of non-tuberculosis-related granulomatous pleuritis are unique in that they frame the need to look for different perspectives and potentiators for pleural pathology. This case is also important given the unique presentation of the post-covid inflammatory response. Since COVID-19 is still so new, the field of post covid syndromes remains largely unknown.

A Rare Case of Hyponatremia and Gallbladder Cancer

Question: A 54-year-old woman with a history of diabetes and hypertension, presented to our hospital with jaundice, nausea, and intense fatigue for 1 month. She denied any abdominal pain, recent medication changes, or sick contacts. On presentation, her laboratory tests were significant for severe hyponatremia of 114 mEq/L, hypokalemia of 2.9 mEq/L, and hypochloremia of 79 mEq/L. Serum glucose was 157 mg/dL, blood urea nitrogen was 44 mg/dL, and serum creatinine was 1.79 mg/dL. Liver biochemistries were as follows: aspartate transaminase 105 IU/L, alanine transaminase 59 IU/L, total bilirubin 26.6 mg/dL, and alkaline phosphatase 1966 IU/L. She also showed mild hypoalbuminemia (2.6 g/dL) and elevated platelet count of 697/microliter.