CT Abdomen Pelvis Research Articles

7650 Thionamide Induced Pancreatitis and Agranulocytosis, a Rare Case of Concurrence

Abstract Disclosure: J. Lin: None. J. Shariff: None. Introduction: Thionamides are considered first line in the treatment of Graves’ Disease due to their efficacy and safety. We present a case of Graves’ in which methimazole resulted in not only agranulocytosis but also pancreatitis. Case Report: A 29yo female was diagnosed with Graves’ 5 months postpartum by her PCP. Her labs at diagnosis revealed a TSH <0.01 uIU/mL, free T4 of 6.4 ng/dL, and positive TRAb. She was started on methimazole 10mg and propranolol 20mg three times a day by her PCP. One month after starting treatment, she presented to the ED due to throat pain/fevers and was diagnosed with tonsilitis. She was given a 10mg dose of dexamethasone and sent home with antibiotics. No labs were drawn that visit. She went to her PCP 3 days later due to persistent symptoms and nausea/vomiting. A CBC revealed she had a WBC of 0.7 K/uL and an absolute neutrophil count (ANC) of 0.1 K/uL. Her last dose of methimazole had been the day prior to seeing her PCP. It was recommended she be seen in the ED due to concern for agranulocytosis where she was started on antibiotics and a CT abdomen pelvis with contrast revealed she had acute pancreatitis. She was admitted and started on filgrastim 5mcg/kg daily for thionamide-induced agranulocytosis. Her pancreatitis improved with conservative measures. Her propranolol was resumed at 30mg three times a day with symptom improvement. On her fifth hospitalization day, her ANC had recovered to 2.22 K/uL, WBC was 6 K/uL. Her free T4 was 1.65 ng/dL, free T3 4.1 pg/mL, TSI >40 IU/L. This change was suspected to be from propranolol, steroids, iodine load from her CT, and prior methimazole use. It was strongly recommended she pursue surgery that hospitalization given inability to treat her Graves’ medically. The patient refused, stating she wished to consider her options further outpatient. She would be seen one week later in a satellite ED. Her free T4 was 5.9 uIU/mL, T3 >30 pg/mL, TSH <0.010 uIU/mL. She left against medical advice. She subsequently declined further endocrine follow-up. Clinical Lessons: Thionamide-induced agranulocytosis is a rare but known complication of use, with some studies showing a prevalence as low as 0.2-0.5% [1]. Pancreatitis is a lesser-known complication of thionamides. There are several case reports of its occurrence, with the European Medicines Agency even listing it in the potential adverse reaction. Absolute risk of occurrence remains low, some studies showing <0.4% [1]. This case shows a rare concurrence of two uncommon complications from thionamide use and brings awareness to both pancreatitis and agranulocytosis as potential adverse events.

8557 Osteitis Fibrosa Cystica as the Initial Manifestation of Severe Primary Hyperparathyroidism: A Case Report

Abstract Disclosure: L.A. Robles Gomez: None. G. Gill: None. A. Vincent, DO: None. A. Mahmoud, MD: None. Introduction: Osteitis fibrosa cystica (OFC) is a pathognomonic yet uncommon finding of hyperparathyroidism seen in less than 2% of patients with primary hyperparathyroidism in Western countries. We present a case of infrequent finding of late-stage severe hyperthyroidism with asymptomatic hypercalcemia and incidental findings of osteolytic bone lesions. Clinical Case: A 28-year-old female with a history of PCOS, fatigue, and chronic abdominal pain presents to the clinic after recent work-up during an ED visit demonstrated incidental findings of osteolytic bone lesions in the setting of mild hypercalcemia. Physical examination was relatively unremarkable except for mild tenderness to palpation on the right lower quadrant. Laboratory significant calcium 10.7 mg/dl (8.6-10.2 mg/dL), albumin 3.6 g/dL, Creatinine 0.56 mg/dL, GFR 127 mL/min, Alkaline phosphatase 187 IU/L (37-127 IU/L), AST 24 IU/L, ALT 45 IU/L, Intact PTH and calcium: PTH 413 pg/mL (15-65 pg/mL), Calcium 11.5 (8.7-10.4 mg/dL), Bone Specific Alkaline Phosphatase: 54.5 mcg/L (4.7-17.8 mcg/L), Phosphorus 2.1 mg/dL (2.4-4.8 mg/dL), Magnesium 1.7 mg/dL (1.5-2.5 mg/dL), Vitamin D 25 10 mg/mL (20-100 ng/mL), TSH 2.12 uIU/mL (0.46-5.05 uIU/mL). CT abdomen pelvis w/o contrast with multiple predominantly lytic expansile bone lesions, mainly in the pelvis, with the most extensive 6.2 cm lesion in the superior, posterior right ilium, the anterior acetabulum, and the posterior right ischium. A prior CT done in 2018 showed a similar distribution of lytic lesions. The patient denied any previous personal or family history of hypercalcemia or parathyroid abnormalities despite a review of prior outside records revealed abnormal labs dating back to 2018 with intact PTH 406 pg/mL, calcium 10.3 mg/dL, Ionized calcium 10.7 mg/dl (3.30-6.0 mg/dL), albumin 3.3g/dL, alkaline phosphatase 288 IU/L. The patient denied prior symptomatology of hypercalcemia, including renal stones, or prior treatment for hypercalcemia. Further work-up was ordered, and the patient was referred to endocrine surgery for management. Conclusion: Osteitis fibrosa cystica (OFC) has become a rare manifestation of primary hyperparathyroidism (PHPT) due to early diagnosis of hypercalcemia by routine lab monitoring. Skeletal findings typically seen on PHPT can vary from bone reabsorption-acroosteolysis, subchondral bone resorption, brown tumors, salt-and-pepper skull, and osteopenia. Subchondral reabsorption around specific joints commonly affects pubic symphysis and sacroiliac joints, as seen in our patient. The mechanism is due to PTH-mediated osteoclastic absorption of bone and surrounding cartilage. Due to the rare presentation of PHPT with associated osteitis fibrosa cystica, diagnosis requires a high degree of clinical suspicion, as delayed diagnosis can lead to avoided manifestation, as described by our report. Presentation: 6/3/2024

S1224 Comparing Findings of CT Abdomen Pelvis Followed by CT Enterography Scans Within 90 Days in Patients With Inflammatory Bowel Disease

S1224 Comparing Findings of CT Abdomen Pelvis Followed by CT Enterography Scans Within 90 Days in Patients With Inflammatory Bowel Disease

Quality improvement project aiming to reduce inappropriate use of abdominal x-rays in the ED

BackgroundThere is compelling evidence that AXRs have limited clinical value in the acute setting. Despite this, they are frequently used in many EDs. This quality improvement project (QIP) aimed to...

EP58 - Gangrenous appendicitis in an incarcerated femoral hernia: A rare case of De Garengeot Hernia

Abstract Aims To present a rare case of gangrenous appendicitis within an incarcerated femoral hernia, discussing its clinical background and highlighting the challenges in its diagnosis and surgical management. Methods We detail a 74-year-old female with a painful, non-reducible groin mass. A CT abdomen pelvis revealed a right femoral hernia with acute reactive inflammatory changes, with no comment made on the appendix (Figure 1 and 2). Emergency open femoral hernioplasty and laparoscopic appendectomy were performed. Results Intraoperatively, a femoral hernia with a gangrenous appendicitis were identified. The appendix was reduced into the abdominal cavity to allow for better evaluation of its base. A laparoscopic appendectomy was performed after identifying the healthy base (Figure 3), followed by a femoral hernioplasty. This case sheds light on the rarity not only of the De Garengeot hernia which is defined by the presence of the vermiform appendix within the femoral hernia sac, but also even rarer the finding of a gangrenous appendix within the sac, with a reported incidence from 0.08-0.13% in cases of acute appendicitis. The case emphasizes the importance of considering an acute appendicitis and its complications within a femoral hernia as a differential diagnosis of painful groin masses with raised inflammatory markers. Conclusion Given the scarcity of literature on the surgical management of acute appendicitis in De Garengeot hernias, this case contributes valuable insights. The absence of established guidelines underscores the need for further exploration of optimal surgical strategies in such cases. Our report aims to enhance awareness of this rare presentation and facilitate future discussions on its management.

Linking NAFLD and Nephrolithiasis: A CT-Based Investigation

Objective: To evaluate the association between NAFLD and renal stone detected on computed tomography. Method: This study encompassed 240 patients who underwent noncontrast CT abdomen-pelvis computed tomography between November 2023 and April 2024. The nonalcoholic fatty liver disease group included those who had a reduced mean Hounsfield unit (HU) of the right lobe, lateral and left medial segment of the liver as compared to that of the spleen. The control group included patients who had liver parenchyma HU larger than spleen HU. All patients were examined for the presence or absence of radiopaque kidney, ureter, or urinary bladder stones, whether symptomatic or not. Results: From 240 patients, 122 were healthy (50.8%) without NAFLD or renal stone disease. NAFLD was found in 88 individuals with a mean age of 46.8±17.7 years, 42 (47.7%) males and 46 (52.3%) women. Renal stone disease was detected in 70 patients, accounting for 29.1% of the total. The average age of these patients was 43.7± 19.3 years, with 32 males and 38 females. Forty individuals with NAFLD had renal stones (45.5%) which was significantly more than the prevalence in those who are NAFLD negative 13 (19.7%), p <0.001. Females with NAFLD had a considerably greater renal stone rate (52.2%) compared to those without NAFLD (16.3%), P < 0.001. Conclusion: Patients with non-alcoholic fatty liver disease (NAFLD) had a significantly higher incidence of renal stone disease compared to persons with a healthy liver, especially among women.

Abstract PO1-11-09: Body composition correlates with BMI and menopausal status in patients with breast cancer

Abstract Background: Obesity is associated with higher risk of breast cancer (BC)-related death, all-cause mortality, and recurrence. While used to estimate body fat, body mass index (BMI) is insensitive to body fat distribution and lean muscle mass. We hypothesized that BMI categories (BMI 18.5-24.9 [healthy], 25-29.9 [overweight], and ≥30 kg/m2 [obesity]) would not correlate with CT-derived body composition. Methods: We retrospectively identified 180 patients diagnosed with new or recurrent Stage I-IV BC who presented to Johns Hopkins from 2015-2018 and were part of an institutional database. We extracted demographics, diagnosis date, cancer characteristics, BMI, and CT abdomen pelvis scans from the medical record. Baseline BMI was defined as the closest measurement to diagnosis between 1 year prior and 1 month after diagnosis. Baseline CT was within 6 months of and closest to the baseline BMI date. Fully automated deep-learning algorithms identified L1 and performed muscle and adipose tissue segmentation and quantification. Body composition data included: cross-sectional areas (CSA) of subcutaneous, visceral, and total adipose tissue; the mean, median, and standard deviation of the average of the muscle attenuation (density); and the body wall musculature CSA. ANOVA tests assessed associations between body composition, BMI, and menopausal status. Results: Among 180 patients, 136 (76%) had early-stage BC, and 44 (24%) had metastatic BC. Most patients were women (98%) and non-Hispanic (94%). Patients identified as White (57%), Black (29%), Asian (6%), and Other Race (8%). Sixty percent were post-menopausal. Hormone receptor-positive, HER2-positive, and triple negative subtypes were 56%, 19% and 22%, respectively. At diagnosis, 24% had a healthy BMI while 36% and 41% had overweight and obesity, respectively. All body composition measures were significantly associated with BMI (Table 1). As BMI increased, the average body wall musculature and subcutaneous, visceral, and total adipose tissue CSAs increased while the average muscle attenuation decreased. Specifically, the average visceral adipose tissue CSAs were 2.7 and 4.0-fold larger for overweight and obesity compared to that of the healthy BMI group, respectively, while their average muscle attenuations were 62.4% and 40.6% of the healthy BMI group. Postmenopausal women had 1.5-fold higher visceral adipose tissue CSA and 44.7% less average muscle attenuation compared to premenopausal women. Conclusion: Body composition correlates with all BMI categories in primarily white, non-Hispanic women with breast cancer. As BMI increases, body composition changes reliably, with increased subcutaneous and visceral adipose tissue, increased muscle area, and decreased muscle density. Muscle density, not size/area, is more associated with muscle performance, which can relate to functional status and outcomes. Despite validity concerns, BMI is an accessible and economical surrogate for body adiposity in patients with breast cancer. Postmenopausal status was also associated with greater visceral and total adiposity and lower muscle density. Further investigation is needed to confirm these findings. Table 1: Correlation between body composition, BMI, and menopausal status in patients with breast cancer All measures of body composition were significantly associated with BMI. Visceral adipose tissue increased and muscle density decreased as BMI increased and with post-menopausal status. Citation Format: Terrence Tsou, Tingchang Wang, Amanda Blackford, Ronald Summers, Vered Stearns, Jennifer Sheng. Body composition correlates with BMI and menopausal status in patients with breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO1-11-09.

Optimizing CT Abdomen-Pelvis Scan Radiation Dose: Examining the Role of Body Metrics (Waist Circumference, Hip Circumference, Abdominal Fat, and Body Mass Index) in Dose Efficiency.

Objective: This study investigates the correlation between patient body metrics and radiation dose in abdominopelvic CT scans, aiming to identify significant predictors of radiation exposure. Methods: Employing a cross-sectional analysis of patient data, including BMI, abdominal fat, waist, abdomen, and hip circumference, we analyzed their relationship with the following dose metrics: the CTDIvol, DLP, and SSDE. Results: Results from the analysis of various body measurements revealed that BMI, abdominal fat, and waist circumference are strongly correlated with increased radiation doses. Notably, the SSDE, as a more patient-centric dose metric, showed significant positive correlations, especially with waist circumference, suggesting its potential as a key predictor for optimizing radiation doses. Conclusions: The findings suggest that incorporating patient-specific body metrics into CT dosimetry could enhance personalized care and radiation safety. Conclusively, this study highlights the necessity for tailored imaging protocols based on individual body metrics to optimize radiation exposure, encouraging further research into predictive models and the integration of these metrics into clinical practice for improved patient management.

The economic impact of short-term imaging with metastatic pancreatic ductal adenocarcinoma.

643 Background: Although modern cancer treatment has significantly improved overall survival, this comes with a high financial cost. Based on an NIH report on Financial Burden of Cancer Care, treating pancreatic adenocarcinoma (PDAC) costs $108K, $18K, and $125K for initial treatment, during follow-up, and in last year of life, respectively. During the course of treatment, patients will visit the hospital for acute symptoms for which cross-sectional imaging is obtained within 45 days of subsequent scheduled follow-up imaging. This presents an opportunity for cost saving if data could be collected to identify an algorithm to avoid unnecessary duplication of imaging in a short interval. The purpose of this pilot study is to evaluate tumor growth trajectory within this short time span of 45 days to guide future trials to clarify the circumstances for which a subsequent follow up study is necessary. Methods: We retrospectively identified patients from our tumor registry from 2016 to 2019 who were diagnosed with metastatic PDAC (mPDAC). Subjects were included for analysis if they met the following criteria: 1) diagnosed with mPDAC; 2) had at least 2 CT abdomen/pelvis (CTAP) within 45 days of each other with one of the studies being obtained in the emergency department; and 3) had at least 1-3 measurable lesions as defined by RECIST 1.1 criteria. Tumor dimension was measured on axial images with the largest cross-section. For our primary outcome we used paired t-tests to evaluate the difference in mean size of all lesions (primary and metastatic). We also performed sub-group analyses comparing mean size of primary and metastatic lesions separately. An alpha level of 0.05 was used to determine statistical significance. Results: We screened 383 subjects from the tumor registry and identified 28 subjects suitable for our study. 18 subjects were female and 10 were male. We identified 69 target lesions, 23 of which were primary and 46 were metastatic. The mean sum of the largest dimension of target lesions was 2.82 cm on the initial study and 3.23 on the latter study (p<0.001). The mean sum of the largest dimension of the primary lesion was 3.62 cm on the initial study and 3.89 on the latter study (p=0.01). For metastatic lesions, the initial sum was 2.38 cm while the latter was 2.85 (p<0.001). Conclusions: Our finding of increase in tumor size in 45 days for mPDAC suggests that mPDAC is aggressive and can grow even in short time span. This suggests that if progression is identified on a study obtained within 45 days of scheduled follow-up, the follow-up study could be cancelled to avoid added cost to the patient. However, if the earlier study is stable or shows response, the scheduled follow-up may still be necessary to demonstrate continued stability/response.

Unraveling the Clinical Spectrum: A Case Study of Classic and Aplasia-Related Paroxysmal Nocturnal Hemoglobinuria

Introduction: Paroxysmal nocturnal hemoglobinuria (PNH) is a rare nonmalignant clonal disorder of hematopoietic stem cells characterized by a phosphatidylinositol glycan protein A (PIGA) gene mutation. This mutation results in the deficiency of glycosylphosphatidylinositol (GPI)-anchored proteins, CD55 and CD59, on the cell surface, rendering red blood cells (RBC) susceptible to complement-mediated destruction. This leads to hemolytic anemia, thromboses, and bone marrow failure. Here we describe two cases of PNH presenting to a tertiary care center. Case 1 A 29-year-old male with a history of polysubstance use presented to the Emergency Department with a 2-day history of progressively worsening left lower quadrant abdominal pain. CT abdomen pelvis showed multiple renal infarcts and findings suggestive of pneumatosis intestinalis. A complete blood count (CBC) revealed pancytopenia with a leukocyte count (WBC) of 3 x 10 9/L, hemoglobin (Hb) of 94 g/L, and platelet count (Plt) of 48 x 10 9/L. Lactate dehydrogenase (LDH) was elevated (900 IU/L), haptoglobin level was low ( <8mg/dL), and direct antiglobulin test (DAT) was negative. Urine was positive for hemosiderin, and flow cytometry showed RBCs (6.7%), granulocytes (97.97%), and monocytes (89.02%) with PNH phenotype. Bone marrow biopsy (BMB) was negative for dysplasia and fibrosis with normal hematopoiesis but showed increased erythroid precursors. Enoxaparin was started for thromboses and levofloxacin for neutropenia. Treatment for PNH was initiated with a loading dose of ravulizumab and meningococcal vaccination. The patient was lost to follow-up after receiving the first maintenance dose. Case 2 An 81-year-old female with a medical history of hypertension and coronary artery disease was hospitalized for gradually worsening shortness of breath and fatigue ongoing for 2 months. She reported easy bruising but denied a history of obvious bleeding from any orifice. Physical exam was significant for petechial rash in her lower extremities. Labs revealed pancytopenia (WBC 1.44 x 10 9/L, Hb 68 g/L, Plt 8 x 10 9/L), low reticulocyte count, LDH of 276 IU/L, and negative DAT. BMB showed marked aplasia, and she became transfusion dependent. Subsequently, flow cytometry revealed PNH phenotype in 1.45% of RBCs, 54% granulocytes, and 54% monocytes. Eculizumab therapy was started for the diagnosis of PNH. However, her transfusion requirements did not decrease. She developed iron overload and showed positive conversion on DAT. Darbepoetin alfa and romiplostim were added. Her Hb stabilized at >70g/L in 3 years, following which she only required romiplostim to maintain Plt >20,000 ( Graph 1). After 5 years, she opted to discontinue all treatment. She is being followed up regularly and has since remained stable. Discussion The two cases above are reflective of how PNH can present in different ways, ranging from the classic triad of symptoms to those with subclinical findings associated with other underlying conditions, such as aplastic anemia or myelodysplastic syndrome. The introduction of complement inhibitors completely changed the natural history of PNH, as patients' median survival shifted from 15-20 years to align with age-matched controls. Indications for treatment include severe anemia, thrombosis, or PNH symptoms like dyspnea, fatigue, and painful paroxysms. Currently, eculizumab and ravulizumab are the only FDA-approved drugs for PNH treatment. Ravulizumab is non-inferior to eculizumab, with the added advantage of less frequent dosing (every 8 weeks versus 2 weeks). Regular monitoring for hemolysis is warranted with treatment. Many patients require long-term therapy, which continues to be a significant challenge, even with the spaced dosing of ravulizumab. Eculizumab protects from terminal complement-mediated damage preventing intravascular hemolysis. However, these cells are still deficient in CD55, making them vulnerable to opsonization by C3 and premature removal in the spleen. As a result, >50% of PNH patients receiving treatment show positive conversion on DAT, as seen in case 2. Heparin is preferred in acute thrombotic states. Most hematologists recommend anticoagulation till a few months after starting complement inhibition.

Abstract 12297: A Rare Case of May-Thurner Syndrome Due to External Compression of the Right and Left Common Iliac Veins

Description of Case: A 54yr male with HTN and CKD stage IIIa presented with asymmetric right greater than left lower extremity (LE) edema. Vital signs were normal. His exam showed asymmetric right greater than left LE edema to the mid-thighs. ECG revealed sinus rhythm. Medical therapy with increasing titration of diuretics was unsuccessful in resolving his asymmetric LE edema. A TTE showed EF of 55-60% with normal bi-ventricular size and function and no significant valve abnormalities. Bilateral duplex US showed no DVT. CT abdomen pelvis showed no hydronephrosis or compressive masses. Right heart catheterization revealed normal bi-ventricular filling pressures. Bilateral peripheral venogram showed bilateral common iliac vein stenosis (Figure 1A). IVUS showed external compression of the right common iliac vein (RCIV) between the right external and internal iliac arteries with external compression of the left common iliac vein (LCIV) by the right common iliac artery (RCIA) against the lumbar spine (Figure 1A). A diagram of the compression observed in this case is included (Figure 1B). The RCIV had an 18mmHg gradient with no significant gradient on the LCIV. The RCIV was stented using an 18x60mm self-expanding stent and balloon dilation. Final IVUS and venogram showed no residual stenosis, edge dissection or perforation (Figure 1D). The patient was discharged on dual-antiplatelet therapy for three months and aspirin thereafter with continued diuretics. He had significant reduction in asymmetric LE edema with marked improvement in ambulation capacity and no further LE asymmetry at the 30-day follow-up visit. Discussion: Here we present a rare case of May-Thurner Syndrome via compression of the LCIV by the RCIA and RCIV by the right internal and external iliac arteries with successful management. We also illustrate the importance of a broad differential diagnosis in patients with persistent asymmetric LE edema refractory to diuretic management

FRI196 Non-Hemorrhagic Adrenal Infarction in Pregnancy with Tuberous Sclerosis

Abstract Disclosure: A. Mahaldar: None. H. Al Jumaili: None. S.R. Campbell: None. M.Z. Baker: None. Background: Non hemorrhagic adrenal infarction is a rare diagnosis in pregnancy with less than 20 cases reported in literature so far. No cases have been reported in patients with tuberous sclerosis. Most patients present with abdominal pain. Clinical Case: 29 year old woman G2P1 presented at 35 weeks gestation with right upper quadrant pain. She reported two episodes of dizziness in first trimester but otherwise had an uneventful pregnancy prior to presentation. First pregnancy was uncomplicated. Past medical history included asymptomatic tuberous sclerosis. No previous history of blood clots. Physical examination revealed a distended abdomen appropriate for gestational age and right upper quadrant tenderness to palpation. Initial laboratory data was unremarkable except for leukocytosis with WBC 16.6 k/mm3 (4-11 k/mm3). Normal electrolytes and liver function tests. Abdominal ultrasound revealed cholelithiasis without evidence of acute cholecystitis and unremarkable renal findings. CT abdomen pelvis with contrast showed thickening with surrounding stranding of right adrenal gland suggesting acute adrenal infarction and multiple pancreatic cysts. 8 am cortisol was 4.9 mcg/dl (4.1-16.6 mcg/dl) and ACTH was 23 pg/ml (7.2-63.3 pg/ml). Patient had received 2 doses of betamethasone due to concern for preterm delivery at 48 hours and 36 hours prior to this blood draw. Hypercoagulable panel was sent prior to starting enoxaparin. Elevated Factor VIII >150% (50 to 150%) was noted as expected in pregnancy. Lupus anticoagulant was weakly positive with LA sensitive PTT 50.1 (0 to 51.9 sec). Anticardiolipin antibody and beta 2 glycoprotein antibody were normal. Patient was treated with hydrocortisone 15 mg by mouth daily and full dose enoxaparin for anticoagulation. At one month follow up 8 am cortisol was 24 mcg/dl. Hydrocortisone replacement was discontinued. Labor was uncomplicated with vaginal delivery at 38 weeks gestation. Day 1 postpartum at 7:30 AM cortisol was 20.94 mcg/dl. Patient was discharged home in a stable condition with continued anticoagulation with enoxaparin and no further hydrocortisone treatment. Conclusion: We present a case of non hemorrhagic adrenal infarction in a pregnant patient with tuberous sclerosis. Adrenal infarction without hemorrhage is rare. Anatomy of adrenal gland makes it prone to microvascular thrombosis and infarction in a thrombotic state because of single draining vein for venous drainage. Pregnancy as a hypercoagulable state has been previously associated with non hemorrhagic adrenal infarction in few case reports. Whether tuberous sclerosis played any role in our patient’s pathogenesis remains unclear as there are no data or case reports linking the two. In conclusion, the diagnosis of non hemorrhagic adrenal infarction needs to be considered in hypercoagulable or pregnant patients presenting with abdominal pain. Presentation: Friday, June 16, 2023

THU361 Diabetic Ketoacidosis As The Initial Presentation Of Pancreatic Adenocarcinoma, A Case Report

Abstract Disclosure: U. Siddiqui: None. M. Ahmad: None. A. Shaikh: None. D. Rosenberg: None. Introduction: Signs and symptoms of pancreatic adenocarcinoma may be vague early in its course and is often discovered when it has quite advanced. Type 2 diabetes has been known to be linked with pancreatic adenocarcinoma with proposed mechanisms of hyperglycemia in these patients including increased insulin resistance, rapid beta cell turnover and oxidative stress. Rarely, diabetic ketoacidosis has been reported as an initial presentation of pancreatic carcinoma. We describe the case of a 61-year-old male with no previous diabetic history presenting with diabetic ketoacidosis (DKA) and found to have pancreatic adenocarcinoma. Case description: A 61-year-old male with no significant past medical history presented to the emergency department (ED) for a one week history of vision changes, nausea, abdominal pain and non-bloody vomiting. He reported heavy alcohol use on weekends, drinking 12 beers a day. He was found to be in DKA with his lab work demonstrating: venous pH 7.0, glucose 717 mg/dL, bicarbonate 7 mmol/L, anion gap 34 and positive beta hydroxybutyrate >60 mg/dL. After fluid resuscitation and IV insulin infusion he eventually had resolution of his DKA. Anti-GAD 65 screen was negative and c-peptide level was 5.71 ng/ml. His hemoglobin A1C was found to be 12.6. CT abdomen-pelvis with contrast demonstrated a patchy hypodensity of with dilation of pancreatic duct and a 2.0 cm pancreatic mass, resulting in pancreatic duct dilation with an MRI confirming these findings. Endoscopic Ultrasound fine needle aspiration confirmed pancreatic adenocarcinoma. The patient proceeded to have distal pancreatectomy and splenectomy. Surgical samples did not show lymph node involvement. After pancreatectomy the patient did have significantly decreased insulin requirements. Discussion: Pancreatic cancer is often discovered late in its course due to its subtle signs and symptoms. Evidence shows that type 2 diabetes is strongly linked with pancreatic cancer, with newly diagnosed type 2 diabetes or glucose intolerance being found in 80% of patients. Insulin resistance caused by pancreatic cancer has been proposed as an etiology of this new-onset diabetes and hyperglycemia. DKA as an initial manifestation of pancreatic cancer, however, is rare. Through this case we hope to highlight this association and suggest, in the right clinical setting, pancreatic cancer workup be considered in adults presenting with new onset type 2 diabetes and DKA. Presentation: Thursday, June 15, 2023

FRI668 Insulinoma As A Cause Of New Onset Hypoglycemic Episodes

Abstract Disclosure: S. Zahra: None. M.A. Abbas: None. R. Subramani: None. F. Manas: None. S. Yavuz: None. 37 years old female with a past medical history of hypothyroidism presented with complaints of shakiness, lightheadedness, and palpitations, relieved by eating. The physical examination was unremarkable. Fasting blood work showed low glucose of 41 mg/dl (70-99 mg/dl), normal insulin levels of 8.4 UIU/ ml (normal:1.9-23 UIU/ml), elevated proinsulin 21.1 pmol/ L (normal:<8.0 pmol/L), normal C Peptide 2.5 ng/ ml (normal:1.1-4.4 ng/ml), and negative for insulin antibody. Serum ACTH and cortisol levels were normal. Blood testing for hypoglycemia-inducing medications was negative. CT and MRI abdomen pelvis contrast was normal. She was prescribed to wear Dexcom to monitor her blood glucose round the clock. She continued to have low blood glucose, sometimes without symptoms and was rescued by the alarm. She underwent endoscopic ultrasound and was found to have a 10mm x 9mm ill-defined rounded pancreatic head mass with diffuse echogenicity of the pancreas. Biopsy of the mass revealed clusters of epithelial cells with neuroendocrine differentiation, compatible with insulinoma. She underwent surgical resection of the mass. She was also referred to genetic testing due to the association of pancreatic tumors with MEN syndrome. The diagnosis of Insulinomas is clinical as well as biochemical with presenting symptoms of Whipple’s Triad along with the presence of the following lab findings: hypoglycemia with plasma glucose of less than 50mg /dl, insulin greater than 5 UIU/L, C-Peptide greater than 0.2 nmol/L (0.6 ng/mL), Insulin/C-Peptide ratio of greater than 1.0, Proinsulin greater than 20pmol/L, and the absence of sulfonylurea metabolites in plasma or urine. Insulinoma is the most common pancreatic neuroendocrine and functional endocrine tumor of the beta cells of the pancreas with a prevalence of 1-4 people per million with equal gender distribution. They are mainly seen in the fifth decade of life but can occur at any age. They can occur sporadically or can be associated with MEN 1. Insulinomas are mostly benign, about 5-10% can be malignant. When to do medical vs surgical management? For benign insulinomas, surgical resection is preferred. For locally invasive and malignant tumors, aggressive surgical resection is performed, unless surgery is contraindicated for any other reason or patient refuses it. Medical treatment is reserved for the patients with diffuse Beta cell disease, multiple insulinoma and unresected malignant insulinoma. In the presence of unresectable metastatic disease; radiofrequency ablation, selective embolization, intraarterial chemotherapy, alone or in combination has been shown to be effective in controlling hypoglycemic episodes and improving quality of life. Octreotide, via inhibiting insulin secretion, normalizes the blood glucose levels. For better detection of hypoglycemia and adequate response to medical therapy, continuous glucose monitoring is helpful. Presentation: Friday, June 16, 2023

THU577 Acth Dependent Cushing Syndrome Identification And Management Challenges

Abstract Disclosure: B.C. Barreto: None. S. Patrick: None. H. Oktaei: None. H.O. Steinberg: None. Endogenous Cushing Syndrome(CS) is rare with an incidence of 0.2-5.0 per million people per year. 70 to 80% of CS is ACTH dependent and subclassified into Cushing Disease, Ectopic ACTH Syndrome and Ectopic CRH Syndrome. Ectopic ACTH secretion(EAS) has a variable clinical presentation. Atypical features like refractory hypokalemia in a patient with a tumoral lesion should raise suspicion. When imaging is inconclusive, differentiating between pituitary or ectopic disease includes invasive and noninvasive methods. We report a case of EAS. Case: A 57-year-old male with history of metastatic small-cell lung-cancer on palliative chemotherapy was admitted for acute coronary syndrome. Endocrinology evaluated the patient’s uncontrolled hypertension, hyperglycemia, and hypokalemia (1.5 mmol/L). He had no suppression with low dose dexamethasone (cortisol>75mcg/dL, ACTH 926pg/mL). Examination was pertinent for an elevated BMI 36.1kg/m2, hyperpigmented anterior thorax but no other stigmata of hypercortisolism. Laboratory analysis showed baseline cortisol 146.1mcg/dL(8.7-22), ACTH 590pg/ml(6-50), 24hr Urine Free Cortisol 736mcg/24h(5-50), which were not suppressed by high dose dexamethasone suppression test(HDDST). Aldosterone and PRA were undetectable. Brain MRI showed an enlarged pituitary gland, but no focal mass. CT abdomen pelvis showed bilateral adrenal hyperplasia, multiple hepatic masses, and bone lesions. Since the patient was a poor surgical candidate, medical therapy was initiated with ketoconazole 200mg TID, aldactone 50mg BID and potassium chloride 40mEq TID. After twelve days cortisol levels decrease to 65.2 mcg/dL, potassium 3.8 mmol/L and glucose 146 mg/dL. Hospitalization was complicated by a small bowel ileus. Medications were held due to poor gastrointestinal absorption and parenteral octreotide 200mcg TID was initiated. Once the ileus resolved, ketoconazole 200mg TID, eplerenone 50mg daily, and dexamethasone 0.5mg daily was started. Despite medical care, the patient eventually expired. Discussion: The HDDST can help distinguish pituitary from an ectopic ACTH overproduction. HDDST with >50% suppression, has been described with sensitivity-specificity of 60 to 100% for pituitary ACTH source. Symptomatic treatment of CS requires rapid normalization of hypercortisolism action. Surgery is the first line approach. When surgery is not an option, medical therapy should be considered. Adrenal steroidogenesis inhibitors, such as ketoconazole, are the first line due to rapid onset of action. Agents such as glucocorticoid receptor antagonists have limited availability in the inpatient setting. Somatostatin analogs and etomidate that inhibit 11-ßhydroxylase are potential options but require close monitoring. Severe hypercortisolism in the critically ill prompts the use of noninvasive evaluation tools and alternative medical approaches. Presentation Date: Thursday, June 15, 2023

FRI204 A Rare Case Of Cushing Syndrome In Pregnancy: Diagnosis And Therapeutic Challenges

Abstract Disclosure: Z. Cardona: None. E.D. Szmuilowicz: None. Introduction: Cushing’s syndrome (CS) rarely occurs during pregnancy, and diagnosis of Cushing’s syndrome in pregnancy is challenging due to physiologic changes during gestation. CS is associated with severe maternal and fetal complications. Clinical Case: A 36-year-old woman presented at 21 weeks gestational age with a known adrenal nodule admitted for evaluation of HTN, bilateral lower extremity edema, transaminitis, hyperglycemia, and acute hypoxemic respiratory failure. Reported proximal muscle weakness, facial swelling, anxiety, depression, perspiration, and headaches associated with HTN. Physical exam notable for mild supraclavicular fat deposition, chest and neck plethora, hypertrichosis, and bruising. CT abdomen pelvis revealed a 2.3-cm left adrenal nodule measuring 30 Hounsfield units. Biochemical evaluation included a plasma renin activity of 0.719 ng/mL/h [ref range: 0.167-5.380 ng/mL/h], aldosterone <1.0 ng/dL [ref range: 0.167-5.380 ng/dL], potassium 2.6 mEq/dL, free plasma metanephrines (MN) < 25 pg/mL [ref range: < or = 57 pg/mL], free normetanephrines (NMN) < 25 pg/mL [ref range: < or = 148 pg/mL, total free MN and NMN < 25 [ref range: < or = 205 pg/mL]. 24-hour urine free cortisol (UFC) was markedly elevated at 1854.1 mcg/24h [ref range: 3.1-50.0 mcg/24h], repeat 2186.2 mcg/24h, ACTH: 1.5 pg/mL [ref range: 7.2-63.6 pg/mL], confirming a diagnosis of ACTH-independent CS. Her case was complicated due to the adrenal nodule location. Patients with left adrenal nodules are at risk of developing inferior vena cava (IVC) syndrome during left adrenalectomies, especially in the third trimester, due to compression exerted by the uterus while lying on the right side during the procedure. She underwent an uncomplicated laparoscopic left adrenalectomy. Was started on hydrocortisone (HC) following surgery. There was concern for transient neonatal adrenal insufficiency at delivery. Measuring adrenal insufficiency in utero is challenging; however, estriol could serve as a surrogate marker of fetal adrenal function. Her estriol was normal, possibly indicating intact fetal adrenal activity. She had an uncomplicated vaginal delivery with no signs of adrenal insufficiency in her baby. Interestingly, she had a severely low alkaline phosphatase (ALP) which completely normalized soon after adrenalectomy. Clinical Lesson: This case depicts the challenges in managing CS in pregnancy and its repercussions regarding maternal, fetal, and delivery outcomes. Additionally, it highlights the importance of implementing a multidisciplinary approach, including obstetricians, endocrinologists, endocrine surgeons, and pediatricians, to ensure the optimization of therapeutic strategies. Presentation: Friday, June 16, 2023

THU387 Euglycemic Diabetic Ketoacidosis And SGLT-2 Inhibitor Use

Abstract Disclosure: N. Abrahimi: None. A. Abrahimi: None. N. Terrigno: None. Background: Diabetic ketoacidosis (DKA) is a known adverse effect of SGLT-2 inhibitors. (1) Incidences of euglycemic diabetic ketoacidosis in patients on SGLT-2 inhibitors are reported on less. Clinical Case: A 39-year-old male past medical history of uncontrolled, non-insulin dependent diabetes mellitus and pancreatitis who presented with abdominal pain, nausea and coffee ground emesis. On initial work up, basic metabolic panel showed blood glucose level of 175 mg/dL with an elevated anion gap of 22 mmol/L. Initial differentials included suspicion for euglycemic diabetic ketoacidosis or acute intraabdominal pathology. Venous blood gas showed metabolic acidosis, with a pH of 7.21 and bicarbonate of 9.7 mmol/L, beta hydroxybutyrate was elevated at 7.83 mmol/L. CT abdomen pelvis found a small hiatal hernia, gastric wall thickening, likely gastritis, and was negative for other intraabdominal pathology. Home medications of the patient included dapagliflozin, semaglutide, metformin, gabapentin, and pantoprazole. Patient was admitted with the diagnosis of suspected euglycemic diabetic ketoacidosis and was started on an insulin drip along with D5 0.45 normal saline. Patient’s anion gap was monitored with basic metabolic panel orders every two hours. The insulin drip was discontinued once the patient had two consecutive normal anion gaps and the patient was subsequently started on a subcutaneous insulin regimen. Conclusion: SGLT-2 inhibitors may cause euglycemic diabetic ketoacidosis based on the physiology of the SGLT-2 transporter and the pharmacology of the SGLT-2 inhibitors. (2) Clinical importance of this case report is to consider euglycemic diabetic ketoacidosis in patients on SGLT-2 inhibitors presenting with nausea, vomiting with normal blood glucose to not delay in the diagnosis and treatment of this life-threatening condition.

SAT331 A Case Of Iatrogenic Cushing’s Syndrome Due To The Concomitant Use Of Cobicistat With An Inhaled Glucocorticoid Followed By Adrenal Insufficiency Upon Discontinuation Of Cobicistat

Abstract Disclosure: L. Noor: None. J. Mullally: None. R. Glassman: None. Cobicistat is an inhibitor of cytochrome P4503A (CYP3A) used to increase the systemic exposure of antiretroviral drugs for treatment of HIV, and because of it’s mechanism of action, can have significant drug interactions. A similar “pharmacologic booster” ritonavir has now been widely reported to cause cases of iatrogenic Cushing’s syndrome when used in combination with glucocorticoids, but the data on this risk with cobicistat is much more limited. This case describes a patient who developed florid Cushing’s syndrome while on cobicistat and inhaled glucocorticoids followed by secondary adrenal insufficiency upon discontinuation of cobicistat. A 60 year old male with past medical history of well-controlled HIV on elvitegravir, cobicistat, emtricitabine and tenofovir, asthma on chronic inhaled fluticasone/salmeterol, presented with several months of progressive abdominal distention, back pain, irritability, easy bruising, proximal muscle weakness and weight gain. On physical exam, he appeared Cushingoid with central obesity, supraclavicular fullness, dorsocervical fat pad, wide violaceous striae on his abdomen and multiple ecchymoses. Iatrogenic Cushing's syndrome was suspected and labs showed undetectable morning serum cortisol and 24 hour urine free cortisol as well as newly elevated A1C of 5.7%. DEXA scan showed osteopenia. CT abdomen pelvis showed small adrenal glands. His HIV medication was switched to a combination of bictegravir, emtricitabine and tenofovir and he subsequently developed significant fatigue, nausea, abdominal discomfort and headaches. He was started on replacement doses of prednisone and his symptoms improved significantly. The prednisone dose is being gradually tapered, with ongoing recovery of the hypothalamic-pituitary-adrenal(HPA) axis, with now low, but detectable cortisol and ACTH levels. We present a unique case of iatrogenic Cushing’s syndrome due to concomitant use of cobicistat with inhaled fluticasone and the subsequent development of secondary adrenal insufficiency upon discontinuation of cobicistat. Cobicistat is an inhibitor of CYP3A which can cause decreased metabolism of exogenous glucocorticoids resulting in HPA axis suppression and exogenous Cushing’s syndrome. Fluticasone causes more cortisol suppression than other inhaled steroids because of it’s long half-life, higher binding affinity for glucocorticoid receptors and high lipophilicity. Concomitant use of cobicistat and glucocorticoids, including inhaled fluticasone, should be avoided and clinicians should be aware of the potential for iatrogenic Cushing’s syndrome and consequent adrenal insufficiency upon discontinuation of cobicistat after use with concomitant glucocorticoids. Presentation: Saturday, June 17, 2023

Clinician survey of current global practice for sarcoma surveillance following resection of primary retroperitoneal, abdominal, and pelvic sarcoma

Introduction– Postoperative surveillance following resection of primary retroperitoneal, abdominal, and pelvic sarcoma (RPS) is standard of care in international sarcoma centres and has rapidly evolved without an evidence base to become highly intensive and prolonged. This clinician survey aims to capture a global, contemporary snapshot of international guidelines used to inform sarcoma surveillance following resection of primary RPS. Materials and methods– Between July 2022 and March 2023, an online, anonymous, clinician survey to assess the current duration, imaging intervals and imaging modalities used for postoperative surveillance following resection of primary RPS was distributed among clinicians working at centres which are members of the TransAtlantic Australasian Retroperitoneal Working Group (TARPSWG). Results– Responses were received from 58 different TARPSWG centres. The majority of centres use institutional guidelines to guide surveillance intensity (n = 43, 74%) and the surveillance imaging modality (n = 39, 67%) used. For surveillance intensity and imaging modality, institutional guidelines are partially or entirely based on international guidelines in 81% (n = 47) and 78% (n = 45) of centres, respectively. Commonly used imaging modalities are contrast-enhanced CT abdomen-pelvis (n = 51, 88%) for abdominal surveillance and non-contrast enhanced CT (n = 25, 43%) for chest surveillance. Imaging intervals, timing of de-escalation of imaging frequency and total duration of surveillance for low-grade and high-grade RPS are reported. Conclusion– This global survey among TARPSWG members demonstrates the heterogeneity in sarcoma surveillance strategies worldwide and emphasises the need for a randomised controlled trial to provide an evidence base for the optimal surveillance schedule following primary resection of RPS.

Investigation of frailty markers including a novel biomarker panel in emergency laparotomy: protocol of a prospective cohort study

BackgroundEmergency laparotomy (EmLAP) is one of the commonest emergency operations performed in the United Kingdom (approximately 30, 000 laparotomies annually). These potentially high-risk procedures can be life changing with frail patients and/ or older adults (≥ 65 years) having the poorest outcomes, including mortality. There is no gold standard of frailty assessment and no clinical chemical biomarkers existing in practice. Early detection of subclinical changes or deficits at the molecular level are essential in improving our understanding of the biology of frailty and ultimately improving patient outcomes. This study aims primarily to compare preoperative frailty markers, including a blood-based biomarker panel, in their ability to predict 30 and 90-day mortality post-EmLAP. The secondary aim is to analyse the influence of perioperative frailty on morbidity and quality of life post-EmLAP.MethodsA prospective single centred observational study will be conducted on 150 patients ≥ 40 years of age that undergo EmLAP. Patients will be included according to the established NELA (National Emergency Laparotomy Audit) criteria. The variables collected include demographics, co-morbidities, polypharmacy, place of residence, indication and type of surgery (as per NELA criteria) and prognostic NELA score. Frailty will be assessed using: a blood sample for ultra-high performance liquid chromatography mass spectrometry analysis; preoperative CT abdomen pelvis (sarcopenia) and Rockwood Clinical Frailty Scale (CFS). Patients will be followed up for 90 days. Variables collected include blood samples (at post operative day 1, 7, 30 and 90), place of residence on discharge, morbidity, mortality and quality of life (EQ-5D-5 L). The frailty markers will be compared between groups of frail (CFS ≥ 4) and non-frail using statistical methods such as regression model and adjusted for appropriate confounding factors.DiscussionThis study hypothesises that frailty level changes following EmLAP in frail and non- frail patients, irrespective of age. We propose that non- frail patients will have better survival rates and report better quality of life compared to the frail. By studying the changes in metabolites/ biomarkers in these patients and correlate them to frailty status pre-surgery, this highly novel approach will develop new knowledge of frailty and define a new area of clinical biomolecular research.Trial registrationClinicalTrials.gov: NCT05416047. Registered on 13/06/2022 (retrospectively registered).