CT Of Abdomen Research Articles

6660 Euglycemic DKA Induced by SGLT-2 Inhibitor Following Administration ofTirzepatide

Abstract Disclosure: K. Gurel: None. S. Mathew: None. M. Zeidan: None. S. Al Barznji: None. F. Alkhankan: None. Introduction Tirzepatide has side effects of diarrhea, nausea, vomiting, and loss of appetite(2). SGLT-2 inhibitors may cause Euglycemic Diabetic ketoacidosis(EDKA) by inducing carbohydrate starvation and volume depletion(1). Clinical Case A 72-year-old male with a past medical history of T2DM(Hg A1c 8.4[≤ 6%]) on empagliflozin, metformin, hyperlipidemia, obesity on tirzepatide who presents with complaining of nausea, vomiting, and abdominal pain. The patient noted that he started experiencing symptoms two days before admission following receiving tirzepatide dose. He takes Tirzepatide every 10 days and he was started on empagliflozin 1 month ago. The patient started to have a loss of appetite, nausea, and vomiting on the day he received his tirzepatide injection. Over the next two days, the patient’s nausea and vomiting worsened and the patient was not able to tolerate food. On admission, ABG demonstrated pure metabolic acidosis (pH of 7.24[7.30-7.40], bicarb of 11.8 [21 - 28 mmol/L] PCO2 of 27.4[ 41 - 51 mmHg]). BMP showed anion gap of 20(3-15 mmol/L) with glucose level of 145(74-106 mg/dl) . Beta-Hydroxybutyrate level was 6.3(0.0 -0.27 mmol/L). UA was only significant for glucose level of >1000(negative) and ketone level of 40(negative). Lipase level was 539(73-393 U/L). CT abdomen ruled out acute pancreatitis. No infection source was identified. Upon admission to the ICU unit, the patient was started on D5 with KCL 20 mEq and Insulin drip. The patient was followed up with a glucose check every hour and BMP every 4 hours. On day 2 of admission, the Anion gap was normalized and the insulin regimen was transitioned to subcutaneous insulin. The patient was placed on carbohydrate consistent diet. On discharge, the patient was advised to avoid taking SGLT-2 inhibitors including empagliflozin. Conclusion Tirzepatide's potential side effects, including diarrhea, vomiting, and appetite loss, may contribute to volume depletion and carbohydrate starvation(2). Individuals using both SGLT-2 inhibitors and Tirzepatide should be closely monitored for these symptoms. Reference 1-)Baggio LL, Drucker DJ. Glucagon-like peptide-1 receptor co-agonists for treating metabolic disease. Mol Metab. 2021 Apr;46:101090. doi: 10.1016/j.molmet.2020.101090. Epub 2020 Sep 25. PMID: 32987188; PMCID: PMC8085566. 2-)Plewa MC, Bryant M, King-Thiele R. Euglycemic Diabetic Ketoacidosis. [Updated 2023 Jan 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554570/ Presentation: 6/2/2024

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.

6963 A Rare Case Presentation of Untreated Congenital Adrenal Hyperplasia with Bilateral Giant Myelolipoma

Abstract Disclosure: F. Omran: None. S. Bromley: None. M. Ilahi: None. M. Zena: None. W. Al-Refaie: None. J. Delto: None. A. Singh,: None. Background: Adrenal myelolipoma is a rare benign neoplasm predominantly composed of mature adipose tissue and intermixed myeloid tissue, often associated with conditions like Congenital Adrenal Hyperplasia. The etiology of this neoplasm is not definitively known although there are numerous hypotheses, including research suggesting that excess ACTH could be responsible for the pathogenesis. Clinical Case: A 40-year-old female with a history of congenital adrenal hyperplasia noncompliant with treatment. She presented with cholelithiasis (s/p laparoscopic cholecystectomy), abdominal imaging revealed incidental finding of a large right retroperitoneal mass. She was noted to have generalized excessive hirsutism in male distribution, small breasts, enlarged clitoris, male body habitus, and amenorrhea after stopping steroids years prior. Laboratory workup showed the following hormonal abnormalities: elevated ACTH (1080 pg/ml), elevated testosterone (243 ng/dl) and free testosterone (31.3 pg/ml), elevated androstenedione (23.431 ng/ml), and low LH (<0.02 miu/ml), low FSH (<0.02 miu/ml). CT abdomen showed right lobulated retroperitoneal mass of 4x14.3x20cm with internal fat and soft tissue components, left lobulated retroperitoneal mass of 13.7x4.7x7.5cm with soft tissue and fat components. CT guided-biopsy showed pathology consistent with adrenal myelolipoma: fatty areas with interspersed hematopoietic tissue components, peripheral rim of normal adrenal cortical tissue. Given the large size of the mass and compressive effects on surrounding organs, patient underwent exploratory laparotomy with resection of right retroperitoneal mass, nephrectomy, and adrenalectomy. Discharged on hydrocortisone and fludrocortisone, instructed to follow up by endocrinologist, always wear medical alert bracelet, and provided with hydrocortisone emergency kit. Conclusion: This case serves as a classic presentation of a rare disease state. Adrenal myelolipomas, a rare benign adrenal neoplasm, have been found in several disorders associated with chronic ACTH hypersecretion including congenital adrenal hyperplasia. Most CAH patients with myelolipomas have untreated or poorly treated CAH. Adrenal myelolipomas that are asymptomatic and <5cm in size are usually monitored if one is certain there is no occult malignancy. If these tumors are symptomatic or >7cm, patients should undergo surgical excision. These patients should be followed by endocrinology. Importantly, further guidelines should be further developed for management. Presentation: 6/3/2024

7305 Pheochromocytoma Presenting With Resistant Hyperglycemia

Abstract Disclosure: M. Economou: None. A. Devine: None. Background: Pheochromocytoma is a rare catecholamine producing tumor arising from the adrenal gland. Impaired glucose tolerance is a well-recognized hormonal and metabolic manifestation of pheochromocytoma caused by catecholamine excess [1]. Insulin resistance requiring very high doses of insulin in association with pheochromocytoma is, however, rare. Here we report a case of pheochromocytoma in a woman with diabetes mellitus that proved difficult to control despite high-dose insulin therapy. Case presentation: A 72-year-old woman with a longstanding history of type 2 diabetes mellitus, uncontrolled hypertension, hyperlipidemia and CVA presented to the hospital after she was found to have a hemoglobin of 7.0 ng/mL on routine labs. Notably, over the past 4 years, her insulin requirement gradually increased from 20 units/day to 50 units/day despite an A1c level of 6.1%. On presentation, our patient was hypertensive to 170/90 with limited response to multiple antihypertensive medications. Additionally, her glucose was severely uncontrolled, fluctuating between 200-500 mg/dL. Within days, the patient’s total daily insulin requirement increased tremendously to as much as 300 units/day. As part of her anemia workup, she underwent a contrast-enhanced CT abdomen & pelvis which identified a left adrenal mass measuring 2.2 x 2.8 x 2.9 cm. Further evaluation with MRI confirmed an adrenal mass suspicious for pheochromocytoma. Evaluation of plasma hormone levels revealed an elevated normetanephrine level of 7.10 nmol/L (normal: less than 0.89 nmol/L). Furthermore, the 24-h urinary normetanephrine level and chromogranin A levels were elevated to 145 mcg/day and 1203 ng/mL, respectively. Initial treatment with alpha and beta blockade improved blood pressure but glucose levels remained persistently elevated. The patient underwent left laparoscopic adrenalectomy and pathology revealed pheochromocytoma, measuring, 3.2 cm in diameter, with stains positive for CD56, synaptophysin and chromogranin. Surgical resection margins were negative for tumor. Postoperatively, insulin requirements returned to roughly that of her baseline, 40 units/day. Conclusion: Impaired glucose tolerance is a known phenomenon associated with pheochromocytoma. Despite this, it is unusual to see an insulin requirement rise as abruptly and drastically as seen in this case. Our patient, with relatively controlled diabetes had an enormous increase in her insulin requirement during her hospital course as evidenced by her insulin regimen which increased sixfold. This case highlights the importance of maintaining a high degree of suspicion for pheochromocytoma in patients with a sudden rise in insulin requirement and uncontrolled hypertension. Reference: (1) Ronen JA, Gavin M, Ruppert MD, Peiris AN. Glycemic Disturbances in Pheochromocytoma and Paraganglioma. Cureus. 2019 Apr 27;11(4): e4551. Presentation: 6/3/2024

6794 Primary Adrenal Insufficiency Following Bilateral Adrenal Hemorrhage Secondary To Antiphospholipid Syndrome

Abstract Disclosure: M. Alameri: None. A.M. Alnuaimi: None. Y. Alabrach: None. A. Abbas: None. S. Baroud: None. M. El Khazendar: None. Introduction: Adrenal insufficiency (AI) is a rare life-threatening complication of antiphospholipid antibody syndrome (APS) accounting for 0.4% to 0.5% of Al cases. Case report: A 26-year-old female with background history of primary antiphospholipid syndrome (PAPS) presented with 3 weeks history of dull abdominal pain and fatigue. Examination revealed dehydration, orthostatic hypotension and hyperpigmented skin. Biochemistry assessment was consistent with primary adrenal insufficiency (hyponatremia 125 mol/L, hyperkalaemia 6.8 mmol/L, low random cortisol 142 mol/L, high ATCH 440 pmol/L [N 1.6-13.9], low aldosterone <1.05 ng/dL and high renin 128 ng/L [N 4-23.7]). She received 100mg hydrocortisone followed by regular IV hydrocortisone q6hrs. CT abdomen revealed bilaterally enlarged hyperdense adrenal glands suggestive of haemorrhage. Adrenal MRI confirmed subacute bilateral adrenal haemorrhage (BAH) replacing whole adrenal glands with hemosiderin depositions and calcifications without evidence of underlying tumor. Anti-21-hydroxylase antibody came back negative. She was discharged on hydrocortisone, fludrocortisone and hydroxychloroquine. Education was given for sick days rule and hydrocortisone emergency kit was provided for adrenal crisis. Discussion and conclusion: We describe a patient with APS, who developed Al due to bilateral subacute adrenal haemorrhages. Adrenal haemorrhage is rare but life-threatening complication of APS. High clinical vigilance is important to consider adrenal haemorrhage in differential diagnosis of Al, specifically in patients with known antiphospholipid antibody syndrome (APS). Presentation: 6/3/2024

7947 Semaglutide Induced Pancreatitis: A Case Report

Abstract Disclosure: T. Altaweel: None. A. Mathew: None. P. Chalasani: None. L. Lawrence: None. S. Hussain: None. N. Aldaoud: None. Introduction/Background: As semaglutide (GLP1 RA) has become a cornerstone in diabetes and weight management, there have been studies indicating pancreatic inflammation with GLP1 RA use. We report a case of acute necrotizing pancreatitis secondary to semaglutide use.Clinical Case: A 52 year old male with a history of hypertension, morbid obesity with BMI of 40 kg/m2, alcohol induced pancreatitis presented to the hospital complaining of epigastric pain. On presentation, he appeared in distress due to pain but was hemodynamically stable. Physical examination revealed a moderately distended abdomen, tender to palpation over the epigastric area without guarding, and negative Murphy’s sign. The patient reported no alcohol consumption, tobacco usage, or recent abdominal injuries. Laboratory workup revealed elevated WBC 14.6 thous/mcL (4.5-10.5) and lipase 1941 U/L (<60). Abdominal ultrasound showed common bile duct 2 mm without gallstones and CT abdomen revealed acute pancreatitis with suspected necrosis in the pancreatic head and the pancreatic tail. Patient was started on aggressive fluid hydration, pain management and admitted to intensive care. Patient reported that he was started on semaglutide three months ago for weight management by his primary care physician. Patient improved symptomatically with pain control and tolerated oral intake. He was discharged home with recommendations not to resume semaglutide. Conclusion: Semaglutide involves direct stimulation of GLP-1 receptors in pancreatic cells, potentially leading to cell overgrowth, increased pancreatic weight, duct occlusion and inflammation. Despite the SUSTAIN-6 trial indicating no increased risk of acute pancreatitis in diabetic patients using semaglutide, atypical presentations of pancreatitis are noted in patients using the medication for weight management. When all identifiable causes of pancreatitis are eliminated, semaglutide-induced pancreatitis should be a primary consideration in the differential diagnosis. Physicians should exercise caution and give careful consideration when prescribing semaglutide for weight management in patients with conditions that increase risk for pancreatitis. Presentation: 6/2/2024

7044 It Is Back, Three Decades Later! When To Stop Glucagonoma surveillance?

Abstract Disclosure: A.T. Wahba: None. J.S. Dillon: Advisory Board Member; Self; Crinetics Pharmaceuticals, CA. A 76-year-old woman presented to the Neuroendocrine Tumor (NET) Clinic for evaluation of sore mouth, perianal area and itchy ankles. She had a medical history notable for glucagonoma, status post distal pancreatectomy and splenectomy in 1988, 32 years prior to her current presentation. She recalled that she had CT imaging post operatively for a few years, but no more recent imaging. She was diagnosed with diabetes mellitus in approximately 2002, with highly variable glucose control. She developed a left leg DVT with pulmonary emboli one year prior to presentation. Shortly after her thromboembolic events, she noted her current presenting complaints. A CT abdomen scan with contrast was reported as normal. Three months later, an abdomen ultrasound for evaluation of right upper quadrant pain and intractable vomiting, showed a liver mass. MRI revealed a contrast enhancing 3.1x2.1x1.8 cm lesion in liver segment 6 and 7. Her plasma Glucagon concentration, which had been undetectable when last checked in 2007, was 382 (N: < 80 pg/ml). CT-guided needle biopsy of the liver lesion confirmed a well differentiated neuroendocrine tumor, immunohistochemically positive for somatostatin receptor 2 (SSTR2A), Islet-1 and PAX6, with low mitotic count and Ki-67 proliferation index of 0.45%. Gallium-68 DOTATATE-PET scan showed a single avid hepatic metastasis, with no other evidence of somatostatin receptor expressing tumor. She was initially started on a combination of short-acting Octreotide 100 mcg TID and monthly 20 mg Sandostatin LAR injections for symptomatic relief. Zinc copper 100 mg capsules were prescribed with significant improvement of skin rash and glossitis within 2-4 months. Repeat MRI abdomen at 3 months and 6 months showed a stable single liver lesion without evidence of additional metastasis. She has continued annual clinic visits and abdomen MRI follow up with stable imaging findings at 3 years. Percutaneous ablation, trans hepatic arterial embolization and surgical resection were discussed, but the patient preferred a more conservative approach of monthly octreotide LAR, which she tolerated well, and which resolved her symptoms. Glucagonoma syndrome presents classically with 5D’s: Dermatitis (Necrolytic Migratory Erythema), DVTs, Diabetes mellitus, Depression, Diarrhea. The National Comprehensive Cancer Network guidelines recommend monitoring glucagonoma patients post-resection for up to 10 years with clinical evaluation, glucagon levels every 6-12 months and imaging studies as clinically indicated. Our case illustrates that recurrence can occur after 30 years from initial resection and that longer surveillance should be considered. Presentation: 6/3/2024

6728 Bilateral Adrenal Hemorrhage: Cause Or Consequence?

Abstract Disclosure: M.N. Rayan: None. R. Horner: None. A. Valenciaga: None. L.E. Ryan: None. Introduction: Before the advent of the CT scan, bilateral adrenal hemorrhage was primarily discovered post-mortem in patients who had succumbed to sepsis, burns, or anticoagulant therapy. Today, non-traumatic hemorrhage is recognized as an infrequent, yet potentially lethal diagnosis causing clinical deterioration in acutely ill patients. Clinical Case: Our patient is a 64-year-old-male with a medical history of Myelodysplastic Syndrome initially presented to an external ED with abdominal pain. CT abdomen revealed hepatomegaly, splenomegaly, and new bilateral adrenal masses—absent in an MRI conducted a year earlier. He was treated conservatively and subsequently discharged. Two weeks later, he returned to the hospital with severe right sided flank pain. His hemoglobin and platelet counts dropped from 11.5 g/dL and 309 K/uL during the previous ED visit to 7.7 g/dL and 80 K/uL, respectively. Additionally, his PT/INR, PTT, fibrinogen, and D-Dimer levels were elevated. A repeat CT scan indicated a significant enlargement of the right adrenal mass, raising suspicion of adrenal hemorrhage. He was appropriately transfused, and a BM biopsy was performed to evaluate for acute transformation of underlying MDS. Cortisol levels were monitored daily for adrenal insufficiency. A complicated hospital course ensued marked by worsening anemia, thrombocytopenia, and coagulopathy, accompanied by high fevers and new-onset atrial fibrillation. Mixing studies showed absence of a factor inhibitor ruling out acquired forms of Hemophilia. Infectious workup including fungal and viral serologies returned negative. A PET scan revealed several small hypermetabolic hypodense liver lesions, and hypermetabolic activity diffusely in the spleen, and adrenal glands leading to suspicion of metastasis. Results of the BM biopsy returned revealing hypercellularity, with aggregates of hemosiderin-laden macrophages replacing the bone marrow space with associated necrosis. Worsening abdominal pain with hematochezia prompted an endoscopy, confirming a diagnosis of metastatic melanoma. Concurrently, seizure activity and altered mentation led to a head CT, revealing new metastatic lesions that confirmed the rapid progression of the disease. Subsequently, the patient was transitioned to comfort care and passed away. Clinical Lesson: It is crucial to review the various causes of adrenal hemorrhage, understand the challenges associated with interpreting adrenal imaging, emphasize the need to monitor adrenal function, and consider the occasional necessity for tissue sampling. In this clinical scenario, metastases with hemorrhage were the most likely etiology. The causes of adrenal hemorrhage are not always apparent; in this presentation, the consequence of the underlying disease state ultimately led to the initial presenting symptom of abdominal pain. Presentation: 6/2/2024

12417 Atypical Patterns Of Hypoglycemia Post-bariatric Surgery Due To Pancreatic Insulinoma

Abstract Disclosure: K.A. Chopra: None. Accurately diagnosing an insulinoma in patients who have had bariatric surgery can be challenging because the autonomic symptoms of palpitations, tremors, anxiety and neuroglycopenic hypoglycemia symptoms of confusion and loss of consciousness may overlap with dumping syndrome or be attributed to non-insulinoma pancreatogenous hypoglycemia. When evaluating hypoglycemia, it is crucial to obtain a detailed history of the pattern and timing of hypoglycemia episodes and collect a critical sample of insulin, proinsulin, c-peptide levels during an episode of low glucose to prevent misdiagnosis. 58-year-old woman with hypertension, obesity, and history of laparoscopic sleeve gastrectomy presented for evaluation of hypoglycemia. The patient lost 100 pounds after her sleeve gastrectomy. Within the past year, the patient had two hospitalizations for severe symptomatic hypoglycemia with associated loss of consciousness. Imaging showed atrophic pancreas and she was discharged with a prescription for daily prednisone without critical sample testing for insulin or c-peptide levels. She sought a second opinion for her hypoglycemia at UCM. Since she was taking prednisone for 10 months prior to initial evaluation at UCM, evaluation for adrenal insufficiency could not be completed initially. She started continuous glucose monitoring which showed multiple daily episodes of hypoglycemia, fasting and at other various timepoints. Fasting labs showed low glucose of 20 mg/dL (RR 60-99 mg/dL), elevated proinsulin 120 pmol/L (RR 3.6- 22 pmol/L), inappropriately normal insulin 16.4 uIU/mL (RR <28.5 uIU/mL), and inappropriately normal c-peptide 0.82 pmol/mL (RR 0.30-2.35 pmol/mL), consistent with insulinoma. CT abdomen showed 1.4 cm arterially enhancing round lesion in the pancreatic body. Endoscopic ultrasound showed 13 mm mass in the pancreatic body with fine needle aspiration with pathology showing a well-differentiated neuroendocrine tumor. She received stress dose hydrocortisone preceding surgery and underwent successful enucleation of 1.6 cm pancreatic neuroendocrine tumor. A few weeks after her surgery, her HPA axis was re-evaluated, and steroids were discontinued. She has had no episodes of hypoglycemia since. Although hypoglycemia can be associated post-bariatric surgery, most patients develop postprandial hypoglycemia due to surgical alterations in alimentary flow leading to increased incretin and insulin secretion (Mulla et al 2016). Therefore, it is important to consider insulinoma in the differential diagnosis of post-bariatric surgery patients presenting without typical postprandial patterns of hypoglycemia. Reference: Mulla CM, Storino A, Yee EU, Lautz D, Sawnhey MS, Moser AJ, Patti ME, Insulinoma After Bariatric Surgery: Diagnostic Dilemma and Therapeutic Approaches. Obes Surg. 2016 Apr;26(4):874-81. Presentation: 6/1/2024

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

8186 Hypoglycemia as an Unusual Presentation of Panhypopituitarism

Abstract Disclosure: P. Chalasani: None. M. Asfaw: None. M. Mansour: None. M. Hammoud: None. T. Altaweel: None. H. Ilyas: None. L. Lawrence: None. Introduction: Hypopituitarism refers to the diminished or complete absence of anterior pituitary function, which may arise from acquired or congenital factors. The symptoms depend on the patient’s age and the hormones affected. We report a case where hypoglycemia led to a new diagnosis of panhypopituitarism in an adult patient. Clinical Case:A 53-year-old female with a past medical history of hypertension was brought to the emergency department after syncope. Patient experienced diaphoresis and loss of consciousness associated with urinary incontinence. She did not have confusion, tongue biting, or muscular weakness after the episode. On presentation, the patient was hypoglycemic with blood glucose of 39 mg/dl and received IV dextrose. No focal neurologic deficits were noted on physical examination. She was mildly hypotensive with blood pressure 98/66 mmHg, and received hydrocortisone 100 mg IV once, and started on IV dextrose infusion. Hypoglycemia workup revealed elevated insulin 16.6 uIU/mL and C-peptide 4.8 ng/mL (1.1-4.4) levels for a blood glucose level of 132 mg/dl, with normal beta-hydroxybutyrate of 0.14 mmol/L (0.02-0.27). Sulfonylurea screen was negative. CT abdomen revealed no pancreatic lesions or abnormalities. Hyperinsulinemia was attributed to insulin resistance in this patient with a BMI of 34 kg/m2. CT head revealed a heterogeneous low-density expansile mass in the sella/suprasellar region measuring approximately 2.5 x 2.3 x 2 cm. MRI brain confirmed a heterogeneous sellar mass with suprasellar extension measuring 3.4 x 2.3 x 2.1 cm abuting the optic chiasm without displacement. Biochemical workup revealed panhypopituitarism with secondary adrenal insufficiency ACTH < 1.5 pg/mL (7.2-63.3) and cortisol 3.63 ug/dL (3.70-19.40); secondary hypothyroidism TSH 0.84 mIU/mL (0.27-4.20) and FT4 < 0.50 ng/dL (0.70-14.8); growth hormone deficiency with low IGF-1 23 ng/mL (65-216); secondary hypogonadism FSH < 1 mIU/mL (46-177), LH < 1 mIU/mL (7.7-59) and estrone < 6 pg/mL (0-125); with normal prolactin 14.1 ng/mL (4.8-23.3). Patient revealed she had been amenorrheic since 23 years old and conceived one child prior. Patient was transitioned to oral hydrocortisone 20 mg AM and 10 mg PM, and started on levothyroxine 50 mcg PO daily. No neurosurgical intervention was recommended. Subsequently, patient requested a second opinion and was transferred to a tertiary center. Conclusion: The link between hypoglycemia and hypopituitarism, may be attributed to hypocortisolism and growth hormone / IGF-1 deficiency. Intriguingly, this patient's initial clinical presentation centered around hypoglycemia, and further evaluation led to the identification of a sellar mass and new diagnosis of panhypopituitarism. This case demonstrates the need to include hypopituitarism in the differential when evaluating hypoglycemic patients. Presentation: 6/2/2024

7940 Insulinoma as a Rare Manifestation of MEN4

Abstract Disclosure: H. Han: None. J. Moalem: None. A.R. Shih: None. B.J. Gigliotti: None. Background/Objective: Multiple endocrine neoplasia 4 (MEN4) is a rare syndrome that is caused by germline mutations in CKDN1B. Its phenotypic expression is similar to multiple endocrine neoplasia 1 (MEN1). Manifestations include primary hyperparathyroidism (PHPT), pituitary adenomas, and pancreatic neuroendocrine tumors (NET). Prevalence of MEN4 is less than one per million. Case Report: A 55-year-old female with history of hypercalcemia presented with symptomatic hypoglycemia. She had a fasting plasma glucose of 41mg/dL, proinsulin of 84.3 pmol/L, insulin level of 24 uIU/mL, c-peptide of 5.2 ng/mL, and beta hydroxybutyrate level of 0.34 mmol/L, consistent with endogenous hyperinsulinism. She was incidentally noted to have PHPT. CT abdomen showed a 1.5 x 1.1 x 1.0 cm pancreatic lesion consistent with an insulinoma. Pathology from subsequent Whipple surgery showed that it was a well-differentiated neuroendocrine tumor with no metastasis. She became normoglycemic after surgery. Germline testing revealed a variant of unknown significance in CDKN1B (p.R93W). Discussion: Increasing evidence suggests that MEN4 exhibits subtle differences in penetrance and natural history compared to MEN1. A recent systemic review of MEN4 cases showed that most gastrointestinal NETs in MEN4 are non-functional NETs and gastrinomas; to date, no insulinomas have been reported. PHPT in MEN4 may exhibit a lower risk of recurrence after parathyroidectomy. This case highlights the importance of germline genetic testing when a patient presents with clinical manifestations of MEN1. Conclusion: This is the first reported case of insulinoma in MEN4. Presentation: 6/3/2024

6701 Bilateral Adrenal Hematomas As Initial Presenting Sign Of Lung Adenocarcinoma

Abstract Disclosure: S. Gumireddy: None. R. Panta: None. Y. Shaikh: None. Introduction: Lung cancer typically presents with dyspnea, chest pain, hemoptysis, weight loss, or recurrent pulmonary infections. This case illustrates primary lung adenocarcinoma presenting with abdominal pain and bilateral adrenal hematomas. Clinical Case: 51-year-old male presented to the emergency department with left sided abdominal pain persisting for one week. CT abdomen showed a left suprarenal mass measuring 4.5 x 5 x 4.3cm indicating an acute adrenal hematoma. An MRI showed a partially solid left adrenal lesion that had hemorrhaged and a 1.3cm hemorrhagic nodule in the right adrenal gland. The patient remained hemodynamically stable. Hormonal evaluation done while patient was in the hospital showed renin level 0.417ng/mL/hr, aldosterone level <1.0ng/dL, epinephrine level 312pg/mL, norepinephrine level 333pg/mL, cortisol 11.3, ACTH level 13, plasma metanephrine levels 93pg/mL, plasma normetanephrine levels 111.7pg/mL, DHEA-S 151mcg/dL, potassium 4.1mmol/L, raising concern for hypersecretion. Patient was discharged with plans for outpatient follow-up but was readmitted in two months due to worsening abdominal pain. Repeat imaging revealed an increase in size of adrenal lesions, measuring 3.3 x 3.6 cm within the right adrenal gland and a 6.7 x 6.3 cm heterogeneously enhancing lesion within the left adrenal gland concerning for metastatic disease to bilateral adrenals and to the ileum causing small bowel obstruction. Chest imaging showed a 2.2cm irregular right apical nodule. Subsequent hormonal evaluation showed normalization of plasma metanephrine levels at 15.8pg/mL, renin level 3.314ng/mL/hr, aldosterone level 4.3ng/dL, deoxycorticosterone level 4.8ng/dL, androstenedione level 40ng/dL, plasma normetanephrines 146.4pg/mL. The patient underwent left adrenal gland mass biopsy which showed metastatic poorly differentiated adenocarcinoma of pulmonary origin. Tumor cells were positive for keratin cocktail, TTF1 and synaptophysin supporting the morphologic interpretation. Patient is currently receiving treatment with carboplatin, pemetrexed, and pembrolizumab. Conclusion: Adrenal masses can be unilateral (85%) or bilateral (15%). While most unilateral adrenal masses are benign and nonfunctional, bilateral adrenal masses are likely to be metastatic disease, hemorrhage, infiltrative disease, congenital adrenal hyperplasia, macronodular Cushing’s syndrome, or bilateral cortical adenomas. Although uncommon, our case highlights the importance of considering metastatic disease to the adrenal glands as a potential initial manifestation of primary cancers. The most likely primary cancers to metastasize to the adrenal glands are breast, lung, colon, kidney, and esophagus. Presentation: 6/1/2024

7491 Post operative Euglycemic Diabetic Ketoacidosis in Type 2 Diabetic patient - A diagnostic challenge

Abstract Disclosure: S. Azmat: None. O. Lodhi: None. H. Ashok: None. M.F. Siddiqui: None. Euglycemic Diabetic Ketoacidosis (EDKA) is a rare but potentially fatal condition that is often difficult to diagnose as underlying ketoacidosis is masked by euglycemia. The diagnosis and management of this condition requires a swift and comprehensive approach to avoid delay. We report a case of 66-year-old female with Insulin-dependent Type 2 DM who developed postoperative euglycemic diabetic ketoacidosis, highlighting the significance of maintaining a high degree of suspicion for EDKA in postoperative patients, whose surgical course may obscure the underlying diabetic ketoacidosis symptoms. Clinical Case: A 66-year-old female with past medical history of Insulin dependent Type 2 DM presented to the emergency department with severe epigastric pain. CT Abdomen revealed perforated gastric ulcer with pneumoperitoneum requiring urgent laparoscopic graham patch repair. Patient’s outpatient medications include Lantus and metformin. She had mild hyperglycemia on admission with blood glucose of 176 mg/dL (140-160mg/dL) without metabolic abnormality. Insulin administration was omitted due to pre and post operative normoglycemia. The patient was NPO followed by initiation of nasogastric tube feeds. Postoperative course was complicated by hypotension, generalized abdominal discomfort and anion gap metabolic acidosis. Graham patch failure, abdominal infection, and post-surgical complications were systematically ruled out. Patient continued to decline with worsening anion gap metabolic acidosis; pH of 7.18 (7.35-7.45), HCO3 < 10 mEq/L (21 mEq/L - 31 mEq/L), anion gap15 mmol/L (8 to 12 mmol/L), blood sugar (147-208 mg/dl). There was no lactic acidosis or renal impairment. Beta hydroxybutyrate levels were elevated at > 4.5 mmol/L. Thus diagnosis of euglycemic DKA was established and treated with insulin drip per DKA protocol and dextrose fluids. EDKA resolved within five days with clinical improvement. She was transitioned to subcutaneous basal bolus insulin. She remained euglycemic and and had good surgical outcomes.Discussion: Euglycemic DKA is rare with only 2.6% to 3.2% of DKA, presenting as euglycemic. It presents as unique diagnostic challenge due to atypical DKA presentation with blood glucose less than 250 mg/dL. The primary driver for EDKA is either a reduction in hepatic glucose production at times of fasting or the overabundance of counter-regulatory hormones resulting in excess glucosuria. Literature has reported the effects short-term fasting on developing EDKA and starvation induced ketosis secondary to extreme ketogenic diets or bariatric surgery primarily among Type 1 diabetics. Clinically patients may exhibit symptoms similar to classic DKA, however, this classic picture may be confounded in a critically ill post-surgical patient, thus delaying recognition. This emphasizes the importance of including EDKA in differentials while evaluating such patients. Presentation: 6/1/2024

8479 A Challenging Case of Hypercortisolism in an Adult Patient With McCune Albright Syndrome

Abstract Disclosure: P. Kesavan Chary: None. S. Jasim: None. Background: McCune Albright Syndrome (MAS) is a rare genetic disorder that occurs due to a spontaneous post-zygotic missense mutation in the GNAS gene resulting in activating gain of function mutations in G-proteins. MAS classically presents as a triad of café-au-lait skin pigmentation, fibrous dysplasia of bone, and precocious puberty. However, continuous autonomous stimulation of endocrine glands can also result in various other endocrinopathies. We present a rare case of hypercortisolism due to bilateral multinodular adrenal hyperplasia (BMAH) in an adult patient with MAS. Case Report: A 38 year old female had MAS, clinically manifested by precocious puberty, renal phosphate wasting with rickets and osteomalacia, fibrous dysplasia of bone with history of multiple fractures, growth hormone excess, and multinodular thyroid status-post total thyroidectomy. A surveillance CT abdomen showed bilateral (right 3.8 x 1.3 cm and left 1.0 x 0.9 cm) adrenal adenomas with low intrinsic attenuation and washout. On diagnosis, the patient had an AM cortisol of 32.5 ug/dL (6.2-19.4 ug/dL) after a low-dose dexamethasone suppression test (DST), and an AM cortisol of 27.3 ug/dL after a high-dose DST. Late night salivary cortisol was 0.518 ug/dL (<0.010-0.090 ug/dL), 24-hour urine cortisol was 78 ug/24hrs (6-42 ug/24hrs), and ACTH was <1.5 pg/mL (7.2-63.3 pg/mL). The patient was initially asymptomatic and monitored for a few months, but subsequently developed easy bruising, recurrent skin infections, and irritability. The patient declined surgical intervention and was initiated on Osilodrostat. Shortly after medication initiation, she was hospitalized for perforated diverticulitis, hypokalemia, and hypomagnesemia. During hospitalization, AM Cortisol was 49 mcg/dL (4.8-19.5 mcg/dL) and 24-hour urine cortisol was 1023 mcg/24hrs (normal range 3.5-45 mcg/24hrs; the patient’s level prior to admission was 170-190 mcg/24hrs). Osilodrostat was held and the patient was initiated on Etomidate infusion. Once plasma cortisol levels normalized, she resumed Osilodrostat prior to discharge. The patient subsequently tried multiple medical therapy options before undergoing a bilateral adrenalectomy as a definitive treatment choice. Conclusion: The gain of function mutations in MAS result in autonomous endocrine gland function that can manifest clinically as various endocrinopathies. While the most common endocrinopathies in MAS are precocious puberty, hyperthyroidism, and pituitary dysfunction, active surveillance is critical to monitor for less common presentations such as hypercortisolism. This is the first report of adrenal Cushing’s in an adult patient with MAS. Presentation: 6/3/2024

Interesting Case Of Congenital Tuberculosis

Background: Mycobacterium tuberculosis (TB) is a global public health problem and is the causative organism of TB. There were 234,000 deaths of children due to tuberculosis. Since most of the pregnant women who have active TB are symptomless, diagnosis of TB is usually delayed2,3. It is difficult to differentiate between true congenital TB and postnatally acquired TB. High suspicion is needed for early diagnosis and treatment. Case: A 30-day-old girl had abdominal distension 1 week before admission and refusal to feed appeared on the 30th day. Clinically, sepsis, TORCH infection was suspected. USG abdomen showed multiple hypoechoic lesions in liver. Ct chest and abdomen showed multiple discrete non-calcified nodules in bilateral lung fields and liver. Gastric aspirate for AFB was negative. Mother was screened for TB; the TSTwas positive and TB QuantiFERON gold came positive. Hence, Tru-cut Liver biopsy was done for neonate and Biopsy for Genexpert showed low level Mycobacterium TB detected. Cerebrospinal fluid analysis for acid-fast bacilli was negative. 4 drug ATT regimen was started. Two weeks after anti-TB medication, the distension completely disappeared. Conclusion: Early diagnosis and treatment is the key for the survival of neonatal TB

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

Impacts of participation in surgical clinical trial on safety and survival outcomes in patients with right-sided colon cancer

Objective: To explore the impact on safety and prognosis in patients with right-sided colon cancer participating in surgical clinical research. Methods: This retrospective cohort study utilized data from a randomized controlled trial (RELARC study) conducted by the colorectal surgery group at Peking Union Medical College Hospital in which laparoscopic complete mesocolic excision (CME) was compared with D2 radical resection for the management of right-sided colon cancer. The eligibility criteria were age 18-75 years, biopsy-proven colon adenocarcinoma, tumor located between the cecum and right 1/3 of the transverse colon, enhanced chest, abdomen, and pelvic CT scans suggesting tumor stage T2-T4N0M0 or TanyN+ M0, and having undergone radical surgical treatment from January 2016 to December 2019. Exclusion factors included multiple primary colorectal cancers, preoperative stage T1N0 or enlarged central lymph nodes, tumor involving surrounding organs requiring their resection, definite distant metastasis or otherwise unable to undergo R0 resection, history of any other malignant tumors within previous 5 years, intestinal obstruction, perforation, or gastrointestinal bleeding requiring emergency surgery, and assessed as unsuitable for laparoscopic surgery. Patients who had participated in the RELARC study were included in the RELARC group, whereas those who met the inclusion criteria but refused to participate in the RELAEC study were included in the control group. The main indicators studied were the patient's baseline data, surgery and perioperative conditions, pathological characteristics, adjuvant treatment, and postoperative follow-up (including average frequency of follow-up within the first 3 years) and survival (including 3-year disease-free survival rate (DFS) and 3-year overall survival rate (OS). Differences in these indicators between the RELARC and control groups were compared. Results: The study cohort comprised 290 patients, 173 in the RELARC group (RELARC-CME group, 82; RELARC-D2 group, 91) and 117 in the control group (CME control group, 72; D2 control group, 45). There was a significantly higher proportion of overweight patients (BMI ≥24 kg/m2) in the RELARC-CME than in the CME control group (67.1% [55/82] vs. 33.3% [24/72], χ2=17.469, P<0.001). There were no other statistically significant differences in baseline characteristics (all P>0.05). No significant disparities were found between the CME and D2 groups in terms of operation duration, intraoperative blood loss, rate of conversion to open surgery, combined organ resection, intraoperative blood transfusion, or intraoperative complications (all P>0.05). There was a trend toward Clavien-Dindo grade II or higher postoperative complications in the RELARC-CME group (24.4% [20/82]) than in the CME control group (18.1% [13/72]); however, this difference was not statistically significant (χ2=0.914, P=0.339). Similarly, the difference in this rate did not differ significantly between the RELARC-D2 group (25.3% [23/91]) and D2 control group (24.4% [11/45], χ2=0.011, P=0.916). The median duration of postoperative follow-up was significantly shorter in the RELARC groups than in the corresponding control groups. Specifically, the median duration of follow-up was 4.5 (4.5, 4.5) months in the RELARC-CME and 7.2 (6.0, 9.0) months in the CME control group (Z=-10.608, P<0.001). Similarly, the median duration of follow-up was 4.5 (4.5, 4.5) months in the RELARC-D2 group as opposed to 8.3 (6.6, 9.0) months in the D2 control group (Z=-10.595, P<0.001). The 3-year DFS rate (91.5%) and OS rate (96.3%) tended to be higher in the RELARC-CME group than in the CME control group (84.7% and 90.3%, respectively). The 3-year DFS rate (87.9%) and OS rate (96.7%) tended to be higher in the RELARC-D2 group than in the D2 control group (81.8% and 88.6%, respectively); however, these differences were not statistically significant (all P>0.05). Subgroup analysis according to pathological stage revealed that patients in the RELARC-D2 group with pN0 stage achieved a significantly superior 3-year OS rate than did those in the D2 control group (100% vs. 88.9%, P=0.008). We identified no statistically significant differences in survival rates between the remaining subgroups (all P>0.05). Conclusions: A high-quality surgical clinical trial with close follow-up can achieve perioperative safety and a trend toward improved survival outcomes.

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...

Rib Fractures in Trauma Patients: Prevalence, Associated Injuries, and Mortality Trends.

Introduction Rib fractures are a common consequence of thoracic trauma, often signaling the presence of additional injuries and increasing the risk of mortality. This study aimed to elucidate the frequency, patterns, and mortality rates associated with rib fractures in multitrauma patients and to explore the association between rib fractures and other systemic injuries. Methods In a retrospective observational study at a tertiary care hospital, electronic medical records of multi-trauma patients over a four-year period were examined. Inclusion criteria encompassed adult patients who had undergone whole-body or chest and abdomen CT imaging. The study evaluated the incidence and location of rib fractures, associated thoracic and intra-abdominal injuries, and the in-hospital mortality rate. Results Among the 1,338 patients analyzed, rib fractures were identified in 273 (20.4%), with a median age of 33 years and 199 (72.9%) were male. Motor vehicle accidents were the most common trauma mechanism with a rate of 52% (n=142). Patients with rib fractures had significantly higher occurrences of pneumothorax (25.3%), hemothorax (20.9%), and intra-abdominal injuries (17.5%) (p<0.001). Notably, patients with six or more rib fractures exhibited a higher frequency of liver, spleen, and kidney injuries (p=0.003, p=0.011, p=0.001, respectively). The in-hospital mortality rate was 5.9% (n=17) for patients with rib fractures, significantly higher than those without (p<0.001). Conclusion Rib fractures in multi-trauma patients are an important indicator of severe concurrent injuries and are associated with a higher mortality rate. These findings advocate for a systemic and immediate evaluation of patients with rib fractures upon presentation in emergency departments to improve survival outcomes.