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Introduction Sustained or proximal hypertension is the most common sign of pheochromocytoma, but approximately 5-15% of pts present with normal blood pressure. We report a case of a patient incidentally found to have a catecholamines secreting adrenal tumor, but was normotensive on admission. Case 30-year-old morbidly obese woman incidentally found to have a 4.8 cm left adrenal gland mass while being worked up for sepsis secondary to atypical pneumonia. Initially, the patient presented with dyspnea, chest pain, palpitation, nausea, and vomiting. Her past medical history is significant for preeclampsia, 200 lb wt loss in 1 year, NSTMI a few months prior to admission discharged on dual antiplatelet and metoprolol which she couldn't tolerate due to hypotensive episodes. On arrival to the ED the patient was afebrile, normotensive SBP 90-110 DBP 57-70 mmHg, HR 86 BPM, RR 20, saturating 98% on room air. Her laboratory workup was significant for leukocytosis, elevated D-dimer, hyperkalemia 5.9 mmol/L, mildly elevated liver enzymes, and mildly elevated troponin. MRI abdomen 4.8×4.4×5. 0 cm complex enhancing mass with eccentric necrosis and/or fibrosis arising from the left adrenal gland. Ur Normetanephrine 5867 mcg/24h, Ur Metanephrine 3017 Mcg/24hr, urine dopamine and norepinephrine were within normal limits. Serum Metanephrine 2.64 nmol/L normetanephrine 13.50 nmol/L, aldosterone, renin, and cortisol levels were normal. Discussion Sustained or proximal hypertension is the most common sign of pheochromocytoma, but approximately 5-15% of pts present with normal blood pressure. Other signs and symptoms that may occur include orthostatic hypotension, visual blurring, papilledema, weight loss, polyuria, polydipsia, constipation, increased ESR, insulin resistance, hyperglycemia, leukocytosis, psychiatric disorders, and, rarely, secondary erythrocytosis due to overproduction of erythropoietin. The beta-adrenergic blocker should never be started first because a blockade of vasodilatory peripheral beta-adrenergic receptors with unopposed alpha-adrenergic receptor stimulation can lead to a further elevation in blood pressure. Our patient was normotensive throughout the hospitalization, and before admission was on metoprolol for NSTMI, however, she was unable to tolerate it due to hypotensive episodes. Conclusion Most patients with pheochromocytoma present with hypertension, however, few cases could present with normotension or even hypotension. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

INTRODUCTION: Calcium channel blocker (CCB) is a significant drug exposure reported to the American Association of Poison centers (1). Medical care of patients poisoned with CCBs can be complex as profound bradycardia and hypotension might be challenging to control, with insufficient evidence on which medical therapy is best (2). Calcium channel blockers directly block calcium L-type channels in the heart and blood vessels leading to hypotension and circulatory collapse in overdose cases. Dihydropyridines are generally less notorious for causing bradycardia than non-dihydropyridine. Amlodipine has a relatively long half-life, and therefore toxicity with amlodipine tends to cause prolonged circulatory collapse (3).This case was particularly challenging since calcium channel blockers were combined with three additional medications, including a benzodiazepine and a GABA receptor agonist (zolpidem). This combination made cardiopulmonary collapse an inevitable consequence.CASE PRESENTATION: A 32-year-old man presented to the emergency department in a stable clinical condition about an hour after intentionally ingesting a total of 300 mg of amlodipine, 1500 mg of bupropion, 3 mg alprazolam, and an unknown amount of zolpidem in a suicidal attempt. Soon after arriving at the emergency room, he started to have slurred speech, and his blood pressure started dropping-treatment initiated with activated charcoal. Subsequently, the patient became more lethargic, requiring emergent sedation, intubation, and mechanical ventilation for airway protection. Additional treatments included hyperinsulinemia euglycemia treatment (HIET), calcium gluconate, sodium bicarbonate, and lipid emulsion.The patient quickly became hemodynamically unstable with a refractory distributive shock requiring high doses of four different vasopressors (norepinephrine, vasopressin, phenylephrine, and epinephrine). Initial laboratory results showed metabolic acidosis (pH of 7.14). Complete blood count and chemistry were unremarkable. Chest x-ray, electrocardiogram, and echocardiogram were essentially normal. After stabilization in the intensive care unit, all vasopressors were successfully weaned off, and the patient was extubated on day 4 of admission. He was transferred out to an inpatient psychiatric unit on day 8 of admission.DISCUSSION: Aside from the initial therapy with intravenous fluids and atropine for bradycardia, there is no agreed-upon algorithms for CCBs toxicity treatment.Hyperinsulinemia euglycemia treatment (HIET) was originally shown to improve survival in dogs poisoned with verapamil in a controlled environment.CONCLUSIONS: Management of calcium channel blocker toxicity is based on maintaining adequate circulation with the use of IV fluids, vasopressors, calcium, high-dose insulin, glucagon, and other therapies that have been documented.

Introduction: Although reported in previous literature, Rhabdomyolysis due to hypothyroidism,without an obvious precipitating factor, is rare. We report a case of severe hypothyroidism leading torhabdomyolysis. Case Report: A 70-year-old man with a history of progressive weakness, myalgia x1 month, statinallergy, pancreatic adenocarcinoma, metastatic melanoma, and acquired hypothyroidism afterreceiving Pembrolizumab for 6 months. He was non-adherent to the levothyroxine, prescribed 1month before hospitalization. He presented to the ED after slipping from his bed onto the floor in aseating position and being unable to get up due to his weakness. Initially, he was afebrile, hypoxic,tachypneic, tachycardic, hypotensive, lethargic, oriented x2, and had a global muscular weakness. Labs were significant for CK of 10,180 (n < 166 IU/L), TSH 136.18(n 0.34-5.6 mU/L), FT4 < 0.25 (n0.6-1.10 ng/dl), FT3 1.4 (n 2.5-3.9 Pg/ml), AKI, leukocytosis, abnormal electrolytes and LFTs. IV fluidsand antibiotics failed to improve the patient’s clinical status in 48 hours. He was started on IVthyroxine and stress steroids with improved weakness and overall clinical picture. Discussion: 4.6 % of people have hypothyroidism per the United States National Health andNutrition Examination Survey. Rhabdomyolysis is defined as the rapid breakdown of skeletal muscle,which may also develop due to hypothyroidism. Most patients with hypothyroidism who developrhabdomyolysis are found to have a clear precipitating risk factor, such as the use of statins orstrenuous exercise. Still, none of these risk factors were present in this case. Our patient acquiredhypothyroidism after a few months of receiving Immunotherapy. It is reported that hypothyroidismoccurs in (9% to 18%) of patients receiving Pembrolizumab. Although the patient was prescribedthyroid replacement therapy, he was not adherent to the medication for 1 month prior topresentation. Although mechanical injury is reported to cause elevated CK levels, mostrhabdomyolysis cases are related to crush injuries. We believe that the fall was probably related tohis progressive generalized weakness due to his noncompliance with medical therapy leading tomyxedema coma and rhabdomyolysis. Conclusion: Screening for hypothyroidism in patients with elevated muscle enzymes should behighly considered since an early diagnosis. Prompt treatment of hypothyroidism is essential toprevent rhabdomyolysis and its consequence.

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