Electrolyte Repletion Research Articles

12201 Ketogenic-diet As A Trigger Of First Episode Diabetic Ketoacidosis In A Woman Living With Type 1 Diabetes Mellitus

Abstract Disclosure: M.E. Chacon Cruz: None. A.N. Gonzalez Bossolo: None. G.J. Mora Osoria: None. A number of dietary patterns have been proposed as an effective method for weight reduction. A keto diet is a strict low-carbohydrate and high-fat diet. The reduction in carbohydrates enables the body to rely on fat as a predominant energy source leading to a state of ketosis. However, a serious but rare complication of the ketogenic diet is ketoacidosis associated with low carbohydrate intake, which should be cautiously monitored in people with a predisposition to the condition, such patient with diabetes mellitus type 1. We report the case of a female patient living with type 1 diabetes mellitus female who developed her first episodes of diabetic ketoacidosis (DKA) as the following the course of ketogenic diet. A 53 y/o Female patient with past medical history diabetes mellitus type 1 and pernicious anemia went emergency department complaining pelvic pain associated with weakness, nausea and vomiting for about 1 day of evolution. Patient also refers that during the past 2 weeks she has been doing a detox and taking some herbal and tea. Other physical examinations were unremarkable except for moderate dehydration. The initial testing revealed patients meet criteria for severe diabetes ketoacidosis (DKA) with a pH: 7.04, CO2 15, serum central bicarbonate in 6 mmol/L and elevated blood glucose in 504 mg/dl and positive urine and serum ketones, C-Peptide less than 0.02 ng/ml. and glycosylated hemoglobin in 8.25%. She was admitted to the intensive care unit and treated with intravenous saline, intravenous insulin infusion, and electrolyte repletion. Blood glucose levels and metabolic acidosis improved. After DKA resolved patient refers that week started with Keto-diet and was restricting carbohydrates. Patient was discharge home with multiple injection insulin and followed by Endocrinologist services in the external clinic for a follow up. This case illustrates the challenges and the importance of dietary history providing clues to the diagnosis. If we had never asked her about her diet, we would not have found the reason that brought her to the DKA. This case demonstrates the development of DKA following ketogenic diet in a patient with type 1 diabetes. It is important for physicians to be aware of this rare potential complication of ketogenic diet which is infrequently reported in literature. Therefore, physicians should be cognizant of the complications and risks, and benefits of the ketogenic diet. Risks and benefits of the ketogenic diet should be discussed with patients before initiation of this diet. The patient was followed in an outpatient clinic with Endocrinologist service for evaluation for an insulin pump. Presentation: 6/1/2024

Hypophosphatemia correction reduces ICANS incidence and duration in CAR T-cell therapy: a pooled clinical trial analysis.

A common complication of chimeric antigen receptor (CAR)-T cell therapy is immune effector cell associated neurotoxicity syndrome (ICANS), which presents with encephalopathy, aphasia, inattention, somnolence, seizures, weakness, or cerebral edema. Despite its significant morbidity, there are currently no effective targeted treatments. Given the clinical similarities between ICANS and the neurological manifestations of acute hypophosphatemia, we retrospectively reviewed 499 patients treated with CD19-targeted CAR-T cell therapy across multiple clinical trials between 2015 and 2020. In addition to clinical toxicities experienced by the patients, we also interrogated the impact of serum electrolyte data and repletion of corresponding electrolyte deficiencies with ICANS incidence, severity, and duration. Hypophosphatemia was a common occurrence in CAR T-cell recipients, and the only electrolyte derangement associated with a significantly higher cumulative incidence of ICANS. Moreover, phosphorus repletion in hypophosphatemic patients was associated with significantly decreased ICANS incidence and duration. Hypophosphatemia was uniquely associated with encephalopathy neurological adverse events, which also showed the strongest positive correlation with both ICANS and CRS severity. These findings suggest that serum phosphorus could be a reliable biomarker for ICANS, and expeditious, goal-directed phosphorus repletion in response to serum hypophosphatemia could be a safe, inexpensive, and widely available intervention for such patients.

Electrolyte Disturbances and Repletion in Orthopaedic and Spine Surgery Patients.

Electrolyte derangement, defined as disorders of clinically impactful physiologic ions such as potassium, sodium, calcium, magnesium, and phosphate, has a variety of clinical manifestations. These electrolytes have narrow windows of normal in vivo concentration before neurologic, cardiac, renal, or gastrointestinal consequences occur. Perioperative disturbances in electrolyte concentration can lead to increased morbidity and mortality, longer length of stay, and higher rates of short and medium-term readmission in orthopaedic and spine surgery postoperatively. To prevent electrolyte related complications, careful monitoring and repletion of at-risk patients must be undertaken. A systematic approach to repletion allows for a safe and efficacious treatment of these disorders.

Association of Physicians of India Expert Recommendations on Oral Fluid, Electrolytes, and Energy Management during Transition Care and Discharge for Hospitalized Patients with Nondiarrheal Illnesses.

Acute nondiarrheal illnesses (NDIs) involve overt or subclinical dehydration, requiring rehydration and electrolyte repletion. Dehydration is frequently under-recognized and under-managed, both in outpatient departments (OPDs) and inpatient departments (IPDs). Postadmission dehydration is associated with longer hospital stays and higher inhospital mortality rates. Recognizing and understanding dehydration in hospitalized patients is necessary due to the adverse outcomes associated with this condition. In this article, we aimed to develop practical consensus recommendations on the role of oral fluid, electrolyte, and energy (FEE) management in hospitalized patients with FEE deficits in NDI. The modified Delphi consensus methodology was utilized to reach a consensus. A scientific committee comprising eight experts from India formed the panel. Relevant clinical questions within three major domains were formulated for presentation and discussion: (1) burden and factors contributing to dehydration in hospitalized patients; (2) assessment of fluid and electrolyte losses and increased energy requirements in hospitalized patients; and (3) management of FEE deficits in hospitalized patients [at admission, during intravenous (IV) therapy, IV to oral de-escalation, and discharge]. The consensus level was classified into agreement (mean score ≥4), no consensus (mean score <4), and exclusion (mean score <4 after the third round of discussion). The questions that lacked agreement were discussed during the virtual meeting. The experts agreed that the most common factors contributing to dehydration in patients with NDI hospitalized in IPDs include decreased oral fluid intake, increased fluid loss due to the illness, insensible fluid loss, and a lack of awareness among doctors about dehydration, which can result in poor fluid intake. Time constraints, discontinuity of care, lack of awareness of the principles of fluid balance, lack of formal procedures for enforcing hydration schemes, and lack of adequate training are most often barriers to the assessment of hydration status in hospital settings. Experts used hydration biomarkers, such as changes in body weight, serum, or plasma osmolality; fluid intake; and fluid balance charts; along with urine output, frequency, quantity, and color, to determine hydration status in hospital settings. Experts agreed that appropriate FEE supplementation in the form of ready-to-drink (RTD) fluids can restore FEE deficits and shorten the length of hospital stays in hospitalized patients at admission, during de-escalation from IV to oral therapy, and at discharge. RTD electrolyte solutions with known concentrations of electrolytes and energy are good choices to avoid taste fatigue and replenish FEE in hospitalized patients during transition care and at discharge.

Profound Alkalosis and Prolonged QT Interval Due to Inappropriate Gastrostomy Tube Loss: A Case Report.

Severe metabolic alkaloses are relatively rare but can carry a high mortality rate. Treatment involves supportive care and treatment of underlying causes. A 55-year-old male dependent on a gastrojejunostomy tube presented to the emergency department for altered mental status. The patient had metabolic alkalosis, electrolyte abnormalities, and prolonged QT interval on electrocardiogram. Examination and history revealed that chronic drainage of gastric fluid via malfunctioning a gastrojejunostomy tube resulted in profound alkalosis. The patient recovered with supportive care, electrolyte repletion, and gastrojejunostomy tube replacement. This case highlights the importance of gastrointestinal acid-base pathophysiology.

Inpatient Management of Hyperemesis Gravidarum.

Hyperemesis gravidarum has a reported incidence of approximately 0.3-3% of pregnancies. Without treatment, refractory hyperemesis gravidarum can result in dehydration, electrolyte deficiencies, and severe nutritional deficiencies, resulting in significant maternal morbidity. The overall goals of inpatient management of refractory hyperemesis gravidarum are the resumption of oral intake to an adequate level to maintain hydration and nutrition, including the ability to tolerate oral pharmacotherapy. Patients initially are stabilized with rehydration and electrolyte repletion. There are numerous pharmacotherapeutics available that can be administered intravenously to control symptoms when oral intake is not an option. However, despite maximizing typical antiemetics, there will be cases refractory to these medications, and alternative pharmacotherapeutics and nutrition-support modalities must be considered. Mirtazapine, olanzapine, corticosteroids, and gabapentin are examples of alternative pharmacotherapeutics, and enteral and parenteral nutrition are alternative therapies that can be used when oral intake is not tolerated for prolonged time periods with ongoing weight loss. In refractory cases of hyperemesis gravidarum, the risks and benefits of these alternative forms of management must be considered, along with the risks of undertreated hyperemesis gravidarum and the overall effect of hyperemesis gravidarum on patients' quality of life.

SGLT2 Inhibitors and Perioperative Euglycemic Diabetic Ketoacidosis

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of diabetes medications that act at the level of the kidney to increase renal glucose clearance. The resultant hypoglycemia suppresses insulin secretion and stimulates glucagon, lipolysis, and ketogenesis, which creates a state of starvation. Since SGLT2 inhibitors also decrease sodium reabsorption, patients are at risk for dehydration. An unusual side effect of this drug class is the development of euglycemic diabetic ketoacidosis (eDKA). A case report describes a patient taking Synjardy® (empagliflozin/metformin) who underwent laparoscopic cholecystectomy and developed perioperative eDKA. It is critical to maintain a high index of suspicion to recognize eDKA and institute immediate therapy tenants of intravenous fluid hydration, insulin infusion, and aggressive electrolyte repletion.

Evaluating the utility of perioperative laboratory tests in primary shoulder arthroplasty

BackgroundThe rising incidence of primary total shoulder arthroplasty (TSA) predicts a $4 billion increase in cost associated with this procedure by 2030. Studies have evaluated sources of cost containment, including inpatient services, namely routine perioperative laboratory tests. This study evaluates the utility of routine perioperative complete blood count (CBC) and basic metabolic panel (BMP) in TSA and identifies predictors of abnormal postoperative laboratory results and the need for medical intervention (NMI). MethodsAll patients undergoing primary TSA from 2013 to 2020 at a single institution were included. Demographics, comorbidities, procedural details, and preoperative and postoperative CBC and BMP values were recorded. Abnormal values were identified for each laboratory parameter. NMI was defined as postoperative blood transfusion, electrolyte repletion, fluid resuscitation, and inpatient medical consultation. Univariate and multivariate analyses were performed to determine independent predictors for abnormal postoperative CBC and BMP (AbBMP) results and NMI. A P value < .05 was considered statistically significant. ResultsA total of 328 patients were included in the study, with 202 (61.6%) female patients and a median age of 70.5 years. Medical intervention was required in 115 (35.1%). There were no differences in rates of NMI based on patient demographics, comorbidities, and preoperative CBC and BMP results, although there was a significant difference in rates of NMI when comparing postoperative serum potassium (4.1 mmol/L in no NMI group; 3.9 mmol/L in NMI group; P = .039). Ultimately, there were no demographic, surgical, or laboratory factors associated with postoperative NMI on predictive modeling. Increasing body mass index (odds ratio [OR] 1.08, 95% confidence interval [CI] 1.01-1.15, P < .03), preoperative serum glucose (OR 1.05, 95% CI 1.02-1.08, P = .003), and preoperative serum blood urea nitrogen (OR 1.12, 95% CI 1.05-1.12, P = .01) are associated with an 8.0%, 5.0%, and 12% increase in odds of an AbBMP, respectively. Preoperative potassium is inversely correlated with odds of AbBMP (OR 0.19, 95% CI 0.05-0.67, P = .01). ConclusionsAlthough postoperative laboratory tests were routinely obtained following primary shoulder arthroplasty, abnormal postoperative CBC and BMP were not associated with NMI. Postoperative BMP tests should be considered in patients with elevated body mass index, elevated preoperative serum glucose, elevated preoperative serum blood urea nitrogen, and those with preoperative serum hypokalemia. Postoperative CBC tests are likely not necessary after primary shoulder arthroplasty.

Rhabdomyolysis After Intravenous Iron Sucrose Infusion During Pregnancy.

Iron infusions have become increasingly common in the treatment of iron-deficiency anemia during pregnancy. Although iron infusions are generally well tolerated, adverse reactions have been reported. A pregnant patient was diagnosed with rhabdomyolysis after receiving a second dose of intravenous (IV) iron sucrose at 32 6/7 weeks of gestation. On admission to the hospital, creatine kinase was 2,437 units/L, sodium was 132 mEq/L, and potassium was 2.1 mEq/L. Intravenous fluids and electrolyte repletion were administered, with improvement of symptoms within 48 hours. Creatinine kinase normalized 1 week after hospital discharge. Rhabdomyolysis can be associated with IV iron infusion during pregnancy.

CE-454610-2 STEREOTACTIC ARRHYTHMIA RADIOABLATION IN VENTRICULAR FIBRILLATION WITH LEFT VENTRICULAR THROMBUS

Stereotactic arrhythmia radioablation (STAR) has been studied for management of refractory ventricular tachycardia (VT) that is not amenable to traditional catheter ablation. We present the case of a patient with recurrent ventricular tachycardia (VT) and left ventricular (LV) thrombus successfully treated with STAR therapy. A 48-year-old man with morbid obesity, paroxysmal atrial fibrillation and infarct related cardiomyopathy was admitted with late presentation of new anterolateral ST elevation myocardial infarction complicated by cardiogenic shock, managed with mechanical circulatory support. He was found to have a 3 x 2.7 cm thrombus in the LV apex (Panel A). He underwent successful percutaneous intervention to an acute left anterior descendinig coronary artery occlusion. During hospitalization, despite aggressive measures, he was noted to have polymorphic ventricular tachycardia (VT), triggered by premature ventricular contractions (PVCs) arising from his LV apical infarct (Panel B). He was treated with multiple antiarrhythmic medications (amiodarone, lidocaine) in addition to electrolyte repletion but unfortunately required repeated external defibrillation for PVC induced VF (Panel C). A dual chamber implantable cardioverter-defibrillator was placed and despite overdrive pacing, he suffered from recurrent life-threatening VT and ventricular fibrillation (VF) requiring additional defibrillation (Panel D). Because he was not a candidate for endocardial ablation, orthotopic heart transplantation, and was deemed too unstable for epicardial ablation, the decision was made to pursue STAR. Surface ECG and 4D computed tomography (Panel E) were used to localize the focus of the VT trigger. A single dose of 25 Gray of radiation was delivered to the LV apex. Our patient has been free of ventricular arrhythmias for 14 months. There has been no clinical evidence of early or late toxicity related to radiotherapy thus far. In challenging cases of PVC induced VT and VF not amenable to traditional therapies, such as our patient, STAR may offer a therapeutic option. Further studies are required.

428: A PERSISTENT CASE OF COVID-19 IN A PATIENT WITH COMPLETE DIGEORGE SYNDROME

Introduction: DiGeorge Syndrome is a relatively common microdeletion syndrome defined by a deletion in chromosome 22 at position 22q11.2 and clinically characterized by T-cell deficiency, unique facial features, congenital heart disease and hypocalcemia. Complete DiGeorge Syndrome refers to a subset that is athymic (< 1%) without any T cell function. The adaptive immune response is then disturbed leading to an increased susceptibility to infections given the lack of cytotoxic response to infected cells. In this population, pathogens can persist and have unique presentations due to the lack of an adaptive immune response. Description: We present a case of persistent COVID-19 in a 3-year-old male with complete DiGeorge syndrome. Two months prior to presentation, he was treated with remdesivir for a symptomatic COVID-19 infection. He later represented with severe persistent hypocalcemia despite aggressive IV electrolyte repletion as well as a new acute hemolytic anemia with positive Coombs and concern for Graft vs Host disease. During his hospital course, he had worsening respiratory status leading to re-intubation. Bronchoscopy with BAL showed significant SARS-CoV-2 viral load and he was started on a repeat course of remdesivir and convalescent plasma. Two weeks after initial bronchoscopy, repeat BAL samples showed unchanged SARS-CoV-2 viral load leading to another course of remdesivir and convalescent plasma. After a month of invasive ventilation, he was able to be successfully extubated and eventually discharged from the hospital, despite having persistently an elevated SARS-CoV-2 viral load and polymerase chain reaction testing positivity. Discussion: This case illustrates a unique situation of COVID-19 in a patient without an adaptive immune response due to complete DiGeorge Syndrome. This patient population is athymic without any T cell function leading to a lack of cytotoxic response and a susceptibility to infections due to the inability to clear infected cells. With COVID’s high mutation rate leading to multiple new strains, we present a case illustrating the possibility of new strain mutations developing due to persistent COVID in a patient with an inability to clear the viral infection.

PSAT220 Severe Vitamin D Deficiency and Hypocalcemia during Pregnancy Masquerading as Thyroid Storm

Abstract Background Hypocalcemic tetany in young female patients is a clinical entity that is well-described in literature. Here we present a potentially life-threatening case of hypocalcemia secondary to severe Vitamin D deficiency and hyperemesis gravidarum mimicking thyroid storm. Case Presentation A 22-year-old Caucasian woman at 21 weeks gestation was transferred to our hospital for suspected thyroid storm with TSH &amp;lt;0.01 mIU/L (0.05-5.7). She had no history of nor risk factors for thyroid disease and presented with severe agitation, hallucinations, and muscle spasms after weeks of vomiting and poor oral intake. In the ambulance her temperature was 106.6F (rectal) and she was tachycardic (216/minute). EKG revealed ventricular arrhythmia with QTc 532 ms. EMS interventions included unsuccessful cardioversion with 100J and 300mg IV amiodarone bolus. In the ED, serum calcium level was 5.9 mmol/L (8.4-10.2), albumin 2.8 g/dL (3.3-4.5), magnesium 1.0 mmol/L (1.7-2.3), potassium 3.1 mmol/L (3.5-4.8), lactic acid 9.5 mmol/L (0.5-2.2), Free T4 1.36 ng/dL (0.58-1.65), troponin 2.21 ng/ml (0.00-0.03), β-hcg 48,775 mIU/ml, CK 9960 U/L (0-188), AST 171 U/L (8-34), ALT 45 (0-24). She received IV calcium gluconate, aggressive IV hydration and electrolyte repletion. Free T3 was drawn prior to initiating empiric thyroid storm treatment (hydrocortisone, propylthiouracil) returned at 3.8 pmol/L (2.5-3.9). Thyroid storm was further ruled out with negative antibodies for TPO and TSI and ultrasound revealing normal-sized gland without nodules and with normal vascularity. Hydrocortisone and Thionamide therapy were discontinued. The patient had rapid improvement in mentation and vitals with continued hydration and electrolyte repletion. 25-hydroxy-Vitamin D level was undetectable and PTH 118 pg/mL (12-88), consistent with secondary hyperparathyroidism. Celiac disease was ruled out with negative tissue transglutaminase IgA and IgG. At her follow-up clinic visit, symptoms had resolved with calcium and Vitamin D supplementation. Discussion Though a common phenomenon in pregnant women, metabolic derangements due to hyperemesis gravidarum can be quite severe and/or life-threatening, as in our case. Literature search revealed an isolated case of hyperemesis gravidarum presenting with severe electrolyte derangement and subsequent paraparesis which resolved after vitamin D and calcium supplementation. Hyperthyroidism is typically associated with hypercalcemia in the Western population. This patient's presenting features of hyperpyrexia, malignant cardiac arrhythmia, hepatitis, and altered mentation were reminiscent of thyroid storm and could easily be attributed to such in a pregnant patient with suppressed TSH. This could lead to continued use of thionamide and further hepatic damage. Thus, it is prudent to consider hypocalcemia in the differential diagnosis of thyrotoxicosis-like presentation, particularly in pregnant patients. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP116 Proton Pump Inhibitor Induced Hypocalcemia - An Overlooked Cause

Abstract Hypocalcemia can be caused by hypoparathyroidism, vitamin D deficiency, GI disorders, or hypomagnesemia. Proton-pump inhibitors (PPIs) which are commonly used for acid reflux symptoms can cause hypomagnesemia leading to hypocalcemia. We report an interesting case of acute hypocalcemia caused by a proton pump inhibitor. A 78-year-old female with a past medical history of follicular thyroid cancer diagnosed in 2008, s/p total thyroidectomy in 2008 followed by radioactive iodine ablation in 2009, was sent to the ER in 2019 for acute hypocalcemia with a calcium level of 6.6 mg/dL found on outpatient labs. Notably, she had no previous history of post-surgical hypoparathyroidism or hypocalcemia after her surgery in 2008. Upon initial evaluation in the ER, she presented with mild numbness, tingling, and weakness preceded by a diarrheal illness. She had concomitant hypokalemia of 3.1 mmol/L and hypomagnesemia of 1. 0 mg/dL for which she received IV and oral electrolyte repletion. She was eventually discharged on oral calcium carbonate, calcitriol, and magnesium. During her outpatient follow up, repeat labs showed persistent hypomagnesemia and low intact parathyroid (PTH) levels. Upon further review of her medication list, she reported continued daily use of omeprazole for acid reflux symptoms for the previous two months prior to her hospitalization. Her magnesium levels remained persistently low despite high doses of replacement. Given her persistently low magnesium and PTH levels, omeprazole was discontinued and she remained on calcium, calcitriol, and magnesium supplementation. Her calcium, and intact PTH levels eventually recovered to normal range and magnesium levels improved. Calcitriol was discontinued. She remained on a low dose of magnesium supplementation. In this patient, the development of her acute hypocalcemia was unlikely related to her remote history of the post-surgical thyroidectomy which occurred eleven years prior. Proton pump inhibitor use is often overlooked when evaluating causes of hypocalcemia. PPIs impair gastrointestinal absorption of magnesium through altering the TRPM6/7 channel affinity of magnesium by decreasing intestinal luminal pH. As a downstream effect, the resulting acute hypomagnesemia is thought to decrease PTH secretion as well as cause PTH resistance, which in turn decreases absorption of calcium, both by the renal and gastrointestinal route. There have been published cases that suggest these electrolyte disturbances commonly occur in elderly women with chronic PPI use. Clinicians should be aware of the effects that PPIs may have on electrolyte abnormalities. As a result, it may be reasonable to monitor magnesium and calcium levels while on a proton pump inhibitor. Presentation: No date and time listed

ODP525 Thyrotoxic Periodic Paralysis

Abstract Thyrotoxic periodic paralysis manifests with painless muscle weakness, mostly in the proximal lower extremities. It is often precipitated byexercise, high carbohydrate meals, and occasionally fasting. Though most cases are hereditary, and affect Asian men disproportionately, some cases may occur sporadically. This thyrotoxicosis is most often attributable to Graves disease and patients typically have symptoms of thyrotoxicosis for months leading up to the episodes of paralysis. This is an 18-year-old Asian man with a history of Autism Spectrum Disorder who presents for evaluation of lower extremity weakness. He was seen two weeks prior for similar complaints. At that time, he had hypokalemia, hypomagnesemia, hypophosphatemia and was repleted and discharged home. The day prior to admission, he had pain in his bilateral posterior legs. On the morning of presentation, he could no longer ambulate which led him to present to the emergency room. Per his collateral, he had lost forty-five pounds in the last 6 months. He has not been tolerating oral food well with early satiety. He denies any diarrhea or constipation, fever/chills, or recent illness. He denies any family history of muscle disorders, thyroid disease, or any other autoimmune disease. He does not smoke tobacco, drink alcohol, or use any illicit substances. On physical exam, he is notably tachycardic to 120 bpm. He has thyromegaly but no palpable nodules. He has no exophthalmos on eye exam. On his neurologic exam, patient has 2/5 strength in his bilateral lower extremities. On laboratory evaluation, patient has fully suppressed TSH &amp;lt;0. 0015 mcunit/mL, free thyroxine of 3.43 ng/dL, total T3 of 463 ng/dL, TSI &amp;gt;40 IU/L, and TSH Receptor Antibody 31 IU/L. His potassium is low at 2.8 with a magnesium of 1.7. His thyroid ultrasound is without evidence of any nodules, has a homogenous parenchymal pattern, with increased vascularity diffusely. Patient is started on methimazole 20mg daily which is then increased to 20mg twice daily as well as propranolol 120mg daily, with plans for definitive therapy in the future. Though mechanism by which thyrotoxicosis can produce electrolyte abnormalities including hypokalemia leading to periodic paralysis is poorly understood, it is thought that thyroid hormone may increase tissue responsiveness to B-adrenergic stimulation like exercise or stress. This may lead to hyperpolarization of the muscle membrane and relative excitability. A variety of other factors play a role in the pathogenesis of thyrotoxic paralysis including insulin and testosterone through activation of the sodium potassium ATPase. Treatment for TPP includes aggressive electrolyte repletion, correction of the underlying cause with methimazole and propranolol-taking advantage of its beta adrenergic blocking ability, and often times planning for definitive therapy. Presentation: No date and time listed

ODP336 Nephrogenic Diabetes Insipidus and Fanconi Syndrome Induced by Ifosfamide in a Patient with Femur Osteosarcoma. A Case Report

Abstract Background Fanconi syndrome and diabetes insipidus are rare adverse effects of ifosfamide. They usually present with high cumulative doses of this medication. They are mainly related to type II proximal renal tubular dysfunction. These complications typically present with severe polydipsia and polyuria accompanied by glycosuria, proteinuria, and some electrolyte abnormalities including hypokalemia, hypophosphataemia, and non-anion gap metabolic acidosis. Clinical case: A 15-year-old male with, a diagnosis of metastatic osteoblastic osteosarcoma in the right distal treated with ifosfamide three years prior to this hospitalization, was admitted to the emergency department complaining of 3 episodes of vomiting, 6 days history of increase volume of the right lower limb and fever. On admission, blood pressure of 80/50 mm Hg, heart rate of 110 beats / minute, respiratory rate of 30 breaths / minute, axillary temperature of 38.3 ° C. It was evident phlogosis at level of the proximal third of the right lower limb. CBC revealed pancytopenia (WBC 5 x10 9 L, Hb 6.8 g/dL, platelets 25×10 3 /mm 3) and ABG and CMP were compatible with mild metabolic acidosis normal AG (pH 7.285, K 1.9 meq / L, Na 156 meq / L, lactate: 0.9 meq / L, HCO3: 17 meq / L). A diagnosis of sepsis was made and the patient was started on meropenem 2g IV every 8 hours, vancomycin 1 g IV every 12 hours, filgastrim 120 ug/daily and one unit of packed RBC. Patient improved after 5 days over the course of his hospitalization. However, on the 18 th day after his hospital admission, he developed a new episode of polyuria, associated with hypocalcemia (7 mg/dL), hypokalemia (2 mEq/L), hypomagnesemia (0.95 mg/dL), hypophosphatemia (0.9 mg/dL) and metabolic acidosis (pH 7.2, bicarbonate 15 mEq/L). Urine analysis revealed glucosuria and proteinuria. Desmopressin test did not showed increase urinary osmolarity thus nephrogenic diabetes insipidus and Fanconi syndrome were diagnosed due to the multiple laboratory abnormalities and sign/symptoms. Patient received electrolyte replacement and ifosfamide was stopped from his chemotherapy regimen. After this, patient recovers and he was discharge at 25 th day of his admission. Conclusion : Ifosfamide causes tubular cell dysfunction leading to both nephrogenic diabetes insipidus and Fanconi syndrome. These complications might event present several years after receiving this chemotherapeutic agent. Full electrolyte repletion and hydration are the gold standard for management The present case report emphasizes the importance of the prevention of nephrotoxicity associated with ifosfamide, since its presentation could increase poor outcomes in patients receiving chemotherapy regimens that include ifosfamide. Presentation: No date and time listed

S1973 A Rare Case of McKittrick Wheelock Syndrome

Introduction: McKittrick Wheelock Syndrome (MWS) is a rare disorder characterized by distal colorectal tumors, most commonly benign secretory villous adenoma leading to secretory diarrhea with electrolyte depletion syndrome. Patients present with volume depletion, severe electrolyte derangement, specifically hyponatremia and hypokalemia, along with acute kidney injury (AKI). We present a rare case of an elderly female with severe electrolyte derangement in setting of MWS. Case Description/Methods: A 71-year-old woman with history of 4 months of watery diarrhea, fatigue, and anorexia presented after a syncopal episode. Notable labs Na 114 mEq/L, K 2.2 mEq/L, WBC 23.5K, and Cr 2.91 mg/dL. Stool electrolytes resulted in Stool Osm Gap 48 mOsm/kg consistent with secretory diarrhea. Of note, patient was hospitalized 3 times in the past 2 months for hyponatremia, hypokalemia, and AKI requiring temporary dialysis secondary to profuse diarrhea. A colonoscopy revealed a large rectal polypoid lesion with pathology consistent with a tubulovillous adenoma (Figure). She had aggressive electrolyte and fluid repletion with a robot assisted abdominoperineal resection. Subsequently, noted to have resolution of her symptoms and complete electrolyte correction upon follow up (Table). Discussion: Villous adenomas, normally a benign condition, can present with a life-threatening electrolyte derangements and volume depletion which makes the ability to diagnose and adequately treat MWS critical. Patients typically have multiple admissions with watery or mucous diarrhea, nausea, and vomiting. Labs significant for hyponatremia, hypokalemia, AKI, and leukocytosis. The tumors are large and often past the splenic flexure and low in the rectum, therefore flexible sigmoidoscopy can be reliably used rather than colonoscopy, which often delays diagnosis due to patients’ inability to prep. Treatment includes aggressive fluid and electrolyte repletion until tumor can be surgically resected. Few case reports suggest using indomethacin or octreotide as a bridge to surgery or as medical management for patients who are not surgical candidates. However, patients who are managed medically have a mortality rate up to ∼61-100%. Surgical management to definitively resolve symptoms, although minimally invasive options are being explored. A high index of suspicion and a systematic approach is critical to diagnose and provide life-saving treatment for MWS patients. Table 1. - Electrolytes: Comparison of Initial Admission vs. Post-Surgical Resection Electrolytes Initial Admission Post-surgical Resection Na 114 137 K+ 2.2 4.8 Cl 79 106 Creatinine 2.91 1.06 Figure 1.: Large rectal polypoid lesion with pathology consistent with a tubulovillous adenoma.

Torsade de Pointes Due to Hypokalemia and Hypomagnesemia.

This scenario was developed to educate emergency medicine (EM) interns but can be used to educate medical students and junior residents. Torsade de Pointes (TdP) is a rare but potentially fatal arrythmia if not quickly diagnosed and properly treated. TdP is defined as a polymorphic ventricular tachycardia (VT) characterized by an oscillatory change in amplitude around an isoelectric line that is associated with a QTc prolongation on the electrocardiogram (ECG).1 It has been well described to predispose to ventricular fibrillation and arrhythmic death. QTc prolongation can be congenital or acquired. Between 1 in 2000 to 20,000 have the genetic mutation for QTc prolongation.1 Acquired QTc is most commonly drug related leading to electrolyte abnormalities. 2 Around 28% of cases of TdP are associated with hypokalemia and hypomagnesemia.2 Several European centers estimate 0.8 to 1.2 per million people per year are drug induced.1 Patients with TdP most commonly presents with syncope, palpitations, and dizziness.2 While 50% are asymptomatic, up to 10% of patients will present in cardiac arrest.1 It is imperative for EM physicians to be able to recognize TdP as it can quickly decompensate into a ventricular fibrillation and sudden death. These patients require management of electrolyte abnormalities, ventricular dysrhythmias, and cardiac death.2 This simulation case will demonstrate treatment strategies for TdP with electrolyte repletion, antiarrhythmics, and defibrillation. By the end of this simulation session, learners will be able to: 1) formulate appropriate work-up for altered mental status (AMS) 2) recognize hypokalemia and associated findings on ECG 3) address hypomagnesemia in a setting to hypokalemia 4) manage pulseless VT by following advanced cardiac life support (ACLS) 5) recognize and address TdP 6) provide care after return of spontaneous circulation (ROSC) 7) consult intensivist and admit to intensive care unit (ICU). This session was conducted using high-fidelity simulation, which was immediately followed by an in-depth debriefing session. Each session had three EM first-year residents and six observers. There was one simulation instructor running the session and one simulation technician who acted as a nurse. After the simulation and debriefing session was complete, an online survey was sent via surveymonkey.com to all the participants. The survey collected responses to the following questions: (1) was the case believable? (2) did the case have the right amount of complexity? (3) did the case help improve medical knowledge and patient care? (4) did the simulation environment gave a real-life experience? (5) did the debriefing session after simulation help improve knowledge? A Likert scale was used to collect the responses. This case was performed once a year for 2 years in a row. There was a total of 19 respondents from both years. One hundred percent of them either agreed or strongly agreed that the case was beneficial in learning and in improving medical knowledge and patient care. All of them found the post-session debrief to be very helpful. Two of them felt neutral about the case being realistic. This high-fidelity simulation was a realistic way of educating learners on how to manage hypokalemia and hypomagnesemia leading to TdP. Cost-effectiveness varies depending on what is available at individual simulation laboratories. Learners are forced to start with a broad differential for the patient who presents with AMS. As they manage the case, the patient quickly decompensates into a fatal arrhythmia due to electrolyte abnormalities. Learners enforced their knowledge on leading ACLS, intubation skills, and treating TdP with electrical conversion and electrolyte repletion. Hypokalemia, hypomagnesemia, torsades de pointes, altered mental status, medical simulation.

37-Year-Old Man With Headache and Nasal Congestion

37-Year-Old Man With Headache and Nasal Congestion

39-Year-Old Woman With Severe Weakness

39-Year-Old Woman With Severe Weakness

Diagnosis and Management of Acute Pancreatitis in Pregnancy.

Acute pancreatitis is rare in pregnancy; however, the associated morbidity and mortality make prompt diagnosis and appropriate management essential. 1,2 Although most cases are mild and improve with limited interventions, severe cases require a multidisciplinary approach in a critical care setting. The main principles of management include identification of an etiology to guide therapy, fluid resuscitation, electrolyte repletion, early nutritional support, and pain management. Antibiotics are not indicated for prophylaxis and should be reserved for cases with a suspected infectious process. Surgical management is indicated in select cases. Management in pregnant patients has few differences which are outlined below.