Aggressive Intravenous Hydration Research Articles

Levetiracetam-induced Rhabdomyolysis - A Rare Complication

Background: Levetiracetam is an anti-epileptic drug that works by modulation of synaptic neurotransmitter release through binding to the synaptic vesicle protein 2A. Levetiracetam is generally well tolerated. Common side effects of levetiracetam include lethargy, drowsiness, headaches, and mood changes. Rhabdomyolysis and an increase in Creatine Kinase (CK) levels are one of the rarely reported effects of levetiracetam. Case presentation: We present a case of a 20-year-old patient with previously known epilepsy (non-compliant with medicine) who presented with a seizure. The patient was given 1 gram of levetiracetam in the emergency department and was kept at a maintenance dose of 500 mg twice a day. The workup revealed acute kidney injury and raised levels of creatinine kinase that peaked at 19,757 IU/L 72 hours after levetiracetam was started. Levetiracetam was later switched to lamotrigine and aggressive intravenous hydration was done. Gradual improvement of CK level was noted accompanied by improvement in renal function. Conclusion: Only a few cases of levetiracetam-induced rhabdomyolysis have been reported worldwide. Our case report highlights the importance of monitoring creatinine and CK levels while treating patients with levetiracetam as rhabdomyolysis can be asymptomatic with a rise in CK levels only.

Post-endoscopic retrograde cholangiopancreatography pancreatitis: a review

Endoscopic retrograde cholangiopancreatography (ERCP) has continued to develop over recent decades with regard to both indications for its use and improvements in technique. The most common complication is post-ERCP pancreatitis (PEP) with incidence rates being reported at ~10%. The exact mechanism of PEP is unknown but is likely multifactorial with papillary edema contributing to the activation of the inflammatory cascade playing an important role. Selected risk factors include patient-related factors (female sex, younger age, sphincter of Oddi dysfunction, and history of PEP) and procedure-related factors (difficult cannulation, multiple pancreatic duct guidewire passes, pancreatic acinarization, multiple pancreatic duct contrast injections, and precut sphincterotomy). Several preventative prophylactic strategies have been posited; however, current guidelines recommend the use of rectal non-steroidal anti-inflammatory drugs (NSAIDs), aggressive intravenous (IV) fluid hydration, and pancreatic duct stents. Appropriate patient selection and the use of noninvasive imaging modalities for diagnosis of pancreaticobiliary abnormalities is a key aspect in prevention. Future studies continue to explore various pharmacologic, procedure-related, and combination strategies for prevention and will be important as the use of ERCP continues to grow.

SAT253 A Rare Case Of Osteolytic Hypercalcemia Of Malignancy In Acute Myeloid Leukemia

Abstract Disclosure: S. Elahi: None. S. Baim: None. Introduction: Acute myeloid leukemia (AML) and other leukemias do not commonly induce hypercalcemia of malignancy (HCM). Limited previous reports of AML-related HCM have largely attributed cases to inflammatory-cytokine-mediated osteoclast activation, with rare reports of calcitriol-mediated HCM and ectopic parathyroid hormone (PTH) production. We describe an unusual case of AML-induced HCM caused by direct leukemic bone invasion, which responded to bisphosphonate therapy. Case Presentation: A 59-year-old female presented with spontaneous bruising and severe leukocytosis concerning for AML. The diagnosis was confirmed by flow cytometry and bone marrow biopsy. Imaging did not reveal any gross destructive bone lesions, but showed soft tissue nodules in the lumbar region which biopsy revealed to be myeloid sarcoma. Prior to initiation of chemotherapy, the patient developed severe hypercalcemia that was treated with aggressive intravenous hydration and zoledronic acid. Intrathecal chemotherapy and high-dose glucocorticoid therapy were initiated thereafter with normalization of serum calcium levels. PTH levels were suppressed. Calcitriol and PTHrP were below normal and undetectable, respectively. Bone turnover markers (C-telopeptide and bone-specific alkaline phosphatase) were significantly elevated prior to administration of zoledronic acid and normalized post-therapy. Calcium levels did not rebound after several interruptions in chemotherapy. Bone marrow biopsy showed focal areas of erosion in trabecular bone consistent with diffuse microscopic osteolytic disease. The patient developed bisphosphonate-induced hypocalcemia following treatment with zoledronic acid, which normalized with treatment with oral calcium carbonate. Discussion: Hypercalcemia of malignancy is a very unusual consequence of AML. No currently-published reports of this phenomenon have described biopsy-proven diffuse microscopic bone erosion associated with AML. We attribute our patient’s severe HCM to large-scale focal bone erosion by AML, independent of and/or associated with concurrent bone resorption mediated by inflammatory cytokines. A single dose of zoledronic acid, a potent suppressor of bone remodeling, achieved long term control of calcium for our patient despite interruption of chemotherapy. Bisphosphonate therapy should be considered an early treatment of HCM in patients with AML due to several potential mechanisms that result in direct calcium release from the skeleton. Presentation: Saturday, June 17, 2023

FRI695 Hypercalcemia Mediated By Granulomatous Disease Due To Polymethylmethacrylate (pmma) Injection Utilization For Gluteal Augmentation

Abstract Disclosure: T. Mishra: None. J. Craven: None. Introduction: While etiologies for hypercalcemia commonly include hyperparathyroidism, malignancy or vitamin D intoxication, unusual causes should also be considered. We present a case that describes a patient who presented with hypercalcemia in the setting of granulomatous reaction to PMMA filler for gluteal augmentation. Clinical case: A 52 year old female with a past medical history of hypertension, stage III chronic kidney disease, nephrolithiasis, depression was admitted to the hospital with a peak calcium of 15.8 mg/dl (n: 8.4-10.4mg/dl). Hypercalcemia was incidentally noted while she was undergoing workup for her chronic kidney disease. Initial testing revealed PTH of 22 pg/ml (n: 22-94). 25 hydroxy vitamin D 24ng/ml, (n: 30-80), 1, 25 dihydroxy D2 markedly elevated at 258 pg/ml (n: 19-79). SPEP/UPEP normal. PTHrp was found to be 5.9 pmol/L(n: 0-3.4pmol/L). High-resolution CT chest did not show evidence of granulomatous disease or lung masses. A PET scan was obtained which showed extensive hypermetabolic activity in the bilateral gluteus medius and maximus muscle consistent with her history of PMMA injection for buttock augmentation. She was placed on aggressive maintenance intravenous fluid hydration. In addition, Lasix, zoledronic acid and calcitonin were administered. With these measures her calcium improved to a level of 10.7mg/dl. She did not tolerate high dose glucocorticoids. With her treatment intolerance and progressive renal disease in mind, plastic surgery has been consulted to explore surgical options for PMMA debulking. Conclusion: This represents a case of hypercalcemia mediated by elevated levels of calcitriol due to granulomatous inflammation caused by a foreign body reaction to PMMA injection. Polymethylmethacrylate is primarily used in South/Central America as a synthetic filling agent in cosmetic procedures, but is not FDA approved for gluteal injection. To our knowledge, there is only one other case report of MMA mediated hypercalcemia in the US. Given the rise in cosmetic tourism and the lag time between PMMA injection and development of hypercalcemia (mean time to presentation of 7 years), this complication is likely to become increasingly prevalent in North America. Presentation: Friday, June 16, 2023

Cinacalcet increases renal calcium excretion in PTHrP-mediated hypercalcemia: a case report

BackgroundIn the acute setting, PTH-independent hypercalcemia is typically treated with anti-resorptive agents such as zoledronic acid or denosumab. When these agents are no longer able to control hypercalcemia, several case reports have shown the utility of cinacalcet. However, it is not known if cinacalcet can be effective in patients naïve to anti-resorptive therapy or how cinacalcet ameliorates the hypercalcemia.Case presentationA 47-year-old male with a history of alcohol-induced cirrhosis was admitted for left cheek bleeding and swelling from an infiltrative squamous cell carcinoma of the oral cavity. On admission, he was found to have an elevated albumin-corrected serum calcium of 13.6 mg/dL, a serum phosphorus of 2.2 mg/dL and an intact PTH of 6 pg/mL (normal 18–90) with a PTHrP of 8.1 pmol/L (normal < 4.3), consistent with PTHrP-dependent hypercalcemia. Aggressive intravenous saline hydration and subcutaneous salmon calcitonin were initiated, but his serum calcium remained elevated. Given tooth extractions scheduled for the next day and possible irradiation to the jaw in the near future, alternatives to antiresorptive therapy were sought. Cinacalcet was initiated at 30 mg twice daily then increased to 60 mg twice daily the following day. The albumin-corrected serum calcium level decreased from 13.2 to 10.9 mg/dL within 48 h. The fractional excretion of calcium increased from 3.7 to 7.0%.ConclusionsThis case demonstrates the utility of cinacalcet for the treatment of PTHrP-mediated hypercalcemia without prior anti-resorptive therapy via increased renal clearance of calcium.

Comparison of clinical outcomes between aggressive and non-aggressive intravenous hydration for acute pancreatitis: a systematic review and meta-analysis

BackgroundCurrent practice guidelines for optimal infusion rates during early intravenous hydration in patients with acute pancreatitis (AP) remain inconsistent. This systematic review and meta-analysis aimed to compare treatment outcomes between aggressive and non-aggressive intravenous hydration in severe and non-severe AP.MethodsThis study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We systematically searched PubMed, Embase and Cochrane Library for randomized controlled trials (RCTs) on November 23, 2022, and hand-searched the reference lists of included RCTs, relevant review articles and clinical guidelines. We included RCTs that compared clinical outcomes from aggressive and non-aggressive intravenous hydration in AP. Meta-analysis was performed using a random-effects model for participants with severe AP and non-severe AP. Our primary outcome was all-cause mortality, and several secondary outcomes included fluid-related complications, clinical improvement and APACHE II scores within 48 h.ResultsWe included a total of 9 RCTs with 953 participants. The meta-analysis indicated that, compared to non-aggressive intravenous hydration, aggressive intravenous hydration significantly increased mortality risk in severe AP (pooled RR: 2.45, 95% CI: 1.37, 4.40), while the result in non-severe AP was inconclusive (pooled RR: 2.26, 95% CI: 0.54, 9.44). However, aggressive intravenous hydration significantly increased fluid-related complication risk in both severe (pooled RR: 2.22, 95% CI 1.36, 3.63) and non-severe AP (pooled RR: 3.25, 95% CI: 1.53, 6.93). The meta-analysis indicated worse APACHE II scores (pooled mean difference: 3.31, 95% CI: 1.79, 4.84) in severe AP, and no increased likelihood of clinical improvement (pooled RR:1.20, 95% CI: 0.63, 2.29) in non-severe AP. Sensitivity analyses including only RCTs with goal-directed fluid therapy after initial fluid resuscitation therapy yielded consistent results.ConclusionsAggressive intravenous hydration increased the mortality risk in severe AP, and fluid-related complication risk in both severe and non-severe AP. More conservative intravenous fluid resuscitation protocols for AP are suggested.Graphical

Prevention of post-ERCP pancreatitis: current strategies and novel perspectives.

Endoscopic retrograde cholangiopancreatography (ERCP) is an advanced endoscopic procedure that might lead to severe adverse events. Post-ERCP pancreatitis (PEP) is the most common post-procedural complication, which is related to significant mortality and increasing healthcare costs. Up to now, the prevalent approach to prevent PEP consisted of employing pharmacological and technical expedients that have been shown to improve post-ERCP outcomes, such as the administration of rectal nonsteroidal anti-inflammatory drugs, aggressive intravenous hydration, and the placement of a pancreatic stent. However, it has been reported that PEP originates from a more complex interaction of procedural and patient-related factors. Appropriate ERCP training has a pivotal role in PEP prevention strategy, and it is not a chance that a low PEP rate is universally considered one of the most relevant indicators of proficiency in ERCP. Scant data on the acquisition of skills during the ERCP training are currently available, although some efforts have been recently done to shorten the learning curve by way of simulation-based training and demonstrate competency by meeting technical requirements as well as adopting skill evaluation scales. Besides, the identification of adequate indications for ERCP and accurate pre-procedural risk stratification of patients might help to reduce PEP occurrence regardless of the endoscopist's technical abilities, and generally preserve safety in ERCP. This review aims at delineating current preventive strategies and highlighting novel perspectives for a safer ERCP focusing on the prevention of PEP.

PSAT200 Parathyroid Crisis Presenting as Failure to Thrive in a Young Man

Abstract Introduction Parathyroid crisis is a serious, life-threatening complication of primary hyperparathyroidism (PHPT) which causes severe symptomatic hypercalcemia and affects multiple organ systems. PHPT is far less common in children and young adults, but they are frequently symptomatic often with kidney and skeletal involvement. We report a case of young adult who presents with severe symptomatic hypercalcemia with classical skeletal findings. Case A 23-year-old man with past medical history of autism spectrum disorder and obesity presented with extreme fatigue, malaise, epigastric pain, nausea and vomiting for 5 days. Patient also reported diffuse bilateral lower extremity pain for 1 year with weakness and difficulty in ambulation for 1 month. He did not see any provider in the last 2 years. He was not on any prescription or over the counter medications. He was found to have severe hypercalcemia with corrected calcium of 14.7 mg/dL, low phosphorus 1.6 mg/dL, low 25 hydroxy vitamin D &amp;lt;4 ng/mL, very high parathyroid hormone (PTH) 1859 pg/mL and high alkaline phosphatase 1167 U/L. No prior history of hypercalcemia. No family history of hypercalcemia, thyroid cancer, pheochromocytoma, pituitary or pancreatic tumor. CT abdomen was performed on admission due to severe gastrointestinal symptoms which revealed left nephrolithiasis, sclerotic changes in the end plates of the spines and multiple lucent lesions throughout femoral necks, symphysis pubis, and sacroiliac joints. It also showed chronic rib fractures. Knee x ray showed bilateral extensive sub-periosteal, sub-tendinous and subligamentous bony resorption and brown tumors. Patient was treated with aggressive intravenous (IV) hydration, calcitonin and IV pamidronate with gradual improvement in serum calcium. Thyroid ultrasound showed left inferior 3.2 cm mass suspicious for parathyroid adenoma. Surgical team was consulted. Patient underwent left inferior parathyroidectomy along with left hemithyroidectomy due to concern for parathyroid cancer. Surgical pathology showed parathyroid adenoma. Patient required aggressive calcium supplementation, along with vitamin D, calcitriol and magnesium to prevent severe hypocalcemia and hungry bone syndrome. He recovered well and was discharged with outpatient follow up. Conclusion Our case highlights that parathyroid crisis is a serious endocrine emergency associated with significant morbidity and urgent surgical intervention after stabilizing serum calcium level leads to a favorable outcome. The finding of parathyroid adenoma is interesting because the constellation of severe skeletal involvement, nephrolithiasis and significantly elevated PTH and calcium in our patient was concerning for parathyroid carcinoma. Clinicians should consider both in patients with severe hypercalcemia and PTH more than 5 times upper limit of normal. The characteristic finding of osteitis fibrosa cystica in our case is rare in United States and is seen in &amp;lt;2% of patients with PHPT due to routine biochemical screening leading to early diagnosis of asymptomatic cases. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP110 Parathyroid Hormone Independent Hypercalcaemia Secondary to Granulomatous Inflammation: Could This Be Melioidosis?

Abstract Background Hypercalcemia has been described in patients with most granulomatous disorders, most commonly in sarcoidosis and tuberculosis, but never in melioidosis. Clinical Case A 45-year-old woman presented with two-day history of abdominal pain, nausea, lethargy and intermittent fevers during Darwin's wet season. Medications included daily methadone, diazepam and mirtazapine. On examination she was febrile with stable hemodynamics and left upper quadrant tenderness. Investigations revealed pancytopenia, deranged liver function tests with a cholestatic pattern, raised CRP of 53 (&amp;lt;5mg/L) and normal serum calcium. Blood cultures were negative but melioidosis serology was positive (indirect hemagglutination antibody (IHA) titer 1: 1280). Abdominal computed tomography demonstrated hepatosplenomegaly with peripheral splenic infarcts and a 7mm intrasplenic aneurysm, but no abscesses. PET showed no hypermetabolic lesions. After extensive investigation, she was treated for presumptive culture-negative melioidosis with intravenous meropenem. Clinically she improved despite gradual elevation in serum calcium which peaked at 3.31 (2.1-2.6mmol/L) five weeks after presentation. Initial biochemical investigations revealed suppressed PTH at 0.5 (1.4-9.1pmol/L), low 25-hydroxy-Vitamin D of 26 (50-150nmol/L), elevated phosphate at 2.43 (0.75-1.5mmol/L) and moderate renal impairment (eGFR 34mL/min/1.73m 2). Hypercalciuria was present with urine calcium to creatinine ratio of 812 (100-580mmol/mol). Her 1,25-dihydroxy-Vitamin D (calcitriol) was elevated at 219 (48-190pmol/L) suggestive of PTH-independent hypercalcemia. The patient remained asymptomatic of hypercalcemia and aggressive intravenous hydration produced minimal biochemical improvement. Renal impairment precluded bisphosphonate use. She was commenced on prednisolone 50mg while continuing intravenous meropenem. Serum calcium normalized in 10 days and prednisolone dose was gradually tapered. A liver biopsy was performed due to persistent liver derangement and histology showed granulomatous inflammation. She completed six weeks of antibiotics for melioidosis and was discharged on day 50, with a planned six months of eradication therapy. Outpatient follow-up demonstrated normal serum calcium after cessation of prednisolone with decreasing IHA titer (1: 320). We hypothesize that this case reflects PTH-independent hypercalcemia secondary to granulomatous inflammation, presumptively caused by melioidosis. The rise in calcium after commencement of antibiotics and normalization following initiation of glucocorticoid therapy, with no rebound post cessation, is consistent with successful therapy of an infection with granulomatous inflammation. Activated macrophages within granulomas have unregulated 1-alpha-hydroxylase expression which is thought to increase conversion of 25-hydroxy-Vitamin D to calcitriol and therefore increase intestinal calcium absorption. Treatment with glucocorticoids inhibits calcitriol synthesis leading to quick resolution of hypercalcemia. While use of glucocorticoids are commonplace in the management of granulomatous disease due to sarcoidosis, they have been increasingly recognized as an important risk factor for melioidosis, considered to result from suppression of innate immunity. However, use of glucocorticoids if required is not contraindicated once antibiotic therapy for melioidosis has commenced. Conclusion In areas where melioidosis is endemic, clinicians should be aware of hypercalcemia and the potential risks associated with its treatment. Presentation: No date and time listed

S66 Aggressive Intravenous Hydration in Patients With Acute Pancreatitis Is Beneficial Only During the First 24 Hours: A Meta-Analysis

Introduction: Early aggressive intravenous hydration (EAIH) remains the only initial treatment specifically for patients with acute pancreatitis. The timing, type, and amount of fluid remains the subject of study, debate, and controversy. In order to define our current state of knowledge of the clinical evidence behind the recommendation for EAIH, we performed a meta-analysis of the published literature. Methods: A Pubmed search to identify all clinical trials evaluating the role of EAIH in patients with acute pancreatitis resulted acute pancreatitis 25 studies, 17 prospective, 18 retrospective, 13 randomized controlled clinical trials (RCT). Studies that evaluated NS to LR were not included. In order to be included in the final analysis, the study needed to have two or more groups defined by different rates of hydration. One group must have included EAIH and define the outcome(s) studied. Outcomes used in our analysis included SIRS, pancreatic necrosis, persistent organ failure, length of stay, ICU admission, and mortality. Any decrease in these outcomes compared to the “control” groups was considered a “benefit”. The weighted mean for each study was defined by the sample size. Results: In a pooled analysis of all studies (n=1865), there was no difference in morbidity or mortality between EAIH and the “control group” (RR 1.1, 95% CI 0.66-1.8). When including only RCT (n=987), there was also no difference in morbidity or mortality (RR 0.88, 95% CI 0.78-1.4). However, when including studies and RCT that focused only on EAIH within the first 24 hours, excluding all studies that defined EAIH as the amount of fluid provided at 48 hours, there was a “benefit” to EAIH (RR 0.62, 95% CI 0.44-0.84). Conclusion: Our results show that the benefit observed in EAIH occurs only within 24 hours of enrollment. While guidelines on the management of acute pancreatitis have generally recommended EAIH, some have suggested that “goal directed therapy” is preferred due to complications. Our study demonstrates that it is important for clinicians caring for patients with acute pancreatitis not miss the “goal” within the first day of managing patients with acute pancreatitis. Our meta-analysis shows aggressive intravenous hydration after the first 24 hours is not beneficial and may be harmful. Based on this analysis, we suggest EAIH be applied to all patients during the first 24 hours and “goal directed” hydration after the first 24 hours.

Systemic loxoscelism induced warm autoimmune hemolytic anemia: clinical series and review

ABSTRACT Objectives Describe the development of warm autoimmune hemolytic anemia warm (AIHA) secondary to a brown recluse spider (Loxosceles reclusa) bite is known as systemic loxoscelism; and review epidemiology, clinical manifestations, diagnostic work-up, pathophysiology, and treatment options associated with warm AIHA secondary to systemic loxoscelism. Methods Cases series of two cases of warm AIHA due to systemic loxoscelism and a review of the current literature: epidemiology, clinical manifestations, diagnostic work-up, pathophysiology, and treatment options associated with warm AIHA secondary to systemic loxoscelism. Results Presented here are two cases of warm AIHA due to systemic loxoscelism. Each patient was generally healthy appearing and presented with symptomatic anemia in the setting of brown recluse spider bites. Both patients were eventually found to have warm AIHA. Upon recognition of the diagnosis, the patients were started on corticosteroids and aggressive intravenous fluid hydration. In addition, they received transfusions of packed red blood cells. Their clinical courses improved, and they recovered to eventually be discharged home. Conclusion Envenomation by a brown recluse spider, Loxosceles reclusa, can result in systemic loxoscelism which can cause warm AIHA. The diagnosis of warm AIHA is confirmed by the direct antiglobulin/Coomb's test. Warm AIHA can be a life-threatening disease process. Hemodynamic support with intravenous fluids and RBC transfusion is the initial step in the management of these patients. Corticosteroids are the mainstay of current management. Second line treatments include rituximab. Rarely patients require splenectomy for refractory disease. Corticosteroids should be tapered over a three-month period.

In vitro fertilization and hypertriglyceridemic pancreatitis: Case report

Few cases of hypertriglyceridemic pancreatitis have been reported in women during a vitro fertilization treatment (IVF) cycle. Here, we describe a 41-year-old woman with primary infertility and a history of acute pancreatitis (of unknown etiology) who was started on high dose ethinyl estradiol to prepare for transfer of cryopreserved embryos. She subsequently presented with nausea, vomiting, and abdominal pain to an emergency room and was found to have hypertriglyceridemic pancreatitis. Her hospitalization involved a prolonged intensive care unit stay in which she underwent three sessions of plasmapheresis. Eventually, with discontinuation of ethinyl estrogen, aggressive intravenous fluid hydration, plasmapheresis, a low-fat diet, and gemfibrozil, she had resolution of severe hypertriglyceridemia and all symptoms related to acute pancreatitis. Our case highlights the possibility that ethinyl estradiol, a commonly used form of estrogen for endometrial preparation during IVF cycles, may cause severe hypertriglyceridemia and acute pancreatitis in certain predisposed individuals. Only seven cases of hypertriglyceridemic pancreatitis during in vitro fertilization have been previously reported, and only one of these prior cases experienced pancreatitis during transfer of cryopreserved embryos like our patient. Our case, along with the few prior reported cases, demonstrate hypertriglyceridemic pancreatitis can occur during IVF. Further work is needed to understand the effects of exogenous estrogen on lipids for women undergoing IVF.

Drug-induced acute pancreatitis in a bodybuilder: a case report

BackgroundUnregulated use of a variety of drugs and supplements by bodybuilders and athletes is common and can lead to severe adverse complications. Only a small proportion of acute pancreatitis cases are drug induced, and case reports are essential for identifying potential drug-related risks for pancreatitis. Here we present the first case report published of acute pancreatitis linked to recreational use of anabolic–androgenic steroids, subcutaneous growth hormone, and clenbuterol in a previously healthy male after excluding all other causes of pancreatitis.Case presentationA 31-year-old Arab male bodybuilder presented with acute abdominal pain associated with nausea and sharp pain radiating to the back. The patient was not using tobacco or alcohol but was using multiple drugs related to bodybuilding, including anabolic–androgenic steroids, subcutaneous growth hormone, clenbuterol, and multiple vitamin supplements. Laboratory studies revealed a normal white blood cell count, elevated C-reactive protein, minimally elevated aspartate aminotransferase and total bilirubin with normal remaining liver tests, and elevated amylase and lipase. The patient had no hypertriglyceridemia or hypercalcemia, and had had no recent infections, abdominal procedures, trauma, or scorpion exposure. Imaging and laboratory investigations were negative for biliary disease and IgG4 disease. Abdominal computed tomography revealed hepatomegaly and diffuse thickening and edema of the body and tail of the pancreas with peripancreatic fat stranding. An abdominal ultrasound showed slight hepatomegaly with no evidence of cholelithiasis. Genetic testing for hereditary pancreatitis-related mutations was negative. A diagnosis of drug-induced acute pancreatitis was made, and he was treated with aggressive intravenous hydration and pain management. The patient has avoided further use of these drugs and supplements and had no further episodes of pancreatitis during 1 year of follow-up.ConclusionsThis case describes a patient with drug-induced acute pancreatitis after the intake of anabolic–androgenic steroids, subcutaneous growth hormone, and clenbuterol, where all other common causes of acute pancreatitis were excluded. Clinicians should be alert to the possibility of drug-induced acute pancreatitis occurring in bodybuilders and athletes using similar drug combinations.

Continuous Infusion of Fluid Hydration Over 24 Hours Does Not Prevent Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis.

Aggressive intravenous fluid hydration, by administering 3500mL of lactated Ringer's solution (LRS) in 9h with a peri-procedural bolus, reduces post-ERCP pancreatitis (PEP) incidence. A concern of this strategy is adverse events related to volume overload; however, the impact of fluid hydration over an extended period without a bolus on PEP is unknown. To assess the effect of continuous infusion of high-volume fluid at a constant rate over 24h on PEP incidence and severity. Two-hundred patients were randomly assigned (1:1) to receive either 3600mL of LRS in 24h starting 2h before the ERCP (high-volume group) or maintenance fluid hydration calculated by the Holliday-Segar method (control group). The mean age of the patients was 50.6 ± 11.6years. The predominant indications were choledocholithiasis (48%) and malignancies (32%). Patient demographics and PEP risk factors were similar in both groups. Patients in the high-volume group received significantly more fluid than the control group (3600 vs. 2413ml, P < 0.001). PEP incidence was not different between the high-volume and the control group (14% vs. 15%; relative risk 0.93: 95% CI 0.48-1.83, P = 0.84). There were no differences in moderate to severe PEP (3% vs. 4%; relative risk 0.75: 95% CI, 0.17-3.27, P = 1.00). Subgroup analysis did not show a benefit in high-risk patients. Only one patient in the control group developed peripheral edema. An infusion of high-volume hydration over 24h is not sufficient to provide optimal hydration for PEP prevention. No. NCT02821546.

TIME-DEPENDENT, LIFE-SAVING SUPPORTIVE TREATMENT IN AN UNORDINARY PULMONARY LEUKOSTASIS PRESENTATION: A CASE REPORT

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Pulmonary leukostasis (PL) is a medical emergency defined by an extremely high white blood cell count (WBC) with pulmonary symptoms with or without imaging findings. This condition is seen more frequently in acute myeloid leukemia or chronic myeloid leukemia during a blast crisis and confers up to 30% mortality. Symptoms usually do not occur unless WBC exceeds 400x10ˆ3 / µL in patients with chronic lymphocytic leukemia (CLL). Here we present an atypical presentation of this dreaded disease. CASE PRESENTATION: An 80-year-old man with a history of atrial fibrillation, benign prostatic hyperplasia, diabetes mellitus, and a recent diagnosis of chronic lymphocytic leukemia came to the emergency room with tachypnea, hypoxia, headache, slurred speech, drowsiness, and confusion. Days before his arrival, he began with bradyphrenia, subjective fever, and dry cough. Vital signs with tachypnea and peripheral oxygen saturation of 90%. Routine laboratories stood out for 95.2 x10ˆ3 / µL white blood cells, with 65% immature blood cells, 17% lymphocytes, 10% neutrophils, and arterial blood gas with metabolic alkalosis and hypoxemia. Supportive therapy began with respiratory therapies every four hours, aggressive intravenous hydration, and empirical antibiotics. Chest radiography and chest computed tomography failed to show effusions, infiltrates, or consolidations. Brain studies negative for intracranial pathology. Debulking and leukoreduction therapies were discussed with the patient who decided to continue with supportive therapy, even with the risk of tumor lysis. After observation and aggressive hydration, there was a significant clinical improvement that correlated with the decrease in WBC from 95.2x10ˆ3 / µL to 69.9x10ˆ3 / µL. Noteworthy, cultures and respiratory panel were negatives. The following days the antibiotics were suspended and the patient was discharged with scheduled chemotherapy. DISCUSSION: Leukostasis is an emergency condition that, if overlooked or misdiagnosed, could be fatal if left untreated. In case of clinical suspicion, expeditious treatment is indicated since the mortality rate is approximately 20 to 40 percent regardless of the leukocytosis. CONCLUSIONS: Although it is less common in CLL and almost unthinkable with WBC less than 100x10ˆ3 / µL; L This case highlights the important role of high clinical suspicion of PL even if not all medical criteria are met and its response to supportive and symptomatic therapy when implemented in a rapid timely manner. REFERENCE #1: Kacar, D., Yarali, N., Candir, M. O., Kara, A., Ozbek, N., & Tunc, B. (2017). Pulmonary Leukostasis. Journal of Pediatric Hematology/Oncology, 39(2), 156–158. doi:10.1097/mph.0000000000000731 REFERENCE #2: Soares, F. A., Landell, G. A. M., & Cardoso, M. C. de M. (1992). Pulmonary leukostasis without hyperleukocytosis: A clinicopathologic study of 16 cases. American Journal of Hematology, 40(1), 28–32. doi:10.1002/ajh.2830400106 REFERENCE #3: Baer, M. R., Stein, R. S., & Dessypris, E. N. (1985). Chronic lymphocytic leukemia with hyperleukocytosis the hyperviscosity syndrome. Cancer, 56(12), 2865–2869. doi:10.1002/1097-0142(19851215)56:12<2865::aid-cncr2820561225>3.0.co;2-6 DISCLOSURES: No relevant relationships by Ian Da Silva Lugo, source=Web Response No relevant relationships by Arelis Febles, source=Web Response No relevant relationships by Juan Feliciano-FIgueroa, source=Web Response No relevant relationships by Heydee Fournier, source=Web Response No relevant relationships by Joel Gonzalez Chaple, source=Web Response No relevant relationships by Juan Santiago, source=Web Response

S41 The Benefit of Aggressive Intravenous Fluid Hydration in Preventing Post-ERCP Pancreatitis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

S41 The Benefit of Aggressive Intravenous Fluid Hydration in Preventing Post-ERCP Pancreatitis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Fluid overload and acute kidney injury in children with tumor lysis syndrome.

Tumor lysis syndrome (TLS) is a common oncologic emergency among patients with pediatric hematologic malignancies. The mainstay of TLS management is aggressive intravenous hydration. However, the epidemiology of fluid overload (FO) and acute kidney injury (AKI) in this population is understudied. In this study, we aimed to describe the incidence, severity, and complications of FO and AKI among pediatric patients with TLS. We completed a single-center retrospective cohort study of pediatric patients with a new diagnosis of hematologic malignancy over a 10-year period. Patients with TLS were analyzed in two groups based on the severity of AKI and FO. Charts were reviewed for complications associated with AKI and FO including hypoxemia, mechanical ventilation, hyponatremia, pulmonary edema, pediatric intensive care (PICU) admission, and need for renal replacement therapy (RRT). We analyzed 56 patients with TLS for FO and AKI. We found severe FO (≥10%) occurred in 35.7% (n=20). PICU admission occurred in 35% of patients with severe FO compared to 8.3% in those with mild/moderate FO <10% (p=.013). Complications of hypoxemia (30% vs. 5.6%, p=.012) and pulmonary edema (25% vs. 2.8%, p=.010) were more common among those with severe FO. AKI occurred in 37.5% (n=21) patients and resulted in a significant increase in PICU admission and requirement for RRT (p=.001 and <.001, respectively). Our results show FO and AKI are common, and often unrecognized complications of TLS associated with increased morbidity. Prospective, multicenter studies are needed to further dissect the burden of FO and AKI within this vulnerable population.

Comparison of aggressive versus standard intravenous hydration for clinical improvement among patients with mild acute pancreatitis: A randomized controlled trial

BackgroundControversy remains regarding fluid management strategy, optimal volume and rate of intravenous fluid in mild acute pancreatitis. We performed a randomized controlled trial to compare clinical improvement and inflammatory markers between aggressive and standard fluid management. MethodsA single center prospective randomized controlled trial was conducted in a tertiary care hospital. We randomized patients with a diagnosis of mild acute pancreatitis using revised Atlanta classification in two groups, the aggressive (20 ml/kg bolus followed by 3 ml/kg/hr) and standard (10 ml/kg bolus followed by 1.5 ml/kg/hr) intravenous hydration with Lactated Ringer's solution. Primary outcome was clinical improvement at 24 and 36 hours. ResultsThe mean age of patients was 46 years and 34 patients (77%) were male. The average volumes of fluid during the first 24 hours in aggressive and standard groups was 4886 ml (71 ml/kg) and 3985 ml (53 ml/kg), respectively; p-value 0.002. Aggressive intravenous hydration did not significantly improve clinical outcome compared with standard intravenous hydration (45.45% vs. 31.82%, respectively; p-value 0.353). However, subgroup analysis between patients with obese and non-obese status, revealed aggressive intravenous hydration significantly improved clinical outcome within the first 24 hours in obese group. ConclusionAggressive intravenous hydration with Lactated Ringer's solution did not improve clinical outcome in mild acute pancreatitis but showed statistically significant improvement only in patients with obese status. Future studies should include a larger sample size to confirm these findings.

Severe Rhabdomyolysis and Acute Renal Failure Due to Noncompliance to Levothyroxine Therapy

Background: Noncompliance to levothyroxine (LT4) is common however only rarely it leads to severe side effects. We report a case of rhabdomyolysis leading to acute kidney injury (AKI) requiring hemodialysis (HD) due to noncompliance to LT4 therapy for one month. Clinical Case: A 68-year-old Caucasian male presented with a 2-week history of worsening fatigue and generalized weakness, accompanied by pain in bilateral lower extremities. Medical history included coronary artery disease, heart failure with reduced ejection fraction, hypertension, dyslipidemia, hypothyroidism, type 2 diabetes mellitus, CKD. Home medications included LT4 200 mcg daily, metoprolol 25 mg daily, doxazosin 2 mg daily, amlodipine 5 mg daily, fluocinonide 40 mg daily, fosinopril 40 mg twice daily, metformin 500 mg twice daily and rosuvastatin 40 mg daily. Further history revealed the patient to be not taking LT4 as “he ran out of it for a month” and only resumed taking it 3 to 4 days before coming to the hospital. On examination, he had proximal muscle weakness with power 3/5 in bilateral lower extremities and mild tenderness on thigh muscles. Labs revealed creatinine 13.1 mg/dL (0.60-1.10 mg/dL), BUN 101 mg/dL (0-30 ng/dL), eGFR 4.0 ml/min/1.73m2, CK 69,500 U/L (22-198 U/L), TSH 55.8 uIU/ml (0.45-4.5 uIU/ml), and FT4 0.61 ug/dL (0.8-1.8 ug/dL). ABG showed metabolic acidosis. Routine labs three months prior revealed normal thyroid function tests (TSH 1.6 uIU/ml and FT4 1.3 ug/dL) on LT4 200 mcg and baseline CKD stage 3b (EGFR 51 ml/min/1.73m2 with baseline creatinine 1.4 mg/dL). The patient was diagnosed with severe rhabdomyolysis secondary to noncompliance with LT4 therapy in presence of concurrent statin use, leading to AKI. Rosuvastatin was stopped and he was treated with aggressive intravenous hydration, sodium bicarbonate, and LT4 200 mcg daily. Despite two days of aggressive treatment, CK remains elevated and hence HD was initiated. The patient underwent three sessions of HD during the course of his hospitalization. Due to lack of renal recovery, outpatient HD was arranged. At 4 weeks of outpatient follow-up, the patient was oliguric and HD dependent. At 8 weeks outpatient follow up, CK, TSH, and FT4 was normal on LT4 200 mcg daily and became dialysis independent. Conclusion: Noncompliance to LT4 therapy along with concomitant use of statin can result in severe rhabdomyolysis induced AKI in patients with CKD.

Hyperleukocytosis and Leukostasis in Acute Myeloid Leukemia: Can a Better Understanding of the Underlying Molecular Pathophysiology Lead to Novel Treatments?

Up to 18% of patients with acute myeloid leukemia (AML) present with a white blood cell (WBC) count of greater than 100,000/µL, a condition that is frequently referred to as hyperleukocytosis. Hyperleukocytosis has been associated with an adverse prognosis and a higher incidence of life-threatening complications such as leukostasis, disseminated intravascular coagulation (DIC), and tumor lysis syndrome (TLS). The molecular processes underlying hyperleukocytosis have not been fully elucidated yet. However, the interactions between leukemic blasts and endothelial cells leading to leukostasis and DIC as well as the processes in the bone marrow microenvironment leading to the massive entry of leukemic blasts into the peripheral blood are becoming increasingly understood. Leukemic blasts interact with endothelial cells via cell adhesion molecules such as various members of the selectin family which are upregulated via inflammatory cytokines released by leukemic blasts. Besides their role in the development of leukostasis, cell adhesion molecules have also been implicated in leukemic stem cell survival and chemotherapy resistance and can be therapeutically targeted with specific inhibitors such as plerixafor or GMI-1271 (uproleselan). However, in the absence of approved targeted therapies supportive treatment with the uric acid lowering agents allopurinol and rasburicase as well as aggressive intravenous fluid hydration for the treatment and prophylaxis of TLS, transfusion of blood products for the management of DIC, and cytoreduction with intensive chemotherapy, leukapheresis, or hydroxyurea remain the mainstay of therapy for AML patients with hyperleukocytosis.