Aggressive Fluid Resuscitation Research Articles

The Role of International Normalized Ratio (INR) in Heart Failure Patient With Sepsis: Hidden in Plain Sight

Heart failure is a clinical syndrome characterized by symptoms and signs caused by a structural and/or functional impairment of the heart. Sepsis in heart failure may cause significant mortality and morbidity rates. Clinically, the presence of heart dysfunction in heart failure worsens outcomes in unstable hemodynamic conditions, for instance, in cases of sepsis, particularly in patients with HFrEF. This research aims to survey the blend of heart failure and sepsis and current updates regarding using the International Normalized Ratio (INR) to detect sepsis. Information was collected from various sources, and updated literature was compiled into a review article. The presence of heart failure with sepsis is associated with horrible clinical results. If fluid alone is insufficient to restore perfusion, the fundamental structure of sepsis includes strong fluid recovery followed by vasopressor association (and possibly inotropic support). In any case, in patients with heart failure, high-portion fluid boluses and vasoactive experts might deteriorate the condition. Heart failure and sepsis can overlap and lead to hemodynamic disturbances and challenging treatment. Meanwhile, aggressive fluid resuscitation is necessary for sepsis; conventional heart failure management requires reducing fluid intake. The International Normalized Ratio (INR) is one of the coagulation parameters that may help determine sepsis in patients with heart failure, thus improving appropriate diagnosis and treatment.

12618 A Rare Case Of Diabetic Ketoacidosis Leading To Severe Hypertriglyceridemia-induced Necrotizing Pancreatitis

Abstract Disclosure: E.R. Perez Roman: None. D.A. Lopez Rodriguez: None. K. Ramirez Gorbea: None. M. Sanchez Cordero: None. Y. Garcia Cruz: None. Acute pancreatitis is an acute inflammatory process of the pancreas that if left untreated can become complicated resulting in multiple organ damage and a fatal outcome in approximately 10%-40% of patients. There are well-known causes that can lead to pancreatitis such as alcohol, hereditary disorders, cholelithiasis, prior pancreatitis, and medications. Less frequently, it can be related to poorly controlled diabetes mellitus and diabetic ketoacidosis (DKA), given that in a state of low or deprived insulin, there is a breakdown of triglycerides into toxic fatty acids by pancreatic lipases; this lipotoxicity can result in the development of acute pancreatitis. We present a case of a 50-year-old woman with a past medical history of untreated hyperlipidemia and previous pancreatitis who was transferred to our institution with acute epigastric pain radiating to the back, nausea, and persistent vomiting. Upon arrival, blood glucose was 299 mg/dL, HbgA1c of 11.4%, lactic acid of 3.6 mmol/L, hypocalcemia of 6.0 mg/dl, hypoalbuminemia, and elevated pancreatic enzymes, amylase 869 U/L and lipase 2,493 U/L. The lipid panel was remarkable for total cholesterol of 1,085 mg/dL and triglycerides of 4,369mg/dL. Abdominopelvic CT scan confirmed acute pancreatitis with extensive peripancreatic and regional mesenteric edema. This patient was treated with aggressive IV fluid resuscitation and treated for DKA as per protocol. Despite prompt treatment, the patient rapidly deteriorated, developing pulmonary effusions and impending respiratory failure requiring mechanical ventilation. Her hyperglycemia was challenging to control and in the setting of severe hypertriglyceridemia, insulin requirements were higher, as intravenous insulin is useful in patients with concomitant findings, in the absence of plasmapheresis availability. Despite the marked reduction of triglyceride to 978 mg/dL and a decrease in pancreatic enzymes, multiorgan failure developed. Unfortunately, the patient died. Repeated abdominopelvic CT imaging revealed the progression of the disease to necrotizing pancreatitis involving the pancreatic head, uncinate process, and neck of the pancreas with evidence of a small hypodense lesion at the level of the tail of the pancreas. This case emphasizes the importance of prompt recognition of acute pancreatitis secondary to uncontrolled hyperglycemia with concomitant severe hypertriglyceridemia since it can lead to a worse clinical outcome as seen in our patient who developed rapid progression to necrotizing pancreatitis. It is paramount not to delay treatment with aggressive fluid resuscitation, continuous insulin infusion, and if available, plasmapheresis; as these treatment strategies in conjunction can be life-saving. Presentation: 6/3/2024

6564 A Case of Severe Hypercalcemia in Carney's Complex

Abstract Disclosure: J. Chippior: None. M. Rayan: None. L. Wright: None. L.S. Kirschner: Grant Recipient; Self; Medpace, Sparrow, Corcept Therapeutics, Corcept, Spruce, CinCor, Crinetics, Adrenas. S.W. Ing: Grant Recipient; Self; Alexion Pharmaceuticals, Inc., Amgen Inc, Radius Health, Inc, Takeda, Ultragenyx, Amolyt, Bridge Bio. Carney complex is a rare syndrome with fewer than 750 reported cases, characterized by lentigniosis, myxomas, and the occurrence of both endocrine and non-endocrine tumors. An inactivating mutation PRKAR1A, which encodes for the type 1A regulatory subunit of Protein kinase A, is responsible for over 70% of familial cases and 37% of sporadic cases. A 31-year-old female with a history of Carney complex, Cushing syndrome due to primary pigmented nodular adrenocortical disease (PPNAD), facial lentigines, spinal Schwannomas, and recent ischemic stroke secondary to embolization of a cardiac atrial myxoma, was transferred to our medical center for hyperemesis and severe hypercalcemia. Albumin-corrected serum calcium measured 15.4 mg/dL (8.6-10.5 mg/dL), ionized calcium 7.8 mg/dL (4.6-5.3 mg/dL) associated with suppressed PTH, normal PTH-related protein, and elevated bone turnover markers, C-telopeptide 4,273 pg/ml (150-635) and Procollagen Type 1 N-terminal Propeptide 222 mcg/L (19-83). Evaluation for etiology of hypercalcemia revealed elevated 1,25 dihydroxy vitamin D at 107.0 pg/ml (20-79) and elevated interleukin-6 at 11 pg/ml (<6.4). IL-6 is expressed by cardiac myxomas. Serum angiotensin-converting enzyme level was 50 U/L (16-85) and infectious workup was negative for potential granulomatous causes of elevated calcitriol (including testing for tuberculosis, histoplasma, blastomyces, bartonella, and coccidioides). CT angiogram of the abdomen and pelvis (completed in preparation of atrial myxoma resection) revealed ground-glass opacities in bilateral posterior lung fields and multiple pulmonary nodules, with the largest measuring 8 mm. After treatment with aggressive intravenous fluid resuscitation, intramuscular calcitonin, and intravenous zoledronic acid, corrected calcium normalized to 9.4 mg/dL at discharge. Urinary cortisol was 6.2 mcg per 24-hr (3.5-45), for which she started hydrocortisone 20 mg daily to treat suspected adrenal insufficiency as excess cortisol secretion in PPNAD may be episodic. Thus remission of hypercortisolism may have unmasked an underlying hypercalcemia, and adrenal insufficiency itself may have contributed to this finding. She had excision of left atrial myxoma and has continued to exhibit normal calcium levels on steroid replacement therapy. Repeat chest CT to further characterize these pulmonary findings is planned. This case illustrates a unique constellation of endocrine features associated with severe hypercalcemia in Carney complex. Presentation: 6/1/2024

6564 A Case Of Severe Hypercalcemia In Carney's Complex

Abstract Disclosure: J. Chippior: None. M. Rayan: None. L. Wright: None. L.S. Kirschner: Grant Recipient; Self; Medpace, Sparrow, Corcept Therapeutics, Corcept, Spruce, CinCor, Crinetics, Adrenas. S.W. Ing: Grant Recipient; Self; Alexion Pharmaceuticals, Inc., Amgen Inc, Radius Health, Inc, Takeda, Ultragenyx, Amolyt, Bridge Bio. Carney complex is a rare syndrome with fewer than 750 reported cases, characterized by lentigniosis, myxomas, and the occurrence of both endocrine and non-endocrine tumors. An inactivating mutation PRKAR1A, which encodes for the type 1A regulatory subunit of Protein kinase A, is responsible for over 70% of familial cases and 37% of sporadic cases. A 31-year-old female with a history of Carney complex, Cushing syndrome due to primary pigmented nodular adrenocortical disease (PPNAD), facial lentigines, spinal Schwannomas, and recent ischemic stroke secondary to embolization of a cardiac atrial myxoma, was transferred to our medical center for hyperemesis and severe hypercalcemia. Albumin-corrected serum calcium measured 15.4 mg/dL (8.6-10.5 mg/dL), ionized calcium 7.8 mg/dL (4.6-5.3 mg/dL) associated with suppressed PTH, normal PTH-related protein, and elevated bone turnover markers, C-telopeptide 4,273 pg/ml (150-635) and Procollagen Type 1 N-terminal Propeptide 222 mcg/L (19-83). Evaluation for etiology of hypercalcemia revealed elevated 1,25 dihydroxy vitamin D at 107.0 pg/ml (20-79) and elevated interleukin-6 at 11 pg/ml (<6.4). IL-6 is expressed by cardiac myxomas. Serum angiotensin-converting enzyme level was 50 U/L (16-85) and infectious workup was negative for potential granulomatous causes of elevated calcitriol (including testing for tuberculosis, histoplasma, blastomyces, bartonella, and coccidioides). CT angiogram of the abdomen and pelvis (completed in preparation of atrial myxoma resection) revealed ground-glass opacities in bilateral posterior lung fields and multiple pulmonary nodules, with the largest measuring 8 mm. After treatment with aggressive intravenous fluid resuscitation, intramuscular calcitonin, and intravenous zoledronic acid, corrected calcium normalized to 9.4 mg/dL at discharge. Urinary cortisol was 6.2 mcg per 24-hr (3.5-45), for which she started hydrocortisone 20 mg daily to treat suspected adrenal insufficiency as excess cortisol secretion in PPNAD may be episodic. Thus remission of hypercortisolism may have unmasked an underlying hypercalcemia, and adrenal insufficiency itself may have contributed to this finding. She had excision of left atrial myxoma and has continued to exhibit normal calcium levels on steroid replacement therapy. Repeat chest CT to further characterize these pulmonary findings is planned. This case illustrates a unique constellation of endocrine features associated with severe hypercalcemia in Carney complex. Presentation: 6/1/2024

7761 Unmasking The Uncommon: A Case Of Primary Adrenal Insufficiency Presenting As Severe Hypercalcemia

Abstract Disclosure: A. Misbah: None. Z. Al-Hiti: None. A. Saleh: None. M. Joda: None. K. Rajamani: None. Adrenal insufficiency is a recognized but uncommon cause of hypercalcemia. The exact mechanism remains unknown; however, it is thought to be a combination of the hypovolemic state in adrenal insufficiency leading to decreased urinary clearance, as well as increased bone resorption. We present a case of primary adrenal insufficiency presenting with severe hypercalcemia. A 41 year old female with a past medical history of osteopenia, recently diagnosed postural orthostatic tachycardia syndrome (POTS), and hyponatremia attributed to SIADH presented with complaints of weakness and poor oral intake. She also reported a history of nausea, vomiting, weight loss, fatigue, and dizziness, for the last few months. She reported feeling well prior to a COVID-19 infection a few months back. At presentation, she was hypotensive with a blood pressure of 70/50 mmHg, while her other vital signs were stable. She appeared ill, and was noted to have dry oral mucous membranes. There was no increased pigmentation noted on exam. Initial laboratory evaluation revealed sodium of 130 (135-145 mmol/L), potassium of 5.3 (3.5-5.1 mmol/L), and creatinine of 1.7 (0.5-0.8 mg/dL). She had severe hypercalcemia with a calcium level of 15.5 (8.3-10.6 mg/dL) and had a blood glucose level of 53 (70-100 mg/dL). Venous blood gas indicated metabolic acidosis. Morning cortisol was low at 1 (3-23 ug/dL). Serum ACTH was elevated at 775 (0-46 pg/mL). Cosyntropin stimulation test confirmed primary adrenal insufficiency. She underwent work-up for hypercalcemia, which revealed a suppressed PTH, normal levels of PTHrP, vitamin D, and vitamin A. Serum and urine protein electrophoresis was normal. She was initially managed in the ICU and received aggressive fluid resuscitation. She was started on stress dose of hydrocortisone, which was then tapered to physiological doses of oral hydrocortisone and fludrocortisone. Subsequent improvements were observed in blood pressure, laboratory abnormalities, and normalized serum calcium levels. She was discharged home on hydrocortisone and fludrocortisone. On follow-up, she was doing well with the resolution of her symptoms. This case highlights the importance of recognizing adrenal insufficiency as one of the causes of hypercalcemia. Although hypercalcemia as a consequence of adrenal insufficiency is well-documented, the exact prevalence is not known but is estimated to be around 6%. After excluding more common diseases such as primary hyperparathyroidism and malignancy, the possibility of adrenal insufficiency should be considered as a cause of hypercalcemia. Treatment involves hormone replacement as well as hydration, bringing resolution to symptoms. Her presentation was unique, also due to the fact that her initial symptoms were diagnosed as POTS as well as SIADH. Given the onset of symptoms after a COVID-19 infection a few months ago, there could also be a potential link between the two. Presentation: 6/3/2024

EP492 - Fulminant Clostridium difficile infection post reversal of ileostomy

Abstract Aims Clostridium difficile infection (CDI) is an important cause of diarrhoea in hospitalized patients, varying from mild to fulminant forms. Fulminant CDI subsequent to the reversal of ileostomy, despite negative C. difficile toxin, is rare. Results We present the case of a 75-year-old male with a history of atrial fibrillation, chronic obstructive pulmonary disease and hypertension, who underwent elective ileostomy reversal following an emergency laparotomy and end ileostomy for acute diverticular bleed two years prior. Initially uncomplicated, the patient developed mild CDI on postoperative day 4 with white cell count of 18.6×109/L, evolving rapidly to severe CDI by day 6, characterized by worsening abdominal pain, worsening leukocytosis (30×109/L), and acute kidney injury stage 1. Patient was started on Vancomycin and Metronidazole, Computed Tomography (CT) scan showed uncomplicated sigmoid colitis. Despite aggressive antibiotic therapy and fluid resuscitation, the patient deteriorated on day 8, presenting with fulminant CDI, hypotension, elevated lactate of 2.6 and leukocytes of 46×109/L. Subsequent CT Imaging revealed pneumatosis coli. At that point, the patient's NELA score was 53.4%. The patient was stabilised by the critical care team prior to emergency subtotal colectomy and end ileostomy due to suspected colonic perforation. Surgical finding showed transverse colon inflammation with a hepatic flexure abscess. Patient required 14-day intensive care unit stay and 13 days of ward management before he is fit for rehab. Conclusion This case highlights the potential for fulminant CDI post-ileostomy reversal and highlights the challenges in managing such complications, necessitating prompt recognition and interventions to mitigate adverse outcomes.

Advancements in Trauma-Induced Acute Kidney Injury: Diagnostic and Therapeutic Innovations.

Acute kidney injury following trauma impacts patient recovery critically, necessitating an integrated approach to emergency care and nephrology. This review aims to provide a comprehensive understanding of trauma-induced nephropathy, highlighting recent advancements in pathophysiological insights, diagnostic techniques, and strategic interventions. Our key findings emphasize the role of biomarkers, like Neutrophil Gelatinase-Associated Lipocalin and Liver Fatty Acid-Binding Protein, and imaging techniques, such as contrast-enhanced ultrasound, in early AKI detection. Preventive strategies, including aggressive fluid resuscitation, avoidance of nephrotoxic agents, and hemodynamic optimization, are essential for mitigating AKI progression. Integrating these approaches into trauma care frameworks aims to enhance patient outcomes and set a foundation for future research and clinical improvements.

Acute pancreatitis in a patient with normal lipase: a case report

This case report highlights the rare occurrence of acute pancreatitis in a patient exhibiting normal lipase levels. The patient presented to the emergency department with abdominal pain and fever. Laboratory tests indicated an acute inflammatory process but a negative lipase value. The diagnosis was established by a CT scan showing necrotizing pancreatic changes with elevated carbohydrate-deficient transferrin (CDT) levels, suggesting alcohol as the etiology. Management involved supportive care, aggressive fluid resuscitation, nutritional support, and empirical antibiotic therapy, which led to clinical improvement. This case emphasizes the importance of a comprehensive clinical assessment beyond standard biochemical markers in diagnosing and managing pancreatitis.

Acute Pancreatitis after EGD: Case Presentation and Literature Review of this Rare Post-Procedure Complication.

Acute pancreatitis is a common cause of hospitalisation characterised by inflammation of the pancreas. While mechanical, toxic and iatrogenic factors typically cause it, post-oesophagogastroduodenoscopy (EGD) pancreatitis is extremely rare. This report examines a case of acute pancreatitis following EGD, aiming to highlight this rare but significant complication. A 46-year-old woman with a history of breast cancer, anxiety, vitamin D deficiency and gastro-oesophageal reflux disease underwent an EGD, which revealed and led to the removal of duodenal polyps. Six hours post-procedure, she presented with severe abdominal pain radiating to her back, accompanied by nausea. Laboratory results indicated elevated lipase levels, and a computed tomography (CT) scan confirmed acute pancreatitis. The patient was managed with aggressive fluid resuscitation, bowel rest and pain management, leading to an improvement in her condition and subsequent discharge. We believe that the pancreatitis was likely caused by the use of cautery during the endoscopic mucosal resection of duodenal polyps. This case underscores the need for clinicians to recognise acute pancreatitis as a potential complication of EGD, especially in the absence of other common risk factors. Acute pancreatitis following oesophagogastroduodenoscopy (EGD) is an uncommon but significant complication.Possible mechanisms include mechanical trauma, gas insufflation or electrical injury during endoscopic mucosal resection.Clinicians should be aware of this potential complication, especially when no typical aetiological factors for pancreatitis are present.

Length of Hospital Stay in Patients Related with Moderate Fluid Resuscitation and Aggressive Fluid Resuscitation in Acute Pancreatitis

Length of Hospital Stay in Patients Related with Moderate Fluid Resuscitation and Aggressive Fluid Resuscitation in Acute Pancreatitis

Management of Refractory Anaphylaxis: An Overview of Current Guidelines.

In this review, we compare different refractory anaphylaxis (RA) management guidelines focusing on cardiovascular involvement and best practice recommendations, discuss postulated pathogenic mechanisms underlining RA and highlight knowledge gaps and research priorities. There is a paucity of data supporting existing management guidelines. Therapeutic recommendations include the need for the timely administration of appropriate doses of aggressive fluid resuscitation and intravenous (IV) adrenaline in RA. The preferred second-line vasopressor (noradrenaline, vasopressin, metaraminol and dopamine) is unknown. Most guidelines recommend IV glucagon for patients on beta-blockers, despite a lack of evidence. The use of methylene blue or extracorporeal life support (ECLS) is also suggested as rescue therapy. Despite recent advances in understanding the pathogenesis of anaphylaxis, the factors that lead to a lack of response to the initial adrenaline and thus RA are unclear. Genetic factors, such as deficiency in platelet activating factor-acetyl hydrolase or hereditary alpha-tryptasaemia, mastocytosis may modulate reaction severity or response to treatment. Further research into the underlying pathophysiology of RA may help define potential new therapeutic approaches and reduce the morbidity and mortality of anaphylaxis.

A rare case of IgA lambda multiple myeloma in a 32-year-old woman with t(14;16) translocation associated with kidney injury and non-albumin proteinuria

BackgroundMultiple myeloma (MM) is a malignant disorder characterized by monoclonal differentiated plasma cells. While it is more commonly diagnosed in elderly individuals, it can also affect younger populations, though with a lower incidence.Case presentationHere, we present the case of a 32-year-old woman diagnosed with IgA lambda MM. She presented with fatigue, nausea, acute kidney injury (AKI) with a rapid increase in creatinine, and anemia. A kidney biopsy was done to rule out a rapidly progressive glomerular disease and a diagnosis was thus reached. A genetic workup revealed t(14;16) translocation and an extra copy of TP53. The patient received aggressive intravenous steroids and intravenous fluid resuscitation, resulting in an improvement in renal function. Treatment with daratumumab in combination with bortezomib, thalidomide, and dexamethasone was initiated and well tolerated. Despite the generally poor prognosis of IgA MM, our case emphasizes the importance of considering MM in young patients with unexplained kidney injury.ConclusionEarly recognition and prompt intervention are essential in managing MM patients, especially in those with high-risk cytogenetic abnormalities. This case serves as a reminder for clinicians to maintain a high index of suspicion for MM, even in younger populations, when presented with unexplained kidney injury.

Rhabdomyolysis Associated with Sedentary Lifestyle, Strenuous Exercise, and Vitamin D3 Deficiency: A Rare Case Report

Rhabdomyolysis can lead to variable clinical presentation and complications putting life at risk. Patients with preexisting low serum 25(OH) Vitamin D are at high risk of exertional rhabdomyolysis during strenuous activities. This aimed to study the pathophysiology of rhabdomyolysis associated with sedentary lifestyle, strenuous exercise, and Vitamin D3 deficiency. A 26-year-old male with chief complaints of cramps in thigh muscles, reduced urine output, and dark coffee-colored urine was presented at Bawa Hospital, Ludhiana. The patient has a history of strenuous exercise and Vitamin D deficiency. Serum creatinine kinase, liver enzymes, and myoglobin in urine were evaluated. The patient was treated with intravenous fluids, sodium bicarbonate, and diuretic. The case was diagnosed as rhabdomyolysis and was treated accordingly. The recovery after 5 days was good following early treatment with fluids and forced alkaline diuresis. The kidney function tests remained normal throughout the treatment period. Aggressive fluid resuscitation is the key management for rhabdomyolysis.

Iliac Vein Stenting and Thrombectomy Result in Limb Salvage in Phlegmasia Caerulea Dolens as a Result of Heavy Fibroid Burden.

Phlegmasia cerulea dolens is a devastating sequelae of propagating deep vein thrombosis causing total venous outflow obstruction of an extremity. It is characterized by significant pain, edema, cyanosis, and critical limb ischemia and may progress toward venous gangrene. Morbidity and mortality rates associated with this phenomenon are high. Treatment options are limited and consist of early and aggressive therapeutic anticoagulation and fluid resuscitation, followed by thrombectomy or thrombolysis if the patient fails to respond clinically in 6-12hours.

Permissive Hypotension in a Patient with Severe Hypernatremia: A Case Report.

Severe hypernatremia is a critical situation, and when coupled with intravascular depletion and hypotension can create a treatment dilemma. We present the case of a medically complex patient who had gradually worsening alteration of mental status and mean arterial pressures in the 50s on presentation to the emergency department. Final diagnoses included severe hypernatremia and hypovolemic shock secondary to poor oral intake. We used judicious fluid repletion with gradual improvement in sodium levels and permissive hypotension to avoid rapid osmotic shifts. Balancing reperfusion and the risk for osmotic effects of aggressive fluid resuscitation can be a challenging situation for the multidisciplinary team.

Prognostic Biomarkers and AKI: Potential to Enhance the Identification of Post-Operative Patients at Risk of Loss of Renal Function.

Acute kidney injury (AKI) is a common complication after surgery and the more complex the surgery, the greater the risk. During surgery, patients are exposed to a combination of factors all of which are associated with the development of AKI. These include hypotension and hypovolaemia, sepsis, systemic inflammation, the use of nephrotoxic agents, tissue injury, the infusion of blood or blood products, ischaemia, oxidative stress and reperfusion injury. Given the risks of AKI, it would seem logical to conclude that early identification of patients at risk of AKI would translate into benefit. The conventional markers of AKI, namely serum creatinine and urine output are the mainstay of defining chronic kidney disease but are less suited to the acute phase. Such concerns are compounded in surgical patients given they often have significantly reduced mobility, suboptimal levels of nutrition and reduced muscle bulk. Many patients may also have misleadingly low serum creatinine and high urine output due to aggressive fluid resuscitation, particularly in intensive care units. Over the last two decades, considerable information has accrued with regard to the performance of what was termed "novel" biomarkers of AKI, and here, we discuss the most examined molecules and performance in surgical settings. We also discuss the application of biomarkers to guide patients' postoperative care.

A315 A QUALITY ASSESSMENT OF THE ADEQUACY OF FLUID REPLACEMENT THERAPY FOR PATIENTS DIAGNOSED WITH ACUTE PANCREATITIS

Abstract Background For acute pancreatitis (AP), aggressive fluid resuscitation therapy (FRT) is the cornerstone for initial management. However, results from the recent WATERFALL study show a higher incidence of fluid overload with aggressive FRT (bolus of 20 ml/kg followed by infusion of 3 ml/kg/hr of Ringer’s lactate [RL]) compared with moderate FRT (infusion of 1.5 ml/kg/hr RL preceded by a bolus of 10 ml/kg only in those with hypovolemia). Given this evidence, we conducted a study to assess whether patients with AP received appropriate fluid therapy and monitoring at our institution. Aims To assess whether fluid replacement therapy in patients with AP was aligned with updated clinical practice at our centre. Methods We completed a chart audit of all adult (≥ 18 years old) patients who presented to the ED from April 1, 2021 through March 31, 2022 and were diagnosed with AP. Patients were identified based on ICD-10 codes for a primary admission or discharge diagnosis of AP. Data variables collected included demographic information, cause of AP, comorbidities, laboratory tests, type and volume of fluids replaced, urine output, complications, and hospital length of stay (HLOS). Severity of AP was categorized as mild, moderate, or severe based on the revised Atlanta classification of AP. Descriptive statistics were completed. Results A total of 250 patients (121 F, 129 M), mean age 53±19 years (range 19-96 years) were diagnosed with AP. Body weight was not available for 4 patients and thus excluded from this analysis. FRT variables stratified for the severity of AP are below in Table 1. Conclusions Our quality assessment has identified a knowledge-to-practice gap in the use of FRT for patients with AP. To assist physicians in the decision-making process, we have developed an algorithm to improve FRT in AP. This will be implemented via an order set to standardize the amount of FRT and to improve monitoring of urine output. This algorithm will be tested using an improvement science approach in collaboration with healthcare professionals. Table 1. Summary of fluid management in AP patients as stratified by severity of disease. Funding Agencies None

The first reported mortality from aluminum phosphide poisoning in Lebanon: a case report

BackgroundAluminum phosphide is a commonly used pesticide, particularly in developing countries where uncontrolled insecticides and pesticides are commonly prevalent. Mortalities have been reported due to accidental and suicidal exposures to aluminum phosphide. To date, there has been no reported mortality case of aluminum phosphide in Lebanon. In addition, there is no specific antidote for aluminum phosphide toxicity and the treatment is mainly supportive. This is why awareness should be spread about this case to include it in the differential diagnoses and enhance prompt management and response in future encounters.Case presentationA previously healthy 37-year-old male, presented to the emergency department of Notre Dame des Secours University Hospital Center for a suicidal attempt after ingesting 5 tablets of pesticide containing 56% aluminum phosphide an hour prior to presentation. Shortly after the presentation, the patient began deteriorating and became clinically unstable. The patient was then intubated and was started on sodium bicarbonate along with aggressive fluid resuscitation. The patient remained hypotensive even after giving vasopressors. He was then later admitted to the intensive care unit for further management. However, the patient further decompensated and developed multiorgan failure. This is the first case of mortality in Lebanon from aluminum phosphide toxicity.ConclusionsEmergency physicians should include aluminum phosphide toxicity in the differential diagnosis when dealing with patients ingesting unknown pesticides especially when they smell the characteristic garlic-like odor. The toxicity from ALP leads to multiorgan failure and death rapidly. Thus, it is of utmost importance to start early, and aggressive resuscitation given that there is no specific antidote.

Combination of substance addiction and Fournier’s gangrenia: a case report

Fournier's gangrene is a bacterial and rapidly progressive necrotizing fasciitis of the perianal and perineal region. It still has high morbidity and mortality. We aimed to present Fournier's gangrene, which developed in a 49-year-old male patient with substance abuse. The patient was brought to the emergency department with complaints of abdominal pain and pain in the perineum and perianal region on the 3rd day after foreign body trauma to the perianal region. Crepitation was detected under the skin in the suprapubic region of the patient. Acute abdomen was present in the abdominal examination. In the abdominal tomography, minimal fluid was detected between the bowel loops in the pelvis. Diffuse edema, heterogeneity and emphysematous changes were observed in the skin and subcutaneous tissues in the perineum, and in the rectus muscle of the anterior abdominal wall. The patient underwent an emergency laparotomy. Abscess material extending from the back of the rectus muscle to the pelvis was seen in the abdomen. Abscess and necrotic areas in the abdomen and perineum were cleaned. A protective Hartman end colostomy was opened to the patient. In the postoperative period, VAC was applied to the perianal region for 3 sessions with 72 hour intervals. Then, the wound in the perineum was closed primarily. After 3 months, his colostomy was taken into the abdomen. Early and aggressive surgical debridement, broad-spectrum antibiotics, and fluid resuscitation are critical in Fournier's gangrene. Because of this patient's late admission to the hospital and his long-term immunosuppression associated with substance abuse, his clinical condition deteriorated rapidly. It should be kept in mind that skin infections in the perianal region may progress to Fournier's gangrene in patients with conditions that may cause immunosuppression, such as substance abuse.

Case Report on a Cocktail Drug Abuser Developing Rhabdomyolysis

Rhabdomyolysis is a medical emergency characterized by the break down of skeletal muscle leading to the release of intracellular contents into the blood stream, which can lead to acute kidney injury and even death. Drug abuse is one of the potential causes of rhabdomyolysis. This case report describes a 18-year-old male with a history of drug abuse who presented to the emergency department with severe muscle pain, weakness, dark and reduced amount of urine. The patient was diagnosed with rhabdomyolysis, which was likely due to a combination of high doses Marijuana, Chlorpheniramine, Dextromethorphan (Corex Syrup), Dicyclomine, Tramadol, Acetaminophen and cigarette smoking over period of 4-5 years, landed up in rhabdomyolysis after joining gym. The patient was immediately started on aggressive intravenous fluid resuscitation, and his urine output and electrolyte levels were closely monitored. Patient required initiation of Hemodialysis over period of 15 days. Patient's muscle pain and weakness gradually improved over the next few days, and he was discharged with a diagnosis of AKI due to Rhabdomyolysis due to drug abuse. Prompt recognition and treatment of rhabdomyolysis are crucial to prevent serious complications, and addiction treatment should be pursued to prevent future episodes of rhabdomyolysis and other drugrelated complications.