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Key Clinical Message: Chronic ketamine use can lead to sphincter of oddi dysfunction (SOD), causing various hepatobiliary complications. Recognizing substance abuse history is vital for early detection. Timely intervention can prevent irreversible liver and pancreas damage. Abstract: Ketamine is commonly abused as a recreational drug worldwide due to its ability to induce euphoria-like effects. Ketamine abuse is associated with many hepatobiliary side effects ranging from cholestasis to biliary sepsis and death. Here we present a case of a young 29-year female with upper abdominal pain due to SOD resulting from chronic use of ketamine. SOD can result in obstruction or dysfunction of the bile and pancreatic ducts. Ketamine induces SOD by activation of the muscarinic receptors in the sphincter of oddi. Detail history of substance abuse is crucial for early identification of ketamine-induced SOD. Early identification and treatment of this rare condition can prevent permanent injury to the liver and pancreas.
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Key Clinical Message: Immune checkpoint inhibitors can rarely lead to occurrence of myositis, myocarditis, and myasthenia gravis (MG). Early recognition and multidisciplinary management are crucial for optimal outcomes. Vigilance for overlapping toxicities is essential in patients receiving combination immunotherapy. Abstract: The use of immune checkpoint inhibitors (ICIs) has revolutionized cancer treatment, but it is associated with immune-related adverse events (IRAEs) affecting various organ systems. The simultaneous occurrence of MG, myocarditis, and myositis highlights the complex nature of IRAEs. Early recognition and comprehensive multidisciplinary management are crucial for optimal patient outcomes. We present a unique case report of a 76-year-old male patient with advanced melanoma who developed concurrent myositis, myocarditis, and MG while receiving combination immunotherapy with Nivolumab and Ipilimumab. This case underscores the significance of recognizing and addressing the "Terrible Triad" of IRAEs in patients receiving ICIs. Healthcare providers should maintain a high index of suspicion for overlapping toxicities and promptly initiate appropriate interventions.
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Immersion pulmonary edema, also known as swimming-induced pulmonary edema (SIPE), manifests with cough, dyspnea, hemoptysis, and hypoxemia from flash pulmonary edema after surface swimming, often in healthy young individuals with no predisposing conditions. SIPE commonly resolves spontaneously within 24-48 hours but can be fatal. Post-mortem findings demonstrate heavy, edematous lungs and frothy airways. Although these pathologic findings are like those seen in patients with drowning, SIPE, by definition, is associated with pulmonary edema that develops with a closed glottis without drowning/aspiration. However, patients who develop SIPE during swimming could lose consciousness and drown. Its pathophysiology is poorly understood, and the medical literature infrequently describes SIPE. Due to the multifactorial and complex pathophysiology and the scarcity of medical literature describing SIPE, the diagnosis could be difficult at presentation. This case report elaborates on diagnosing and treating swimming-induced pulmonary edema in a hypertensive and obese female who presented to our emergency room with an acute onset of shortness of breath after recreational swimming in a pool.
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Diabetic ketoacidosis (DKA) is a life-threatening metabolic emergency traditionally associated with Type 1 diabetes but is increasingly recognized in Type 2 diabetes, particularly with the use of sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Euglycemic DKA, characterized by near-normal blood glucose levels, is a distinct variant that has gained attention. This case report highlights a unique presentation of euglycemic DKA in a 56-year-old female with a past medical history of Type 2 Diabetes Mellitus who presented to the emergency department with a one-week history of chest pain.
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This case report explores the intricate diagnostic challenges encountered in a 30-year-old male patient with abdominal pain, jaundice, and a history of acetaminophen use. Initially presenting as a potential case of drug-induced hepatitis due to acetaminophen overdose, the diagnosis took an unexpected turn when the patient tested positive for hepatitis B surface antigen. The case highlights the complexity of diagnosing acute hepatitis, considering multiple potential etiologies, including viral and drug-induced factors. Differential diagnoses for this case involve considering drug-induced hepatitis, autoimmune hepatitis, various viral hepatitis types, and the potential contribution of cocaine-induced hepatitis as individual possibilities or in combination. This case emphasizes the need for a comprehensive evaluation, the consideration of multiple potential causes, and the importance of ongoing monitoring and follow-up to ensure optimal patient care in cases of acute hepatitis.