Primary gastric squamous cell carcinoma is a very rare disease. A 53-year-old male with history of hypertension, alcoholism, and nicotine abuse presented to the hospital after a syncopal episode. He complained of bloating abdominal pain, early satiety, and poor appetite. A CT of his abdomen and pelvis revealed a gastric mass with diffuse hepatic metastasis. A gastric mass was seen on upper endoscopy and biopsies revealed gastric squamous cell carcinoma. There was no involvement of the esophagus. This case should add to the limited literature and serve as a reminder that while this is a rare malignancy, it must be considered when evaluating a gastric mass.

We present a 71-year-old white man with active ileocolonic Crohn's disease, recently started on budesonide therapy, who presented with extreme weakness and muscle aches. He was diagnosed with hypokalemia-induced rhabdomyolysis, 3 weeks after starting budesonide therapy. His symptoms and laboratory values improved with budesonide discontinuation and appropriate fluid and electrolyte replacement. This is only the second case of hypokalemia-induced rhabdomyolysis secondary to budesonide.

Introduction: Acute esophageal necrosis (AEN), commonly referred to as black esophagus due to the striking circumferential blackening of the esophageal mucosa, is a rare clinical condition with a prevalence of up to 0.2%. The etiology of this condition is unclear but thought to involve the interplay of ischemia and gastric outlet obstruction with gastroesophageal reflux. As this condition carries with it a mortality rate of nearly 40%, prompt recognition and aggressive management is of the utmost importance to prevent perforation or stricture. Considering this, AEN should be recognized as a possible outcome of an ischemic event and considered a potential cause of spontaneous esophageal perforation. Case Description/Methods: A 43-year-old female with a history of epithelioid hemangioendothelioma status post resection, Crohn's colitis in remission, and recent hospitalization for a complicated urinary tract infection and abdominopelvic ascites concerning for malignancy with hospitalization complicated by cardiopulmonary arrest presented to the emergency department 8 days after discharge following a near syncopal episode. She was found to be hypotensive with tachycardia concerning for shock. She was started on broad spectrum antibiotics, 3 vasopressors, intubated, and admitted to the ICU. A CT scan of her chest, abdomen, and pelvis showed extensive pneumomediastinum concerning for esophageal perforation and pneumatosis intestinalis. Perforation was confirmed utilizing serial chest x-rays with contrast demonstrating a right-sided esophageal leak at the gastroesophageal junction. Both cardiothoracic surgery and gastroenterology were consulted, she was not deemed a surgical candidate and endoscopy with covered stent placement was planned. Endoscopy revealed a black esophagus consistent with an ischemic process throughout the entire esophagus and pneumatosis intestinalis suggesting small bowel ischemia. Stenting was aborted and the findings were discussed with the patient's family who decided to pursue comfort measures. The patient died the following day (Figure). Discussion: It has been demonstrated that critically ill patients often experience low flow states, poor nutritional status, and disruption of intrinsic repair mechanisms. Coupled together, these insults increase the risk of developing AEN and must be acknowledged as a possible complication in this patient population. Although this is a rare condition, it should be recognized as a potential outcome of an ischemic event.[2450] Figure 1. Images A-D depicts a diffusely abnormal mucosa throughout the esophagus, characterized by black/brown tissue consistent with ischemia.

INTRODUCTION: Here we present the case of a 71-year-old white male with active ileocolonic Crohn's disease, recently started on budesonide therapy, who presents with extreme weakness and muscle aches. He was diagnosed with hypokalemia induced rhabdomyolysis, three weeks after starting budesonide therapy. CASE DESCRIPTION/METHODS: We present the case of a 71-year-old male with hypertension and ileocolonic stricturing crohn's disease (CD) presents with severe muscle weakness and malaise. He presented for a five-month history of worsening watery diarrhea and unintentional weight loss. Colonoscopy to neoterminal ileum revealed Rutgeerts score of i3. He was started on oral 9 mg budesonide and began to experience weakness and muscle aches to a point where he was unable to walk or lift his arms above his head. He presented to the hospital and labs revealed hypomagnesemia 0.8 mg/dL, hypokalemia of potassium 1.7 mmol/L, creatinine 1.52 mg/dL, creatine phosphokinase (CPK) 15913 IU/L, hypocalcemia 7.1 mg/dL, normal albumin 3.7 g/dL. Urinalysis showed 3+ blood and 0-3 red blood cells. Labs two months prior were unremarkable (Table 1). He was diagnosed with rhabdomyolysis. DISCUSSION: Budesonide has long been accepted as induction therapy for mild-to-moderate CD. Hypokalemia induced rhabdomyolysis is due to laxative abuse, chronic diarrhea, renal tubular acidosis, diuretics use is well reported. Hypokalemia is a known side effect of budesonide. 1 Rhabdomyolysis is a syndrome which is characterized by muscle necrosis with CPK four times more than the upper limit of normal. 1 During a muscle contraction, potassium is released from the intracellular to extracellular space mediating the vasodilation and more blood flow to the muscle. When a patient has hypokalemia, there is a decrease in blood flow to the contracting muscles. This leads to constriction of arterioles causing ischemia of the muscles and myocytes destruction. The breakdown of the myofibril causes muscle necrosis and an increase in intracellular CPK and myoglobin, which is released into the blood circulation. 2 In this patient, several factors were taken into account for the cause of hypokalemia induced rhabdomyolysis. The patient rapidly responded to intervenous fluid and discontinuation of the budesonide.

No abstract