RESUMO
Cameron lesions are rare causes of upper gastrointestinal bleeding (UGIB). The lesions are linear erosions or ulcers that develop in the sac of a hiatal hernia, which often go unnoticed in the upper gastrointestinal system, and are a prevalent cause of anemia resulting from iron deficiency. Postponed treatment can result in severe consequences such as potentially fatal hemorrhaging. Here, we present a case of a young woman who presented to the emergency room with recurrent gastrointestinal bleeding and severe microcytic anemia. The chest X-ray revealed a partial intrathoracic stomach, and a large hiatal hernia was subsequently confirmed in the CT scan of the abdomen and pelvis. The esophagogastroduodenal endoscopy indicated Los Angeles Classification System grade A reflux esophagitis and an 8 cm hiatal hernia with multiple Cameron ulcers with pigmented material and chronic non-erosive gastritis. Biopsies of the gastric body and antrum showed Helicobacter pylori-associated chronic active gastritis and intestinal metaplasia. An esophagus biopsy showed squamous esophageal mucosa with mild chronic inflammation. The patient was treated with a transfusion of three units of red blood cells, iron replenishment, and pantoprazole infusion and underwent hiatal hernia repair with mesh and Toupet fundoplication without any complications. After that, the patient was discharged and scheduled for follow-up with general surgery at the outpatient clinic.
RESUMO
Aortoesophageal fistula (AEF) is an uncommon complication of esophageal cancer and can be extremely fatal if left untreated. Compared to open repair, thoracic endovascular aortic repair (TEVAR), a less invasive technique, is the initial recommended treatment in cases of hemorrhagic shock secondary to AEF, as this procedure showed a favorable outcome in controlling the overt bleeding. Here, we present a case of a patient with a history of stage IV esophageal cancer being treated with chemotherapy and an esophageal stent due to a previous tracheoesophageal fistula who presented to the emergency room due to severe gastroesophageal bleeding and hemorrhagic shock. A CT angiography of the chest revealed an AEF. The patient was subsequently resuscitated and treated with TEVAR. After the procedure, the hemorrhage was managed, and the patient was discharged with palliative radiation therapy. However, after one month, the patient had a major gastrointestinal hemorrhage, which caused her death. This example indicates the necessity of early detection and surgical intervention in AEF patients with unstable hemodynamics who have underlying unresectable esophageal cancer and chemotherapy. TEVAR should be conducted as soon as possible before the open surgery to achieve the best outcome for patients.
RESUMO
Hypernatremia, characterized by a plasma sodium concentration above 145 mmol/L, is frequently observed in critically ill patients, often due to factors such as gastrointestinal losses, dehydration, and diabetes insipidus. Psychiatric patients, particularly those with major depressive disorder, are also at risk of developing hypernatremia due to abnormalities in thirst sensation, mineralocorticoid excess, or medication side effects. Severe hypernatremia in psychiatric patients is associated with a high mortality rate, presenting challenges in diagnosis and management. The treatment of chronic hypernatremia (>48 hours) typically involves administering isotonic saline to hypovolemic patients until normalization of vital signs, followed by dextrose 5% in water (D5W) based on water deficit and losses. The goal is to decrease plasma sodium by 8-10 mmol/day. Acute hypernatremia (<48 hours) is corrected with a plasma sodium reduction of 1 mmol/L/hour in the first six to eight hours. While there are no clear guidelines for sodium correction in severe hypernatremia, the literature suggests a safe correction rate of 8-10 mmol/day for chronic hypernatremia and 1 mmol/L/hour for acute cases. In a specific case, a 51-year-old female with severe depression and reduced oral intake was admitted. She exhibited signs of dehydration and was found to have severe hypernatremia (191 mmol/L) with acute kidney injury. Treatment involved D5W, followed by D5W/half-normal saline at 150 mL/hr. Within 24 hours, her plasma sodium decreased to 178 mmol/L and gradually normalized to 143 mmol/L without neurological complications. This case highlights the challenges and underscores the importance of early recognition and management of severe hypernatremia in psychiatric patients. The primary treatment approach addresses water deficits and losses and administers D5W. Recent findings suggest that rapid correction of the condition is acceptable.
