Amebic liver abscesses (ALAs) are the most commonly encountered extraintestinal manifestation of human invasive amebiasis, which results from Entamoeba histolytica ( E. histolytica ) spreading extraintestinally. Amebiasis can be complicated by liver abscess in 9% of cases, and ALAs led to almost 50000 fatalities worldwide in 2010. Although there have been fewer and fewer cases in the past several years, ALAs remain an important public health problem in endemic areas. E. histolytica causes both amebic colitis and liver abscess by breaching the host’s innate defenses and invading the intestinal mucosa. Trophozoites often enter the circulatory system, where they are filtered in the liver and produce abscesses, and develop into severe invasive diseases such as ALAs. The clinical presentation can appear to be colitis, including upper-right abdominal pain accompanied by a fever in ALA cases. Proper diagnosis requires nonspecific liver imaging as well as detecting anti- E. histolytica antibodies; however, these antibodies cannot be used to distinguish between a previous infection and an acute infection. Therefore, diagnostics primarily aim to use PCR or enzyme-linked immunosorbent assay to detect E. histolytica . ALAs can be treated medically, and percutaneous catheter drainage is only necessary in approximately 15% of cases. The indicated treatment is to administer an amebicidal drug (such as tinidazole or metronidazole) and paromomycin or other luminal cysticidal agent for clinical disease. Prognosis is good with almost universal recovery. Establishing which diagnostic methods are most efficacious will necessitate further analysis of similar clinical cases.

BACKGROUND Dextromethorphan is a prevalent antitussive agent that can be easily obtained as an over-the-counter medication. There has been a growing number of reported cases of toxicity in recent years. Generally, there are numerous instances of mild symptoms, with only a limited number of reports of severe cases necessitating intensive care. We presented the case of a female who ingested 111 tablets of dextromethorphan, leading to shock and convulsions and requiring intensive care that ultimately saved her life. CASE SUMMARY A 19-year-old female was admitted to our hospital via ambulance, having overdosed on 111 tablets of dextromethorphan (15 mg) obtained through an online importer in a suicide attempt. The patient had a history of drug abuse and multiple self-inflicted injuries. At the time of admission, she exhibited symptoms of shock and altered consciousness. However, upon arrival at the hospital, the patient experienced recurrent generalized clonic convulsions and status epilepticus, necessitating tracheal intubation. The convulsions were determined to have been caused by decreased cerebral perfusion pressure secondary to shock, and noradrenaline was administered as a vasopressor. Gastric lavage and activated charcoal were also administered after intubation. Through systemic management in the intensive care unit, the patient’s condition stabilized, and the need for vasopressors ceased. The patient regained consciousness and was extubated. The patient was subsequently transferred to a psychiatric facility, as suicidal ideation persisted. CONCLUSION We report the first case of shock caused by an overdose of dextromethorphan.

BACKGROUND Esophageal submucosal hematoma is a rare condition. Although the exact etiology remains uncertain, vessel fragility with external factors is believed to have led to submucosal bleeding and hematoma formation; the vessel was ruptured by a sudden increase in pressure due to nausea, and the hematoma was enlarged by antiplatelet or anticoagulant therapy. Serious conditions are rare, with a better prognosis. We present the first known case of submucosal esophageal hematoma-subsequent hemorrhagic shock due to Mallory-Weiss syndrome. CASE SUMMARY A 73-year-old female underwent endovascular treatment for an unruptured cerebral aneurysm. The patient received aspirin and clopidogrel before surgery and heparin during surgery, and was well during the surgery. Several hours after returning to the ICU, she complained of chest discomfort, vomited 500 mL of fresh blood, and entered hemorrhagic shock. Esophageal submucosal hematoma with Mallory-Weiss syndrome was diagnosed through an endoscopic examination and computed tomography. In addition to a massive fluid and erythrocyte transfusion, we performed a temporary compression for hemostasis with a Sengstaken-Blakemore (S-B) tube. Afterwards, she became hemodynamically stable. On postoperative day 1, we performed an upper gastrointestinal endoscopy and confirmed no expansion of the hematoma nor any recurring bleeding; therefore, we removed the S-B tube and clipped the gastric mucosal laceration at the esophagogastric junction. We started oral intake on postoperative day 10. The patient made steady progress, and was discharged on postoperative day 33. CONCLUSION We present the first known case of submucosal esophageal hematoma subsequent hemorrhagic shock due to Mallory-Weiss syndrome.