Non-traumatic esophageal perforation: A case report on Boerhaave’s syndrome

Boerhaave’s syndrome is a potentially fatal condition characterized by spontaneous perforation of a previously healthy esophagus, due to severe vomiting or straining. It often presents with non-specific symptoms such as fever, pain, and vomiting and hence may go undiagnosed. The Makler’s triad, consisting of vomiting, chest pain, and subcutaneous emphysema, may be seen in only 50% of cases. Delayed diagnosis may result in complications such as sepsis, mediastinitis, pneumothorax, and multi-organ dysfunction. In general, patients presenting later than 48 h are conservatively managed with esophageal stenting. Surgical repair is usually reserved for those patients who present within 24 h, or are managed conservatively and develop complications. Mortality rises from 0% if treated within 24 h to about 29% if delayed more than 48 h. We present a case of Boerhaave’s syndrome in a 35-year-old male who presented with spontaneous respiratory distress and hemodynamic instability, about 36 h after the onset of vigorous vomiting. The case was managed initially with endoscopic insertion of a self-expanding metallic stent, followed later by surgical closure of the esophageal perforation. The patient, however, developed post-operative septic complications and died after a week

Atypical hemolytic uremia syndrome in a young adult male

Atypical hemolytic uremia syndrome (aHUS) is a rare and life-threatening disease, characterized by the same triad of hemolytic anemia, thrombocytopenia, and renal failure as seen in HUS. It differs in its etiology, being caused by a dysregulation of the complement pathway rather than Shiga-like toxin-producing Escherichia coli. Prognosis is poor, with 50% of cases progressing to end-stage renal disease (ESRD) and 25% succumbing in the acute phase. The treatment of choice is therapeutic plasma exchange which can lower mortality. Monoclonal antibody drugs such as eculizumab, which suppress the dysregulated complement pathway, help to prevent complement-mediated kidney injury. We report the case of a young adult male who presented with thrombocytopenia and worsening acute kidney injury and was diagnosed with aHUS based on high lactic dehydrogenase, low complement C3, and haptoglobin, as well as renal biopsy showing thrombotic microangiopathy

Liver transplantation for fulminant hepatic failure in yellow phosphorus poisoning

Yellow phosphorus (YP) containing rodenticides is a readily available poison that may be accidentally or deliberately ingested, leading to symptoms ranging from simple gastrointestinal symptoms to fulminant hepatic failure, depending on the amount ingested. As there is no specific antidote, the treatment requires early gastric lavage and institution of supportive measures such as acetyl cysteine infusion and Vitamin K. Progression to fulminant hepatic failure is characterized by rapid deterioration of liver function tests, worsening coagulopathy, and sensorium. The only definitive treatment at this stage is a liver transplant and therapeutic plasma exchange (TPE) can serve as a bridge therapy until a compatible liver donor is found. We present a case of YP-containing rodenticide poisoning, in which the patient progressed to fulminant hepatic failure despite aggressive supportive therapy and was successfully managed with TPE until liver transplantation.