A 54‐year‐old HIV‐positive male patient with history of cocaine abuse presented to the emergency room with a 1‐day duration of chest and epigastric pain. He had poor medication compliance, with a low CD4 count of 113 cells/mm3. He denied nausea, vomiting, dysphagia, odynophagia, and dyspnea. He admitted to cocaine use the previous day. Physical exam was normal. Initial laboratory parameters, cardiac markers, and EKG were normal; a chest x‐ray showed minimal left lower lobe alveolar infiltrate. A CT angiogram of the chest ruled out pulmonary embolism and aortic dissection. The following day he had acute severe respiratory distress and worsening chest pain with nausea and vomiting. Repeated chest x‐ray revealed a large new hydropneumothorax. A chest tube was placed, and pleural fluid analysis revealed elevated amylase, indicating a possible spontaneous esophageal rupture (SER). The patient underwent thoracotomy with repair of a 1.5‐cm transmural rupture at the esophagogastric junction. A large periesophageal abscess abutting the left lower lobe of the lung was drained along with decortication of that lobe. GMS stain showed budding yeast with pseudohyphae suggestive of Candida species, cultures were negative, and tissue biopsy showed fat necrosis with no malignant changes. He recovered from esophageal repair but died later from renal failure complications.
Spontaneous esophageal rupture is a surgical emergency associated with 90% mortality if diagnosis and treatment are delayed. It is not commonly seen in HIV; however, opportunistic infections may play a role in approximately 30% of the spontaneous ruptures. Herman Boerhaave first described SER in 1724. SER usually occurs in the absence of preexisting esophageal disease. It is characterized by Meckler's triad of symptoms — vomiting, lower chest pain, and cervical subcutaneous emphysema, often following overindulgence in food or alcohol. It is usually a result of ejection of gastric contents in a nonrelaxed esophagus against a closed glottis. The presence of Candida in the biopsy raises the question of perforated esophageal candidiasis; however, transmural fungal infection is extremely rare. HIV disease can directly cause esophageal mucosal cell dysfunction and decrease the ability of mucosal cells to repair themselves and thus with advanced opportunistic infections may lessen the mechanical strength of the esophagus, making it prone to perforation. HIV patients may also have an esophageal motility disorder independent of symptoms and/or the presence of mucosal lesions. Cocaine has been shown to cause ulceration and subsequent perforation of the GI tract as a result of vasoconstriction by alpha adrenergic activation. By its anticholinergic effects, it produces gastric hypomotility, delays gastric emptying, and prolongs exposure to gastric hydrochloric acid, all of which contributes to ulcer formation.
We illustrate the multifactorial causation of spontaneous esophageal rupture probably triggered by cocaine consumption.
R. Prasad, none; S. Somasundara, none; M. Rodriguez, none.
To cite this abstract:Nanjundappa R, Somasundara S, Rodriguez M. Spontaneous Esophageal Rupture in HIV. Abstract published at Hospital Medicine 2008, April 3-5, San Diego, Calif. Abstract 160. Journal of Hospital Medicine. 2008; 3 (suppl 1). https://www.shmabstracts.com/abstract/spontaneous-esophageal-rupture-in-hiv/. Accessed May 26, 2019.