Mallory-Weiss Syndrome Without Vomiting Following Cardiopulmonary Resuscitation With a Laryngeal Tube.

Mallory-Weiss syndrome (MWS) is characterized by longitudinal mucosal lacerations at the esophagogastric junction and is an established cause of nonvariceal upper gastrointestinal bleeding (UGIB), classically triggered by forceful vomiting, retching, or coughing. We report a case of MWS occurring after cardiopulmonary resuscitation (CPR) with a laryngeal tube (LT) in the complete absence of antecedent vomiting. A 77-year-old woman with no history of vomiting, alcohol use, or gastrointestinal disease experienced out-of-hospital cardiac arrest (OHCA). Emergency medical services initiated resuscitation and, after approximately 15 minutes of assisted bag-valve-mask ventilation followed by cardiopulmonary resuscitation, secured the airway with a size-3 LT (Smiths Medical Japan, Tokyo, Japan), a standard LT that lacks a gastric drainage channel. Defibrillation shocks were delivered for ventricular tachycardia, and return of spontaneous circulation (ROSC) was achieved after approximately 29 minutes of CPR. On arrival, the patient was hemodynamically unstable with a blood pressure of 89/56 mmHg and a Glasgow Coma Scale (GCS) score of 3. Contrast-enhanced CT, performed because of unexplained hemodynamic instability, revealed active contrast extravasation into the gastric lumen. A nasogastric (NG) tube subsequently yielded bloody aspirate, and emergent upper gastrointestinal endoscopy identified a longitudinal mucosal laceration at the gastric cardia, confirming MWS. Because CT preceded NG tube insertion, iatrogenic injury from NG tube placement was excluded as the cause of the laceration. Endoscopic hemostasis was achieved, and the patient received four units of packed red blood cells and four units of fresh frozen plasma. Despite successful hemostasis, she developed severe hypoxic-ischemic encephalopathy and was transitioned to comfort-focused care; she died on hospital day 21. We hypothesize that impaired gastric decompression due to the esophageal occlusion balloon of the LT, combined with repeated increases in intra-abdominal pressure during chest compressions, may have contributed to mucosal laceration at the esophagogastric junction in the absence of vomiting. However, because this is a single case, a causal relationship cannot be established, and this mechanism remains purely hypothesis-generating. This report highlights the need to consider MWS in the differential diagnosis of unexplained anemia or upper gastrointestinal bleeding after CPR, particularly when an LT has been used, and supports prompt evaluation even in the absence of antecedent emesis.