An 18-year-old man with no history of significant illness or injury was transferred from an outlying facility after a chest CT revealed SPM. His symptoms included chest pain, shortness of breath, and abdominal pain radiating to the back. The day before admission to our ICU, he experienced 10-15 episodes of forceful vomiting over a 24-hour period that filled two trash cans. The vomitus consisted primarily of food contents with occasional blood streaks but no clots. He had no history of pancreatitis, NSAID use, or peptic ulcer disease. He reported a six-month history of intermittent marijuana use, with recurrent episodes of nausea and vomiting partially relieved by hot showers, and a history of occasional alcohol use, with his last alcohol intake (reported as three drinks) occurring four to five days prior.

On arrival at our facility the following day, he was hemodynamically stable and not vomiting. He was alert and oriented, in no acute distress, with clear breath sounds bilaterally and a regular cardiac rhythm. His abdomen was soft, nondistended, and nontender. No subcutaneous crepitus was appreciated, and his skin and neurologic examinations were normal.

Initial imaging was obtained at an outside local facility (OLF) before transfer. A contrast-enhanced chest CT angiography performed there showed no evidence of pulmonary embolism and reported nonspecific pneumomediastinum in the middle mediastinum with air surrounding the mainstem bronchi. A repeat noncontrast chest CT at the admitting hospital demonstrated a small amount of pneumomediastinum with air extending into the right minor fissure (Figure 1). Laboratory studies on admission were largely unremarkable. He was admitted with a diagnosis of pneumomediastinum secondary to persistent vomiting, likely attributable to CHS.

During hospitalization, he was kept NPO with plans to advance his diet gradually and was placed on IV piperacillin-tazobactam for mediastinitis prophylaxis while esophageal perforation was being excluded. A cardiothoracic surgeon evaluated the patient and reviewed the noncontrast chest CT performed at the admitting hospital. The surgeon identified findings consistent with a Mallory-Weiss tear and possible microperforation of the esophagus. Contrast was observed within the esophagus without evidence of extravasation, effectively excluding a gross esophageal perforation.

Serial laboratory testing showed no biochemical evidence of evolving mediastinitis. At the OLF, the patient’s initial lactate level was elevated at 3.2 mmol/L, and the reflex repeat lactate normalized. A C-reactive protein level obtained at the same facility was mildly elevated (18.9 mg/L). An extended viral panel at the OLF was negative. At the OLF, the white blood cell count was elevated (20.3 × 10⁹/L); however, on admission to our hospital, the white blood cell count was normal at 9.3 × 10⁹/L and continued to trend downward to 7.8 × 10⁹/L on hospital day 2, arguing against an acute infectious process (Table 1). Hemoglobin, hematocrit, electrolyte, renal function, and glucose levels remained stable, and no metabolic abnormalities emerged. He remained afebrile and hemodynamically stable throughout hospitalization, without tachycardia, hypotension, or worsening chest pain. Physical examination revealed no new crepitus, dysphagia, tracheal tenderness, or respiratory deterioration. These stable laboratory and clinical parameters supported discontinuation of empiric piperacillin-tazobactam.

The patient was discharged two days after admission with instructions for outpatient follow-up, including a repeat esophagram in two weeks and further evaluation of his chronic insomnia. At his follow-up visit one week later, he remained asymptomatic, had resumed a normal diet, and reported no recurrent symptoms.