Endocrine Abstracts

A 22-year-old male presented to the Emergency Department with nausea and vomiting. He reported thirst, polyuria, reduced appetite and weight loss. He did not have pre-existing medical conditions and did not take regular medications. On examination, he appeared pale and clammy. He was apyrexial, tachycardic and tachypnoeic with normal blood pressure and oxygen saturation. His chest was clear and abdomen generally tender. A venous blood gas revealed pH 6.94, base excess −29 mmol/l, bicarbonate 3.2 mmol/l and glucose 27 mmol/l. His capillary blood ketone concentration was 4.9 mmol/l. Diabetic Ketoacidosis (DKA), secondary to undiagnosed type 1 diabetes, was diagnosed. He was treated with fluid resuscitation and insulin infusion. As clinical and metabolic statuses improved, Radiology alerted the medical team about the presence of subcutaneous emphysema and pneumomediastinum on chest radiograph. Vomiting-induced subcutaneous emphysema and pneumomediastinum raised suspicion of spontaneous oesophageal perforation. The patient was started on antimicrobials, antifungals and high-dose proton-pump inhibitors, transferred to a tertiary referral gastro-oesophageal centre and scheduled for urgent feeding tube insertion. However, CT scan with oral contrast showed the absence of pleural effusions and contrast extravasation. After discussion, the Surgical and Endocrinology teams agreed on conservative management: the patient remained NBM until an unremarkable contrast swallow on day 5. He was discharged with outpatient follow-up. Spontaneous pneumomediastinum occurs due to increased intra-alveolar pressure and alveolar rupture (Hamann’s syndrome): it is a benign, self-limiting condition. In DKA, it may arise from vomiting and Kussmaul breathing. Treatment is conservative, and it is important to differentiate it from oesophageal rupture (Boerhaave’s syndrome).