Boerhaave syndrome is rare, has an non-specific clinical presentation and most commonly develops after persistent vomiting. Septic shock dominates the clinical picture as a result of extensive infection of the mediastinum and pleural and abdominal cavities. The current management of Boerhaave syndrome includes conservative, endoscopic and surgical treatments. The authors present the case of a 94-year-old man admitted to hospital with community-acquired pneumonia with mild respiratory insufficiency complicated by oesophageal perforation after an episode of vomiting and the development of a large left pleural effusion. An endoscopic approach with the placement of an oesophageal prosthesis was chosen given the advanced age of the patient. The hospital stay was complicated by pleural effusion infection requiring broad-spectrum antibiotics and prosthesis substitution. The patient was discharged after 60 days of hospitalization, without the need for oxygen supplementation, and scoring 80% on the Karnofsky Performance Status Scale. The increase in average life expectancy requires a case-by-case approach, where the benefits of invasive manoeuvres and likelihood of discharge are weighed against an acceptable quality of life, aiming to prevent futile medical treatment.LEARNING POINTSBoerhaave syndrome is a complete rupture of the oesophageal wall secondary to a sudden increase in intraluminal oesophageal pressure, often in the lower third and left lateral position of the oesophagus.The management of Boerhaave syndrome depends on the time of diagnosis and clinical presentation and includes conservative, endoscopic and surgical approaches.Curative, aggressive approaches focused on the treatment of disease are often not appropriate for an aging population, hence the need for a case-by-case approach, where the benefits of invasive manoeuvres and likelihood of discharge are weighed against an acceptable quality of life, aiming to prevent futile medical treatment.

Mauriac syndrome, first described in 1930, is typically diagnosed in young patients with poorly controlled type 1 diabetes mellitus and growth retardation, delayed puberty, Cushingoid features, hypercholesterolaemia and hepatomegaly. However, the sole presenting feature of Mauriac syndrome can be hepatic glycogenosis in both adults and children. The mainstay of treatment for hepatic glycogenosis is strict control of glucose levels, with an excellent prognosis with improved glycaemic control. The authors present the case of a 22-year-old female patient with type 1 diabetes mellitus and a history of poor glycaemic control who was admitted with diabetic ketoacidosis (DKA). She complained of episodes of right upper quadrant abdominal pain associated with nausea and vomiting for the last 2 months with worsening in the last 48 hours. Physical examination was remarkable for short stature and tenderness over the hepatic area with a mildly enlarged liver. The patient had elevated liver enzymes and persistent hyperlactacidaemia despite DKA resolution. Liver imaging suggested diffuse fat infiltration. The clinical suspicion of hepatic glycogenosis was confirmed by liver biopsy. After glycaemic control was improved, liver enzymes normalized and the episodes of abdominal pain, nausea and vomiting subsided.LEARNING POINTSHepatic glycogenosis can be the sole presenting feature of Mauriac syndrome.Hepatic glycogenosis is an under-recognized cause of abdominal pain in patients with type 1 diabetes mellitus.Hepatic glycogenosis may be confused with non-alcoholic fatty liver disease, with important therapeutic implications and a distinct prognosis.The mainstay of treatment for hepatic glycogenosis is strict glycaemic control with an excellent prognosis when achieved.