P042 Spontaneous gallbladder perforation: a rare complication of eosinophilic granulomatosis with polyangiitis
Authors: Ochogwu Joanna , Madathil Afsar , Mazin Hamed , Makkuni Damodar 
Published: April 2022

Abstract

Background/Aims
Gallbladder (GB) perforation is a serious clinical condition, caused by cholecystitis with or without cholelithiasis. Although there have been reports of bowel perforation in many cases of vasculitis, we report to the best of our knowledge, the first case of spontaneous gallbladder perforation following a diagnosis of EGPA. This alerts the clinician to a unique complication of EGPA.

Methods
A 48-year-old man presented initially to haematology with weight loss and marked eosinophilia, investigations (bone marrow aspirate and trephine, CT chest, abdomen and pelvis) at the time showed no evidence of haematological causes. Subsequently, he developed worsening weakness and paraesthesia of the upper and lower limbs, ongoing for 4 months. He had a background of asthma, and hay fever, which were well-controlled. On examination, he had progressive quadriparesis with extensive muscle wasting. His abdomen was soft non-tender, and he had no skin changes, although he later revealed a photograph of a vasculitic rash affecting the limbs when the symptoms initially presented.

Results
Laboratory findings revealed raised white blood cells of 46.9 (4-10 x109/L), raised eosinophils of 29.4 (0.01-0.5 x109/L), thrombocytosis of 757 (150-410 x109/L), raised CRP of 172 (0-10mg/L), raised IgE 179(&lt;107 kU/L), and IgG 20.8(6-16 g/L). An extensive infectious screen was performed including HIV, and hepatitis (A-E), which were all negative. Vasculitic screen was negative for PR3 and MPO ANCA. However, nerve conduction studies showed evidence of confluent mononeuritis mimicking acute demyelinating sensory motor neuropathy. Following this, a CT scan was requested to exclude underlying neoplasms and infection which revealed a GB perforation with defect in the distended GB wall. He had no typical symptoms of cholecystitis, favouring an underlying gallbladder necrotizing vasculitis as the cause of GB perforation. The patient was commenced on IV cyclophosphamide and maintained on prednisolone, and azathioprine. A percutaneous cholecystostomy was inserted and immunosuppression continued with antibiotic cover. He had excellent response to therapy and his mobility improved following physiotherapy and rehabilitation. However, he continues to have significant residual weakness of the small muscles of his hand (median and ulnar nerve palsies). An MRCP was later requested, this revealed a contracted GB with no evidence of cholelithiasis or ongoing inflammation. He remained asymptomatic of GB perforation, and as a result, surgeons decided not to proceed with a cholecystectomy.

Conclusion
Gallbladder vasculitis (GV) can occur as a single organ vasculitis or as part of a systemic vasculitis. In the rare occasion of its occurrence, it mainly presents as symptoms of cholecystitis. Spontaneous GB perforation as a complication of GV has been noted in patients with other vasculitides like Henoch-Schonlein Purpura. However, this is the first report of a spontaneous gallbladder perforation in a patient with EGPA.

Disclosure
J. Ochogwu: None. A. Madathil: None. H. Mazin: None. D. Makkuni: None.