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A 16 year old girl, with known advanced cirrhosis, portal hypertension and polysplenia, secondary to Biliary Atresia, post Kasai, presented with sudden onset left upper quadrant pain of one week duration. The pain was aggravated by lying flat, eating, coughing, mobilising and on deep inspiration. She required oral morphine for her pain. She reported her urine was more dark and her sclera were more jaundiced than normal. She was pyrexial 390C, tender in left upper quadrant with otherwise stable splenomegaly. There was no haemodynamic disturbance. Blood Investigations showed CRP of 79 (< 5); serum bilirubin 97 umol/L , ALT 48 (10–40); GGT 56 (< 38); ALP 168 (54–130). She had thrombocytopaenia 106, marginally improved to her usual level of 76 (secondary to hypersplenism). Prothrombin time was increased 19.1 (10.0–14.1) and haemaglobin was stable at 132 g/l. Lipase and chest x ray were normal.In view history of previous Kasai, altered liver tests and pyrexia, she was commenced on IV Tazocin for possible cholangitis. An abdominal USS was requested to look for possible splenic infarct, which was not identified, although splenic varices were seen and portal vein was patent. After further discussion, a CT Angiogram mesenteric artery was requested, which showed multiple splenic artery aneurysms (SAA) ranging from 7 mm to 27 mm and presence of fluid around the region, concerning for a recent aneurysmal bleed.She remained haemodynamically stable.Local Interventional radiology (IR), suggested embolisation of anuerysm(s) with consideration of splenectomy. She was well known to paediatric Liver centre and transferred for further assessment and management with a concern of potential acute liver decompensation if further aneurysmal bleed or secondary to intervention. She had a further bleed 10 days later and underwent repeat CT scan, which showed formation of a pseudoaneurysm and was embolised by IR, along with a few others. Following emobilisation she complained of left upper quadrant pain, likely due to splenic infarct but did not develop pancreatitis. There was a concern liver function was further compromised.Reviewing the literature, SAA occurs more commonly in cirrhotic patients and are at a heightened risk of rupture peri liver transplant with potentially fatal consequences up to 57% mortality reported in one paper.1 However, there is no consensus regarding optimal management of asymptomatic SAA pre transplantation. A systematic review by Du Phan et al 2 reported on 159 patients with SAA, of whom 121 had asymptomatic SAA, diagnosed pre liver transplant and subsequently underwent liver transplantation. 37/121 patients diagnosed pre transplant had treatment instigated (28 surgically and 8 radiologically). Post-transplant rupture was noted in 2/28 patients treated surgically with no fatality. No rupture was observed in the radiologically treated group, although 1 patient died of splenic abscess and sepsis after embolization. Post-transplant rupture was recorded 4/86 untreated patients, (2/4 resulted in fatality). They concluded treatment should be considered regardless of aneurysmal size because of the risk of rupture post transplantation.References Gaglio PJ, Regenstein F, Slakey D. a-1 antitryspin deficiency and splenic artery aneurysm rupture: an association? Am J of Gastroenteroly. Jun 2000;95(6):1531–1534.Du Phan, Furtadoa R, Laurence J. Splenic artery aneurysm management in the cirrhotic patient listed for liver transplantation:a systematic review. Transplantation Proceedings Apr 2022;54(3):706–714.