A 55-year-old man with a background of alcoholic liver cirrhosis (Child-Pugh Class B) presented with a two-day history of fresh per-rectal bleeding and postural dizziness. Whilst he had a history of vomiting, he did not have hematemesis. As a known patient with oesophageal varices, he was on oral propranolol, 10 mg twice daily.
On examination, the patient was jaundiced with conjunctival pallor. Clubbing was present and a fine tremor was observed in both hands. His abdomen was soft with mild tenderness, and a per-rectal examination revealed fresh blood.
At the time of admission, the patient was alert and orientated, haemodynamically stable with a blood pressure of 135/98 mmHg, borderline tachycardic with a heart rate of 101 bpm, had oxygen saturations of 100% on air, and a temperature of 36.7 °C. Laboratory tests revealed haemoglobin 6.0 g/dl, platelets 134, albumin 25, bilirubin 50, ALP 91, ALT 59, AST 104, GGT 121, pro-thrombin time 10.8 and INR 1.03.
The patient was transferred to the intensive care unit where he was intubated, and oesophago-gastro-duodenoscopy was subsequently performed. This revealed four columns of grade 2–3 oesophageal varices with red wale signs (i.e. longitudinal red streaks on the varices), portal hypertensive gastropathy and a small duodenal ulcer, but no active bleeding. As the patient had fresh per-rectal bleeding of unknown aetiology, he was referred for computed tomography (CT).
Triphasic (non-contrast, arterial and porto-venous phases post 85mls of Omnipaque 350 mg/ml delivered at a rate of 4 ml/s with bolus tracking performed on a Siemens Somatom Diefinition Flash) CT showed multiple right para-colic portosystemic collaterals around the hepatic flexure and ascending colon (Fig. 1), in addition to the known cirrhosis and features of portal hypertension. No active extravasation was noted, and the patient was given a somatostatin infusion, 500 mcg/h, before colonoscopy was performed. Colonoscopy confirmed fresh blood in the colon up to the caecum, with a submucosal varix deemed the most likely source of haemorrhage. Endoscopic clips were placed adjacent to the varix to act as markers to guide subsequent therapy.
The patient was administered intravenous vasopressin (Terlipressin 2 mg 4-hourly), a beta blocker (Carvedilol titrated up to 18.75 mg twice daily) and multiple units of platelets, packed cells and fresh frozen plasma. His haemoglobin improved to 8.4 g/dl and he remained haemodynamically stable for the next few days. After multi-disciplinary team discussion, he underwent balloon-occluded retrograde transvenous obliteration as TIPS was potentially technically difficult due to left portal vein thrombosis and a small right portal venous system.
Balloon-occluded retrograde transverse obliteration (BRTO)
The procedure was performed under general anaesthesia in the Interventional Radiology angiography suite. The right internal jugular vein was accessed, through which free and wedged hepatic venous pressures were measured with a calculated hepatic venous pressure gradient of 15 mmHg. The decision for BRTO was re-affirmed, considering his overall morbidities. Right renal venogram was performed with a 4Fr catheter confirming the large colo-renal shunt with multiple tortuous pericolic varices around the caecum and ascending colon. The large colo-renal shunt was catheterised via the right renal vein using a reverse curve catheter. A stiff wire was advanced deep into the tortuous shunt and the catheter was exchanged for an occlusion balloon catheter (6Fr, 8.5–11.5 mm) (Berentstein, Boston Scientific, Natick, MA, USA). Balloon occlusion venography (Fig. 2), in which a balloon catheter is inflated to occlude the venous shunt and contrast subsequently injected upstream/retrogradely, was performed to delineate the anatomy of the pericolic porto-systemic collaterals and drainage pattern. With the balloon inflated to achieve relative stasis of blood and prevent efflux of sclerosant, a microcatheter was advanced through the occlusion balloon catheter deep into the varix before injecting 3% sodium tetradecyl sulphate (STS) sclerosant with the aim of filling the entire varix. The occlusive balloon remained in situ for approximately 4 h until there was satisfactory stasis of sclerosant. Small residual variceal collaterals were embolised with N-Butyl cyanoacrylate (NBCA) glue. Venograms confirmed satisfactory embolisation of the abnormal pericolic varices. The balloon catheter was then deflated and removed.
The patient remained hemodynamically stable following the procedure and experienced an uneventful post-procedure recovery. His Hb levels remained stable at 8.7 g/dl and there were no further episodes of gastrointestinal bleeding. An outpatient follow-up bi-phasic (portovenous and delayed post contrast with 70mls of Omnipaque 350 mg/ml) CT 2 months later confirmed thrombosed varices (Fig. 3).