Spontaneous Rupture of a Pseudoaneurysm of the Right Hepatic Artery Causing Massive Upper Gastrointestinal Bleeding

Autor: Kiran Verma, Abuajela Sreh, Muhammad Hafiz Kamarul Bahrin, Muhammad Bin Farid
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: European Journal of Case Reports in Internal Medicine (2019)
European Journal of Case Reports in Internal Medicine
Popis: We describe the case of an 84-year-old woman who presented with right lower chest pain, anaemia and newly deranged liver function which was followed by massive upper gastrointestinal (GI) bleeding with no source of bleeding found on upper GI endoscopy. CT angiography of the GI tract confirmed rupture of a pseudoaneurysm of the right hepatic artery (RHA) that was treated successfully with trans-arterial embolization of the RHA. LEARNING POINTS If upper gastrointestinal (GI) endoscopy fails to identify the source of upper GI bleeding, CT angiography is required to search for rare causes such as pseudoaneurysm of the right hepatic artery (RHA) with fistula formation with the GI and biliary tract, along with other causes such as aorto-enteric fistula. Pseudoaneurysm of the RHA is commonly secondary to recent surgery or trauma and spontaneous occurrence is very rare. Endovascular repair using transcatheter arterial embolization is the treatment of choice but if it fails, emergency laparotomy should be considered. Keywords: Pseudoaneurysm, right hepatic artery, RHA, gastrointestinal, GI, bleeding CASE DESCRIPTION An 84-year-old woman was brought to hospital by ambulance with acute right lower chest pain, unexplained anaemia and newly deranged liver function. The patient denied any history of cough, shortness of breath or palpitations. She had no history of venous thromboembolism (VTE) and denied risk factors for VTE. She did not have abdominal pain, vomiting, urinary symptoms, active bleeding or melena. She had normal stool habits. However, she had a history of hypertension, osteoarthritis, ischaemic heart disease with previous coronary artery bypass graft surgery many years previously, and chronic kidney disease stage 3. She was taking aspirin, and anti-hypertensive and anti-angina medication as well as a glyceryl trinitrate (GTN) spray. She had a good performance status, lived alone independently and was helped by carers only twice a week. On examination, the patient was alert and fully conscious. Her vital signs were stable with a respiratory rate of 16 and saturating 100% on air, blood pressure of 105/59 mmHg, heart rate of 75 bpm and temperature of 36.8°C. Auscultation revealed normal heart sounds with no murmurs, and bilateral good air entry with right basal crepitations. The abdomen was soft and non-tender, bowel sounds were normal, and digital rectum examination revealed normal stool colour with no signs of fresh blood or melena. The calves were soft and non-tender and no focal neurological deficits were demonstrated. Blood results initially showed a raised white cell count of 14×109/l (normal 4.0–10.0×109/l) and a C-reactive protein (CRP) level of 28 mg/l (0–5). Haemoglobin was 89 g/l (120–150) compared to a previous haemoglobin of 127 g/l approximately 2 months previously. Mean corpuscular volume (MCV) was 86 fl (83–101) and liver enzymes were newly deranged as follows: bilirubin 15 μmol/l (0–21), alanine aminotransferase (ALT) 304 U/l (0–33) and alkaline phosphatase (ALP) 507 U/l (30–130). We also noted urea of 11.8 mmol/l (2.5–7.8) and creatinine of 92 μmol/l (44–80). Chest x-ray showed mild haziness in the right lower zone consistent with infective changes. Initially the patient was treated for right basal pneumonia with associated pleurisy. Because of the new anaemia, raised urea level and newly deranged liver function, she underwent urgent oesophagogastroduodenoscopy (OGD) and ultrasound of the abdomen. At this stage she was stable. OGD showed hiatus hernia and severe oesophagitis but no source of active bleeding. Two hours later, the patient started passing a large amount of melena and her systolic blood pressure dropped to 70 mmHg despite initial intravenous fluid boluses. On arrival of the emergency team, the patient was spontaneously ventilating, on 4 l/min of oxygen saturating 98%, with good air entry bilaterally, a blood pressure of 70/48 mmHg and receiving continuous intravenous fluid resuscitation, a heart rate of 117 bpm, and a capillary refill time of 3 seconds. Blood sugars were normal and the Glasgow Coma Scale (GCS) score was 15/15. The patient was complaining of abdominal pain with a distended abdomen, generalised abdominal tenderness, involuntary guarding and sluggish bowel sounds. There were also weak peripheral pulses and no sign of VTE. Management at this stage was for massive upper GI bleeding and included fluid resuscitation, activation of the massive haemorrhage protocol (transfusing Group O negative blood until matched bloods became available and fresh frozen plasma), proton pump inhibitor infusion, tranexamic acid 1 g and terlipressin 2 mg given on the basis of deranged liver function. A CT angiogram of the abdomen and pelvis was arranged once the patient was haemodynamically stable, and surgical review was sought for a possible perforated bowel. A CT angiogram of the abdomen (portal, venous and arterial phases) suggested a suspected pseudoaneurysm in the right hepatic artery, with surrounding fluid indicating potential active bleeding and suspected haemorrhagic content in the distended biliary tree (Fig. 1). Open in a separate window Figure 1 (A) A suspected pseudoaneurysm in the right hepatic artery, with surrounding fluid (likely active bleeding). (B) suspected haemorrhagic content in the distended biliary tree.
Databáze: OpenAIRE
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