Hepatic artery pseudo aneurysm rupture precipitated by pneumonia: an unusual case.
G Muthukumarasamy¹, D Watt¹, A Davidson¹, A Newland¹.
¹Department of General Surgery, Crosshouse Hospital, Kilmarnock
Correspondence
Girivasan Muthukumarasamy
Speciality trainee,
Department of surgery
Crosshouse hospital
Kilmarnock
KA2 0BE
Email: mgirivasan@hotmail.com
Key Words: hepatic artery, pseudo aneurysms, coiling
Abstract
We present a unique case of hepatic artery pseudo aneurysm rupture associated with pneumonia. A 67 year old woman admitted to our hospital with productive cough, pleuritic chest pain and shortness of breath. She was diagnosed to have community acquired pneumonia and was treated with antibiotics. On third day of admission she developed acute abdominal pain and haemorrhagic shock. Contrast CT scan showed left hepatic artery pseudo aneurysm rupture, a rare emergency condition associated with high mortality rate. She underwent percutaneous endovascular coiling and made a complete recovery.
Introduction
Hepatic artery aneurysm (HAA) is a rare entity and first described by Wilson in 18091. They represent approximately 20% of all visceral artery aneurysm. Approximately half of them are pseudo or false aneurysm2. The aetiology for hepatic artery pseudo aneurysm (HAP) formation are varied and occur commonly after penetrating or blunt trauma, surgical intervention and inflammation. The mortality from HAPs rupture is 40%, so early diagnosis and appropriate treatment is vital3. Systemic infection or sepsis may result in formation and rupture of pseudo aneurysm. We present an unusual case of HAP rupture precipitated by community acquired pneumonia and its successful management by endovascular coiling.
Case report
A 67 year old lady was admitted to our hospital with three day history of productive cough, left sided pleuritic chest pain, shortness of breath and fever. There was no significant past medical history other than an open cholecystectomy about 30 years ago. She was a smoker and does not take any regular medications. On examination, she was pyrexial (39.5° C), tachycardic and tachypnoeic. Further examination revealed reduced air entry in left lower base. The cardiovascular and abdomen was unremarkable. Initial blood tests showed raised inflammatory markers WCC of 30.2, CRP of 340 and normal liver function tests. Blood culture was reported as no growth after five days of incubation. Chest x-ray revealed patchy infiltrates and consolidation in left lower lobe of the lung (Fig 1). A clinical diagnosis of community acquired pneumonia was made and she was treated with appropriate antibiotics. Symptomatic improvement was gradually achieved in next two days.
Figure 1
On the third day after her admission she developed sudden onset of severe abdominal pain and hypotension. The full blood count showed a drop in haemoglobin from 12.4 to 8.0 gms/dl. The abdomen was grossly tender with signs of peritonism. The CT scan of the abdomen revealed pseudo aneurysm of the left hepatic artery measuring about 12 mm in diameter in the lateral aspect of left lobe of the liver with free fluid in the abdomen(Fig 2). The diagnosis of left hepatic pseudo aneurysm rupture was made. She was resuscitated, transfused and transferred to tertiary care hospital for emergency endovascular treatment for the rupture. The endovascular coiling embolisation of the left hepatic artery pseudo aneurysm was done (Fig 3, 4). She recovered quite well from the procedure without any complications. The chest infection got better with systemic antibiotics and she was discharged home after 4 days of hospital stay.
Figure 2
Figure 3
Figure 4
Discussion
HAA is a rare occurrence and the incidence in hospital admission was reported to be as low as 0.002%3. True HAAs are secondary to atherosclerosis, hypertension and vasculitis. Seventy to seventy five percent of true HAA is extra hepatic. Pseudo aneurysm occurs in 50 % of the HAA cases of which 95 % occur in the right hepatic artery and 25 % are intra hepatic4. In our case, HAP was in the left hepatic artery and intra hepatic site.
Pseudo aneurysm occur secondary to injury to the vessels either by trauma or by inflammation. The causes of hepatic artery pseudo aneurysm formation are blunt or penetrating trauma, iatrogenic or hepatobiliary interventional procedures, liver transplantation and laparoscopic cholecystectomy. Infective or mycotic aneurysm constitutes for only 4% of HAPs2. Infective endocarditis, intravenous drug abuse and liver transplantation are predominant causes for mycotic aneurysms. In liver transplant, local infection secondary to bile leak can lead to pseudo aneurysm formation5. Liver abscesses has also been reported to cause mycotic HAP6
There are also few reports of HAPs secondary to pancreatitis7, cholecystitis8and tuberculous infections9 in the literature. Otah et al also suggested local infection after interventional procedures may lead to formation and rupture of HAPs10.
Periarterial inflammation and resulting weakness of the vessel wall is the cause for aneurysm formation in case of systemic infection11. Pseudo aneurysm formation is due to increased proteolysis of extracellular matrix proteins by bacteria12. The only significant past history in our case is open cholecystectomy about 30 years ago. In literature there is no report of HAPs formation after such long period of time. The CT scan in our case did not show any atherosclerotic changes or periarterial signs of mycotic aneurysm. The systemic infection due to pneumonia has precipated the formation and rupture of HAP in our patient.
HAAs are common in males and in sixth decade of life. The HAA is mostly asymptomatic and the ruptured ones present as severe abdominal pain with or without haemorrhagic shock13. The rupture of hepatic artery aneurysm was reported as 21% to 80%14, 15. Nearly 60% of HAPs are asymptomatic and incidental finding and they have high risk of rupture10. The Quincke’s triad of gastrointestinal pain, haemobilia or gastrointestinal haemorrhage and obstructive jaundice occur in of ruptured HAA16. This is present in only 30% of cases. HAPs may rupture into the peritoneal cavity or to adjacent portal or biliary system. The mortality for patients in shock secondary to HAP rupture is 50%16.The patient in our report had severe abdominal pain and was in haemorrhagic shock. There was no abnormal liver function test or obstructive jaundice at any stage.
Contrast enhanced CT scans is a useful modality to demonstrate the HAP and rupture. The digital subtraction angiography is the diagnostic and gives valuable information regarding the feeding vessels, fistulae and multiple aneurysms. The common image findings of mycotic aneurysms are irregular vessel wall, peri-aneurysmal oedema and mass. The contrast enhanced CT scan of abdomen demonstrated the left HAPs and intra peritoneal haemorrhage in our case.
Treatment depends on the cause and anatomical location of HAPs. Open surgical treatment options are ligation, excision, venous grafting, synthetic grafting and liver resections. Intra hepatic aneurysms can be treated with resection, ligation or embolisation3. Berceli et al recommends endovascular embolisation for all intrahepatic pseudo aneurysms17. The success rate for embolisation in un-ruptured HAPs is 75%-100%. In ruptured cases, 37% of the cases need re- embolisation18. In our case we successfully managed to perform percutaneous embolisation using a micro coil without any complications.
We conclude that HAP rupture is an acute emergency, early recognition and appropriate initiation of management are important for good clinical outcome. Systemic infection secondary to pneumonia can be a precipitating factor for rupture of these rare aneurysms.
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