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Post-traumatic Hepatic Arterioportal Fistula.


Hepatic arterioportal fistulae (APF) are abnormal communications between a hepatic arterial branch and a portal venous branch. The most common causes of hepatic APFs are trauma, interventional procedures, and vascular malformations. (1) They can result in portal hypertension and other hemodynamic imbalances. (1) Portal hypertension occurs due to creation of an inflow block resulting from the interruption of portal venous flow by the inflow of arterial blood with subsequent increased pressure in portal vein radicals. Hepatic APFs are usually small and self-limiting, however, in rare cases, fistulae can enlarge with time and become clinically symptomatic (e.g. esophageal varices and ascites) (1). Cross-sectional imaging using CT and magnetic resonance imaging (MRI) has a role in characterizing these fistulas and their imaging appearances have been described in detail. (2-4) Digital subtraction angiography (DSA) is the gold standard in the diagnosis and treatment of APFs. (8) In this report, we present a patient with APF secondary to a gunshot injury to the epigastrium which led to transection of the right branch of the hepatic artery, injury to the right portal vein, and creation of a fistula between them. This was confirmed on DSA and treated surgically.


A 26-year-old male was brought to the emergency room (ER) with history of gunshot injury to the upper abdomen about one hour before presentation. Patient had a GCS (Glasgow Coma Scale) of 13 when he was brought to the ER (hospital day one), the airway was maintained, he had tachycardia with a heart rate of 130 beats/minute, and he was hypotensive with systolic blood pressure in the low 90s. An entry wound was visible in the epigastrium, without a definite exit wound. Intravenous access was obtained in bilateral antecubital veins and the right femoral vein. Two units of packed RBCs and 1000 ml of intravenous fluids (0.9% saline) were administered. The patient was then sedated and intubated in the ER. The initial hematocrit was 30% and later increased to 35% and 41%, after resuscitation. Initial laboratory tests revealed: BUN 10.0 mg/dl, Creatinine 0.73 mg/dl, total protein 5.4 mg/dl, total bilirubin 1.7 mg/dl, AST (Aspartate Aminotransferase) of 1524 U/L, ALT (Alanine Aminotransferase) of 1258 U/L, alkaline phosphatase of U/L, findings consistent with liver injury. Patient was then intubated and transferred to the operating room for an emergent exploratory laparotomy (indicated for suspected bowel perforation from the gunshot injury) which showed the hepatic segment 4 entry of the bullet and exit from the caudate lobe. Injury to the superior pole of the right kidney was also seen. A cholecystectomy was performed (to visualize the bullet tract but no injury was noted to the gall bladder), a drain was placed at the site of the right superior renal pole injury, and the patient was then transferred to the intensive care unit (ICU).

Thereafter, a CT scan was performed (about eight hours after the laparotomy to look for additional injuries) using the trauma protocol. CT of the chest, abdomen, and pelvis was acquired 60 seconds after the administration of 145 ml of IV contrast (Visipaque 320 mg/ml) and delayed images acquired at five minutes. CT showed a grade 4 injury (AAST liver injury scale) with hepatic laceration extending from segment 4 to the caudate lobe (Figure 1).

It also showed intrahepatic right hepatic artery transection and a suspected abnormal communication between the transected right hepatic artery and the right branch of the portal vein (arterioportal fistula), with more intense enhancement of the right-sided portal venous system (Figure 2). Other findings were right-sided hemothorax and hemoperitoneum, with no evidence of active blood or urine extravasation. Right renal laceration (grade III per AAST kidney injury scale) was also seen. The ballistic fragment was seen in the subcutaneous right-lower chest (Figure 1).

Angiogram was performed about 36 hours after the CT scan to further characterize and possibly treat the vascular injury and the shunt. Aortogram was followed by selective catheterization of the superior mesenteric artery (SMA) and celiac arteries (using a 5 Fr Rosch-Celiac catheter) and their DSA, followed by super selective catheterization of the hepatic artery (using a microcatheter and microwire) and DSA evaluation. A total of 60 ml of Visipaque 270 was used and the fluoroscopy time was 4.7 minutes. Transection of the distal proper hepatic artery was seen along with early visualization of the right portal system, confirming the arterioportal fistula (Figure 3 and 4). Injury of the right portal was suspected. There was no evidence of active extravasation. Findings were communicated to the surgery team who contemplated further exploration and surgical management.

A repeat laparotomy was then performed on day four when the transected right hepatic artery was ligated and a right trisegmentectomy was performed as there was no flow in the right portal vein after the ligation of the right hepatic artery, which would predispose the patient to liver necrosis. Patient tolerated the surgeries well, but was later found to have developed a right subphrenic abscess which was treated with percutaneous drainage on day 14. A right ureteric stent was also placed for the right renal injury on day 10 and a tracheotomy was performed on day 25 due to prolonged intubation. Patient continues to recover without any further complications, at the time of writing of this manuscript.


Hepatic arterioportal fistulas (APF) are the most common intrahepatic vascular shunts, consisting of a communication between a hepatic arterial branch and a portal venous branch. The most common causes of hepatic APFs are trauma, interventional procedures, and vascular malformations. (1) Spontaneous small arterioportal shunts may be associated with hepatocellular carcinoma and hemangiomas. (2) In a series by Vauthey et al., trauma as the most common cause accounted for 28%, interventional procedures 16%, congenital vascular malformations 15%, tumor 15%, and aneurysm 14% of all reviewed cases. (1) APF exposes the portal vascular bed to high arterial pressures and this also leads to interruption of the portal venous flow, which causes portal hypertension and its complications, if not treated early. The common presentations of symptomatic intrahepatic APFs include gastrointestinal bleeding, ascites, congestive heart failure, abdominal pain, and diarrhea. (1)

The first case of APF secondary to liver biopsy was reported by Preger in 1967. (5) APFs after liver biopsy have been reported with a frequency of about 5.4-10%. Most resolve spontaneously within 12 weeks as they are small and peripheral. Rarely they may be centrally located and grow, leading to clinical symptoms development. (6) Doppler ultrasound is typically employed as an initial screen, with high-flow velocities and arterial waveforms in the portal vein. Turbulence with reversal of flow may also be present in the portal vein.

Cross sectional imaging using dynamic contrast enhanced CT and MRI can diagnose and characterize APFs. Due to the fistula, there is an early increased attenuation of a peripheral and central portal vein compared with the main portal vein, and "double-barrel" or "rail-tract" signs. A segmental area of transient hepatic enhancement is seen during the arterial phase as a wedge-shaped geographic area of hyperenhancement, due to high-pressure arterial blood passing into a low-pressure portal vein branch. (2-4,7) Guzman et al. introduced a classification system for APF with therapeutic implications. Small, peripheral, intrahepatic APFs (Type 1) with minimal physiologic consequences are most commonly caused by percutaneous liver biopsies. They usually resolve spontaneously and thus can be observed with ultrasound imaging, as they tend to thrombose within one month. Large, central APFs (Type 2) can be intrahepatic or extrahepatic and are often caused by abdominal trauma and erosion of a splenic artery aneurysm into the portal system. They can cause increased portal venous pressure with enough flow and thus require treatment by transcatheter embolization with surgical approach reserved only for complex cases. Congenital APFs (Type 3) tend to be diffuse and intrahepatic and difficult to manage, requiring varying transcatheter and often surgical treatments. (8)

Digital subtraction angiography is the gold standard in the diagnosis, treatment planning, and follow-up of APFs. APFs were treated with surgical ligation of the supplying artery in the past, however, endovascular transcatheter arterial embolization is now the treatment of choice. Embolization is directed towards selective closure of the fistula and preservation of adjacent normal vasculature. (9) Various embolization agents have been used such as: stainless-steel coils, detachable balloons, onyx, and cyanoacrylate glue. (10)

Our patient developed the APF due to a gunshot injury to the liver, leading to a communication between the right hepatic artery and the right branch of portal vein. The fistula developed because of direct injury to the right branch of portal vein and the right hepatic artery. The right branch of the portal vein was supplied only by the fistula without any portal venous perfusion. The ligation of the transected right hepatic artery would have caused liver necrosis, so a right hepatic trisegmentectomy was performed to treat this large APF.


We describe a case of a large APF secondary to gunshot injury, CT and DSA imaging features of this rare pathology, and subsequent surgical treatment. DSA is the gold standard in the diagnosis and treatment, but surgery may be needed for large hepatic arterio-fistulas.


(1.) Vauthey JN, Tomczak RJ, Helmberger T, et al. The arterioportal fistula syndrome: clinicopathologic features, diagnosis, and therapy. Gastroenterology 1977;113:1390-1401.

(2.) Nguyen CT, Saksobhavivat N, Shanmuganathan K, Steenburg SD, Moeslein FM, Mirvis SE, Chiu W. MDCT diagnosis of post-traumatic hepatic arterioportal fistulas. Emerg Radiol. 2013;20(3):225-32.

(3.) Sunnapwar A, Katre R, Prasad SR, Chintapalli K, Philips S. Spectrum of multidetector computed tomography/magnetic resonance imaging findings in intrahepatic vascular shunts: classification, characterization, and management. Curr Probl Diagn Radiol 2012;41(5):189-197.

(4.) Elsayes KM, Shaaban AM, Rothan SM, Javadi S, Madrazo BL, Castillo R P, Casillas VJ, Menias CO. A Comprehensive Approach to Hepatic Vascular Disease. Radiographics. 2017 May-Jun;37(3):813-836.

(5.) Preger L. Hepatic arteriovenous fistula after percutaneous liver biopsy. Am J Roentgenol Radium Ther Nucl Med 1967;101:619-620.

(6.) Piccinino F, Sagnelli E, Pasquale G, Giusti G. Complications following percutaneous liver biopsy. A multicenter retrospective study on 68,276 biopsies. J Hepatol 1986;2:165-173.

(7.) Semelka RC, Lessa T, Shaikh F, Miller FH, Elazzazi M, Dyson M. MRI findings of posttraumatic intrahepatic vascular shunts. J Magn Reson Imaging 2009;29(3): 617-620.

(8.) Guzman EA, McCahill LE, Rogers FB. Arterioportal fistulas: introduction of a novel classification with therapeutic implications. J Gastrointest Surg 2006;10:543-550.

(9.) Kumar A, Ahuja CK, Vyas S, et al. Hepatic arteriovenous fistulae: role of interventional radiology. Dig Dis Sci 2012;57:2703-2712.

(10.) Tasar M, Gulec B, Bozlar U, Saglam M, Ugurel M, Ucoz T. Intrahepatic arterioportal fistula and its treatment with detachable balloon and transcatheter embolization with coils and microspheres. Clin Imaging 2005;29:325-330.

Peeyush Bhargava, MD, Guillermo Sangster, MD, and Chaitanya Ahuja, MD are associated with Louisiana State University Health Sciences Center-Shreveport, Department of Radiology in Shreverport, LA. Quyen Chu, MD is affiliated with Louisiana State University Health Sciences Center-Shreveport, Department of Surgery in Shreveport, LA.

Peeyush Bhargava, MD, Guillermo Sangster, MD, Chaitanya Ahuja, MD, Quyen Chu, MD
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Author:Bhargava, Peeyush; Sangster, Guillermo; Ahuja, Chaitanya; Chu, Quyen
Publication:The Journal of the Louisiana State Medical Society
Article Type:Clinical report
Geographic Code:1USA
Date:May 1, 2018
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