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Posttraumatic Hemobilia: A Nonoperative Treatment

D. Dobanovacki, S. Radojkovic*, B. Vujosevic**, R Jokic, V. Pekovic-Zrnic

Pediatric Surgery Clinics Institute for Child And Adolescent Health Care in Vojvodina, Novi Sad, Serbia

* Department of Radiology Academy for Military Medicine Belgrade, Serbia

** Department of Radiology Institute for Oncology Sremska Kamenica, Serbia

 

Abstract

We present a case of haemobilia due to severe liver injury in pediatric patient. A boy of six year old suffered a liver fracture and life threatening intraabdominal haemorrhage. Tenth day after the accident and liver sutures the diagnosis of haemobilia was confirmed. Selective hepatic angiography discovered a communication with the biliary tree to the rupture, and embolisation was performed. The patient’s recovery was satisfying. Selective embolisation is a treatment of choice for haemobilia.

Key words: posttraumatic haemobilia, embolisation.

 

Correspondence

Dusanka Dobanovacki

Pediatric Surgery Clinics Institute for Child And Adolescent Health Care in Vojvodina

21 000 Novi Sad, Hajduk Veljkova 10.

e-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.

 

Introduction

Posttraumatic haemobilia is a complication of liver injury. It develops as consequence of necrosis of an intrahepatic haematoma. The main clinical features are biliary colic followed by gastrointestinal bleeding that manifest by haemetemesis and/or melena. Hepatic arteriography discloses the
bleeding site and a transcatheteral embolisation should always be attempted in the same procedure. If embolisation fails liver resection is a therapeutic method of choice (1).

Case Presentation

A six year old boy injured by car was admitted fully unconscious, intubated for brain contusion, and in the state of hypovolemic shock. Physical examination revealed blunt abdominal trauma and ultrasonography showed a profuse life threatening intra-abdominal haemorrhage due to the liver rupture. An emergency exploration by laparotomy was done at the moment when the arterial pressure and pulse were not notable. Extensive rupture of the right liver lobe was noticed deep through parenchyma (grade V of AAST Liver Injury Grading Scale). Combination of Pringle manoeuvre, manual compression and deep parenchyma sutures made possible to stop the bleeding. Blood from the right pleural cavity was drained by chest tube.

The postoperative recovery was as expected for the first six days, and the state improved so that he became able to communicate.

Tenth day after accident syncope and melena appeared, suddenly followed by the decrease of blood count. An abdominal CT scan disclosed a large cavity in the right liver lobe (Fig. 1). Duodenoscopy revealed blood flowing from the biliary tree through the ampula of Vater. A diagnosis of posttraumatic haemobilia was obvious.

A selective hepatic angiography by transfemoral approach discovered that one of the right hepatic artery branches communicated with billiary tree (Fig. 2). That artery was superselectively engaged by catheter 5F Cordis-Cobra 1, and a couple of Gealfoam-torpedoes (20x3x3 mm) soaked in contrast media were injected. The bleeding artery was completely occluded (Fig. 3). Haemorrhage ceased and the child’s condition was stable.

Two days after embolisation, serum bilirubin levels rapidly increased to 133 mmol/l but returned to normal values in the next couple of days spontaneously.

Four weeks after accident and two weeks after liver artery embolisation child’s general condition permitted dismissal from the hospital. All laboratories results were normal and there were no traces of blood in his stools.

Now, sixteen years later the boy is a healthy and well developed young men with good liver function and no complaints.

hemobilia 1 hemobilia 2
Figure 1. CT scan of the liver: a large defect in the parenchyma of the right lobe. Figure 2. Selective hepatic angiography: contrast leaks through the rupture of one of the right hepatic artery communicate with biliary tree.

hemobilia 3
Figure 3.  Angiography after embolisation: the stump of the right hepatic artery is outlined. Arrows delineate the cavity.

Discussion

Although posttraumatic haemobilia accounts for 50% of all haemobilia cases, it is seen only in 2, 5% of all liver trauma cases.

Diagnosis of haemobilia is not difficult to obtain if it is suspected. A typical clinical picture of gastrointestinal bleeding, biliary colic and obstructive jaundice is met only in about 1/3 of the patients; anaemia in 70%, and only sporadically fever and palpable mass with dull pain are found (2). A hypovolemic shock is not rare. If the blood loss is slow, anaemia may be the single symptom. Sometimes a time lapse of several weeks or even months can happen between the injury and the development of bleeding signs. In our case, it was only nine days because the large branch of right hepatic artery was ruptured. Imaging procedures (ultrasound, CT, percutaneous transhepatic cholangiography) can detect filling defect in the biliary tree as an indirect sign. A definitive diagnosis is obtained by doing a fibroscopy and finding evidence of direct blood flow through the Vater’s ampulla, which was performed in our case. A selective angiography of the liver could reveal extravasations of contrast media into the biliary tree.

Until Walter et al. in 1976 first described a successful transcatheteral control of haemobilia, the standard method of treatment was the surgical one. Transcatheteral embolisation can control haemobilia in almost every case (3). Most often, Gelfoam particles are sufficient but in cases of very large fistulae Gianturco spring-coils of detachable balloons are needed. It should always be attempted to catheterize and occlude the most distal part of the bleeding artery so as to prevent possible necrosis of liver tissue as in the case presented.

A dual vascular irrigation of the liver is responsible for a very low complication rate of embolisation. Major complications are rare and associated with obstructive jaundice.

An elevation of serum liver enzymes concentration is a normal feature in about 20 per cent of embolised patients. We were surprised by the elevation of the bilirubin level up to 133mmol/l in our patient. The explanation of this phenomenon is a speculative one; necrosis of liver tissue, developed due to Gelfoam particles injected, and contrast media, both enlarging the traumatic cavity in the liver parenchyma, provoking the compression of the right biliary duct – fact confirmed by post-procedural ultrasound. Fortunately, the condition soon improved spontaneously – the clot swelling diminished, leading to the desobstruction of biliary branch and, three months later, to thrombus scarring in the traumatic cavity. In cases when embolisation fails liver resection is a therapeutic method of choice.

 

REFERENCES

1. Burch JM, Moore EE., Injuries to the Liver. In Trauma and Thermal Injury Section 7 Chapter 6 2006

2. Gupta LB, Puri AS., Management of Traumatic Haemobilia with Embolisation. Indian Pediatrics, Editorial 2006; 43:825-827

3. Walter JF, Paaso BI, Cannon BW, Successful Transcatheteral Embolic Control of Massive Haemobilia Secundary to Liber Biopsy. AJR 1976; 127:847