Traumatic injury to the portal triad

INTRODUCTION — The portal triad contains the extrahepatic segments of the portal vein, hepatic artery, and bile ducts. Injury to the portal triad is uncommon but is one of the most difficult to manage traumatic injuries associated with high morbidity and mortality.

Deaths are due to exsanguinating hemorrhage often from more than one source and a challenging exposure. Furthermore, attempts to control bleeding with vascular ligation of the portal vein or hepatic artery may result in complete bowel ischemia or liver necrosis, respectively. Ductal injuries are difficult to identify, and postreconstruction complications of leak, sepsis, and death are not uncommon.

The clinical features, diagnosis, and management of portal trial injuries are reviewed. The initial approach to management of abdominal trauma is reviewed separately. (See "Overview of inpatient management of the adult trauma patient" and "Initial evaluation and management of blunt abdominal trauma in adults" and "Initial evaluation and management of abdominal stab wounds in adults".)

ANATOMY — The portal triad is contained within the hepatoduodenal ligament and contains the portal vein (posterolateral), hepatic artery (medial), and bile ducts (lateral) (figure 1). Variations in portal triad anatomy are relatively common (figure 2) [1].

The portal vein forms at the confluence of the splenic vein and superior mesenteric vein (figure 3). The inferior mesenteric vein can insert into the splenic vein (figure 4) or at the confluence of portal vein and superior mesenteric vein, which is posterior to the neck of the pancreas [2].

The classic hepatic artery anatomy (Michels [1] or Hiatt [3] classification Type 1) of left and right hepatic arteries branching from the common hepatic artery occurs in roughly 80 percent of people [4]. Variants to the arterial system include a replaced left hepatic artery that is off the left gastric artery in 3 to 10 percent of people. A replaced right hepatic artery originates from the superior mesenteric artery in 11 to 21 percent of people. This can be identified by placing a finger in the foramen of Winslow and palpating a pulse posterior to the portal vein.

The typical pattern of left and right hepatic ducts forming a common hepatic duct occurs in 50 to 60 percent of people. One common variation is the right posterior sectorial can drain into the left hepatic duct or confluence of the left and right hepatic ducts [5].

INCIDENCE AND ETIOLOGY — Injury to any structure in the portal triad is rare, and thus, most data on portal trial injuries come from small, single-center case series over the course of decades. In an 11-year retrospective series from Harborview Medical Center, injuries to the portal triad comprised only 0.21 percent of all trauma admissions [6]. The mechanism was penetrating injury in 62 percent, and the patients were predominantly male with a median age of 35. In a series of 302 abdominal vascular injuries over a six-year period in another urban level 1 trauma center, portal vein injuries occurred in 14 (5 percent) [7].

Concomitant injuries — Concomitant injuries to the portal vein, hepatic arteries, and bile ducts can occur; however, there are no apparent patterns with respect to the number of structures or combination or mechanism of injury (ie, penetrating, blunt). In the largest multicenter, retrospective review of 99 patients with portal triad injuries, 84 patients (88 percent) had one structure injured, 15 (16 percent) had two or more structures injured, and 4 patients had all three structures injured [8].

Associated injuries — Given the proximity of the portal triad to other anatomic structures, nearly all patients have an additional solid organ (liver, pancreas, right kidney, right adrenal gland), hollow viscous (stomach, duodenum, colon, gallbladder), or vascular injury (vena cava, aorta, renal vessels). In a series of 21 portal triad injuries, the most common solid organ injury was the liver (62 percent) followed by the pancreas (29 percent). The most common vascular injury was the vena cava (14 percent) and the aorta (9 percent) [9]. In another series of porta hepatis injuries, an average of 3.6 additional injuries per patient were present [10].

CLINICAL FEATURES

Hemorrhagic shock — The majority of patients with portal triad injuries will present with hemorrhagic shock. In a series of 21 patients with portal triad injuries from mostly penetrating mechanisms, 85 percent arrived in shock and were taken immediately to the operating room [9]. Among patients who arrived with a systolic blood pressure <80 mmHg, the mortality rate was 91 percent [11].

Abdominal pain or peritoneal signs — The presence of abdominal pain or peritoneal signs are nonspecific. In the context of portal triad injury, these can be related to:

●Blood in the abdomen from portal venous injury or hepatic artery injury

●Bile in the abdomen from bile duct injury

●Intestinal congestion related to mesenteric venous thrombosis

DIAGNOSIS — Hemorrhagic shock and signs of intra-abdominal injury are nonspecific, and the diagnosis of portal trial injury relies upon demonstration of the injury on direct examination of the portal structures in the operating room, or on imaging features that strongly suspect portal triad injury or demonstrate injury in the vicinity of the portal triad that are highly associated with portal triad injury.

●For patients with blunt abdominal trauma, hypotension with a positive Focused Assessment with Sonography for Trauma exam (commonly in the right upper quadrant) is an indication for immediate abdominal exploration. Other indications for immediate laparotomy in blunt abdominal trauma may include the presence of free air on plain radiography or computed tomography (CT) of the abdomen or signs of peritonitis from associated adjacent hollow viscus injury.

●For patients with penetrating trauma and hemodynamic compromise or concern for portal triad injury based on a penetrating intrabdominal trajectory, urgent exploratory laparotomy is indicated.

●For hemodynamically stable patients with blunt trauma, cross-sectional imaging using a CT scan with intravenous (IV) contrast might be able to identify hepatic artery or portal vein injuries, but the data on this are sparse.

Features of hepatic artery injury may include intimal irregularity, pseudoaneurysm, and free contrast extravasation, and are all dependent on the timing of contrast injection and scanning. Delayed portal venous images may show portal venous thrombus or extravasation.

The American Association for the Surgery of Trauma (AAST) classification of extrahepatic biliary injury (table 1) and abdominal vascular injury (table 2) are shown in the tables. Using a classification system is essential in comparing outcomes and can be helpful in determining management strategies. This classification system should be incorporated into the clinical record (eg, imaging study, operative report) for every patient with portal triad injury.

SURGICAL MANAGEMENT — Surgical management of portal triad injury usually occurs under damage control principles but can occur under less urgent circumstances (eg, isolated bile duct injury).

General principles — For patients with hemorrhagic shock, portal triad injury may or may not be the main source of bleeding. When it is, the portal venous or hepatic artery bleeding is controlled first and then managed after quick control of other sources of bleeding and control of gastrointestinal contamination. If more urgent bleeding is from another source (eg, kidney, iliac artery), the portal triad is packed and managed once bleeding is controlled, and the patient is resuscitated according to damage control principles. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Damage control laparotomy'.)

A "damage control" approach to portal triad injury is recommended. For patients with vascular injury, hemorrhage control is the first priority of management. With portal venous injury, the surgeon is faced with bleeding from a structure that normally has an average of nearly 1 liter of blood flow per minute. In a Western Trauma Association review of portal triad injuries, exsanguination from the portal vein was responsible for 79 percent of early or operative deaths, and the overall mortality rate was 55 percent [8].

Control hemorrhage — Inflow control can be achieved with a Pringle maneuver (figure 5). This involves encircling the hepatoduodenal ligament using vascular clamps or using a Rommel tourniquet for proximal control. A "double Pringle maneuver" can be achieved as well, with a second clamp near the liver for distal control (figure 6) [11]. Packing may also be used.

Clamp time of the Pringle maneuver should be limited to what is necessary for hemorrhage control, and the clamp should be intermittently released, if possible, in 15-minute intervals. In a trial that randomly assigned patients to intermittent clamping of 15-minute intervals or ischemic preconditioning (20 minutes of ischemic preconditioning followed by inflow clamping for at least 30 minutes during transection) in patients undergoing elective liver resection, intermittent clamping was associated with lower blood loss [12]. (See "Open hepatic resection techniques", section on 'Vascular control'.)

Expose the portal triad — Following control of hemorrhage, optimal exposure is key. A wide Kocher maneuver (figure 7) with take-down and medial mobilization of the hepatic flexure of the colon and medial rotation of the duodenum will assist in exposure of the more proximal portal structures. It is important to leave the kidney and adrenal gland in their native locations. Identification and lateral retraction of the uninjured bile duct will protect it from potential iatrogenic injury. One of the most challenging portal vein injury locations to manage is behind the pancreas. In this situation, division of the pancreas will expose the retropancreatic portal vein and the confluence of the superior mesenteric vein and splenic vein. However, some authors reserve this heroic maneuver only when distal pancreatectomy is indicated [2]. (See "Management of pancreatic trauma in adults", section on 'Operative management of pancreatic injury'.)

Portal venous injury — Following vascular control and exposure, the surgeon is faced with the decision to repair or reconstruct the injury, provide a temporary shunt, or to ligate the vein.

Whenever possible, primary repair or reconstruction of the portal vein should be performed. In the Western Trauma Association multicenter series, survival was significantly increased for those in whom primary repair via lateral venorrhaphy was performed compared with venous ligation (58 versus 10 percent) [8].

Nevertheless, ligation of the portal vein rather than attempts at complex reconstruction may be expedient and appropriate in the hemodynamically unstable patient. The decision to ligate must be made early in the operative course, before shock and coagulopathy set in. In a series of 83 patients, those treated from 1958 to 1973 only underwent ligation as a last resort and only 13 percent survived; however, after 1974, they proceeded directly with ligation if simple lateral repair of the vein was impractical, and survival increased to 80 percent [13].

Shunting the portal vein is another option if the injury is not amenable to lateral repair, with delayed reconstruction using a saphenous vein or prosthetic vascular graft. However, there have been no large series or long-term work to guide any details of portal vein shunting. In a 2015 multicenter American Association for the Surgery of Trauma study, among 213 vascular shunts, only two were placed in the portal or superior mesenteric veins [14].

Second-look operation — When a second-look surgery is planned, the timing of surgery should be within 48 hours, but earlier if there is any concern for bowel ischemia. Temporary abdominal closure using a transparent adhesive dressing over the incision allows for inspection of congested bowel and prevents the occurrence of abdominal compartment syndrome. (See "Management of the open abdomen in adults" and "Abdominal compartment syndrome in adults".)

The second-look surgery will also identify additional injuries that may have been missed during a hectic index operation. Nonviable bowel is resected, as needed.

If the portal vein was ligated, portal venous pressure increases abruptly. Collateral blood flow may develop over the ensuing days to weeks. In the interim, large-volume resuscitation is needed to compensate for portal sequestration [15].

Postoperative surveillance for portal venous thrombosis — Abdominal duplex ultrasound should be used for routine surveillance for portal vein thrombus following portal venous repair or reconstruction. In a small series, 33 percent of patients had portal vein thrombosis on routine ultrasound surveillance following venous repair [16].

Systemic anticoagulation should be initiated in patients who develop portal vein thrombosis, provided other injuries do not contraindicate its use. (See "Acute portal vein thrombosis in adults: Clinical manifestations, diagnosis, and management".)

Hepatic artery injury — The hepatic artery is the least commonly injured portal triad structure. In the Western Trauma Association series, most hepatic artery injuries were due to blunt trauma [8]. The common, proper, left, and right hepatic arteries were affected equally. Abdominal exploration is indicated for active bleeding (eg, exsanguination, contrast blush seen on computed tomographic imaging) [8].

For most hepatic artery injuries causing bleeding, the hepatic artery can be ligated. If the hepatic artery is ligated, flow in the cystic artery, which provides the predominant blood supply to the gallbladder, will severely diminish, and as such, the gallbladder should be removed. Repair or reconstruction of the hepatic artery at any location (eg, common, proper, branches) can be time-consuming, and the repair is prone to thrombosis, given bleeding and shock. While there may be concern that ligation of the hepatic artery will lead to liver failure from ischemic hepatopathy, with isolated hepatic artery injury, this complication is unusual since the portal vein should contribute 80 percent of hepatic blood flow [2].

For patients with injuries to both the hepatic artery and portal vein, repair of at least one is mandatory, with efforts preferentially focused on the portal vein (see 'Portal venous injury' above). Liver perfusion can be evaluated intraoperatively using with laser-assisted fluorescence angiography (LAFA). If ischemia is confirmed after hepatic artery ligation, hepatic arterial inflow can be restored and/or any ischemic liver debrided.

In the Western Trauma Association series, 28 of 99 patients had a hepatic artery injury [8]. About two-thirds (68 percent) underwent ligation of the artery. Over 90 percent of survivors had ligation as the treatment of choice. All patients with a concomitant portal vein injury who underwent attempted primary repair of the hepatic artery died.

Bile duct injury — Injury to the extrahepatic bile ducts is unusual; however, the complications can be severe. In a Western Trauma Association series, only 35 patients had a bile duct injury over a 60-year cumulative experience [8]. Given the rarity of these injuries, the literature on the management of laparoscopic bile duct injuries is helpful for providing management, including the preferred type of repair (eg, primary repair, biliary-enteric reconstruction) and timing of repair.

Bile staining during laparotomy is suggestive of biliary tree injury. Intraoperative cholangiography or magnetic resonance cholangiopancreatography following index operation can also be used.

The size of the injury influences the type of repair. Partial or small injuries of the larger bile ducts can be primarily repaired, potentially over T-tube drainage or internal stent. In one of the largest series of intraoperatively identified bile duct injuries (nonthermal injury) during laparoscopic cholecystectomy, 10 of 19 patients underwent primary repair with or without a T-tube [17]. Biliary reconstruction is recommended for complex bile duct injuries, including those with segmental tissue loss, injuries greater than 50 percent circumference laceration. In the Western Trauma Association series, 9 of 10 patients with complex extrahepatic bile duct injuries underwent biliary-enteric anastomoses [8]. Biliary-enteric anastomotic reconstruction may be preferable to end-to-end reconstruction due to lower the rate of stricture. (See "Repair of common bile duct injuries".)

The timing of bile duct repair is critical for optimal outcome. The biliary enteric anastomosis should be performed with optimal physiology, especially in the face of a combined hepatic arterial injury and/or shock. In a series of 200 patients transferred to a tertiary referral center with bile duct injuries from laparoscopic cholecystectomy, the median time to repair was 10 weeks, and most patients (98 percent) underwent Roux-en-Y hepaticojejunostomies [18].

In the rare scenario of destruction of the distal common bile duct, a pancreaticoduodenectomy can be performed. In a series of patients requiring pancreaticoduodenectomy for trauma, the most common indication for the procedure was massive injury to the distal bile ducts and pancreatic head [19]. (See "Surgical resection of lesions of the head of the pancreas".)

POSTOPERATIVE CARE — Nearly every patient will undergo a second-look operation to evaluate for bowel edema and viability. Any patient with abdominal complaints following a laparotomy and surgical intervention on the portal triad should undergo an abdominal computed tomography (CT) scan to evaluate for abscess, leak, or missed injury. A duplex ultrasound of the portal vein and/or hepatic artery can be used to identify thrombosis and intervention with medical therapy instituted as indicated.

MORBIDITY AND MORTALITY — Morbidity and mortality related to portal triad injury is high. Despite improvements in survival for most other injury types, there has been little to no improvement in survival over the last 25 years due to the high degree of blood loss, frequency of associated injuries, and high complication rate.

A Western Trauma Association multi-institution series of portal triad injuries published in 1995 reported an overall mortality rate of 51 percent [8]. A later review of the Trauma Quality Improvement Program national database study demonstrated a 46 percent mortality rate [20]. Another institutional series reported similar mortality rates for portal venous and superior mesenteric venous injuries in 26 patients [21].

Complications — For survivors of portal triad injury, there is a substantial complication rate. In a single-center study of 15 portal vein injuries, 78 percent of patients had postoperative complications, most commonly sepsis [22]. In the nationwide Trauma Quality Improvement Program study of portal vein injuries, the most common complication was pneumonia (8.2 percent), followed by acute kidney injury (7.8 percent) and deep venous thrombosis (6.4 percent) [20].

Complications unique to the injury include postoperative liver failure and postoperative bowel ischemia if the portal venous or hepatic arterial systems are injured and especially in the setting of preoperative shock. Bile duct injuries pose their own unique set of morbidity, including stricture, cholangitis, leak, and sepsis.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Traumatic abdominal and non-genitourinary retroperitoneal injury".)

SUMMARY AND RECOMMENDATIONS

●Anatomy and incidence – The portal triad contains the extrahepatic segments of the portal vein, hepatic artery, and bile ducts. Injury to any the structures in the portal triad is overall rare. Given the proximity of these structures, injury to more than one portal trial structure frequently occurs. A penetrating injury mechanism is more common than blunt injury. Anatomic variations to the portal triad structures are common (figure 2) and can make an already difficult exposure even more challenging. (See 'Anatomy' above and 'Incidence and etiology' above.)

●Clinical features – Most patients with portal triad injuries have symptoms and signs of intra-abdominal injury (eg, pain, peritoneal signs) and are in hemorrhagic shock. Because of anatomic proximity, nearly all patients with portal triad injury will have an associated solid organ (liver, pancreas, right kidney, right adrenal gland), hollow viscous (stomach, duodenum, colon, gallbladder), or vascular injury (vena cava, aorta, renal vessels) that contributes to their symptomatology. (See 'Clinical features' above and 'Associated injuries' above.)

●Diagnosis – Hemorrhagic shock and other signs of intra-abdominal injury are nonspecific. A definitive diagnosis of portal triad injury relies upon demonstration of the injury on direct examination of the portal structures in the operating room in patients with indications for abdominal exploration. In hemodynamically stable patients, findings on computed tomography (CT) of the abdomen may confirm a clinical suspicion for portal triad injury. (See 'Diagnosis' above.)

●Damage control surgery – For patients in hemorrhagic shock, a "damage control" approach to portal triad injury should be used. The portal triad injury may or may not be the main source of bleeding. If it is, portal venous or hepatic arterial bleeding is controlled first using the Pringle maneuver (figure 6) and then managed after control of other sources of bleeding and control of gastrointestinal contamination. If more urgent bleeding is from another source (eg, kidney, iliac artery), the portal triad is packed and managed once other serious bleeding controlled and the patient has been resuscitated. Following a damage control approach, a second-look procedure is recommended. (See 'General principles' above.)

●Surgical repair – Once hemorrhage is controlled, the portal structures are exposed. Division of the pancreas may be required to expose retropancreatic portal vein injury; however, this is generally performed only when distal pancreatectomy is also indicated due to injury.

•Portal venous injury – Options for managing portal venous injury include primary repair, ligation, or shunting with delayed reconstruction. Ligation is less desirable but may be a necessary lifesaving maneuver. (See 'Portal venous injury' above.)

•Hepatic artery injury – Options for managing hepatic arterial injury include ligation or repair. Ligation of the hepatic artery is well tolerated provided any associated portal venous injury can be repaired. If the hepatic artery is ligated, the gallbladder should also be removed. (See 'Hepatic artery injury' above.)

•Bile duct injury – Non-iatrogenic traumatic injury to the extrahepatic bile ducts is unusual. Drainage with delayed repair is commonly used to manage these injuries. Depending on the size of the injury, options for repair include repair over a T-tube or biliary reconstruction (eg, end-to-end repair, biliary-enteric anastomosis). Severe distal bile duct injuries with concomitant injury to the head of the pancreas may mandate pancreaticoduodenectomy and reconstruction (ie, Whipple procedure). (See 'Bile duct injury' above.)

●Postoperative surveillance – Worsening pain or new abdominal complaints following surgery for portal triad injury should prompt an abdominal CT scan to evaluate for abscess, leak, or missed injury. For patients who have undergone portal venous repair, we suggest routine duplex surveillance for portal vein thrombus. (See 'Postoperative care' above.)

●Complications – Complications are common for survivors of portal triad injuries. Following control of serious bleeding from the portal vein or hepatic artery, patients can experience bowel ischemia or liver necrosis, respectively, requiring further surgery. Even with successful biliary reconstruction, complications such as bile leak, cholangitis, and sepsis are not uncommon. (See 'Complications' above.)

●Mortality – Despite improvements in survival for most other injury types, there has been little to no improvement in survival over the last 25 years due to the high degree of blood loss, frequency of associated injuries, and high complication rates. (See 'Morbidity and mortality' above.)