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LIVER TRANSPLANTATION 14:1204-1210, 2008

ORIGINAL ARTICLE

Emergency Liver Transplantation Following Severe Liver Trauma Olga N. Tucker, Paul Marriott, Mohamed Rela, and Nigel Heaton Institute of Liver Studies, King’s College London School of Medicine, King’s College Hospital, London, United Kingdom

Liver trauma is a major cause of mortality after major blunt and penetrating abdominal trauma. The need for life-saving emergency hepatectomy and liver transplantation is extremely rare. We report the management of 2 patients who required urgent liver transplantation for liver trauma. One patient developed hepatic failure following global ischemia after a gunshot injury. The second patient developed a severe postreperfusion injury following removal of a perihepatic pack after blunt abdominal trauma. We highlight the difficulties in the management of severe liver trauma with an emphasis on the clinical features, radiological investigations, and surgical treatment of these complex patients. Liver Transpl 14:1204-1210, 2008. © 2008 AASLD. Received January 2, 2008; accepted May 9, 2008.

Liver injury is the main cause of death following major blunt abdominal trauma with a mortality rate of 10% to 31%.1-4 Patients with a severe blunt liver injury have a higher reported mortality of up to 58%.1,2,5,6 Furthermore, injury to the main hepatic veins or retrohepatic cava is associated with mortality rates of 50% to 100%.3,7-9 Significant blunt liver trauma is associated with other intra-abdominal and/or extra-abdominal injuries in 69% to 90% of cases, which may be important in determining the outcome.1-3,10 Isolated penetrating liver injury is becoming more prevalent and is the commonest mode of injury in some parts of the world.5,9,11 Prompt assessment and treatment following major blunt or penetrating abdominal injury are key to determining the outcome. This report describes successful outcomes in 2 patients with severe liver injury after emergency liver transplantation (LT) following the failure of conventional management. One patient developed progressive acute liver failure (ALF) from global liver ischemia after a high-velocity gunshot injury. The second developed a life-threatening postreperfusion injury of the liver after perihepatic pack removal following blunt abdominal trauma.

CASE 1 A 34-year-old male was admitted to a district general hospital with penetrating thoracoabdominal injuries from multiple gunshot wounds. On initial assessment, he was alert, oriented, and normotensive with a blood pressure (BP) of 130/60 mm Hg, but he was tachycardiac at 130 beats/minute. Multiple bullet entry wounds were visible in the right hemithorax, with further entry and exit wounds along the left anterior hemithorax, upper abdomen, and right upper limb. Abdominal examination revealed diffuse abdominal tenderness. An intercostal drain was inserted to drain a right hemopneumothorax. Three units of blood, 1 unit of colloid, and 2 L of crystalloid were administered. A thoracoabdominal computed tomography (CT) scan demonstrated a penetrating liver injury and a right hemopneumothorax. The patient was transferred to our liver intensive care unit (LICU). On arrival (within 4 hours of the injury), he was agitated, confused, tachypnoeic, and hemodynamically unstable. His abdomen was distended with diffuse tenderness and guarding. Resuscitative measures were commenced. Echocardiography

Abbreviations: ALF, acute liver failure; ARF, acute renal failure; BP, blood pressure; CMV, cytomegalovirus; CT, computed tomography; CVVHF, continuous veno-veno hemofiltration; HSV, herpes simplex virus; LICU, liver intensive care unit; LT, liver transplantation; MAP, mean arterial pressure; n/a, not available; NOM, nonoperative management; POD, postoperative day. Address reprint requests to Olga N. Tucker, Institute of Liver Studies, King’s College London School of Medicine, King’s College Hospital, Denmark Hill, London SE5 9RS, United Kingdom. Telephone: ⫹44-20-73463762; FAX: ⫹44-20-73463575; E-mail: [email protected] DOI 10.1002/lt.21555 Published online in Wiley InterScience (www.interscience.wiley.com).

© 2008 American Association for the Study of Liver Diseases.

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Figure 1. Contrast-enhanced axial abdominal and pelvic computed tomography scan after a penetrating liver injury demonstrating a laceration (arrow) extending from the posterior right liver and exiting the anterior left liver with active contrast extravasation and an extensive centrally located hematoma. Abbreviations: L, left liver; R, right liver; S, stomach.

excluded cardiac tamponade. Following hemodynamic stabilization, a contrast-enhanced abdominal CT scan was performed, demonstrating a hemoperitoneum and a liver laceration corresponding to the bullet track extending from the posterior right liver and exiting the anterior left liver (Fig. 1). Active bleeding was seen at the center of the liver laceration, with further bleeding tracking along the lesser curve of the stomach with pooling at this site. The retrohepatic inferior vena cava was compressed. Visceral angiography demonstrated disruption of the left hepatic artery with active bleeding, which was embolized. An extensive hematoma was seen centrally within the liver, but no portal venous disruption was identified. However, he continued to be hemodynamically unstable and underwent emergency laparotomy within 4 hours of admission. At surgery, there was extensive parenchymal injury to both lobes with active hemorrhage from the entry and exit wounds. Because of the patient’s unstable hemodynamic status and extensive parenchymal damage with active bleeding from the entry, exit, and bullet tract wounds, liver resection was not considered, and hemostasis was achieved with perihepatic packing. Closure was performed with a conventional mass closure technique. Postoperatively, he remained hemodynamically unstable with ongoing transfusion requirements, coagulopathy (international normalized ratio ⫽ 2.7), hypofibrinogenemia, thrombocytopenia, transaminitis with an aspartate aminotransferase of 3426 IU/L, hypothermia, increasing ventilatory support requirements with an acute lung injury, and refractory metabolic acidosis requiring continuous veno-veno hemofiltration (CVVHF). A repeat laparotomy was undertaken within 24 hours of transfer for abdominal compartment syndrome with an intra-abdominal pressure of 35 mm Hg associated with anuria and hypoxemia. Following perihepatic pack

removal, the liver was edematous, with ongoing bleeding from the left lobe. As the liver was viable, a decision to perform total hepatectomy was not taken. To achieve hemostasis, perihepatic packs were placed, and the abdominal wall was closed with a silastic mesh. Despite the achievement of hemostasis, the patient’s clinical condition continued to deteriorate with increasing vasopressor requirements, rising intra-abdominal pressure, metabolic and lactic acidosis, established acute renal failure (ARF), respiratory failure, and an indocyanine green clearance of 4.2%. The patient was listed for LT and transplanted 24 hours later. At laparotomy, the liver was ischemic (Fig. 2). Following the creation of a portocaval shunt, hepatectomy and piggyback LT were performed with a Roux-en-Y hepaticojejunostomy. The abdomen was closed with a silastic mesh. Examination of the explanted liver demonstrated a grade V cavitation injury and diffuse nonviable ischemic necrosis (Fig. 2). His postoperative recovery was complicated by a prolonged LICU stay with an acute lung injury, rhabdomyolysis, ARF, slow respiratory wean, and liver graft and gut dysfunction. He was discharged from LICU 45 days post-LT. Other postoperative morbidity included left radial nerve palsy, critical illness myopathy with bilateral foot drop, and pressure sores on both heels. He is currently well with excellent graft function 3 years following LT.

CASE 2 A 14-year-old boy was admitted to a district general hospital following a road traffic accident. On arrival, he was hemodynamically stable with a distended diffusely tender abdomen. An abdominal CT scan demonstrated a grade IV liver injury. A laparotomy was performed because of hemodynamic instability. Following temporary portal triad clamping, perihepatic packing and conventional abdominal closure, the patient was transferred, arriving at our LICU 13 hours after the accident. Prior to transfer, he received 25 units of blood, 7 units of fresh frozen plasma, 4 units of platelets, 4 L of colloid, and 2 L of crystalloid. On arrival, he was well oxygenated and hemodynamically stable without vasopressor support. His liver function tests were deranged with an international normalized ratio of 1.74, serum lactate of 2.7 mmol/L, and aspartate aminotransferase of 129 IU/L. Selective hepatic angiography demonstrated disruption of the right hepatic artery, and coil embolization was successfully performed. Seventeen hours following admission, he became oliguric, acidotic, and hyperlactatemic and was commenced on buffer-free CVVHF employing prostacyclin. Norepinephrine (0.05 ␮g/kg/minute) and dopexamine (1 ␮g/kg/minute) were also administered. After 27 hours in LICU, the patient underwent an exploratory laparotomy. After the opening of the abdomen and within 1 minute of commencement of perihepatic pack removal, the mean arterial pressure (MAP) fell to 35 mm Hg with a tachycardia of 128 beats/minute, and the central venous pressure fell to 12 mm Hg in the absence of hemorrhage. The initial hypotension was managed with col-

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Figure 2. Representative intraoperative images at the time of liver transplantation after a penetrating liver injury. (A) Diffuse parenchymal liver ischemia with areas of infarction. (B) Explant demonstrating the bullet track entering the right lobe and exiting the left with extensive intervening parenchymal cavitation injury with necrosis and hematoma.

loids and 100-␮g bolus doses of epinephrine followed by a continuous norepinephrine infusion to maintain a MAP ⬎ 60 mm Hg after adequate volume replacement. The liver was dusky, with improvement in color once pack removal was complete. There was a further fall in BP accompanied by an increase in peak inspiratory pressures and increased oxygen requirements. Tension pneumothorax and cardiac tamponade were excluded. Auscultation of the lungs revealed fine crepitations at both bases. The liver was repacked, and the abdomen

was partially closed. A thorough physical examination, chest X-ray, transthoracic echocardiogram, and electrocardiogram were normal apart from evidence of pulmonary edema. Continuous pulse contour analysis using the PiCCO system (Pulsion Medical Systems, Munich) indicated a high cardiac index with a low systemic vascular resistance index. A diagnosis of severe postreperfusion injury of the liver was made. The patient continued to deteriorate with worsening gas exchange, rising pulmonary inflation pressures, and progressive hemodynamic instability. Following multidisciplinary discussion and consultation with the patient’s family, a decision was taken to proceed to hepatectomy and listing for LT. On re-exploration, the patient had severe pulmonary edema. The liver was markedly ischemic. Hepatectomy was performed with oversewing of the hepatic veins and formation of a portocaval shunt. Following excision, there was an improvement in the patient’s physiological variables, with a reduction in pulmonary edema fluid and vasopressor support. On his return to LICU, CVVHF was recommenced, and a continuous infusion of N-acetyl cysteine was administered as a free-radical scavenger. Cardiac output monitoring was continued with the PiCCO system, and fluid administration was guided by intrathoracic blood volume index estimation and central venous pressure. Sedation was maintained with fentanyl and lorazepam infusions titrated to optimal effect. A cadaveric liver became available the following day, and implantation was performed 35 hours after total hepatectomy. All vasopressor support was discontinued within 9 hours, and extubation was performed on postoperative day 8, with discharge from LICU on postoperative day 17. He was readmitted 2 days later for 5 days of ventilation for infective complications. Histopathological analysis of the explanted liver demonstrated a 14-cm-long and 4-cm-deep laceration of the right lobe with extensive hepatic hemorrhagic necrosis and gallbladder infarction. His postoperative course was complicated by ARF requiring renal support for 22 days, myocardial ischemia, and a methicillin-resistant Staphylococcus aureus wound infection. He was discharged home after an in-hospital stay of 43 days. Subsequently, he developed steroid-induced diabetes mellitus, renal impairment, depression, and poor compliance with immunosuppressant therapy, with chronic graft rejection necessitating 2 further cadaveric liver transplants 1 and 3 years later. He is currently well with good liver graft function.

DISCUSSION Since the early 1990s, nonoperative management (NOM) of hemodynamically stable patients with blunt liver trauma has become the standard of care.2,12 Approximately 85% of patients with blunt liver injury are stable at presentation, and NOM is associated with reduced transfusion requirements, ICU stay, intra-abdominal infections, and length of hospital stay.2,13 Successful outcome following NOM has been reported in

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TABLE 1. Indications for Transfer of Patients to a Specialist Liver Unit After Major Liver Trauma Severe liver injury: ⱖgrade 3 Penetrating liver injury: any grade Lack of expertise locally: any grade Anticipation of surgical intervention Major vessel injury Major biliary injury Hemostasis with perihepatic packing Requirement of specialist radiological techniques, including angiography and angioembolization Requirement of specialist interventional endoscopic techniques, including biliary stenting Evolving acute liver failure

85% to 100% of patients, regardless of liver injury grade.3,13-17 Although conservative management of hemodynamically stable patients following penetrating abdominal trauma has been reported, laparotomy is indicated in the presence of peritonitis.11,18 In hemodynamically unstable patients, early control of ongoing hemorrhage is key as the majority of intraoperative deaths are due to uncontrolled bleeding, and an expeditious laparotomy can be life-saving.3,15 Perihepatic packing is an effective technique for achieving hemostasis after severe liver trauma, with or without retrohepatic venous injury.3,6 Other options such as hepatorrhaphy, selective hepatic artery ligation, resectional debridement, and anatomical resection are less effective in achieving hemostasis and invariably result in loss of functioning liver tissue. Total vascular occlusion, venovenous bypass, or atriocaval shunting may be required for repair of retrohepatic venous injuries. Major resection of the damaged parenchyma after severe liver injury is not recommended in hemodynamically unstable patients. Increased mortality rates have been demonstrated in association with a higher number of resected segments and increased intraoperative blood loss.1,8,19,20 Operative management of patients with severe liver trauma in specialized units is associated with lower mortality and morbidity rates in comparison with nonspecialist centers.10,21 Early communication with a specialist unit, hemostasis with perihepatic packing, and prompt transfer to a tertiary care facility once the patient is hemodynamically stable for further management are recommended (Table 1).20,22 Early stabilization with immediate laparotomy and perihepatic packing prior to transfer was a lifesaving measure in our 14-year-old patient. Patients requiring operative management have a significantly higher injury severity score, lower Glasgow coma scale score, lower initial BP, higher initial heart rate, higher fluid and blood transfusion requirements, and higher liver-related mortality.15,20 Selective hepatic artery embolization is an important additional therapeutic option in patients with ongoing bleeding after perihepatic packing or a primary measure when active bleeding is demonstrated on contrastenhanced CT and/or selective hepatic angiogra-

phy.23-28 Both of our patients underwent selective hepatic angiography for ongoing bleeding with identification of a source of active blood loss with effective hemostasis with coil embolization. An increased survival benefit has been demonstrated with the combination of damage-control laparotomy, perihepatic packing, and embolization versus early laparotomy with attempted hemostasis.29 LT is the only therapeutic option for progressive ALF. In the setting of major trauma, indications include uncontrollable hemorrhage (in experienced hands), severe grade IV-V injury, irreversible liver failure after initial treatment, and life-threatening postreperfusion injury.30,31 The requirement for LT after major liver trauma is rare, with only 19 reported cases, the majority occurring after blunt trauma with a variable outcome (Table 2).30,31-37,44 One of our patients had irreversible ALF secondary to liver necrosis from a diffuse parenchymal cavitational and major hilar injury after a gunshot injury. The presence of multiorgan failure involving 3 to 4 major organs in association with complete liver necrosis may give rise to toxic liver syndrome. In a series of 32 patients who underwent thirty-four 2-stage LTs by Ringe at al.,38 toxic liver syndrome was present in 27 and was due to a variety of causes, including primary graft nonfunction, acute rejection, fulminant hepatitis, postoperative liver failure, delayed graft failure, hepatic artery thrombosis, postnecrotic cirrhosis, and massive liver trauma. Our second patient developed a severe postreperfusion injury following perihepatic pack removal. The postreperfusion syndrome is a systemic response to a reperfusion injury.39 The term was first used by Aggarwal et al.39 in 1987 to describe the profound changes in recipient cardiovascular status following graft reperfusion during LT. It is defined as a fall in MAP of ⬎30% from baseline for at least 1 minute within 5 minutes of graft reperfusion. It differs from an ischemia-reperfusion injury, which is a process of continued or accelerated local damage occurring in a previously ischemic organ or body region following restoration of blood supply.40 The postreperfusion syndrome is associated with life-threatening cardiovascular and respiratory decompensation, including bradyarrythmias, hypotension, reduced systemic vascular resistance, increased cardiac filling pressures, and high pulmonary arterial pressures.39,41 Other causes of acute intraoperative cardiovascular decompensation in a patient following major multisystem trauma need to be excluded. More common causes include hypovolemia, cardiac tamponade, tension pneumothorax, air or fat embolism, myocardial injury, sepsis, and anaphylactoid reactions to administered drugs or blood products.40 In our patient, the significance of the injury was indicated by the difficulties in achieving hemostasis, progressive liver failure, and liver hypoperfusion on pack removal. The precipitous clinical deterioration in the absence of another identifiable cause indicated severe postreperfusion syndrome. Emergency hepatectomy, on the basis of previous experiences, was considered the only therapeutic option. This action helped to stabilize the patient to allow for LT. Once a decision has been reached to proceed with LT

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TABLE 2. Outcome After Liver Transplantation Following Abdominal Trauma

Year

Trauma Type

Transplant

Esquivel et al.

1987

Blunt

n⫽2

Angstadt et al.34

1989

Blunt

n⫽1

Jeng et al.37 Ringe et al.31

1993 1995

Blunt Blunt

n⫽1 n⫽8

Demirbas et al.36

1997 Penetrating

Dominguez et al.32 Chiumello et al.33

2001 2002

n/a Blunt

n ⫽ 2 (1 retransplant for hepatic artery thrombosis n⫽2 n⫽1

Veroux et al.30 Boggi et al.44

2003 2006

Blunt Blunt

n⫽1 n⫽1

Authors 35

Survival/Follow-Up (Time from First Transplant) n ⫽ 1: died in week 7. n ⫽ 1: alive at 16 months n ⫽ 1: discharged on POD40 n ⫽ 1: died on POD25 n ⫽ 2: alive at 49 and 67 months n ⫽ 2: alive at 9 and 14 months

n⫽2 n ⫽ 1: alive at 6 months n ⫽ 1: alive at 8 years n ⫽ 1: died on POD2

Cause of Death CMV, sepsis, pulmonary and hepatic failure

Sepsis Sepsis, multiorgan failure

Sepsis

Respiratory failure, HSV infection

Abbreviations: CMV, cytomegalovirus; HSV, herpes simplex virus; n, patient number; n/a, not available; POD, postoperative day.

for major liver trauma, a number of surgical options exist. The first is a 2-stage procedure, with total hepatectomy and portocaval shunt followed by LT when a suitable donor organ becomes available. Another option is continued supportive management while the patient waits for a suitable donor graft with subsequent standard LT.32,33,42 The first successful 2-stage procedure was performed by Ringe et al.38,43 in 1986, who reported dramatic clinical improvement after rendering patients with failing livers anhepatic, and they employed this technique successfully in the emergency management of massive and otherwise unsalvageable liver trauma. In the Ringe series published in 1988, thirty-four 2-stage procedures were performed in 32 patients. The indications were broadly divided into 2 categories: multiorgan failure due to acute hepatic necrosis with toxic shock syndrome and liver only failure due primarily to hemorrhage.38 Both surgical options were employed in our patients, being dictated by the severity of their clinical condition. It is impossible to accurately define a maximal duration of anhepatic tolerance. The anhepatic time in case 2 was 35 hours, and time periods of up to 41 hours have been described.38 However, survival depends on the clinical status of the patient at hepatectomy and the effectiveness of LICU supportive management. For major venous injuries, liver explantation, extracorporeal repair, and autotransplantation have been reported. However, although technically successful, the patient died 48 hours later.44 Iatrogenic complications after interventional procedures to achieve hemostasis following major liver trauma rarely necessitate LT. LT for ischemia after common hepatic artery coil emboli-

zation has been described for grade V liver injury bleeding following failed perihepatic packing.45 Although the presence of infection is a contraindication to transplantation, a successful outcome after LT for progressive liver failure with generalized sepsis has been reported for a 26-year-old patient after left hepatectomy and primary repair of multiple caval lacerations.46 Liver trauma is a frequent and preventable cause of mortality in the young. Although the majority of injuries can be successfully managed conservatively, laparotomy is indicated in the hemodynamically unstable patient following blunt abdominal trauma or in the hemodynamically stable patient with peritonitis following penetrating abdominal trauma. The aim of surgery is to arrest bleeding. Perihepatic packing is quick and generally effective. Selective embolization is an important adjunct for achieving hemostasis and preserving the liver parenchyma. Total hepatectomy should be performed only as a life-saving measure when hemorrhage is uncontrollable, for irreversible liver failure, or for life-threatening postreperfusion injury. Early communication with a regional LT center is advised. Extracorporeal repair of liver injury and autotransplantation for hepatic venous or retrohepatic caval injuries may be an option in experienced centers.

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