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Fatal hepatic hemorrhage after trauma
Fatal Hepatic Hemorrhage After Trauma
Steven C. Elerding, MD, Denver Colorado G. E. Aragon, MD, Denver Colorado Ernest E. Moore, MD, Denver Colorado
Despite protection from the lower rib cage, the liver is the second most commonly injured intraabdominal organ. The management of hepatic trauma has undergone significant revision over the past half century, resulting in a progressive reduction in mortality from 66 per cent in World War I, to 27 per cent in World War II, to 14 per cent in the Korean War, to 9 per cent in Vietnam [l-3]. However, the improvement in survival rate has now reached a plateau with the inability to control massive hemorrhage as the leading cause of death. Recent civilian reviews of liver injuries report mortality rates of 10 to 20 per cent and cite intractable bleeding as a major cause of death in 31 to 76 per cent of the cases (Table I) [4-IO]. The purpose of this review is to critically analyze a series of patients who died from exsanguination associated with hepatic trauma to help identify those at risk for this lethal complication and to establish a management plan to avert uncontrollable hemorrhage. Material and Methods Patients. Two hundred twenty-five patients with significant hepatic injuries underwent laparotomy at the Denver General Hospital from January 1, 1973 to December 31, 1978. Thirty-four patients (15 per cent) died, 28 (82 per cent) intraoperatively from hemorrhage and 6 (18 per cent) from associated injuries or multiple organ failure. The 28 exsanguinating injuries form the basis of this review; 15 (54 per cent) resulted from penetrating injuries and 13 (46 per cent) from blunt trauma. The 18 men and 10 women ranged in age from 3 to 60 years (average 30). initial Management. All patients were brought to the emergency department within 25 minutes of injury, where
From the Department of Swgety, Denver General Hospital and the University of Colorado Medical Center. Denver. Colorado. Reprint reWe?JS should be addressed to Ernest E. Moore, MD, Department of Surgery, Denver General Hospital, Denver, Colorado 80204. Presented at the 31st Annual Meeting of the Southwestern Surgical Congress, Las Vegas, Nevada, April 23-26, 1979.
Volume 138, December 1979
initial evaluation and resuscitation were performed. Central venous and multiple peripheral intravenous lines, a Foley catheter, and a nasogastric tube were immediately placed. Endotracheal intubation was carried out promptly when airway control was needed. Associated injuries were evaluated and managed as indicated. Warmed Ringer’s lactate was the initial resuscitative fluid in all patients with a detectable blood pressure. When the Ringer’s lactate replacement exceeded 50 cc/kg, transfusion of type-specific blood was begun as soon as available. Low liter 0 negative blood was given only to patients whose condition deteriorated to the point of cardiac arrest. Blood warmers and filters were used routinely. All patients were taken to the operating room within 45 minutes of arrival at the emergency department. Associated Injuries (Table II). Significant extraabdominal injuries were present in 8 (53 per cent) of the 15 patients with penetrating injuries. Six of these patients had associated thoracic trauma; one required thoracotomy in the operating room for a cardiac wound. Two other patients had significant extremity injuries. Eight patients (62 per cent) in the blunt trauma group had concomitant extraabdominal injuries. There were six extremity injuries, five chest wounds, three pelvic fractures, and two closed head injuries. An average of 2.4 associated intraabdominal organ injuries were encountered with penetrating trauma and 1.5 with blunt injuries. Four patients (27 per cent) in the penetrating injury group and three (23 per cent 1with blunt trauma had isolated liver injuries. The classification’of these lethal hepatic injuries is indicated in Table III. All injuries were grade IV or V. The retrohepatic vena cava was involved in eight patients (24 per cent) and the portal vein in five (15 per cent). Operative Management. Emergency thoracotomy before laparotomy was performed in one case. A midline incision was initially made and then extended across the costal margin into the right chest. Direct suture ligation of bleeding vessels was attempted in all cases. Temporary occlusion of the porta hepatis, the Pringle maneuver, was performed in 10 patients (26 per cent). Fifteen patients (54 per cent) underwent left anterolateral thoracotomy for internal cardiac massage and cross clamping of the descending aortic after intraoperative cardiac arrest.
883
Elerding
et al
TABLE I
study Ben Taub (1939-74) [ 41 Detroit Genera) (1961-76) [ 5] Parkland (1963-7 1) [ 61 Charity (1964-76) [ 71 San Francisco (1966-71) [ 81 San Antonio (1970-75) [ 91 Louisville (1973-76) [ IO] Denver General (1973-78)
1,590 1,404 811 546 285 233 178 225
13 12 13 10 19 11 20 15
58 63 76 35 56 31 58 82
Total
5.271
14
55
Mortality (“/)
(%)
-.
injuries Associated With Lethal Hepatic Trauma No. of Injuries
Location of Injury
In 15 Patients With Penetrating Trauma
In 13 Patients With Blunt Trauma
6 2 0 0
5 6 3 2
8 6 5 5 5 4 3
4 5 4 4 0 2 0
Extraabdominal Chest Extremity Pelvis Head lntraabdominal Small bowel Pancreas Kidney Spleen Stomach Vascular Colon
Hepatic
lobar resection
was carried out in 14 patients
per cent), to gain access to retrohepatic
Ciassitication of Lethal Hepatic injuries Penetrating Injury Group
Exsanguination
No. of Patients
TABLE ii
TABLE iii
Mortality Associated With Hepatic Trauma
(50
vena caval wounds
in 3. Repair of retrohepatic vena caval injuries was attempted in five patients without the use of a shunt and in three with shunting devices described by Schrock et al [I I J or Pilcher et al [IZ].
Class
I. Capsular tears II. Nonbleeding parenchymal tears
Blunt Trauma Group
0 0
0 0
0
0
8
12
7
1
bleeding, each patient had received more than 10 units of banked blood; however, none received platelet concentrates, fresh frozen plasma, or fresh whole blood. The characteristic picture was then massive uncontrollable hepatic hemorrhage as well as diffuse bleeding from all exposed surfaces. Only 11 patients (39 per cent) ultimat.ely received fresh frozen plasma and none underwent coagulation studies. In eight patients (29 per cent) arterial blood gases were measured to determine the magnitude of associated acidosis; the average pH was 7.11. Core temperature was obtained to ascertain the severity of hypothermia in only six patients (21 per cent); the average temperature was 32.2”C. Autotransfusion was utilized in one patient hut without blood component replacement.
Results All patients arrived at the emergency department with significant hypotension. Four had no obtainable blood pressure and 24 (84 per cent) presented with a systolic blood pressure of 60 to 90 mm Hg. Initial fluid resuscitation with Ringer’s lactate increased the systolic blood pressure to greater than 100 mm Hg in 22 patients (92 per cent). Blood pressure remained undetectable in one patient, who underwent thoracotomy for resuscitation in the emergency department. Of the 22 patients whose blood pressure improved to a systolic level greater than 100 mm Hg, systolic pressure subsequently decreased to less than 80 mm Hg in 20 (91 per cent) during their evaluation or transfer to the operating room. Exploration of these patients was undertaken immediately. By the time packs had been placed to t.amponade the hepatic se.4
Comments More than 85 per cent of liver injuries are minor and can be dealt with by simple techniques. The successful treatment of severe hepatic trauma, however, demands instant recognition and a preplanned course of action as well as mature surgical skill. Too often delay in judgment is fatal. Critical analysis of our hepatic injuries has identified a group of patients who died from exsanguination but who might have been saved by an aggressive orderly management plan. The typical patient arrived in the emergency department with a systolic blood pressure of 60 to 90 mm Hg after sustaining severe blunt or penetrating trauma. Initial fluid resuscitation increased the pressure to 100 mm Hg. The suspicion of a devastating injury was then lost and the surgeon often The Amerlcen Journal of Surgery
Fatal Hepatic Hemorrhage After Trauma
procrastinated by obtaining further roentgenographic studies and awaiting formal cross matching of blood. Recurrent hypotension was difficult to reverse, and the patient was quickly transported to the operating room and exploration undertaken. The surgeon found hemostasis impossible to achieve despite vigorous suturing, clamping, and packing. The potential therapeutic benefit as well as diagnostic aid of temporary porta hepatis occlusion was frequently overlooked. The anesthesiologist was preoccupied with efforts to replete volume and gave little attention to increasing acidosis and hypothermia. The blood bank, too, was ill prepared for the challenge, and consequently none of the patients received blood component or fresh blood replacement until more than 10 units of banked blood had been administered. In a desperate attempt to halt the torrential blood loss from the injured liver, the surgeon often resorted to major resection. This precipitated massive diffuse blood loss from the raw surface of the liver as well as from the incision and associated injuries. With the patient’s condition further deteriorating, thoracotomy was performed in a heroic but futile effort to revive the heart. This scenario should be preventable with a more aggressive but orderly approach. Early diagnosis is extremely important. Significant liver injuries associated with lower chest or upper abdominal penetrating wounds are usually not difficult to recognize. Any patient who is hypotensive on arrival at the emergency department after abdominal trauma must be suspected of having a severe liver injury. Rib fractures of the right lower thoracic cage, especially the posterior segments of the 9th through the 12th ribs, should raise suspicion. If multiple injuries occur or the patient’s mental status is altered, diagnostic peritoneal lavage is extremely reliable in identifying hemoperitoneum [13]. Ringer’s lactate, warmed to 4O”C, should be infused through central venous and large bore upper extremity intravenous lines. If more than 3 liters of Ringer’s lactate are required to normalize the blood pressure, type-specific blood should be obtained and the patient quickly transferred to the operating room. Additional chest x-rays and intravenous pyelograms may have to be obtained intraoperatively. Although disseminated intravascular coagulation, excessive fibrinolysis, and defective clotting factor synthesis have been incriminated in the pathogenesis of “nonmechanical” hemorrhage in severe liver injury, Clagett and Olsen [14] have indicated that massive transfusion of stored blood is the most important causative factor. They observed a significant coagulation defect in 17 (52 per cent) of 33 patients with grade IV and V hepatic trauma and recommend Volume 139, December 1979
the prophylactic use of blood component replacement. If the patient remains hypotensive after the 2nd unit of blood has been transfused, fresh frozen plasma should be administered then and with every 4th unit thereafter. Prothrombin time and partial thromboplastin time should be determined after administration of each unit of fresh frozen plasma, and additional quantities should be given to maintain the prothrombin and partial thromboplastin times within normal limits. Five units of platelet concentrate should be given with the 5th unit of blood and with each successive 10 units of blood. Platelet counts should be obtained after every 5th unit of blood transfusion and additional platelets given if the total count falls below 60,000. If coagulopathy persists despite normalization of the prothrombin and partial thromboplastin times and the platelet count exceeds 60,000, bleeding time is measured and additional platelets are administered until this value is within normal limits. Despite an adequate platelet, count, a coagulation defect may exist because of impaired platelet function [15]. Should bleeding persist despite normal prothrombin, partial thromboplastin, and bleeding times, fresh whole blood is given. Calcium chloride (1 g) should probably be given after every 5th unit of blood transfused as well as for electrocardiographic changes indicating hypocalcemia. Autotransfusion may be a useful adjuvant but is associated with consumptive coagulopathy [ 16,171 and platelet dysfunction [ 181. Therefore, blood component replacement is essential. Hypothermia can also induce coagulation changes [19]. A warming blanket should be placed on the operating table before the patient’s arrival. An. esophageal or high rectal probe is positioned and the core temperature monitored continually. Ringer’s lactate, incubated at 4O”C, is used and blood is administered through warming devices. If the core temperature falls below 32”C, lavage of the thoracic and abdominal cavities should be undertaken with warm Ringer’s lactate. Ideally an arterial line should be placed in the operating room to monitor systemic arterial pressure and obtain serial arterial blood gases. Sodium bicarbonate should be administered to maintain the arterial pH above 7.20 [20]. The operative plan is outlined in Figure 1. If the patient fails to respond to initial fluid resuscitation in the emergency department, a rapid left anterolateral thoracotomy is performed through the 5th intercostal space. The descending aorta is temporarily cross-clamped above the diaphragm until volume replacement can be established [ZZ]. If cardiac arrest occurs the pericardium is opened anterior a85
Elerding et al
to the phrenic nerve and internal cardiac massage performed. Before the induction of anesthesia, the patient is draped widely to include the chest, the entire abdomen, the flanks, and the upper thighs. If the systolic and blood pressure is less than 80 mm Hg after the induction of anesthesia despite the blood and crystalloid replacement, left thoracotomy and aortic cross clamping is performed before laparotomy in anticipation of release of the abdominal wall tamponade on incision [22]. A long midline abdominal incision is made, blood is quickly evacuated from the abdomen, and injuries
are assessed. If severe hepatic trauma is the dominant injury, large gauge packs are placed and firm compression is applied. If brisk bleeding continues, the porta hepatis, including the hepatic artery and portal vein, is temporarily occluded with a tourniquet or vascular clamp, the Pringle maneuver. Although it has generally been accepted that the human liver cannot tolerate ischemia longer than 15 minutes, recent evidence suggests hepatic warm ischemia may be extended to 1 hour in man [23]. If massive hemorrhage continues, major hepatic vein or retrohepatic vena caval injury must be suspected. Characteristically, a strong torrent of blood descends from the
O-Blood A
I
I
Cardiac Arrest
Type Specific Blood SUSPECTED LIVER INJURY
S.B.P. < 60 mn Hg
Failure to Improve
c
I
S.B.P. < 80 Ringer's Lactate via CVP and Upper Extremities S.B.P. > 80 nunHg Anesthesia
S.B.P. > 80 m
B
SelectiveHepatic ArterialOcclusion \
/
Hg'
Successful*~l
\ Fails
Fails Individual Temporary Hemrrhage+Vessel Ligation t succe+u1 $ Control
SelectivePortal Vein Occlusion
1 S.P.V.L. ( SEVERE HEPATIC INJuRYcoNFImEll
Pack ' PringleManeuver
l-+
I
\
Core Temperature ArterialpH CoagulationStudies
HEPATIC LoBECD%Y (RetrohepaticIVC and/or, Median Stermtomy Hemorrhage ___) Not Controlled HepaticVein Injury) I.V.C. Shunt
REPAIR I.V.C. & I
HEPATICVEINS J
Figure 1. Management plan for severe hepatk trauma. A, preoperative plan. 6, intraoperative plan. CVP = central venous pressure line; IVC = inferior vena cava; O.R. = operating room: S.&P. = systolic blood pressure; SHAL = selective hepatk arterial tigation; S, P. V.L. = selective portal vein Kgatfon.
886
The American Journal of Surgery
Fatal Hepatic Hemorrhage After Trauma
dome of the liver or the lateral aspect of the right lobe after downward displacement of the liver [24]. In such a case the midline incision is extended into a median sternotomy in preparation for right hepatic lobectomy. A vena caval shunt is inserted through the right atrium as proposed by Schrock et al [I I] or by way of the saphenofemoral junction as described by Pilcher et al [ 221. With total vascular exclusion and containment of the hemorrhage, the right hepatic lobe is quickly removed and the hepatic vein and vena caval defects are closed. Although traumatic retrohepatic vena caval injuries have been successfully approached without the use of intracaval shunts, most of these severely hypovolemic patients will suffer cardiac arrest when the inferior vena cava is abruptly occluded. Major hepatic vein ligation without parenchymal resection has been reported 1251,but the opportunity to approach such an injury in this manner is unusual. If occlusion of the porta hepatis controls bleeding from the liver, an orderly approach using conservative methods to effect hemostasis should be undertaken. With simple fractures individual ligation of severed intrahepatic vessels should be attempted. Success with this method is periodically checked by releasing the Pringle maneuver. If local control cannot be achieved, a trial of selective devascularization is pursued [26,27]. First the artery of the involved lobe is occluded and, if that is successful, ligated. If lobar dearterialization fails, selective occlusion of the branch of the portal vein to the involved lobe is tried. If successful, the branch is ligated. If hemost,asis has been accomplished by local ligation or selective lobar occlusion, devitalized tissue is then removed. If both hepatic arterial and portal venous occlusions are required to control hemorrhage, these vessels are ligated and anatomic resection is completed [28]. Large hemostatic clamps have been designed to facilitate hepatic resection [29], but success with these devices has been variable. With extensive bilobar injury, common hepatic arterial occlusion should be considered. In rare instances extensive bilobar hepatic injuries cannot be dealt with by selective devascularization and are not amenable to resectional therapy. In such instances extensive packing alone may provide satisfactory hemostasis with the packing removed in the operating room :Sto 7 days later [.5]. The management of hemorrhage associated with severe liver injuries remains a formidable challenge. Patient survival hinges on exemplary surgical care. Early diagnosis, prompt hemostasis and restoration of blood volume, close attention to coagulation fac-
Volume 138. December 1979
tors including prevention of profound hypothermia and acidosis, and the precise application of surgical techniques are crucial in saving the patient. Summary
Two hundred twenty-five cases of acute hepatic trauma were reviewed. Thirty-four patients died, 28 (82 per cent) as a direct result of exsanguination. The successful management of hemorrhage associated with severe liver injuries requires early diagnosis, prompt hemostasis and restoration of blood volume, close attention to coagulation factors, and the precise application of surgical techniques. References 1. Madding GF, Kennedy PA: Trauma to the liver. Major Problems in Clinical Surgery: III. Philadelphia, WB Saunders, 1971. 2. Noer RJ: Acute injuries of the liver (Scudder Oration of Trauma). Am Co/l Surg Bull, Jan-Feb 1969. 3. Hardaway RM: Vietnam wound analvsis. J Trauma 18: 635. 1978.. 4. Defore WW, Mattox KL, Jordan GL, Beall AC: Management of 1590consecutive cases of liver trauma. Arch Surg 111: 493, 1976. 5. Walt AJ: The mythology of hepatic trauma-or Babel revisited. Am J Surg 135: 12, 1978. 6. Trunkey DD, Shires GT, McClelland R: Management of liver trauma in 811 consecutive patients. Ann Surg 179: 722. 1974. 7. Levin A, Gover P, Nance FC: Surgical restraint in the management of hepatic injury: a review of Charity Hospital experience. J Trauma 18: 399, 1978. 8. Lim RC, Knudson J, Steele M: Liver trauma: current method of management. Arch Surg 104: 544, 1972. 9. Mclnnis WD, Richardson JD. Aust JB: Hepatic trauma: pitfalls in management. Arch Surg 112: 157, 1977. 10. Flint LM, Mays TE, Aaron WS, Fulton RL, Polk HC: Selectivity in the management of hepatic trauma. Ann Surg 185: 613, 1977. 11. Schrock T, Blaisdell W, Mathewson C: Management of blunt trauma to the liver and hepatic veins. Arch Surg 96: 698, 1968. 12. Pilcher DB, Harmon PK, Moore EE: Retrohepatic vena cava balloon shunt introduced via the sapheno-femoral function. J Trauma 17: 837, 1977. 13. Fischer RP, Beverlin BC, Engrave LH, Benjamin GI, Perry JF: Diagnostic peritoneal lavage: fourteen years and 2586 patients later. Am J Surg 136: 701, 1978. 14. Clagett GP, Olsen WR: Non-mechanical hemorrhage in severe liver injury. Ann Surg 187: 369, 1978. 15. Lim RC, Olcott C, Robinson A, Blaisdell FW: Platelet response and coagulation changes following massive blood replacement. J Trauma 13: 577, 1973. 16. Rakower SR, Worth MH. Berman I, Lackner H: Hemostatic and homeostatic changes following massive autotransfusion in the dog. J Trauma 14: 594, 1974. 17. Stillman RM, Wrezlewicz WW, Stanczewski B, Chapa L, Fox MJ. Sawyer PN: The haematological hazards of autotransfusions. Br J Surg 63: 651, 1976. 18. Moore EE, Dunn EL, Breslich DL, Galloway WB: Platelet abnormalities following autotransfusion. Submitted to J Trauma. 19. Johansson BW. Nilsson JM: The effect of heparin and E-aminocaproic acid on the coagulation in hypothermic dogs. Acta phvsiol Stand 60: 267, 1964.
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et al
20. Dunn EL, Moore EE, Breslich DL, Galloway WB: Acidosis induced coagulopathy. Surg Forum, 1979. 21. Moore EE, Moore JB, Galloway AC, Eiseman BE: Post injury thoracotomy: a critical analysis. Surgery, in press. 22. Ledgerwood AM, Kagmens M, Lucas CE: The role of thoracic aortic occlusion for massive hemoperitoneum. J Trauma 16: 610. 1976. 23. Huguef C, Nordlinger B, Conard J: Tolerance of the human liver to prolonged normothermic ischemia. Arch Surg 113: 1448, 1978. 24. Aragon GE, Eiseman B, Norton L: Liver trauma: review of 300 cases. La Pr@nsa Medica Argentina 61: 600, 1974. 25. Depinto DJ, Mucha SJ, Powers PC: Major hepatic vein ligation necessitated by blunt abdominal trauma. Ann Surg 183: 243, 1976. 26. Lewis FR, Lim RC, Blaisdell WF: Hepatic artery ligation: adjunct in the management of massive hemorrhage from the liver. J Trauma 14: 743, 1974. 27. Mays TE: Lobar dearterialization for exsanguinating wounds of the liver. J Trauma 12: 397, 1972. 28. Starzl TE, Bell EH, Beart RW, Putnam CW: Hepatic trisegmentectomy and other liver resections. Surg Gynecol Obstet 141: 429,1975. 29. Storm FK Longmire WP: A simplified clamp for hepatic resection. Surg Gynecol Obstet 133: 103, 1971.
David V. Feliciano (Houston, TX): A plateau in the survival rate has been reached, and it is time to rethink this problem. In an experienced trauma institution like Denver General, only 11 of 28 patients received fresh frozen plasma despite massive transfusion requirements. Only 6 of 28 patients had intraoperative temperature monitoring, and only 1 of 28 had intraoperative autotransfusion. All three of these critical resuscitative maneuvers are essentially out of the hands of the surgeon and depend on extensive anesthesia support. If trauma institutions are to save more of these patients, blood component replacement coupled with temperature and pH control will have to be improved first. Practically speaking, one nurse anesthetist cannot handle these patients without staff assistance. One other practical point mentioned in the paper is the use of packs for extensive bilobar injuries, subcapsular hematomas that are expanding and oozing when the patient is cold. Packs have proved to be lifesaving recently in several of our patients at Ben Taub. Fourteen of 28 patients underwent hepatic lobectomy. This proportion seems high in comparison with other reported series. In recent years has your approach to these injuries become more conservative? Second, do you now recommend the Pringle maneuver and autotransfusion in all of these patients? Finally, I think that some surgeons who handle trauma would probably quarrel with the use of emergency room thoracotomy in patients who respond to early fluid resuscitation. Perhaps simultaneous thoracotomy and laparotomy in the operating room under good
conditions is better than emergency room thoracotomy certain patients.
in
Claude H. Horgan, Jr (Omaha, NE): If institutions really want to handle major trauma, then they must have a higher level of resident surgeon on call at the hospital, and senior staff surgeons will have to get in the trenches. Comparative randomized studies have shown that the complication rate is significantly different when senior surgeons are in the field, particularly in biliary tract sur-
gery. Every new method of diagnosis or treatment adds potential complications. In the last year I have seen three patients who underwent thoracotomy with cross clamping of the aorta and who ended up with empyema, which is a serious complication. Melvin Twiest (Albuquerque, NM): I note that three of the patients who died were managed with vena caval shunts. Were any of the survivors managed in that way? Ernest E. Moore (closing): It is imperative that the blood bank be intimately involved in these cases and be available 24 hours daily to perform coagulation studies so that factors are appropriately replenished. Contrary to former recommendations, we believe that fresh frozen plasma and platelets should be given prophylactically for these severe injuries. The number of major hepatic lobectomies performed in this series was excessive, and we readily admit that this was a serious error. As you can see from our algorithm for patient management, lobectomy is the last resort. We hope that by adhering to a management plan in the future we can decrease the number of patients subjected to this devastating surgical procedure. The Pringle maneuver, we agree, is a crucial step in the treatment of severe hepatic injuries. However, we differ in our enthusiasm for autotransfusion. We have demonstrated in our laboratory not only a consumptive coagulopathy but also platelet dysfunction induced by autotransfusion. This work was done with the Sorenson device, which is probably the most feasible system for use in emergency situations. We have questioned the indiscriminate use of emergency department thoracotomy, but we strongly believe selected trauma victims will benefit from this heroic measure. In regard to the inferior vena caval shunt, we have used either the approach proposed by S&rock or, more recently, a technique we developed with Dr. Pilcher from Vermont of introducing the catheter via the saphenofemoral junction. In the last year two of our patients with major right hepatic venous and retrohepatic vena caval injuries survived with the aid of these inferior vena caval shunts.
The American Journal of Surgery
Steven C. Elerding, MD, Denver Colorado G. E. Aragon, MD, Denver Colorado Ernest E. Moore, MD, Denver Colorado
Despite protection from the lower rib cage, the liver is the second most commonly injured intraabdominal organ. The management of hepatic trauma has undergone significant revision over the past half century, resulting in a progressive reduction in mortality from 66 per cent in World War I, to 27 per cent in World War II, to 14 per cent in the Korean War, to 9 per cent in Vietnam [l-3]. However, the improvement in survival rate has now reached a plateau with the inability to control massive hemorrhage as the leading cause of death. Recent civilian reviews of liver injuries report mortality rates of 10 to 20 per cent and cite intractable bleeding as a major cause of death in 31 to 76 per cent of the cases (Table I) [4-IO]. The purpose of this review is to critically analyze a series of patients who died from exsanguination associated with hepatic trauma to help identify those at risk for this lethal complication and to establish a management plan to avert uncontrollable hemorrhage. Material and Methods Patients. Two hundred twenty-five patients with significant hepatic injuries underwent laparotomy at the Denver General Hospital from January 1, 1973 to December 31, 1978. Thirty-four patients (15 per cent) died, 28 (82 per cent) intraoperatively from hemorrhage and 6 (18 per cent) from associated injuries or multiple organ failure. The 28 exsanguinating injuries form the basis of this review; 15 (54 per cent) resulted from penetrating injuries and 13 (46 per cent) from blunt trauma. The 18 men and 10 women ranged in age from 3 to 60 years (average 30). initial Management. All patients were brought to the emergency department within 25 minutes of injury, where
From the Department of Swgety, Denver General Hospital and the University of Colorado Medical Center. Denver. Colorado. Reprint reWe?JS should be addressed to Ernest E. Moore, MD, Department of Surgery, Denver General Hospital, Denver, Colorado 80204. Presented at the 31st Annual Meeting of the Southwestern Surgical Congress, Las Vegas, Nevada, April 23-26, 1979.
Volume 138, December 1979
initial evaluation and resuscitation were performed. Central venous and multiple peripheral intravenous lines, a Foley catheter, and a nasogastric tube were immediately placed. Endotracheal intubation was carried out promptly when airway control was needed. Associated injuries were evaluated and managed as indicated. Warmed Ringer’s lactate was the initial resuscitative fluid in all patients with a detectable blood pressure. When the Ringer’s lactate replacement exceeded 50 cc/kg, transfusion of type-specific blood was begun as soon as available. Low liter 0 negative blood was given only to patients whose condition deteriorated to the point of cardiac arrest. Blood warmers and filters were used routinely. All patients were taken to the operating room within 45 minutes of arrival at the emergency department. Associated Injuries (Table II). Significant extraabdominal injuries were present in 8 (53 per cent) of the 15 patients with penetrating injuries. Six of these patients had associated thoracic trauma; one required thoracotomy in the operating room for a cardiac wound. Two other patients had significant extremity injuries. Eight patients (62 per cent) in the blunt trauma group had concomitant extraabdominal injuries. There were six extremity injuries, five chest wounds, three pelvic fractures, and two closed head injuries. An average of 2.4 associated intraabdominal organ injuries were encountered with penetrating trauma and 1.5 with blunt injuries. Four patients (27 per cent) in the penetrating injury group and three (23 per cent 1with blunt trauma had isolated liver injuries. The classification’of these lethal hepatic injuries is indicated in Table III. All injuries were grade IV or V. The retrohepatic vena cava was involved in eight patients (24 per cent) and the portal vein in five (15 per cent). Operative Management. Emergency thoracotomy before laparotomy was performed in one case. A midline incision was initially made and then extended across the costal margin into the right chest. Direct suture ligation of bleeding vessels was attempted in all cases. Temporary occlusion of the porta hepatis, the Pringle maneuver, was performed in 10 patients (26 per cent). Fifteen patients (54 per cent) underwent left anterolateral thoracotomy for internal cardiac massage and cross clamping of the descending aortic after intraoperative cardiac arrest.
883
Elerding
et al
TABLE I
study Ben Taub (1939-74) [ 41 Detroit Genera) (1961-76) [ 5] Parkland (1963-7 1) [ 61 Charity (1964-76) [ 71 San Francisco (1966-71) [ 81 San Antonio (1970-75) [ 91 Louisville (1973-76) [ IO] Denver General (1973-78)
1,590 1,404 811 546 285 233 178 225
13 12 13 10 19 11 20 15
58 63 76 35 56 31 58 82
Total
5.271
14
55
Mortality (“/)
(%)
-.
injuries Associated With Lethal Hepatic Trauma No. of Injuries
Location of Injury
In 15 Patients With Penetrating Trauma
In 13 Patients With Blunt Trauma
6 2 0 0
5 6 3 2
8 6 5 5 5 4 3
4 5 4 4 0 2 0
Extraabdominal Chest Extremity Pelvis Head lntraabdominal Small bowel Pancreas Kidney Spleen Stomach Vascular Colon
Hepatic
lobar resection
was carried out in 14 patients
per cent), to gain access to retrohepatic
Ciassitication of Lethal Hepatic injuries Penetrating Injury Group
Exsanguination
No. of Patients
TABLE ii
TABLE iii
Mortality Associated With Hepatic Trauma
(50
vena caval wounds
in 3. Repair of retrohepatic vena caval injuries was attempted in five patients without the use of a shunt and in three with shunting devices described by Schrock et al [I I J or Pilcher et al [IZ].
Class
I. Capsular tears II. Nonbleeding parenchymal tears
Blunt Trauma Group
0 0
0 0
0
0
8
12
7
1
bleeding, each patient had received more than 10 units of banked blood; however, none received platelet concentrates, fresh frozen plasma, or fresh whole blood. The characteristic picture was then massive uncontrollable hepatic hemorrhage as well as diffuse bleeding from all exposed surfaces. Only 11 patients (39 per cent) ultimat.ely received fresh frozen plasma and none underwent coagulation studies. In eight patients (29 per cent) arterial blood gases were measured to determine the magnitude of associated acidosis; the average pH was 7.11. Core temperature was obtained to ascertain the severity of hypothermia in only six patients (21 per cent); the average temperature was 32.2”C. Autotransfusion was utilized in one patient hut without blood component replacement.
Results All patients arrived at the emergency department with significant hypotension. Four had no obtainable blood pressure and 24 (84 per cent) presented with a systolic blood pressure of 60 to 90 mm Hg. Initial fluid resuscitation with Ringer’s lactate increased the systolic blood pressure to greater than 100 mm Hg in 22 patients (92 per cent). Blood pressure remained undetectable in one patient, who underwent thoracotomy for resuscitation in the emergency department. Of the 22 patients whose blood pressure improved to a systolic level greater than 100 mm Hg, systolic pressure subsequently decreased to less than 80 mm Hg in 20 (91 per cent) during their evaluation or transfer to the operating room. Exploration of these patients was undertaken immediately. By the time packs had been placed to t.amponade the hepatic se.4
Comments More than 85 per cent of liver injuries are minor and can be dealt with by simple techniques. The successful treatment of severe hepatic trauma, however, demands instant recognition and a preplanned course of action as well as mature surgical skill. Too often delay in judgment is fatal. Critical analysis of our hepatic injuries has identified a group of patients who died from exsanguination but who might have been saved by an aggressive orderly management plan. The typical patient arrived in the emergency department with a systolic blood pressure of 60 to 90 mm Hg after sustaining severe blunt or penetrating trauma. Initial fluid resuscitation increased the pressure to 100 mm Hg. The suspicion of a devastating injury was then lost and the surgeon often The Amerlcen Journal of Surgery
Fatal Hepatic Hemorrhage After Trauma
procrastinated by obtaining further roentgenographic studies and awaiting formal cross matching of blood. Recurrent hypotension was difficult to reverse, and the patient was quickly transported to the operating room and exploration undertaken. The surgeon found hemostasis impossible to achieve despite vigorous suturing, clamping, and packing. The potential therapeutic benefit as well as diagnostic aid of temporary porta hepatis occlusion was frequently overlooked. The anesthesiologist was preoccupied with efforts to replete volume and gave little attention to increasing acidosis and hypothermia. The blood bank, too, was ill prepared for the challenge, and consequently none of the patients received blood component or fresh blood replacement until more than 10 units of banked blood had been administered. In a desperate attempt to halt the torrential blood loss from the injured liver, the surgeon often resorted to major resection. This precipitated massive diffuse blood loss from the raw surface of the liver as well as from the incision and associated injuries. With the patient’s condition further deteriorating, thoracotomy was performed in a heroic but futile effort to revive the heart. This scenario should be preventable with a more aggressive but orderly approach. Early diagnosis is extremely important. Significant liver injuries associated with lower chest or upper abdominal penetrating wounds are usually not difficult to recognize. Any patient who is hypotensive on arrival at the emergency department after abdominal trauma must be suspected of having a severe liver injury. Rib fractures of the right lower thoracic cage, especially the posterior segments of the 9th through the 12th ribs, should raise suspicion. If multiple injuries occur or the patient’s mental status is altered, diagnostic peritoneal lavage is extremely reliable in identifying hemoperitoneum [13]. Ringer’s lactate, warmed to 4O”C, should be infused through central venous and large bore upper extremity intravenous lines. If more than 3 liters of Ringer’s lactate are required to normalize the blood pressure, type-specific blood should be obtained and the patient quickly transferred to the operating room. Additional chest x-rays and intravenous pyelograms may have to be obtained intraoperatively. Although disseminated intravascular coagulation, excessive fibrinolysis, and defective clotting factor synthesis have been incriminated in the pathogenesis of “nonmechanical” hemorrhage in severe liver injury, Clagett and Olsen [14] have indicated that massive transfusion of stored blood is the most important causative factor. They observed a significant coagulation defect in 17 (52 per cent) of 33 patients with grade IV and V hepatic trauma and recommend Volume 139, December 1979
the prophylactic use of blood component replacement. If the patient remains hypotensive after the 2nd unit of blood has been transfused, fresh frozen plasma should be administered then and with every 4th unit thereafter. Prothrombin time and partial thromboplastin time should be determined after administration of each unit of fresh frozen plasma, and additional quantities should be given to maintain the prothrombin and partial thromboplastin times within normal limits. Five units of platelet concentrate should be given with the 5th unit of blood and with each successive 10 units of blood. Platelet counts should be obtained after every 5th unit of blood transfusion and additional platelets given if the total count falls below 60,000. If coagulopathy persists despite normalization of the prothrombin and partial thromboplastin times and the platelet count exceeds 60,000, bleeding time is measured and additional platelets are administered until this value is within normal limits. Despite an adequate platelet, count, a coagulation defect may exist because of impaired platelet function [15]. Should bleeding persist despite normal prothrombin, partial thromboplastin, and bleeding times, fresh whole blood is given. Calcium chloride (1 g) should probably be given after every 5th unit of blood transfused as well as for electrocardiographic changes indicating hypocalcemia. Autotransfusion may be a useful adjuvant but is associated with consumptive coagulopathy [ 16,171 and platelet dysfunction [ 181. Therefore, blood component replacement is essential. Hypothermia can also induce coagulation changes [19]. A warming blanket should be placed on the operating table before the patient’s arrival. An. esophageal or high rectal probe is positioned and the core temperature monitored continually. Ringer’s lactate, incubated at 4O”C, is used and blood is administered through warming devices. If the core temperature falls below 32”C, lavage of the thoracic and abdominal cavities should be undertaken with warm Ringer’s lactate. Ideally an arterial line should be placed in the operating room to monitor systemic arterial pressure and obtain serial arterial blood gases. Sodium bicarbonate should be administered to maintain the arterial pH above 7.20 [20]. The operative plan is outlined in Figure 1. If the patient fails to respond to initial fluid resuscitation in the emergency department, a rapid left anterolateral thoracotomy is performed through the 5th intercostal space. The descending aorta is temporarily cross-clamped above the diaphragm until volume replacement can be established [ZZ]. If cardiac arrest occurs the pericardium is opened anterior a85
Elerding et al
to the phrenic nerve and internal cardiac massage performed. Before the induction of anesthesia, the patient is draped widely to include the chest, the entire abdomen, the flanks, and the upper thighs. If the systolic and blood pressure is less than 80 mm Hg after the induction of anesthesia despite the blood and crystalloid replacement, left thoracotomy and aortic cross clamping is performed before laparotomy in anticipation of release of the abdominal wall tamponade on incision [22]. A long midline abdominal incision is made, blood is quickly evacuated from the abdomen, and injuries
are assessed. If severe hepatic trauma is the dominant injury, large gauge packs are placed and firm compression is applied. If brisk bleeding continues, the porta hepatis, including the hepatic artery and portal vein, is temporarily occluded with a tourniquet or vascular clamp, the Pringle maneuver. Although it has generally been accepted that the human liver cannot tolerate ischemia longer than 15 minutes, recent evidence suggests hepatic warm ischemia may be extended to 1 hour in man [23]. If massive hemorrhage continues, major hepatic vein or retrohepatic vena caval injury must be suspected. Characteristically, a strong torrent of blood descends from the
O-Blood A
I
I
Cardiac Arrest
Type Specific Blood SUSPECTED LIVER INJURY
S.B.P. < 60 mn Hg
Failure to Improve
c
I
S.B.P. < 80 Ringer's Lactate via CVP and Upper Extremities S.B.P. > 80 nunHg Anesthesia
S.B.P. > 80 m
B
SelectiveHepatic ArterialOcclusion \
/
Hg'
Successful*~l
\ Fails
Fails Individual Temporary Hemrrhage+Vessel Ligation t succe+u1 $ Control
SelectivePortal Vein Occlusion
1 S.P.V.L. ( SEVERE HEPATIC INJuRYcoNFImEll
Pack ' PringleManeuver
l-+
I
\
Core Temperature ArterialpH CoagulationStudies
HEPATIC LoBECD%Y (RetrohepaticIVC and/or, Median Stermtomy Hemorrhage ___) Not Controlled HepaticVein Injury) I.V.C. Shunt
REPAIR I.V.C. & I
HEPATICVEINS J
Figure 1. Management plan for severe hepatk trauma. A, preoperative plan. 6, intraoperative plan. CVP = central venous pressure line; IVC = inferior vena cava; O.R. = operating room: S.&P. = systolic blood pressure; SHAL = selective hepatk arterial tigation; S, P. V.L. = selective portal vein Kgatfon.
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The American Journal of Surgery
Fatal Hepatic Hemorrhage After Trauma
dome of the liver or the lateral aspect of the right lobe after downward displacement of the liver [24]. In such a case the midline incision is extended into a median sternotomy in preparation for right hepatic lobectomy. A vena caval shunt is inserted through the right atrium as proposed by Schrock et al [I I] or by way of the saphenofemoral junction as described by Pilcher et al [ 221. With total vascular exclusion and containment of the hemorrhage, the right hepatic lobe is quickly removed and the hepatic vein and vena caval defects are closed. Although traumatic retrohepatic vena caval injuries have been successfully approached without the use of intracaval shunts, most of these severely hypovolemic patients will suffer cardiac arrest when the inferior vena cava is abruptly occluded. Major hepatic vein ligation without parenchymal resection has been reported 1251,but the opportunity to approach such an injury in this manner is unusual. If occlusion of the porta hepatis controls bleeding from the liver, an orderly approach using conservative methods to effect hemostasis should be undertaken. With simple fractures individual ligation of severed intrahepatic vessels should be attempted. Success with this method is periodically checked by releasing the Pringle maneuver. If local control cannot be achieved, a trial of selective devascularization is pursued [26,27]. First the artery of the involved lobe is occluded and, if that is successful, ligated. If lobar dearterialization fails, selective occlusion of the branch of the portal vein to the involved lobe is tried. If successful, the branch is ligated. If hemost,asis has been accomplished by local ligation or selective lobar occlusion, devitalized tissue is then removed. If both hepatic arterial and portal venous occlusions are required to control hemorrhage, these vessels are ligated and anatomic resection is completed [28]. Large hemostatic clamps have been designed to facilitate hepatic resection [29], but success with these devices has been variable. With extensive bilobar injury, common hepatic arterial occlusion should be considered. In rare instances extensive bilobar hepatic injuries cannot be dealt with by selective devascularization and are not amenable to resectional therapy. In such instances extensive packing alone may provide satisfactory hemostasis with the packing removed in the operating room :Sto 7 days later [.5]. The management of hemorrhage associated with severe liver injuries remains a formidable challenge. Patient survival hinges on exemplary surgical care. Early diagnosis, prompt hemostasis and restoration of blood volume, close attention to coagulation fac-
Volume 138. December 1979
tors including prevention of profound hypothermia and acidosis, and the precise application of surgical techniques are crucial in saving the patient. Summary
Two hundred twenty-five cases of acute hepatic trauma were reviewed. Thirty-four patients died, 28 (82 per cent) as a direct result of exsanguination. The successful management of hemorrhage associated with severe liver injuries requires early diagnosis, prompt hemostasis and restoration of blood volume, close attention to coagulation factors, and the precise application of surgical techniques. References 1. Madding GF, Kennedy PA: Trauma to the liver. Major Problems in Clinical Surgery: III. Philadelphia, WB Saunders, 1971. 2. Noer RJ: Acute injuries of the liver (Scudder Oration of Trauma). Am Co/l Surg Bull, Jan-Feb 1969. 3. Hardaway RM: Vietnam wound analvsis. J Trauma 18: 635. 1978.. 4. Defore WW, Mattox KL, Jordan GL, Beall AC: Management of 1590consecutive cases of liver trauma. Arch Surg 111: 493, 1976. 5. Walt AJ: The mythology of hepatic trauma-or Babel revisited. Am J Surg 135: 12, 1978. 6. Trunkey DD, Shires GT, McClelland R: Management of liver trauma in 811 consecutive patients. Ann Surg 179: 722. 1974. 7. Levin A, Gover P, Nance FC: Surgical restraint in the management of hepatic injury: a review of Charity Hospital experience. J Trauma 18: 399, 1978. 8. Lim RC, Knudson J, Steele M: Liver trauma: current method of management. Arch Surg 104: 544, 1972. 9. Mclnnis WD, Richardson JD. Aust JB: Hepatic trauma: pitfalls in management. Arch Surg 112: 157, 1977. 10. Flint LM, Mays TE, Aaron WS, Fulton RL, Polk HC: Selectivity in the management of hepatic trauma. Ann Surg 185: 613, 1977. 11. Schrock T, Blaisdell W, Mathewson C: Management of blunt trauma to the liver and hepatic veins. Arch Surg 96: 698, 1968. 12. Pilcher DB, Harmon PK, Moore EE: Retrohepatic vena cava balloon shunt introduced via the sapheno-femoral function. J Trauma 17: 837, 1977. 13. Fischer RP, Beverlin BC, Engrave LH, Benjamin GI, Perry JF: Diagnostic peritoneal lavage: fourteen years and 2586 patients later. Am J Surg 136: 701, 1978. 14. Clagett GP, Olsen WR: Non-mechanical hemorrhage in severe liver injury. Ann Surg 187: 369, 1978. 15. Lim RC, Olcott C, Robinson A, Blaisdell FW: Platelet response and coagulation changes following massive blood replacement. J Trauma 13: 577, 1973. 16. Rakower SR, Worth MH. Berman I, Lackner H: Hemostatic and homeostatic changes following massive autotransfusion in the dog. J Trauma 14: 594, 1974. 17. Stillman RM, Wrezlewicz WW, Stanczewski B, Chapa L, Fox MJ. Sawyer PN: The haematological hazards of autotransfusions. Br J Surg 63: 651, 1976. 18. Moore EE, Dunn EL, Breslich DL, Galloway WB: Platelet abnormalities following autotransfusion. Submitted to J Trauma. 19. Johansson BW. Nilsson JM: The effect of heparin and E-aminocaproic acid on the coagulation in hypothermic dogs. Acta phvsiol Stand 60: 267, 1964.
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20. Dunn EL, Moore EE, Breslich DL, Galloway WB: Acidosis induced coagulopathy. Surg Forum, 1979. 21. Moore EE, Moore JB, Galloway AC, Eiseman BE: Post injury thoracotomy: a critical analysis. Surgery, in press. 22. Ledgerwood AM, Kagmens M, Lucas CE: The role of thoracic aortic occlusion for massive hemoperitoneum. J Trauma 16: 610. 1976. 23. Huguef C, Nordlinger B, Conard J: Tolerance of the human liver to prolonged normothermic ischemia. Arch Surg 113: 1448, 1978. 24. Aragon GE, Eiseman B, Norton L: Liver trauma: review of 300 cases. La Pr@nsa Medica Argentina 61: 600, 1974. 25. Depinto DJ, Mucha SJ, Powers PC: Major hepatic vein ligation necessitated by blunt abdominal trauma. Ann Surg 183: 243, 1976. 26. Lewis FR, Lim RC, Blaisdell WF: Hepatic artery ligation: adjunct in the management of massive hemorrhage from the liver. J Trauma 14: 743, 1974. 27. Mays TE: Lobar dearterialization for exsanguinating wounds of the liver. J Trauma 12: 397, 1972. 28. Starzl TE, Bell EH, Beart RW, Putnam CW: Hepatic trisegmentectomy and other liver resections. Surg Gynecol Obstet 141: 429,1975. 29. Storm FK Longmire WP: A simplified clamp for hepatic resection. Surg Gynecol Obstet 133: 103, 1971.
David V. Feliciano (Houston, TX): A plateau in the survival rate has been reached, and it is time to rethink this problem. In an experienced trauma institution like Denver General, only 11 of 28 patients received fresh frozen plasma despite massive transfusion requirements. Only 6 of 28 patients had intraoperative temperature monitoring, and only 1 of 28 had intraoperative autotransfusion. All three of these critical resuscitative maneuvers are essentially out of the hands of the surgeon and depend on extensive anesthesia support. If trauma institutions are to save more of these patients, blood component replacement coupled with temperature and pH control will have to be improved first. Practically speaking, one nurse anesthetist cannot handle these patients without staff assistance. One other practical point mentioned in the paper is the use of packs for extensive bilobar injuries, subcapsular hematomas that are expanding and oozing when the patient is cold. Packs have proved to be lifesaving recently in several of our patients at Ben Taub. Fourteen of 28 patients underwent hepatic lobectomy. This proportion seems high in comparison with other reported series. In recent years has your approach to these injuries become more conservative? Second, do you now recommend the Pringle maneuver and autotransfusion in all of these patients? Finally, I think that some surgeons who handle trauma would probably quarrel with the use of emergency room thoracotomy in patients who respond to early fluid resuscitation. Perhaps simultaneous thoracotomy and laparotomy in the operating room under good
conditions is better than emergency room thoracotomy certain patients.
in
Claude H. Horgan, Jr (Omaha, NE): If institutions really want to handle major trauma, then they must have a higher level of resident surgeon on call at the hospital, and senior staff surgeons will have to get in the trenches. Comparative randomized studies have shown that the complication rate is significantly different when senior surgeons are in the field, particularly in biliary tract sur-
gery. Every new method of diagnosis or treatment adds potential complications. In the last year I have seen three patients who underwent thoracotomy with cross clamping of the aorta and who ended up with empyema, which is a serious complication. Melvin Twiest (Albuquerque, NM): I note that three of the patients who died were managed with vena caval shunts. Were any of the survivors managed in that way? Ernest E. Moore (closing): It is imperative that the blood bank be intimately involved in these cases and be available 24 hours daily to perform coagulation studies so that factors are appropriately replenished. Contrary to former recommendations, we believe that fresh frozen plasma and platelets should be given prophylactically for these severe injuries. The number of major hepatic lobectomies performed in this series was excessive, and we readily admit that this was a serious error. As you can see from our algorithm for patient management, lobectomy is the last resort. We hope that by adhering to a management plan in the future we can decrease the number of patients subjected to this devastating surgical procedure. The Pringle maneuver, we agree, is a crucial step in the treatment of severe hepatic injuries. However, we differ in our enthusiasm for autotransfusion. We have demonstrated in our laboratory not only a consumptive coagulopathy but also platelet dysfunction induced by autotransfusion. This work was done with the Sorenson device, which is probably the most feasible system for use in emergency situations. We have questioned the indiscriminate use of emergency department thoracotomy, but we strongly believe selected trauma victims will benefit from this heroic measure. In regard to the inferior vena caval shunt, we have used either the approach proposed by S&rock or, more recently, a technique we developed with Dr. Pilcher from Vermont of introducing the catheter via the saphenofemoral junction. In the last year two of our patients with major right hepatic venous and retrohepatic vena caval injuries survived with the aid of these inferior vena caval shunts.
The American Journal of Surgery