Decreasing Morbidity after Liver Trauma A. David Drezner, MD, PhD, Hartford, Connecticut James H. Foster, MD, Hartford, Connecticut
Historically liver trauma has been a lethal lesion. Near the turn of the century Edler [I] and Thole [2] reported on a large series of patients with liver injuries. Mortality rates were high whether or not patients were treated surgically. These results were not significantly changed during World War I nor during the interval between the wars [3-51. During this time, surgical treatment consisted of packing the fractured liver bed. The first significant reduction in mortality was recorded by Madding, Lawrence, and Kennedy [6] in a review of World War II experience. They reported 829 liver injuries with an over-all mortality of 27 per cent. Among the reasons cited for this success were a change from packing wounds to suture ligation of bleeding sites, antibiotics, improved blood replacement, and appropriate drainage. After World War II, reports by Sparkman [7], DeBakey [8], Shires [9], Walt [IO], and their coworkers all documented further improvements in survival. However, blunt trauma continued to carry a high mortality (20 to 40 per cent) when compared with penetrating lesions (10 to 15 per cent). The Vietnam experience showed a 4.5 per cent mortality for American casualties with liver injuries, mainly from high velocity missile wounds [11,12]. Lim, Knudson, and Steele [13] have reported a reduction in mortality to 15 per cent from blunt liver injury, representing approximately one third of their 285 cases, whereas their operative mortality for major resection was 56 per cent. More recently the Parkland Hospital series [14] has been updated and now includes more than 800 patients. A mortality of 13 per cent was described
From the Department of Surgery, Hartford Hospital, Hartford, Connacticut. Reprint requests should be addressed to James H. Foster, MO, Department of Surgery, Hartford Hospit~~l.60 Seymour Street, Hartford, Connecticut 06115. Presented at the Fifty-Fifth Annual Meeting of the New Englarni Surgical Society, WaterviNe Valley, New Hampshire, September 26-26, 1974.
vollana 129, Apru 1975
with an operative mortality for major resection of 47 per cent. This report describes a four year experience (1969 to 1973) at Hartford Hospital with fifty-one patients with various degrees of hepatic injury, mostly from blunt trauma resulting from automobile accidents, By using appropriate drainage, avoiding large hepatic mattress sutures, resecting all devitalized hepatic tissue while preserving viable liver, avoiding some newer operative technics, and applying close clinical support in the postoperative period, we believe we have achieved a significant reduction in the mortality and morbidity for this group of seriously ill patients. Clinical Material All patients with liver trauma proved by laparotomy or autopsy between June 1969 and May 1973 were included in this study. No patient was excluded. The average age was twenty-eight years with a range of two to sixty years. There were forty male and eleven female patients Of the fifty-one liver injuries, four were secondary to gunshot wounds, five were due to stab wounds, and forty-two were caused by blunt trauma. All patients undergoing laparotomy had positive abdominal taps before surgery. The administration of antibiotics was started pre- or intraoperatively in thirty-eight patients. Cephalosporin was used in thirty patients and ampicillin in eight patients Three other patients died in the emergency room and had no operative treatment other than efforts at resuscitation. Forty-five patients had preoperative central venous pressure catheters and urinary drainage. With an x-ray cassette beneath the patient, exploration was performed through a midline incision in all patients. When it was necessary to obtain more central vena caval control, the incision was usually extended into the right side of the chest. Although separate left thoracotomies were used occasionally, they were done for separate trauma rather than for liver injuries per se. Nonresected hepatic injuries were most often treated by drainage alone. Sutures for closure of lacerations not
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actively bleeding and the use of absorbable hemostatic fabrics were avoided if possible. If adequate hemostasis could not be achieved or bile leakage could not be controlled, the wounds were carefully explored. Specific blood vessels or ducts were isolated and ligated, which often required enlargement of the traumatic wound. Devitalized tissue, usually recognized by a darker color and firmer consistency, was removed using meticulous blunt technic with small ties or metal clips, but all viable liver tissue was preserved. When major bleeding was encountered, the porta hepatis was compressed to differentiate injury of the hepatic vein from that of the portal vein or hepatic artery. If the hemorrhage was appreciably slowed by this maneuver [15], the hepatic peritoneal attachments were mobilized and some type of resection or debridement was completed to obtain hemostatic control with removal of devitalized tissue. If the major hepatic veins were involved, packs were placed over the open injury. The liver was then mobilized, the right side of the chest entered, and the porta hepatis and the pre- and posthepatic inferior vena cava were controlled so that the liver could be isolated from its blood supply. The packs were then removed after vascular control was obtained, and liver tissue was rapidly debrided until the injury was identified and repaired with vascular sutures. This could usually be accomplished in less than thirty minutes. Inflow occlusion was tolerated without problem for up to twenty minutes. Deliberate hypothermia [16,17] was not used although massive transfusion may have lowered body temperature somewhat. Inferior vena cava shunts as suggested by Shires [14], Allen [18], Bricker [I9], Brown [ZO], Timmis [21], Blaisdell [22], Schrock [23], and Donovan [24], and their coworkers were not used nor was ligation of the hepatic artery as advocated by Madding and Kennedy [25] and Mays [26,27]. T tube decompression of the common bile duct as described by Merendino, Dillard, and Cammock [28] was used in only one patient, a child of six whose gallbladder required removal. It was never used for diagnostic studies. Three patients underwent cholecystostomy. All of the wounds were drained. Primary use was made of soft rubber Penrose drains about the liver and in other areas when indicated. Hard plastic sump drains were avoided; occasionally, soft rubber suction tubes were used, but they would frequently clot within twenty-four hours. Raw liver edges were not covered with peritoneal flaps or any other material if hemostasis was secure; occasionally, the falciform ligament was used to improve hemostasis. In general, major resection was performed for one of three reasons: (1) deep lacerations with involvement of a major vascular structure or bile ducts; (2) nonviable liver segments; (3) massive hemorrhage associated with vena cava or hepatic vein injury. Something short of segmental resection was frequently performed to insure that all nonviable liver tissue had been removed. Postoperative care was based on an effort to treat prophylactically anticipated complications. Patients undergoing major resection were left intubated for at least
484
twenty-four hours until we were confident that posttraumatic pulmonary insufficiency would not be a problem. Antibiotics were usually maintained for three days after which they were discontinued unless a specific organism was being treated. Patients were closely watched for pulmonary emboli (both fat and clot), pancreatitis, clotting abnormalities, and gastrointestinal bleeding. Any signs of cardiac decompensation were treated aggressively with digitalis. Liver function was closely monitored and patients were routinely given hyperglycemic solutions in the immediate postoperative period.
Results Eight of the fifty-one patients with liver injury died. One patient with head injury died of neurologic problems after abdominal exploration for a minor liver laceration. Another patient died of head injury without operation; subsequent autopsy showed a minor hepatic injury. Three patients died or were declared dead in the emergency room, subsequent autopsy showing massive hepatic injury. The final three deaths occurred in the operating room, all from exsanguination before control of hemorrhage could be established. No patient who survived laparotomy for major hepatic trauma died. Of the fifty-one patients, nineteen were considered as having had “major” hepatic injury based on the amount of devitalized tissue and the magnitude of resection performed. Thirteen patients underwent “major” resection defined as left lateral segmentectomy or right or left lobectomy. Three died in the emergency room and three in the operating room. As has been demonstrated by many a direct relationship existed others [7-10,13,29], between the number and degree of associated injuries and survival. There were various types of morbidity in these patients, but in general they fell into six categories: (1) pulmonary emboli, (2) post-traumatic pulmonary insufficiency, (3) acute tubular necrosis, (4) coagulopathy, as defined by a persistent abnormality in prothrombin time, partial thromboplastin time, or platelet count, (5) pancreatitis, and (6) abscess. The complications seen in thirty patients with nonresected hepatic injuries, defined as those usually requiring drainage only with occasional hemostatic suture and minimal debridement, included: pulmonary emboli, one patient (5 per cent); post-traumatic pulmonary insufficiency, two patients (6 per cent); coagulopathy, two patients (6 per cent); pancreatitis, four patients (13 per cent). However, one patient in this group had fracture of the liver completeiy down the major fissure
The American Journal of Surgery
Morbidity
TABLE _____
I
Patient Number
Analysis of Morbidity Number of Days
in Thirteen
Pulmonary Emboli
Survivors
Acute Tubular Necrosis No No No No No No No No No No Yes
Yes Yes Yes Yes
Yes No No No Yes Yes Yes Yes Yes Yes Yes
No No
No Yes
No No
117%
10177%
91 11 80 31 54 50 31 58 50 97 122
Suspected Yes, fat No Suspected Yes. fat
Yes, No No No No Yes No Yes Yes No Yes
45 46
19 44
Suspected Suspected
No No
727156
4/30%
5138%
Liver
Trauma
Resection
Post-Traumatic Pulmonarv lnsufficien~y
1 3 5 6 7 8 10 15 30 39 44
Yes No Suspected Suspected Suspected Yes
of Major Hepatic
after
Coagulopathy Yes Yes Yes No Yes Yes
Pancreatitis
8/60%
Abscess No No No No No No No No No No Pelvic, subhepatic (Klebsiella and Proteus) No Subhepatic (enterococci) 2115%
W85%,)
through the gallbladder bed into the fossa of the inferior vena cava. There were no hepatic vein injuries and the only treatment required was cholecystectomy for an avulsed gallbladder. The average hospital stay after nonresected liver injury was twenty-one days, most of which related to associated injuries rather than the liver insult per se. The average hospital stay in thirteen patients who survived major hepatic resection was fifty-six days. (Table I.) The most frequently documented complication was an abnormal prothrombin time, partial thromboplastin time, or thrombocytopenia below 50,000 cells per mm3. These clotting abnormalities occurred during the immediate postoperative period and uniformly cleared with appropriate therapy before the end of the first postoperative week. There were no cases of disseminated intravascular coagulopathy as documented by reduced fibrinogen or increased fibrin split product level. In those patients demonstrating a hematologic abnormality, there was an unequivocal increase in postoperative morbidity. (Table II.) The incidence of clotting abnormalities is related to the number of units of blood given as shown in Table III. All types of morbidity were significantly reduced in patients receiving 5 units of blood or less. Pulmonary emboli were documented either by radioisotope scanning or arteriography in four of thirteen patients with “major” liver injury and in only one of the patients with nonresected hepatic trauma. Two episodes of fat embolism resulted from associated fracture. If, however, we included
Volume 129, April 1975
patients who had clinical signs highly suggestive of this entity, such as persistent pleural effusions, pulmonary infiltrates, and arterial blood gases with a pop less than 70 mm Hg on room air and who also had equivocal scans without arteriography or could not be studied because of traction or other logistical problems, the incidence rises to over 80 per cent. Certainly pulmonary complications such as effusions, infiltrates, and pneumonitis were one of the more common problems encountered by this group, although frank post-traumatic pulmonary insufficiency was documented in only five or 38 per cent. Five patients demonstrated hyperamylasemia on admission with a return to normal levels within three days of operation. In three other patients, hyperamylasemia developed from one to three weeks after operation and was associated with sepsis but not with the classic clinical findings of pancreatitis. In no patient with a nonresected “hepatic” injury did an intra-abdominal abscess develop. Two patients who had resection had this problem, one relatively late after the initial insult. A pelvic abscess was drained forty-four days after the initial operation in one patient and he required subsequent drainage of a subhepatic abscess secondary to a failed pyloroplasty ninety-five days post injury. In the second patient a subhepatic abscess was drained sixteen days after emergency resection of the left lateral segment of the liver. This patient had had reoperation for postoperative surgical
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TABLE
Effect of Transfusions
II
Patients Twelve patients with coagulopathy Thirty-one patients with normal clotting
Bleeding
Abscess
Pancreatitis
Post-Traumatic Pulmonary Insufficiency
11.6
4 (33%)
2 (17%)
7 (59%)
4 (33%)
2.3
1 (3%) 0.005
0 0.025
5 (16%) 0.005
3 (9%) 0.05
Number of Units Given in Operating Room
studies
P
TABLE
III
Relation between
Number
of Units of Blood Transfused
Units of Blood
Reoperation
Given in Operating Room
for Bleeding
Five or less (29 patients) Six or more P
(14 patients)
Reoperation for
0 5 35.5% 0.001
bleeding. This latter instance represents the only abscess we thought was related to the initial hepatic surgery and occurred despite the use of proNo intrahepatic or subphylactic antibiotics. phrenic abscesses were identified. Although fever often persisted for several weeks postoperatively, we could not relate it to the subsequent clinical course. A stress ulcer develoljed in one patient who was treated with vagotomy and pyloroplasty. Nasogastric antacids were used sporadically during the first three years of this study and routinely thereafter. Liver enzyme levels were routinely followed throughout the postoperative period. They were persistently elevated in those patients undergoing major resection. The alkaline phosphatase level remained elevated for as long as four months after operation. However, there was no correlation between the development of abscess and the serum protein levels, the prothrombin times, the bilirubin levels, or the alkaline phosphatase levels. Comments Only four of forty-seven patients (5 per cent) who reached the operating room died, a figure considerably lower than that reported by others [610,13,14,24,29] despite a high proportion of cases of blunt trauma. We believe that part of this reduction is attributable to specific technics used in intra- and postoperative care. Most investigators would agree with conservative resection of devital-
486
and Clotting Abnormalities Post-Traumatic Pulmonary
Abscess 0
Pancreatitis 4
2 14.3% 0.05
13.8% 8 57.1% 0.005
Insufficiency 3 10.3% 4 28.6% 0.1
Coagulopathy 2 6.8% 10 71.4% 0.001
ized liver tissue, adequate drainage, and avoidance of large mattress sutures. Yet many are also advocating the use of inferior vena cava bypass [14,18-22,241, hypothermia (16,171, hepatic artery ligation [25-271, parietal flaps to cover raw liver area [22], extrahepatic biliary decompression [ 17,24,28-301, and even nonoperative therapy for known liver trauma [31]. Although we do not necessarily disagree with all of these suggestions, we believe they can often present as many problems as they solve. A case in point is extrahepatic biliary decompression after hepatic trauma [28]. Although generally utilized after its initial reporting in 1963, this treatment presently seems to be losing favor [17,32,33]. It may even contribute to increased morbidity in the form of gastrointestinal bleeding [ 12,34,35]. Our findings with respect to hematologic complications in these patients suggest that bleeding parameters should be monitored closely. Abnormalities should be treated as soon as they are noted. Fresh frozen plasma is used with each transfusion of 5 units of whole blood, and platelet packs are given when the thrombocyte count drops below 50,000 per mm3. The clotting abnormalities probably reflect dilution of clotting factors due to rapid and large volume transfusions with accompanied blood loss, a “washout” phenomenon. Yet they represent entities that should be treated aggressively since they can contribute to increased blood loss and be related to other complications. Calcium levels are likewise monitored closely and
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Morbidity after Liver Trauma
are appropriately given during the intra- and postoperative periods. Pulmonary emboli in these patients represent a most difficult therapeutic problem. No specific treatment was given for fat emboli, and patients with the more common clot emboli were given anticoagulants only when they had documented emboli and normal clotting studies and at least three days had elapsed since surgery. In those instances, only low dose heparin, that is, 3,000 units every six hours, was used. This was appropriately increased depending on the postoperative time and degree of pulmonary insufficiency. Usually no site of phlebitis was identified and therefore it was difficult to gauge an end point for therapy, which was usually continued a week after symptoms cleared. Patients were not maintained on Coumadin@ therapy. The relatively high incidence of hyperamylasemia in this series may be attributable to direct trauma to the pancreas although gross evidence of pancreatic laceration was not found. This frequently presented as a chemical entity without clinical signs. No specific therapy was given, and in the asymptomatic patient feedings were started. No morbidity was encountered with this approach. The low incidence of intra-abdominal abscess was encouraging. We believe that antibiotic therapy begun in the preoperative period and continued for a limited time in the postoperative period is very important, but that the details of operative technic are most important in preventing localized collections of necrotic or purulent debris. Body temperature and liver function test results in the postoperative period were always abnormal for various lengths of time. No correlation could be made with the presence or absence of intra-abdominal abscess, and thus these parameters were valueless with respect to postoperative therapeutic decisions. Although ligation of the hepatic artery probably can and will help to avoid some major hepatic resections, it may decompensate liver tissue with borderline circulation, probably one of the more important factors in the induction of intrahepatic abscess. We favor ligation of specific vessels or ducts. We also avoid the use of hard drains as we believe that these contribute to hepatic necrosis through pressure. These desperately ill patients often require all of the technical and medical expertise the surgeon has to offer. Our data represent an argument for a conservative surgical approach to these patients with which we may hope to reduce both morbidity and mortality.
Votume 129, April 1975
Summary Fifty-one patients with significant recognized hepatic trauma were treated at Hartford Hospital during a four year period ending May 1973. Seventy-five per cent of the injuries were the result of blunt trauma. Many patients had severe associated injuries and three died in the emergency room before operation could be undertaken. Forty-eight patients underwent laparotomy and various types of repair including sixteen resections of significant volumes of nonviable liver. Three patients died in the operating room, but no patient who left the operating room alive after resection died. Hematologic, pulmonary, renal, and gastrointestinal complications are analyzed in detail. There were no postoperative intrahepatic or subphrenic abscesses in patients undergoing resection and we believe that this is attributable to changes in technic. This review stresses the technical details of the operations as they may relate to the apparent improvement in morbidity and mortality. Acknowledgment: We wish to thank Esther Kronstadt, Mary Beth O’Brien, and Tama Zimmerman for their assistance and patience in the preparation of this manuscript.
References 1. Edler L: Die traumatischen Verletzungen der Parenchymatosen Unterleibsarga. Arch Klin Chir 34: 343. 1887. 2. Thole F: Die Verletzungen der Luber und der Gallenwege. Stuttgart, Verlag Von Ferdinand Enke, 19 12. 3. Lamb C: Rupture of the liver. N EnglJ Aded221: 855, 1939. 4. O’Neill J: Traumatic rupture of liver. California & West Med 54: 88, 1941. 5. Alhn A: Internal injuries without penetration. N Engl J A&d 205: 34, 1931. 8. Madding G. Lawrence K, Kennedy P: Forward surgery of the severely injured, p 307. Monograph No. 1, Second Auxillary Surgical Group. Washington, DC, US Government Printing Office, 1942-1945. 7. Sparkman l?. Fogelman M: Wounds of the liver. Ann Surg 139: 890. 1954. 8. Crosthwait R, Allen J, Murga F, Beall A, DeBakey M: The surgical management of 840 consecutive liver injuries in civil&n practice. Surg Gyneco/ Obstet 114: 850, 1982. 9. McClelland Ft. Shires T: Management of liver trauma in 259 consecutive patients. Ann Surg 161: 248, 1965. 10. Lucas C. Walt A: Critical decisions in liver trauma. Arch Surg 101: 277, 1970. 11. Pilcher D: Penetrating injuries of the liver in Vietnam. Ann Surg 170: 793, 1969. 12. Carroll C, Cass K, Whelan T: Wounds of the liver in Vietnam: a critical analysis of 254 cases. Ann Surg 177: 385, 1973. 13. Lim R, Knudson J, Steele M: Liver trauma. Arch Surg 104: 544, 1972. 14. Trunkey D, Shires T. McClelland R: Management of liver
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15. 18.
17. 18. 19. 20. 21. 22.
23.
24. 25. 26. 27.
28.
29. 30. 31. 32. 33.
34.
35.
trauma in 811 consecutive patients. Ann Surg 179: 722, 1974. Pringle J: Notes on the arrested hepatic hemorrhage due to trauma. Ann Surg 48: 541, 1908. Madding G, Kennedy P: Trauma to the liver, pp 58. 78. Major Problems in Clinical Surgery, vol 3 (Madding G, Kennedy P, ed). Philadelphia. Saunders, 197 1. Longmire W; Cleveland R: Surgical anatomy and blunt trauma of the liver. Surg C/in North Am 52: 887, 1972. Allen R, Blaisdell F: Injuries to the inferior vena cava. Surg C/in North Am 52: 899, 1972. Bricker R, Morton J. Okies J: Surgical management of injuries to the inferior vena cava. J ktuma 11: 725, 1971. Brown R. Bovd D. Matsuda T: Temporary internal shunt for retrohepatic vena cava injury. J fraud 12: 736, 1971. Timmis f-f, Rosanova A, Larkin W: Bloodless hepatic resection with an internal caval shunt. Surgery 65: 109, 1969. Blaisdell F, Lim R: “Liver resection” in trauma to the liver, p 131. Major Problems in Clinical Surgery, vol 3 (Madding G, Kennedy P, ed). Philadelphia, Saunders, 197 1. Schrock T, Blaisdell F, Mathewson C: Management of blunt trauma of the liver and hepatic veins. Arch Surg 96: 698, 1968. Donovan A, Michaelian M, Yellin A: Anatomical lobectomy in trauma. Surgery 73: 833, 1973. Madding G, Kennedy P: Hepatic artery ligation. Surg C/in North Am 52: 719, 1972. Mays E: Observation and management after hepatic artery ligation. Surg Gynecol Obstet 124: 801, 1967. Mays T: Demonstration of collateral arterial flow after interruption of hepatic arteries in man. N Engl J Med 290: 993. 1974. Merendino K, Dillard D. Cammock E: The concept of surgical biliary decompression in the management of liver trauma. Surg Gynecol Obstet 117: 285, 1983. Amerson J, Stone H: Experiences in the management of hepatic trauma. Arch Surg 100: 150, 1970. Mays E: Hepatic lobectomy. Arch Surg 103: 2 16, 197 1. Popovsky J: Liver trauma: conservative management and the liver scan. Arch Surg 108: 184, 1974. Lucas C, Lenaghan R. Walt A: Biliary drainage and liver trauma. Surg Forum 20: 388, 1989. Lucas C: Prospective clinical evaluation of biliary drainage in hepatic trauma: an interim report. Ann Surg 174: 830, 1971. Foster J. Lawler M, Welborn, M, Holcomb G, Sawyers J: Recent experiences with major hepatic resection. Ann Surg 167: 651, 1968. Bowen J: Upper gastrointestinal bleeding associated with biliary diversion after hepatic injury. Ann Surg 177: 402, 1973.
Discussion George Wilson (New Haven, Conn): We recently treated a very interesting late thoracic complication of a ruptured liver. A fifty year old man had fallen from a horse in 1967. One year later, while in New York City, he developed an acute abdomen. At Bellevue Hospital, through a thoracoabdominal incision, a delayed rupture of the liver was found. A one year delay in rupture of a subcapsular hematoma is unusual. In 1973 we examined the patient to evaluate a lesion of the right side of the chest which was thought to be attached to the chest wall in the anterior axillary line about the level of the sixth rib. The lesion had grown as noted from earlier films that had been taken in 1970 and 1971. At exploration a fragment of liver tissue was found
growing on the chest wall. At pathologic examination, hyperplastic liver tissue was identified with no bile ducts, but blood vessels were present. We have found no similar case in the world literature. Paul Mellish (Burlington, Vt): The management of liver trauma presents a changing spectrum. Over the years, treatment has progressed from extensive packing of wounds, to deep ligation of liver tissue, to extensive resection and, recently, to ligation of the hepatic artery. For the surgeon who performs hepatic surgery, the anatomic studies of the liver by Nicholas Michels deserve a great deal of attention. He has shown that the liver has some twenty-six possible collateral arterial pathways if the hepatic artery is tied off. However, he concludes: “That the liver has collateral pathways should by no means of deductive reasoning give rise to the impression that ligation of a major hepatic artery can be performed with impunity.” Doctor Drezner and his colleagues have used multiple methods of dealing with liver injuries in a practical manner. I would like to ask if they think their resection rate might be a little high. In Merendino’s series there were thirteen resections in a total of 400 cases. I would like to show slides of an unusual liver injury that we have seen in three children, namely, traumatic fissure of the liver through the major central vein. (Slide) This demonstrates venous drainage of the liver. From this aspect the liver is a trilobate organ. In these children the liver was split between the major right and left lobes through this central vein area, one by a large tractor, another by the wheels of a bus, and one by a metal post after diving off a swing. In all three cases the blood loss was extensive and in all three it was possible to repair the liver by compressing and suturing the two halves together. (Slide) This liver scan shows diminished uptake in this area of split. In conclusion, I support the concepts of careful surgical technic in the care of liver injuries as expressed by the authors. Gerald 0. Strauch (Stamford, Conn): In a paper given at our annual meeting two years ago, the results of a statewide study of major abdominal injuries in Connecticut were presented. The year 1971 covered in that study cuts right through the time period of the report just presented. In that study, eighty liver injuries, fifty of which were from blunt injury and thirty from perforating wounds, were found and treated. Fifteen liver resections were performed among these cases, and the total mortality among all liver injuries was 17.3 per cent. Sixteen per cent of the patients in our entire study were from Hartford Hospital, so that you can see the kind of contribution Hartford Hospital makes to trauma surgery in Connecticut. What impresses me most about the present report and the previous Connecticut study is the necessity and real value of aggressive management of the bleeding problem during operation for liver injuries.
The AmericanJournal of Surgery
Morbidity after Liver Trauma
When we analyzed the mortality in our cases of liver injury, eight deaths occurred either in the operating room during operation or during the twenty-four hours after operation; six of those eight deaths occurred from uncontrolled or uncontrollable hemorrhage. Five late postoperative deaths occurred from delayed hemorrhage in two, brain damage in two, and pulmonary complications in one. The lesson that we learn from these numbers is that we have to get very aggressive and able to control hemorrhage from the liver at the time of operation, and certainly Hartford Hospital sets a good example in this regard. We encountered seven intra-abdominal abscesses after operation for liver injury, and I would certainly subscribe to the belief that many of these are preventable by proper attention to technical principles at the time of operation. James H. Foster (closing): We appreciate the opportunity to bring a conservative message to this Society. There are many articles written about new clamps, complicated shunts, hypothermia, arterial ligation, and other operative gimmicks to be used in the care of patients with liver trauma. We believe that in many in-
Volume 129, Apdl 1975
stances these technics may actually be harmful. Our results may justify a restoration of faith in the older technics of adeq’uate debridement and hemostasis with the use of fine sutures or clips and avoidance of large mattress sutures. There will not be an opportunity for transfer of many patients with hemorrhage from liver injury to large centers. Most general surgeons should be prepared to evaluate and treat such patients. Liver tissue that is firm and blue should be resected but normal appearing liver tissue, even if severely lacerated, should be left unless resection is essential to obtain hemostasis. Anatomic lobectomy will rarely be indicated since major bleeding rarely occurs from a central fissure unless the major hepatic veins and inferior vena cava are involved. The incidence of only one perihepatic abscess suggests that most nonviable liver was resected and that our operative technic did not further compromise liver tissue. Many patients had postoperative fever, often for prolonged periods, but our experience suggests that such fevers should not be an indication for re-exploration. Most will subside in a week or two. We urge your reattention to the basic principles for handling tissue common to all wounded organs.
489
Historically liver trauma has been a lethal lesion. Near the turn of the century Edler [I] and Thole [2] reported on a large series of patients with liver injuries. Mortality rates were high whether or not patients were treated surgically. These results were not significantly changed during World War I nor during the interval between the wars [3-51. During this time, surgical treatment consisted of packing the fractured liver bed. The first significant reduction in mortality was recorded by Madding, Lawrence, and Kennedy [6] in a review of World War II experience. They reported 829 liver injuries with an over-all mortality of 27 per cent. Among the reasons cited for this success were a change from packing wounds to suture ligation of bleeding sites, antibiotics, improved blood replacement, and appropriate drainage. After World War II, reports by Sparkman [7], DeBakey [8], Shires [9], Walt [IO], and their coworkers all documented further improvements in survival. However, blunt trauma continued to carry a high mortality (20 to 40 per cent) when compared with penetrating lesions (10 to 15 per cent). The Vietnam experience showed a 4.5 per cent mortality for American casualties with liver injuries, mainly from high velocity missile wounds [11,12]. Lim, Knudson, and Steele [13] have reported a reduction in mortality to 15 per cent from blunt liver injury, representing approximately one third of their 285 cases, whereas their operative mortality for major resection was 56 per cent. More recently the Parkland Hospital series [14] has been updated and now includes more than 800 patients. A mortality of 13 per cent was described
From the Department of Surgery, Hartford Hospital, Hartford, Connacticut. Reprint requests should be addressed to James H. Foster, MO, Department of Surgery, Hartford Hospit~~l.60 Seymour Street, Hartford, Connecticut 06115. Presented at the Fifty-Fifth Annual Meeting of the New Englarni Surgical Society, WaterviNe Valley, New Hampshire, September 26-26, 1974.
vollana 129, Apru 1975
with an operative mortality for major resection of 47 per cent. This report describes a four year experience (1969 to 1973) at Hartford Hospital with fifty-one patients with various degrees of hepatic injury, mostly from blunt trauma resulting from automobile accidents, By using appropriate drainage, avoiding large hepatic mattress sutures, resecting all devitalized hepatic tissue while preserving viable liver, avoiding some newer operative technics, and applying close clinical support in the postoperative period, we believe we have achieved a significant reduction in the mortality and morbidity for this group of seriously ill patients. Clinical Material All patients with liver trauma proved by laparotomy or autopsy between June 1969 and May 1973 were included in this study. No patient was excluded. The average age was twenty-eight years with a range of two to sixty years. There were forty male and eleven female patients Of the fifty-one liver injuries, four were secondary to gunshot wounds, five were due to stab wounds, and forty-two were caused by blunt trauma. All patients undergoing laparotomy had positive abdominal taps before surgery. The administration of antibiotics was started pre- or intraoperatively in thirty-eight patients. Cephalosporin was used in thirty patients and ampicillin in eight patients Three other patients died in the emergency room and had no operative treatment other than efforts at resuscitation. Forty-five patients had preoperative central venous pressure catheters and urinary drainage. With an x-ray cassette beneath the patient, exploration was performed through a midline incision in all patients. When it was necessary to obtain more central vena caval control, the incision was usually extended into the right side of the chest. Although separate left thoracotomies were used occasionally, they were done for separate trauma rather than for liver injuries per se. Nonresected hepatic injuries were most often treated by drainage alone. Sutures for closure of lacerations not
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actively bleeding and the use of absorbable hemostatic fabrics were avoided if possible. If adequate hemostasis could not be achieved or bile leakage could not be controlled, the wounds were carefully explored. Specific blood vessels or ducts were isolated and ligated, which often required enlargement of the traumatic wound. Devitalized tissue, usually recognized by a darker color and firmer consistency, was removed using meticulous blunt technic with small ties or metal clips, but all viable liver tissue was preserved. When major bleeding was encountered, the porta hepatis was compressed to differentiate injury of the hepatic vein from that of the portal vein or hepatic artery. If the hemorrhage was appreciably slowed by this maneuver [15], the hepatic peritoneal attachments were mobilized and some type of resection or debridement was completed to obtain hemostatic control with removal of devitalized tissue. If the major hepatic veins were involved, packs were placed over the open injury. The liver was then mobilized, the right side of the chest entered, and the porta hepatis and the pre- and posthepatic inferior vena cava were controlled so that the liver could be isolated from its blood supply. The packs were then removed after vascular control was obtained, and liver tissue was rapidly debrided until the injury was identified and repaired with vascular sutures. This could usually be accomplished in less than thirty minutes. Inflow occlusion was tolerated without problem for up to twenty minutes. Deliberate hypothermia [16,17] was not used although massive transfusion may have lowered body temperature somewhat. Inferior vena cava shunts as suggested by Shires [14], Allen [18], Bricker [I9], Brown [ZO], Timmis [21], Blaisdell [22], Schrock [23], and Donovan [24], and their coworkers were not used nor was ligation of the hepatic artery as advocated by Madding and Kennedy [25] and Mays [26,27]. T tube decompression of the common bile duct as described by Merendino, Dillard, and Cammock [28] was used in only one patient, a child of six whose gallbladder required removal. It was never used for diagnostic studies. Three patients underwent cholecystostomy. All of the wounds were drained. Primary use was made of soft rubber Penrose drains about the liver and in other areas when indicated. Hard plastic sump drains were avoided; occasionally, soft rubber suction tubes were used, but they would frequently clot within twenty-four hours. Raw liver edges were not covered with peritoneal flaps or any other material if hemostasis was secure; occasionally, the falciform ligament was used to improve hemostasis. In general, major resection was performed for one of three reasons: (1) deep lacerations with involvement of a major vascular structure or bile ducts; (2) nonviable liver segments; (3) massive hemorrhage associated with vena cava or hepatic vein injury. Something short of segmental resection was frequently performed to insure that all nonviable liver tissue had been removed. Postoperative care was based on an effort to treat prophylactically anticipated complications. Patients undergoing major resection were left intubated for at least
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twenty-four hours until we were confident that posttraumatic pulmonary insufficiency would not be a problem. Antibiotics were usually maintained for three days after which they were discontinued unless a specific organism was being treated. Patients were closely watched for pulmonary emboli (both fat and clot), pancreatitis, clotting abnormalities, and gastrointestinal bleeding. Any signs of cardiac decompensation were treated aggressively with digitalis. Liver function was closely monitored and patients were routinely given hyperglycemic solutions in the immediate postoperative period.
Results Eight of the fifty-one patients with liver injury died. One patient with head injury died of neurologic problems after abdominal exploration for a minor liver laceration. Another patient died of head injury without operation; subsequent autopsy showed a minor hepatic injury. Three patients died or were declared dead in the emergency room, subsequent autopsy showing massive hepatic injury. The final three deaths occurred in the operating room, all from exsanguination before control of hemorrhage could be established. No patient who survived laparotomy for major hepatic trauma died. Of the fifty-one patients, nineteen were considered as having had “major” hepatic injury based on the amount of devitalized tissue and the magnitude of resection performed. Thirteen patients underwent “major” resection defined as left lateral segmentectomy or right or left lobectomy. Three died in the emergency room and three in the operating room. As has been demonstrated by many a direct relationship existed others [7-10,13,29], between the number and degree of associated injuries and survival. There were various types of morbidity in these patients, but in general they fell into six categories: (1) pulmonary emboli, (2) post-traumatic pulmonary insufficiency, (3) acute tubular necrosis, (4) coagulopathy, as defined by a persistent abnormality in prothrombin time, partial thromboplastin time, or platelet count, (5) pancreatitis, and (6) abscess. The complications seen in thirty patients with nonresected hepatic injuries, defined as those usually requiring drainage only with occasional hemostatic suture and minimal debridement, included: pulmonary emboli, one patient (5 per cent); post-traumatic pulmonary insufficiency, two patients (6 per cent); coagulopathy, two patients (6 per cent); pancreatitis, four patients (13 per cent). However, one patient in this group had fracture of the liver completeiy down the major fissure
The American Journal of Surgery
Morbidity
TABLE _____
I
Patient Number
Analysis of Morbidity Number of Days
in Thirteen
Pulmonary Emboli
Survivors
Acute Tubular Necrosis No No No No No No No No No No Yes
Yes Yes Yes Yes
Yes No No No Yes Yes Yes Yes Yes Yes Yes
No No
No Yes
No No
117%
10177%
91 11 80 31 54 50 31 58 50 97 122
Suspected Yes, fat No Suspected Yes. fat
Yes, No No No No Yes No Yes Yes No Yes
45 46
19 44
Suspected Suspected
No No
727156
4/30%
5138%
Liver
Trauma
Resection
Post-Traumatic Pulmonarv lnsufficien~y
1 3 5 6 7 8 10 15 30 39 44
Yes No Suspected Suspected Suspected Yes
of Major Hepatic
after
Coagulopathy Yes Yes Yes No Yes Yes
Pancreatitis
8/60%
Abscess No No No No No No No No No No Pelvic, subhepatic (Klebsiella and Proteus) No Subhepatic (enterococci) 2115%
W85%,)
through the gallbladder bed into the fossa of the inferior vena cava. There were no hepatic vein injuries and the only treatment required was cholecystectomy for an avulsed gallbladder. The average hospital stay after nonresected liver injury was twenty-one days, most of which related to associated injuries rather than the liver insult per se. The average hospital stay in thirteen patients who survived major hepatic resection was fifty-six days. (Table I.) The most frequently documented complication was an abnormal prothrombin time, partial thromboplastin time, or thrombocytopenia below 50,000 cells per mm3. These clotting abnormalities occurred during the immediate postoperative period and uniformly cleared with appropriate therapy before the end of the first postoperative week. There were no cases of disseminated intravascular coagulopathy as documented by reduced fibrinogen or increased fibrin split product level. In those patients demonstrating a hematologic abnormality, there was an unequivocal increase in postoperative morbidity. (Table II.) The incidence of clotting abnormalities is related to the number of units of blood given as shown in Table III. All types of morbidity were significantly reduced in patients receiving 5 units of blood or less. Pulmonary emboli were documented either by radioisotope scanning or arteriography in four of thirteen patients with “major” liver injury and in only one of the patients with nonresected hepatic trauma. Two episodes of fat embolism resulted from associated fracture. If, however, we included
Volume 129, April 1975
patients who had clinical signs highly suggestive of this entity, such as persistent pleural effusions, pulmonary infiltrates, and arterial blood gases with a pop less than 70 mm Hg on room air and who also had equivocal scans without arteriography or could not be studied because of traction or other logistical problems, the incidence rises to over 80 per cent. Certainly pulmonary complications such as effusions, infiltrates, and pneumonitis were one of the more common problems encountered by this group, although frank post-traumatic pulmonary insufficiency was documented in only five or 38 per cent. Five patients demonstrated hyperamylasemia on admission with a return to normal levels within three days of operation. In three other patients, hyperamylasemia developed from one to three weeks after operation and was associated with sepsis but not with the classic clinical findings of pancreatitis. In no patient with a nonresected “hepatic” injury did an intra-abdominal abscess develop. Two patients who had resection had this problem, one relatively late after the initial insult. A pelvic abscess was drained forty-four days after the initial operation in one patient and he required subsequent drainage of a subhepatic abscess secondary to a failed pyloroplasty ninety-five days post injury. In the second patient a subhepatic abscess was drained sixteen days after emergency resection of the left lateral segment of the liver. This patient had had reoperation for postoperative surgical
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TABLE
Effect of Transfusions
II
Patients Twelve patients with coagulopathy Thirty-one patients with normal clotting
Bleeding
Abscess
Pancreatitis
Post-Traumatic Pulmonary Insufficiency
11.6
4 (33%)
2 (17%)
7 (59%)
4 (33%)
2.3
1 (3%) 0.005
0 0.025
5 (16%) 0.005
3 (9%) 0.05
Number of Units Given in Operating Room
studies
P
TABLE
III
Relation between
Number
of Units of Blood Transfused
Units of Blood
Reoperation
Given in Operating Room
for Bleeding
Five or less (29 patients) Six or more P
(14 patients)
Reoperation for
0 5 35.5% 0.001
bleeding. This latter instance represents the only abscess we thought was related to the initial hepatic surgery and occurred despite the use of proNo intrahepatic or subphylactic antibiotics. phrenic abscesses were identified. Although fever often persisted for several weeks postoperatively, we could not relate it to the subsequent clinical course. A stress ulcer develoljed in one patient who was treated with vagotomy and pyloroplasty. Nasogastric antacids were used sporadically during the first three years of this study and routinely thereafter. Liver enzyme levels were routinely followed throughout the postoperative period. They were persistently elevated in those patients undergoing major resection. The alkaline phosphatase level remained elevated for as long as four months after operation. However, there was no correlation between the development of abscess and the serum protein levels, the prothrombin times, the bilirubin levels, or the alkaline phosphatase levels. Comments Only four of forty-seven patients (5 per cent) who reached the operating room died, a figure considerably lower than that reported by others [610,13,14,24,29] despite a high proportion of cases of blunt trauma. We believe that part of this reduction is attributable to specific technics used in intra- and postoperative care. Most investigators would agree with conservative resection of devital-
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and Clotting Abnormalities Post-Traumatic Pulmonary
Abscess 0
Pancreatitis 4
2 14.3% 0.05
13.8% 8 57.1% 0.005
Insufficiency 3 10.3% 4 28.6% 0.1
Coagulopathy 2 6.8% 10 71.4% 0.001
ized liver tissue, adequate drainage, and avoidance of large mattress sutures. Yet many are also advocating the use of inferior vena cava bypass [14,18-22,241, hypothermia (16,171, hepatic artery ligation [25-271, parietal flaps to cover raw liver area [22], extrahepatic biliary decompression [ 17,24,28-301, and even nonoperative therapy for known liver trauma [31]. Although we do not necessarily disagree with all of these suggestions, we believe they can often present as many problems as they solve. A case in point is extrahepatic biliary decompression after hepatic trauma [28]. Although generally utilized after its initial reporting in 1963, this treatment presently seems to be losing favor [17,32,33]. It may even contribute to increased morbidity in the form of gastrointestinal bleeding [ 12,34,35]. Our findings with respect to hematologic complications in these patients suggest that bleeding parameters should be monitored closely. Abnormalities should be treated as soon as they are noted. Fresh frozen plasma is used with each transfusion of 5 units of whole blood, and platelet packs are given when the thrombocyte count drops below 50,000 per mm3. The clotting abnormalities probably reflect dilution of clotting factors due to rapid and large volume transfusions with accompanied blood loss, a “washout” phenomenon. Yet they represent entities that should be treated aggressively since they can contribute to increased blood loss and be related to other complications. Calcium levels are likewise monitored closely and
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Morbidity after Liver Trauma
are appropriately given during the intra- and postoperative periods. Pulmonary emboli in these patients represent a most difficult therapeutic problem. No specific treatment was given for fat emboli, and patients with the more common clot emboli were given anticoagulants only when they had documented emboli and normal clotting studies and at least three days had elapsed since surgery. In those instances, only low dose heparin, that is, 3,000 units every six hours, was used. This was appropriately increased depending on the postoperative time and degree of pulmonary insufficiency. Usually no site of phlebitis was identified and therefore it was difficult to gauge an end point for therapy, which was usually continued a week after symptoms cleared. Patients were not maintained on Coumadin@ therapy. The relatively high incidence of hyperamylasemia in this series may be attributable to direct trauma to the pancreas although gross evidence of pancreatic laceration was not found. This frequently presented as a chemical entity without clinical signs. No specific therapy was given, and in the asymptomatic patient feedings were started. No morbidity was encountered with this approach. The low incidence of intra-abdominal abscess was encouraging. We believe that antibiotic therapy begun in the preoperative period and continued for a limited time in the postoperative period is very important, but that the details of operative technic are most important in preventing localized collections of necrotic or purulent debris. Body temperature and liver function test results in the postoperative period were always abnormal for various lengths of time. No correlation could be made with the presence or absence of intra-abdominal abscess, and thus these parameters were valueless with respect to postoperative therapeutic decisions. Although ligation of the hepatic artery probably can and will help to avoid some major hepatic resections, it may decompensate liver tissue with borderline circulation, probably one of the more important factors in the induction of intrahepatic abscess. We favor ligation of specific vessels or ducts. We also avoid the use of hard drains as we believe that these contribute to hepatic necrosis through pressure. These desperately ill patients often require all of the technical and medical expertise the surgeon has to offer. Our data represent an argument for a conservative surgical approach to these patients with which we may hope to reduce both morbidity and mortality.
Votume 129, April 1975
Summary Fifty-one patients with significant recognized hepatic trauma were treated at Hartford Hospital during a four year period ending May 1973. Seventy-five per cent of the injuries were the result of blunt trauma. Many patients had severe associated injuries and three died in the emergency room before operation could be undertaken. Forty-eight patients underwent laparotomy and various types of repair including sixteen resections of significant volumes of nonviable liver. Three patients died in the operating room, but no patient who left the operating room alive after resection died. Hematologic, pulmonary, renal, and gastrointestinal complications are analyzed in detail. There were no postoperative intrahepatic or subphrenic abscesses in patients undergoing resection and we believe that this is attributable to changes in technic. This review stresses the technical details of the operations as they may relate to the apparent improvement in morbidity and mortality. Acknowledgment: We wish to thank Esther Kronstadt, Mary Beth O’Brien, and Tama Zimmerman for their assistance and patience in the preparation of this manuscript.
References 1. Edler L: Die traumatischen Verletzungen der Parenchymatosen Unterleibsarga. Arch Klin Chir 34: 343. 1887. 2. Thole F: Die Verletzungen der Luber und der Gallenwege. Stuttgart, Verlag Von Ferdinand Enke, 19 12. 3. Lamb C: Rupture of the liver. N EnglJ Aded221: 855, 1939. 4. O’Neill J: Traumatic rupture of liver. California & West Med 54: 88, 1941. 5. Alhn A: Internal injuries without penetration. N Engl J A&d 205: 34, 1931. 8. Madding G. Lawrence K, Kennedy P: Forward surgery of the severely injured, p 307. Monograph No. 1, Second Auxillary Surgical Group. Washington, DC, US Government Printing Office, 1942-1945. 7. Sparkman l?. Fogelman M: Wounds of the liver. Ann Surg 139: 890. 1954. 8. Crosthwait R, Allen J, Murga F, Beall A, DeBakey M: The surgical management of 840 consecutive liver injuries in civil&n practice. Surg Gyneco/ Obstet 114: 850, 1982. 9. McClelland Ft. Shires T: Management of liver trauma in 259 consecutive patients. Ann Surg 161: 248, 1965. 10. Lucas C. Walt A: Critical decisions in liver trauma. Arch Surg 101: 277, 1970. 11. Pilcher D: Penetrating injuries of the liver in Vietnam. Ann Surg 170: 793, 1969. 12. Carroll C, Cass K, Whelan T: Wounds of the liver in Vietnam: a critical analysis of 254 cases. Ann Surg 177: 385, 1973. 13. Lim R, Knudson J, Steele M: Liver trauma. Arch Surg 104: 544, 1972. 14. Trunkey D, Shires T. McClelland R: Management of liver
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15. 18.
17. 18. 19. 20. 21. 22.
23.
24. 25. 26. 27.
28.
29. 30. 31. 32. 33.
34.
35.
trauma in 811 consecutive patients. Ann Surg 179: 722, 1974. Pringle J: Notes on the arrested hepatic hemorrhage due to trauma. Ann Surg 48: 541, 1908. Madding G, Kennedy P: Trauma to the liver, pp 58. 78. Major Problems in Clinical Surgery, vol 3 (Madding G, Kennedy P, ed). Philadelphia. Saunders, 197 1. Longmire W; Cleveland R: Surgical anatomy and blunt trauma of the liver. Surg C/in North Am 52: 887, 1972. Allen R, Blaisdell F: Injuries to the inferior vena cava. Surg C/in North Am 52: 899, 1972. Bricker R, Morton J. Okies J: Surgical management of injuries to the inferior vena cava. J ktuma 11: 725, 1971. Brown R. Bovd D. Matsuda T: Temporary internal shunt for retrohepatic vena cava injury. J fraud 12: 736, 1971. Timmis f-f, Rosanova A, Larkin W: Bloodless hepatic resection with an internal caval shunt. Surgery 65: 109, 1969. Blaisdell F, Lim R: “Liver resection” in trauma to the liver, p 131. Major Problems in Clinical Surgery, vol 3 (Madding G, Kennedy P, ed). Philadelphia, Saunders, 197 1. Schrock T, Blaisdell F, Mathewson C: Management of blunt trauma of the liver and hepatic veins. Arch Surg 96: 698, 1968. Donovan A, Michaelian M, Yellin A: Anatomical lobectomy in trauma. Surgery 73: 833, 1973. Madding G, Kennedy P: Hepatic artery ligation. Surg C/in North Am 52: 719, 1972. Mays E: Observation and management after hepatic artery ligation. Surg Gynecol Obstet 124: 801, 1967. Mays T: Demonstration of collateral arterial flow after interruption of hepatic arteries in man. N Engl J Med 290: 993. 1974. Merendino K, Dillard D. Cammock E: The concept of surgical biliary decompression in the management of liver trauma. Surg Gynecol Obstet 117: 285, 1983. Amerson J, Stone H: Experiences in the management of hepatic trauma. Arch Surg 100: 150, 1970. Mays E: Hepatic lobectomy. Arch Surg 103: 2 16, 197 1. Popovsky J: Liver trauma: conservative management and the liver scan. Arch Surg 108: 184, 1974. Lucas C, Lenaghan R. Walt A: Biliary drainage and liver trauma. Surg Forum 20: 388, 1989. Lucas C: Prospective clinical evaluation of biliary drainage in hepatic trauma: an interim report. Ann Surg 174: 830, 1971. Foster J. Lawler M, Welborn, M, Holcomb G, Sawyers J: Recent experiences with major hepatic resection. Ann Surg 167: 651, 1968. Bowen J: Upper gastrointestinal bleeding associated with biliary diversion after hepatic injury. Ann Surg 177: 402, 1973.
Discussion George Wilson (New Haven, Conn): We recently treated a very interesting late thoracic complication of a ruptured liver. A fifty year old man had fallen from a horse in 1967. One year later, while in New York City, he developed an acute abdomen. At Bellevue Hospital, through a thoracoabdominal incision, a delayed rupture of the liver was found. A one year delay in rupture of a subcapsular hematoma is unusual. In 1973 we examined the patient to evaluate a lesion of the right side of the chest which was thought to be attached to the chest wall in the anterior axillary line about the level of the sixth rib. The lesion had grown as noted from earlier films that had been taken in 1970 and 1971. At exploration a fragment of liver tissue was found
growing on the chest wall. At pathologic examination, hyperplastic liver tissue was identified with no bile ducts, but blood vessels were present. We have found no similar case in the world literature. Paul Mellish (Burlington, Vt): The management of liver trauma presents a changing spectrum. Over the years, treatment has progressed from extensive packing of wounds, to deep ligation of liver tissue, to extensive resection and, recently, to ligation of the hepatic artery. For the surgeon who performs hepatic surgery, the anatomic studies of the liver by Nicholas Michels deserve a great deal of attention. He has shown that the liver has some twenty-six possible collateral arterial pathways if the hepatic artery is tied off. However, he concludes: “That the liver has collateral pathways should by no means of deductive reasoning give rise to the impression that ligation of a major hepatic artery can be performed with impunity.” Doctor Drezner and his colleagues have used multiple methods of dealing with liver injuries in a practical manner. I would like to ask if they think their resection rate might be a little high. In Merendino’s series there were thirteen resections in a total of 400 cases. I would like to show slides of an unusual liver injury that we have seen in three children, namely, traumatic fissure of the liver through the major central vein. (Slide) This demonstrates venous drainage of the liver. From this aspect the liver is a trilobate organ. In these children the liver was split between the major right and left lobes through this central vein area, one by a large tractor, another by the wheels of a bus, and one by a metal post after diving off a swing. In all three cases the blood loss was extensive and in all three it was possible to repair the liver by compressing and suturing the two halves together. (Slide) This liver scan shows diminished uptake in this area of split. In conclusion, I support the concepts of careful surgical technic in the care of liver injuries as expressed by the authors. Gerald 0. Strauch (Stamford, Conn): In a paper given at our annual meeting two years ago, the results of a statewide study of major abdominal injuries in Connecticut were presented. The year 1971 covered in that study cuts right through the time period of the report just presented. In that study, eighty liver injuries, fifty of which were from blunt injury and thirty from perforating wounds, were found and treated. Fifteen liver resections were performed among these cases, and the total mortality among all liver injuries was 17.3 per cent. Sixteen per cent of the patients in our entire study were from Hartford Hospital, so that you can see the kind of contribution Hartford Hospital makes to trauma surgery in Connecticut. What impresses me most about the present report and the previous Connecticut study is the necessity and real value of aggressive management of the bleeding problem during operation for liver injuries.
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Morbidity after Liver Trauma
When we analyzed the mortality in our cases of liver injury, eight deaths occurred either in the operating room during operation or during the twenty-four hours after operation; six of those eight deaths occurred from uncontrolled or uncontrollable hemorrhage. Five late postoperative deaths occurred from delayed hemorrhage in two, brain damage in two, and pulmonary complications in one. The lesson that we learn from these numbers is that we have to get very aggressive and able to control hemorrhage from the liver at the time of operation, and certainly Hartford Hospital sets a good example in this regard. We encountered seven intra-abdominal abscesses after operation for liver injury, and I would certainly subscribe to the belief that many of these are preventable by proper attention to technical principles at the time of operation. James H. Foster (closing): We appreciate the opportunity to bring a conservative message to this Society. There are many articles written about new clamps, complicated shunts, hypothermia, arterial ligation, and other operative gimmicks to be used in the care of patients with liver trauma. We believe that in many in-
Volume 129, Apdl 1975
stances these technics may actually be harmful. Our results may justify a restoration of faith in the older technics of adeq’uate debridement and hemostasis with the use of fine sutures or clips and avoidance of large mattress sutures. There will not be an opportunity for transfer of many patients with hemorrhage from liver injury to large centers. Most general surgeons should be prepared to evaluate and treat such patients. Liver tissue that is firm and blue should be resected but normal appearing liver tissue, even if severely lacerated, should be left unless resection is essential to obtain hemostasis. Anatomic lobectomy will rarely be indicated since major bleeding rarely occurs from a central fissure unless the major hepatic veins and inferior vena cava are involved. The incidence of only one perihepatic abscess suggests that most nonviable liver was resected and that our operative technic did not further compromise liver tissue. Many patients had postoperative fever, often for prolonged periods, but our experience suggests that such fevers should not be an indication for re-exploration. Most will subside in a week or two. We urge your reattention to the basic principles for handling tissue common to all wounded organs.
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