Liver anatomy
Manual Compression and Hepatic Packing (Fig. 7.2)
Upon initial entry into the abdominal cavity, control of hemorrhage can be temporarily achieved by manually compressing the injured liver with laparotomy pads. This temporary control of hemorrhage allows the anesthesia team to “catch up” in the resuscitation of the patient before embarking on more definitive means of hemorrhage control or repair.
Initial hepatic packing can be achieved by placing laparotomy pads above the liver, ensuring that packing is done above the dome of the liver and as posterior as possible. Another set of laparotomy pads are placed below the liver in an effort to sandwich the liver and provide temporary hemostatic control with compression. Division of the falciform ligament allows for optimal superior packing and later evaluation of the superior and lateral lobes of the liver.
In the event of more severe hepatic trauma, further mobilization of the liver is needed to provide more direct manual compression to control hemorrhage by realigning the liver parenchyma to its normal anatomic position. This mobilization is accomplished by dividing the right and left triangular ligaments. The freely mobilized liver can then be optimally manually compressed by pushing left and right lobes together with the surgeon’s or assistant’s hands. The liver can also be compressed posteriorly and superiorly to tamponade any posterior hepatic bleeding.
Other techniques for hepatic compression include the use of absorbable mesh to circumferentially wrap around the liver. The goal is to create a tamponade effect by restoring the liver to its normal anatomical state. This technique is best utilized on burst injuries in which the parenchymal edges are still viable.
Caution should be taken if hematomas are noted in either ligament, as hepatic vein or caval injuries may be present. In cases of retrohepatic venous injuries, division of the triangular ligaments and mobilization of the liver may negate the tamponade effect provided by hepatic compression and release further sites of uncontrolled hemorrhage.
Manual compression and hepatic packing
Finger Fracture and Direct Suture Ligation (Fig. 7.3)
Higher grade or deeper hepatic lacerations may not respond to manual compression alone. Superficial laceration may be amenable to hemostatic control with direct suturing to approximate the liver parenchyma. Utilization of a large blunt tip 0-chromic suture is preferred in order to avoid tearing Glisson’s capsule when reapproximating the tissue. However, this technique is not advised in deeper hepatic laceration, because blindly suturing these lacerations may injure intrahepatic bile ducts and vasculature and cause larger areas of hepatic necrosis from ischemia, intrahepatic hematomas, or hemobilia.
In cases of more severe lacerations, direct ligation of larger bleeding hepatic artery or portal vein branches is necessary for hemostatic control. This is accomplished by gently separating the edges of the fractured liver to expose the depth of the wound. Any visible injured or bleeding vessels can be ligated at this time. Careful dissection through the liver parenchyma can be accomplished via finger fracture technique to identify injured vessels. These vessels can then be ligated via suture ties or clips.
Finger fracture and direct suture ligation
Resection (Fig. 7.4)
Major hepatic trauma can often result in friable or partially devascularized tissue at the liver periphery or within a hepatic laceration. Non-anatomic resection of the devascularized tissue can be accomplished by various techniques. Devitalized tissue can be removed by finger fracturing through the hepatic parenchyma, ligating vasculature to the tissue, and using electrocautery to resect. Liver clamps can also be applied to either side of the injured tissue that requires resection. Mattress sutures can be applied for hemostasis prior to resection of the tissue. The use of linear stapling devices offers a more expedient option for resection of devitalized liver.
Additional electrocautery or argon beam can be utilized to cauterize oozing from the remaining liver edges. Once major bleeding has been controlled, a pedicle flap of viable omentum can be placed within a deep liver laceration to provide further hemostasis and protect against bile leakage from unidentified injuries to minor bile duct branches.
Resection
Balloon Tamponade (Fig. 7.5)
In the case of a penetrating hepatic injury, bleeding from the penetrating tract within the liver can be difficult to access and visualize. Internal tamponade of bleeding from a penetrating tract can be achieved via balloon tamponade with a red rubber catheter or a Foley and Penrose drain. Holes are cut in the red rubber catheter and a Penrose drain is slipped over the catheter tied at each end. The holes cut in the catheter then serve to inflate the Penrose drain like a balloon. This is inserted into the penetrating tract and inflated to serve as an internal tamponade device. Once in the optimal position, the device can be left in place for 24–48 hours and re-evaluated upon return to the operating room.
Balloon tamponade
Vascular Control (Fig. 7.6)
When hemorrhage control cannot be achieved with hemostatic agents or compression/packing, occlusion of the portal triad can effectively reduce bleeding from the liver and provide time to identify and provide a more definitive method of hemorrhage control. The Pringle maneuver is achieved by encircling the portal triad initially with a finger through the epiploic foramen and then clamping with a vascular clamp or Rummel tourniquet. Warm hepatic ischemia can be tolerated from 30 to 60 minutes [2, 3].
If further bleeding is noted after vascular inflow occlusion via the Pringle maneuver, then retrograde bleeding from the retrohepatic inferior vena cava or portal veins must be suspected. In the evident of major retrohepatic venous injury, the infrahepatic and suprahepatic inferior vena cava and portal triad can be occluded to achieve hepatic vascular isolation. Atriocaval shunts to shunt blood from the inferior vena cava to the heart and bypass the liver were first described by Schrock and colleagues in 1968 [4]. These shunts have been associated with overall high mortality rates.
