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Edit Comment Close By: aakashdeeparora (29 month(s) ago) trauma day Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Journal Club26 February 2010 : Management of Liver Trauma Dr. Stephanie HY Lau & Dr. Lai Kang Yiu Intensive Care Unit CME Program Queen Elizabeth Hospital Journal Club26 February 2010 Liver Trauma : Liver Trauma Largest solid abdominal organ , fixed position, partially protected by ribs Extraordinary regeneration capacity; Huge redundancy Double vascular supply: Vascular: blood flow 1.5L/min Second most common injured, but most common cause of death after abdominal trauma Liver Trauma : Liver Trauma Types of injuries Subcapsular hematoma or intrahepatic hematoma. Laceration Contusion Hepatic vascular disruption Bile duct injury Gallbladder injuries rare, with contusions being most common, avulsions next most. Traumatic hemobilia (4-6 wks post injury) Upper or lower GI bleeding Colicky abd pain Jaundice 100% mortality if untreated Liver Trauma : Liver Trauma Penetrating vs blunt trauma Differences in incidence around the world Blunt MVA most common Mortality 4%-5%, 73% with other visceral injuries Blunt liver trauma = 10X more fatal than penetrating Conservative: paradigm shift Before 1993, routine operative treatment Between 1993 - 1994, selective non operative management Between 1994 - 1998, non operative management standard practice 80% adults, 97% children-conservative treatment Slide 6: Evolution in the Management of Hepatic Trauma: A 25-Year Perspective J. David Richardson, ANNALS OF SURGERY 2000 Vol. 232, No. 3, 324–330 Slide 7: Major Reduction in Death due to Haemorrhage Liver Trauma : Liver Trauma Decreased transfusion requirement with haemostatic resuscitation protocol, early use of Novo VII, radiological intervention, permissive hypotension, damage control laparotomy, correction and avoidance of lethal triad and intensive care. Significant changes in management over last two decades with significant improvement in outcome Recovery potential Mild hepatic injuries involving < 25% of one lobe heal in 3 months. Moderate injuries involving 25-50% of one lobe heal in 6 months. Severe injuries require 9-15 months to heal. Slide 10: Compensation hepatic hypertrophy after hepatic resection Extraordinary regeneration capacity Liver AnatomyFrom morphological anatomy to functional anatomy : Liver AnatomyFrom morphological anatomy to functional anatomy Morphological (Classical) Anatomy The ligamentum falciforme divides the liver into the right and left anatomic lobes. A plane from GB fossa to IVC divides liver functionally into two halves Slide 13: Functional Division of liver Anatomical Division of Liver Slide 14: Vascular supply & Bile Duct of Liver Slide 15: 25% 75% Liver has dual Blood supply Slide 16: Bismuth's classification (popular in the U.S.A.) Anatomy : Anatomy The 8 liver segments are numbers clockwise on the frontal view. Slide 18: Couinaud developed 4 sectors and 8 segments, divided into vertical and oblique planes, defined by the 3 main hepatic veins and transverse plane through right and left portal branches. Caudate lobe : Caudate lobe The caudate lobe or segment 1 is located posteriorly and is anatomically different from other lobes in that it often has direct connections to the IVC through hepatic veins, that are separate from the main hepatic veins. The caudate lobe may be supplied by both right and left branches of the portal vein. Due to a different blood supply the caudate lobe is spared from the disease process of cirrhosis and hypertrophied to compensate for the loss of normal liver parenchyma. Slide 20: Why is the liver so susceptible to injury ? Anatomy of liver : Anatomy of liver Relatively fragile parenchyma contained within thin Glisson’s capsule. Very susceptible to blunt and penetrating trauma Wide-bore, thin-walled vessels with high blood flow Injury associated with significant blood loss Anatomy of liver : Anatomy of liver Fixed position in relation to spine Right lobe gets hit more since its larger, and closer to ribs. 85% injuries involve segments 6,7,8 from compression against ribs, spine, abdominal wall. Shear forces at attachments to diaphragm Transmission through right hemithorax. Rib fragment penetration into the liver parenchyma Anatomy of liver : Anatomy of liver Liver injured easily in children since ribs are compliant, force transmitted. Liver not as developed in children, with weaker connective tissue framework. Slide 24: Injury can lead to capsular tears and bile leaks, fistulas, hemoperitoneum. Slide 25: (1964) (1973) Change in pattern of injury after motor vehicle accidents after introduction of seat belt in the U.S.A. Slide 26: Seat Belt Sign Seat Belt Sign : Seat Belt Sign The incidence of perforated small bowel injury in patients presenting with a seatbelt sign is 37.6%. The incidence of perforated small bowel in patients wearing a seat belt is 21.1%. The mechanism of injury is attributed to acceleration/deceleration forces applied to the abdomen with resultant crush of the bowel between the lap belt and the vertebrae. This, along with sudden increases in abdominal pressures within the bowel, can result in tearing along fixed points, i.e., bowel mesentery. A unique pattern of injury secondary to seatbelt-related blunt abdominal trauma. Munshi IA. Patton W. Journal of Emergency Medicine. 27(2):183-5, 2004 Aug. Presence of seat belt sign in children was associated with a significantly increased risk for intraabdominal injury (30% vs. 10%; relative risk, 2.9). Most of the increase in risk was attributed to injuries to the gastrointestinal tract (26% vs. 2%; RR, 12.8) and pancreas (7.0% vs. 0.3%; RR, 22.4). Sokolove PE et al. Association between the "seat belt sign" and intra-abdominal injury in children with blunt torso trauma. Acad Emerg Med 2005 Sep; 12:808-13. Mechanism of Hepatic Injury : Mechanism of Hepatic Injury Blunt: Rapid deceleration Fall from heights, road traffic accident Central crush injury Rupture of Glisson’s capsule, parenchymal fracture Venous/arterial bleeding, bile duct disruption, devitalized liver Penetrating: Direct trauma Gunshot, stab or impalement injury Minimal parenchymal disruption, venous/arterial bleeding, bile duct division. Devitalized liver rare Blunt Abdominal Trauma : Blunt Abdominal Trauma Mechanisms Direct impact Acceleration-deceleration forces Shearing forces No correlation between size of contact area and resultant injuries. Abdomen = potential site of major blood loss. Penetrating Abdominal Trauma : Penetrating Abdominal Trauma Evaluation Any penetrating wound between nipples and gluteal crease = potential intra-abdominal injury. Stab wounds: stratify based on location GSW: higher potential for serious injury. Mechanisms of Injury : Blunt Trauma Deceleration injury (RTA, fall from height) Tears at sites of fixation to diaphragm and abdominal wall Typically fracture between posterior sector (segment VI and VII) and anterior sector (segment V and VIII) of right lobe Significant vascular injury due to tear of right hepatic vein Mechanisms of Injury Mechanisms of Injury : Blunt Trauma Central crush injury (Direct blow from fist or weapon) Extensive satellite-type laceration involving segments IV, V and VIII Major vascular injury with disruption of hepatic arteries, portal veins and major hepatic veins +/- bleeding from caudate lobe Mechanisms of Injury Mechanisms of Injury : Penetrating Trauma Stab injury Major bleeding from one of the three hepatic veins or vena cava (+/- portal vein/hepatic artery if hilum involved) Gunshot injury Major vessel disruption, cavitation effect particularly from high velocity weapons Mechanisms of Injury Transhepatic bullet tract Pseudoaneurysm arising from anterior branch of right hepatic artery. Grading of Liver Injuries : Several classification systems in use Most widely used American Association for the Surgery of Trauma Grading of Liver Injuries Grade I-II: Minor, no operative treatment needed Slide 37: Grade I-II: Minor, no operative treatment needed (94% success with non-operative management) Slide 38: Grade III-V: Severe, require operative treatment (Nonoperative management success rate only 20% for grade III –IV) Slide 39: Avoiding disturbance of new clot in liver lacerations/fractures is the main reason for the improvement in mortality since adoption of this paradigm shift in NOMLI. Haemostatic resuscitation 85% specific for arterial vascular injury Poletti et al. Radiology 216:416, 2000 Slide 40: Selective Management of Abdominal Stab Wounds Robert M. Shorr Arch Surg 1988;123:1141-1145 Assessment and Initial Investigation : High index of suspicion especially in those with shock and trauma to right side Limit crystalloid with early use of fresh whole blood. Permissive hypotension before definitive radiological or surgical intervention to stop the bleeding. Aggressive correction of acute traumatic coagulopathy with massive transfusion protocol using transfusion ratio of RBC:FFP:Platelet in 1:1:1 ratio with additional cryoprecipitate and early use of Novo VII. Avoid lethal triad of hypothermia, coagulopathy and acidosis Assessment and Initial Investigation Assessment and Initial Investigation (2) : In unstable (SBP<90mmHg) despite fluid resuscitation Immediate operation is indicated In stable patients Proceed with investigative and therapeutic modalities such as USG, CT and IR techniques Assessment and Initial Investigation (2) Acute Traumatic Coagulopathy Implication to Massive Transfusion Protocol for Hepatic Trauma : Acute Traumatic Coagulopathy Implication to Massive Transfusion Protocol for Hepatic Trauma Dr. Lai Kang Yiu Intensive Care Unit Queen Elizabeth Hospital Major Shift In Trauma Care : Major Shift In Trauma Care “Damage Control Resuscitation represents the most important advance in trauma care for hospitalized civilian and military casualties from this war.” Cordts, Brosch and Holcomb, J Trauma, 2008 Slide 45: Activation of the anticoagulant protein C pathway by elevated thrombomodulin Hyperfibrinolysis Massive Blood Loss Replacement of patient’s blood volume within 24 hours Transfusion of more than 10 units of red cells in 24 hours Replacement of more than 50% of the patient’s blood volume in 3 hours Blood loss more than 150 mL/ minute in an adult Haemorrhage is the major potentially treatable cause of death in the initial 24 hours Slide 47: Acute coagulopathy of trauma: mechanism, identification and effect Karim Brohia, Mitchell J. Cohenb and Ross A. Davenport Curr Opin Crit Care 13:680–685. Only 2% of patients with a base deficit under 6mEq/l had prolonged clotting times, compared with 20% of patients with a base deficit over 6mEq/l. Not reversed with pH neutralization Slide 48: Acute coagulopathy of trauma: mechanism, identification and effect Karim Brohia, Mitchell J. Cohenb and Ross A. Davenport Curr Opin Crit Care 13:680–685. Trauma + Shock Slide 49: Trauma, induces the initiation of coagulation Tissue factor (TF) is exposed and binds to FVIIa or FVII which is subsequently converted to FVIIa The complex between TF and FVIIa activates FIX and FX FXa binds to FVa on the cell surface Normal Haemostasis: Initiation Phase Slide 50: Normal Haemostasis: Amplification phase The FXa/FVa complex converts small amounts of prothrombin into thrombin The small amount of thrombin generated activates FVIII, FV, FXI and platelets locally. FXIa converts FIX to FIXa Activated platelets bind FVa, FVIIIa and FIXa Slide 51: Normal Haemostasis : Propagation Phase The FVIIIa/FIXa Complex activates FX on the surfaces of activated platelets FXa in association with FVa converts large amounts of prothrombin into thrombin creating a “thrombin burst”. The “thrombin burst” leads to the formation of a stable fibrin clot. Slide 52: Thrombin is generated primarily via the ‘extrinsic’ pathway with multiple feed-forward loops. When thrombomodulin (TM) is presented by the endothelium, it complexes thrombin which is no longer available to cleave fibrinogen. This anticoagulant thrombin activates protein C which reduces further thrombin generation through inhibition of cofactors V and VIII. Anticoagulation Slide 53: Tissue plasminogen activator (tPA) is released from the endothelium by injury and hypoperfusion and cleaves plasminogen to initiate fibrinolysis. Activated protein C (aPC) consumes plasminogen activator inhibitor-1 (PAI-1) when present in excess, and reduced PAI-1 leads to increased tPA activity and hyperfibrinolysis. Hyperfibrinolysis Slide 54: Activated protein C pathway Thrombin binds Thrombomodulin The complex Thrombin- Thrombomodulin activates Protein C APC decreases FVIIIa and FVa and induces D-dimers production Slide 55: Direct thrombin generation even in the absence of FVIII and FIX Increase Xa Direct activate IX on activated platelet Potential Role of FVIIa in Acute Traumatic Coagulopathy FVIIa Inhibit Fibrinolysis The Lethal TriadPrevention Is Better Than Cure : The Lethal TriadPrevention Is Better Than Cure Hypothermia Acidosis Coagulopathy Death If this “lethal triad“ is present ..... surgical control of bleeding is unlikely to be successful! Development of Resuscitation Protocol For Major Haemorrhagic Shock : Development of Resuscitation Protocol For Major Haemorrhagic Shock World War II Mid 70’ - 2003 2008 - Chimerism Acute coagulopathy of trauma Fresh Whole Blood Saves Life Crystalloid Colloid Packed cells Slide 58: Limit crystalloids Early Use of Blood Product Give products in a ratio of PRBC:FFP:platelets 1:1:1 Early use of Novo VII Traditionally, FFP & platelet concentrates are given as “needed” Slide 59: Arrest of Haemorrhage Provide volume that also restores the haemostatic cascade Minimize crystalloid Permissive hypotension Small volume resuscitation Stop the bleeding Stay out of trouble Component Therapy vs Fresh Whole Blood : Component Therapy vs Fresh Whole Blood So Component Therapy Gives You 1U PRBC + 1U PLT + 1U FFP + 10 pk Cryo = 660 COLD mL Hct 29% Plt 87K Coag activity 65% 750 mg fibrinogen 500 mL Warm Hct: 38-50% Plt: 150-400K Coags: 100% 1500 mg Fibrinogen Slide 63: Systolic BP < 90 mmHg BE > - 6 mmol/L INR > 1.5 T < 96 °F (35.6 °C) Hb < 11 g/dL Slide 64: Management of Trauma Patient Requring Massive Transfusion Role of ICU (OT) Ambulance & A&E Department Slide 65: FAST USS Examination Control External Bleeding + Diagnostic Adjunct to locate source of internal bleeding F.A.S.T. Blunt Abdominal Trauma : Blunt Abdominal Trauma The Role of FAST Scan and Contrast Ultrasound : The Role of FAST Scan and Contrast Ultrasound Ultrasonography : Largely replaced diagnostic peritoneal lavage FAST (Focused Assessment Sonography for Trauma) Non-invasive, easily accessible and less costly Highly operator dependent Very accurate for blunt and penetrating abdominal injuries, specificity 95-100% & sensitivity 63-100% Ultrasonography Negative FAST scan does not safely rule out injury Cannot determine extent of hepatic parenchymal or vascular injury Morrison’s Pouch : Morrison’s Pouch Ultrasound probe is placed in the right mid- to posterior axillary line at the level of the 11th and 12th ribs Slide 71: Morison’s Pouch: space between Glisson’s capsule and Gerota’s fascia Appearance of blood : Appearance of blood Fresh blood Anechoic (black) Coagulating blood First hypoechoic Later hyperechoic Free fluid DDx Blood Ascites Urine from ruptured bladder Lavage fluid Ruptured Ovarian Cyst Slide 73: Liver Kidney Diaphragm Pleural effusion or haemothorax Slide 74: Contrast agents have been developed for ultrasound. They are small, gas-filled microbubbles, around 3 µm in size, which can be given intravenously safely. Microbubble-specific software can image the microcirculation, and we anticipated that this could facilitate detection of traumatized tissue. Ultrasound contrast media are biologically inert, with no significant toxicity (not nephrotoxic) , so that follow-up scans may be performed as often as needed. Microbubble ultrasound demonstrates liver trauma.Kraemer N. Cosgrove D. Blomley M. Journal of Trauma-Injury Infection & Critical Care. 56(4):913-4, 2004 Apr. Slide 75: Contrast-enhanced ultrasound 3 days after trauma, showing details of liver lacerations US 3 days after trauma. A haematoma is seen, but no details Contrast–enhanced ultrasound in trauma European Radiology Supplements 2004 (14, Supplement 8) P 43-52 Slide 76: US 16 days after trauma, showing no obvious lesion Contrast-enhanced ultrasound 16 days after trauma, showing small remaining rift Contrast–enhanced ultrasound in trauma European Radiology Supplements 2004 (14, Supplement 8) P 43-52 Slide 77: Baseline ultrasound of the liver. No evidence of intrahepatic lesion. Contrast USS Late phase. Lack of perfusion at the segment IV of the liver, corresponding with the knife track (arrow). Contrast USS Late phase. Lack of perfusion at the subcapsular area (arrow), perpendicular to the knife track, corresponding with heamatoma. Lacerated area at the segment IV (black arrow), Subcapsular hematoma (white arrow) perpendicular to the knife track. Is Contrast Enhanced Ultrasound an Essential Tool for Liver Trauma? Kalogeropoulou, C P. MD; Ceccotti, P C. MD; Leen, E MD, FRCR; Horgan, P PhD, FRCSThe Journal of Trauma: Injury, Infection, and Critical Care Issue: Volume 60(1), January 2006, pp 233-236 Contrast-enhanced ultrasound in blunt abdominal trauma (Pierre Alexandre Poletti; Lars Thorelius; Kalogeropoulou) : Contrast-enhanced ultrasound in blunt abdominal trauma (Pierre Alexandre Poletti; Lars Thorelius; Kalogeropoulou) It is cheap, portable and noninvasive and does not use radiation (children, pregnancy) or iodinated contrast media (renal failure, iodine contrast allergy) It has a vascular phase and a late sinusoidal phase that last for 6 minutes. Repeated doses of contrast can be injected to investigate the possibility of active bleeding of every suspected area during the vascular phase enhancement. In the sinusoidal phase, the normal liver becomes brighter and it can distinguish hepatic laceration or hematomas that are isoechoic to the normal liver. Cannot replace CT to exclude the presence of a solid organ traumatic injury. Could be a useful alternative to CT to detect delayed splenic pseudoaneurysms. Could be a complement to CT to differentiate contusion from lacerations. Could be useful for frequent followed up and monitoring of patient with risk of transportation and impaired renal function. Slide 79: CT Scan of abdomen Slide 80: CT 3D portal venous angiogram CT angiogram Coronal 3D CT cholangiogram Liver Laceration Subcapsular haematoma Computerized Tomography : Standard evaluation modality for stable patients with abdominal injury High sensitivity (92-97%) and specificity (98.7%) for liver injuries (improves with increasing time between injury and scanning) Computerized Tomography Exposure of ionising radiation, use of IV contrast which may compromise renal function Computerized Tomography : Type and extent of liver injury Volume of haemoperitoneum & presence of ongoing haemorrhage Clotted blood (45-70HU), active bleeding (30-45HU) Extravasation of contrast material is strong predictor of failure of non-surgical management Invaluable for detection of associated intraperitoneal and retroperitoneal injuries Follow-up of complications (delayed haemorrhage, bile leaks, abscess formation) Computerized Tomography CT Scans : CT Scans Accurate in localizing the site of liver injury, associated injuries. Used to monitor healing. CT criteria for staging liver trauma uses AAST liver injury scale Grades 1-6 Hematoma,laceration,vascular,acute bleeding,gallbladder injury,biloma. CT Scan Classification : CT Scan Classification I-Subcapsular hematoma<1cm, superficial laceration<1cm deep. II-Parenchymal laceration 1-3cm deep, subcapsular hematoma1-3 cm thick. III-Parenchymal laceration> 3cm deep and subcapsular hematoma> 3cm diameter. IV-Parenchymal/supcapsular hematoma> 10cm in diameter, lobar destruction, or devasularization. V- Global destruction or devascularization of the liver. VI-Hepatic avulsion Slide 85: Grade 1 hepatic injury in a 21-year-old man with a stabbing injury to the right upper quadrant of the abdomen. Axial, contrast-enhanced computed tomography (CT) scan demonstrates a small, crescent-shaped subcapsular and parenchymal hematoma less than 1 cm thick. (arrow) Grade 1 - Subcapsular hematoma less than 1 cm in maximal thickness, capsular avulsion, superficial parenchymal laceration less than 1 cm deep, and isolated periportal blood tracking Slide 86: A 20-year-old man with systemic lupus erythematosus presented with grade 2 liver injury after minor blunt abdominal trauma. Nonenhanced axial CT scan at the level of the hepatic veins shows a subcapsular hematoma 3 cm thick. Grade 2 - Parenchymal laceration 1-3 cm deep and parenchymal/subcapsular hematomas 1-3 cm thick Slide 87: A 20-year-old man with systemic lupus erythematosus presented with grade 2 liver injury after minor blunt abdominal trauma (same patient as in Images above). Axial CT image through the inferior aspect of the right lobe of the liver demonstrates multiple low-attenuation lesions in the liver consistent with parenchymal contusion. Grade 2 Grade 2 Liver InjuryParenchymal laceration 1-3cm deep, subcapsular hematoma1-3 cm thick. : Grade 2 Liver InjuryParenchymal laceration 1-3cm deep, subcapsular hematoma1-3 cm thick. Slide 89: Grade 3 liver injury in a 22-year-old woman after blunt abdominal trauma. Contrast-enhanced axial CT scan through the upper abdomen shows a 4-cm-thick subcapsular hematoma associated with parenchymal hematoma and laceration in segments 6 and 7 of the right lobe of the liver. Free fluid is seen around the spleen and left lobe of the liver consistent with hemoperitoneum. Grade 3 - Parenchymal laceration more than 3 cm deep and parenchymal or subcapsular hematoma more than 3 cm in diameter Slide 90: Laceration > 3 cm Subcapsular hematoma > 3 cm. Grade III Liver Injury Slide 91: Grade 3 Liver Injury Laceration > 3 cm Slide 92: Grade 3 liver injury (arrows) with areas of high attenuation (arrowheads) within the laceration due to active extravasation. Slide 93: Grade 4 - Parenchymal/subcapsular hematoma more than 10 cm in diameter, lobar destruction, or devascularization Image obtained in a 35-year-old male bouncer after blunt abdominal injury). Nonenhanced axial CT scan of the abdomen demonstrates a large subcapsular hematoma measuring more than 10 cm. The high-attenuating areas within the lesion represent clotted blood. The injury was classified as a grade 4 liver injury. Slide 94: Contrast-enhanced axial CT scan in a 39-year-old man with a grade 4 liver injury shows a large parenchymal hematoma in segments 6 and 7 of the liver with evidence of an active bleed. Note the capsular laceration and large hemoperitoneum Slide 95: Multisegment infarct (segments 2, 3, 4a, and 4b) in a 40-year-old man who was in a motor vehicle accident and underwent emergency segmental resection of the right lobe. Note the sharply demarcated wedge-shaped area of infarction; hence, the classification as grade 4. Slide 96: Grade 4: Massive central subcapsular hematoma >10 cm lobar destruction/devitalization Slide 97: Transverse CT scan shows a grade 4 liver laceration (arrows) in the right lobe of the liver with two high-attenuating areas (arrowheads), which represent active bleeding. Slide 98: CT scan shows a focal area of normally enhancing hepatic parenchyma (straight arrow) within a grade 4 right liver lobe laceration (curved arrows) mimicking a site of active hemorrhage. The selective hepatic angiogram (not shown) did not show evidence of hepatic bleeding. Slide 99: Branch of the portal vein mimicking a hepatic pseudoaneurysm in a 31-year-old man admitted following a blunt abdominal trauma. At initial interpretation of the transverse CT scan, a well-circumscribed focal area of high attenuation (arrow) seen within a grade 4 hepatic laceration (arrowheads) was falsely considered to be a hepatic pseudoaneurysm. The selective hepatic angiogram (not shown) did not demonstrate a hepatic arterial pseudoaneurysm. Slide 100: Grade 5 - Global destruction or devascularization of the liver Grade 5 injury in a 36-year-old man who was involved in a motor vehicle accident demonstrates global injury to the liver. Bleeding from the liver was controlled by using Gelfoam. Slide 101: Grade 5 injury in a 36-year-old man who was involved in a motor vehicle accident (same patient as in Images above). Axial CT scan shows a hematoma around the right kidney and inferior vena cava consistent with renal and inferior vena cava injury. Slide 102: Active hemorrhage/extravasation Gd V Slide 103: Oral and intravenous contrast-enhanced computed tomography image of the upper abdomen of case 2 demonstrates the complex liver laceration, pseudoaneurysm (curved arrow), and extravasated intravenous contrast in the perihepatic space (straight arrow). Slide 104: Digital subtraction common hepatic arteriogram from case 2 demonstrates a pseudoaneurysm from a peripheral branch of the right hepatic artery (arrow). Slide 105: Periportal Tracking Slide 106: Multidetector CT and MRI findings in periportal space pathologies. Karcaaltincaba M. Haliloglu M. Akpinar E. Akata D. Ozmen M. Ariyurek M. Akhan O. European Journal of Radiology. 61(1):3-10, 2007 Jan. Slide 107: Axial CT image shows normal fat tissue around umbilical segment of left portal vein which is a frequently seen normal appearance. Presence of fat probably indicates extrahepatic course of left portal vein. Slide 108: Hepatic fracture Blood Slide 109: Laceration Periportal Tracking Slide 110: Liver haematoma Periportal tracking surrounding anterior segment of right portal vein Slide 111: Haematoma at bare area of liver Periportal tracking at right lobe of liver Posterior right rib fracture Slide 112: Unsuspected child abuse revealed by delayed presentation of periportal tracking and myoglobinuria. DiGiacomo JC. Frankel H. Haskell RM. Rotondo MF. Schwab CW. Journal of Trauma-Injury Infection & Critical Care. 49(2):348-50, 2000 Aug. Periportal tracking in pediatric blunt abdominal trauma. Correlation with liver enzymes and liver injury. Vade A. Demos TC. Salvino C. Korach JL. Clinical Imaging. 18(3):189-94, 1994 Jul-Sep. : Periportal tracking in pediatric blunt abdominal trauma. Correlation with liver enzymes and liver injury. Vade A. Demos TC. Salvino C. Korach JL. Clinical Imaging. 18(3):189-94, 1994 Jul-Sep. Periportal tracking (PPT) was divided into four grades (0-3) depending upon the distribution of decreased attenuation adjacent to the portal vessels. Circumferential PPT extending to the periphery of the liver (grade 3) was found in 20/243 children. They had a higher incidence of liver parenchymal injury seen on CT 20% versus 0.5% in combined PPT grades 0-2. Sixteen children with grade 3 PPT and no liver injury had significantly elevated liver enzymes as compared to children with combined 0-2 grade PPT. Eleven of the 20 children with grade 3 PPT had no other CT evidence of intraabdominal injury and none of these patients developed intraabdominal hemorrhage. Thus, grade 3 periportal tracking as an isolated abnormality did not indicate a clinically significant liver injury in any patient. Computed tomography in blunt hepatic trauma. Davis KA. Brody JM. Cioffi WG. Archives of Surgery. 131(3):255-60, 1996 Mar. : Computed tomography in blunt hepatic trauma. Davis KA. Brody JM. Cioffi WG. Archives of Surgery. 131(3):255-60, 1996 Mar. The finding of periportal tracking on the admission CT scan is not clinically significant and does not preclude nonoperative management of patients with blunt hepatic injury. Routine follow-up CT scans are not indicated, as treatment is not influenced by their results. Rather, follow-up CT scans should be obtained as dictated by the patient's clinical course. Extrapolation of these findings to all patients with blunt hepatic trauma in the United States would result in considerable savings of health care dollars, without negatively affecting patient care. Slide 115: Multidetector CT evaluation of active extravasation in blunt abdominal and pelvic trauma patients.Hamilton JD. Kumaravel M. Censullo ML. Cohen AM. Kievlan DS. West OC. Radiographics. 28(6):1603-16, 2008 Oct. Sentinel Clot Sign : Sentinel Clot Sign The "sentinel clot sign" has been described by Orwig and Federle as representing localized intra-abdominal blood adjacent to an organ and implies that that organ is the source of bleeding. Clotted blood can be distinguished from nonclotted blood by CT, because clotted blood has a higher density and hemoglobin content. Free intraperitoneal blood usually has a CT-measured density of 35-45 Hounsfield units (H), whereas clotted blood usually exceeds 60 H. In the absence of measured Hounsfield densities, a sentinel clot is recognized as a focal area that is visibly more dense than the surrounding fluid and much more dense than would be encountered if the contrast were leaking from gastrointestinal or genitourinary sites. Slide 117: Sentinel clot sign. (a) Contrast-enhanced CT image shows a sentinel clot secondary to laceration along the fissure for the ligamentum teres (arrow), in the perihepatic space and lesser sac. Slide 118: Contrast-enhanced CT image obtained in a patient who was undergoing anticoagulation therapy for a protein C deficiency shows a sentinel clot (arrow) surrounding the spleen. Slide 119: Surgically confirmed splenic Injury wIth perisplenic hematomas. CT scan shows hyperdense clot (C) relative to lower density of lysed blood (B) surrounding liver. Localized clotted blood as evidence of visceral trauma on CT: the sentinel clot sign. Orwig D. Federle MP. AJR. American Journal of Roentgenology. 153(4):747-9, 1989 Oct. Slide 120: Hepatic artery pseudo-aneurysm Embolization Slide 121: Contrast-enhanced CT image shows a large liver laceration with internal pooling of high-attenuation material (arrow), a finding suggestive of an aneurysm or pseudo-aneurysm. Angiogram shows a pseudoaneurysm (arrow). Slide 122: Combined hepatic pseudoaneurysm and active extravasation. (a, b) Initial 1-minute delayed image (a) shows a large nonenhancing area within the left hepatic lobe, a finding that represents a grade III laceration (7), and a central oval area of high attenuation (arrow), which represents a pseudoaneurysm. The high attenuation decreases on the 5-minute delayed image (b). (c) Coronal reformatted image reveals a small jet of active extravasation (curved arrow) inferior to the pseudoaneurysm (straight arrow). Both findings and the enhancement of the hematoma within the laceration are better seen with the coronal reformation from the initial image data after 1-minute delay compared with the 5-minute delayed image. Multidetector CT evaluation of active extravasation in blunt abdominal and pelvic trauma patients. Hamilton JD. Kumaravel M. Censullo ML. Cohen AM. Kievlan DS. West OC. Radiographics. 28(6):1603-16, 2008 Oct. Slide 123: Venous Injuries Slide 124: Transverse CT scan shows right lobe liver lacerations (arrows) extending to the right and middle hepatic veins at their confluence with the inferior vena cava Slide 125: Wedge-shaped, low-attenuating area (open arrows) in the right hepatic lobe drained by the middle hepatic vein (thrombosed and not enhanced in CT). Free intraperitoneal blood (arrowheads) is seen around the inferior vena cava and the liver. At surgery, the middle hepatic vein was avulsed from the inferior vena cava and actively bleeding. Role of Radiological Intervention in Hepatic Trauma : Role of Radiological Intervention in Hepatic Trauma Arterial embolization Interventional Vascular Radiological Technique : Multidisciplinary approach involving use of arterial embolisation and transhepatic venous stenting Useful adjunct in stable patients managed non-operatively or those who have been stabilized by perihepatic packing or has rebleed after initial period of stability Interventional Vascular Radiological Technique Slide 128: Hepatic angiogram Trauma Angiography and Embolization : Trauma Angiography and Embolization Goals Stop bleeding Prevent future bleeding (delayed rupture) Diminish complications of organ injury Percutaneous Rx when best approach Advances DSA for rapid, accurate diagnostic angio Coaxial microcatheters and microcoils Slide 135: Mechanisms of arterial injury and radiological appearance Liver CT Screening for AngiographyCT Criteria for Management of Blunt Liver Trauma: Correlation with Angiographic and Surgical Findings Poletti, et al Radiology 2000; 216:418-427 : Liver CT Screening for AngiographyCT Criteria for Management of Blunt Liver Trauma: Correlation with Angiographic and Surgical Findings Poletti, et al Radiology 2000; 216:418-427 Vascular lesion (pseudoaneurysm, extravasation) helps predict positive angiogram Sens 56%, Spec 83%, PPV 64%, NPV 83% Grade 4 or 5 injury with hepatic vein/IVC involvement Helps predict (+) arteriogram even without CT findings of arterial injury Higher incidence of failure of NOM Role of angiogram in grade 4 or 5 injuries without vascular lesion or major hepatic vein involvement? Embolotherapy Principles : Embolotherapy Principles Selectivity: More is generally better but… Not if deteriorating hemodynamics Consequences of tissue loss and non-target embo (CNS > Kidney > pelvis ) Expendability, dual supply, collaterals Durability: Temporary agent, gelfoam works; Coils if hole large, specific placement, mechanical blockade Simultaneous patient management and support – avoid coagulopathy, maintain perfusion and clotting factors Embolotherapy principles : Embolotherapy principles What causes late failure? Spasm masking injury, choose too small coil, partial thrombosed Back bleeding from collaterals Recanalization, pseudoaneurysm formation Coagulopathy Venous bleeding Hepatic Trauma Embolotherapy Outcomes : Hepatic Trauma Embolotherapy Outcomes Technical success rates 90-100% Beware of rebleed in patients with HV/IVC injury Delayed complications are less common with embolization (see more bilomas) than surgery (mostly infection) Drainage Slide 140: Raised Intrahepatic Pressure Abdominal Compartment Syndrome (ACS) Yang, et al J Trauma 2002;52:982-986 : Abdominal Compartment Syndrome (ACS) Yang, et al J Trauma 2002;52:982-986 Because mortality with high grade liver injuries is high, consider NOM with embolization whenever possible Instances of ACS have occurred at SFGH (previously seen only in operative series) Successful treatment by draining accumulated blood from the abdomen – has not resulted in feared loss of tamponade Classification of Traumatic Biliary InjuriesStein and Batistella, Seminar Interventional Radiology 2003;20:141-149 : Classification of Traumatic Biliary InjuriesStein and Batistella, Seminar Interventional Radiology 2003;20:141-149 Nonoperative and Operative Management : Nonoperative and Operative Management Nonoperative Management : Most significant paradigm shift 1908: Pringle packing of liver injury Non-operative management first reported in surgical literature in 1972 Pringle packing fell out of favour, not used in Vietnam war 1981: Feliciano 90% survival by packing in severe liver injury 1983: Stone abbreviated laparotomy, 11/17 survivors Rotundo: damage control surgery, 1990s Recognition that 50-80% of liver injuries stop bleeding spontaneously 2003, acute traumatic coagulopathy recognized with major change in blood transfusion protocol for massive transfusion, early use of novo VII and radiological intervention. Nonoperative Management Nonoperative Management : Selection criteria Mechanism of injury Haemodynamic stability after resuscitation Absence of signs of other visceral or retroperitoneal injuries that require surgery Availability of multidisciplinary team (good quality CT, intensive care facilities and experienced surgeons) Grade of injury and volume of haemoperitoneum is considered less significant Nonoperative Management Failure of Nonoperative Management : Most common: Coexisting abdominal injury such as delayed bleeding from spleen or kidney Rarely due to delayed liver bleeding (0-3.5%) Other predictors Age, haemoglobin, blood pressure, active extravasation on CT and need for blood transfusion Failure of Nonoperative Management Factors of failure for nonoperative management of blunt liver and splenic injuries. Ochsner MG. World Journal of Surgery. 25(11):1393-6, 2001 Nov. : Factors of failure for nonoperative management of blunt liver and splenic injuries. Ochsner MG. World Journal of Surgery. 25(11):1393-6, 2001 Nov. Nonoperative management should not be considered unless the patient meets the following criteria: (1) hemodynamic stability, with or without minimal fluid resuscitation; (2) no demonstrable peritoneal signs on abdominal examination; and (3) the absence on computed tomography (CT) scan of any intraperitoneal or retroperitoneal injuries that require operative intervention. (4) Liver injury of American Association for the Surgery of Trauma grades I-III (5) Pooling of contrast on CT scan. Formerly thought to be a predictor of failure of nonoperative management, periportal tracking has not been cited as such in recent reports of hepatic injuries. Signs of failure of nonoperative management of a hepatic injuryHEPATIC TRAUMA D. V. Feliciano, G. S. Rozycki Scandinavian Journal of Surgery 91: 72–79, 2002 : Signs of failure of nonoperative management of a hepatic injuryHEPATIC TRAUMA D. V. Feliciano, G. S. Rozycki Scandinavian Journal of Surgery 91: 72–79, 2002 Decreased hematocrit in combination with tachycardia with or without hypotension in the first 48 hours of observation, especially in the absence of orthopaedic injuries >2–4 units packed RBC transfusion in the first 24–48 hours of observation, especially in the absence of orthopaedic injuries Increasing abdominal pain, tenderness, and onset of diffuse peritonitis Expansion of subcapsular or intrahepatic hematoma on a followup CT Subcapsular or intrahepatic hematoma becomes a septic focus Development of a symptomatic perihepatic fluid collection (infected hematoma or biloma) Slide 149: Operative Management of Severe Liver Injury Operative Management – Incision : Midline laparotomy Extended either with oblique incision or right subcostal incision Bilateral subcostal incision Sometimes favoured if there is obvious penetrating through and through liver injury Operative Management – Incision Initial Control of Bleeding : Immediate control of bleeding is an absolute priority Liver manually closed and compressed followed by packs If unsuccessful, proceed with Pringle manoeuvre Both diagnostic and therapeutic Generally can tolerate 1 hour occlusion time Initial Control of Bleeding Slide 153: Pringle manoeuvre Pringle JH. Notes on the arrest of hepatic hemorrhage due to trauma. Ann Surg 1908; 48:541-49. A large haemostat is used to clamp the hepatoduodenal ligament interrupting the flow of blood through the hepatic artery and the portal vein and thus helping to control bleeding from the liver. Damage Control Surgery : 3 principle phases Phase 1: Initial control of haemorrhage and contamination followed by packing and rapid wound closure Minimise metabolic insult (hypothermia, coagulopathy and acidosis), limit operating time and avoidance of opening of body cavities that have not been traumatized Temp <34C, nonsurgical oozing/prothrombin time >50% above normal and acidosis pH <7.2 despite adequate volume resuscitation Phase 2: Further resuscitation and stabilisation in ICU for 24-48hr period till normal physiological parameters (e.g. acidosis, hypothermia and coagulopathy) have been restored Phase 3: Re-exploration and definitive repair Damage Control Surgery Slide 155: Hepatic Packing Perihepatic Packing : Controls profuse haemorrhage in up to 80% patients Allows intraoperative resuscitation Particularly useful for extensive injuries (grade III-V) and when transfer to trauma centres/hepatobiliary units is needed Perihepatic Packing Perihepatic Packing (2) : Large folded laparotomy packs inserted over diaphragmatic surface to produce tamponade effect between liver and abdominal wall/thoracic cage “Six pack technique” by Krige et al. Avoid: Forcing packs into liver fractures extend the injury and cause venous tears and increased bleeding Excessive packing/Infrahepatic packs vena caval and renal vein compression abdominal compartment syndrome Close upper part of wound to enhance tamponade effect while leaving lower 2/3 open temporarily covered with silastic sheet Perihepatic Packing (2) Perihepatic Packing (3) : Administer broad spectrum antibiotics to reduce risk of sepsis (occurs in 10-30%) Exact timing of removal of packs controversial Packs removed after 36-48 hours Premature removal of packs (<24 hours) increases bleeding and is related to worse outcome Delayed removal (up to 1 week) is not associated with increased incidence of organ-specific or systemic complications Some surgeons advocate insertion of plastic sheets between the liver and packs to reduce rebleeding during removal Perihepatic Packing (3) Definitive Procedures : Needed when bleeding persists despite initial control Hepatotomy and selective vascular suture or ligation Hepatorrhaphy Selective hepatic artery ligation Nonanatomical resection (resectional debridement) Anatomical resection Total vascular exclusion Venovenous bypass Atriocaval shunt Definitive Procedures Hepatotomy and selective vascular suture or ligation : Preferred method for major vascular injuries in many centres Under Pringle control, involves finger fracture or Kelly clamp extension of laceration to allow suture or ligation of bleeding vessels Hepatotomy and selective vascular suture or ligation Hepatorrhaphy : One of the earliest techniques Wide placement of large sutures in the parenchyma to compress it and tamponade bleeding vessels Risks parenchymal ischemia and necrosis no longer recommended Hepatorrhaphy Slide 162: Mattress and Buttress Selective hepatic artery ligation : Once widely used but now largely replaced by other methods Persistent arterial bleeding from hepatic wounds was encountered in approximately 10% of severe liver injuries. Compression of the porta hepatis will result in cessation of bleeding in such patients and subsequent ligature of the appropriate lobar artery will provide permanent, safe control of bleeding. Failures of selective hepatic artery ligation commonly result from incomplete diagnosis of the extent of injury to portal veins and hepatic veins. Selective hepatic artery ligation: limitations and failures. Flint LM Jr, Polk HC Jr J Trauma. 1979 May;19(5):319-23. Selective hepatic artery ligation Slide 167: Mass Ligation of Inflow Pedicle Nonanatomical resection : Removal of devitalised parenchyma using the line of injury as the boundary of resection Patient should be haemodynamically stable and does not have coagulopathy Nonanatomical resection Anatomical resection : Involves resection along standard anatomical planes Extensive anatomical resection was associated with very high mortality, also goes against principles of conservative surgery and damage control Rarely practised now, only in 2-4% major liver trauma cases Removes source of bleeding and sepsis especially when a lobe is shattered or presence of proximal ductal injury with devascularisation in which repair will inevitably fail Anatomical resection Total Vascular Exclusion : Involves clamping of portal triad and infra and suprahepatic IVC Requires experience with mobilisation of liver as in liver resection and transplantation Total Vascular Exclusion Major drawback: Caval clamping results in decreased venous return leading to severe hypotension and circulatory collapse in a already hypovolaemic patient Venovenous Bypass : Involves shunting of blood via a vortex pump from common femoral and mesenteric veins to axillary to internal jugular veins Usually limited to units with specialist transplantation experience Venovenous Bypass Atriocaval Shunt : Caval control obtained above and below the liver while venous return from IVC to right atrium maintained Involves opening the chest via median sternotomy and passing a shunt down into IVC via right atrial appendage. Supra and infrahepatic IVC controlled by tapes and Pringle clamp applied Balloon shunts introduced via saphenofemoral junction allows the avoidance of sternotomy Very poor survival figures – “More authors than survivors”! Atriocaval Shunt Liver Transplantation : Transplantation has been reported in a small number of patients with massive liver damage How do we keep the patient alive during the anhepatic phase while waiting for a suitable graft? Venovenous bypass Temporary end-to-side portocaval shunt Remains a limited option due to obvious logistic problems Liver Transplantation Slide 174: Traumatic Haemobilia Traumatic HaemobiliaHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. : Traumatic HaemobiliaHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. Accidental liver injury is the second commonest cause of haemobilia, exceeded only by iatrogenic causes Less than 3% of liver injuries Haemobilia is usually arterial in origin and may occur either acutely after simultaneous perforation of closely approximated intrahepatic bile ducts and blood vessels, or, more commonly, may have a delayed presentation due to gradual erosion of a pseudoaneurysm into a bile duct. Present 4-6 wks post injury [23.5 (range 1–120) days M. V. Forlee 2004] Upper or lower GI bleeding- life threatening with melena (90%) and haematemesis (72%) Colicky abd pain (70%) Jaundice (60%) 100% mortality if untreated Traumatic Haemobilia: InvestigationsHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. : Traumatic Haemobilia: InvestigationsHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. ERCP showed ampulla of Vater in 12–40% of patients with haemobilia USS showed show blood clot or intraluminal echogenic material in the biliary tree or gallbladder Computed tomography can detect common bile duct obstruction, false aneurysms and identify intrahepatic cavities that may require operative debridement. Selective coeliac axis and superior mesenteric angiography the diagnostic procedure of choice when haemobilia cannot be established by gastroduodenoscopy, or when severe gastrointestinal bleeding is life-threatening. Traumatic Haemobilia: TreatmentHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. : Traumatic Haemobilia: TreatmentHaemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Forlee MV. Krige JE. Welman CJ. Beningfield SJ. Injury. 35(1):23-8, 2004 Jan. Hepatic artery embolisation can usually be performed safely if the portal vein is patent and the hepatic artery has not been ligated. Success rates of HAE above 95% and mortality and morbidity rates lower than following surgery have been reported. Complications include ischaemic infarction of normal structures, liver abscess formation, migration of the occluding device, ischaemic cholecystitis and local puncture site complications. Rebleeding may occur in some patients when gelatin sponge or even coils have been used as embolization material because gelatin sponge usually reabsorbs within a few weeks. Surgical operation has a high complication rate. In addition, surgical ligation of the hepatic artery may not be effective in controlling haemobilia as a result of extensive collaterals Slide 178: Haemobilia Blood clot in the gallbladder (arrow). Traumatic false aneurysm of the left hepatic artery (arrow). Post-embolic occlusion of the left hepatic artery with microcoils (arrow). Liver Trauma Summary : Liver Trauma Summary Significant evolvement of management of liver injuries in past two decades Establishment of nonoperative techniques for management of grade IV-V injuries although higher failure rates compared with grade I-III injuries Advancement in new haemostatic transfusion protocol (limited crystalloid, use whole fresh blood, transfuse blood,FFP, platelet at 1:1:1 ratio, use of novo VII, avoidance of lethal triad) addressing acute traumatic coagulopathy for patient at risk of massive blood transfusion. Interventional radiological techniques in those managed nonoperatively or those stabilized with perihepatic packing Liver Trauma Summary : In unstable patients, immediate control of bleeding is crucial Manual compression, Pringle manoevre, perihepatic packing Definite move away from major, time-consuming procedures towards conservative surgery and damage control For inaccessible bleeding within a laceration, rapid finger hepatotomy and direct suture or ligation remains the preferred technique In persistently unstable patients or at first signs of coagulopathy, definitive perihepatic packing should be employed at an early stage Liver Trauma Summary Liver Trauma Summary : Packing is also recommended for the inexperienced surgeon to allow control and stabilization prior to transfer Nonanatomical resection is recommended when there is unviable parenchyma Anatomical resection reserved for devascularised lobe with major ductal injury Hepatorrhaphy, selective arterial ligation, atriocaval shunting are no longer recommended Liver Trauma Summary Liver Trauma Prognosis : Liver Trauma Prognosis Overall mortality 10% for operatively managed liver trauma Grade III/IV injury: 10% Grade V/VI injury > 75% Management of traumatic liver injuries. Br J Surg. 80:86-88 Blunt trauma mortality 27% Vs penetrating trauma mortality 11% S Afr J Surg, 1997, 35 : 10-15. Liver Trauma : Liver Trauma Take Home Message Current massive transfusion protocol and early use of Novo VII that address acute traumatic coagulopathy together with early radiological intervention at high risk group have improve the success of nonoperative management of blunt liver trauma. Patients that are haemodynamically stable with liver trauma alone do not require surgery Hepatic CT that suggests vascular disruption : Angiography Delayed angiography and or embolization are performed in: Hemobilia Bleeding from abdominal drains Pseudoaneurysm or extravasation of contrast in follow-up CT Success rate for non-operative care is high ( > 85% ) Slide 184: Thank you for your attention. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.