Injuries to major abdominal vessels are uncommon but highly lethal vascular crises. Predictably, exsanguinating hemorrhage is the most important cause of early death. Intra-abdominal vascular injuries are associated with extremely rapid rates of blood loss and pose challenges of exposure during celiotomy,[1, 2, 3] given the posterior position of the major abdominal vascular structures (except for the portal vein and the hepatic artery).
Essential to the successful management of these injuries is a thorough knowledge of intra-abdominal vascular anatomy and a familiarity with the techniques of proximal and distal control combined with selective application of primary repair, bypass, or ligation as indicated.
See the following for more information:
The following anatomic locations should be distinguished:
In blunt trauma, rapid deceleration during a motor vehicle accident (MVA) results in an avulsion of the small branches of major vessels (eg, mesenteric tear). Another mechanism of injury is related to a direct crush or blow to the major vessels, resulting in an intimal tear with thrombosis or vessel rupture and hemorrhage.
Penetrating injuries directly disrupt the vessel wall or create intimal flaps secondary to the blast effect. Because of the anatomical position of the major vascular structures in the abdomen, injuries to these vessels have a high probability of association with other major injuries in the abdomen, particularly to the small bowel.
Hemorrhagic shock from intra-abdominal hemorrhage often leads to metabolic acidosis accompanied by coagulopathy and hypothermia—the so-called lethal triad of trauma. The use of systolic blood pressure at any predefined cutoff value when considered out of context with other potential indicators of shock is neither particularly specific, nor sufficiently sensitive, to be useful clinically for the diagnosis of shock. In contrast, the shock index (ie, heart rate divided by systolic blood pressure) may suggest compensated shock when either heart rate or blood pressure considered separately do not. Metabolic acidosis in trauma patients is the result of lactate overproduction, most often from decreased oxygen delivery as a result of hypovolemic shock.
Acidosis adds to the overall lethality of preexisting injury primarily by depression of myocardial contractility and by impairment of coagulation. Furthermore, hypothermia (below 34°C) inhibits platelet function and slows coagulation factor activation. This self-perpetuating cycle is responsible for 80% of deaths in patients with major vascular injury and must be rapidly corrected to prevent a dismal outcome.
Patients also present in a hyperfibrinolytic state, which exacerbates the coagulopathy associated with the lethal triad of trauma.[4]
The incidence of abdominal vascular injuries in military conflicts is surprisingly low: generally less than 5% of all vascular injuries. In contrast, approximately 30% of all vascular injuries observed in civilians occur in the abdomen. This striking difference between combat and noncombat vascular trauma can be attributed to the low energy of missiles from civilian handguns and the short prehospital transit times in urban settings, which make it more likely that a civilian with penetrating abdominal vascular injury will survive long enough to reach surgical care.
The incidence of abdominal vessel injury in patients with blunt trauma is estimated at approximately 5-10%. A similar incidence of 10.3% is reported in patients with penetrating stab wounds to the abdomen. Patients with gunshot wounds (GSWs) to the abdomen will have major vessel injury in 20-25% of cases.
Mortality rates for abdominal vascular trauma vary depending on the vessel or vessels injured, as follows:
Clinical data obtained from emergency medical services (EMS) can be crucial and may be the only patient information available. In inner city hospitals, GSWs and stab wounds predominate. Mechanism of injury, vital signs at the scene of the accident, and transit time are essential data. The amount of intravenous (IV) fluid the patient received in the field and during transport should also be elicited from EMS. Penetrating trauma to the chest below the nipple line should also be considered as penetrating trauma to the abdomen.
Patients without recorded vital signs at the scene of injury and blunt trauma victims without vital signs at the time of arrival in the emergency department (ED) rarely survive after resuscitation, with or without ED thoracotomy.
Hemodynamically unstable patients with positive results, including pericardial effusion, on focused assessment with sonography for trauma (FAST) or diagnostic peritoneal lavage (DPL) require surgery.
Hemodynamically stable blunt trauma patients who have peritoneal signs or positive computed tomography (CT) findings require exploration.
Hemodynamically unstable patients should be transported immediately to the operating room (OR) if the airway is secure and ventilation is adequate, preferably within 5 minutes of arrival in the ED.
Stable patients with posterior wounds and most patients with anterior stab wounds should be evaluated with triple-contrast (eg, oral, IV, rectal) CT scanning, diagnostic laparoscopy to exclude peritoneal penetration, and/or FAST examination to exclude hemoperitoneum. Patients with GSWs to the abdomen require celiotomy for evaluation and treatment, although some trauma surgeons prefer selective nonoperative evaluation of abdominal GSWs in stable patients.[5]
Early complications of abdominal vascular injuries include ongoing bleeding, coagulopathy, and abdominal compartment syndrome. Late complications include, but are not limited to, intra-abdominal infections, wound dehiscence, acute respiratory distress syndrome (ARDS), and pneumonia.
Hemodynamically unstable patients with penetrating trauma should be transported immediately to the operating room (OR); no imaging studies are necessary.
The assessment of hemodynamically unstable patients with blunt trauma to the abdomen may include focused assessment with sonography for trauma (FAST) or diagnostic peritoneal lavage (DPL) to confirm hemoperitoneum as well as portable chest radiography only if expeditious transport to the OR is not to be interrupted.
Abdominal exploration is indicated in essentially all patients with a GSW to the abdomen.
Stable patients with stab wounds may undergo laparoscopy to confirm peritoneal penetration. If time permits, chest and pelvic radiography may be beneficial to exclude bleeding into the chest and pelvic fracture.
Hemodynamically stable patients with blunt trauma and suspected abdominal vascular injuries may benefit from abdominal computed tomography (CT) scanning, which helps localize a hematoma and evaluate solid organ injuries.[6, 7, 8, 9, 10]
A retrospective study by Benjamin et al suggested that negative CT finding for an asymptomatic patient after blunt abdominal trauma is sufficient to exclude major intra-abdominal injury.[11, 12]
Angiography with or without embolization may be considered in stable patients, particularly in patients with blunt trauma.
Also see Focused Assessment with Sonography in Trauma (FAST).
Once exposure and proximal and distal control have been obtained, all abdominal vascular injuries should be graded according to the American Association for the Surgery of Trauma Organ Injury Scale (AAST-OIS) for vascular injuries (see the table below).
Table 1. American Association for the Surgery of Trauma Organ Injury Scale for Vascular Injuries
View Table | See Table |
Essential to the successful management of these injuries is a thorough knowledge of intra-abdominal vascular anatomy and a familiarity with the techniques of proximal and distal control combined with selective application of primary repair, bypass, or ligation as indicated.
In the treatment of ruptured abdominal aortic aneurysm, Kimball et al conducted a retrospective study comparing standard primary abdominal closure with the initial use of the open abdomen using the vacuum-pack technique followed by delayed abdominal closure.[13] The investigators identified 3 ischemia-reperfusion criteria that predicted mortality and which were also useful as surrogate clinical markers for abdominal compartment syndrome: preoperative hypotension, estimated blood loss of 6 L or greater, or intraoperative resuscitation with 12 L or more.
Patients who had at least 1 of the 3 ischemia-reperfusion criteria had higher in-hospital mortality (43% vs 10%).[13] Of those who had at least 1 criterion, the initial 24-hour mortality as well as the 30-day mortality was higher in those in the primarily closed abdomen group relative to those in the 47% open abdomen group.
In a hypothermic traumatic shock swine model, Ding et al demonstrated that temporary intravascular shunts may improve survival in superior mesenteric artery (SMA) injuries compared with repair by primary vascular anastomosis.[14] Relative to pigs in the primary vascular anastomosis group, the animals treated with temporary shunting required less resuscitation fluid, retained higher superior mesenteric artery flow rates, normalized lactate levels faster, suffered less severe intestine histopathology, and had greater early survival.[14]
Although the investigators caution that further research is needed, they believe that in the setting of superior mesenteric artery transection, temporary intravascular shunts show promise for better management of damage control surgery than primary vascular anastomosis.
See the following for more information:
Initial resuscitation of a patient with abdominal vascular injuries depends on his or her condition at arrival in the emergency department (ED). Insert multiple large-bore catheters into the upper extremities, or, if necessary, obtain central venous access for rapid infusion of warm isotonic fluid. Because a possibility of intra-abdominal venous injury exists, lower extremity venous access is not recommended. Massive transfusion by protocol may be required for patients presenting with a shock index of greater than 0.9 or those that fail to respond to initial crystalloid resuscitation.[15, 16]
In the agonal patient with a distended abdomen suggesting major intraperitoneal bleeding, ED thoracotomy with cross-clamping of the descending aorta may be necessary. This is usually associated with a poor prognosis and low survival rates.
Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a minimally invasive alternative to resuscitative thoracotomy that seems to show promise for the patient in extremis.[17] After femoral artery access is obtained, the balloon catheter is advanced and inflated to achieve proximal occlusion of the aorta.
Perform blood replacement during resuscitation with type-specific blood if time permits receiving this blood in the ED. If time does not permit, use O-negative blood (or O-positive blood for males), which should be immediately available in the ED. Centers that potentially receive patients with these types of injuries should have in place massive transfusion protocols that direct administration of blood components (red blood cells, fresh frozen plasma, platelets) in a fixed ratio (eg, 1:1:1) or by point-of-care coagulation testing with viscoelastic technology. Start efforts to limit hypothermia as soon as the patient arrives. Ensure that prewarmed fluids, high-flow blood warmers, and prewarmed blankets are available.
Place the patient on a warming blanket, and make every effort to reduce heat loss. Drape the patient to expose chest and both thighs in the event that a thoracotomy or vein harvest is required. Perform a generous midline incision from the xiphoid to well below the umbilicus, which can be extended to the pubis if needed to improve exposure. Aggressively administer blood replacement therapy. A radial arterial line may be helpful for monitoring blood pressure and arterial blood gases.
Enter the peritoneal cavity through a midline incision. Quickly evacuate blood and clots and perform 4-quadrant packing. After initial stabilization, systematically remove the packing and evaluate the injuries. Injuries to major abdominal vessels can be grouped into 5 regions, as follows.
Midline supramesocolic hemorrhage or hematoma (superior to the transverse mesocolon) is usually from an injury to the suprarenal aorta, celiac axis, proximal SMA, or proximal renal artery. Use aortic compression to obtain proximal aortic control at the hiatus. Once aortic control is achieved, gain direct access to the vessels through retroperitoneal mobilization and medial rotation of all left-side abdominal viscera (the Mattox maneuver) or an extensive Kocher maneuver on the right side. An injured celiac axis may be safely ligated in critical situations.
View Video | Mattox Maneuver Motion Graphic Simulation. By Matthew Bacchetta, ColumbiaDoctors, New York, NY. Video courtesy of ColumbiaDoctors. https://www.columbiadoctors.org/ |
Access to the SMA and the superior mesenteric vein (SMV) may require transection of the pancreas. Primary repair of this major vessel is usually the first choice; however, ligation, particularly of the venous structures, may be a better option. Significant venous congestion can compromise viability of the bowel.
Midline inframesocolic hemorrhage or hematoma results from infrarenal aortic or inferior vena cava (IVC) injury.
Obtain exposure by incising the posterior peritoneum in the midline after evisceration of the small bowel and cephalic retraction of the transverse mesocolon, or divide the white line of Toldt adjacent to the cecum and extend cephalad through the hepatic flexure, then rotate the right colon and small bowel medially (the Cattel-Braasch maneuver). Place an aortic clamp just below the left renal vein, and apply a distal clamp near the aortic bifurcation. Repair the injury primarily.
If the aorta is intact, suspect injury to the IVC, and obtain access to the infrahepatic IVC by mobilizing the right colon and duodenum. Preferably, repair anterior injuries in a transverse fashion. Posterior injuries can be repaired from inside the IVC. Both approaches require proximal and distal control of the vessel. Apply a Satinsky clamp or Judd Alyce clamp to the injury. Large IVC defects may be repaired by using a autologous vein, synthetic, or peritoneal patch. Ligation of the suprarenal IVC will lead to renal failure and should be avoided. However, in patients with multiple injuries and exsanguinating hemorrhage, ligation of the infrarenal IVC may be indicated.
Lateral perirenal hematoma or hemorrhage suggests injury to the renal vessels or kidneys. Exploration after blunt trauma is not necessary in patients with a negative result on abdominal computed tomography (CT) scanning, preoperative intravenous pyelography (IVP), or arteriography or if the hematoma is not expanding.
Penetrating injury usually indicates a necessity for exploration. Obtain vascular control of the ipsilateral renal artery. Expose the kidney and clamp the renal vessels if active bleeding from the kidney or expanding retroperitoneal hematoma is present. Only 30-40% of kidneys with arterial injuries can be salvaged. Before performing a nephrectomy, assess the viability of the contralateral kidney.
Lateral pelvic hematoma or hemorrhage suggests injury to the iliac artery, the iliac vein, or both. Obtain vascular control at the aortic bifurcation proximally and close to the inguinal ligament distally. If an injury to the right common iliac vein is present, it may require a division of the overlying right common iliac artery. For best visualization of the internal iliac artery, elevate the common and external iliac arteries on vascular tapes. Repair injuries to the common or external iliac arteries. Treat injuries to the iliac veins with lateral venorrhaphy or ligation.
Once initial control of the hemorrhage is completed and gross contamination is controlled, terminate the procedure, and transfer the patient to the recovery room for further resuscitation. Measurement of abdominal compartment pressure may be needed.
Hepatoduodenal ligament hematoma suggests injury to the portal vein, the hepatic artery, or both. Obtain vascular control by clamping the porta hepatis with vascular clamps proximal and distal to the injury (the double-Pringle maneuver).
Portal vein ligation may be required to manage portal vein injuries expeditiously if the patient is exsanguinating, though primary repair may be attempted. Hepatic artery injuries are generally managed by ligation. If portal vein inflow is compromised, the liver should be assessed for ischemia, and restoration of hepatic arterial inflow or resectional debridement of the ischemic section should be undertaken or staged.
Patients may require aggressive resuscitation involving the correction of acidosis, active rewarming, and massive blood transfusion (>10 U of blood within 24 h). Fresh frozen plasma, platelets, cryoprecipitate, or prothrombin complex concentrate may be required on an individual basis to correct coagulopathy induced by massive transfusion. In addition, aminocaproic acid or tranexamic acid may be given as inhibitors of trauma-associated hyperfibrinolysis if used early. A planned reoperation 24-48 hours after the initial procedure is done to complete a damage control sequence.
The most important aspects of medical therapy for patients with vascular injuries are adequate oxygen delivery and crystalloid fluid administration. Although colloid solution is mentioned, the mortality benefit of colloid over crystalloid has never been proven. Blood transfusion may also be beneficial for patients with low hemoglobin concentrations.
Clinical Context: NS restores interstitial and intravascular volume. It is used in initial volume resuscitation.
Clinical Context: LR restores interstitial and intravascular volume. It is used in initial volume resuscitation.
Isotonic sodium chloride (normal saline [NS]) and lactated Ringer (LR) are isotonic crystalloids, the standard intravenous (IV) fluids used for initial volume resuscitation. They expand the intravascular and interstitial fluid spaces. Typically, about 30% of administered isotonic fluid stays intravascular; therefore, large quantities may be required to maintain adequate circulating volume.
Both fluids are isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with the administration of large quantities of either fluid, for practical purposes and in most situations, the differences are clinically irrelevant. No demonstrable difference in hemodynamic effect, morbidity, or mortality exists between resuscitation with NS or LR.
Clinical Context: Albumin is used for certain types of shock or impending shock. It is useful for plasma volume expansion and maintenance of cardiac output. A solution of NS and 5% albumin is available for volume resuscitation. Five percent solutions are indicated to expand plasma volume, whereas 25% solutions are indicated to raise oncotic pressure.
Colloids are used to provide oncotic expansion of plasma volume. They expand plasma volume to a greater degree than isotonic crystalloids and reduce the tendency of pulmonary and cerebral edema. About 50% of the administered colloid stays intravascular.
OIS
Grade*Artery Injured Vein Injured II Hepatic
Splenic
Gastric
Gastroduodenal
Inferior mesenteric
Primary named vessels of superior mesentericSplenic
Inferior mesentericIII Renal
Iliac
HypogastricSuperior mesenteric
Renal
Iliac
Hypogastric
Vena cava (infrarenal)IV Superior mesenteric (trunk)
Celiac axis
Aorta (infrarenal)Vena cava (infrahepatic) V Aorta (suprarenal) Vena cava (suprahepatic)
Vena cava (retrohepatic)
Portal
Hepatic (extrahepatic)* Grade I injury includes the following: No named superior mesenteric artery or superior mesenteric vein branches; nonnamed inferior mesenteric artery or inferior mesenteric vein branches; phrenic artery/vein; lumbar artery/vein; gonadal artery/vein; ovarian artery/vein; other nonnamed small arterial or venous structures requiring ligation.