Abdominal Major Vascular Injury, Anesthesia for
Synonyms
Definition
The abdominal major vascular injuries are usually caused by penetrating abdominal traumas, gunshot wounds, or stab wounds. The blunt abdominal trauma may also cause major vascular injuries by rapid deceleration mechanism, direct anteroposterior crushing, or direct laceration. In a prospective study of vascular abdominal trauma caused by gunshot injuries in 217 patients who underwent exploratory laparotomy, the incidence of vascular trauma was 14.3 % (Demetriades et al. 1997). The incidence of vascular injuries in patients undergoing laparotomy for stab wounds was 10 % (Feliciano et al. 2000). In a review of 302 abdominal vascular injuries, the most commonly injured abdominal vessel was the inferior vena cava (accounted for 25 % of injuries), followed by aorta (21 %), the iliac arteries (20 %), the iliac veins (17 %), the superior mesenteric vein (11 %), and the superior mesenteric artery (10 %) (Asensio et al. 2000).
Preexisting Conditions
Retroperitoneal vascular zones
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Zone 1 (upper, central box) is the upper midline retroperitoneum, from the aortic hiatus to the aortic bifurcation longitudinally and laterally from renal hilum to renal hilum. This zone is subdivided into supramesocolic and inframesocolic regions. It contains the midline vessels, the aorta, the celiac artery, the superior and inferior mesenteric arteries and veins, the renal arteries and veins, as well as the inferior vena cava.
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Zone 2 (upper left and right boxes) is the lateral perinephric area, encompassing the upper lateral retroperitoneum from the renal hilum laterally. It contains the renal vessels.
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Zone 3 (lower box) is the pelvic retroperitoneum from the aortic bifurcation inferiorly. It contains the iliac vessels.
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Zone 4 is the perihepatic area, which contains the hepatic artery and veins, the portal vein, and the retrohepatic inferior vena cava.
Anatomic Location of Hemorrhage
Midline supramesocolic hemorrhage or hematoma (superior to the transverse mesocolon) is usually caused by injury to the suprarenal aorta, the celiac axis, the proximal superior mesenteric artery, or the proximal renal artery. Midline inframesocolic hemorrhage or hematoma results from infrarenal aorta or inferior vena cava injury. Lateral perirenal hematoma or hemorrhage suggests injury to the renal vessels or kidneys. Lateral pelvic hematoma or hemorrhage indicates injury to the iliac artery, the iliac vein, or both. Hepatoduodenal ligament hematoma or hemorrhage indicates injury to the portal vein, the hepatic artery, or both. Injury of the aorta above or involving superior mesenteric artery will produce abdominal pain, pararenal involvement may lead to hematuria, or injury to the infrarenal aorta may manifest as unilateral or bilateral lower extremity ischemia.
Resuscitation
Patients sustaining major vascular injury usually present with severe physiologic derangements due to hemorrhage, tissue hypoxia, and the sequelae of anaerobic metabolism. Severe hemorrhage may lead to “lethal triad” of trauma: hypothermia, coagulopathy, and acidosis. Patients require massive transfusion, generally defined as requiring greater than twenty units of packed red blood cells (PRBCs) within 24 h or more than 4–5 units within an hour. Many current prehospital resuscitation protocols recommend insertion of peripheral intravenous lines and resuscitation with isotonic crystalloid solution as soon as possible following trauma. On arrival to the emergency department the patient should have inserted a minimum of two large caliber intravenous lines (if not already placed in prehospital setting) and an arterial line inserted in the upper extremities. If adequate peripheral intravenous access is not possible to obtain, central line should be inserted at thoracic inlet (internal jugular or subclavian veins). The access site should be above the diaphragm in any patient with possibility of abdominal or pelvic bleeding. At the time of line insertion, blood should be drawn for type and crossmatch, arterial blood gas, and laboratory studies (CBC, chemistry, and coagulation). Blood bank should be contacted and massive transfusion protocol should be activated. Monitoring used during the resuscitation phase includes electrocardiography, blood pressure monitoring, pulse oximetry, and capnography in intubated patient. Placement of urinary and nasogastric catheters is also considered part of the resuscitation phase. Diagnostic testing, radiologic examination, and essential laboratory tests should not delay patient’s resuscitation and transfer to the operating room as indicated.
Trauma room preparation should include setting up all equipment necessary for the management of major trauma: rapid transfusion device, fluid warmers, autologous cell saver device, difficult intubation cart, equipment necessary for the placement of invasive monitors, and infusion pumps as necessary. The operating room environment should be maintained as warm as possible, and the infused fluid should be prewarmed to 40–42 °C. Blood and blood products should be immediately available in the operating room. If patient is hemodynamically unstable and crossmatched blood is not available, blood transfusion should be initiated with uncrossmatched blood (O Rh negative PRBC). If uncrossmatched blood transfusion was initiated, transfusion should be converted to type-specific blood as soon as that one becomes available. Serial measurement of hematocrit, ionized calcium, and coagulation parameters is necessary for guiding transfusion of blood products (PRBC, fresh frozen plasma, platelets, and cryoprecipitate).
Application
Anesthetic Management
Monitoring
Besides the American Society of Anesthesiologists standard monitoring, invasive monitoring is necessary for abdominal major vascular injury cases: arterial line, central venous pressure, and potentially transesophageal echocardiography. Arterial line is important for hemodynamic management on induction and during maintenance of anesthesia and should be placed prior to induction of anesthesia.
Induction of Anesthesia
These patients are considered “full stomach” with high risk of aspiration. An adequate preoxygenation, rapid sequence induction and intubation with cricoid pressure, and in-line stabilization of cervical spine are recommended approaches for the endotracheal tube placement. Airway management may take place in the emergency department or the operating room (if not already performed in the prehospital setting). Capnography is the most reliable method for confirmation of endotracheal tube placement.
Etomidate and ketamine are the preferred induction agents in hypotensive patients with major abdominal vascular injury. Etomidate (0.1–0.2 mg/kg) has the advantage of inducing less hemodynamic changes in comparison to other induction agents. Ketamine (0.25–1.0 mg/kg) may cause hypertension and tachycardia from endogenous catecholamine release, which may be advantageous in patients with hemorrhagic shock. It is important to recognize that both induction agents can cause hypotension and decrease in cardiac output in trauma patients; thus, conventional dosages should be reduced. Succinylcholine (1.0–1.5 mg/kg) is a neuromuscular blocker of choice for rapid sequence induction, due to its rapid onset (less than 1 min) and short duration (5–10 min). If succinylcholine is contraindicated, rocuronium (1.0–1.2 mg/kg) is recommended neuromuscular-blocking agent for rapid sequence induction. Cricoid pressure should be applied throughout induction and attempts at intubation. However, cricoid pressure can be released to ease intubation or insertion of laryngeal mask airway if necessary. Waking up the patient is not the choice in patient with abdominal vascular injury, and trauma team should be ready to rapidly proceed with invasive airway in the case of unsuccessful intubation and “cannot intubate, cannot ventilate” scenario.
The patients with major abdominal vascular injury have high abdominal pressure from hemoperitoneum. Thus, patient’s abdomen and thorax should be “prepped and draped” before the induction of anesthesia because the latter is often associated with rapid hemodynamic decompensation in this patient group. After rapid sequence induction and intubation, a rapid midline incision is made to enter the abdomen. Intraperitoneal blood is evacuated and abdomen is rapidly packed in all four quadrants with laparotomy pads. The surgery is then temporarily suspended to allow anesthesia team to catch up with the patient’s resuscitation as needed. Once the patient is sufficiently hemodynamically stable, a systemic exploration of the entire abdomen is accomplished. Proximal and distal control should be obtained for any vascular injury.
Maintenance of Anesthesia
It is often very challenging to meet all objectives of anesthetic maintenance and to provide adequate depth of general anesthesia in a hemodynamically unstable patient such as a patient with major abdominal vascular injury. General anesthesia is usually maintained with a combination of volatile agent, benzodiazepines, and narcotics. Isoflurane, sevoflurane, and desflurane all decrease arterial blood pressure through reduction in systemic vascular resistance. Thus, in hypotensive bleeding patient, minimum alveolar concentration (MAC) of volatile agent must be decreased, and the anesthetic agent titrated to maintain minimum necessary blood pressure and adequate tissue perfusion. MAC of 0.3–0.5 is often used in addition to midazolam to prevent recall of intraoperative events. Small boluses of midazolam may be administered repeatedly throughout the surgery to assure amnesia. Fentanyl is another adjuvant anesthetic and is usually administered in increments throughout the procedure. However, fentanyl alone does not guarantee amnesia.
Aortic Cross-Clamping and Unclamping
Temporary clamping of the abdominal aorta may be required during the surgery for abdominal major vascular injuries, and adequate preparation is essential to prevent severe hemodynamic changes and decompensation. Application of aortic cross-clamp results in a sudden increase in afterload and systemic blood pressure. Increased afterload results in increased left ventricular end-systolic wall stress. These changes are accompanied with decrease in cardiac output. A sudden increase in afterload can lead to left ventricular failure, especially in patients with noncompliant left ventricle. All these changes are more profound in the case of a supraceliac cross-clamp placement. The addition of inotrope may be necessary in the case of left ventricular failure. After the removal of aortic cross-clamp, systemic vascular resistance and arterial blood pressure decrease dramatically, as a result of peripheral vasodilation. Vasodilation can become systemic as the lactic acid is washed out of the extremities into central circulation. In order to minimize hypotensive response, volume loading prior to cross-clamp release is necessary to raise filling pressures to slightly above normal. Acidosis should be corrected and calcium replaced immediately after the removal of aortic cross-clamp (Gelman 1995). The patient may require temporary pharmacologic support to achieve an acceptable blood pressure. Ephedrine, an indirect alpha- and beta-receptor-stimulating agent can be used. Other options include appropriate dosing of direct alpha- and beta-receptor agonists such as epinephrine, norepinephrine, and dopamine. Phenylephrine, a pure alpha1 receptor agonist, can be also used to increase patient’s blood pressure. However, phenylephrine has not been shown to improve end-organ perfusion and may result in end-organ ischemia, especially bowel ischemia, in hypovolemic patients (Thiele et al. 2011). Transesophageal echocardiography can be useful in differentiating between myocardial ischemia and cardiac failure versus continuous hemorrhage and consequent hypovolemia. Myocardial ischemia or cardiac failure results in elevated filling pressures, while hemorrhage results in low filling pressures.
Damage Control Surgery (DCS)
DCS refers to a limited surgical procedure or set of procedures with very discrete, life-saving goals and the intent to defer more definitive repair until resuscitation has occurred (Sagraves et al. 2006). The basic principles of DCS include rapid surgical control of bleeding, control of sources of contamination, and deferral of definitive procedure until patient is more stable. Patients with major abdominal vascular injuries may benefit from early damage control and definitive reconstruction at a later stage after resuscitation and stabilization in the ICU. Damage control approach should be considered before the patient becomes severely hypotensive and coagulopathic. With the damage control approach, any large vessel bleeding should be surgically controlled and repaired in an expeditious fashion. Any source of contamination, such as injury of gastrointestinal tract, should be controlled as well. If possible, vascular continuity should be restored by either expeditious definitive repair or temporizing measure such as vascular shunt. The abdomen is closed temporarily with vacuum dressing techniques in order to prevent abdominal compartment syndrome. The damage control strategy has been shown to lead to better than expected survival rates for abdominal trauma.
Abdominal Compartment Syndrome (ACS)
All patients with severe abdominal trauma, especially vascular trauma, are at risk of developing ACS. Major risk factors include massive blood transfusion, prolonged hypotension, hypothermia, aortic cross-clamping, damage control procedures, and tight closure of abdominal wall. ACS is characterized by a tense abdomen, tachycardia with or without hypotension, respiratory dysfunction with high peak inspiratory pressure in mechanically ventilated patients, and oliguria. After damage control procedures, the abdominal wall should never be closed under tension because postoperative bowel edema results in ACS in most patients. When the bowel edema improves, usually within 2–3 days, the patient is returned to the operating room for definitive vascular repair and abdominal wall closure. Knowledge of ACS is important, and necessary measures for prevention of this complication should be undertaken whenever possible.
Cross-References
References
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- Demetriades D, Velmahos G, Cornwell EE et al (1997) Selective nonoperative management of gunshot wounds of the anterior abdomen. Arch Surg 132:178–183PubMedCrossRefGoogle Scholar
- Feliciano DV, Burch JM, Graham JM (2000) Abdominal vascular injury. In: Mattox KL, Feliciano DV, Moore EE (eds) Trauma, 4th edn. McGraw-Hill, New York, pp 783–806Google Scholar
- Gelman S (1995) The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 82:1026–1060PubMedCrossRefGoogle Scholar
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