Clinical Anesthesia Procedures

Abdominal Aortic Surgery

Infrarenal Aortic Surgery

  1. Abdominal aortic surgery may be required for atherosclerotic occlusive disease or aneurysmal dilation. These processes can involve any portion of the aorta and its major branches and lead to ischemia, rupture, and exsanguination. Ninety-five percent of all abdominal aortic aneurysms (AAAs) occur below the level of the renal arteries. Patients with AAAs more than 5 cm in diameter, especially those shown to be expanding, have a better prognosis if they undergo elective resection. The annual risk of rupture of an expanding 5-cm aneurysm is about 4%. The operative mortality for elective AAA resection is less than 2%, while the overall mortality of aneurysm rupture is 70% to 80%.
  2. Surgical technique. Compared with a transabdominal approach, the retroperitoneal approach may result in a lower incidence of postoperative ileus, pulmonary complications, cardiovascular complications, and fluid shifts. The approach is technically advantageous in morbidly obese patients and in those who have had previous abdominal procedures.
  3. Monitoring. A large peripheral IV (14 gauge), electrocardiogram (ECG) (leads II and V5), a central venous catheter, arterial line, and Foley catheter, in addition to the standard monitoring, are required. PA catheters are used when indicated, as outlined in Chapter 10. Most monitoring catheters (except the Foley) are inserted before induction, and initial baseline values are obtained to guide anesthetic and postoperative management. A central venous catheter can be placed after induction and is usually dictated by the patient's comorbidities. Vasoactive agents (e.g., nitroglycerin and phenylephrine) must be available for every case. Other vasoactive agents should be available based on a patient's comorbid conditions.
  4. Anesthetic technique
    1. General considerations. Most patients receive combined general and epidural anesthesia using a midthoracic epidural catheter. Although general anesthesia alone is acceptable, a combined technique reduces anesthetic requirements, facilitates immediate extubation, and provides for postoperative analgesia.
    2. Induction. The epidural catheter is injected with 2% lidocaine, and a sensory level is confirmed before administration of general anesthesia. Reduced blood pressure associated with the onset of epidural anesthesia is treated with phenylephrine. General anesthesia is induced in a slow and controlled fashion, titrating drugs to the desired hemodynamic and anesthetic effect. Because immediate postoperative extubation is usually planned, high-dose opioid techniques are generally avoided.
    3. Maintenance
      1. Anesthesia is provided primarily by epidural blockade with 2% lidocaine. This is supplemented by nitrous oxide, muscle relaxants, and a low inspired concentration of a volatile anesthetic. A continuous epidural infusion of dilute 0.1% bupivacaine with an opioid (dilaudid or fentanyl) is often started during the procedure.
      2. Heat conservation. Heat loss during aortic procedures may be considerable. Strategies for heat conservation are discussed in Chapter 18. Forced air warmers should never be used below the level of aortic cross-clamp as severe burns may develop on the ischemic tissue.
      3. Bowel manipulation is necessary to gain access to the aorta during a transabdominal approach and may be accompanied by skin flushing, decreased systemic vascular resistance, and profound hypotension. These changes may be caused by release of prostaglandins and vasoactive peptides from the bowel and last for 20 to 30 minutes. Treatment consists of IV phenylephrine, volume expansion, and reducing anesthetic depth.
      4. Fluid management. Intravascular volume is depleted by hemorrhage, insensible losses into the bowel and peritoneal cavity, and evaporative losses associated with large abdominal incisions.
        1. Crystalloid solutions are used for volume replacement at an approximate rate of 5 to 7 mL/kg/hour.
        2. Colloid solutions are rarely necessary and are reserved for patients who are unresponsive or intolerant of large amounts of crystalloid.
        3. Serum hemoglobin should be maintained above the 9-g/dL range. With blood losses greater than 2,000 mL, coagulation profiles should be monitored and platelets, clotting factors, and calcium replaced, guided by laboratory evaluation.
        4. Autotransfusion devices should be used intraoperatively to scavenge shed blood. Autotransfused blood is deficient in plasma, clotting factors, and platelets.
      5. Aortic cross-clamping
        1. Heparin (5,000 units IV) is given several minutes before applying an aortic cross-clamp.
        2. Increased afterload following aortic cross-clamping is well tolerated by patients with normal hearts. Those with compromised left ventricular function may exhibit a decreased cardiac output and/or myocardial ischemia. The use of nitroglycerin or, rarely, nitroprusside may improve myocardial oxygen supply–demand balance.
      6. Renal preservation. The incidence of renal failure is 1% to 2% for infrarenal aortic surgery. Preoperative angiographic dye studies and preexisting renal disease increase this risk. Patients with chronically elevated creatinine levels (>2 mg/dL) have substantially greater morbidity and mortality after vascular surgery. Renal cortical blood flow and urine output may decrease with infrarenal aortic cross-clamping, possibly because of circulatory derangements, effects on the renin–angiotensin system, and microembolization. Maintenance of adequate hydration and urine flow is extremely important. If the urine output falls in spite of adequate hydration, IV mannitol, furosemide, or fenoldopam (3 µg/kg/minute) may be given.
      7. Aortic unclamping. Intravascular volume must be maintained in the normal to slightly hypervolemic range, anticipating a fall in systemic vascular resistance and venous return after release of the aortic cross-clamp. Volume loading, decreasing anesthetic depth, discontinuing vasodilators, infusing a vasopressor, and a slow, controlled release of the aortic cross-clamp will minimize hypotension. Reperfusion of the lower extremities, resulting in the washout of anaerobic products and systemic acidosis, may produce a negative inotropic effect, which is related to the duration of the cross-clamp time and the degree of collateral flow. Sodium bicarbonate administration is rarely necessary. Minute ventilation can be adjusted to allow for more CO2 elimination if deemed necessary.
      8. Emergence. Most patients are extubated at the end of the procedure. Patients with unstable cardiac or pulmonary function, ongoing bleeding, or severe hypothermia (<33°C) are left intubated. Hypertension, tachycardia, pain, and shivering should be anticipated and treated.
      9. Transport. All patients should receive supplemental oxygen and continuous monitoring of blood pressure and ECG.

Suprarenal Abdominal Aortic Surgery

The surgical procedure may involve cross-clamping of the aorta at various levels above the renal arteries. Anesthetic considerations are similar to those for infrarenal aortic surgery (see section V.A), with the following caveats:

  1. PA catheters are used more frequently.
  2. Blood loss is potentially greater.
  3. Renal perfusion is at greater risk because of longer cross-clamp times and potential for cholesterol embolization.
  4. Cross-clamping above the celiac and superior mesenteric arteries can produce visceral ischemia and profound acidosis. In these cases, sodium bicarbonate is given routinely during the cross-clamping before opening.
  5. IV mannitol and fenoldopam are administered before cross-clamping with the aim of minimizing ischemic renal injury.

Renal Artery Surgery

Renal artery stenoses or aneurysms are repaired with a variety of techniques. Aortorenal bypass and transaortic endarterectomy require aortic cross-clamping; hepatorenal (right) and splenorenal (left) bypass procedures avoid cross-clamping. The anesthetic considerations are the same as for abdominal aortic surgery (see section V.A). Postoperative concerns include ongoing hypertension and deterioration in renal function.

Endovascular Abdominal Aneurysm Repair (EVR)(Fig. 22.1)

Endovascular graft repair of an infrarenal AAA.

(From Kaufman JA, Geller SC, Brewster DC, et al. Endovascular repair of abdominal aortic aneurysm: current status and future directions. Am J Roentgenol 2000;175:289–302, reprinted with permission.)

  1. EVR of an AAA or thoracoabdominal aortic aneurysm (TAA) involves deployment of an expandable, prosthetic graft within the lumen of the aneurysm, thus excluding the aneurysm from the circulation and reducing the risk of its rupture. The graft is typically deployed, under fluoroscopic guidance, from sheaths placed in the femoral arteries via cutdown arteriotomies. Compared with conventional AAA repair, EVR involves less blood loss and a lower incidence of perioperative morbidity, including pulmonary, cardiovascular, and renal complications. The use of EVR has resulted in fewer postoperative intensive care unit admissions, earlier ambulation, and shorter hospital stays and may lower perioperative mortality.
  2. Patient selection and stent graft sizing depend on detailed preoperative imaging. Up to 60% of patients with known infrarenal AAAs may be amenable to EVR.
  3. Monitoring. In addition to standard monitors (Chapter 10), a large peripheral IV (14 to 16 gauge), arterial catheter, and Foley catheter are used. Conversion to an open procedure is relatively rare, but each case should be set up for the possibility of an emergent AAA repair (see below).
  4. Anesthetic technique. Most patients receive an epidural or combined spinal and epidural anesthetic. IV sedation with propofol and/or benzodiazepines and short-acting narcotics is titrated to patient comfort.
  5. Complications of EVR include failure to exclude the AAA from the arterial system (endoleak), embolism, arterial injury, graft kinking, limb ischemia, and infection. Patients with impaired renal function are at risk for CIN, and both N-acetylcysteine and sodium bicarbonate infusion are given routinely.

Emergency Abdominal Aortic Surgery

Patients present with a wide spectrum of signs and symptoms and can be divided into two groups:

  1. The hemodynamically stable patient with an expanding contained rupture has the same anesthetic considerations as described above (see section V.A), but the preoperative preparation must proceed expeditiously.
    1. Foley catheter and nasogastric tube insertion should be delayed until after induction, to avoid Valsalva maneuvers (or hypertension) that may aggravate bleeding or cause frank rupture. Placement of a central venous pressure or PA line is often undertaken while the patient is awake.
    2. Induction proceeds after preoxygenation, using placement of cricoid pressure and careful titration of hypnotic agents, opioids, and muscle relaxants. Hypertension must be avoided and anesthesia may be supplemented with vasoactive drugs.
  2. The hemodynamically unstable patient (ruptured aneurysm) requires resuscitative measures. Mortality can be limited by restoration of intravascular volume, judicious use of vasoconstrictors, and rapid surgical control. Under the best of situations, there is a 40% to 50% mortality, usually resulting from the physiologic consequences of hypotension and massive blood transfusion. The incidence of MI, acute renal failure, respiratory failure, and coagulopathy is high.
    1. General considerations
      1. Large-bore IV access is paramount.
      2. Blood samples should be sent immediately for cross-matching and any other pertinent laboratory studies. Blood components should be ordered immediately, but universal donor-type blood (type O-negative in women of childbearing age and type O-positive in all others) and FFP (type AB) should be obtained if type-specific blood and FFP are unavailable. Colloid solutions should be available. The autotransfusion team should be notified and equipment set up.
    2. Surgical technique. The immediate surgical priority will be to control bleeding by cross-clamping the aorta in the chest or abdomen.
    3. Monitoring. Minimum monitoring standards (see Chapter 10) should be applied during the initial volume resuscitation, followed by placement of invasive monitors as time and hemodynamics permit. Placement of monitors and fluid resuscitation should not delay definitive surgical control of a rupture in an unstable patient. Coordination of the patient care priorities should be accomplished by direct communication between the surgical and anesthesia team.
    4. Anesthetic technique
      1. Induction
        1. In moribund patients, endotracheal intubation should be performed immediately.
        2. In hypotensive patients, a rapid careful induction is indicated, but the patient may be able to tolerate only small doses of scopolamine, ketamine, etomidate, and/or a benzodiazepine and a relaxant.
      2. Maintenance
        1. Once the aorta has been clamped to control bleeding, resuscitative efforts should continue until hemodynamic stability is achieved. Incremental doses of opioid and supplemental anesthetics are given as tolerated.
        2. Blood products (including FFP and platelets) are administered when available. Serial laboratory studies should guide further management. Fluid warmers capable of infusing large volumes should be available.
        3. Hypothermia is common and contributes to the acidosis, coagulopathy, and myocardial dysfunction that complicate aortic aneurysm repair. Methods of heat conservation and warming are discussed in 18.
        4. To prevent renal failure, aggressive efforts should be made to preserve urine output with volume replacement, mannitol, and fenoldopam. Mortality in patients developing renal failure following a ruptured AAA is high.
      3. Emergence. Large fluid shifts; hypothermia; and acid-base, electrolyte, and coagulation abnormalities make the immediate postoperative period complex. Most patients remain intubated and mechanically ventilated at the end of the procedure and transported to the ICU for postoperative care.


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