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Basics

Description
Epidemiology

Incidence

  • AAA is present in 5–10% of patients >65 years old (1) [C].
  • Estimated to occur in 7.7 to 26.8 per 100,000 person-years in recent large European study (remarkable variation was noted across countries).

Morbidity

  • Respiratory insufficiency (5–10%)
  • Myocardial infarction (10–15%)
  • Renal insufficiency (2–5%)
  • GI complications (3–4%)
  • Lower extremity ischemia (2–5%)

Mortality

  • rAAA is the 13th leading cause of death in the US, with up to 15,000 deaths annually.
  • 30–50% of patients with a rAAA do not survive transport to a hospital.
  • Operative mortality after rupture ~ 50%
Etiology/Risk Factors
Physiology/Pathophysiology
Anesthetic Goals/Guiding Principles

Diagnosis

Symptoms

Back, chest, or abdominal pain

History

  • Comorbidities are common.
    • Atherosclerosis associated with coronary artery disease, stroke, peripheral vascular disease, and renal insufficiency
    • Smoking associated with obstructive pulmonary disease
  • Presence of connective tissue disease
  • Medical optimization is not feasible due to the emergent nature of the surgery.

Signs/Physical Exam

  • Pulsatile abdominal mass
  • Hypotension
Treatment History

Pre-existing vascular grafts or repairs

Medications
Diagnostic Tests & Interpretation

Labs/Studies

  • Baseline and serial cardiac biomarkers, BUN/Cr, CBC with platelets, coagulation profile, and TEG if available
  • ECG may be normal or show nonspecific ST segment or T wave changes, left ventricular hypertrophy, ischemia, or infarction.
  • Chest radiograph may suggest concomitant pulmonary disease.
  • CT angiography is quick, highly sensitive, and specific; 64-slice multidetector CT with cardiac gating may allow for simultaneous evaluation of pulmonary and coronary arteries.
  • TEE allows rapid evaluation of cardiac function, volume status, and valvular integrity.
  • MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but is more time-consuming and contraindicated with metallic implants.
Concomitant Organ Dysfunction
Circumstances to Delay/Conditions

None; rAAA has a mortality that exceeds 80% if not repaired.

Classifications

Treatment

PREOPERATIVE PREPARATION

Premedications

  • Analgesia: Small incremental doses of opioids
  • Sedation: Avoid in hemodynamically unstable patients
  • Bronchodilators: Symptomatic patients with COPD
  • Antihypertensive/anti-anginal: Continued until time of surgery if hemodynamically stable
  • Blood products: pRBCs, platelets, FFP, cryoprecipitate
INTRAOPERATIVE CARE

Choice of Anesthesia

  • General endotracheal anesthesia
  • Continuous epidural anesthesia may be considered if rupture is contained and coagulation status is normal. However, placement should not occur in hemodynamically unstable patients or if it will delay surgery.

Monitors

  • ECG with ST-segment analysis
  • Arterial line: Pre-induction placement in radial artery is commonly performed. Femoral artery insertion may permit monitoring of distal perfusion pressures.
  • Central venous access is appropriate for monitoring pressures and administration of vasoactive medications.
  • TEE facilitates continuous evaluation of intravascular volume, valvular integrity, and ventricular function.
  • Pulmonary artery catheterization provides SvO2, SVR, CO, PAP.
  • Temperature (central and peripheral sites if bypass is to be used)
  • Foley catheter
  • Cell salvage, rapid infuser

Induction/Airway Management

  • Slow, controlled titration of induction medications: In patients at risk for pulmonary aspiration, the decision to proceed with an RSI should be balanced against the potential for hypertension.
    • Control of hypertensive response to laryngoscopy and intubation can be accomplished with moderate-dose narcotics.
    • Avoid hypotension which may contribute to cardiac ischemia and further deterioration of peripheral perfusion.
  • Single-lumen endotracheal tube is sufficient for surgery contained to the abdominal cavity. Lung isolation with a double-lumen tube or bronchial blocker is preferred for procedures extending into the thorax.
  • Positive pressure ventilation may decrease venous return and further decrease cardiac output and peripheral perfusion.

Maintenance

  • Position: Supine with transperitoneal approach; the lateral decubitus position and retroperitoneal approach may be preferred in certain situations.
  • Thermoregulation: forced air and fluid warming systems are necessary due to significant heat loss with open procedures.
  • Fluid management: Maintenance of intravascular volume may be challenging due to significant hemorrhage and evaporative losses; no specific colloid or crystalloid strategy has emerged as superior.
  • Coagulation: Consumption and dilution of coagulation factors and platelets may be significant; replacement is guided by conventional coagulation studies as well as TEG, if available.
  • Renal protection: Maintenance of renal blood flow and urine output is essential. IV sodium bicarbonate, mannitol, and fenoldapam may decrease the risk of kidney injury (mannitol and fenoldapam should not be used in hemodynamically unstable patients).
  • Placement of aortic cross-clamp
    • Increase in left ventricle (LV) afterload and potential for cardiac collapse. Acute increases in systemic vascular resistance (SVR) can be mitigated with vasodilators (nitroprusside, nitroglycerin, calcium channel blockers, propofol).
    • Decrease in venous return: Gentle administration of IV fluids may augment preload.
    • Suprarenal clamping decreases renal perfusion. Consider administration of mannitol (0.25–0.5 g/kg) prior to clamping.
  • Removal of aortic cross-clamp
    • Release of vasoactive metabolites into the central circulation can lead to hypotension and cardiac arrhythmias.
    • Decreases in the SVR are mitigated with IV fluids and vasopressors (phenylephrine or epinephrine). Profound, unresponsive hypotension can be temporarily treated with re-instigation of the aortic clamp.

Extubation/Emergence

  • Ongoing cardiac or pulmonary instability, bleeding, hypothermia, or neurologic injury may necessitate continued mechanical ventilation; otherwise patients may be extubated at the conclusion of the procedure.
  • Pain, hypertension, and tachycardia should be anticipated and addressed.

Follow-Up

Bed Acuity
Complications

References

  1. Assar A , Zairians C. Ruptured abdominal aortic aneurysm: A surgical emergency with many clinical presentations. Postgrad Med J. 2009;85:268273.
  2. Brattheim BJ , Elkemo TA , Altreuther M , et al. Regional disparities in incidence, handling and outcome of patients with symptomatic ruptured abdominal aortic aneurysms in Norway. Eur J Endovasc Surg. 2012.
  3. Wozniak F , LaMuraglia GM , Musch G , et al. Anesthesia for open abdominal surgery. Int Anesth Clin. 2005;43(1):6178.
  4. Thompson R , Geaghty P , Lee J. Abdominal aortic aneurysms: Basic mechanisms and clinical implications. Curr Probl Surg. 2002;39:110130.
  5. Adam van der Vliet J , Boll A. Abdominal aortic aneurysms. Lancet. 1997;349:863866.
  6. Bernstein E , Chan E. Abdominal aortic aneurysm in high risk patients: Outcome of selective management based on size and expansion rate. Ann Surg. 1984;200(3):255263.
  7. Falk J , Rackow EC , Blumenberg R , et al. Hemodynamic and metabolic effects of abdominal aortic cross-clamping. Am J Surg. 1981;142:174177.
  8. Subramaniam B , Singh N , Roscher C , et al. Innovations in treating aortic diseases: The abdominal aorta. J Cardiothorac Vasc Anesth. 2011 (article in press).
  9. Gelman S. The pathophysiology of aortic cross clamping and unclamping. Anesthesiology. 1995;82(4):10261060.

Additional Reading

See Also (Topic, Algorithm, Electronic Media Element)

Codes

ICD9

441.3 Abdominal aneurysm, ruptured

ICD10

I71.3 Abdominal aortic aneurysm, ruptured

Clinical Pearls

Author(s)

John W. Hoffman, Jr ., DO, MS

Shawn T. Beaman , MD