Aortic dissection is characterized by the development of a tear in the aortic intima that allows blood to enter a false lumen and cause a separation in the layers of the vessel wall.
It is the most common aortic catastrophe, occurring with a frequency exceeding that of abdominal aortic aneurysm rupture.
Most acute dissections (80%) develop in the absence of a pre-existing aneurysm; thus, distinction should be made between the terms "dissection" and "aneurysm."
The diagnosis of aortic dissection is missed in up to 40% of patients at initial presentation as physical findings may be absent or nonspecific or mimic conditions for which the therapeutic strategy is dissimilar (e.g., myocardial ischemia).
Epidemiology
Incidence
Peak incidence in the 6th and 7th decades with the mean age of diagnosis at 63 years
Males account for 65% of cases
Circadian and seasonal patterns have been described with peak frequency between 8:00 AM and 9:00 AM and during winter months.
3.5 per 100,000 persons per year (US data)
Prevalence
Actual prevalence unknown since many patients (~20%) die prior to hospital presentation. Autopsy series report 1 acute aortic dissection for every 128 to 745 autopsies.
Morbidity
Neurologic complications are the main cause of disability among survivors.
Mortality
Acute dissection of the ascending aorta has a 30-day mortality rate of 20% with surgical repair and 50% with medical therapy alone.
Death most often results from aortic rupture, cardiac tamponade, stroke, and visceral ischemia.
Etiology/Risk Factors
Hypertension (72%)
Atherosclerosis (31%)
Smoking
Bicuspid aortic valve
Coarctation
Deceleration trauma
Cocaine/crack
Pregnancy
Iatrogenic (percutaneous cardiac and aortic or valvular surgical procedures)
Hereditary fibrillinopathies (Marfan, EhlersDanlos, annuloaortic ectasia, and familial aortic dissection)
The development of a tear in the intimal layer of the aorta exposes the medial layer to the force of intraluminal blood flow. Entry of blood cleaves the intima and media longitudinally in an anterograde and/or retrograde direction; this serves to create a second or "false" lumen, separated from the true lumen by an intimal flap.
Propagation of aortic dissection is linked to mean, peak, and diastolic recoil arterial pressure as well as the rate of rise of aortic pressure (aortic dP/dt).
Malperfusion of branch vessels can occur due to occlusion by the intimal flap or by compression of the true lumen by expansion of the false lumen.
Most originate in the ascending aorta (65%), followed by the descending aorta (20%), aortic arch (10%), and abdominal aorta (5%).
Anesthetic Goals/Guiding Principles
Hemodynamic stabilization, pain control, and blood pressure optimization are priorities of initial management. In general, systolic blood pressure should be maintained at 100120 mm Hg or the lowest level that maintains effective end-organ perfusion.
In the past, uncomplicated distal aortic dissection (Stanford B, DeBakey III) was managed medically; however, endovascular techniques are increasingly being applied.
Uncomplicated distal aortic dissection (Stanford B, DeBakey III) was historically managed medically; however, endovascular techniques are increasingly being applied.
Diagnosis⬆⬇
Symptoms
Sudden, severe chest, back, and abdominal pain are the most common symptoms (>90%).
Syncope (up to 20%) with or without a history of pain
Acute heart failure (7%) due to myocardial ischemia or acute aortic insufficiency
Limb ischemia
Hoarseness (due to recurrent laryngeal nerve compression)
History
96% of acute aortic dissections are identified with the following prediction model:
Aortic pain with immediate onset, a tearing or ripping character, or both
Mediastinal widening, aortic widening, or both on chest radiography
Pulse differentials (absence of a proximal extremity or carotid pulse), blood pressure differentials (systolic pressure difference >20 mm Hg between arms), or both
Signs/Physical Exam
Hypertension (69% of distal and 36% of proximal dissections)
Hypotension, shock, or tamponade (27% of proximal dissections)
Pulse or blood pressure differentials (20%)
Focal neurologic deficits (12%)
Murmur of aortic insufficiency (32%)
Pleural effusion (left > right)
Horner syndrome
Superior vena cava syndrome
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 (~30%) or show nonspecific ST-T changes (40%), left ventricular hypertrophy (26%), ischemia (15%), or infarction (10%).
Chest radiograph findings include mediastinal widening (61%), abnormal aortic contour (49%), pleural effusion (19%), displacement/calcification of aorta (14%). Normal findings are present in 12% of patients.
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 is highly sensitive for ascending aortic dissection and allows rapid evaluation of hemodynamic instability (tamponade, coronary dissection, valvular regurgitation, tension hemothorax, etc.).
MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but is more time-consuming and contraindicated with metallic implants.
Aortography: Previously the reference standard, this is performed less often and rarely as the initial study.
CONCOMITANT ORGAN DYSFUNCTION
Compromise of aortic branches and subsequent malperfusion can affect several systems:
Cardiovascular: Acute aortic valvular insufficiency due to aortic root dilation or leaflet disruption; ischemia/infarction (dissections often arise from right sinus of Valsalva causing inferior wall myocardial infarction); limb ischemia from subclavian or iliac arteries
Neurologic: Syncope, stroke (innominate or common carotid arteries), spinal cord ischemia (radicular arteries), peripheral ischemic neuropathy
Pulmonary: Left pleural effusion/hemothorax
Renal: Ischemia, infarction, acute renal failure
Gastrointestinal: Abdominal organ ischemia (celiac, mesenteric arteries)
Circumstances to delay/Conditions
Delays are associated with increased mortality; thus, evaluation should be limited to the acquisition of appropriate diagnostic studies and evaluation of conditions that will alter surgical candidacy or affect perioperative management.
Pericardiocentesis as a temporizing measure for tamponade has been associated with increased risk of PEA arrest and death compared to immediate sternotomy and surgical control of the aorta.
Classifications
Acute (<2 weeks) or chronic (>2 weeks)
Stanford:
Type A: Ascending aorta involved
Type B: Ascending aorta not involved (distal to takeoff of left subclavian artery)
DeBakey:
Type I: Ascending aorta, arch, descending aorta
Type II: Ascending aorta only
Type IIIa: Descending aorta only
Type IIIb: Descending and abdominal aorta
Treatment⬆⬇
PREOPERATIVE PREPARATION
Premedications
Short-acting drugs permit rapid termination of effect, if desired, and should be considered.
Morphine, beta-blockers, and vasodilating drugs can be used to control pain and blood pressure. Esmolol is ultra-short-acting and has organ-independent elimination (metabolized within red blood cells).
Sodium nitroprusside may cause an increase in aortic dP/dt; it is generally added only after a negative inotrope is administered.
Nicardipine may be preferred in patients intolerant of beta-antagonists and does not cause a reflex tachycardia.
Enalaprilat may be useful in refractory hypertension due to renal artery compromise.
Phenylephrine and norepinephrine are preferred pressors due to a relative lack of associated increase in aortic dP/dt.
INTRAOPERATIVE CARE
Choice of Anesthesia
No superiority has been demonstrated with any given anesthetic technique.
for open repair, GETA is typically employed, alone or in combination with epidural anesthesia; epidural placement may be precluded by hemodynamic instability.
Evoked-potentials monitoring may influence technique (i.e., volatile anesthetic concentration, use of muscle relaxant).
for endovascular repair, local, regional, and general techniques may be used.
Monitors
ECG with ST-segment analysis
Temperature (central and peripheral sites if bypass is to be used)
Foley catheter
Arterial line: Right radial artery may be preferred if blood flow to the left subclavian artery is disrupted due to dissection or cross-clamp placement. Femoral artery insertion may permit monitoring of distal perfusion pressures.
Central venous access may be appropriate for IV access and administration of vasoactive medications.
Pulmonary artery catheterization can provide SvO2, SVR, CO, PAP.
TEE aids in diagnosis, anatomic localization, identification of complications, and characterization of valvular and ventricular function in real time.
Lumbar drains and evoked-potentials may be placed for patients at risk for spinal cord ischemia.
The potential for catastrophic hemorrhage necessitates appropriate vascular access, availability of blood products, rapid infuser system, and autologous red cell salvage.
Induction/Airway Management
Slow, controlled titration of medications to the desired effect can help maintain hemodynamic stability. Hypertension and tachycardia increase shear stress and risk of rupture.
Single-lumen ETT may be typically placed for a median sternotomy approach.
Lung isolation with a double lumen tube or bronchial blocker aids in the exposure of the descending aorta and is preferred for procedures using the lateral thoracotomy approach.
Maintenance
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 mannitol and fenoldopam can be employed to reduce the risk of kidney injury.
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.
ClouseWD, HallettJr JW, SchaffHV, et al.Acute aortic dissection: Population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004;79:176180.
HaganPG, NienaberCA, IsselbacherEM, et al.The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA. 2000;283:897903.
PencoM, PaparoniS, DagiantiA, et al.Usefulness of transesophageal echocardiography in the assessment of aortic dissection. Am J Cardiol. 2000;86:53G56G.
von KodolitschY, SchwartzAG, NienaberCA.Clinical prediction of acute aortic dissection. Arch Intern Med. 2000;160:29772982.
NienaberCA, EagleKA.Aortic dissection: New frontiers in diagnosis and management. Part I: From etiology to diagnostic strategies. Circulation. 2003;108:628635.
NienaberCA, EagleKA.Aortic dissection: New frontiers in diagnosis and management. Part II: Therapeutic management and follow-up. Circulation. 2003;108:772778.
See Also (Topic, Algorithm, Electronic Media Element)
Acute dissection of the proximal aorta is a surgical emergency, and preoperative evaluation should be expedited.
Preoperative management is directed at the reduction of arterial pressure and aortic dP/dt.
Monitoring is essential to anesthetic management and should be individualized to the specifics of the patient, nature of dissection, and surgical procedure.