Emergent Management of Asystole

Background

Asystole is cardiac standstill with no cardiac output and no ventricular depolarization, as shown in the image below; it eventually occurs in all dying patients.

Rhythm strip showing asystole.

Pulseless electrical activity (PEA) is the term applied to a heterogeneous group of dysrhythmias unaccompanied by a detectable pulse. Bradyasystolic rhythms are slow rhythms; they can have a wide or narrow complex, with or without a pulse, and are often interspersed with periods of asystole. When discussing pulseless electrical activity, ventricular fibrillation (VF) (see the following image) and ventricular tachycardia (VT) are excluded.

Rhythm strip showing ventricular fibrillation. NextPathophysiology

Asystole can be primary or secondary. Primary asystole occurs when the heart's electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (ie, sclerosis) of the sinoatrial (SA) node or atrioventricular (AV) conducting system. Primary asystole is usually preceded by a bradydysrhythmia due to sinus node block-arrest, complete heart block, or both.

Reflex bradyasystole/asystole can result from ocular surgery,[1, 2] retrobulbar block, eye trauma, direct pressure on the globe, maxillofacial surgery, hypersensitive carotid sinus syndrome, or glossopharyngeal neuralgia. Episodes of asystole and bradycardia have been documented as manifestations of left temporal lobe complex partial seizures.[3] These patients experienced either dizziness or syncope. No sudden deaths were reported, but the possibility exists if asystole were to persist. The longest interval was 26 seconds.

Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia with metabolic acidosis. Asystole or bradyasystole follows untreated ventricular fibrillation and commonly occurs after unsuccessful attempts at defibrillation. This forebodes a dismal outcome.

PreviousNextEtiology

Causes of primary and secondary asystole are briefly reviewed in this section.

Primary asystole

Primary asystole develops when cellular metabolic functions are no longer intact and an electrical impulse cannot be generated. With severe ischemia, pacemaker cells cannot transport the ions necessary to affect the transmembrane action potential. Implantable pacemaker failure may also be a cause of primary asystole.

Proximal occlusion of the right coronary artery can cause ischemia or infarction of both the sinoatrial (SA) and the atrioventricular (AV) nodes. Extensive infarction can cause bilateral bundle-branch block (ie, infranodal complete heart block).

Idiopathic degeneration of the SA or AV node can result in sinus arrest-block and/or AV heart block, respectively. This process is slow and progressive, but the symptoms may be acute and asystole may result. An implantable pacemaker is usually required for these conditions.

Occasionally, asystolic sudden death occurs from congenital heart block, local tumor, or cardiac trauma.[4]

Asystole can occur following an indirect lightning strike (ie, direct current [DC]) that depolarizes all the cardiac pacemakers. A rhythm may return spontaneously or shortly after cardiopulmonary resuscitation (CPR) is initiated. These patients may survive intact if given immediate attention. Alternating current (AC) from man-made sources of electrical current usually results in ventricular fibrillation (VF).

Secondary asystole

Examples of common conditions that can result in secondary asystole include suffocation, near drowning, stroke, massive pulmonary embolus, hyperkalemia, hypothermia, myocardial infarction (MI) complicated by VF or ventricular tachycardia (VT) that deteriorates to asystole, post defibrillation, and sedative-hypnotic or narcotic overdoses leading to respiratory failure.

Hypothermia is a special circumstance, because asystole can be tolerated for a longer period under such conditions and can be reversed with rapid rewarming while CPR is being performed. If available, institute cardiopulmonary bypass immediately, because it can accomplish both of these goals. Most survivors have received cardiopulmonary bypass.

PreviousNextEpidemiology

The number of US adults in cardiopulmonary arrest who had bradyasystole as the initial arrest rhythm is difficult to measure accurately. Reports vary and may be skewed by the patient population studied and/or by the method of reporting the initial rhythm. For example, in a 1991 study of 185 patients in cardiopulmonary arrest at the time of arrival to the emergency department, 9% had survived to hospital admission but none were discharged alive.[5] This study was not limited to patients with asystole.[5] In one study from Goteborg, Sweden, asystole was the presenting rhythm in the field in 35% of patients with cardiac arrest.[6]

Race is not a significant factor in asystole except as it relates to the underlying conditions that may lead to a cardiac arrest, such as chronic hypertension, renal failure, coronary artery disease, congestive heart failure, or cardiac dysrhythmias.

Individuals with low CAD incidence

When the incidence of coronary artery disease (CAD) in the population of a country is relatively low, asystole is relatively more common as a manifestation of cardiopulmonary arrests. This is because cardiac ischemia more frequently results in ventricular fibrillation (VF).

Children

The prevalence of asystole as the presenting cardiac rhythm is lower in adults (25-56%) than in children (90-95%). In fact, asystole is most likely to be found in cardiopulmonary arrests occurring in children; this is usually secondary to another noncardiac event (ie, respiratory arrest due to sudden infant death syndrome [SIDS], infection, choking, drowning, or poisoning).[7] Infants are more statistically likely to suffer a cardiac arrest than older children or adolescents.

The Resuscitation Outcomes Consortium Epistry-Cardiac Arrest trial, nontraumatic cardiac arrest occurred at a rate of 72.1 per 100,000 infants versus 3.73 per 100,000 in children and 7.37 per 100,000 in adolescents.[8] Investigators found the adult rate of cardiac arrest was 126.52 per 100,000 when they evaluated 25,405 adults and 624 patients younger than 20 years.

Pediatric patients with VF or ventricular tachycardia (VT) were 4 times more likely to survive an out-of-hospital cardiac arrest (20%) than those with asystole (5%), and patients younger than 20 years had an overall better survival rate than adults when all rhythms are included and traumatic arrests are excluded.[8]

Women

The frequency of asystole, as a percentage of all cardiopulmonary arrests, is higher in women than in men; however, the frequency of cardiac arrest in general is proportional to the underlying incidence of heart disease, which is more common in males until around age 75 years.

PreviousNextPrognosis

The prognosis in asystole depends on the etiology of the asystolic rhythm, timing of interventions, and success or failure of advanced cardiac life support (ACLS).

Resuscitation is likely to be successful only if it is secondary to an event that can be corrected immediately, such as a cardiac arrest due to choking on food (a cafe coronary), and only if an airway can be established and the patient may be rapidly reoxygenated. Occasionally, primary asystole can be reversed if it is due to pacemaker failure, which could be either intrinsic or extrinsic, and this is corrected immediately by external pacing.

Generally, the prognosis is dismal regardless of its initial cause; in particular, individuals with postcountershock asystole have an even worse survival rate.[9, 10] In the Termination of Resuscitation study, when no shock was advised in patients with unwitnessed cardiac arrest, there were no survivors.[11, 12] In the Goteborg, Sweden, study, 10% of 1,635 asystolic patients survived to hospital admission, but 2% survived to hospital discharge.[6]

The most recent American Heart Association guidelines to improve cardiocerebral resuscitation (CCR) have validated studies that show improved outcomes in all adults with out-of-hospital cardiac arrest in ventricular tachycardia and ventricular fibrillation only.[13]

Complications

Complications from asystole include permanent neurologic impairment and complications from cardiopulmonary resuscitation (CPR) or invasive procedures (eg, liver laceration, fractured ribs, pneumothorax, hemothorax, air embolus, aspiration, gastric/esophageal rupture). Death often occurs.

PreviousNextPatient Education

Advice about electrical storm safety and prevention of hypothermia is appropriate for those likely to be exposed to these conditions.

For patient education information, see Heart Health Center as well as Cardiopulmonary Resuscitation (CPR), Heart Attack, and Coronary Artery Disease.

PreviousProceed to Clinical Presentation , Emergent Management of Asystole

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Tube Thoracostomy Management

Overview

The mechanics of ventilation relate to the negative intrathoracic pressure that draws air into the lungs during spontaneous respiration. This negative pressure is best maintained in the pleural space, which is the potential space between the parietal and visceral layers of the pleura. Collections of air, fluid, or blood in the pleural space not only compress the lung tissue but also cause the pleural pressures to become positive, causing inappropriate ventilation.

(See the video below, showing chest tube insertion.)

Insertion of chest tube. Video courtesy of Therese Canares, MD, and Jonathan Valente, MD, Rhode Island Hospital, Brown University.

Chest drains are inserted to remove pathological collections of air or fluid in the pleural space, to allow the re-creation of the essential negative pressures in the chest, and to permit complete expansion of the lung, thereby restoring normal ventilation. Chest drains are very simple and effective tools in the management of thoracic and pleural pathology. They need proper safe insertion and correct management. Chest drains are lifesaving in critical care.

Chest drainage systems work by combining the following 3 efforts:

Expiratory positive pressure from the patient helps push air and fluid out of the chest (eg, cough, Valsalva maneuver).Gravity helps fluid drainage as long as the chest drainage system is placed below the level of the patient’s chest.Suction can improve the speed at which air and fluid are pulled from the chest.

Any catheter inserted through the chest wall to remove air or fluid from the pleural space may be called a chest tube or chest drain. Crosswell Hewitt is credited as being the first to use a chest drain, in 1876, when he used a red rubber catheter to drain an empyema thoracis.[1] Ideally, the chest tubes (also called thoracic catheters) must be nontoxic, nonthrombogenic, and soft but with thick resilient walls. The traditional red rubber tubes have most of these features but, being opaque, tend to be quickly occluded by encrustation and fibrinous secretions.

Today, chest tubes are made of clear plastic (vinyl or silastic). They are available in varying diameters, sized in multiples of 4 on the French scale (eg, 12F, 16F, 20F, up to 36F). They have multiple side holes to allow effective drainage and have length markers to help note the distance of the lowest hole from the skin surface. A radiopaque strip lines the tube to help easy visualization on chest radiography.[2] Some tubes are mounted on stylets or trocars that act as guides to help insertion and proper placement of tubes.

The standard of care with chest tubes has evolved with experience gained with their use for chest trauma during the Korean War of the 1950s and the Vietnam War thereafter.[3] Improper management of inserted chest tubes results in premature removal or delayed removal, both of which lead to increased hospital stay and costs.

When caring for and maintaining a patient with a chest tube, the following steps are important: Keep chest tubes patent, note the presence of drainage and fluctuations, and observe the patient's vital signs and levels of comfort. The chest dressing status and type of suction must be noted.

Next, Tube Thoracostomy Management

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Emergent Management of Acute Aortic Dissection

Overview

Aortic dissection is the most common catastrophe of the aorta, 2-3 times more common than rupture of the abdominal aorta. When left untreated, about 33% of patients die within the first 24 hours, and 50% die within 48 hours. The 2-week mortality rate approaches 75% in patients with undiagnosed ascending aortic dissection.

The establishment of the International Registry of Acute Aortic Dissection in 1996, which gathers information from 24 centers in 11 countries, has helped in the development of an understanding of the complexity of aortic dissection.

Dissections of the thoracic aorta have been classified anatomically by 2 different methods. The more commonly used system is the Stanford classification, which is based on involvement of the ascending aorta and simplifies the DeBakey classification.

Go to Aortic Dissection for complete information on this topic.

Stanford classification

The Stanford classification divides dissections into 2 types, type A and type B. Type A involves the ascending aorta (DeBakey types I and II); type B does not (DeBakey type III).

This system helps to delineate treatment. Usually, type A dissections require surgery, while type B dissections may be managed medically under most conditions.

DeBakey classification

The DeBakey classification divides dissections into 3 types, as follows:

Type I involves the ascending aorta, aortic arch, and descending aortaType II is confined to the ascending aortaType III is confined to the descending aorta distal to the left subclavian artery

Type III dissections are further divided into IIIa and IIIb. Type IIIa refers to dissections that originate distal to the left subclavian artery but extend proximally and distally, mostly above the diaphragm.

Type IIIb refers to dissections that originate distal to the left subclavian artery, extend only distally, and may extend below the diaphragm.

Thoracic aortic dissections should be distinguished from aneurysms (ie, localized abnormal dilation of the aorta) and transections, which are caused most commonly by high-energy trauma.

NextPrehospital Care

Assure adequate breathing, maintain oxygenation, treat shock, and obtain useful historical information.

Establishing the diagnosis in the field is usually difficult or impossible, but certain salient features of aortic dissection may be observed. It is life threatening if not quickly recognized and treated.

Radio communication with the receiving hospital permits the medical control physician to direct care and select a capable destination hospital, while permitting the emergency department (ED) to mobilize appropriate resources.

In the rare event that the diagnosis can be made based on prehospital information, the physician directing prehospital care should request transport to a facility capable of operative treatment of an aortic dissection.

PreviousNextEmergency Department Care

The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48 hours. Initial therapy should begin when the diagnosis is suspected. This includes 2 large-bore intravenous lines (IVs), oxygen, respiratory monitoring, and monitoring of cardiac rhythm, blood pressure, and urine output.

Clinically, the patient must be assessed frequently for hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes, and development or progression of carotid, brachial, and femoral bruits.

Aggressive management of heart rate and blood pressure should be initiated.

Beta blockers should be given initially to reduce the rate of change of blood pressure (dP/dt) and the shear forces on the aortic wall.

The target heart rate should be 60-80 beats per minute.

The target systolic blood pressure should be 100-120 mm Hg.

End organ perfusion should be evaluated. Balancing the risks of dP/dt on the aortic wall versus the benefits of acceptable end organ perfusion may be a difficult clinical decision.

Retrograde cerebral perfusion may increase the protection of the central nervous system during the arrest period.

The mortality rate from aortic arch dissections is about 10-15%, with significant neurologic complications occurring in another 10% of patients. The mortality rate is influenced by the patient's clinical condition.

The American College of Radiology has established ACR Appropriateness Criteria for the diagnosis and treatment of suspected aortic dissection.[1]

Type A dissections

Urgent surgical intervention is required in type A dissections.

The area of the aorta with the intimal tear usually is resected and replaced with a Dacron graft.

The operative mortality rate is usually less than 10%, and serious complications are rare with ascending aortic dissections.

The development of more impermeable grafts, such as woven Dacron, collagen-impregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated Carbo-Seal Ascending Aortic Prothesis (Sulzer CarboMedics, Austin, Tex), has greatly enhanced the surgical repair of thoracic aortic dissections.

With the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion, the morbidity and mortality rates associated with this highly invasive surgery have decreased.

Dissections involving the arch are more complicated that those involving only the ascending aorta, because the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest usually is required. If the arrest time is less than 45 minutes, the incidence of central nervous system complications is less than 10%.

Aortic stent grafting is a challenging technique. It may prove feasible and has offered good results in a small series of patients. It may be a reasonable alternative in high-risk patients in the near future.

Type B dissections

The definitive treatment for type B dissections is less clear.

Uncomplicated distal dissections may be treated medically to control blood pressure. Distal dissections treated medically have a mortality rate that is the same as or lower than the mortality rate in patients who are treated surgically.

Surgery is reserved for distal dissections that are leaking, ruptured, or compromising blood flow to a vital organ.

Acute distal dissections in patients with Marfan syndrome usually are treated surgically.

Inability to control hypertension with medication is also an indication for surgery in patients with a distal thoracic aortic dissection.

Patients with a distal dissection are usually hypertensive, emphysematous, or older.

Long-term medical therapy involves a beta-adrenergic blocker combined with other antihypertensive medications. Avoid antihypertensives (eg, hydralazine, minoxidil) that produce a hyperdynamic response that would increase dP/dt (ie, alter the duration of P or T waves).

Survivors of surgical therapy also should receive beta-adrenergic blockers.

A series of patients with type B dissections demonstrated that aggressive use of distal perfusion, CSF drainage, and hypothermia with circulatory arrest improves early mortality and long-term survival rates.

Endovascular stenting remains an option for treatment of some type B dissections. Some studies recommend that patients with complicated acute type B dissections undergo endovascular stenting with the goal of covering the primary intimal tear.[2]

Definitive treatment

Definitive treatment involves segmental resection of the dissection, with interposition of a synthetic graft.

When thoracic dissections are associated with aortic valvular disease, replace the defective valve.

With combined reconstruction–valve replacement, the operative mortality rate is approximately 5%, with a late mortality rate of less than 10%.

Operative repair of the transverse aortic arch is technically difficult, with an operative mortality rate of 10% despite induction of hypothermic cardiocirculatory arrest.

Repair of the descending aorta is associated with a higher incidence of paraplegia than repair of other types of dissections because of interruption of segmental blood supply to the spinal cord.

The operative mortality rate is approximately 5%.

In a study by Mimoun et al of patients with Marfan syndrome who had acute aortic dissection, the patients were found to have a better event-free survival when there were no dissected portions of the aorta remaining after surgery.[3]

PreviousNextConsultations

Once a thoracic dissection is suspected, consult a thoracic surgeon. Because many patients with this disorder have concomitant medical illness, consult the patient's primary care provider to expedite preoperative preparation. Early consultation is encouraged when ordering further imaging studies if the patient requires rapid operative intervention.

Consult a radiologist prior to obtaining aortography.

PreviousNextInpatient Care

Patients with symptomatic dissection should undergo immediate repair, especially if it is leaking or expanding.

Symptomatic patients require admission to a center experienced in cardiopulmonary bypass and operative care.

Completely asymptomatic patients may have their repair performed electively but may require admission to expedite their evaluation or for preoperative stabilization of their condition.

Patients with chest pain should undergo serial echocardiograms (ECGs) and creatine kinase (CK) determinations if acute myocardial infarction (AMI) is indicated.

PreviousNextOutpatient Care

Follow-up examinations with radiologic studies are recommended at 3-month intervals for the first year and every 6 months for the next 2 years.

After this, follow up annually.

PreviousNextTransfer

Symptomatic patients require care at a facility equipped to perform cardiopulmonary bypass with aortic and/or valvular repair.

Contact the receiving physician as soon as possible to transfer patients before their condition deteriorates.

Early airway management is indicated in the presence of hemoptysis or stridor.

If coronary insufficiency is suspected, nitrates may be used, but therapy with thrombolytic agents and aspirin should be avoided.

Patients should be monitored and accompanied by personnel capable of resuscitation.

If a prolonged ground transport time is anticipated, consider air transport.

Previous, Emergent Management of Acute Aortic Dissection

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Emergent Management of Abdominal Aortic Aneurysm Rupture

Introduction to AAA

The decision to treat an unruptured abdominal aortic aneurysm (AAA) is a complex one, based on operative risk, the risk of rupture, and the patient’s estimated life expectancy. Ruptured AAA is a life-threatening condition that requires emergent surgery. For other discussions on AAA, see Abdominal Aortic Aneurysm and Bedside Ultrasonography Evaluation of Abdominal Aortic Aneurysm.

History of the procedure

Vesalius described the first AAA in the 16th century. Before the development of a surgical intervention for the process, attempts at medical management failed. The initial attempts at surgical control used ligation of the aorta, with the expected consequences.

In 1923, Matas performed the first successful aortic ligation on a patient. Attempts were made to induce thrombosis by inserting intraluminal wires. In 1948, Rea wrapped reactive cellophane around the aneurysm in order to induce fibrosis and limit expansion. This technique was used on Albert Einstein in 1949, and he survived 6 years before succumbing to rupture. In 1951, Charles Dubost performed the first AAA repair using a homograft.

Prior to this, aortic aneurysms were treated using a variety of methods, including ligation, intraluminal wiring, and cellophane wrapping. Unfortunately, early homografts became aneurysmal because of preservation techniques. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (ie, nylon). Later, these grafts were replaced by Dacron and GORE-TEX (ie, polytetrafluoroethylene [PTFE]) fabrics. The final advance was abandonment of silk sutures, which degenerate, in favor of braided Dacron, polyethylene, and PTFE (ie, GORE-TEX) sutures, all of which retain tensile strength.

Postoperative surgical mortality rates initially remained high (>25%) because the aneurysm sac generally was excised. Nearly simultaneously in 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy (see the images below). This advancement dramatically reduced mortality. Today, operative mortality rates range from 1.8-5%.

Aneurysm with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis. Endoaneurysmorrhaphy.

In the late 1980s, Parodi et al described endovascular repair using a large Palmaz stent and unilateral aortofemoral and femorofemoral crossover Dacron grafts.[1] Currently, many devices are used for the endovascular treatment of AAA (see the image below).

Endovascular grafts. NextEpidemiologyUnited States statistics

Ruptured abdominal aortic aneurysm (AAA) causes an estimated 15,000 deaths per year. The frequency of rupture is 4.4 cases per 100,000 persons. The reported incidence of rupture varies from 1-21 cases per 100,000 person-years.

International statistics

The frequency of rupture is 6.9 cases per 100,000 persons in Sweden, 4.8 cases per 100,000 persons in Finland, and 13 cases per 100,000 persons in the United Kingdom.

PreviousNextPrognosis

The prognosis is guarded in patients who suffer AAA rupture prehospital. More than 50% do not survive to the ED; of those who do, survival rate drops by about 1% per minute. However, survival rate is good in the subset of patients who are not in severe shock and who receive timely, expert surgical intervention.

In 1988, 40,000 surgical reconstructions for abdominal aortic aneurysm (AAA) were performed in the US, with substantial mortality differences between elective versus emergency operations. As elective aneurysm repair has a mortality rate drastically lower than that associated with rupture, the emphasis must be on early detection and repair free from complications.

The long-term prognosis is related to associated comorbidities. Long-term survival is shortened by chronic heart failure and chronic obstructive pulmonary disease. Rupture of associated thoracic aneurysms is also an important cause of late death. Overall, AAA repair is very durable, with few long-term complications ([2, 3]

PreviousNextPathophysiology

Aneurysm diameter is an important risk factor for rupture. In general, abdominal aortic aneurysms (AAAs) gradually enlarge (0.2-0.8 mm/y) and eventually rupture. Hemodynamics play an important role. Areas of high stress have been found in AAAs and appear to correlate with the site of rupture. Computer-generated geometric factors have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications in determining which AAAs require surgical repair.

AAA rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. Wall tension can be calculated using the Laplace Law for wall tension: P × R/W, where P = mean arterial pressure (MAP), R = radius of the vessel, and W = wall thickness of the vessel.

AAA wall tension is a significant predictor of pending rupture. The actual tension in the AAA wall appears to be a more sensitive predictor of rupture than aneurysm diameter alone. For these reasons, the clinician may wish to achieve acute blood pressure control in patients with AAA and elevated blood pressure.

PreviousNextClinical Presentation

Persons with abdominal aortic aneurysms (AAAs) that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, or flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.

Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture.

Patients with a ruptured AAA may present in frank shock as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital.

It is important to note progressive symptoms (eg, abdominal or back pain, vomiting, syncope, claudication). These should alert the clinician to the possibility of expansion with imminent rupture.

Peripheral emboli and claudication

Atheroemboli from small AAAs produce livedo reticularis of the feet or blue toe syndrome (see the image below). Occasionally, small AAAs thrombose, producing acute claudication.

Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of the feet (ie, blue toe syndrome). Aortocaval fistulae

AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia.

Aortoduodenal fistulae

Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.

PreviousNextIndications

Even patients who do not have symptoms from their abdominal aortic aneurysms (AAAs) may eventually require surgical intervention because the result of medical management in this population is a mortality rate of 100% over time due to rupture. In addition, these patients have a high likelihood of limb loss from peripheral embolization.

The decision to treat an unruptured abdominal aortic aneurysm (AAA) is based on operative risk, the risk of rupture, and the patient’s estimated life expectancy. In 2003, the Society for Vascular Surgery (SVS) published a series of guidelines for the treatment of AAAs based on these principles.[4] The operative risk is based on patients’ comorbidities and hospital factors.

Abdominal ultrasonography can provide a preliminary determination of aneurysm presence, size, and extent. Rupture risk is in part indicated by the size of the aneurysm (see Table 1, below).

Table 1. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture (Open Table in a new window)

AAA Diameter (cm) Rupture Risk (%/y) 04-50.5-55-63-156-710-207-820-40>830-50

In addition to aneurysm diameter, risk of rupture is also an expression of sex, aneurysm expansion rate, family history, and chronic obstructive pulmonary disease (COPD) (see Table 2, below).

Table 2. Risk of Abdominal Aortic Aneurysm Rupture (Open Table in a new window)

Low Risk Average Risk High Risk Diameter5-6 cm>6 cmExpansion0.3-0.6 cm/y>0.6 cm/ySmoking/COPDNone, mildModerateSevere/steroidsFamily historyNo relativesOne relativeNumerous relativesHypertensionNormal blood pressureControlledPoorly controlledShapeFusiformSaccularVery eccentricWall stressLow (35 N/cm2Medium (40 N/cm2High (45 N/cm2)Sex...MaleFemale

The operative risk (see Table 3, below) is based on patients’ comorbidities and hospital factors. Patient characteristics, including age, sex, renal function, and cardiopulmonary disease are perhaps the most important. However, lower-volume hospitals and surgeons are associated with higher mortality.[5]

Table 3. Operative Mortality Risk of Open Repair of Abdominal Aortic Aneurysm (Open Table in a new window)

Lowest RiskModerate RiskHigh RiskAge Age 70-80 yAge 80 yPhysically activeActiveInactive, poor staminaNo clinically overt cardiac diseaseStable coronary disease; remote MI;

LVEF >35%

Significant coronary disease; recent MI;

frequent angina; CHF; LVEF
No significant comorbiditiesMild COPDLimiting COPD; dyspnea at rest; O2

dependency; FEV1
...Creatinine 2.0-3.0 mg/dL...Normal anatomyAdverse anatomy or AAA

characteristics

Creatinine >3 mg/dLNo adverse AAA characteristics...Liver disease (↑ PT; albumin Anticipated operative mortality, 1%-3%Anticipated operative mortality, 3%-7%Anticipated operative mortality, at least

5%-10%; each comorbid condition

adds ~3%-5%

mortality risk

CHF – chronic heart failure; COPD – chronic obstructive pulmonary disease; LVEF – left ventricular ejection fraction; MI – myocardial infarction; PT – prothrombin time

With AAAs smaller than 5.5 cm, elective repair has not been shown to improve survival.[6]

Prospective studies have concluded that following aneurysms larger than 5.5 cm with serial ultrasounds or CT scans is safe. A slightly higher rupture rate in women exists, and this threshold may be lower.

Thus, the decision to repair an AAA is a complex one in which the patient must play an important role. In some very elderly patients or patients with limited life expectancy, aneurysm repair may not be appropriate. In these patients, the consequences of rupture should be frankly discussed. If rupture occurs, no intervention should be performed.

PreviousNextContraindications

Contraindications for operative intervention of abdominal aortic aneurysms (AAAs) include severe chronic obstructive pulmonary disease (COPD), severe cardiac disease, active infection, and medical problems that preclude operative intervention. These patients may benefit best from endovascular stenting of the aneurysm.

In many patients, the decision to operate is a balance between risks and benefits. In an elderly patient (>80 y) with significant comorbidities, surgical repair may not be indicated. However, the decision to intervene should not be based on age alone, even with rupture. The decision is best based on the patient's overall physical status, including a positive attitude toward the surgery.

Patients with known cancer that has an indolent course (eg, prostate cancer) may merit aneurysm repair if their estimated survival is 2 years or longer.

PreviousNextWorkupLaboratory studies

A complete blood count with differential is used to assess transfusion requirements and the possibility of infection. A metabolic panel (including kidney and liver function tests) is indicated for ascertaining the integrity of renal and hepatic function, in order to assess operative risk and guide postoperative management.

Type and crossmatch blood to prepare for the possibility of transfusion, including clotting factors and platelets.

Because synthetic material is used in the intervention, assess and eliminate potential foci of infection preoperatively by urinalysis.

Assessment of pulmonary function is part of the preoperative workup, to determine operative risk and postoperative care. Patients who can climb a flight of stairs without excessive shortness of breath generally do well. If the patient's pulmonary status is in question, blood gas measurement and pulmonary function tests are helpful.

Chest radiography

Chest radiography is used to gain a preliminary assessment of the status of the heart and lungs. Concurrent pulmonary or cardiac disease may need to be addressed prior to treating the aneurysm.

Computed tomography

Preoperative CT scanning helps more clearly define the anatomy of the aneurysm and other intra-abdominal pathologies. Nonenhanced CT scanning is used to size aneurysms.[7] Although sizing the aneurysm is important, the anatomic relationships important to surgery are also determined. These include the location of the renal arteries, length of the aortic neck, condition of the iliac arteries, and anatomic variants such as a retroaortic left renal vein or horseshoe kidney.

Enhanced spiral CT scanning of the abdomen and pelvis with multiplanar reconstruction and CT angiography is the test of choice for preoperative evaluation for open and endovascular repair (see the image below).

Enhanced spiral CT scans with multiplanar reconstruction and a CT angiogram.

Of AAA cases, 10-20% have focal outpouchings or blebs visible on CT scans that are thought to contribute to the potential for rupture. The wall of the aneurysm becomes laminated with thrombus as the blebs enlarge. This can give the appearance of a relatively normal intraluminal diameter in spite of a large extraluminal size.

Magnetic resonance angiography

Magnetic resonance angiography (MRA) is quickly replacing the traditional angiographic assessment of aneurysms. The study provides excellent anatomical definition and 3-dimensional assessment of the problem. Gadolinium-enhanced MRA can provide excellent images, even though regional variations in quality are reported.

Conventional angiography

Angiography remains the criterion standard for the diagnosis of AAA, and it is indicated in the presence of associated renal or visceral involvement, peripheral occlusive disease, or aneurysmal disease. Angiography is also essential with any renal abnormality (eg, horseshoe kidney, pelvic kidney). (See the image below.)

Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac. Echocardiography

Because of the fluid shift involved during the operative repair of AAA, cardiac function should be assessed using echocardiography. By ascertaining the ejection fraction of the patient, the operative intervention can be planned and cardiac protective measures can be instituted as needed. This study is particularly indicated in patients with a history of CHF or known cardiac enlargement.

Pulmonary assessment

Assessment of pulmonary function is of paramount importance in these patients. Because surgical intervention requires an abdominal incision, preoperative assessment of the patient's pulmonary status allows for tailored postoperative care.

Cardiac assessment

Assess cardiac status in all patients with vascular disease. If one vascular bed is involved with an atherosclerotic process, then consider that others also may be involved. Electrocardiography findings provide a baseline assessment of cardiac rhythm and old disease processes.

A stress test can be performed to uncover unsuspected cardiac ischemia. Significant coronary disease may need to be addressed before the AAA can be repaired.

PreviousNextTreatment & Management

Abdominal aortic aneurysms (AAAs) are typically repaired by an operative intervention. The possible approaches are the traditional open laparotomy, newer minimally invasive methodologies, or by the placement of endovascular stents.

Preoperative details

Preoperatively, obtain a careful history and perform a physical examination and laboratory assessment. These basic assessments provide the information for estimating perioperative risk and life expectancy after the proposed procedure.

Carefully consider whether the patient's current quality of life is sufficient to justify the operative intervention. In the case of elderly persons who may be debilitated or may have mental deterioration, this decision is made in conjunction with the patient and family.

Once the decision is made, identify comorbidities and risk factors that increase the operative risk or decrease survival. Ascertain the patient's activity level, stamina, and stability of health. Perform a thorough cardiac assessment tailored to the patient's history, symptoms, and results from preliminary screening tests such as the electrocardiogram and stress test.

Because COPD is an independent predictor of operative mortality, assess lung function by performing a room-air arterial blood gas measurement and pulmonary function tests. In patients with abnormal test results, preoperative intervention in the form of bronchodilators and pulmonary toilet often can reduce operative risks and postoperative complications.

Preoperative intravenous antibiotics (usually a cephalosporin) are administered to reduce the risk of infection. Arranging for appropriate intravenous accesses to accommodate blood loss, arterial pressure monitoring through an arterial line, and Foley catheter placement to monitor urine output are routine preparations for surgery.

For patients at high risk because of cardiac compromise, a Swan-Ganz catheter is placed to assist with cardiac monitoring and volume assessment. Transesophageal echocardiography can be useful to monitor ventricular volume and cardiac wall motion and to provide a guide with respect to fluid replacement and pressor use.

Prepare for blood replacement. The patient should have blood available for transfusion. Intraoperative Cell Saver use and preoperative autologous blood donation have become popular.

Maintain a normal body temperature during the operative intervention to prevent coagulopathy and maintain normal metabolic function. To prevent hypothermia, place a recirculating, warm forced-air blanket on the patient and warm any intravenous fluids and blood before administration.

In summary, the following are standard preoperatively:

Type and crossmatch bloodAdminister prophylactic antibiotics (cefazolin, 1 g intravenous piggyback)Insert a Foley catheterEstablish large-bore intravenous accessMonitor central venous pressure or establish Swan-Ganz catheterization (if indicated)Prepare the skin from the nipples to the mid thighAdminister general anesthesia (with or without epidural anesthesia)Cell Saver use has become popularInsert a nasogastric tubeIntraoperative details

The aorta may be approached either transabdominally or through the retroperitoneal space. Approach juxtarenal and suprarenal aortic aneurysms from the left retroperitoneal space.

Self-retaining retractors are used. Keep the bowel warm and, if possible, not exteriorized. The abdomen is explored for abnormalities (eg, gallstones, associated intestinal or pancreatic malignancy).

Depending on the patient's anatomy, the aorta can be reconstructed with a tube graft, an aortic iliac bifurcation graft, or an aortofemoral bypass.

For proximal infrarenal control, first identify the left renal vein. Occasionally (

Regarding pelvic outflow, in most instances, the inferior mesenteric artery is sacrificed. Therefore, to prevent colon ischemia, make every attempt to restore at least one hypogastric (internal iliac) artery perfusion. If the hypogastric arteries are sacrificed (associated aneurysms), reimplant the inferior mesenteric artery.

For supraceliac aortic control, first divide the ligaments to the left lateral segment of the liver and then retract the segment. The crura of the diaphragm are separated, and the aorta is bluntly dissected. Supraceliac control is recommended for inflammatory aneurysms.

The aorta is reconstructed from within using PTFE or Dacron. The aneurysm sac is closed, and the graft is put into the duodenum to prevent erosion.

Special considerations

Inflammatory aneurysms require supraceliac control, minimal dissection of the duodenum, and balloon occlusion of the iliac arteries. In patients with inflammatory aneurysms or large iliac artery aneurysms, identify the ureters; occasionally, ureteral stents are recommended in patients with inflammatory aneurysms.

Prevention of distal embolization

The patient is heparinized (5000 U intravenously) prior to aortic cross-clamping. If significant intraluminal debris, juxtarenal thrombus, or prior peripheral embolization is present, the distal arteries are clamped first, followed by aortic clamping.

Before restoring lower extremity blood flow, both forward flow (aortic) and back flow (iliac) are allowed to remove debris. The graft is also irrigated to flush out debris.

The colon is inspected prior to closure, and the femoral arteries are palpated. Before the patient leaves the operating room, determine lower extremity circulation. If a clot was dislodged at the time of aortic clamping, it can be removed with a Fogarty embolectomy catheter. Heparin reversal is not usually required.

PreviousNextPostoperative Details

Fluid shifts are common following aortic surgery. Fluid requirements may be high in the first 12 hours, depending on the amount of blood loss and fluid resuscitation in the operating room. Monitor the patient in the surgical intensive care unit for hemodynamic stability, bleeding, urine output, and peripheral pulses. A postoperative electrocardiogram and chest radiograph are needed. Prophylactic antibiotics (eg, cefazolin at 1 g) are administered for 24 hours.

The patient is seen in 1-2 weeks for suture or skin staple removal, then yearly thereafter.

PreviousNextPatient Education

For patient education information, see the Circulatory Problems Center and Cholesterol Center, as well as Aortic Aneurysm, High Cholesterol, and Cholesterol FAQs.

PreviousNextComplications

The following are potential complications of abdominal aortic aneurysms:

Death - 1.8-5% if elective and 50% if rupturedPneumonia - 5%Myocardial infarction - 2-5%Groin infection - Less than 5%Graft infection - Less than 1%Colon ischemia - Less than 1% if elective and 15-20% if rupturedRenal failure related to preoperative creatinine level, intraoperative cholesterol embolization, and hypotensionIncisional hernia - 10-20%Bowel obstructionAmputation from major arterial occlusionBlue toe syndrome and cholesterol embolization to feetImpotence in males - Erectile dysfunction and retrograde ejaculation (>30%)Paresthesias in thighs from femoral exposure (rare)Lymphocele in groin - Approximately 2%Late graft enteric fistulaPreviousNextEndovascular Stent Grafts

Endovascular stent grafts for the treatment of abdominal aortic aneurysm (AAA) are a less invasive form of treatment. Patients are discharged 1-2 days following surgery. The graft is placed through 2 small incisions. In September 2000, 2 grafts were approved by the US Food and Drug Administration (FDA). Since then, several more devices have received FDA approval.[8] Recently, the FDA has recommended careful follow-up because of persistent endoleaks and late ruptures.

In some instances, endoleaks represent continued pressurization of the sac (see image below). Aneurysm sacs may also demonstrate elevated pressure despite the absence of a demonstrable endoleak. This has been described as "endotension."

Persistently elevated aneurysm sac pressure, whether secondary to endoleak or endotension, is worrisome because it may progress to AAA rupture. Early data demonstrated a need for secondary interventions, via endovascular techniques, in as many as 10% of patients per year following endovascular aneurysm repair, compared with 2% in the first 5 years for open repair. Improvement has been made in the rate of secondary interventions following endovascular repair, but long-term durability has yet to be determined.

Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.

Informing the patient about these potential problems is important prior to implanting these grafts. In addition, patients with endografts require follow-up evaluation with serial CT scanning on a schedule that demands more office visits than are required for patients who receive conventional grafts.

Currently, endovascular repair is advocated for patients at increased risk for open aneurysm repair, but until results from randomized controlled trials are available, patient preference is the strongest determinant in deciding between endovascular and open aneurysm repair.

Previous, Emergent Management of Abdominal Aortic Aneurysm Rupture

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