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shear forces upon the aortic wall leading to disruption of the intima (Singh, Khaja, & Alpert, 2010).
Dissection is caused by rupture in the intimal layer. A rupture may occur through adventitia or into
the lumen through the intima, allowing blood to reenter the main channel and resulting in chronic
dissection (e.g., pseudoaneurysm) or occlusion of branches of the aorta.
As the separation progresses, the arteries branching from the involved area of the aorta shear and occlude. The
tear occurs most commonly in the region of the aortic arch, with the highest mortality rate associated with
ascending aortic dissection (Dixon, 2011). The dissection of the aorta may progress backward in the direction of
the heart, obstructing the openings to the coronary arteries or producing hemopericardium (effusion of blood into
the pericardial sac) or aortic insufficiency, or it may extend in the opposite direction, causing occlusion of the
arteries supplying the gastrointestinal tract, kidneys, spinal cord, and legs.

Clinical Manifestations
Onset of symptoms is usually sudden. Severe and persistent pain, described as tearing or ripping, may be reported.
The pain is in the anterior chest or back and extends to the shoulders, epigastric area, or abdomen. Aortic
dissection may be mistaken for an acute myocardial infarction, which could confuse the clinical picture and initial
treatment. Cardiovascular, neurologic, and gastrointestinal symptoms are responsible for other clinical
manifestations, depending on the location and extent of the dissection. The patient may appear pale. Sweating and
tachycardia may be detected. Blood pressure may be elevated or markedly different from one arm to the other if
dissection involves the orifice of the subclavian artery on one side.

Assessment and Diagnostic Findings

Arteriography, multidetector computed tomography angiography (MDCTA), TEE, duplex ultrasonography, and
MRA, while limited in terms of expediency during an emergency situation, may aid in the diagnosis.

Medical Management
The medical or surgical treatment of a dissecting aorta depends on the type of dissection present and follows the
general principles outlined for the treatment of thoracic aortic aneurysms.

Nursing Management
A patient with a dissecting aorta requires the same nursing care as a patient with an aortic aneurysm requiring
surgical intervention, as described earlier in this chapter. Interventions described in Chart 30-3 are also
appropriate.

Arterial Embolism and Arterial Thrombosis

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Acute vascular occlusion may be caused by an embolus or acute thrombosis. Acute arterial occlusions may result
from iatrogenic injury, which can occur during insertion of invasive catheters such as those used for arteriography,
PTA or stent placement, or an intra-aortic balloon pump, or it may occur as a result of IV drug abuse. Other causes
include trauma from a fracture, crush injury, and penetrating wounds that disrupt the arterial intima. The accurate
diagnosis of an arterial occlusion as embolic or thrombotic in origin is necessary to initiate appropriate treatment.

Pathophysiology
Arterial emboli arise most commonly from thrombi that develop in the chambers of the heart as a result of atrial
fibrillation, myocardial infarction, infective endocarditis, or chronic heart failure. These thrombi become detached
and are carried from the left side of the heart into the arterial system, where they lodge in and obstruct an artery
that is smaller than the embolus. Emboli may also develop in advanced aortic atherosclerosis because the
atheromatous plaques ulcerate or become rough. Acute thrombosis frequently occurs in patients with preexisting
ischemic symptoms.

Clinical Manifestations
Symptoms of arterial emboli depend primarily on the size of the embolus, organ involvement, and the state of
collateral vessels. The immediate effect is cessation of distal blood flow. The blockage can progress distal and
proximal to the site of the obstruction. Secondary vasospasm can contribute to the ischemia. The embolus can
fragment or break apart, resulting in occlusion of distal vessels. Emboli tend to lodge at arterial bifurcations and
areas narrowed by atherosclerosis. Cerebral, mesenteric, renal, and coronary arteries are often involved in addition
to the large arteries of the extremities.
The symptoms of acute arterial embolism in extremities with poor collateral flow are acute, severe pain and a
gradual loss of sensory and motor function. The six Ps associated with acute arterial embolism are pain, pallor,
pulselessness, paresthesia, poikilothermia (coldness), and paralysis. Eventually, superficial veins may collapse
because of decreased blood flow to the extremity. Because of ischemia, the part of the extremity distal to the
occlusion is markedly colder and paler than the part proximal to the occlusion.
Arterial thrombosis can also acutely occlude an artery. A thrombosis is a slowly developing clot that usually
occurs where the arterial wall has become damaged, generally as a result of atherosclerosis. Thrombi may also
develop in an arterial aneurysm. The manifestations of an acute thrombotic arterial occlusion are similar to those
described for embolic occlusion. However, treatment is more difficult with a thrombus because the arterial
occlusion has occurred in a degenerated vessel and requires more extensive reconstructive surgery to restore flow
than is required with an embolic event.

Assessment and Diagnostic Findings

An arterial embolus is usually diagnosed on the basis of the sudden nature of the onset of symptoms and an
apparent source for the embolus. Two-dimensional transthoracic echocardiography or TEE, chest x-ray, and
electrocardiography (ECG) may reveal underlying cardiac disease. Noninvasive duplex and Doppler
ultrasonography can determine the presence and extent of underlying atherosclerosis, and arteriography may be
performed.

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Medical Management
Management of arterial thrombosis depends on its cause. Management of acute embolic occlusion usually requires
surgery because time is of the essence. Because the onset of the event is acute, collateral circulation has not
developed, and the patient quickly moves through the list of six Ps to paralysis, the most advanced stage. Heparin
therapy is initiated immediately to prevent further development of emboli and to prevent the extension of existing
thrombi. Typically, an initial IV bolus of 60 U/kg body weight is administered, followed by a continuous infusion
of 12 U/kg/h until the patient undergoes interventional treatment or surgery.

Minimally Invasive Interventional Management

Emergency embolectomy is the procedure of choice if the involved extremity is viable (Fig. 30-13). Arterial
emboli are usually treated by insertion of an embolectomy catheter. The catheter is passed through a groin incision
into the affected artery and advanced past the occlusion. The catheter balloon is inflated with sterile saline
solution, and the thrombus is extracted as the catheter is withdrawn. This procedure involves incising the vessel
and removing the clot.

Endovascular Management

Percutaneous mechanical thrombectomy devices may also be used for the treatment of an acute thrombosis. All
endovascular devices necessitate obtaining access to the patient’s arterial system and inserting a catheter into the
patient’s artery to obtain access to the thrombus. The approach is similar to that used for angiograms in that it is
made through the groin to the femoral artery. Some devices require that a small incision be made into the patient’s
artery. These devices may use (1) a jet of fluid to disrupt the thrombus and then aspirate the particles; (2) a
rotating, sinusoidal-shaped wire that mixes a thrombolytic agent that simultaneously dissolves the clot; or (3)
high-frequency, low-energy ultrasound to dissolve an occlusive thrombus. Complications arising from the use of
any of the endovascular devices may include arterial dissection or distal artery embolization.

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FIGURE 30-13 • Extraction of an embolus by balloon-tipped

embolectomy catheter. The deflated balloon-tipped catheter is
advanced past the embolus, inflated, and then gently withdrawn,
carrying the embolic material with it. Adapted with permission from
Rutherford, R. B. (2005). Vascular surgery (6th ed., Vols. I and II).
Philadelphia: Elsevier.

Pharmacologic Therapy

When the patient has adequate collateral circulation, treatment may include IV anticoagulation with heparin,
which can prevent the thrombus from spreading and reduce muscle necrosis. Intra-arterial thrombolytic
medications are used to dissolve the embolus. Fibrin-specific thrombolytic medications (e.g., tissue plasminogen
activator [t-PA, alteplase, Activase] and single-chain urokinase-type plasminogen activator [scu-PA,
prourokinase]) do not deplete circulating fibrinogen and plasminogen, which prevents the development of
systemic fibrinolysis. Other thrombolytic medications are reteplase (r-PA, Retavase) and tenecteplase (TNKase)
(Rivera-Bou, Cabanas, Villanueva, et al., 2012). Although these agents differ in their pharmacokinetics, they are
administered in a similar manner: A catheter is advanced under x-ray visualization to the clot, and the
thrombolytic agent is infused.
Thrombolytic therapy should not be used when there are known contraindications to therapy or when the
extremity cannot tolerate the several additional hours of ischemia that it takes for the agent to lyse (disintegrate)
the clot. Contraindications to peripheral thrombolytic therapy include active internal bleeding, cerebrovascular
hemorrhage, recent major surgery, uncontrolled hypertension, and pregnancy.

Nursing Management
Before an intervention or surgery, the patient remains on bed rest with the affected extremity level or slightly
dependent (15 degrees). The affected part is kept at room temperature and protected from trauma. Heating and
cooling pads are contraindicated because ischemic extremities are easily traumatized by alterations in temperature.

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If possible, tape and ECG electrodes should not be used on the extremity; sheepskin and foot cradles are used to
protect an affected leg from mechanical trauma (Gist, Tio-Matos, Falzgraf, et al., 2009).
If the patient is treated with thrombolytic therapy, the dose is based on the patient’s weight. The patient is
admitted to a critical care unit for continuous monitoring. Vital signs are taken initially every 15 minutes and then
at progressively longer intervals if the patient’s status remains stable. The patient is closely monitored for
bleeding. The nurse minimizes the number of punctures for inserting IV lines and obtaining blood samples, avoids
intramuscular injections, prevents any possible tissue trauma, and applies pressure at least twice as long as usual
after any puncture is performed. If t-PA is used for the treatment, heparin is usually administered to prevent
another thrombus from forming at the site of the lesion. The t-PA activates plasminogen on the thrombus, but it
does not decrease the clotting factors as much as other thrombolytic therapies, so patients receiving t-PA can make
new thrombi more readily than if they receive other thrombolytics.
During the postoperative period, the nurse collaborates with the surgeon about the patient’s appropriate activity
level based on the patient’s condition. Generally, every effort is made to encourage the patient to move the

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