ARTERIAL EMBOLISM AND ARTERIAL THROMBOSIS
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. 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 appropri-ate treatment.
Arterial emboli arise most commonly from thrombi that develop in the chambers of the heart as a result of atrial fibrillation, myo-cardial 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 ob-struct an artery that is smaller than the embolus. Emboli may also develop in advanced aortic atherosclerosis because the atheroma-tous plaques ulcerate or become rough. Acute thrombosis fre-quently occurs in patients with preexisting ischemic symptoms.
The symptoms of arterial emboli depend primarily on the size of the embolus, the organ involved, and the state of the collateral ves-sels. The immediate effect is cessation of distal blood flow. The blockage can progress above and below the obstruction. Secondary vasospasm can contribute to the ischemia. The embolus can frag-ment or break apart, resulting in occlusion of distal vessels. Em-boli 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 ar-terial embolism are pain, pallor, pulselessness, paresthesia, poi-kilothermia (coldness), and paralysis. Eventually, superficial veins may collapse because of decreased blood flow to the extremity. The part of the extremity below the occlusion is markedly colder and paler than the part above the occlusion because of ischemia.
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 ath-erosclerosis. 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, treat-ment is more difficult with a thrombus because the arterial oc-clusion has occurred in a degenerated vessel and requires more extensive reconstructive surgery to restore flow than is required with an embolic event.
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 echocardiography or transesophageal echocardiography, chest x-ray, and electrocardiography may re-veal underlying cardiac disease. Noninvasive duplex and Doppler ultrasonography can determine the presence and extent of un-derlying atherosclerosis, and arteriography may be performed.
Management of arterial thrombosis depends on its cause. Man-agement of acute embolic occlusion usually requires surgery be-cause 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, which is the most advanced stage. Heparin therapy is initiated immediately to prevent further development of emboli and to hamper the exten-sion of existing thrombi. Typically, an initial bolus of 5,000 to 10,000 units is administered intravenously, followed by a con-tinuous infusion of 1,000 units per hour until the patient is able to undergo surgery.
Emergency embolectomy is the procedure of choice only if the involved extremity is viable (Fig. 31-15). Arterial emboli are usually treated by insertion of an embolectomy catheter. The catheter is passed through a groin incision into the affected artery and ad-vanced past the occlusion. The 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.
When the patient has collateral circulation, treatment may in-clude intravenous anticoagulation with heparin, which can prevent the thrombus from spreading and reduce muscle necrosis. The use of intra-arterial thrombolytic medications helps to dissolve the embolus. Fibrin-specific thrombolytic medications (eg, tissue plas-minogen activator [t-PA, alteplase, Activase] and single-chain urokinase-type plasminogen activator [scu-PA, pro-urokinase]) avoid systemic depletion of circulating fibrinogen and plasmino-gen, which prevents the development of systemic fibrinolysis.
Other thrombolytic medications are reteplase (r-PA, Retavase), tenecteplase (TNKase), and staphylokinase (Moore, 2002). Al-though 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 can-not tolerate the several additional hours of ischemia that it takes for the agent to lyse (disintegrate) the clot. Contraindications to thrombolytic therapy include active internal bleeding, CVA (brain attack, stroke), recent major surgery, uncontrolled hyper-tension, and pregnancy.
Before surgery, the patient remains on bed rest with the 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. If possible, tape and electrocardiogram electrodes should not be used on the ex-tremity; sheepskin and foot cradles are used to protect the leg from mechanical trauma.
If the patient is treated with thrombolytic therapy, she or he is accurately weighed in kilograms, and the dose of thrombolytic therapy is determined based on the patient’s weight. The patient is admitted to a critical care unit for continuous monitoring. Vital signs are taken every 15 minutes for 2 hours, then every 30 min-utes for the next 6 hours, and then every hour for 16 hours. Bleeding is the most common side effect of thrombolytic therapy, and the patient is closely monitored for any signs of bleeding. The nurse also minimizes the number of punctures for inserting in-travenous lines, avoids intramuscular injections, prevents any possible tissue trauma, and applies pressure at least twice as long as usual after any puncture that 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 acti-vates plasminogen on the thrombus more than circulating plas-minogen, but it does not decrease the clotting factors as much as other thrombolytic therapies, so patients receiving t-PA are able to make new thrombi more easily than with some of the 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 en-courage the patient to move the leg to stimulate circulation and prevent stasis. Anticoagulant therapy may be continued after surgery to prevent thrombosis of the affected artery and to di-minish the development of subsequent thrombi at the initiating site. The nurse assesses for evidence of local and systemic hemor-rhage, including mental status changes, which can occur when anticoagulants are administered. Pulses, Doppler signals, ABI, and motor and sensory function are assessed every hour for the first 24 hours, because significant changes may indicate reocclu-sion. Metabolic abnormalities, renal failure, and compartment syndrome may be complications after an acute arterial occlusion.
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