RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 9. Vascular Disorders

Vascular disorders can affect the arteries, the veins, or both types of vessels. Arterial disorders include aneurysms, which result from a weakening of the arterial wall; arterial occlusive disease, which commonly results from atherosclerotic narrowing of the artery's lumen; and Raynaud's disease, which may be linked to immunologic dysfunction. Thrombophlebitis, a venous disorder, results from inflammation or occlusion of the affected vessel.

ABDOMINAL AORTIC ANEURYSM

Abdominal aortic aneurysm (AAA), an abnormal dilation in the arterial wall, generally occurs in the aorta between the renal arteries and iliac branches. Rupture, in which the aneurysm breaks open, resulting in profuse bleeding, is a common complication that occurs in larger aneurysm. Dissection occurs when the artery's lining tears and blood leaks into the walls.

AAA is four times more common in men than in women and is most prevalent in whites ages 40 to 70. Less than half of people with a ruptured AAA survive.

Pathophysiology

Aortic aneurysms develop slowly. First, a focal weakness in the muscular layer of the aorta (tunica media), caused by degenerative changes, allows the inner layer (tunica intima) and outer layer (tunica adventitia) to stretch outward. Blood pressure within the aorta progressively weakens the vessel walls and enlarges the aneurysm.

Nearly all AAAs are fusiform, which causes the arterial walls to balloon on all sides. The resulting sac fills with necrotic debris and thrombi.

About 95% of abdominal aneurysms result from arteriosclerosis or atherosclerosis; the rest, from cystic medial necrosis, trauma, hypertension, blunt abdominal injury, syphilis, and other infections.

Complications

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Rupture

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Obstruction of blood flow to other organs

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Embolization to a peripheral artery

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Diminished blood supply to vital organs resulting in organ failure (with rupture)

Assessment findings

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Most patients with abdominal aneurysms are asymptomatic until the aneurysm enlarges and compresses surrounding tissue.

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A large aneurysm may produce signs and symptoms that mimic renal calculi, lumbar disk disease, and duodenal compression.

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The patient may complain of gnawing, generalized, steady abdominal pain or low back pain that's unaffected by movement. He may have a sensation of gastric or abdominal fullness caused by pressure on the GI structures.

ff2-b01382759RED FLAG

Sudden onset of severe abdominal pain or lumbar pain that radiates to the flank and groin from pressure on lumbar nerves may signify enlargement and imminent rupture. If the aneurysm ruptures into the peritoneal cavity, severe and persistent abdominal and back pain, mimicking renal or ureteral colic, occurs. If it ruptures into the duodenum, GI bleeding occurs with massive hematemesis and melena.

·

The patient may have a syncopal episode when an aneurysm ruptures, causing hypovolemia and a subsequent drop in blood pressure. Once a clot forms and the bleeding stops, he may again be asymptomatic or have abdominal pain because of bleeding into the peritoneum.

·

Inspection of the patient with an intact abdominal aneurysm usually reveals no significant findings. However, if the patient isn't obese, you may notice a pulsating mass in the periumbilical area.

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If the aneurysm has ruptured, you may notice signs of hypovolemic shock, such as skin mottling, decreased level of consciousness (LOC), diaphoresis, and oliguria.

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The abdomen may appear distended, and an ecchymosis or hematoma may be present in the abdominal, flank, or groin area.

·

Paraplegia may occur if the aneurysm rupture reduces blood flow to the spine.

·

 

·

Palpation of the abdomen may disclose some tenderness over the affected area. A pulsatile mass may be felt; however, avoid deep palpation to locate the mass because this may cause the aneurysm to rupture.

·

Palpation of the peripheral pulses may reveal absent pulses distal to a ruptured aneurysm.

Diagnostic test results

Because an abdominal aneurysm seldom produces symptoms, it's typically detected accidentally on an X-ray or during a routine physical examination.

Several tests can confirm suspected abdominal aneurysm:

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Abdominal ultrasonography or echocardiography can help determine the size, shape, and location of the aneurysm.

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Anteroposterior and lateral X-rays of the abdomen can be used to detect aortic calcification, which outlines the mass, at least 75% of the time.

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A computed tomography scan can be used to visualize the aneurysm's effect on nearby organs, particularly the position of the renal arteries in relation to the aneurysm.

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Aortography shows the condition of vessels proximal and distal to the aneurysm and the extent of the aneurysm, but the diameter of the aneurysm may be underestimated because aortography shows only the flow channel and not the surrounding clot.

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Magnetic resonance imagining can be used as an alternative to aortography.

Treatment

Usually, abdominal aneurysm requires resection of the aneurysm and Dacron graft replacement of the aortic section. If the aneurysm is small and produces no symptoms, surgery may be delayed; however, small aneurysms can rupture. A beta-adrenergic receptor blocker may be given to decrease the rate of growth of the aneurysm. Regular physical examination and ultrasound checks help monitor progression of the aneurysm. Large aneurysms or those that produce symptoms risk rupture and require immediate repair. In asymptomatic patients, surgery is advised when the aneurysm is 5 to 6 cm in diameter. In symptomatic patients, repair is indicated regardless of size. In patients with

poor perfusion distal to the aneurysm, external grafting may be done. (See Repairing abdominal aortic aneurysms with endovascular grafting.)

REPAIRING ABDOMINAL AORTIC ANEURYSMS WITH ENDOVASCULAR GRAFTING

Endovascular grafting is a minimally invasive procedure used to repair abdominal aortic aneurysms. Such grafting reinforces the walls of the aorta to prevent rupture and prevents expansion of the aneurysm.

The procedure is performed with fluoroscopic guidance, with a delivery catheter with an attached compressed graft inserted through a small incision into the femoral or iliac artery over a guide wire. The delivery catheter is advanced into the aorta, where it's positioned across the aneurysm. A balloon on the catheter expands the graft and affixes it to the vessel wall. The procedure generally takes 2 to 3 hours to perform. Patients are instructed to walk the first day after surgery and are discharged from the facility in 1 to 3 days.

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For patients with acute dissection, emergency treatment before surgery includes resuscitation with fluid and blood replacement, I.V. propranolol (Inderal) to reduce myocardial contractility, I.V. nitroprusside (Nitropress) to reduce and maintain blood pressure to 100 to 120 mm Hg systolic, and an analgesic to relieve pain. An arterial line and indwelling urinary catheter are inserted to monitor the patient's condition.

Nursing interventions

IN A NONACUTE SITUATION

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Allow the patient to express his fears and concerns. Help him identify effective coping strategies as he attempts to deal with his diagnosis.

·

 

 

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Before elective surgery, weigh the patient, insert an indwelling urinary catheter and an I.V. line, and assist with insertion of the arterial line and pulmonary artery catheter to monitor hemodynamic balance.

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Give a prophylactic antibiotic as ordered.

IN AN ACUTE SITUATION

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Monitor the patient's vital signs on his admission to the intensive care unit (ICU).

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Insert an I.V. line with at least a 18G needle to facilitate blood replacement.

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Obtain blood samples for kidney function tests (such as blood urea nitrogen, creatinine, and electrolyte levels), a complete blood count with differential, blood typing and crossmatching, and arterial blood gas (ABG) levels.

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Monitor the patient's cardiac rhythm strip. Insert an arterial line to allow for continuous blood pressure monitoring. Assist with insertion of a pulmonary artery line to monitor for hemodynamic balance.

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Give drugs, such as an antihypertensive and a beta-adrenergic receptor blocker to control aneurysm progression and an analgesic to relieve pain.

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Look for signs of rupture, which may be immediately fatal. Watch closely for signs of acute blood loss (such as decreasing blood pressure, increasing pulse and respiratory rates, restlessness, decreased sensorium, and cool, clammy skin).

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If rupture occurs, get the patient to surgery immediately. Medical antishock trousers may be used while transporting him to surgery.

AFTER SURGERY

·

 

·

Assess fluid status, and replace fluids as needed to ensure adequate hydration.

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Watch for signs of bleeding (such as increased pulse and respiratory rates, and hypotension), which may occur retroperitoneally from the graft site.

·

Check abdominal dressings for excessive bleeding or drainage. Assess the wound site for evidence of infection. Be alert for temperature elevations and other signs of infection. Use sterile technique to change dressings.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH AN ABDOMINAL AORTIC ANEURYSM

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Review incisional care.

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Instruct the patient to look at his incision daily and report any signs or symptoms of infection to the surgeon.

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Make sure the patient knows when to see the surgeon for follow-up care.

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Instruct the patient to take all drugs as prescribed and to carry a list of drugs at all times, in case of an emergency.

·

Tell the patient not to push, pull, or lift heavy objects until the practitioner indicates that it's okay to do so.

·

After nasogastric intubation for intestinal decompression, irrigate the tube frequently to ensure patency. Record the amount and type of drainage.

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Large amounts of blood may be needed during the resuscitative period to replace blood loss. Thus, renal failure due to ischemia is a major postoperative complication, possibly requiring hemodialysis.

ff2-b01382759RED FLAG

Assess for return of severe back pain, which can indicate that the graft is tearing.

·

Mechanical ventilation is required after surgery. Assess the depth, rate, and character of respirations and breath sounds at least every hour. Have the patient cough, or suction the endotracheal tube, as needed, to maintain a clear airway. If the patient can breathe unassisted and has good breath sounds and adequate ABG levels, tidal volume, and vital capacity 24 hours after surgery, he will be extubated and will require oxygen by mask.

·

Weigh the patient daily to evaluate fluid balance.

·

Provide frequent turning, and help the patient walk as soon as he's able (generally the second day after surgery). (See Teaching the patient with an abdominal aortic aneurysm.)

FEMORAL AND POPLITEAL ANEURYSMS

Because femoral and popliteal aneurysms occur in the two major peripheral arteries, they're also known as peripheral arterial aneurysms.

This condition is most common in men older than age 50. Elective surgery before complications arise greatly improves the prognosis.

Causes

Femoral and popliteal aneurysms may be fusiform (spindle-shaped) or saccular (pouchlike). Fusiform types are three times more common. Aneurysms may be singular or multiple segmental lesions, in many instances affecting both legs, and may accompany other arterial aneurysms located in the abdominal aorta or iliac arteries.

Femoral and popliteal aneurysms usually result from progressive atherosclerotic changes in the arterial walls (medial layer). Rarely, they result from congenital weakness in the arterial wall. They may also result from blunt or penetrating trauma, bacterial infection, or peripheral vascular reconstructive surgery (which causes pseudoaneurysms, also called false aneurysms, where a blood clot forms a second lumen).

Complications

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Thrombosis

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Emboli

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Gangrene

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Poor tissue perfusion to areas distal to the aneurysm may require amputation

Assessment findings

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The patient may report pain in the popliteal space when a popliteal aneurysm is large enough to compress the medial popliteal nerve.

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Inspection may reveal edema and venous distention if the vein is compressed.

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Femoral and popliteal aneurysms can produce signs and symptoms of severe ischemia in the leg or foot resulting from acute thrombosis within the aneurysmal sac, embolization of mural thrombus fragments and, rarely, rupture.

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A patient with acute aneurysmal thrombosis may report severe pain.

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Inspection may reveal distal petechial hemorrhages from aneurysmal emboli. The affected leg or foot may show loss of color.

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Palpation of the affected leg or foot may indicate coldness and a loss of pulse. Gangrene may develop.

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DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH FEMORAL AND POPLITEAL ANEURYSM

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Tell the patient to report recurrence of symptoms immediately because the saphenous vein graft replacement can fail or another aneurysm may develop.

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Explain to the patient with popliteal artery resection that swelling may persist for some time. If using antiembolism stockings, make sure they fit properly, and teach the patient how to apply them. Warn against wearing constrictive apparel.

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If the patient is receiving an anticoagulant, suggest measures to prevent accidental bleeding such as using an electric razor. Tell the patient to report signs of bleeding immediately (for example, bleeding gums, tarry stools, and easy bruising). Explain the importance of follow-up blood studies to monitor anticoagulant therapy. Warn the patient to avoid trauma, tobacco, and aspirin.

Diagnostic test results

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Arteriography or ultrasonography may help resolve doubtful situations. Arteriography may also detect associated aneurysms, especially those in the abdominal aorta and the iliac arteries.

·

Ultrasonography may also help determine the size of the femoral or popliteal artery.

Treatment

Femoral and popliteal aneurysms require surgical bypass and reconstruction of the artery, usually with an autogenous saphenous vein graft replacement. Arterial occlusion that causes severe ischemia and gangrene may require leg amputation.

Nursing interventions

BEFORE ARTERIAL SURGERY

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Assess and record the patient's circulatory status, noting the location and quality of peripheral pulses in the affected leg.

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Give a prophylactic antibiotic or anticoagulant.

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Discuss expected postoperative procedures, review the explanation of the surgery, and answer the patient's questions.

AFTER ARTERIAL SURGERY

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Carefully monitor the patient for early signs and symptoms of thrombosis or graft occlusion (such as loss of pulse, decreased skin temperature and sensation, and severe pain) and infection (such as fever).

 

·

Palpate distal pulses at least every hour for the first 24 hours and then as often as ordered. Correlate these findings with the preoper-ative circulatory assessment. Mark the sites on the patient's skin where pulses are palpable to facilitate repeated checks.

·

Help the patient walk soon after surgery to prevent venous stasis and, possibly, thrombus formation. (See Teaching the patient with femoral and popliteal aneurysm.)

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Peripheral arterial occlusive disease is an obstruction or narrowing of the lumen of the aorta and its major branches, which interrupts blood flow, usually to the legs and feet. Arterial occlusive disease may affect the carotid, vertebral, innominate, subclavian, mesenteric, and celiac arteries. (See Possible sites of major artery occlusion, page 452.)

Peripheral arterial occlusive disease is more common in men than in women. The prognosis depends on the location of the occlusion, the development of collateral circulation to counteract reduced blood flow and, in patients with acute disease, the time elapsed between the development of the occlusion and its removal.

Pathophysiology

Peripheral arterial occlusive disease is almost always the result of atherosclerosis in which fatty, fibrous plaques narrow the lumen of blood vessels. This occlusion can occur acutely or progressively over 20 to 40 years, with areas of vessel branching, or bifurcation, being the most common sites. The narrowing of the lumens reduces the blood volume that can flow through them, causing arterial insufficiency to the affected area. Ischemia usually occurs after the vessel lumens have narrowed by at least 50%, reducing blood flow to levels which no longer meet the needs of tissues and nerves.

Arterial occlusive disease is a common complication of atherosclerosis. The occlusive mechanisms may be endogenous, due to emboli formation or thrombosis, or exogenous, due to trauma or fracture. (See What causes acute arterial occlusion? page 453.)

Predisposing factors include smoking; aging; conditions such as hypertension, hyperlipidemia, and diabetes mellitus; and family history of vascular disorders, myocardial infarction, or stroke.

ff1-b01382759AGE AWARE

Aging causes sclerotic changes in blood vessels, which leads to decreased elasticity and narrowing of the lumen, further contributing to the development of peripheral arterial occlusive disease. In people older than age 70, the prevalence of the disease is estimated to be 10% to 18%.

POSSIBLE SITES OF MAJOR ARTERY OCCLUSION

Listed below are some of the possible sites of major artery occlusions.

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WHAT CAUSES ACUTE ARTERIAL OCCLUSION?

The most common cause of acute arterial occlusion is obstruction of a major artery by a clot. The occlusive mechanism may be endogenous, resulting from emboli formation, thrombosis, or plaques, or exogenous, resulting from trauma or fracture.

Embolism

Often the obstruction results from an embolus originating in the heart. Emboli typically lodge in the arms and legs, where blood vessels narrow or branch. In the arms, emboli usually lodge in the brachial artery but may occlude the subclavian or axillary arteries. Common leg sites include the iliac, femoral, and popliteal arteries. Emboli originating in the heart can cause neurologic damage if they enter the cerebral circulation.

Thrombosis

In a patient with atherosclerosis and marked arterial narrowing, thrombosis may cause acute intrinsic arterial occlusion. This complication typically arises in areas with severely stenotic vessels, especially in a patient who also has heart failure, hypovolemia, polycythemia, or traumatic injury.

Plaques

Atheromatous debris (plaques) from proximal arterial lesions may also intermittently obstruct small vessels (usually in the hands or feet). These plaques may also develop in the brachiocephalic vessels and travel to the cerebral circulation, where they may lead to transient cerebral ischemia or infarction.

Exogenous causes

Acute arterial occlusion may stem from insertion of an indwelling arterial catheter or intra-arterial drug abuse.

Extrinsic arterial occlusion can also result from direct blunt or penetrating trauma to the artery.

Complications

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Severe ischemia and necrosis

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Skin ulceration

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Gangrene, which can lead to limb amputation

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Impaired nail and hair growth

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Stroke or transient ischemic attack

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Peripheral or systemic embolism

Assessment findings

Varied assessment findings depend on the vessel involved. (See Signs and symptoms of peripheral arterial occlusive disease, pages 454 and 455.)

SIGNS AND SYMPTOMS OF PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

A patient with arterial occlusive disease may have a wide variety of signs and symptoms depending on which portion of the vasculature is affected by the disorder.

SITE OF OCCLUSION

SIGNS AND SYMPTOMS

 

Transient ischemic attacks (TIAs) due to reduced cerebral circulation produce unilateral sensory or motor dysfunction (transient monocular blindness, hemiparesis), possible aphasia or dysarthria, confusion, decreased mentation, and headache (these recurrent clinical features usually last for 5 to 10 minutes but may persist for up to 24 hours and may herald a stroke; absent or decreased pulsation with an auscultatory bruit over the affected vessels)

Vertebral and basilar arteries

TIAs of brain stem and cerebellum (less common than carotid TIA), producing binocular visual disturbances, vertigo, dysarthria, and falling down without loss of consciousness

Innominate (brachiocephalic) artery

Signs and symptoms of vertebrobasilar occlusion, indications of ischemia (claudication) of right arm, possible bruit over right side of neck

 

Subclavian steal syndrome characterized by backflow of blood from the brain through the vertebral artery on the same side as the occlusion, into the subclavian artery distal to the occlusion, clinical effects of vertebrobasilar occlusion and exercise-induced arm claudication, possible gangrene (usually limited to the digits)

Mesenteric artery

Bowel ischemia, infarct necrosis, and gangrene; sudden, acute abdominal pain; nausea and vomiting; diarrhea; leukocytosis; shock due to massive intraluminal and plasma loss

Aortic bifurcation (saddle block occlusion, a medical emergency associated with cardiac embolization)

Sensory and motor deficits (muscle weakness, numbness, paresthesia, paralysis), signs and symptoms of ischemia (sudden pain; cold, pale legs with decreased or absent peripheral pulses) in both legs

Iliac artery (Leriche's syndrome)

Intermittent claudication of lower back, buttocks, and thighs, relieved by rest; absent or reduced femoral or distal pulses; shiny, scaly skin, subcutaneous tissue loss, and no body hair on affected limb; nail deformities; increased capillary refill time; blanching of feet on elevation; possible bruit over femoral arteries; impotence in males

Femoral and popliteal arteries (associated with aneurysm formation)

Intermittent claudication of the calves on exertion; ischemic pain in feet; pretrophic pain (heralds necrosis and ulceration); leg pallor and coolness; shiny, scaly skin, subcutaneous tissue loss, and no body hair on affected limb; nail deformities; increased capillary refill time; blanching of feet on elevation; gangrene; no palpable pulses distal to occlusion (auscultation over affected area may reveal a bruit)

Peripheral cute arterial occlusion occurs suddenly, in many cases without warning. However, peripheral occlusion can usually be recognized by the five Ps:

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Pain, the most common symptom, occurs suddenly and is localized to the affected arm or leg.

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Pallor results from vasoconstriction distal to the occlusion.

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Paralysis and paresthesia occur in the affected arm or leg from disturbed nerve endings or skeletal muscles.

A sixth P, known as poikilothermy, refers to temperature changes that occur distal to the occlusion, making the skin feel cool.

Diagnostic test results

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Arteriography demonstrates the type, location, and degree of obstruction and the establishment of collateral circulation. It's particularly useful for monitoring patients with chronic disease and for evaluating candidates for reconstructive surgery.

 

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Ultrasonography and plethysmography are noninvasive tests that, in patients with acute disease, show decreased blood flow distal to the occlusion.

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Doppler ultrasonography typically reveals a relatively low-pitched sound and a monophasic waveform.

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Segmental limb pressures and pulse volume measurements help evaluate the location and extent of the occlusion.

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Ophthalmodynamometry helps determine the degree of obstruction in the internal carotid artery by comparing ophthalmic artery pressure with brachial artery pressure on the affected side. More than a 20% difference between pressures suggests arterial insufficiency.

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Electroencephalography and a computed tomography scan may be necessary to rule out brain lesions.

Treatment

In patients with mild chronic disease, treatment usually consists of supportive measures: smoking cessation, hypertension control, walking, and foot and leg care. In patients with carotid artery occlusion, antiplatelet therapy may begin with dipyridamole (Persantine) and aspirin or clopidogrel (Plavix). For those patients with intermittent claudication caused by chronic peripheral arterial occlusive disease, pentoxifylline (Trental) may improve blood flow through the capillaries. This drug is particularly useful for those who aren't good surgical candidates.

Thrombolytics—such as urokinase (Abbokinase), streptokinase (Streptase), and alteplase (Activase)—can dissolve clots and relieve the obstruction caused by a thrombus.

Acute peripheral arterial occlusive disease usually requires surgery, such as:

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embolectomy. A balloon-tipped catheter is used to remove thrombotic material from the artery. Embolectomy is used mainly for mesenteric, femoral, or popliteal artery occlusion.

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thromboendarterectomy. This involves the opening of the artery and removal of the obstructing thrombus and the medial layer of the arterial wall. Plaque deposits remain intact. Thromboendarterectomy is usually performed after angiography and is commonly used with autogenous vein or Dacron bypass surgery (femoropopliteal or aortofemoral).

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atherectomy. Plaque is excised using a drill or slicing mechanism.

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balloon angioplasty. The obstruction is compressed using balloon inflation.

 

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laser angioplasty. Excision and a hot-tip laser are used to vaporize the destruction.

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stents. A mesh of wires that stretch and mold to the arterial walls are inserted to prevent reocclusion.

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combined therapy. Any of the above treatments may be used concomitantly.

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percutaneous transluminal coronary angioplasty (PTCA). Using fluoroscopy and a special balloon catheter, the stenosis or occluded artery is dilated to a predetermined diameter without overdistending it.

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laser surgery. An excimer or a hot-tip laser obliterates the clot and plaque by vaporizing it.

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patch grafting. This involves removal of the thrombosed arterial segment and replacement with an autogenous vein or Dacron graft.

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bypass graft. Blood flow is diverted through an anastomosed autogenous or woven Dacron graft to bypass the thrombosed arterial segment.

Amputation may be necessary if arterial reconstructive surgery fails or if gangrene, uncontrollable infection, or intractable pain develops.

Other therapy includes heparin to prevent emboli (for embolic occlusion) and bowel resection after restoration of blood flow (for mesenteric artery occlusion).

Nursing interventions

FOR PATIENTS WITH CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

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Prevent trauma to the affected extremity. Use minimal pressure mattresses, heel protectors, a foot cradle, or a footboard to reduce pressure that could lead to skin breakdown. Keep the arm or leg warm, but never use heating pads. If the patient is wearing socks, remove them frequently to check the skin.

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Avoid using restrictive clothing such as antiembolism stockings.

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Give an analgesic to relieve pain.

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Allow the patient to express fears and concerns, and help him identify and use effective coping strategies.

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Assess the patient's circulatory status by checking for the most distal pulses and by inspecting his skin color and temperature.

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Give an analgesic to relieve pain.

 

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Give heparin or a thrombolytic by continuous I.V. drip. Use an infusion pump to ensure the proper flow rate.

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Wrap the patient's affected foot in soft cotton batting, and reposition it frequently to prevent pressure on one area.

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Strictly avoid elevating or applying heat to the affected leg.

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Watch for signs of fluid and electrolyte imbalance, and monitor intake and output for signs of renal failure (such as urine output of less than 30 ml/hour).

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If the patient has carotid, innominate, vertebral, or subclavian artery occlusion, monitor him for signs of stroke, such as numbness in an arm or a leg and intermittent blindness.

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Monitor the patient's vital signs. Continuously assess his circulatory function by assessing skin color and temperature and by checking for distal pulses. In charting, compare earlier assessments and observations. Watch closely for signs of hemorrhage (such as tachycardia and hypotension), and check dressings for excessive bleeding.

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If the patient has a carotid, innominate, vertebral, or subclavian artery occlusion, assess neurologic status frequently for changes in level of consciousness, pupil size, and muscle strength.

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If the patient has a mesenteric artery occlusion, connect a nasogastric tube to low intermittent suction. Monitor intake and output (low urine output may indicate damage to renal arteries during surgery). Check bowel sounds for the return of peristalsis. Increasing abdominal distention and tenderness may indicate extension of bowel ischemia with resulting gangrene, necessitating further excision, or it may indicate peritonitis.

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If the patient has a saddle block occlusion, check distal pulses for adequate circulation. Watch for signs of renal failure and mesenteric artery occlusion (severe abdominal pain) and for cardiac arrhythmias, which may precipitate embolus formation.

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If PTCA was performed, sheath (catheter) care must be done. The line must be kept open with a heparin infusion; monitor the insertion site for bleeding. Keep the catheterized leg immobile, and keep the patient on strict bed rest. Monitor and record pulses in the catheterized leg. Provide an analgesic for back pain associated with catheter placement.

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If the patient has an iliac artery occlusion, monitor urine output for signs of renal failure from decreased perfusion to the kidneys as a result of surgery. Provide meticulous catheter care.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

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When preparing the patient for discharge, instruct him to watch for signs and symptoms of recurrence (such as pain, pallor, numbness, paralysis, or absence of pulse) that can result from graft occlusion or occlusion at another site. Caution against wearing constrictive clothing, crossing legs, bumping affected limbs, and wearing garters.

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Warn the patient to avoid all tobacco products.

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Tell the patient to avoid temperature extremes. If he must go outside in the cold, remind him to dress warmly and take special care to keep his feet warm.

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Instruct the patient to wash his feet daily and inspect them for signs of injury or infection. Remind him to report abnormalities to the practitioner.

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Advise the patient to wear sturdy, properly fitting shoes. Refer him to a podiatrist for foot problems.

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Teach the patient about preventive measures, such as smoking cessation, regular exercise, weight control, reduction of dietary fat intake, and avoidance of pressure and constriction to extremities. These measures may reduce the risk of arterial occlusive disease, especially in patients with a history of cardiovascular disease.

·

If the patient has a femoral or popliteal artery occlusion, assist with early ambulation, and don't allow the patient to sit for an extended period.

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When caring for a patient who has undergone amputation, check the stump carefully for drainage. If drainage occurs, note and record its color and amount, and the time. Elevate the stump, if indicated, and give an analgesic as needed. Because phantom limb pain is common, explain this phenomenon to the patient. (See Teaching the patient with peripheral arterial occlusive disease.)

RAYNAUD'S DISEASE

Raynaud's disease—also known as vasospastic arterial disease—is one of several primary arteriospastic disorders. These disorders are characterized by episodic vasospasm in the small peripheral arteries and arterioles precipitated by exposure to cold or stress.

Raynaud's disease occurs bilaterally and usually affects the hands or, less commonly, the feet and, rarely, the earlobes and the tip of the nose. The disease is five times more common in women than in men, particularly between late adolescence and age 40. The disorder is benign, requiring no specific treatment and with no serious effects.

CAUSES OF RAYNAUD'S PHENOMENON

Patients with the primary or idiopathic form of Raynaud's phenomenon have Raynaud's disease. Raynaud's phenomenon, on the other hand, may occur secondary to the following diseases and conditions as well as with the use of certain drugs.

Collagen vascular disease

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Dermatomyositis

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Polymyositis

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Rheumatoid arthritis

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Scleroderma

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Systemic lupus erythematosus

Arterial occlusive disease

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Acute arterial occlusion

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Atherosclerosis of the extremities

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Thoracic outlet syndrome

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Thromboangiitis obliterans

Neurologic disorders

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Carpal tunnel syndrome

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Invertebral disk disease

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Poliomyelitis

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Spinal cord tumors

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Stroke

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Syringomyelia

Blood dyscrasias

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Cold agglutinins

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Cryofibrinogenemia

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Myeloproliferative disorders

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Waldenström's disease

Trauma

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Cold injury

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·

 

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Keyboarding

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Piano playing

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Drugs

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Beta-adrenergic receptor blockers

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Bleomycin

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Cisplatin

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Ergot derivatives such as ergotamine

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Methysergide

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Vinblastine

Other

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Pulmonary hypertension

Raynaud's phenomenon, however, is a condition commonly associated with several connective tissue disorders, such as scleroderma, systemic lupus erythematosus, and polymyositis. The concurrent disorders have a progressive course, leading to ischemia, gangrene, and amputation. (For other disorders and conditions associated with Raynaud's phenomenon, see Causes of Raynaud's phenomenon.)

Pathophysiology

Although the cause is unknown, several conditions account for the reduced blood flow to the digits: intrinsic vascular wall hyperactivity to cold, ineffective basal heat production, increased vasomotor tone from sympathetic stimulation, stress, and an antigen-antibody immune response (the most probable theory because abnormal immunologic test results accompany Raynaud's phenomenon).

Complications

·

Ischemia, gangrene, and amputation resulting from severe, persistent vasoconstriction

·

 

Assessment findings

·

The patient with Raynaud's disease may report skin color changes induced by cold or stress.

·

The response to cold and stress is typically triphasic. Initially, the skin of affected areas appears markedly pale from severe vasoconstriction. During this phase, the patient may report numbness and tingling. In the second phase, the skin appears cyanotic, resulting from dilation of cutaneous arterioles and venules.

Because vasoconstriction is diminished, reactive hyperemia results, so the skin in the third phase appears red and feels warm. During this phase, the patient may report a throbbing, burning, and painful sensation.

·

Between attacks, the affected areas usually appear normal, although they may feel cool and perspire excessively. In patients with long-standing disease, you may notice trophic changes, such as sclerodactyly and ulcerations.

Diagnostic test results

·

Diagnosis is based primarily on presenting symptoms. Before Raynaud's phenomenon can be diagnosed, secondary diseases, such as chronic arterial occlusive disease and connective tissue disease, must be ruled out.

·

Arteriography and digital photoplethysmography may also help diagnose the presence of Raynaud's disease or phenomenon.

Treatment

Initially, treatment consists of avoidance of cold, mechanical, or chemical injury; cessation of smoking; and reassurance that symptoms are benign. Because adverse reactions to drugs, especially vasodilators, may be more bothersome than the disease itself, drug therapy is reserved for unusually severe signs and symptoms. Such therapy may include phenoxybenzamine (Dibenzyline), nifedipine (Procardia), or reserpine and prazosin (Minipress). Biofeedback therapy may be useful if signs and symptoms are caused by stress.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH RAYNAUD'S DISEASE

·

Warn against exposure to the cold. Tell the patient to wear mittens or gloves in cold weather or when handling cold items or defrosting the freezer.

·

Advise the patient to avoid stress and to stop smoking. Refer her to a smoking-cessation program if needed.

·

Instruct the patient to inspect her skin frequently and to seek immediate care for signs of skin breakdown or infection.

·

Teach the patient about prescribed drugs, their proper use, and their adverse effects. Tell her to report adverse reactions to her practitioner.

Sympathectomy may be helpful when conservative treatment fails to prevent ischemic ulcers (occurring in less than 25% of patients).

Nursing interventions

·

If signs and symptoms are caused by stress, help the patient identify stress-producing areas of her life and effective coping strategies. If appropriate, refer her to a biofeedback program to help control signs and symptoms related to stress.

·

Provide psychological support and reassurance to allay the patient's fear of amputation and disfigurement.

·

Teaching the patient with Raynaud's disease.)

THORACIC AORTIC ANEURYSM

Thoracic aortic aneurysm is a potentially life-threatening disorder characterized by abnormal widening of the ascending, transverse, or descending part of the aorta. The aneurysm may be saccular, an outpouching of the arterial wall, with a narrow neck, involving only a portion of the vessel circumference; or fusiform, a spindle-shaped enlargement, encompassing the entire aortic circumference.

Dissection of the aneurysm is the circumferential or transverse tear of the aortic wall intima, usually within the medial layer. It occurs in about 60% of patients, is usually an emergency, and has a poor prognosis. (See Classifying aortic dissection.)

CLASSIFYING AORTIC DISSECTION

These drawings illustrate the DeBakey classification of aortic dissections (shaded areas) according to location. Dissections can also be classified by their location in relation to the aortic valve. Thus, types I and II are proximal; type III, distal.

In type I, the most common and lethal type of dissection, intimal tearing occurs in the ascending aorta, and the dissection extends into the descending aorta.

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Type II

In type II, which appears most commonly with Marfan syndrome, dissection is limited to the ascending aorta.

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Type III

Type III dissection includes two formations. In the first, type Illa, the intimal tear is located in the descending aorta with distal propagation of the dissection that's confined to the thorax. The second, type Illb, has the same origin site, but may extend beyond the diaphragm.

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The ascending thoracic aorta is the most common site for the aneurysm, which occurs predominantly in men younger than age 60 who have coexisting hypertension. Descending thoracic aortic aneurysms are most common in younger patients who have had chest trauma.

Pathophysiology

Commonly, ascending thoracic aortic aneurysm results from atherosclerosis, which weakens the aortic wall and gradually distends the lumen in this area. It's also closely associated with cigarette smoking and hypertension.

Descending thoracic aortic aneurysm usually occurs after blunt chest trauma that shears the aorta transversely (acceleration-deceleration injury), such as in a motor vehicle accident, or after a penetrating chest injury, such as a knife wound. It may also be caused by hypertension.

Mycotic aneurysm develops from staphylococcal, streptococcal, or salmonella infections, usually at an atherosclerotic plaque.

Cystic medial necrosis caused by degeneration of the collagen and elastic fibers in the media of the aorta causes aneurysms during pregnancy and in patients with hypertension and Marfan syndrome. However, it can also be the cause without any underlying condition.

Other causes include congenital disorders, such as coarctation of the aorta, syphilis infection, and rheumatic vasculitis.

Complications

·

Rupture of untreated thoracic dissecting aneurysm into the pericardium, with resulting cardiac tamponade

·

Thoracic aortic aneurysms fail to produce signs and symptoms until they expand and begin to dissect. Pain and other symptoms result from compression of the surrounding structures or from dissection of the aneurysm. (See Clinical characteristics of thoracic dissection.)

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The patient may complain of hoarseness, dyspnea, throat pain, dysphagia, and a dry cough when a transverse aneurysm compresses the surrounding structures.

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Dissection of the aneurysm causes sudden pain and possibly syncope.

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CLINICAL CHARACTERISTICS OF THORACIC DISSECTION

AORTA

DESCENDING

AORTA

TRANSVERSE

AORTA

CHARACTERISTIC OF PAIN

Severe, boring, ripping, extending to neck, shoulders, lower back, and abdomen (rarely to jaw and arms); more severe on right side

Sudden onset; sharp, tearing, usually between the shoulder blades; may radiate to the chest; most diagnostic feature

Sudden onset; sharp, boring, tearing; radiates to shoulders

OTHER SYMPTOMS AND EFFECTS

If dissection involves carotid arteries, abrupt onset of neurologic deficit (usually intermittent); bradycardia, aortic insufficiency, and hemopericardium detected by pericardial friction rub; unequal intensity of right and left carotid pulses and radial pulses; difference in blood pressure, especially systolic, between right and left arms

Aortic insufficiency without murmur, hemopericardium, or pleural friction rub; carotid and radial pulses and blood pressure in both arms typically equal

Hoarseness, dyspnea, pain, dysphagia, and dry cough from compression of surrounding structures

DIAGNOSTIC FEATURES

CHEST X-RAY

Best diagnostic tool; shows widening of mediastinum, enlargement of ascending aorta

Widening of mediastinum; descending aorta larger than ascending section

Widening of mediastinum; descending aorta larger than ascending section; widened transverse arch

AORTOGRAPHY

False lumen; narrowing of lumen of aorta in ascending section

False lumen; narrowing of lumen of aorta in descending section

False lumen; narrowing of lumen of aorta in transverse arch

TREATMENT

Surgical repair needed; this is a medical emergency that requires immediate aggressive treatment to reduce blood pressure (usually with nitroprusside or trimethaphan)

Surgical repair required but less urgent than for the ascending dissection; to control hypertension, nitroprusside and propranolol may be used if bradycardia and heart failure are absent

Immediate surgical repair (mortality as high as 50%), control of hypertension

 

·

In dissecting descending aneurysm, the pain is sharp, tearing, and located between the shoulder blades, and in many cases radiates to the chest.

·

In dissecting transverse aneurysm, the pain is sharp, boring, and tearing and radiates to the shoulders.

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In a patient with a thoracic aortic aneurysm, you may find pallor, diaphoresis, dyspnea, cyanosis, leg weakness or transient paralysis, and an abrupt onset of intermittent neurologic deficits.

·

Palpation of peripheral pulses in dissecting ascending aneurysm may disclose abrupt loss of radial and femoral pulses and right and left carotid pulses.

·

In dissecting descending aneurysm, carotid and radial pulses may be present and equal bilaterally.

·

Percussion of the chest may reveal an increasing area of flatness over the heart, suggesting cardiac tamponade and hemopericardium.

·

 

 

·

 

·

In dissecting descending aneurysm, systolic blood pressure is equal bilaterally, and you hear no murmur of aortic insufficiency or pericardial friction rub. You may detect bilateral crackles and rhonchi if pulmonary edema is present.

Diagnostic test results

In an asymptomatic patient, the diagnosis commonly occurs accidentally, through posteroanterior and oblique chest X-rays showing widening of the aorta and mediastinum.

Several tests can help confirm the aneurysm:

·

Aortography, the most definitive test, shows the lumen of the aneurysm, its size, and its location.

·

Magnetic resonance imaging and computed tomography scanning help confirm and locate the presence of aortic dissection.

·

Electrocardiography (ECG) helps rule out the presence of MI as the cause of the symptoms, and echocardiography may help identify dissecting aneurysm of the aortic root.

·

Transesophageal echocardiography can be used to measure the aneurysm in both the ascending and the descending aorta.

·

Hemoglobin levels may be normal or decreased, resulting from blood loss from a leaking aneurysm.

Treatment

For long-term treatment, beta-adrenergic receptor blockers and other agents can control hypertension and cardiac output. In an emergency, antihypertensives such as nitroprusside, negative inotropic agents such as propanolol, oxygen for respiratory distress, opioids for pain, I.V. fluids, and whole blood transfusions, if needed, may be used.

In dissecting ascending aortic aneurysm—an extreme emergency—surgical resection of the aneurysm can restore normal blood flow through a Dacron or Teflon graft replacement. With aortic valve insufficiency, surgery consists of replacing the aortic valve.

Postoperative measures include careful monitoring and continuous assessment in the intensive care unit, antibiotics, insertion of endotracheal (ET) and chest tubes, ECG monitoring and, in many instances, pulmonary artery catheterization and monitoring.

Nursing interventions

·

In a nonemergency situation when a patient is diagnosed with a thoracic aneurysm, allow him to express his fears and concerns. Help him identify and use effective coping strategies.

·

Offer the patient and his family psychological support. Answer all questions honestly and provide reassurance.

·

In an acute situation, monitor blood pressure, pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP). Assess pain, breathing, and carotid, radial, and femoral pulses.

·

Give analgesics to relieve pain.

·

Explain diagnostic tests. If surgery is scheduled, explain the procedure and expected postoperative care (I.V. lines, ET and drainage tubes, cardiac monitoring, and ventilation).

·

Make sure laboratory tests include a complete blood count with differential, electrolyte measurements, typing and crossmatching for whole blood, arterial blood gas analysis, and urinalysis.

·

Insert an indwelling urinary catheter to monitor hourly outputs. Give dextrose 5% in water or lactated Ringer's solution, and antibiotic. Carefully monitor nitroprusside I.V.; use a separate I.V. line for infusion. Adjust the dose by slowly increasing the infusion rate. Meanwhile, check blood pressure every 5 minutes until it stabilizes. With suspected bleeding from an aneurysm, give whole blood transfusions as ordered.

AFTER REPAIR OF THORACIC ANEURYSM

·

Carefully assess the patient's level of consciousness. Monitor vital signs, pulmonary artery pressure, CVP, PAWP, pulse rate, urine output, and pain.

·

Check respiratory function. Carefully observe and record type and amount of chest tube drainage, and assess heart and breath sounds frequently.

·

Monitor I.V. therapy and intake and output to determine the adequacy of renal function.

·

Give an analgesic, especially before the patient performs breathing exercises or is moved.

·

After stabilization of vital signs, encourage and assist the patient in turning, coughing, and deep breathing. If necessary, provide intermittent positive-pressure breathing to promote lung expansion. Help the patient walk as soon as he's able. (See Teaching the patient with thoracic aortic aneurysm.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH THORACIC AORTIC ANEURYSM

·

Ensure compliance with antihypertensive therapy by explaining the need for such drugs and the expected adverse effects.

·

Direct the patient to call the practitioner immediately if he experiences sharp pain in the chest or back of the neck.

·

Teach the patient how to monitor his blood pressure.

·

Refer him to community agencies for continued support and assistance as needed.

·

Watch for signs of infection, especially fever, and excessive drainage on the dressing. Monitor for signs that resemble those of the initial dissecting aneurysm, suggesting a tear at the graft site.

·

Assist with range-of-motion exercises of legs to prevent thromboemboli from venostasis during prolonged bed rest.

THROMBOPHLEBITIS

Thrombophlebitis is an acute condition characterized by inflammation and thrombus formation. It may occur in deep or superficial veins. Deep vein thrombosis (DVT) affects small veins, such as the lesser saphenous vein, or large veins, such as the vena cava and the iliac, femoral, and popliteal veins. It's more serious than superficial vein thrombophlebitis because it affects the veins deep in the leg musculature that carry most of the venous outflow from the leg. (See Major venous pathways of the leg, page 470.) Thrombophlebitis is typically progressive, leading to pulmonary embolism, a potentially life-threatening complication. Superficial thrombophlebitis is usually self-limiting and seldom leads to pulmonary embolism. Thrombophlebitis typically begins with localized inflammation alone (phlebitis), but such inflammation rapidly provokes thrombus formations. Rarely, venous thrombosis develops without associated inflammation of the vein (phlebothrombosis).

Causes

A thrombus occurs when an alteration in the epithelial lining causes platelet aggregation and consequent fibrin entrapment of red and white blood cells and additional platelets. Thrombus formation is more rapid in areas where blood flow is slower, resulting from greater contact between platelet and thrombin accumulation. The rapidly expanding thrombus initiates a chemical inflammatory process in the vessel epithelium, which leads to fibrosis. The enlarging clot may occlude the vessel lumen partially or totally, or it may detach and embolize to lodge elsewhere in systemic circulation.

MAJOR VENOUS PATHWAYS OF THE LEG

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Deep vein thrombophlebitis may be idiopathic, but it usually results from endothelial damage, accelerated blood clotting and reduced blood flow, such as in predisposing factors of prolonged bed rest, trauma, surgery, childbirth, and use of hormonal contraceptives such as estrogens. It's also more likely to occur in the presence of certain diseases, treatments, injuries, or other factors, such as:

·

hypercoagulable states—cigarette smoking; circulating lupus anticoagulant; deficiencies of antithrombin III, protein C, or protein S; disseminated intravascular coagulation; estrogen use; dysfibrinogenemia; myeloproliferative diseases; and systemic infection

·

intimal damage—infection, infusion of irritating I.V. solutions, trauma, or venipuncture

·

neoplasms—of the lung, ovary, pancreas, stomach, testicles, or urinary tract

·

surgery—abdominal, genitourinary, orthopedic, or thoracic

·

fracture—of the spine, pelvis, femur, or tibia

·

venous stasis—acute myocardial infarction, heart failure, dehydration, immobility, incompetent vein valves, postoperative convalescence, or stroke

·

venulitis—Behçet's disease, homocystinuria, or thromboangiitis obliterans

·

other—pregnancy or previous deep vein thrombosis.

Complications

·

Pulmonary embolism

·

Chronic venous insufficiency (see Dealing with chronic venous insufficiency, page 472)

Assessment findings

·

In both deep vein and superficial vein thrombophlebitis, clinical features vary with the site of inflammation and length of the affected vein. Up to 50% of patients with deep vein thrombophlebitis may be asymptomatic, but others may complain of some tenderness, aching, or severe pain in the affected leg or arm, fever, chills, and malaise. Complete your physical examination carefully because much of the patient's subsequent care depends on your findings.

·

Inspection may reveal redness, swelling, and cyanosis of the affected leg or arm.

·

Some patients with deep vein thrombophlebitis of a leg vein may have a positive Homans' sign (pain on dorsiflexion of the foot), but this is considered an unreliable sign.

·

A positive cuff sign (elicited by inflating a blood pressure cuff until pain occurs) may be present in deep vein thrombophlebitis of either the arm or leg.

·

When palpated, the affected leg or arm may feel warm.

·

Patients with superficial vein thrombophlebitis may also be asymptomatic, or they may complain of pain localized to the thrombus site.

Chronic venous insufficiency results from the valvular destruction of deep vein thrombophlebitis, usually in the iliac and femoral veins and occasionally in the saphenous veins. It's commonly accompanied by incompetence of the communicating veins of the ankle, causing increased venous pressure and fluid migration into the interstitial tissue.

Signs and symptoms

Chronic venous insufficiency causes chronic swelling of the affected leg from edema, leading to tissue fibrosis and induration, skin discoloration from extravasation of blood in subcutaneous tissue, and stasis ulcers around the ankle.

Treatment

Appropriate treatment for small stasis ulcers is bed rest, elevation of the legs, warm soaks, and antimicrobial therapy for infection.

Treatment to counteract increased venous pressure, the result of reflux from the deep venous system to superficial veins, may include compression dressings or a zinc gelatin boot (Unna boot). This therapy begins after massive swelling subsides.

Large stasis ulcers unresponsive to conservative treatment may require excision and skin grafting. Care includes daily inspection to assess healing and measures similar to those for varicose veins.

·

Inspection may disclose redness and swelling at the site and surrounding area.

·

When palpated, the area feels warm, and a tender, hard cord extends over the affected vein's length.

·

Extensive vein involvement may cause lymphadenitis.

·

 

Diagnostic test results

Diagnosis must rule out arterial occlusive disease, lymphangitis, cellulitis, and myositis. Diagnosis of superficial vein thrombophlebitis is based on physical findings, whereas diagnosis of deep vein thrombophlebitis is based on the following characteristic test findings:

·

Doppler ultrasonography identifies reduced blood flow to a specific area and obstruction to venous flow, particularly in iliofemoral deep vein thrombophlebitis.

 

·

Plethysmography shows decreased circulation distal to the affected area; it's more sensitive than ultrasonography in detecting deep vein thrombophlebitis.

·

Phlebography usually confirms the diagnosis and shows filling defects and diverted blood flow.

·

D-dimer results indicate an abnormally high level of fibrin degradation products, reflective of significant clot formation and breakdown in the body; however, it doesn't reveal location or cause.

Treatment

In deep vein thrombophlebitis, treatment includes bed rest, with elevation of the affected arm or leg; application of warm, moist compresses to the affected area; and analgesics. After the acute episode subsides, the patient may begin to ambulate while wearing antiembolism stockings (applied before he gets out of bed).

Treatment may include anticoagulants (initially, heparin; later, warfarin) to prolong clotting time. However, the full anticoagulant dose must be discontinued during surgery to avoid the risk of hemorrhage. After some types of surgery, especially major abdominal or pelvic operations, prophylactic doses of anticoagulants may reduce the risk of deep vein thrombophlebitis.

For lysis of acute, extensive deep vein thrombophlebitis, treatment should include streptokinase or urokinase, if the risk of bleeding doesn't outweigh the potential benefits of thrombolytic treatment.

Rarely, deep vein thrombophlebitis may cause complete venous occlusion, which necessitates venous interruption through simple ligation to vein plication, or clipping. Embolectomy may be done if clots are being shed to the pulmonary and systemic vasculature and other treatment is unsuccessful. Caval interruption with transvenous placement of an umbrella filter can trap emboli, preventing them from traveling to the pulmonary vasculature.

Therapy for severe superficial vein thrombophlebitis may include an anti-inflammatory drug such as indomethacin along with antiembolism stockings, warm compresses, and elevating the patient's leg.

Nursing interventions

·

Enforce bed rest as ordered, and elevate the patient's affected arm or leg. If you plan to use pillows for elevating the leg, place them so they support its entire length to avoid compressing the popliteal space.

·

Apply warm compresses or a covered aquamatic K pad to increase circulation to the affected area and to relieve pain and inflammation. Give analgesics to relieve pain as ordered.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH THROMBOPHLEBITIS

·

Before discharge, emphasize the importance of follow-up blood studies to monitor anticoagulant therapy.

·

If the patient is being discharged on heparin therapy, teach him or his family how to give subcutaneous injections. If he requires further assistance, arrange for a home health care nurse.

·

Tell the patient to avoid prolonged sitting or standing to help prevent a recurrence.

·

Teach the patient how to properly apply and use antiembolism stockings. Tell him to report complications such as cold, blue toes.

·

To prevent bleeding, encourage the patient to use an electric razor and to avoid drugs that contain aspirin.

·

Mark, measure, and record the circumference of the affected arm or leg daily, and compare this measurement with that of the other arm or leg. To ensure accuracy and consistency of serial measurements, mark the skin over the area, and measure at the same spot daily.

·

Give I.V. heparin with an infusion monitor or pump to control the flow rate if necessary.

·

Measure partial thromboplastin time regularly for the patient on heparin therapy. Measure prothrombin time for the patient on warfarin (therapeutic anticoagulation values for both are 1½ to 2 times control values).

·

Watch for signs and symptoms of bleeding, such as tarry stools, coffee-ground vomitus, and ecchymoses. Watch for oozing of blood at I.V. sites, and assess gums for excessive bleeding.

·

Be alert for signs of pulmonary emboli (such as crackles, dyspnea, hemoptysis, sudden changes in mental status, restlessness, and hypotension).

·

To prevent thrombophlebitis in high-risk patients, perform range-of-motion exercises while the patient is on bed rest, use intermittent pneumatic calf massage during lengthy surgical or diagnostic procedures, apply antiembolism stockings postoperatively, and encourage early ambulation. (See Teaching the patient with thrombophlebitis.)