DIAGNOSIS.

The physician must distinguish between the symptoms of arteriosclerotic PVD, such as intermittent claudication and coldness of the feet, and symptoms of venous disease, because occlusive arterial disease usually contraindicates the operative management of varicosities below the knee. When the two conditions coexist, the reduced blood flow caused by the atherosclerosis may even improve the varicosities by reducing blood flow through the veins.

Visual inspection and palpation identify varicose veins of the legs, and Doppler ultrasonography or the duplex scanner is useful in detecting the location of incompetent valves. Endoscopy or radiographic diagnosis identifies esophageal varices, rectal examination or proctoscopy is used to diagnose hemorrhoids, and palpation identifies varicocele (scrotal swelling).

TREATMENT.

Treatment of mild varicose veins is conservative, consisting of periodic daily rest periods with feet elevated slightly above the heart. Client education as to the importance of promoting circulation is stressed, including instructions to make frequent changes in posture, a daily exercise program, and the appropriate use of properly fitting elastic stockings.

When varicosities have progressed past the stage at which conservative care is helpful, surgical intervention and compression sclerotherapy may be considered. In the past, surgical treatment of varicose veins consisted of removing the varicosities and the incompetent perforating veins (ligation and stripping), a procedure sometimes referred to as stripping the veins or miniphlebectomy.

Other procedures for varicose veins have been developed, including radiofrequency (radio waves used to seal off the vein), sclerotherapy (injections of a hardening, or sclerosing, solution; over several months’ time, the injected veins atrophy and blood is channeled into other veins), and laser therapy (noninvasive use of near-infrared wavelengths). Ligation and stripping of the greater saphenous vein prevent its use as a source for future CABGs, motivating researchers to develop effective intervention techniques that salvage large veins.

Oral dietary supplementation has been adopted by some individuals as an addition to traditional management of varicose veins. The loss of vascular integrity associated with the pathogenesis of both hemorrhoids and varicose veins may be aided by several botanical extracts shown to improve microcirculation, capillary flow, and vascular tone while strengthening the connective tissue of the perivascular substrate.²⁰⁴

PROGNOSIS.

Good results with relief of symptoms are usually possible in the majority of cases. Early conservative care for varicose veins during initial stages may help prevent the condition from worsening, but advanced disease may not be prevented from recurring, even with surgical intervention or sclerotherapy. Although surgery for varicose veins can improve appearance, it may not reduce the physical discomfort, suggesting that most lower limb symptoms may have a nonvenous cause. A high mortality is associated with ruptured, bleeding esophageal varices (see Chapter 16).

DIAGNOSIS AND PROGNOSIS.

Diagnosis is usually made by clinical presentation and past medical history. Raynaud’s disease is diagnosed by a history of symptoms for at least 2 years with no progression and no evidence of underlying cause. Raynaud’s disease must be differentiated from the numerous possible disorders associated with Raynaud’s phenomenon. Untreated and uncontrolled Raynaud’s may damage or destroy the affected digits. Rarely, necrosis, ulceration, and gangrene result. Even with intervention, the person with Raynaud’s disease or phenomenon may experience disability and loss of function.

PREVENTION AND TREATMENT.

Treatment for Raynaud’s disease is limited to prevention or alleviation of the vasospasm because no underlying cause or condition has been discovered, although pharmacologic agents for primary and secondary Raynaud’s phenomenon are under investigation. Clients are encouraged to avoid stimuli that trigger attacks, such as cool or cold temperatures, changes in temperature, and emotional stress, and to eliminate use of nicotine, which has a constricting effect on blood vessels.

Physical or occupational therapy is often prescribed and should include client education about managing symptoms through protective skin care and cold protection (see Box 12-14), biofeedback, stress management and relaxation techniques, whirlpool or other gentle heat modalities, and exercise. Large movement arm circles in a windmill fashion can restore circulation in some people. The individual will have to experiment with the speed at which to move the arms; some people benefit from slow, gentle movement, whereas others find greater success with fast rotations.

Calcium channel blockers are the treatment of choice. Pharmacologic management may also include nonaddicting analgesics for pain. Therapists can be instrumental in teaching physiologic modulation starting with hand warming. A hand-held device to measure fingertip temperature combined with self-guided or audio-guided relaxation can be very effective and is available.¹⁵⁶

When conservative care fails to relieve symptoms and the condition progresses clinically, sympathetic blocks followed by intensive therapy may be helpful. Sympathectomy may be necessary for persons who only temporarily benefit from the sympathetic blocks.

Treatment for Raynaud’s phenomenon consists of appropriate treatment for the underlying condition or removing the stimulus causing vasospasm. The clinical care described for Raynaud’s disease may also be of benefit. In addition, the use of antioxidants as an effective treatment of Raynaud’s phenomenon as well as the role of therapeutic angiogenesis (regeneration of vessels) remains under investigation.

Vascular Neoplasms

Malignant vascular (i.e., involving the blood vessels) neoplasms are extremely rare and include angiosarcoma, hemangiopericytoma, and Kaposi’s sarcoma. Angiosarcomas (hemangiosarcomas) can occur in either gender and at any age, most commonly appearing as small, painless, red nodules on the skin, soft tissue, breast, bone, liver, and spleen. Almost one half of all people with angiosarcoma die of the disease.

Hemangiopericytoma arises from the smooth muscle cells that are external to the walls of capillaries and arterioles. Most commonly located on the lower extremities and retroperitoneum (space between the peritoneum lining the walls of the abdominal and pelvic cavities and the posterior abdominal wall), these tumors are composed of spindle cells with a rich vascular network. Metastasis to the lungs, bone, liver, and lymph nodes occurs in 10% to 50% of cases, but the majority of hemangiopericytomas are removed surgically without having invaded or metastasized.

Kaposi’s sarcoma in association with AIDS most likely occurs as a result of loss of immunity. One form of the tumor resembles a simple hemangioma with tightly packed clusters of capillaries, most often visible on the skin. Although Kaposi’s sarcoma is malignant and may be widespread in the body, it is not usually a cause of death.

Arteriovenous Malformations

Arteriovenous malformations (AVMs) are congenital vascular malformations of the cerebral vasculature. AVMs are the result of localized maldevelopment of part of the primitive vascular plexus consisting of abnormal arteriovenous communications without intervening capillaries. There is a central tangled mass of fragile, abnormal blood vessels called the nidus that shunts blood from cerebral feeding arteries directly into cerebral veins. The loss of the normal capillary network between the high-pressure arterial system and the low-pressure venous system results in a faster flow and elevated pressure within the delicate vessels of the AVM. The lack of a gradient pressure system predisposes the lesion to rupture.

AVMs vary in size, ranging from massive lesions that are fed by multiple vessels to lesions too small to identify. Perfusion to adjacent brain tissue may be impaired because blood flow is diverted to the AVM, a phenomenon referred to as vascular stealing. AVMs may occur in any blood vessel, but the most common sites include the brain, GI tract, and skin. Approximately 10% of cases present with aneurysms. Small AVMs are more likely to bleed than large ones, and once bleeding occurs, repeated episodes are likely.

Clinical presentation depends on the location of the malformation and may relate to hemorrhage from the malformation or an associated aneurysm or to cerebral ischemia caused by diversion or stasis of blood. Seizures, migrainelike headaches unresponsive to standard therapy, and progressive neurologic deficits may develop.

Diagnostic testing and planned intervention rely on cerebral angiography to show the AVM size, location, feeding vessels, nidus, and venous outflow vessels. Other tests may include MRI, x-rays, ultrasound, electroencephalogram (EEG), and arteriogram. Treatment options are individualized depending on the size and location of the lesion as well as any other surgical risks present.

In the last 15 years, endovascular embolization and stereotactic radiosurgery (delivery of extremely precise doses of radiation to destroy abnormal blood vessels) have increased survival outcomes, especially for lesions previously considered inoperable or in cases of high surgical risk factors. Prognosis is guarded, since there is a 2% to 4% chance of hemorrhage with the concomitant risk of permanent neurologic deficit or even death.

The Lymphatic Vessels

The lymphatic system (see also the section on The Lymphatic System in Chapter 13) is part of the circulatory system that collects excess tissue fluid and plasma that has leaked out of capillaries into the interstitial space and returns it to the bloodstream.

The lymphatic system consists of lymphatic vessels and lymph nodes and functions to remove impurities from the circulatory system and to produce cells of the immune system (lymphocytes) that are vital in fighting bacteria and viruses. The lymph nodes are also part of the lymphoid system, the organs and tissues of the immune system. All the lymphoid organs link the hematologic and immune systems in that they are sites of residence, proliferation, differentiation, or function of lymphocytes and mononuclear phagocytes (mononuclear phagocyte system).

Disorders of the lymphatic system may result from inflammation of a lymphatic vessel (lymphangitis), inflammation of one or more lymph nodes (lymphadenitis), an increased amount of lymph (lymphedema), or enlargement of the lymph nodes (lymphadenopathy). There are also three forms of lymph vascular insufficiency that can occur.

The first, dynamic insufficiency, occurs when the lymphatic load exceeds the lymphatic transport capacity. In this situation, the anatomy of the lymphatic system and its function are normal but are overwhelmed. A second form of insufficiency of the lymph vascular system is caused by a reduction of the lymphatic transport capacity below the level of a normal lymphatic protein load. This reduction results in low lymph flow failure called mechanical insufficiency.

A third form of lymph vascular insufficiency occurs when the lymphatic system has a reduced transport capacity, leading to an overflowing of lymph. This form is called safety valve insufficiency. For a complete discussion of the lymphatic system, see Chapter 13.

The Cardiac Client and Surgery

Persons with previously diagnosed cardiac disease undergoing general or orthopedic surgery are at risk for additional postoperative complications. Anesthesia and surgery are often associated with marked fluctuations of heart rate and blood pressure, changes in intravascular volume, myocardial ischemia or depression, arrhythmias, decreased oxygenation, and increased sympathetic nervous system activity. In addition, changes in medications, surgical trauma, wound healing, infection, hemorrhage, and pulmonary insufficiency may overwhelm the diseased heart. All these factors place an additional stress on the cardiac client during the perioperative period.

Cardiac surgery via median sternotomy requires a longitudinal incision and disruption of the sternum. During the operative procedure, the bone is rewired with stainless steel wire and fixed with low separation strength and security of closure approximately 5% of normal (this increases to 90% of normal strength at 6 weeks for most people).²¹⁴

A single-lung transplantation requires a posterolateral thoracotomy, whereas a double-lung transplant requires bilateral anterior thoracotomies referred to as a “clam shell.” In this latter procedure, the rib cage and sternum are lifted perpendicularly as the hood of a car would be lifted. The heart-lung procedure is still done by open sternotomy.

Complications following a sternotomy include mediastinitis, poor wound healing, chronic pain, posttraumatic stress disorder, and, more rarely, brachial plexus injury. Risk factors for these complications may include obesity, osteoporosis, diabetes or other comorbidities, large breasts in women (the weight of both breasts puts additional traction on sutures), and client noncompliance or poor compliance.

Development of a less invasive means of performing cardiac surgery may be possible with recent advances in technology, especially videoscopic visualization and the ability to provide myocardial protection. Surgeons are examining alternate techniques in hopes of reducing operative stress, postoperative pain, and postoperative recovery time.

New procedures are being developed that eliminate the use of a sternotomy, such as the minithoracotomy or “keyhole” thoracotomy via a small incision that allows surgeons to operate on a beating heart. These alternate surgical techniques involve passing instruments through small incisions in the skin and muscle and between the ribs. Surgeons can suture bypass vessels around blocked coronary arteries without shutting down the heart and rerouting the blood through a bypass machine.

Cardiogenic Shock

Shock is acute, severe circulatory failure associated with a variety of precipitating conditions. Regardless of the cause, shock is associated with marked reduction of blood flow to vital organs, eventually leading to cellular damage and death. See Table 14-1 for categories and causes of shock.

The therapist may see a client in one of three stages of shock. Stage 1, compensated hypotension, is characterized by reduced cardiac output that stimulates compensatory mechanisms that alter myocardial function and peripheral resistance. During this stage, the body tries to maintain circulation to vital organs such as the brain and the heart and clinical symptoms are minimal. Blood pressure may remain normotensive.

In stage 2, compensatory mechanisms for dealing with the low delivery of nutrients to the body are overwhelmed, and tissue perfusion is decreased. Early signs of cerebral, renal, and myocardial insufficiency are present. Cardiogenic shock (inadequate cardiac function) may result from disorders of the heart muscle, valves, or electrical pacing system. Shock associated with MI or other serious cardiac disease carries a high mortality rate. The therapist is only likely to see this type of client in a CCU setting.

Stage 3 is characterized by severe ischemia with damage to tissues by toxins and antigen-antibody reactions. The kidneys, liver, and lungs are especially susceptible; ischemia of the GI tract allows invasion by bacteria with subsequent infection.

Clinical manifestations of shock may include (in early stages) tachycardia, increased respiratory rate, and distended neck veins. In early septic shock (vascular shock caused by infection), there is hyperdynamic change with increased circulation, so that the skin is warm and flushed and the pulse is bounding rather than weak.

In the second phase of shock (late septic shock) hypoperfusion (reduced blood flow) occurs with cold skin and weak pulses, hypotension (systolic blood pressure of 90 mm Hg or less), mottled extremities with weak or absent peripheral pulses, and collapsed neck veins. This phase is usually irreversible; the client is unresponsive, and cardiovascular collapse eventually occurs. The therapist should be aware that some healthy adults may have blood pressure levels this low without ill effects or with only minor symptoms of orthostatic hypotension when changing positions quickly.

Treatment is directed toward both the manifestations of shock and its cause.

The Cardiac Client and Pregnancy

Normal physiologic changes during pregnancy can exacerbate symptoms of underlying cardiac disease, even in previously asymptomatic individuals. The most common cardiovascular complications of pregnancy are peripartum cardiomyopathy, aortic dissection, and pregnancy-related hypertension.

Peripartum cardiomyopathy or cardiomyopathy of pregnancy is discussed briefly earlier in the chapter (see the section on Cardiomyopathy). Pregnancy predisposes to aortic dissection, possibly because of the accompanying connective tissue changes. Dissection usually occurs near term or shortly postpartum in the arteries (including coronary arteries) or the aorta, and special implications are the same as for aneurysm.

The Heart in Collagen Vascular Diseases

Collagen vascular diseases (now more commonly referred to as diffuse connective tissue disease) (Box 12-17) often involve the heart, although cardiac symptoms are usually less prominent than other manifestations of the disease.

Cardiac Complications of Cancer and Cancer Treatment²²⁷

Many treatments for cancers are also known to be cardiotoxic. People with cancer experience all the usual cardiac problems that occur in the general population in addition to complications of cancer and its therapy. Tumor masses can cause compression of the heart and great vessels resulting in pericardial effusions and tamponade. Certain tumors can cause arrhythmias and may secrete mediators that are directly toxic to the heart. Pericardial effusions and tamponade can follow surgery, radiation, or chemotherapy.

Cardiac toxicity may occur following chest irradiation, especially when combined with the administration of many chemotherapeutic agents. Chest radiation for any type of cancer (e.g., Hodgkin’s disease, non-Hodgkin’s lymphoma, esophageal cancer, lung cancer, breast cancer) exposes the heart (and lungs) to varying degrees and doses of radiation. Previous mediastinal radiation and increasing cumulative doses of chemotherapy or irradiation are known risk factors for the development of cardiotoxicity.

Radiation exposure can cause considerable scarring within the subendocardial adipose tissue, endocardial thickening, and interstitial fibrosis.²⁸⁴ Collectively the latter three defects would make the heart less capable of expanding during systole. Pericardial effusion is the most common manifestation of radiation heart disease, but coronary arteries are known to become fibrotic and undergo luminal narrowing, resulting in hypertension, angina, and MI.

Doxorubicin (Adriamycin) was identified as being cardiotoxic during the early drug trials in the 1970s, but it took 5 to 6 years of actual use for the full extent of cardiac damage to become obvious. Today, cumulative doses of doxorubicin are limited to approximately 550 mg/m² because the drug can cause fatal CHF in doses above this amount. Often these effects are not seen until years or decades after treatment with the drug has been completed. Many other chemotherapeutic agents are cardiotoxic but not to the extent of doxorubicin, and these effects tend be more acute than chronic.³⁶⁶

Chemotherapy agents may prompt acute and chronic heart failure (e.g., anthracycline antibiotics, mitoxantrone, doxorubicin combined with paclitaxel used in the treatment of breast cancer)²⁶² or coronary spasm leading to angina, MI, arrhythmias, or sudden death (e.g., 5-fluorouracil). Anthracycline effects on the heart reduce exercise tolerance. Endocarditis also occurs in cancer clients with vascular access devices and immune compromise.

Recombinant technology has resulted in the development of biologic response modifiers, including the interferons, interleukins, and tumor necrosis factor, which also have some adverse cardiovascular effects. Hypotension and tachycardia are the most common problems, although there have been some reports of myocardial ischemia and infarction. These adverse effects appear to be caused by significant alterations in fluid balance rather than any dysrhythmic or cardiotoxic properties of the drugs. Fortunately, many of the cardiac complications associated with chemotherapeutic agents and biologic response modifiers are transient and reversible.¹⁵⁰

The most common manifestations of cardiotoxicity are cardiac arrhythmias or acute or chronic pericarditis. Other cardiac problems that may develop include blood pressure changes, thrombosis, ECG changes, myocardial fibrosis with a resultant restrictive cardiomyopathy, conduction disturbances, CHF, accelerated and radiation-induced CAD, and valvular dysfunction. These may occur during or shortly after treatment or within days or weeks after treatment; or they may not be apparent until months and sometimes years after completion of chemotherapy.²⁵¹

Although only a small percentage of persons develop serious problems or obvious symptoms of cardiotoxicity, many people have functional limitations that are not clinically apparent because they are physically inactive. A number of risk factors may predispose someone to cardiotoxicity, including total daily dose, increasing cumulative dose, schedule of administration, concurrent administration of cardiotoxic agents, prior chemotherapy, mediastinal radiation, age (younger than 18 years or older than 70 years), female gender, history of preexisting cardiovascular disorders or other comorbidities such as diabetes, and presence of electrolyte imbalances (e.g., hypokalemia, hypomagnesemia).²⁵¹

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