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VASaJLAR SYSTEM AND HEMATOLOGY

395

Table 6-14. Causes of Secondary Hypertension

Origin

Descri ption

Coarcration of the aOrta

Congenital constriction of the aorta at

the level of the ductus arteriosus,

which results in increased pressure

(proximal to the area) of constriction

and decreased pressure (distal to the

area) of constriction

Cushing's disease or syndrome

See Pituitary Gland in Chapter 11

Oral conrraceprives

May be related to an increased secretion of glucocorticoids from adrenal

or pituitary dysfunction

Pheochromocytoma

Tumor of the adrenal medulla causing

increased catecholamine secretion

Primary aldosteronism

Increased aldosterone secretion primarily as result of an adrenal tumor

Renin-secreting tumors

See Adrenal Gland in Chapter 11

Renovascular disease

Parenchymal disease, such as acme

and chronic glomerulonephritis

Narrowing stenosis of renal arrery as a

result of atherosclerosis or congenital fibroplasia

Source: Data from 8 Bullock (cd). Pathophysiology: Adaptations and Aherations in

Function (4th cd). Philadelphia: Lippincott-Raven, t 996;5 t 7.

• Review and clarify any strict blood pressure parameters

that the physician has designated for the patient, as some

patients need to have higher or lower systolic pressures

than expected normal ranges.

Systemic Vasclilitis

Systemic vasculitis is a general term referring to the inflammation of

arteries and veins that progresses to necrosis, leading ro a narrowing

of the vessels. The precise etiology is unknown; however, an autoimmune mechanism is suspected and is becoming more delineated. The secondary manifestations of vasculitis are numerous and may include

thrombosis, aneurysm formation, hemorrhage, arterial occlusion,

weight loss, fatigue, depression, fever, and generalized achiness that is

396 AClITE CARE HANDBOOK FOR PHYSICAL THERAPISn

worse in the morning. The recognized forms of vasculitis arc discussed in the following sections.IJ,14,29.JO

Polyarteritis Nodosa Polyarteritis nodosa (PAN) is a disseminated

disease with focal transmural arterial inflammation, resulting in

necrosis of medium-sized arteries. Most of the cases present with an

unknown etiology; however, the hepatitis B virus has been evolving as

one of the more common causative factors.29 The most frequently

involved organs are the kidney, heart, liver, and gastrointestinal tract,

with symptOms representative of the dysfunction of the involved

organ. Aneurysm formation with destruction of the medial layer of

the vessel is the hallmark characteristic of PAN. Pulmonary involvement can occur; however, most cases of vasculitis in the respiratory tract are associated with Wegener's granulomatosis.

Current management of PAN includes corticosteroid therapy

with or wirhout concurrent cytoxic therapy with cyclophosphamide

(Cytoxan). Antiviral agents may also be used if there is an associated viral infection. Elective surgical correction of PAN is not feasible, given its diffuse nature. Patients diagnosed with PAN have a 5-year survival rate of 12 % without medical treatment and 80% with

treatmenr.IJ·29

Wegener's Granulomatosis Wegener's granulomatosis is a granulomatous, necrotizing disease that affects small- and medium-sized blood vessels rhroughout the body, with primary manifestations in the

upper respiratory tract, lungs, and kidneys. The etiology is unknown;

diagnosis and treatment are still in development. Onset of symptoms

generally occurs after 40 years of age and is slightly more common in

men. Pulmonary signs and symptoms mimic those of pneumonia (i.e.,

fever, productive cough at times with negative sputum cultures, and

chest pain).26,29 The J -year mortality rate is 90% without therapy,

50% with corticosteroid therapy, and 10% with combined corticosteroid and cytotoxic therapy.'·

Treatment of Wegener's granulomatosis may consist of a combination of immunosuppressive agents and corticosteroids (methotrexate and prednisone, respectively). Anti-infective agents may also be prescribed if there is associated respiratory tract infection.16.29

Thromboangiitis Obliterans Thromboangiitis obliterans (Buerger's

disease) is a clinical syndrome that is found mainly in young men ages

20-45 years and is directly correlated to 3 heavy smoking history.l.U."

The disease is characterized by segmental thrombotic occlusions of the

VASCULAR SYSTEM AND HEMATOLOGY 397

small� and medillm�sized arteries in the distal lower and upper extremities. The thrombotic occlusions consist of microabscesses that are inAammarory in nature, suggesting a collagen or autoimmune origin,

although the exact etiology is still unknown.I3·21 Rest pain is common,

along with intermittent claudication that occurs more in the feet than in

the calf regionJ

Treatment of Buerger's disease can include smoking cessation, corticosteroids, prostaglandin EI infusion, vasodilators, hemorheologic agents, antiplatelet agents, and anticoagulants.IJ,21

Giant Cell Arteritis Giant cell arteritis (GCA) is another granulomatous inflammatory disorder of an unknown etiology. It predominantly affects the large arteries and is characterized by destruction of the

internal elastic lamina. Two clinical presentations of GCA have been

recognized: temporal arteritis and Takayasu's arteritis.21

Temporal arteritis is a more common and mild presentation of GCA

that occurs after 50 years of age. The primary signs and symptoms are

persistent headache (temporal and occipital areas), transient visual disturbances (amaurosis fugax and graying or blurring of vision), and iaw and tongue pain. Polymyalgia rheumatica, a clinical syndrome characterized by pain on active motion and acute onset of proximal muscular stiffness, is frequently associated with temporal arteritis. The primary

treatment for temporal arteritis is prednisone.18,29

Takayasu's arteritis generally affects young Asian women but has

been known to occur in both genders of blacks and Hispanics as

well. It is a form of generalized GCA that primarily involves the

upper extremities and the aOrta and its major branches. Lowerextremity involvement is less common. Management of Takayasu's arteritis may consist of prednisone and cyclophosphamide, along

with surgical intervention if the disease progresses to aneurysm,

gangrene, or both.18

RaYllaud's Disease

Raynaud's disease is a form of intermittent arteriolar vasoconstriction

that occurs in patients who have concurrent immunologic disease. The

exact etiology is unknown but may be linked to defects in the sympathetic nervous system. Evidence exists for and against the theory of sympathetic overactiviry, which is said to lead to Raynaud's disease. Women 16-40 years of age are mOSt commonly affected, especially in cold climates or during the wimer season. Other than cold hypersensitivity, emotional factors can also trigger the sudden vasoconstriction. Areas

generally affected are the fingertips, roes, and the tip of the nose.3,18,26

398

AClJfE CARE HANDBOOK FOR PHYSICAL THERAPISTS

Raynaud's Phenomenon Raynaud's phenomenon may result from

Raynaud's disease and is the term used to describe the localized

and intermittent episodes of vasoconstriction that cause unilateral

color and temperature changes in the fingertips, toes, and tip of

nose. The color changes of the affected skin progress from white to

blue to red (reflecting the vasoconstriction, cyanosis, and vasodilation process, respectively). Numbness, tingling, and burning pain may also accompany the color changes. However, despite these

vasoconstrictive episodes, peripheral pulses remain palpable.

Raynaud's phenomenon can also be associated with diseases such

as scleroderma, systemic lupus erythematosus, rheumatoid arthritis, and obstructive arterial disease and trauma.3.1 8.26

Management of Raynaud's disease and phenomenon may consist

of any of the following: conservative measures to ensure warmth of

the body and extremities; regular exercise; diet rich in fish oils and

antioxidants (vitamins C and E); pharmacologic intervention,

including calcium channel blockers and sympatholytics; conditioning and biofeedback; acupuncture; and sympathectomy.18,31

Reflex Sympathetic Dystrophy

Reflex sympathetic dystrophy is constant, extreme pain that occurs

after the healing phase of minor or major trauma, fracrures, surgery, or any combination of these. Injured sensory nerve fibers may transmit constant signals to the spinal cord that result in increased

sympathetic activity to the limbs. Affected areas initially present as

dry, swollen, and warm but then progress to being cold, swollen,

and pale or cyanotic. Raynaud's phenomenon can occur later on.18

Management of reflex sympathetic dystrophy may consist of any

of the following1 8,32-J5:

• Physical or occupational therapy, or both

• Pharmacologic sympathetic blocks

• Surgical sympathectomy

• Spinal cord electrical stimulation

• Badofen drug administration

• Prophylactic vitamin C administration after sustaining fractu res