Physical Examination Vascular Evaluation
D- Dimer The dimer assay provides (a highly specific)
measurement of the amount of fibrin degradation. D-dimer tests have high sensitivity (95% to 99%) but are nonspecific (40% to 60%). Thrombotic problems such as DVT, pulmonary embo- lism (PE), and thrombosis of malignancy are associated with high levels of D-dimer. The test accurately identifies patients with DVT because its high sensitivity translates into a high negative predictive value. In other words, if the D-dimer test result is negative, the patient has a very low likelihood of having DVT. However, a positive D-dimer test result is less helpful because there are multiple conditions that may lead to elevated D-dimer titers, including advanced age, recent surgery, infec- tion, inflammatory states and elevated liver enzyme levels. It is a simple and confirmatory test for disseminated intravascular coagulation (DIC). Levels of D-dimer can increase when a fibrin clot is lysed by thrombolytic therapy.11,23
Lymphatic Evaluation
Relevant history should include cancer and/or cancer treatment, trauma, and surgery, and onset of swelling at birth and/or puberty (primary lymphedema).3 Clinical evaluation should include a detailed description of skin integrity, use of body diagrams, both anterior-posterior (AP) and lateral to draw unusual body contours. This description should also include presence of edema or fibrosis on the trunk quadrants, the head, and the neck, as well as on the limbs, and the location and condition of scars, fibrotic area, and open wounds. Circumfer- ential measurements accurately assess the shape and contour of a limb. Circumferential measurements should be taken at con- sistent locations/sites relative to the anatomical landmarks for reliable comparison between limbs and overtime. Volumetric measurement is a useful to measure the actual volume of the limb and is more helpful in cases of bilateral extremity edema, when no “normal” limb can be used for comparison. Both volu- metric measurements and girth measurements have been shown to be reliable, but the two methods cannot be reliably interchanged.24
Health Conditions
This section is divided into a discussion of vascular, hemato- logic, and lymphatic disorders.
Vascular Disorders
Vascular disorders are classified as arterial, venous, or combined arterial and venous disorders. Clinical findings differ between arterial and venous disorders, as described in Table 7-13. Arterial Disorders
Atherosclerosis. Atherosclerosis is a diffuse and slowly
progressive process characterized by areas of hemorrhage and the cellular proliferation of monocytes, smooth muscle, connec- tive tissue, and lipids. The development of atherosclerosis begins early in life. In addition to the risk factors listed in Box 7-1, a high level of an inflammatory biomarker, C-reactive protein, has been identified as a good predictive marker for early identification of atherosclerosis.25 Waist circumference and weight gain are the strongest predictors of early atherosclerosis in healthy adults.26
Atherosclerosis is the underlying cause of approximately 90% of all myocardial infarction and a large proportion of strokes and ischemic gangrenes.27
Clinical manifestations of atherosclerosis result from decreased blood flow through the stenotic areas. Signs and symptoms vary according to the area, size, and location of the lesion, along with the age and physiologic status of the patient. As blood flows through a stenotic area, turbulence will occur beyond the stenosis, resulting in decreased blood perfusion past the area of atherosclerosis. Generally, a 50% to 60% reduction in blood flow is necessary for patients to present with symptoms (e.g., pain). Turbulence is increased when there is an increase in blood flow to an area of the body, such as the lower extremities during exercise. When atherosclerosis develops slowly, collateral circulation develops to meet the needs.24 A patient with no complaint of pain at rest may therefore experience leg pain (intermittent claudication [IC]) during walking or exercise as a result of decreased blood flow and the accumulation of meta- bolic waste (e.g., lactic acid).4,28,29
BOX 7-1 Risk Factors for Atherosclerosis
Reversible Irreversible
Hypertension (controlled) Glucose intolerance and Diabetes
(controlled)
Lipid abnormalities (controlled) High LDL cholesterol Low HDL cholesterol Hypertriglyceridemia Cigarette smoking Obesity Sedentary lifestyle Cocaine Depression Male gender Strong family history Genetic abnormalities
HDL, High-density lipoprotein; LDL, low-density lipoprotein.
Data from Bryant RA, Nix DP: Acute and chronic wounds, ed 3, St Louis, 2007, Mosby; Kumar V: Robbins and Cotran pathologic basis of disease, ed 7, St Louis, 2005, Saunders; Crawford MH, DiMarco JP, Paulus WJ: Crawford: Cardiology, ed 3, St Louis, 2009, Mosby, Inc.
These symptoms are referred to as pseudoclaudication or neu- rologic claudication. Table 7-14 outlines the differences between true claudication and pseudoclaudication.31
All patients with claudication should be strongly advised to stop smoking. The beneficial effect of exercise training in patients with IC is well proven. The improvement in walking distance has been reported to be between 30% and 200%. A specific exercise program gives a more marked improvement than if the patient tries to exercise on his or her own. The great- est improvement in walking distance until pain develops seems to occur with an exercise duration of longer than 30 minutes per session and a frequency of at least three sessions per week. Walking should be used as a mode of exercise, and it should be performed at nearly maximum pain. The program should last at least 6 months.27
Medications that have been used in managing intermittent claudication include pentoxifylline and cilostazol.32
Treatment of atherosclerotic disease is based on clinical pre- sentation and can range from risk-factor modifications (e.g., low-fat diet, increased exercise, and smoking cessation) to pharmacologic therapy (e.g., anticoagulation and thrombolyt- ics) to surgical resection and grafting. Modification of risk factors has been shown to be the most effective method to lower the risk of morbidity (heart attack or stroke) from atherosclerosis.33,34
Aneurysm. An aneurysm is a localized dilatation or out-
pouching of the vessel wall that results from degeneration and weakening of the supportive network of protein fibers with a concomitant loss of medial smooth muscle cells. Aneurysms The following are general signs and symptoms of
atherosclerosis30:
• Peripheral pulses that are slightly reduced to absent. • Presence of bruits on auscultation of major arteries (i.e.,
carotid, abdominal aorta, iliac, and femoral).
• Coolness and pallor of skin, especially with elevation. • Presence of ulcerations, atrophic nails, and hair loss. • Increased blood pressure.
• Subjective reports of continuous burning pain in the lower extremities at rest that is aggravated with elevation (isch- emic pain) and relieved with placing the leg over the edge of the bed.24 Pain at rest is usually indicative of severe (80% to 90%) arterial occlusion.
• Subjective reports of calf or lower-extremity pain, ache or cramp induced by walking (intermittent claudication) and relieved by rest.
TABLE 7-13 Comparison of Clinical Findings of Arterial and Venous Disorders
Clinical Finding Arterial Disorders Venous Disorders
Edema May or may not be present Present
Worse at the end of the day Improves with elevation
Muscle mass Reduced Unaffected
Pain Intermittent claudication Cramping
Worse with elevation
Aching pain
Exercise improves pain Better with elevation Cramping at night
Paresthesias, pruritus (severe itching) Leg heaviness, especially at end of day
Pulses Decreased to absent
Possible systolic bruit Usually unaffected, but may be difficult to palpate if edema is present
Skin Absence of hair
Small, painful ulcers on pressure points, especially lateral malleolus
Normal toenails Tight, shiny skin Thickened toenails
Broad, shallow, painless ulcers of the ankle and lower leg
Color Pale
Dependent cyanosis Brown discolorationDependent cyanosis
Temperature Cool May be warm in presence of thrombophlebitis
Sensation Decreased light touch
Occasional itching, tingling, and numbness Pruritus
Data from Black JM, Matassarin-Jacobs E, editors: Luckmann and Sorensen’s medical-surgical nursing: a psychophysiologic approach, ed 4, Philadelphia, 1993, Saunders, p 1261. CLINICAL TIP The distance a person can walk before the onset of pain indi- cates the degree of circulatory inadequacy (e.g., two blocks or more is mild, one block is moderate, one half block or less is severe).24 Progression of ambulation distance in the patient with intermittent claudication can be optimized if ambulation is per- formed at short, frequent intervals (i.e., before the onset of claudicating pain).
Symptoms similar to intermittent claudication may have a neurologic origin from lumbar canal stenosis or disc disease.
FIGURE 7-4
True and false aneurysms. Center, Normal vessel. Left, True aneurysm. The wall bulges outward and may be attenuated but is intact. Right, False aneurysm. The wall is ruptured, and there is a collection of blood (hema- toma) that is bounded externally by adherent extravascular tissues. (From Kumar V: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
Normal vessel False aneurysm
Extravascular connective tissue Extravasation of blood Hematoma True aneurysm
TABLE 7-14 Differentiating True Intermittent Claudication from Pseudoclaudication
Characteristic of Discomfort Intermittent Claudication Pseudoclaudication
Activity-induced Yes Yes or no
Location Unilateral buttock, hip, thigh, calf, and foot Back pain and bilateral leg pain
Nature Cramping
Tightness Tiredness
Same as with intermittent claudication or presence of tingling, weakness, and clumsiness
Occurs with standing No Yes
Onset Occurs at the same distance each time with
walking on level surface Occurs at variable distance each time with walking on level surfaces Unchanged or decreased distance walking uphill Increased distance when walking uphill Unchanged or increased distance walking
downhill Decreased distance walking downhill
Relieved by Stopping activity Sitting
Data from Young JR, Graor RA, Olin JW et al, editors: Peripheral vascular diseases, St Louis, 1991, Mosby, p 183; Fritz JM: Spinal stenosis. In Placzek JD, Boyce DA, editors: Orthopaedic physical therapy secrets, Philadelphia, 2001, Hanley & Belfus, p 344.
most commonly occur in the abdominal aorta or iliac arteries, followed by the popliteal, femoral, and carotid vessels.28,33,35,36 The exact mechanism of aneurysm formation is not fully under- stood but includes a combination of the following:
• Genetic abnormality in collagen (e.g., with Marfan’s syndrome)
• Aging and natural degeneration of elastin • Increased proteolytic enzyme activity
• Atherosclerotic damage to elastin and collagen
A true aneurysm is defined as a 50% increase in the normal diameter of the vessel36 and involves weakening of all three layers of the arterial wall. True aneurysms are also generally fusiform and circumferential in nature. False and saccular aneu- rysms are the result of trauma from dissection (weakness or separation of the vascular layers) or clot formation (Figure 7-4). They primarily affect the adventitial layer.35
Abdominal aortic aneurysm is dilatation of the abdominal aorta to more than 3 cm in diameter. These aneurysms can be infrarenal, juxtarenal or suprarenal, according to the relation- ship to the renal arteries.27
Approximately 80% of the aneurysms are identified inciden- tally on abdominal ultrasound, computed tomography (CT) scan, magnetic resonance imaging (MRI), or plain x-ray.37 Aneurysms will rupture if the intraluminal pressure exceeds the tensile strength of the arterial wall. Rupture is mostly likely to occur in aneurysms that are 5 cm or larger.24
CLINICAL TIP
Abdominal aortic aneurysms are frequently referred to as AAA,
A3, or triple A in the clinical setting.
Physical Therapy Considerations. The following are addi- tional clinical manifestations of aneurysms:
• Popliteal aneurysm presents as a pulsating mass, 2 cm or more in diameter. Femoral aneurysms presents as a pulsating mass in the femoral area on one or both sides.24 In thin individuals, an aortic aneurysm may be seen as a pulsating swelling in the upper abdomen.27
because of widening of the aortic annulus or actual disrup- tion of the aortic valve leaflets.
• Pleural effusions: Pleural effusion, which occur most fre- quently in the left chest, can be caused by the rupture of the dissection into the pleural space or by weeping of fluid from the aorta as the result of an inflammatory reaction to the dissection.41
• Neurological manifestations (cerebrovascular accident and, rarely, altered consciousness, coma).
• Ischemic manifestations (described earlier in the Atheroscle- rosis section), if the aneurysm impedes blood flow. Most abdominal aneurysms are asymptomatic, but intermittent or constant pain in the form of mild to severe mid-abdominal or lower back discomfort is present in some form in 25% to 30% of cases. Groin or flank pain may be experienced because of increasing pressure on other strutures.24 Most of the aneurysms are relatively asymptomatic until an embolus dislodges from the aneurysm or the aneurysm ruptures.36
• Cerebral aneurysms, commonly found in the circle of Willis, present with increased intracranial pressure and its sequelae (see Chapter 6 for more information on intracranial pressure).35
• Aneurysms that result in subarachnoid hemorrhage are also discussed in Chapter 6.
• Low back pain (aortic aneurysms can refer pain to the low back).
• Dysphagia (difficulty swallowing) and dyspnea (breathless- ness) resulting from the enlarged vessel’s compressing adja- cent organs.
Surgical resection and graft replacement are generally the desired treatments for aneurysms.38 However, endovascular repair of abdominal aneurysms is demonstrating favorable results. Endovascular repair involves threading an endoprosthe- sis through the femoral artery to the site of the aneurysm. The endoprosthesis is then attached to the aorta, proximal to the site of the aneurysm, and distal to the iliac arteries. This effectively excludes the aneurysm from the circulation, which minimizes the risk of rupture.36 Non–surgical candidates must have blood pressure and anticoagulation management.38
Aortic Dissection. Aortic dissection is caused by an intimal
tear, which allows creation of a false lumen between the media and adventitia. A history of Marfan’s syndrome or hypertension is usually present.39 Aortic dissection occurs at least twice as frequently in men than in women.7 Signs and symptoms gener- ally reflect the type of aortic dissection (whether type A or type B [Figure 7-5]) and the extent of cardiovascular involvement.40 Signs and symptoms of aortic dissection include40:
• Pain: Sudden and excruciating pain in the chest (90% of the patients) or the upper back is the most common initial symptom. Another important characteristic of the pain is its tendency to migrate to the neck, abdomen, or groin, gener- ally following the path of dissection.
• Shock: Cardiogenic or hypovolemic shock may be secondary to cardiac tamponade from aortic rupture into the pericar- dium, dissection or compression of the coronary arteries, acute aortic regurgitation, or acute blood loss.
• Syncope.
• Hypertension: More than 50% of patients with distal dissec- tion are hypertensive, and severe hypertension with diastolic pressure as high as 160 mm Hg may be encountered with distal dissection. Severe hypertension may be due to renal ischemia.
• Reduced or absent pulses.
• Murmur of aortic regurgitation. This may be present in 50% of the patients with proximal dissection and may occur
FIGURE 7-5
Classification of aortic dissections. A, Dissection of ascending aorta (type A). B, Dissection of descending aorta (type B). (From Kumar V: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
Type B Type A
DeBakey I DeBakey II DeBakey III
CLINICAL TIP
The pain of aortic dissection may mimic that of myocardial ischemia.41
The chest radiograph may be the first clue to the diagnosis of aortic dissection, but the findings on the chest radiograph are nonspecific, subject to interobserver variability and in many cases completely normal.7
Electrocardiogram (ECG) findings in these patients are non- specific.7,39 Transesophageal echocardiography (TEE) and CT scan are the primary diagnostic tests used by most institutions to diagnose aortic dissection.42 TEE is highly accurate for the evaluation and diagnosis of acute aortic dissection, with sensi- tivity (98%) and specificity (94% to 97%). Contrast CT is also highly accurate for diagnosing aortic dissection, with sensitivity and specificity of 95% to 98%. MRI is a highly accurate non- invasive technique for evaluating aortic dissection but is rarely used as the initial test for diagnostic evaluation of acute dissec- tion. MRI is known to have high sensitivity (95% to 100%) and specificity (94% to 98%) for the detection of aortic dissection.7
Hypertension is frequently asymptomatic; this creates a sig- nificant health risk for affected people.24 Signs and symptoms that can result from hypertension and its effects on target organs are described in Table 7-17.
Two general forms of hypertension exist: essential and sec- ondary. Essential or idiopathic hypertension is an elevation in blood pressure that results without a specific medical cause but is related to the following risk factors35,45:
• Genetic predisposition • Smoking • Sedentary lifestyle • Type A personality • Obesity • Diabetes mellitus
• Diet high in fat, cholesterol, and sodium • Atherosclerosis
• Imbalance of vasomediator production, nitric oxide (vasodi- lator), and endothelin (potent vasoconstrictor)
Secondary hypertension results from a known medical cause,
such as renal disease and others listed in Table 7-18. If the causative factors are treated sufficiently, systolic blood pressure may return to normal limits.35
A rise in diastolic blood pressure from a sitting to standing position suggests essential hypertension, whereas a fall in blood pressure from the sitting to standing position indicates second- ary hypertension.9
Management of hypertension consists of behavioral (e.g., diet, smoking cessation, activity modification) and pharmaco- logic intervention to maintain blood pressure within acceptable parameters. Pharmacologic treatment can likely be deferred in hypertensive patients who regularly participate in aerobic exer- cise. Exercise high in intensity and duration has a beneficial effect in the management of hypertension, and the antihyper- tensive effect of regular training can be maintained as long as 3 years.46 The primary medications used are diuretics and Management includes stabilizing the patient, aggressive
control of blood pressure, and pain control. Patients may be managed medically or surgically, depending on the site of the dissection and the patient’s comorbidities.
Arterial Thrombosis. Arterial thrombosis occurs in areas of
low or stagnant blood flow, such as atherosclerotic or aneurys- mal areas. The reduced or turbulent blood flow in these areas leads to platelet adhesion and aggregation, which then activates the coagulation cycle to form a mature thrombus (clot). Blood flow may then be impeded, potentially leading to tissue isch- emia with subsequent clinical manifestations.35,38
Arterial Emboli. An arterial embolus is a fragment of
thrombus, fat, atherosclerotic plaque, bacterial vegetation, or air that mobilizes within the arterial vessels and obstructs flow distal to the embolus.43 Arterial emboli arise from areas of stagnant or disturbed blood flow in the heart or aorta. Acute arterial embolus is a surgical emergency. The likelihood of limb salvage decreases after 4 to 6 hours.42 The most common sources of arterial emboli are listed in Table 7-15.
Areas in which arterial emboli tend to lodge and interrupt blood flow are arterial bifurcations and areas narrowed by ath- erosclerosis (especially in the cerebral, mesenteric, renal, and coronary arteries). Signs and symptoms of thrombi, emboli, or both depend on the size of the occlusion, the organ distal to the clot, and the collateral circulation available.35
When arterial thrombosis or embolism is suspected, the affected limb must be protected by proper positioning below the horizontal plane, and protective skin care must be provided. Heat or cold application and massage are to be avoided.24 Treat- ment of thrombi, emboli, or both includes anticoagulation with or without surgical resection of the atherosclerotic area that is predisposing the formation of thrombi, emboli, or both. Medical management of arterial thrombosis can also include antithrom- botic drugs (e.g., tissue factor or factor Xa inhibitors) or com- bined antithrombotic therapy with aspirin, a thienopyridine and warfarin, or both.44
Hypertension. Hypertension is an elevated arterial blood
pressure, both systolic and diastolic, that is abnormally sus- tained at rest (Table 7-16).
From Belkin M, Owens CD, Whittemore AD et al: Peripheral arterial occlusive disease. In Townsend CM, Beauchamp RD, Evers BM et al, editors: Sabiston textbook of surgery: the biological basis of modern surgical practice, ed 18, Philadelphia, 2007, Saunders.
TABLE 7-15 Sources of Peripheral Emboli
Source Percentage Cardiac 80% Atrial fibrillation 50%