Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology

Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology Acute care handbook for physical therapists (fourth edition) chapter 7 vascular system and hematology

Review the vascular and hematologic evaluation, including physical examination and diagnostic and labora-3 Describe vascular, hematologic, and lymphatic health conditions, including clinical findings, medical and surgical management, and physical therapy intervention

PREFERRED PRACTICE PATTERNS

The most relevant practice patterns for the diagnoses discussed in this chapter, based on the

American Physical Therapy Association’s Guide to Physical Therapist Practice, second edition,

are as follows:

• Arterial Disorders (Atherosclerosis, Aneurysm, Aortic Dissection, Hypertension, Raynaud’s Disease), Chronic Regional Pain Syndrome, Compartment Syndrome: 4C, 4J, 6D, 7A

• Venous Disorders (Varicose Veins, Venous Thrombosis, Pulmonary Embolism, Chronic Venous Insufficiency): 4C, 6D, 7A

• Combined Arterial and Venous Disorders (Arteriovenous Malformations): 4C, 6D, 7A

• Hematologic Disorders (Erythrocytic Disorders [Anemia], Polycythemia), cytic Disorders: 4C, 6D

Thrombo-• Lymphatic Disorders (Lymphedema): 4C, 6D, 6HPlease refer to Appendix A for a complete list of the preferred practice patterns, as individual patient conditions are highly variable and other practice patterns may be applicable

Alterations in the integrity of the vascular and hematologic systems can alter a patient’s ity tolerance The physical therapist must be aware of the potential impact that a change in blood composition or blood flow has on a multitude of body functions, including cardiac output, hemostasis, energy level, and healing

activ-Body Structure

The network of arteries, veins, and capillaries composes the vascular system Living blood cells and plasma within the blood vessels are the structures that compose the hematologic system The lymphatic system assists the vascular system by draining unabsorbed plasma from tissue spaces and returning this fluid (lymph) to the heart via the thoracic duct, which empties into the left jugular vein The flow of lymph is regulated by intrinsic contractions of the lymph vessels, muscular contractions, respiratory movements, and gravity.1

Vascular System StructureAll blood vessels are composed of three similar layers (Figure 7-1 and Table 7-1) Blood vessel diameter, length, and wall thickness vary according to location and function (Table 7-2) Note

CHAPTER OUTLINE

Body Structure

Vascular System Structure

Hematologic System Structure

Lymphatic System Structure

Blood Product Transfusion

Vascular Surgical Procedures

Physical Therapy Management

for Patients with Vascular and

Hematologic Disorders

FIGURE 7-1 Structure of the arteries and veins (From Lewis SL, Heitkepmer M, Dirksen S et al: Medical-surgical nursing:

assessment and management of clinical problems, ed 7, St Louis, 2007, Mosby.)

Artery Vein

Endothelium (tunica intima)

Elastic membrane (thinner in veins)

Smooth muscle layer (tunica media) (thinner in veins) Connective tissue (tunica advenitia) Valve

TABLE 7-1 Blood Vessel Layers

Tunica intima Innermost layer: Endothelial layer over a basement membrane Provides a smooth surface for laminar

blood flow Tunica media Middle layer: Smooth muscle cells and elastic connective tissue

with sympathetic innervation Constricts and dilates for blood pressure regulation Tunica adventitia Outermost layer: Composed of collagen fibers, lymph vessels, and

the blood vessels that supply nutrients to the blood vessel Protects and attaches blood vessels to nearby structures

Data from Marieb EN: Human anatomy and physiology, ed 3, Redwood City, CA, 1995, Benjamin-Cummings.

TABLE 7-2 Characteristics of Blood Vessels

Artery Large or elastic arteries—aorta and its large

branches and pulmonary artery.

Medium or muscular arteries—composing other branches of aorta (i.e., coronary arteries).

Small arteries and arterioles.

Thick tunica media layer allows arteries to readily accommodate to pressure changes from the heart.

Vein Small, medium, or large in diameter.

Thin tunica media and thick tunica adventitia.

Valves prevent backflow of blood to maintain venous return to the heart.

Capillary

network The interface of the arterial and venous systems where blood cells, fluids, and gases are

exchanged.

Capillary beds can be open or closed, depending

on the circulatory requirements of the body.

Data from Marieb EN: Human anatomy and physiology, ed 3, Redwood City,

CA, 1995, Benjamin-Cummings; Kumar V: Robbins and Cotran pathologic

basis of disease, ed 7, Philadelphia, 2005, Saunders.

that the arteries are divided into three types, depending on their size and structural features

Hematologic System StructureBlood is composed of living cells (Table 7-3) in a nonliving plasma solution and accounts for 8% of total body weight, or

4 to 5 liters in women and 5 to 6 liters in men Plasma is posed almost completely of water and contains more than 100 dissolved substances The major solutes include albumin, fibrin-ogen, protein globules, nitrogenous substances, nutrients, elec-trolytes, and respiratory gases.2

com-Lymphatic System StructureThe lymphatic system includes lymph vessels, lymph fluid, and lymph tissues and organs (lymph nodes, tonsils, spleen, thymus, and the thoracic duct) The lymphatic system is parallel to and works in concert with the venous system Lymphatics are fragile and are more likely to collapse under pressure than the veins Lymphatics are located in all portions of the body except the central nervous system and cornea Lymph moves throughout the body through a number of mechanisms, and the excess

lymph is transported to the thoracic duct and emptied into the

jugular vein trunks Lymph fluid is first absorbed at the

capil-lary level, then channeled through the small vessels and finally

picked up by the larger valved vessels.3

Body Function

The function of the blood vessels is to carry blood throughout

the body to and from the heart (Table 7-4) Normal alterations

in the vessel diameter will occur, depending on circulating

blood volume and the metabolic needs of the tissues

The function of the lymphatic system is to (1) protect the

body from infection and disease via the immune response and

TABLE 7-3 Blood Cell Types

An oxygen molecule attaches to each iron atom to become oxyhemoglobin.

(platelet; Plt) Cell fragment responsible for clot formation.

Data from Marieb EN: Human anatomy and physiology, ed 3, Redwood City,

CA, 1995, Benjamin-Cummings.

TABLE 7-4 Functions of Blood

Oxygen and carbon dioxide

transport Binding to hemoglobin; dissolved in plasma

Nutrient and metabolite

transport Bound to plasma proteins; dissolved in plasma

Hormone transport In plasma

Transport of waste products to

kidneys and liver In plasma

Transport of cells and substances

involved in immune reactions In plasma to site of infection or foreign body

Clotting at breaks in blood

Maintenance of fluid balance Blood volume regulation

Body temperature regulation Peripheral vasoconstriction

or dilation Maintenance of acid-base balance Acid-base regulation

Data from Nettina S: The Lippincott manual of nursing practice, ed 8,

Phila-delphia, 2005, Lippincott Williams & Wilkins.

(2) to facilitate movement of fluid back and forth between the bloodstream and the interstitial spaces, removing excess fluid, blood waste, and protein molecules in the process of fluid exchange.3

The vascular and hematologic systems are intimately linked, and the examination of these systems is often similar For the purpose of this chapter, however, the evaluations of the vascular and hematologic systems are discussed separately

Physical Examination

Vascular EvaluationHistory

In addition to the general chart review (see Chapter 2), it is important to gather the following information during examina-tion of the patient with a suspected vascular disorder4-8:

• Relevant medical history that includes diabetes mellitus, hypertension, hyperlipidemia, syncope or vertigo, and non-healing ulcers

• Relevant social history that includes exercise and dietary habits, as well as the use of tobacco or alcohol

• History of recent prolonged bed rest and/or surgery or a long flight

• Pain in arms and legs (Visceral pain and arthritis pain may radiate to the extremities.)

• Presence of intermittent claudication (pain, ache, sense of fatigue, or other discomfort that occurs in the affected muscle group with exercise, particularly walking, and resolves with rest.) The speed, distance, and the site of the pain, including what relieves the pain, should be noted

• Buttock, hip, or thigh claudication typically occurs in patients with obstruction of the aorta and iliac arteries Calf claudication characterizes femoral and popliteal artery steno-sis The gastrocnemius muscle consumes more oxygen during walking than other muscle groups in the leg and hence causes the most frequent symptom reported by patients

• Presence of nocturnal pain that can develop as the vascular occlusion worsens This type of pain occurs when the patient

is in bed and is caused by a combination of leg elevation and reduced cardiac output

• Presence of rest pain refers to pain that occurs in the absence

of activity and with legs in a dependent position Rest pain signals advanced occlusive disease, typically greater than 90% occlusion

• Presence or history of acute or chronic peripheral edema If chronic, what is the patient’s baseline level of edema?

• Precautions, such as weight bearing or blood pressure eters after vascular surgery

CLINICAL TIP

Intermittent claudication is often abbreviated in the clinical setting as IC

Peripheral pulses can be assessed in the following arteries (see Chapter 3, Figure 3-6):

Inspection

Observation of the following features can help delineate the

location and severity of vascular disease and help determine

whether these manifestations are arterial or venous in origin1,4,5,9:

• Skin color: Note the presence of any discoloration of the

distal extremities/nail bed, which is indicative of decreased

blood flow (e.g., mottled skin)

• Hair distribution: Patchy hair loss on the lower leg may

indicate arterial insufficiency

• Venous pattern: Dilation or varicosities—dilated, purplish,

ropelike veins, particularly in the calf

• Edema or atrophy: Peripheral edema from right-sided

con-gestive heart failure occurs bilaterally in dependent areas;

edema from trauma, lymphatic obstruction, or chronic

venous insufficiency is generally unilateral Refer to Table

3-5 for grading of pitting edema Measurement of the

extremities may help to identify the edema or atrophy With

a flexible tape, measure:

• The forefoot

• The smallest possible circumference above the ankle

• The largest circumference at the calf

• The mid-thigh, a measured distance above the patella

with the knee extended

A difference greater than 1 cm just above the ankle or 2 cm

at the calf is suggestive of edema

• Presence of cellulitis

• Presence of petechiae: Small, purplish, hemorrhagic spots on

the skin

• Skin lesions: Ulcers, blisters, or scars

• Digital clubbing: Could be indicative of poor arterial

oxy-genation or circulation

• Gait abnormalities

Palpation

During the palpation portion of the examination, the physical

therapist can assess the presence of pain and tenderness, strength

and rate of peripheral pulses, respiratory rate, blood pressure,

skin temperature, and limb girth (if edematous) Changes in

heart rate, blood pressure, and respiratory rate may correspond

to changes in the fluid volume status of the patient For example,

a decrease in fluid volume may result in a decreased blood

pressure that results in a compensatory increase in heart and

respiratory rates The decreased fluid volume and resultant

increased heart rate in this situation may then result in a

decreased strength of the peripheral pulses on palpation A

decreased or absent pulse provides insight into the location of

arterial stenoses.7 In patients with suspected or diagnosed

peripheral vascular disease, monitoring distal pulses is more

important than monitoring central pulses in the larger, more

proximal vessels.4

The following system/scale is used to grade peripheral

pulses10:

• 0: Absent, not palpable

• 1: Diminished, barely palpable

• 2: Brisk, expected

• 3: Full, increased

• 4: Bounding

Physical Therapy Considerations

• In patients who have disorders resulting in vascular mise (e.g., diabetes mellitus, peripheral vascular disease, or hypertension), pulses should be monitored before, during, and after activity not only to determine any rate changes, but, more important, to determine any changes in the strength of the pulse

compro-• Notation should be made if the strength of pulses is lated to complaints of pain, numbness, or tingling of the extremity

corre-• Compare the two extremities for color, temperature, and swelling Bilateral coldness is most often due to cold envi-ronment and/or anxiety.5

• Carotid arteries should never be palpated simultaneously, as excessive carotid sinus massage can cause slowing of the pulse, cause a drop in blood pressure, and compromise blood flow to the brain If the pulse is difficult to palpate, the patient’s head should be rotated to the side being examined

to relax the sternocleidomastoid.10Auscultation

Systemic blood pressure and the presence of bruits (whooshing sound indicative of turbulent blood flow from obstructions) are assessed through auscultation.4 Bruits are often indicative of accelerated blood flow velocity and flow disturbance at sites

of stenosis.7 Bruits are typically assessed by physicians and nurses (see Chapter 3 for further details on blood pressure measurement)

Vascular TestsVarious tests that can be performed clinically to evaluate vas-cular flow and integrity are described in Table 7-5 These tests can be performed easily at the patient’s bedside without the use

of diagnostic equipment The Wells Clinical Decision Rule for Deep Venous Thrombosis is described in Table 7-6

TABLE 7-5 Vascular Tests

Capillary refill time * To assess vascular perfusion

and indirectly assess cardiac output.

Nail beds of fingers or toes are squeezed until blanching (whitening) occurs, and then they are released.

Blanching should resolve (capillary refill) in less than 2 seconds.

Elevation pallor To assess arterial perfusion

Normally color should not change A gray (dark- skinned individuals) or pale/pallor (fair-skinned individuals) discoloration will result from arterial insufficiency or occlusion.

A limb is elevated 30-40 degrees for 15-60 seconds, and color changes are observed over 60 seconds.

Observe the amount of time it takes for pallor to appear: Pallor within 25 seconds indicates severe occlusive disease Pallor within 25-40 seconds indicates moderate occlusive disease.

Pallor within 40-60 seconds indicates mild occlusive disease.

Trendelenburg’s test/

Retrograde filling

test

To determine if superficial or deep veins and their valves are involved in causing varicosities.

To do Trendelenburg’s test, mark the distended veins with a pen while the patient stands Then have the patient lie on the examination table and elevate his or her leg for about a minute to drain the veins

Next, have the patient stand while you measure venous filling time.

If the veins fill in less than 30 seconds, have the patient lie on the examination table again, and elevate his or her leg for 1 minute

Then apply a tourniquet around his

or her upper thigh Next, have the patient stand.

Next, remove the tourniquet.

To pinpoint incompetent valve location, repeat this procedure by applying the tourniquet just below the knee and then around the upper calf.

Competent valves take at least 30 seconds to fill.

If leg veins still fill in less than

30 seconds, suspect incompetent perforating vein and deep vein valves (functioning valves block retrograde flow).

If the veins fill again in less than

30 seconds, suspect incompetent superficial vein valves that allow backward blood flow.

Manual compression

test To detect competent valves in the veins. Palpate the dilated veins with the fingertips of one hand With

the other hand, firmly compress the vein at a point at least 8 inches (20.3 cm) higher Palpate the impulse under your finger.

With a competent valve, there will be no detectable impulse

A palpable impulse indicates incompetent valves in the vein segment between the two hands.

Allen’s test To assess the patency of the

radial and ulnar arteries,

to ensure the collateral circulation of the hand.

Flex the patient’s arm with the hand above level of the elbow Then compress the radial and ulnar arteries at the level of the wrist while the patient clenches his or her fist The patient then opens his

or her hand and either the radial or the ulnar artery is released The process is repeated for the other artery.

When the patient opens the hand, the blanched area should flush within seconds if collateral circulation is adequate If the blanched area does not flush quickly, then it may indicate that collateral circulation is inadequate to support circulation to the hand.

Homans’ sign † To detect the presence of deep

vein thrombosis. The calf muscle is gently squeezed, or the foot is quickly dorsiflexed. Pain that is elicited with either squeezing or dorsiflexing may

indicate a deep vein thrombosis.

Continued

Test Indication Description Normal Results and Values

Ankle-brachial index

(ABI) ‡ To compare the perfusion pressures in the lower leg

with the upper extremity using a blood pressure cuff and Doppler probe This test is commonly used to screen patients for evidence of significant arterial insufficiency.

Place the patient in supine at least 10 minutes before the test Obtain the brachial pressure in each arm, and record the highest pressure Obtain the ankle pressure in each leg

Place the cuff around the lower leg 2.5 cm above the malleolus Apply acoustic gel over the dorsalis pedis

or posterior tibialis pulse location

Hold the Doppler probe lightly over the pedal pulse Inflate the cuff to a level 20-30 mm Hg above the point at which the pulse is no longer audible Slowly deflate the cuff while monitoring for the return of the pulse signal; the point at which the arterial signal returns is recorded as the ankle pressure Calculate the ABI by dividing the higher of the two ankle systolic pressures by the higher of the brachial systolic pressures.

The diagnosis of peripheral arterial disease is based on the limb symptoms or an ABI Interpretation of ABI ABI ≥ 1.0-1.3: normal range §

ABI ≥ 0.7-0.8: borderline perfusion.

ABI ≤ 0.5: severe ischemia, wound healing unlikely ABI ≤ 0.4: critical limb ischemia.

*Variability is found in defining the time by different individuals, so capillary refill time should not be considered an observation with exquisite sensitivity and specificity and should be used more to confirm clinical judgment.

†A 50% false-positive rate occurs with this test Vascular laboratory studies are more sensitive.

‡ABI measurements may be of limited value in anyone with diabetes because calcification of the tibial and peroneal arteries may render them noncompressible.

§An ABI of less than 0.95 is considered abnormal and is 95% sensitive for the angiographically verified peripheral arterial stenosis.

TABLE 7-5 Vascular Tests—cont’d

Data from Seidel HM, Ball JW, Dains JE et al: Mosby’s guide to physical examination, ed 7, St Louis, 2010, Mosby; Lanzer P, Rosch J, editors: Vascular diagnostics: noninvasive and invasive techniques, peri-interventional evaluations, Berlin, 1994, Springer Verlag; Springhouse: Handbook of medical-surgical nursing, ed 4, Phila- delphia, 2005, Lippincott Williams & Wilkins; Newberry L, Sheehy S, editors: Sheehy’s emergency nursing: principles and practice, ed 6, St Louis, 2009, Mosby; Dormandy JA, Rutherford RB: Management of peripheral arterial disease (PAD) TASC Working Group, J Vasc Surg 31:S1–S296, 2000; Hallet JW, Brewster DC, Darling RC, editors: Handbook of patient care in vascular surgery, ed 3, Boston, 1995, Little, Brown; Goodman CC: The hematologic system In Goodman CC, Boisonnault WG, editors: Pathology: implications for the physical therapist, ed 3, Philadelphia, 2009, Saunders.

Diagnostic Studies

Noninvasive Laboratory Studies Various noninvasive

proce-dures can examine vascular flow The phrases lower-extremity

noninvasive studies and carotid noninvasive studies are general

descriptions that are inclusive of the noninvasive tests described

in Table 7-7

Invasive Vascular Studies The most common invasive

vascu-lar study is arteriography, typically referred to as contrast

angi-ography (Figure 7-2) This study is performed by injecting

radiopaque dye into the femoral, lumbar, brachial, or axillary

arteries, followed by radiographic viewing Blood flow

dynam-ics, abnormal blood vessels, vascular anomalies, normal and

abnormal vascular anatomy, and tumors are easily seen during

the radiographic viewing With the use of digital-subtraction

angiography (DSA), bony structures can be obliterated from the

picture DSA is useful when adjacent bone inhibits visualization

of the blood vessel to be evaluated.11 An angiogram is a picture

produced by angiography Angiography is generally performed

before or during therapeutic interventions, such as percutaneous

angioplasty, thrombolytic therapy, or surgical bypass grafting

Postangiogram care includes the following12:

• Bed rest for 4 to 8 hours

• Pressure dressings to the injection site with assessment for

hematoma formation

• Intravenous fluid administration to help with dye excretion Blood urea nitrogen (BUN) and creatinine are monitored to ensure proper renal function (refer to Chapter 9 for more information on BUN and creatinine)

• Frequent vital sign monitoring with pulse assessments

• If a patient has been on heparin before angiography, the drug

is not resumed for a minimum of 4 hours.12The complications of arteriography can be due to the catheterization or due to the contrast agent that is injected (Table 7-8)

Hematologic EvaluationThe medical workup of the patient with a suspected hemato-logic abnormality includes the patient’s medical history and laboratory studies, in addition to the patient’s clinical presentation

History

In addition to the general chart review (see Chapter 2), the lowing questions are especially relevant in the evaluation of the patient with a suspected hematologic disorder13-15:

fol-• What are the presenting symptoms?

• Was the onset of symptoms gradual, rapid, or associated with trauma or other disease?

TABLE 7-6 Wells Clinical Decision Rule (CDR) for Deep Venous Thrombosis

Active cancer (treatment ongoing within previous 6 mo or palliative) 1 Paralysis, paresis, or recent plaster immobilization of the lower extremities 1 Recently bedridden for more than 3 days or major surgery, within 4 weeks 1 Localized tenderness along the distribution of the deep venous system 1

Calf swelling by more than 3 cm when compared with the asymptomatic leg (measured 10 cm below tibial tuberosity) 1

Alternative diagnosis as likely as or more likely than deep vein thrombosis −2

*−2 to 0: Low probability of DVT (3%); 1 to 2: Moderate probability of DVT (17%); 3 or more: High probability of DVT (75%) Medical consultation is advised

in the presence of low probability; medical referral is required with moderate or high score.

From Wells PS, Anderson DR, Bormanis J et al: Value of assessment of pretest probability of deep-vein thrombosis in clinical management, Lancet

350(9094):1795-1798, 1997.

TABLE 7-7 Noninvasive Vascular Studies

Doppler ultrasound High-frequency and low-intensity (1-10 MHz) sound waves are applied to the skin with a Doppler probe

(and acoustic gel) to detect the presence or absence of blood flow, direction of flow, and flow character over arteries and veins with an audible signal Low-frequency waves generally indicate low-velocity blood flow Ultrasound examination has a sensitivity and specificity of approximately 95%.

Color duplex scanning or

imaging Velocity patterns of blood flow along with visual images of vessel and plaque anatomy can be obtained by combing ultrasound with a pulsed Doppler detector Distinctive color changes indicate blood flow

through a stenotic area.

Plethysmography Plethysmography is a noninvasive test that provides measurement of changes in the volume of the blood

distal to the affected area indicating an occlusion and specifically for the amount of time required for the veins to refill after being emptied.

Exercise testing Exercise testing is performed to assess the nature of claudication by measuring ankle pressures and pulse

volume recordings (PVRs) after exercise.

A drop in ankle pressures can occur with arterial disease.

This type of testing provides a controlled method to document onset, severity, and location of claudication Screening for cardiorespiratory disease can also be performed, as patients with peripheral vascular disease often have concurrent cardiac or pulmonary disorders (see Chapter 3).

Computed tomography (CT) CT is used to provide visualization of the arterial wall and its structures.

Indications for CT include diagnosis of abdominal aortic aneurysms and postoperative complications of graft infections, occlusions, hemorrhage, and abscess.

Magnetic resonance imaging

(MRI) MRI has multiple uses in evaluating the vascular system and is now more commonly used to visualize the arterial system than arteriograms Specific uses for MRI include detection of deep venous thrombosis and

evaluation of cerebral edema.

(Serial MRIs can also be used to help determine the optimal operative time for patients with cerebrovascular accidents by monitoring their progression.)

Magnetic resonance

angiography (MRA) MRA uses blood as a physiologic contrast medium to examine the structure and location of major blood vessels and the flow of blood through these vessels The direction and rate of flow can also be quantified

MRA minimizes complications that may be associated with contrast medium injection Figure 7-2

illustrates the MRA of the aorta and lower extremity.

Data from Black JM, Matassarin-Jacobs E, editors: Luckmann and Sorensen’s medical-surgical nursing: a psychophysiologic approach, ed 4, Philadelphia, 1993, Saunders, p 1286; Bryant RA, Nix DP: Acute and chronic wounds Current management concepts, ed 4, St Louis, 2012, Mosby; Lanzer P, Rosch J, editors: Vascular diagnostics: noninvasive and invasive techniques, peri-interventional evaluations, Berlin, 1994, Springer Verlag; Kee JL, editor: Laboratory and diagnostic tests with nursing implications, ed 8, Stamford, CT, 2009, Appleton & Lange, p 606; Malarkey LM, Morrow ME, editors: Nurses manual of laboratory tests and diagnostic procedures, ed 2, Philadelphia, 2000, Saunders, p 359; Mettler FA: In Essentials of radiology, ed 2, Philadelphia, 2005, Saunders; Fahey VA, editor: Vascular nursing,

ed 4, Philadelphia, 2003, Saunders; McCance KL, Huether SE, editors: Pathophysiology: the biologic basis for disease in adults and children, ed 6, St Louis, 2009, Mosby, p 1001; George-Gay B, Chernecky CC: In Clinical medical-surgical nursing: a decision-making reference, ed 1, Philadelphia, 2002, Saunders; Schroeder ML: Principles and practice of transfusion medicine, ed 10 In Lee GR, Foerster J, Lukens J et al, editors: Wintrobe’s clinical hematology, vol 1, Baltimore, 1999, Lip- pincott Williams & Wilkins, pp 817-874.

FIGURE 7-2

Magnetic resonance angiography (MRA) of the aorta and lower extremity

arterial circulation (From Adam A: Grainger & Allison’s diagnostic

radiol-ogy, ed 5, London, 2008, Churchill Livingstone.)

TABLE 7-8 Complications of Contrast Arteriography

Puncture site or catheter

related Hemorrhage/hematomaPseudoaneurysm

Arteriovenous fistula Atheroembolism Local thrombosis Contrast agent related Major (anaphylactoid) sensitivity

reaction Minor sensitivity reactions Vasodilation/hypotension Nephrotoxicity

Hypervolemia

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.

• Is the patient unable to complete daily activities secondary

to fatigue?

• Is there a patient or family history of anemia or other blood

disorders, cancer, hemorrhage, or systemic infection?

• Is there a history of blood transfusion?

• Is there a history of chemotherapy, radiation therapy, or other

drug therapy?

• Has there been an environmental or occupational exposure

to toxins?

• Have there been night sweats, chills, or fever?

• Is the patient easily bruised?

• Is wound healing delayed?

• Is there excessive bleeding or menses?

Other relevant data include the patient’s diet (for the ation of vitamin- or mineral-deficiency anemia), history of weight loss (as a warning sign of cancer or altered metabolism), whether the patient abuses alcohol (a cause of anemia with chronic use), and race (some hematologic conditions have a higher incidence in certain races)

evalu-InspectionDuring the hematologic evaluation, the patient is observed for the following13,16,17:

• General appearance (for lethargy, malaise, or apathy)

• Degree of pallor or flushing of the skin, mucous membranes, nail beds, and palmar creases Pallor can be difficult to assess

in dark-skinned individuals In these individuals, lips, tongue, mucosa, and nail beds should be monitored

• Presence of petechiae (purplish, round, pinpoint, nonraised spots caused by intradermal or subcutaneous hemorrhage) or ecchymosis (bruising)

• Respiratory ratePalpation

The examination performed by the physician includes palpation

of lymph nodes, liver, and spleen as part of a general physical examination For specific complaints, the patient may receive more in-depth examination of a body system Table 7-9 summarizes abnormal hematologic findings by body system on physical examination

The physical therapist may specifically examine the following:

• The presence, location, and severity of bone or joint pain using an appropriate pain scale (see Chapter 21)

• Joint range of motion and integrity, including the presence

of effusion or bony abnormality

• Presence, location, and intensity of paresthesia

• Blood pressure and heart rate for signs of hypovolemia (see Palpation in the Vascular Evaluation section for a description

of vital sign changes with hypovolemia)Laboratory Studies

In addition to the history and physical examination, the clinical diagnosis of hematologic disorders is based primarily on labora-tory studies

Complete Blood Cell Count The standard complete blood

cell (CBC) count consists of a red blood cell (RBC) count, white blood cell (WBC) count, WBC differential, hematocrit (Hct) measurement, hemoglobin (Hgb) measurement, and platelet (Plt) count (Table 7-10) Figure 7-3 illustrates a common method used by the medical-surgical team to document por-tions of the CBC in progress notes If a value is abnormal, it is usually circled within this “sawhorse” figure

Physical Therapy Considerations

• The most important thing to consider when looking at hemoglobin values is the patient’s oxygen supply versus

• Hct is approximately three times the Hgb value.

• A low Hct may cause the patient to experience weakness, dyspnea, chills, or decreased activity tolerance, or it may exacerbate angina

• Patients with cancer such as leukemia or patients who are receiving cancer treatment will most likely present with lower Hct and Hgb values; therefore the therapist should proceed with caution in these patients

• The term pancytopenia refers to a significant decrease in RBCs,

all types of WBCs, and platelets

• The term neutropenia refers to an abnormal decrease in WBCs,

Erythrocyte Indices RBC, Hct, and Hgb values are used

to calculate three erythrocyte indices: (1) mean corpuscular volume (MCV), (2) mean corpuscular Hgb, and (3) mean cor-puscular Hgb concentration (Table 7-11) At most institutions, these indices are included in the CBC

Erythrocyte Sedimentation Rate The erythrocyte

sedi-mentation rate (ESR), often referred to as the sed rate, is a

TABLE 7-9 Signs and Symptoms of Hematologic Disorders by Body System

Palpitations Anemia, hypovolemia

Sternal tenderness Leukemia, sickle cell disease

Syncope Severe anemia, polycythemia Vertigo, tinnitus Severe anemia

Paresthesia Vitamin B 12 anemia, malignancy Confusion Severe anemia, malignancy, infection

Blindness Thrombocytopenia, anemia Gastrointestinal, urinary, and

reproductive DysphagiaAbdominal pain Iron-deficiency anemiaLymphoma, hemolysis, sickle cell disease

Splenomegaly or hepatomegaly Hemolytic anemia Hematemesis, melena Thrombocytopenia and clotting disorders Hematuria Hemolysis and clotting disorders Menorrhagia Iron-deficiency anemia

Ecchymosis Hemolytic, pernicious anemia

Data from Black JM, Matassarin-Jacobs E, editors: Medical-surgical nursing: clinical management for continuity of care, ed 5, Philadelphia, 1997, Saunders.

FIGURE 7-3

Illustration of portions of the complete blood cell count in shorthand

format Hct, Hematocrit; Hgb, hemoglobin; Plt, platelet; WBC, white

blood cell

demand Decreased Hgb levels can reduce oxygen transport

capacity and subsequently reduce the oxygen supply, which

can reduce a patient’s endurance level

• It is important to consider the trends in the Hgb and Hct

levels If Hct/Hgb levels are low at baseline, these patients

may be able to tolerate activity However, patients with

acutely low levels of Hct/Hgb may or may not tolerate

increased activity

• A physical therapist should be aware of signs and symptoms

of hypoxia to major organs: brain, heart, and kidneys

• Monitoring of tolerance and modifications in the therapeutic

plan may be indicated with low levels of Hct/Hgb.18 Hct is

accurate in relation to fluid status; therefore Hct may be

falsely high if the patient is dehydrated and falsely low if the

patient is fluid overloaded.11

TABLE 7-10 Complete Blood Cell Count: Values and Interpretation*

Red blood cell

(RBC) count Number of RBCs per µl of blood Female: 4.2-5.4 million/µlMale: 4.7-6.1 million/µl Blood loss, anemia, polycythemia.Elevated RBC count may increase risk of venous

stasis or thrombi formation.

Increased: polycythemia vera, dehydration, severe chronic obstructive pulmonary disease, acute poisoning.

Decreased: anemia, leukemia, fluid overload, recent hemorrhage.

White blood cell

(WBC) count Number of WBCs per µl of blood 5-10 × 10

3 (5000-10,000) Presence of infection, inflammation, allergens, bone

marrow integrity.

Monitors response to radiation or chemotherapy Increased: leukemia, infection, tissue necrosis.

Decreased: bone marrow suppression.

WBC differential Proportion (%) of the

different types of WBCs (out of 100 cells)

Presence of infectious states.

Detect and classify leukemia.

Hematocrit (Hct) Percentage of RBCs in

whole blood Female: 37%-47%Male: 42%-52% Blood loss and fluid balance.Increased: polycythemia, dehydration.

Decreased: anemia, acute blood loss, hemodilution Hemoglobin

(Hgb) Amount of hemoglobin in 100 ml of blood Female: 12-16 g/100 mlMale: 14-18 g/100 ml Blood loss, bone marrow suppression.Increased: polycythemia, dehydration.

Decreased: anemia, recent hemorrhage, fluid overload Platelets (Plt) Number of platelets in

µl of blood 150-450 × 10

9 150,000-450,000 µl Thrombocytopenia.Increased: polycythemia vera, splenectomy,

malignancy.

Decreased: anemia, hemolysis, DIC, ITP, viral infections, AIDS, splenomegaly, with radiation or chemotherapy.

AIDS, Acquired immunodeficiency syndrome; DIC, disseminated intravascular coagulation; ITP, idiopathic thrombocytopenic purpura.

*Lab values vary among laboratories RBC, hemoglobin, and platelet values vary with age and gender.

Data from Elin RJ: Laboratory reference intervals and values In Goldman L, Bennett JC, editors: Cecil textbook of medicine, vol 2, ed 21, Philadelphia, 2000, Saunders, p 2305; Matassarin-Jacobs E: Assessment of clients with hematologic disorders In Black JM, Matassarin-Jacobs E, editors: Medical-surgical nursing: clinical management for continuity of care, ed 5, Philadelphia, 1997, Saunders, p 1465; Mosby’s diagnostic and laboratory test reference, ed 8, St Louis, 2007, Mosby.

TABLE 7-11 Erythrocyte Indices: Values and Interpretation*

Mean corpuscular volume

(MCV) (Hct × 10/RBC) Mean size of RBCs in a sample of blood 80-100 µm 3 Increased by macrocytic, folic acid, or vitamin B 12 deficiency

anemias; liver disease; and recent alcohol use.

Decreased by microcytic, iron-deficiency, and hypochromic anemias; thalassemia; and lead poisoning.

Mean corpuscular hemoglobin

(MCH) (Hgb × 10/RBC) Amount of Hgb in one RBC 26-34 pg/cell Increased by macrocytic anemia.Decreased by microcytic anemia.

Low mean corpuscular hemoglobin indicates Hgb deficiency Mean corpuscular hemoglobin

concentration (MCHC)

(Hgb/Hct × 100)

Proportion of each RBC occupied

by Hgb

31-37 g/dl Increased by spherocytosis (small round RBC).

Decreased by microcytic, hypochromic, and iron-deficiency anemias and thalassemia.

Hct, Hematocrit; Hgb, hemoglobin; RBC, red blood cell.

*Lab values vary among laboratories.

Data from Elin RJ: Laboratory reference intervals and values In Goldman L, Bennett JC, editors: Cecil textbook of medicine, vol 2, ed 21, Philadelphia, 2000, Saunders, p 2305; Matassarin-Jacobs E: Assessment of clients with hematologic disorders In Black JM, Matassarin-Jacobs E, editors: Medical-surgical nursing: clinical management for continuity of care, ed 5, Philadelphia, 1997, Saunders, p 1466; and Pagana KD, Pagana TJ: Mosby’s diagnostic and laboratory test reference, ed 10,

St Louis, 2011, Mosby, pp 830-833.

measurement of how fast RBCs fall in a sample of

anticoagu-lated blood Normal values vary widely according to laboratory

method According to the Westergren method, the normal

value for males is up to 15 mm per hour and the normal value

for females is up to 20 mm per hour.11

The ESR is a reflection of acute-phase reaction in

inflamma-tion and infecinflamma-tion A limitainflamma-tion of the test is that it lacks

sen-sitivity and specificity for disease processes In addition, ESR

cannot detect inflammation as quickly or as early as some other

tests.19

ESR may be elevated in systemic infection, collagen vascular

disease, and human immunodeficiency virus It is a fairly

reli-able indicator of the course of disease In general, as the disease

worsens, the ESR increases; as the disease improves, the ESR

decreases.11 ESR may be decreased in the presence of sickle cell

disease, polycythemia, or liver disease or carcinoma

CLINICAL TIP

ESR is often normal in patients with connective tissue disease

or neoplasms; heparin falsely increases the results.19

Peripheral Blood Smear A blood sample may be

exam-ined microscopically for alterations in size and shape of the

RBCs, WBCs, and platelets RBCs are examined for size, shape,

and Hgb distribution WBCs are examined for proportion and

the presence of immature cells Finally, platelets are examined

for number and shape.20 Peripheral blood smear results are

cor-related with the other laboratory tests to diagnose hematologic

disease

CLINICAL TIP

ment of coagulation levels, the INR value is used more often than PT

Because INR is more reliable and provides consistent measure-The PT, PTT, and INR are used in clinical conditions in which an increased risk of thrombosis is present—for example, treatment of deep venous thrombosis (DVT), thrombosis associ-ated with prosthetic valves, and atrial fibrillation (Table 7-12).22

Coagulation Profile Coagulation tests assess the blood’s

ability to clot The tests used to determine clotting are thrombin time (PT) and partial thromboplastin time (PTT)

pro-An adjunct to the measurement of PT is the international normalized ratio (INR) The INR was created to ensure reliable and consistent measurement of coagulation levels among all laboratories The INR is the ratio of the patient’s PT to the standard PT of the laboratory, raised by an exponent (the sen-sitivity index of the reagent) provided by the manufacturer.21

TABLE 7-12 Coagulation Profile

Prothrombin time (PT) Examines the extrinsic and

common clotting factors I,

II, V, VII, and X

PT 11-12.5 seconds Used to assess the adequacy of warfarin

(Coumadin) therapy or to screen for bleeding disorders

Increased: Coumarin therapy, liver diseases, bile duct obstruction, diarrhea, salicylate intoxication, DIC, hereditary factor deficiency, alcohol use, or drug interaction

Decreased: Diet high in fat or leafy vegetables, or drug interaction INR Reflects standardized reporting

of prothrombin time (PT) so that results are comparable among laboratories

0.8-0.11 Refer to Prothrombin time (PT)

Partial thromboplastin time

disorders Increased: Heparin or coumarin therapy, liver disease, vitamin K or congenital clotting factor deficiency, DIC Decreased: Extensive cancer, early DIC

DIC, Disseminated intravascular coagulation.

*Values for PT and PTT vary between laboratories.

Data from Pagana KD, Pagana TJ: Blood studies In Mosby’s manual of diagnostic and laboratory tests, St Louis, 1998, Mosby; Mosby’s diagnostic and laboratory test reference, ed 8, St Louis, 2007, Mosby.

CLINICAL TIP

When confirming an order for physical therapy in the cian’s orders, the therapist must be sure to differentiate between the order for physical therapy and the blood test (i.e., the abbreviations for both physical therapy and prothrombin time are PT)

D-Dimer The D-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 DisordersVascular 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 Box7-1, 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.26Atherosclerosis 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

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 rologic claudication Table 7-14 outlines the differences between true claudication and pseudoclaudication.31

neu-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.27Medications that have been used in managing intermittent claudication include pentoxifylline and cilostazol.32

Treatment of atherosclerotic disease is based on clinical 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

pre-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

Worse at the end of the day Improves with elevation

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

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

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.

Symptoms similar to intermittent claudication may have a

neurologic origin from lumbar canal stenosis or disc disease

Extravasation of blood

Hematoma True aneurysm

TABLE 7-14 Differentiating True Intermittent Claudication from Pseudoclaudication

Location Unilateral buttock, hip, thigh, calf, and foot Back pain and bilateral leg pain

Tightness Tiredness

Same as with intermittent claudication or presence of tingling, weakness, and clumsiness

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

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 tally on abdominal ultrasound, computed tomography (CT) scan, magnetic resonance imaging (MRI), or plain x-ray.37Aneurysms 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

because of widening of the aortic annulus or actual tion of the aortic valve leaflets.

disrup-• Pleural effusions: Pleural effusion, which occur most 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

fre-• 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

• 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

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 specific.7,39 Transesophageal echocardiography (TEE) and CT scan are the primary diagnostic tests used by most institutions

non-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 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.

sig-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:

(vasodi-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,

Diastolic)

Hypertensive Blood Pressure (Systolic/ Diastolic)

Teenagers (age 12-17 years) 115/70 130/80Adults ≥18 years <120/<80 (Prehypertension)

120-139/80-89 (Stage 1 hypertension) 140-159/90-99 (Stage 2 hypertension)

≥160/≥100

Data from Bullock B: Pathophysiology: adaptations and alterations in function,

ed 4, Philadelphia, 1996, Lippincott-Raven, p 517; Chobanian A, et al: The seventh report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure The JNC 7 report, Hyper- tension 2003, 42:1206-1252, 2003.

angiotensin-converting enzyme inhibitors along with beta blockers, calcium channel blockers, and vasodilators.35,47-49 A summary of these medications, their actions, and their side effects can be found in Chapter 19, Tables 19-3 and 19-3a.Hypertensive crisis is a medical emergency It occurs when the blood pressure is high enough to threaten target organs acutely Hypertensive emergency requires admission to an intensive care unit and parenteral therapy.50

Physical Therapy Considerations

• Hypertension is a risk factor for heart attack, stroke, and kidney failure

• Systolic blood pressure gradually increases through life stolic blood pressure increases until 50 to 60 years of age

Dia-• Women typically have lower blood pressure than men until after menopause.51

• Physical exertion increases blood pressure acutely and decreases resting blood pressure over time.51

• Blood pressure is usually lowest in the morning when bolic rate is the lowest, rises throughout the day, and peaks

meta-in late afternoon when the person is mentally awake and physically active.51

• Knowledge of medication schedule may facilitate activity tolerance by having optimal blood pressures at rest and with activity

• Review and clarify any strict blood pressure parameters that the physician has designated for patient because some patients need to have higher or lower systolic pressures than expected normal ranges

• When the blood pressure measurement reveals an elevated blood pressure, make sure the cuff size is right for the patient’s arm, take the blood pressure in the opposite extrem-ity, and then notify the team

TABLE 7-17 Hypertensive Effects on Target Organs

Brain Cerebrovascular accident Area of brain involved dictates presentation May include severe occipital headache,

paralysis, speech and swallowing disturbances, or coma Encephalopathy Rapid development of confusion, agitation, convulsions, and death Eyes Blurred or impaired vision Nicking (compression) of retinal arteries and veins, at the point of their junction

Encephalopathy Hemorrhages and exudates on visual examination

Papilledema Heart Myocardial infarction Electrocardiographic changes

Enzyme elevations Congestive heart failure Decreased cardiac output

Auscultation of S3 or gallop Cardiomegaly on radiograph Myocardial hypertrophy Increased angina frequency

ST- and T-wave changes on electrocardiogram Dysrhythmias Ventricular or conduction defects

Kidneys Renal insufficiency Nocturia

Proteinuria Elevated blood urea nitrogen and creatinine levels Renal failure Fluid overload

Accumulation of metabolites Metabolic acidosis

Data from Bullock B: Pathophysiology: adaptations and alterations in function, ed 4, Philadelphia, 1996, Lippincott-Raven, p 522.

TABLE 7-18 Causes of Secondary Hypertension

Coarctation 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 10

Oral contraceptives 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 10

Renovascular disease Parenchymal disease, such as acute

and chronic glomerulonephritis Narrowing stenosis of renal artery

as a result of atherosclerosis or congenital fibroplasia

Data from Bullock B: Pathophysiology: adaptations and alterations in function,

ed 4, Philadelphia, 1996, Lippincott-Raven, p 517.

medium-sized blood vessels throughout the body, with primary manifestations in the upper respiratory tract, lungs, and kidneys The etiology is unknown; diagnosis and treatment are still in development It occurs most commonly in the fourth and fifth decades of life and affects men and women with equal fre-quency.39 Pulmonary signs and symptoms mimic those of pneu-monia (i.e., fever, productive cough at times with negative sputum cultures, and chest pain).47,54 The 1-year mortality rate

is 90% without therapy, 50% with corticosteroid therapy, and 10% with combined corticosteroid and cytotoxic therapy.54Treatment of Wegener’s granulomatosis may consist of a combination of immunosuppressive agents and corticosteroids (methotrexate and prednisone, respectively) Antiinfective agents may also be prescribed if there is associated respiratory tract infection.31,34

Thromboangiitis Obliterans Thromboangiitis obliterans

(Buerger’s disease) is a vasculitis (inflammatory and thrombotic process) affecting the peripheral blood vessels (both arteries and veins), primarily in the extremities.24 It is found mainly in young men ages 20 to 45 years and is directly correlated with

a heavy smoking history.4,35,53 If abstinence from tobacco is adhered to, the disease takes a favorable course If smoking is continued, the disease progresses, leading to gangrene and small-digit amputations.57 The disease is characterized by seg-mental thrombotic occlusions of the small- and medium-sized arteries in the distal lower and upper extremities The throm-botic occlusions consist of microabscesses that are inflammatory

in nature, suggesting a collagen or autoimmune origin, although the exact etiology is still unknown.35,53 Rest pain is common, along with intermittent claudication that occurs more in the feet than in the calf region.3 The diagnosis is made by invasive and noninvasive methods The noninvasive methods include physical exam, Doppler ultrasound, plethysmography, and ankle-brachial index (ABI) The invasive methods include mag-netic resonance angiography (MRA), other forms of angiogra-phy, and spiral CT.58

Treatment of Buerger’s disease can include smoking cessation, corticosteroids, prostaglandin E1 infusion, vaso-dilators, hemorheologic agents, antiplatelet agents, and anticoagulants.35,53

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 sentations of GCA have been recognized: temporal arteritis and Takayasu’s arteritis.35 Temporal artery biopsy (TAB) is the “gold standard” for the diagnosis of GCA and ESR, C-reactive protein, and platelet count are the primary serologic markers Color ultrasonography of the temporal arteries detects characteristic signs of vasculitis with a high sensitivity and specificity Vision loss is the most dreaded complication of GCA, and when it occurs it tends to be profound and permanent.59

pre-Temporal arteritis is a more common and mild presentation

of GCA that occurs after 50 years of age The onset of arteritis

is usually sudden, with severe, continuous, unilateral, throbbing headache and temporal pain as the first symptoms The pain may radiate to the occipital area, face, or side of the neck Visual

• In certain patient populations (e.g., patients who have had

mastectomies, patients with a peripherally inserted central

catheter [PICC] line) there are restrictions on taking blood

pressure in the upper extremities In these cases, blood

pres-sure can be taken in the lower extremities

• In patients receiving antihypertensive therapy, keep in mind

the signs and symptoms of low blood pressure, such as

diz-ziness, confusion, syncope, restlessness, or drowsiness,

espe-cially in elderly patients

• Patients can present with an elevated blood pressure when

they are apprehensive, in pain, and under stress Keep this

in mind, and try to calm the patient (by applying a wet

washcloth on the forehead and/or neck and by distracting

the patient through talking) Repeat the measurement in

a few minutes for an accurate representation of blood

pressure

Systemic Vasculitis Systemic vasculitis is a general term

referring to the inflammation of arteries and veins that

pro-gresses to necrosis, leading to a narrowing of the vessels

Although the specific cause of many of these disorders is not

known, infectious organisms, drugs, tumors, and allergic

reac-tions are some of the defined triggers Pathogenetic factors

include immune complex disease, antineutrophil cytoplasmic

antibodies, anti–endothelial cell antibodies, and cell-mediated

immunity The major ischemic manifestations of vasculitis are

defined by the type and size of blood vessels involved and the

tissue and organ damage caused by the ischemia related to the

vascular occlusion.52 The secondary manifestations of vasculitis

are numerous and may include thrombosis, aneurysm

forma-tion, hemorrhage, arterial occlusion, weight loss, fatigue,

depression, fever, and generalized achiness that is worse in the

morning The recognized forms of vasculitis are discussed in the

following sections.29,53-55

Polyarteritis Nodosa Polyarteritis nodosa (PAN) is an

acute necrotizing vasculitis of medium-sized and small

arter-ies.52 Most cases present with an unknown etiology; however,

the hepatitis B virus has been emerging as one of the more

common causative factors.54 PAN usually begins with

nonspe-cific symptoms, which may include malaise, fatigue, fever,

myalgias, and arthralgias Skin lesions are common, and a

majority of patients have vasculitic neuropathy.56 The most

frequently involved organs are the kidney, heart, liver, and

gas-trointestinal tract, with symptoms representative of the

dys-function 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 without concurrent cytotoxic therapy with

cyclophos-phamide (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 treatment.53,54

Wegener’s Granulomatosis Wegener’s granulomatosis is

a granulomatous necrotizing disease that affects small- and

progress to atrophy of the terminal fat pads and development

of fingertip gangrene Women 16 to 40 years of age are most commonly affected, especially in cold climates or during the winter season Raynaud’s disease is usually benign, causing mild discomfort on exposure to cold and progressing very slightly over the years The prognosis of Raynaud’s phenomenon is that

of the associated disease.39 Areas generally affected are the gertips, toes, and the tip of the nose.4,31,47

fin-Management of Raynaud’s disease and Raynaud’s enon may consist of any of the following: conservative measures

phenom-to ensure warmth and protection 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 biofeed-back; acupuncture; and sympathectomy.31,39,60

Complex Regional Pain Syndrome Complex regional

pain syndrome (CRPS) is a rare disorder of the extremities characterized by autonomic and vasomotor instability Use of the former name of this entity, reflex sympathetic dystrophy (RSD), is now discouraged because the precise role of the sym-pathetic nervous system is unclear and dystrophy is not an inevitable sequela of the syndrome

The presenting symptom is constant, extreme pain that occurs after the healing phase of minor or major trauma, frac-tures, 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 It occurs in all age groups and equally in both sexes and can involve either the arms or the legs.39

Three stages have been defined (Steinbrocker classification), although all patients may not have evolved through the stages

or proceed in a temporal fashion.52,57

• Stage 1 (acute—occurring within hours to days after the injury): Pain, tenderness, edema, and temperature changes predominate

• Stage 2 (dystrophic—3 to 6 months after the injury): Pain extends beyond the area affected; loss of hair and dystrophic nails become apparent Muscle wasting, osteoporosis, and decreased range of motion may occur

• Stage 3 (atrophic or chronic—6 months after injury): Atrophy, demineralization, functional impairment, and irre-versible damage are present

Management of CRPS may consist of any of the following31,61-64:

• Physical or occupational therapy, or both (cornerstone therapy)

• Pharmacologic sympathetic blocks

• Surgical sympathectomy

• Spinal cord electrical stimulation

• Baclofen drug administration

• Prophylactic vitamin C administration after sustaining fractures

• Bisphosphonate administrationThe prognosis partly depends on the stage in which the lesions are encountered and the extent and severity of associated

disturbances range from blurring to diplopia to visual loss

Irreversible blindness may occur in the course of the disease

from involvement of the ophthalmic artery

Other symptoms include enlarged, tender temporal artery,

scalp sensitivity, and jaw claudication (pain in response to

chewing, talking or swallowing) when involvement of the

exter-nal carotid artery causes ischemia of the masseter muscles; pain

is relieved by rest.59 Polymyalgia rheumatica, a clinical

syn-drome 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.31,54

Takayasu’s arteritis generally affects young Asian women but

has been known to occur in both genders in African Americans

and Hispanics as well It is a form of generalized GCA that

primarily involves the upper extremities and the aorta and its

major branches The pulmonary circulation is involved in

approximately 50% of cases of Takayasu’s artertitis.56

Lower-extremity involvement is less common Management of

Takaya-su’s arteritis may consist of prednisone and cyclophosphamide,

along with surgical intervention if the disease progresses to

aneurysm, gangrene, or both.31

Raynaud’s Disease Raynaud’s disease is an episodic

vaso-spastic disorder characterized by digital color change (white to

blue to red—reflecting the vasoconstriction, cyanosis, and

vasodilation process, respectively) with exposure to cold

environment or emotional stress Numbness, tingling, and

burning pain may also accompany the color changes However,

despite these vasoconstrictive episodes, peripheral pulses

remain palpable If idiopathic, it is called Raynaud’s disease If

associated with a possible precipitation systemic or regional

disorder (autoimmune diseases, myeloproliferative disorders,

multiple myeloma, cryoglobulinemia, myxedema,

macroglob-ulinemia, or arterial occlusive disease), it is called Raynaud’s

phenomenon.4,31,47

In Raynaud’s disease, the disease is symmetric by rule; in

Raynaud’s phenomenon, the changes may be most noticeable in

one hand or even in one or two fingers only Infrequently, the

feet and toes are involved Between attacks, the affected

extrem-ities may be entirely normal The incidence of disease is

esti-mated to be as high as 10% in the general population An

abnormality of the sympathetic nervous system has long been

implicated in the etiology of Raynaud’s disease; recently,

research has focused on the theory of up-regulation of vascular

smooth muscle α2-adrenergic receptors The distinction between

Raynaud’s disease and Raynaud’s phenomenon is meant to

reflect a difference in prognosis Whereas Raynaud’s disease is

benign and often controllable, Raynaud’s phenomenon may

CLINICAL TIP

At the time of an exacerbation, gently rewarm fingers or toes as

soon as possible by placing hands in the axilla, wiggle fingers

or toes, and move or walk around to improve circulation If

possible, run warm water over the affected body part until

normal color returns.24