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PERIPHERAL VASCULAR DISEASE


ANATOMY
GENERAL FEATURE OF BLOOD VESSELS
Blood vessels outside of the heart can be placed in two classes:
SYSTEMIC VESSELS
Transport blood through all parts of the body from the left ventricle
and back to the right atrium.
Blood flowing through the systemic circulation supplies oxygen and
nutrients to all tissues of the body and carries away carbon dioxide
and waste.
PULMONARY VESSELS
Transport blood from the right ventricle through the lungs and back
to the left atrium.
Blood flowing through the pulmonary circulation takes up oxygen
through the lungs and release carbon dioxide.
LAYERS OF BLOOD VESSEL WALL
TUNICA INTIMA
Consists of endothelium composed of simple squamous epithelial
cells and small amount of connective tissue.
TUNICA MEDIA
Consists of smooth muscle cells arranged circularly around the
blood vessel.
It also contains variable amounts of elastic and collagen fibers,
depending on the size and type of vessel.
TUNICA ADVENTITIA
Composed of connective tissue, which varies from dense
connective tissue adjacent to the tunica media to loose connective
tissue toward the outer portion of blood vessel wall.
ARTERIES
Are blood vessels that carry blood away from the heart. Blood is pumped
from the ventricles of the heart into large elastic arteries, which branch
repeatedly to form progressively smaller arteries. As they become smaller,
the arteries undergo a gradual transition from having walls containing
more elastic tissue than smooth muscle to having walls with more smooth
muscle than elastic tissue. Although the arteries form a continuum from
the largest to the smallest branch they are normally classified as:
Elastic Arteries (Aorta and large arteries)
Are the largest diameter arteries and have the thickest wall.
Stretched when the ventricles of heart pump blood into them. The
elastic tissue allows them to distend during systole to
accommodate the stroke volume with only a moderate increase in
pressure.
The elastic recoil prevents blood pressure from falling rapidly and
maintains blood flow while the ventricles are relaxed.
Function as WINKESSEL VESSELS.
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Muscular Arteries
Included medium-sized and small-diameter arteries.
Medium-sized arteries are frequently called distributing arteries
because the smooth muscle tissue enables these vessels to control
blood flow to different regions of the body by either constricting or
dilating. It supplied blood to small-diameter arteries.
Small-diameter arteries have about the same structure as the
medium-sized arteries except for its diameter.
Arterioles
Transport blood from the small arteries to capillaries and are
smallest arteries in which the three tunics can be identified.
When the smooth muscles of the small arteries and arterioles are
activated, they allow the vessels to constrict their lumen, causing an
increase in the pressure centrally and decrease the pressure peripherally.
These vessels function as RESISTANCE VESSEL.

CAPILLARIES
Capillaries have thinner walls, blood flow through them more slowly, and
there are far more of them than any other blood vessel type.
The capillary wall consists of endothelium and is surrounded by delicate
layer of loose connective tissue. Capillaries are 0.5 to 1mm long, and they
branch without a change in their diameter.
Function as EXCHANGE VESSELS.
Capillaries branch off from the metaterioles. Metaterioles branch off from
the arterioles at right angles. They serve as through-channels to the
venules or high resistance tubes between arterioles and veins. Blood flow
from arterioles into capillaries, which branch to form networks. Red blood
cells flow through most capillaries in single file and are frequently folded
as they pass through the smaller diameter capillaries. Blood flow through
the capillaries is regulated by smooth muscle cells called PRECAPILLARY
SPHINCTERS located at the origin of the branches. These sphincters
serve as the main control over capillary flow, and such function is
SPHINCTER VESSELS. As blood flows through the capillaries, blood
gives up oxygen and nutrients to the tissue spaces and takes up carbon
dioxide and other byproducts of metabolism.
VEINS
The walls of the vein and venules are very thin, with only small amounts of
elastin and limited smooth muscle. They contain about four times more
blood than the arterial system because of their great distensibility.
They function as CAPACITANCE VESSELS.
Venules
Are tubes with a diameter larger than capillaries and are composed
of endothelium resting on a delicate connective tissue membrane.
The structure of venules, except for their diameter, is very similar to
capillaries.

Small Veins
Are slightly larger in diameter than venules, and their walls contain
a continuous layer of smooth muscle cells.
Medium-Sized Veins
Collect blood from small vein and deliver it to large veins.
Veins having diameter greater than 2 mm contain valves. The valves
allow blood to flow toward the heart but not in the opposite direction.
There are many valves in the medium-sized veins. There are more valves
in veins of the legs than in veins of the arms. This prevents the flow of
blood toward the feet in response to the pull of gravity.
Large Veins
Contains the largest blood volume in the circulation.
ARTERIOVENOUS ANASTOMOSES
Short channels that connect arterioles to venules, bypassing the
capillaries.
Predominant in the palms, fingers, and ear lobes.
Abundantly innervated by vasoconstrictor nerve fibers.
Function as SHUNT VESSELS.

PHYSIOLOGY
BLOOD PRESSURE
Refers to the force the blood exerts against a vessel wall.
Because liquid flows only from a higher to a lower pressure, the pressure
is highest in the arteries, lower in the capillaries, and lowest in the veins.
SYSTOLIC PRESSURE
The highest pressure exerted by the blood against the
arterial walls during cardiac contraction.
DIASTOLIC PRESSURE
The lowest pressure exerted by the blood against the arterial
wall during cardiac relaxation.
PULSE PRESSURE
Difference between systolic pressure and diastolic pressure.
REGULATORY MECHANISMS
LOCAL CONTROL OF BLOOD VESSELS
Local control of blood flow is achieved by periodic contraction and
relaxation of the precapillary sphincter. Because of t he contraction and
relaxation of the precapillary sphincters, blood flow through the capillaries
is cyclic. The precapillary sphincters are controlled by the metabolic needs
of the tissues. Blood flow increase when oxygen levels decrease, or to a
lesser degree, when glucose, amino acids, fatty acids, and other nutrients
decrease. Blood flow also increase when byproducts of metabolism build
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up in tissue spaces. An increase in carbon dioxide or decrease in pH


causes the precapillary sphincters to relax.
NERVOUS CONTROL OF BLOOD VESSELS
AFFERENT RECEPTORS
BARORECEPTORS (Pressoreceptors)
Stimulated by stretch of the vessel wall from alteration in pressure.
CAROTID SINUSES
Baroreceptors that are located at the carotid arteries.
Monitor the blood pressure to the brain.
AORTIC SINUSES
Baroreceptors that are located at the aortic arch.
Responsible for monitoring the blood pressure throughout
the body.
If there will be an increase in blood pressure, the baroreceptors will
send an input to the vasomotor center which will results to inhibition
of the vasoconstrictor center of the medulla and excitation of the
vagal center. This results in decrease heart rate, decrease force of
cardiac contraction, vasodilation, and subsequent decrease in
blood pressure. When there is a drop in blood pressure the
opposite mechanism will happen.
CHEMORECEPTORS
Stimulated by reduction of arterial oxygen concentrations, increase
in carbon dioxide tension, and increased hydrogen ions
concentration.
CAROTID BODIES
Chemoreceptors located at the carotid arteries.
AORTIC BODIES
Chemoreceptors located at the aortic arch.
Impulses from these receptors travel to the brain (cardioregulatory
and vasomotor center) via afferent pathways in the vagus and
glossopharyngeal nerves. Efferent impulse from these centers, in
response to alterations in blood pressure, will alter the heart rate,
strength of cardiac contractions, and size of blood vessel.
VASOMOTOR CENTER
Is located bilaterally in the lower pons and upper medulla. It
transmits impulses through sympathetic nerves to all vessels of the
body. The vasomotor center is tonically active, producing a slow,
continual firing in all vasoconstrictor nerve fibers. It is this slow,
continual firing that maintains a partial state of contraction of blood
vessels and provides a normal VASOMOTOR TONE. The
vasomotor center assist in providing a stable arterial pressure
required to maintain blood flow to body tissue and organs. This
occurs because of its close connection to the cardiac controlling
center in the medulla. Additionally, the vasomotor and cardiac
controlling centers require input from afferent receptors.

HORMONAL CONTROL OF BLOOD VESSELS


ADRENAL MEDULLARY MECHANISM
Epinephrine released from the adrenal medulla as a result of
sympathetic stimulation increase heart rate, stroke volume, and
vasoconstriction.
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
Renin is released by the kidneys in response to lower blood
pressure. Renin promotes the production of angiotensin which,
when activated, causes vasoconstriction and increase in
aldosterone secretion. Aldosterone reduces urine output.
VASOPRESSIN MECHANISM
Antidiuretic hormone (vasopressin) released from the posterior
pituitary causes vasoconstriction and reduces urine output.
ATRIAL NATRIURETIC MECHANISM
Atrial natriuretic factor is released from the heart when atrial blood
pressure increases. It stimulates an increase in urine production,
causing a decrease in blood volume and blood pressure.
FACTORS THAT INFLUENCE BLOOD PRESSURE
Blood volume
Elasticity of blood vessels
Cardiac output
Age
Exercise
Valsalva maneuver
Blood viscosity
Positioned between the layers of endothelial cells and perivascular nerves are
the smooth muscle cells responsible for the control of arterial and venous tone
and distribution of blood flow throughout the body. The connections between the
arteries and veins can be divided into the resistance vessels (arterioles),
exchange vessels (capillaries), and capacitance vessels (venules). The
regulatory mechanism in the above components involves humoral and nervous
mechanisms, with complex interactions between smooth muscle cells,
perivascular nerves, and endothelium and the local metabolic products. The
smooth muscle cells form circular layers around the vessels and are innervated
by perivascular nerve fibers. Transmitters released by these fibers activate
receptors on the vascular smooth muscle cell membrane with resultant
vasoconstriction or vasodilation. The major neurologic control of blood vessel
tone is accomplished by sympathetic nerves and norepinephrine is the principal
neurotransmitter that causes vasoconstriction via alpha adrenoreceptors, along
with receptor-operated calcium channels. The amount of neurotransmitter
release depends on the degree of stimulation of the sympathetic fibers and the
presence of local metabolic and circulating vasoactive substances as well as
autoregulation.
Newer research has shown the role of endothelial cells in the regulation of blood
flow. Endothelial cells respond to various stimuli regulating the tone of the in the
smooth muscle cells. These stimuli include substances such as endotheliumderived relaxing factor, prostacyclin, endothelium-derived contracting factor, and
angiotensin II, which effect platelet aggregation, platelet adhesion, and smooth
muscle proliferation.
In order to develop strategies for prevention and treatment of vascular diseases,
it is imperative to understand how vascular smooth muscle cells contract and

relax in response to physical and chemical stimulation, the role that endothelium
plays in this complex process, and the pathophysiology of the disease processes
that disturb the fine balance in this regulation.

PATHOPHYSIOLOGY
Congenital or acquired defects in endothelial cell function could lead to
imbalance to imbalance between relaxing and contracting factors, which is
one of the major factors leading to pathophysiologic changes in the
function of blood vessel walls. Endothelial dysfunction has been
demonstrated in the several diseases of the peripheral blood vessels,
including hypertension, diabetes, atherosclerosis, hyperlipidemia, and
vasospasm.
Changes in the morphology and histology of the vascular system may
range from thickening of capillary basement membrane, a decrease in the
density of the microvessels, endothelial cell degeneration, and increased
platelet adhesion and aggregation in diabetes mellitus, to endothelial
injury, endothelial fat accumulation with fatty streak formation, and smooth
muscle proliferation in atherosclerosis.

ETIOLOGY
There are many causes of arterial occlusive disease, the most common of
which is atherosclerosis obliterans (ASO). Other disease processes
include thromboangitis obliterans (Buergers disease), vasospastic
disorders (Raynauds phenomenon, livedo reticularis, and acrocyanosis),
thrombosis, embolism, dissection, vasculitis and fibromuscular dysplasia.
ATHEROSCLEROSIS
Atherosclerosis in its advanced form is a systemic disorder involving the
coronary, cerebral, pulmonary, renal, and peripheral vessels. The earliest
manifestation of atherosclerosis appears to be the intimal streak, although
the eventual progression of streaks to fibrous or complicated plaques
remains uncertain. The plaques tend to develop at branch points,
bifurcations, zones of rapid tapering, and areas where arteries follow a
tortuous course. Arherosclerosis typically involves multiple level of the
arterial tree; however, it tends to be a segmental disease in which
intervening arterial segments can be remarkably free of involvement or
minimally involved. Associated conditions can affect the location of
disease. In diabetics, atherosclerosis occurs with equal frequency in both
femoral and tibial arteries, whereas in nondiabetics the most common
sites of severe disease are the abdominal aorta and iliac and femoral
arteries. Potentially reversible factors that increase the risk of
atherosclerosis include smoking, hyperlipidemia, hypertension, diabetes,
and obesity. Most people younger than 65 years who have atherosclerosis
have one or more identifiable risk factors. The presence of multiple risk
factors further increases the risk of atherosclerosis. Cigarette smoking is
by far the most common risk factor, competing with juvenile diabetes
mellitus and certain rare congenital hyperlipidemias as the most serious.
Smoking acts synergistically with other risk factors such as hypertension,
or hypercholesterolemia to enhance progression of atherosclerotic lesions.

The calculated risk of developing claudication is 15 times higher in male


smokers than in nonsmokers, 7 times higher in female smokers than in
nonsmokers, and directly related to the number of cigarette smoked.
Atherosclerosis of the arteries in the lower limbs is one of the strongest
indicators of atherosclerosis in other vessels in the body, such as the
coronary and cerebral blood vessels. In the lower extremities it involves
mostly the large and medium sized arteries. Lesions tend to develop at
major arterial bifurcations and sites of acute vessel angulation. The
disease does not affect all arteries to the same extent but shows a
predilection for coronary arteries, carotid bifurcation, aortoiliac and lower
extremity vessels. The lower extremity site most commonly affected is the
arterial segment between the superficial femoral and popliteal arteries in
Hunters canal. In nondiabetics, aortoiliac disease is the second most
likely location, whereas in diabetics, popliteal and tibial disease are more
likely to follow femoral disease.
RISK FACTORS
A number of factors predispose to the development or acceleration of
atherosclerosis:
1. Clinical and experimental studies have established that elevated plasMa concentration of lipoproteins, particularly low-density lipoproteins,
Increase the risk and rate of progression of atherosclerosis.
Cholesterol is a major constituent of advanced lesions. In patients with
significant atherosclerosis, the mean plasma cholesterol was found to
be more than 50 mg/dl higher than in controls.
2. Smoking is described as the single most powerful risk factor for
peripheral vascular disease. Relative risk of smoking in the
development of leg arterial disease ranges from 1.4 to more than 10
times depending on age, sex, definition of a smoker, and methods of
evaluation of arterial disease. Three quarters of cases of intermittent
claudication could eventually be attributed to smoking.
3. Hypertension exacerbates atherosclerosis with each incremental
increase in pressure, directly increasing the risk of coronary artery
disease. Systolic blood pressure appears to be a better predictor of
arterial disease than diastolic blood pressure. Hypertension was found
in 25 % of patient with symptomatic disease of the aortoiliac and
femoral popliteal arteries, but was found in only 9 % of age-matched
controls. The mechanism appears to be related to endothelial injury
from hypertensive pressure or hemodynamic shearing.
4. Diabetes mellitus is associated with the earlier onset of atherosclerosis
and a more rapid disease progression. The obstructive disease of the
large arteries in diabetes, usually designated as macroangiopathy, is
commonly held as indistinguishable from atherosclerosis in
nondiabetes. In diabetes, distal vessels are more involved than are
aortoiliac vessels; proposed mechanisms include disturbance of
normal platelet, endothelial, and smooth muscle cell function,
secondary to hyperglycemia, causing vasoconstriction and smooth
muscle proliferation.
5. Other risk factors for generalized atherosclerosis include obesity,
hyperuricemia, sedentary life-style, and a positive family history.

COMMON PERIPHERAL VASCULAR DISEASES


ARTERIAL DISEASES
CHRONIC ARTERIAL DISEASE
1. THOMBOANGITIS OBLITERANS
A disease involving thrombosis and inflammation of small
peripheral arteries and veins. The process tends to begin in the
smaller peripheral arteries of the extremities. Lesions are usually
located distal to the knee or elbow. Most theories implicate some
component of cigarette smoking that predisposes the arterial wall
to inflammation, possibly through the formation of immune
complexes.
It initially occurs in the small arteries of the feet and hands and
progresses proximally and results in vasoconstriction, decreased
arterial circulation to the extremities, ischemia, and eventual
necrosis and ulceration of soft tissues.
The inflammatory reaction and resulting signs and symptoms can
be controlled if the patient stops smoking.
This is predominantly seen in young, male patient who smoke,
involves an inflammatory reaction of the arteries to nicotine.
The pathology responsible for the clinical symptoms of decreased
temperature and eventual tissue necrosis, is an inflammatory
process in the veins and arteries that appears to be directly related
to tobacco use. Nicotine is also a very potent vasoconstrictor and is
responsible for the more immediate decrease in skin temperature
seen in smokers.
2. ARTERIOSCLEROSIS OBLITERANS
Other names:
Chronic arteriosclerotic vascular disease
Atherosclerotic occlusive disease
Progressive arterial occlusive disease
The circulation progressively deteriorates because of narrowing,
fibrosis, and occlusion of the large and medium arteries, usually in
the lower extremities.
It is the most common of all arterial disease affecting the lower
extremities.
It is a manifestation of the generalized disease,
ATHEROSCLEROSIS.
The disease is most often seen in elderly patients and is common
associated with DIABETES MELLITUS.
Since it is a slowly developing, degenerative process, its
manifestations occur insidiously. The disease begins with
monocytes adherence to the endothelial wall following some form
of physical damage such as trauma, hypertension, or a biochemical
process. A fatty streak begins to develop and subsequently results

in the production of an atheromatous plaque in the intima of the


artery. As the plaque increases in size the lumen is narrowed and
linear flow of blood is impaired.
CLINICAL PRESENTATION:
Intermittent claudication(earliest presenting symptom)
As the disease progresses, the arterial flow may
become impaired to the point that pain is present
even at rest.
Diminished/absent pedal pulse
Positive sign for rubor dependency
Trophic changes(more pronounced disease)
Ulceration
3. DIABETIC ANGIOPATHY
Diabetes mellitus is a major risk factor in peripheral vascular
disease. Diabetes presents with both metabolic and vascular
components, which are likely strongly interrelated.
Metabolically, there is an inappropriate elevation in the blood
glucose level, which is associated with a disturbed lipid and protein
metabolism.
The vascular dysfunction involves an accelerated version of
atherosclerotic process.
The alteration in the coetaneous sensation becomes a major
problem, as patients tend to develop neurotrophic ulcers due to an
inability to perceive pressure on the body parts, particularly the feet.
4. TAKAYASUSS DISEASE
Pulseless disease
Primary Aortic Arteritis
An idiopathic inflammatory condition of the aorta and its branches
that results to absence in the arterial pulse.
Affects the tunica intima and tunica adventitia of the artery
Common in young adults
5. MONCKEBERGS MEDIAL SCLEROSIS
A condition characterized by isolated rings of calcification in the
tunica media with normal tunica intima.
Common in the elderly and affects large arteries in the lower
extremities
ACUTE ARTERIAL DISEASES
1. RAYNAUDS PHENOMENON
Is a vascular spasm of unknown etiology.
Raynaud described the attack of digital ischemia in women those
results from cold exposure and emotional stress. Specific
hypotheses for the etiology include abnormal sympathetic activity,
abnormal digital vessels or an immunologic process.

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Most frequently involves the hands but can also affect the feet. With
exposure to cold or emotional stress, spasm of the small arteries
and arterioles of the fingers results in ischemia (pallor or cyanosis),
pain, and subsequent vasodilation with hyperemia. It can be
idiopathic or occur as a manifestation of a potentially serious
underlying systemic disease.
It is caused by an abnormality of the sympathetic nervous system
and is usually seen in young adults.
Symptoms are slowly relieved by warm.
DIAGNOSIS
Vasospasm precipitated by cold and emotional stress
Symptoms for more than 2 years
Bilateral involvement
Minimal or absent gangrene of fingertips
Absence of other diseases associated with vasospastic
attack
CLINICAL FEATURES
Classic triad:
Digital pallor with numbness
Cyanosis
Reactive hyperemia and rubor of skin
Sensitivity to cold
Blanching and cyanosis of the fingertips and nailbeds
Severe pain, sensory loss(tingling or numbness),
decrease function in the hand
Gangrene(rare)
Atrophic changes:
Atrophy of the skin
Wasting of tissues in the finger pads
Irregular nail growth
TREATMENT
Treatment is directed primarily at symptom relief.
For majority of patient with Raynauds, maintaining local
and general body warmth is adequate. Avoidance of cold,
nicotine, and exacerbating drugs is essential.
Biofeedback benefits some individuals by teaching them
to warm their hands or dilate the blood vessels.
Additional measures include relaxation training and
stress management if stress is the inciting factor.
2. ACUTE ARTERIAL OCCLUSION
It is usually caused by thrombus formation, embolism, or trauma to
an artery.
The most common location of an arterial embolus is at the femoral
popliteal bifurcation.
An occlusion will result in absent or diminished pulses and
complete or partial interruption of circulation to an extremity.

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The severity of the problem is dependent upon the location and


size of the occlusion and the availability of collateral circulation. If
little or no collateral circulation is available, an acute arterial
occlusion will cause tissue ischemia and possibly gangrene of the
distal limb.
ARTERIAL EMBOLISM
Most frequently encountered form of acute arterial disease.
Emboli can arise from any numerous sites and be composed
of various substances. Probably, one of the most frequently
occurring types results from the dislodging of a preexisting
thrombus in the heart. The thrombus then migrates to a
peripheral arterial vessel.
ARTERIAL THROMBUS
Usually occur in the area of a previously existing
atherosclerotic lesion.
When the arterial lumen narrows in the presence of an
atherosclerotic lesion, the blood flow becomes turbulent.
This swirling motion of blood slows its passage through the
area and permits platelets to collect. The platelets
aggregate, together with significant amounts of fibrin, leads
to the development of the thrombus.
VASOSPASTIC DISEASE
Characterized by changes in skin color and temperature.
The arterial spasm that occurs appears to be localized to the
small arteries and arterioles.
3. CRITICAL LEG ISCHEMIA
Critical leg ischemia is initially defined by Rutherford included
patients with ischemic ulcers or rest pain whose ankle systolic
pressure was below 40-60 mmHg.
Chronic critical leg ischemia in both diabetic and nondiabetic
patients is defined by either of the following two criteria:
Persistent recurring ischemic rest pain requiring regular adequate
analgesia for at least 2 weeks, with an ankle systolic pressure no
more than 50 mmHg, and or a toe systolic pressure no more than
30 mmHg.
Ulceration or gangrene of the foot or toes, with an ankle systolic
pressure no more than 50 mmHg or toe systolic pressure of no
more than 30 mmHg.
MANAGEMENT
Management depends on the severity of the arterial disease and
ability of the patient to tolerate certain treatment options.
Candidates for medical management
Patient with mild to moderate disease and only
symptoms of claudication Patients with recent onset of
disease who do not have fully developed collaterals
Patients who have failed vascular reconstruction or are
high surgical risk
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EDUCATION
The patient must be educated about the disease to improve
understanding and compliance with treatment and alleviate the fear
of amputation.
RISK REDUCTION
Smoking is the major contributing factor, in terms operative risk and
promotion of disease progression. Patient must stop smoking.
Hypertension must be controlled.
Reduction in calories and possibly cholesterol intake to control
body weight
TREATMENT OF ASSOCIATED DISEASE
Attention on the associated disease that exacerbates
atherosclerosis.
Congestive heart failure should be treated to maximize heart
function and reduced peripheral edema
Diabetes must be controlled because of the association of arterial
disease progression and neuropathy
FOOT CARE
Attention on the lower extremity especially the foot
Overall the tissue oxygen demand should be decreased by
avoiding trauma, inflammation, and heat.
Meticulous foot care is essential
EDEMA CONTROL
Edema can decrease arterial perfusion
Elevating the head of the bed 6 to 8 inches allow pain-free sleep
with minimal edema formation.
Vascular stockings are not too tight and constricting also help
resolve edema.
MEDICAL MANAGEMENT
The goal of treatment is restoration of function and relief of pain,
along with the treatment of any treatable associated disease. The
long term goal is to prevent progression and promote regression.
Analgesics (Acetamenophen)
For reduction of pain
Antiplatelet agents (aspirin)
Reduces platelet aggregation and are effective in low doses
Ticlopidine
Increase cutaneous temperature and transcutaneous partial
pressure of oxygen.
Hemorrheologic agents
Affect RBC flexibility and have been associated with
significant increase in walking distances in a double blinded
study of patient with intermittent claudication
Protanoids

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Treatment option for patient who are not candidate for


reopening procedure
Heparin
Best manage acute thrombosis or acute arterial embolus
followed by arteriography to define the lesion.
SURGICAL MANAGEMENT
It is indicated in:
Intractable ischemic pain
Severe ischemia with nonhealing ulcer or gangrene
Increase disability
The following surgical options may be exercised:
Reopening procedures
Angioplasty is indicated for focal stenosis or short segmental
occlusion with relative disease-free adjacent vessels.
Advantages of this procedure include:
Short inpatient stay
Low incidence of morbidity
Fairly successful long-term results
Limb Salvage Procedures
Bypass surgery, which uses prosthetic materials.
Indicated for diffuse arterial disease
Amputation
Primary Amputation
Indicated in patients with failed bypass surgery or spreading
infection or toxemia.
Delayed Elective Amputation
Performed in the later stage of the disease to achieve a
more pain-free functional status after a careful review of riskto-benefit and cost-to-benefit ratios.
PHYSICAL REHABILITATION
EXERCISE
This is important at all stages of the disease.
Mechanisms of beneficial effect of exercise:
Improve peripheral utilization of oxygen
Increase patency of collateral circulation
Improve oxidative and glycolytic capacity
Exercise therapy is contraindicated in the presence of an ischemic
ulcer or rest pain. A baseline treadmill exercise test should be
performed in the absence of contraindications. Training may consist
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of walking, jogging, bicycling, or swimming; the upright exercise


posture is preferable to the horizontal because it improves lower
extremity perfusion.
Walking programs should be individualized considering the
precautions and contraindications in each case. Standard
prescription includes a gradual increase in duration from 30 to 60
minutes three to five times a week at 2 miles per hour, as tolerated,
with the provision of rest when claudication develops.
In program of group therapy three times per week with each
session including walking, jogging, leg stretching, and leg
relaxation, the patients doubled their walking distance after 3
months.
Low-level pain-free endurance training is also effective in
increasing walking distance, exercise time, and energy expenditure.
PROPER SHOE WEAR
Proper shoe wear should prescribe as needed. New shoe should
be broken in slowly and carefully.
ORTHOTICS
Although infrequently used, an ankle-foot orthosis may decrease
improvement and increase in walking distances. Occasionally a
patient who refuses amputation for ischemic ulcers may ambulate
safely with patellar tendon-bearing orthosis.

CLINICAL SIGNS AND SYMPTOMS OF ARTERIAL DISEASE


CHANGES IN THE SKIN
Pallor- a chalky, white color, blanching of the skin
Shiny and waxy appearance of the skin
Decreased hair growth distal to the insufficiency
Decreased skin temperature
Dryness of the skin
Ulceration(weight bearing areas)
Gangrene
SENSORY DISTURBANCES
Decreased tolerance to hot or cold temperature
Paresthesia
Tingling and eventual numbness in the distal portion of the
extremities
PAIN
Intermittent Claudication (exercises pain)
Occur when there is insufficient blood supply and ischemia in
an exercising muscle.
Cramping occurs in musculature distal to the occluded
vessel.
Most common site is the calf muscle because of the
occlusion of the femoral artery.
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Pain slowly diminishes at rest


Exercise tolerance progressively decreases, and ischemic
pain occurs more readily as the disease progresses.
Pain at Rest
A burning, tingling pain in the extremities occurs as a result
of severe ischemia.
It frequently occurs at night because the heart rate and blood
volume flow to the extremities decreases with rest.
Partial or complete relief of pain may be achieved if the leg is
placed in a dependent position.
Elevation of the limb will cause an increase in pain.
PARALYSIS
Loss of motor function
Atrophy of muscles
CLINICAL EVALUATION OF ARTERIAL DISORDERS
HISTORY AND CLINICAL FINDINGS
ACUTE ARTERIAL OCCLUSION
The clinical presentation in acute arterial occlusion includes:
Sudden onset of toe, foot, and leg pain
Absence of pulse
Skin discoloration
Six Ps
Pulselessness
Pain
Polar (cold)
Pallor
Paresthesia
Paralysis
The most common cause of acute arterial embolism is cardiac
(atrial fibrillation, recent myocardial infarction, cardiomyopathy,
native or prosthetic heart valve replacement, and rarely, atrial
myxoma)
CHRONIC ARTERIAL OCCLUSION
The most common symptom is intermittent claudication.
The site of claudication is of rough value for indicating the level of
occlusion. Patients with occlusion at or above the ankle can present
with claudication in the arch of the foot. Calf claudication suggests
occlusion at or above the calf. Patients with isolated aortoiliac
disease generally present with buttock pain or sexual dysfunction.
As the disease process advances, resting blood flow rates are
affected, and ischemia at rest and impaired skin metabolism result.
Clinical findings of ischemia can include:
Trophic changes
Dependent rubor
Paresthesia
Cutaneous ulceration

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PALPATION OF PULSES
Basis of any integrity of the arterial system in distal portion of the
extremities
Pulselessness is a sign of severe arterial insufficiency
SKIN TEMPERATURE
Temperature of the skin can be grossly assessed by palpation. A limb with
diminished arterial blood flow will be cool to the touch.
SKIN INTEGRITY ANG PIGMENTATION
Diminished or absent arterial blood flow to an extremity causes trophic
changes in the skin periphery.
The patients skin is dry and color is diminished.
Hair loss and a shiny appearance to the skin also occur.
Skin ulceration may also be present.
VASCULAR TESTING
Testing may be needed for the following reasons:
To establish a diagnosis
To determine the severity of the disease
To confirm failure or success of treatment
To document the disease process
NONINVASIVE STUDIES
TEST FOR RUBOR
Changes in skin color that occurs with elevation and dependency of
the limb as the result of altered blood flow.
Procedure:
The legs are elevated for several minutes above the level of
the heart while the patient is lying supine.
Pallor of the skin will occur in the feet within 1 minute or less
if arterial circulation is poor.
The time necessary for blanching to develop is noted.
The legs are then placed in a dependent position, and the
color of the feet is noted.
Normally, a pinkish flush appears in the feet after several
seconds.
In occlusive arterial disease, a bright reddening or rubor of
the distal legs and feet occurs.
The rubor may take as long as 30 seconds to appear.
Reactive Hyperemia
Evaluated by temporary restricting the blood flow to the distal
portion of the lower extremity with blood pressure cuff.
This restriction causes an accumulation of CO2 and lactic acid in
the distal extremity. These metabolites are vasodilators and affect
the vascular bed of the blood flow (deprived area)
When the cuff is released and blood flow resumes to the extremity,
a normal hyperemia(flushing) of the extremity should occur within
10 seconds.
In arteriosclerotic vascular disease it may take as long as 1 to 2
minutes for a flush to appear.

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CLAUDICATION TIME
The amount of time a patient can exercise before experiencing
cramping and pain in the distal musculature.
A common test is to have the patient walk at a slow predetermined
speed on a level treadmill(1 to 2 mph). The time that the patient is
able to walk before the onset of pain or before pain prohibits further
walking is noted.
This measurement should be taken to determine a BASELINE for
exercise tolerance before initiating a program to improve exercise
tolerance.
SEGMENTAL PRESSURE
Arterial pressure is recorded from different segments of the lower
extremity arterial tree and referenced against brachial pressure to
create a pressure index.
VENOUS FILLING TIME
This test measures the time necessary for the superficial veins to
refill after emptying. The test is only of use in persons with normal
venous system since any valvular problems could permit retrograde
venous flow and not give a good picture of filling via the normal
arterial pathway.
The patient is placed supine for this test also, and the legs are
elevated and milked of venous blood. After this has been
accomplished, the patient hangs the legs over the edge of the
table. The time necessary for the veins to refill is noted. A time
greater than 10 to 15 seconds indicates arterial insufficiency.
PLETHYSMOGRAPHY
Used to measure mean blood flow by recording the rate of increase
in limb volume after sudden interruption of venous outflow.
To perform a plethysmographic flow measurement, the limb is
placed in a neutral, relaxed position and the venous occlusion cuff
is rapidly inflated. Blood that flows into the limb becomes trapped,
and the limb expands. The rate at which expansion occurs is
measured by the plethysmograph, from which arterial inflow can be
estimated.
DUPLEX ULTRASONOGRAPHY
Combines a pulsed Doppler with real-time-B mode scanning.
Duplex scanning combines exact anatomical localization of disease
with physiological blood flow studies to define the hemodynamic
significance of the lesion.
DOPPLER ULTRASONOGRAPHY
A non-invasive assessment that uses the Doppler principle to
determine the relative velocity of blood flow in the major arteries
and veins.
A sound head, covered with coupling gel, is placed on the skin
directly over the artery to be evaluated. An ultrasonic beam is
directed transcutaneously to the artery. Blood cells moving in the
path of the beam cause a shift in the frequency of the reflected
sound. The frequency of the reflected sound emitted varies with the
velocity of blood flow. This information is transmitted visually, onto
an oscilloscope or printed tape or audibly, via a loudspeaker or
stethoscope.

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TRANSCUTANEOUS OXYGEN TENSION


Is an objective indicator of ischemia of the skin in a patient with
peripheral occlusive arterial disease.

INVASIVE STUDY
ARTERIOGRAPHY
This is an invasive procedure and is usually the last test to be
performed.
A radiopaque dye is injected in an artery. A series of x-ray
examinations are taken to detect any restriction of movement of the
dye, indicating a complete or partial occlusion of blood flow. It gives
the most accurate picture of the location and extent of arterial
obstruction.
TREATMENT OF ARTERIAL DISORDERS
ACUTE ARTERIAL OCCLUSION
THROMBOSIS
Acute thrombosis is generally best managed with an initial course
of HEPARIN therapy followed by arteriography to define the lesion
and the status of the inflow and outflow vessels.
Early intervention can prevent neuromuscular injury, enhance limb
salvage, and avoid myonecrosis, myogobinuria, and associated
renal failure.
EMBOLIC ISCHEMIA
HEPARIN should be given as soon as the diagnosis of acute
arterial embolus is suspected.
Large doses of heparin are required to inhibit coagulation and to
prevent clot propagation in patients in whom thrombus is already
present.
DISSECTION
It depends on the location:
ASCENDING AORTA (Stanford type A)
Management includes control of arterial systolic blood pressure and
emergency surgical repair to correct or prevent cardiac tamponade,
acute aortic insufficiency, or coronary artery occlusion.
DESCENDING THORACIC/ABDOMINAL AORTA (Stanford type B)
Medical management of pain and arterial blood pressure is usually t
he treatment of choice
Postoperative care by the physical therapist centers on preventing
pressure, monitoring pulse, and temperature, and enhancing venous
return. The patient should be checked to assure there is no binding
clothing to impede blood flow. A turning schedule should be instituted
making sure that the surgical site is always visible.

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CHRONIC ARTERIAL OCCLUSION


General Management:
1. Goals:
Develop effective therapy that prevents progression of
the disease process.
Promotes regression of existing lesions.
Improve circulation
Instruct the patient in home management
2. Patient and family education
3. Protection from trauma
4. Orthoses
5. Exercise
6. Risk factor modifications
7. Behavioral modifications
9. Diet
10. Behavioral modifications
11. Diet

VENOUS DISEASES
ETIOLOGY AND PATHOGENESIS
Thumb frequently arises from clot formation in the cusp of venous valves,
with thrombi then propagating out of the cusp into the major venous
channels.
Another site of thrombus development is at the entrance of a tributary
vein. The thrombus can go on to occlude a major venous channel by
prograde or retrograde propagation.
RISK FACTORS
Virchows Triad:
1. Changes in blood flow
2. Alteration in the vessel wall
3. Variation in the coagulability of blood
Prior history of deep vein thrombosis
Immobilization
Postoperative state
Age(older than 40 years)
Cardiac disease
Limb trauma
Post-thrombotic state or coagulation abnormalities
Hormonal therapy
Pregnancy and postpartum state
Obesity
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Neoplasm

CHRONIC VENOUS DISORDERS


1. CHRONIC VENOUS INSUFFICIENCY
Previously termed as VENOUS STASIS
Is usually the result of congenital or acquired valvular
incompetence and, less frequently, obstruction of the veins.
PATHOPHYSIOLOGY
The basic underlying pathophysiologic mechanism is increased
pressure in the deep venous system. This venous hypertension is
caused either by blocking of outflow or backflow.
Usually manifested by:
Dilated veins(most common initial sign and is most
apparent along the dependent portion of the limb)
Leg pain(limb heaviness or aches)
Chronic edema
Cutaneous changes
It can be the result of:
Venous occlusion
Valvular defect
Problems in the calf muscle pumping mechanism
CHARACTERISTICS
Dependent edema
Associated with standing and sitting for prolonged
period of time
Usually worse at the end of the day
Edema decreases if the leg is elevated while the
patient lies supine
Aching or tiredness in the leg
Increase pigmentation and stasis of the limb
Skin ulceration and secondary infection, which can lead
to cellulitis
Chronic venous insufficiency results in:
Chronic edema
Scarring
Obliteration of cutaneous lymphatics
Decreased skin integrity
Hemosiderin deposition(resultant brownish discoloration)
Dermatitis
Ulceration

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CHRONIC VENOUS INSUFFICIENCY


STAGE

SYMPTOMS

PHYSICAL FINDINGS
Superficial varicosities
Edema along perimalleolar are

Pain
Heaviness
Mild swelling

II

Heaviness
Pigmentation, pruritis
Moderate to severe
swelling

Moderate varicosities
Pigmentation
Dermatitis
Moderate to severe edema

III

Ulceration
Severe swelling
Calf pain with or
without venous
claudication

Multiple varicusitis
Marked skin pigmentation
Ulceration
Severe edema

MANAGEMENT
It is important to have patient education.
Conservative Therapy for Chronic Venous Insufficiency
STAGE I
Custom-fitted elastic compression stockings
Ace wrap or variant
Circ-aid
Intermittent external pneumatic compression
Skin care
STAGE II
Custom-fitted elastic compression stockings
Skin care with water-based lotion
Topical steroids for dermatitis
Surgical consultation
STAGE III
Ulcer care
Wet to dry saline dressings
Douderm
Unna boot
Four-layer high compression bandage
Custom fitted elastic compression stockings
2. VARICOSE VEINS

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TYPES OF VARICOSE VEIN


Hereditary Varicosities
Often have family history and are predominantly female
Connective tissue laxity is believed to be the underlying
mechanism, and terminal valve incompetence of the greater
and lesser saphenous veins is the major abnormality.

Acquired varicosities (secondary)


Associated with chronic abnormalities of the deep venous
system and are the result of ambulatory venous
hypertension.
Result from proximal obstruction to venous return, as seen
with pregnancy of a pelvic mass.
The increase in pressure placed on the venous system leads
to valve failure and the tortuous appearance noted in the
more superficial veins.
ACUTE VENOUS DISORDERS
1. ACUTE THROMBOPHLEBITIS
An acute inflammatory condition with occlusion of a superficial or
deep vein by a thrombus.
Superficial venous thrombosis
If blood clot is lodged in one of the superficial veins, the
condition usually resolves without long-term complications.
MANAGEMENT
Elevation
Appropriate compressive stockings (30-40 mmHg)
Aspirin/NSAIDs
Deep Venous Thrombosis
Thrombophlebitis of one of the deeper veins can result in a
pulmonary embolism and is life threatening.
The pathogenesis of DVT is related to the VIRCHOWS
TRIAD.
STASIS or altered blood flow in the lower limb deep veins
results from immobility, paralysis or surgery. The stasis
contributes to venous thrombosis by preventing the activated
coagulation factors being diluted by non-activated blood,
preventing clearance and mixing with naturally occuring
inhibitors.
INJURY TO VESSEL WALL has been suggested to be the
strongest risk factor for venous thrombosis. The damage
endothelium leads to platelet adhesion, aggregation, and
platelet release, with activation of components of both
intrinsic and extrinsic pathways of coagulation.
HYPERCOAGULABILITY

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Results in imbalance between thrombosis and hemorrhage.


MANAGEMENT
Standard therapy for acute DVT consist of:
Anticoagulation
Bed rest
Elevation
Support of the extremity
Patients with calf vein thrombosis are confined to bed for 72
hours, followed by gradual mobilization.
Patients with proximal venous thrombosis require 4 to 7 days
of bed rest t with gradual mobilization when pain and
swelling has subsided
All patients wear gradient elastic stockings when they are
mobilized.
Phlebothrombosis
Used to describe the occlusion of a vein by a blood clot.
RISKS FACTORS ASSOCIATED WITH THROMBOPHLEBITIS
1.
2.
3.
4.
5.
6.
7.
8.
9.

Immobility and bed rest over a prolonged period


Obesity
Age of the patient
Orthopedic injuries
Postoperative patients
Congestive heart failure
Malignancy
Use of oral contraceptives
Pregnancy

EVALUATION OF VENOUS DISORDERS


PHLEBOGRAPHY
An invasive procedure similar to angiography
Using an X-ray study and radiopaque dye injected into the venous
system.
The procedure is used to detect a venous thrombosis.
GIRTH MEASUREMENT
The girth of the involved extremity may be compared with the girth
of the uninvolved extremity.
One accepted method is to take circumferential measurements
every 10 cm along the entire length of the extremity.
PERCUSSION TEST
A test used for varicose vein.
Procedure:
Ask the patient to stand until the varicosities in the leg fill with
blood.
Palpate a portion of the saphenous vein below the knee and then
sharply percuss the vein above the knee.

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If a thrust of blood is felt with the palpating finger below the knee,
the valves are incompetent.
HOMAN SIGN
With patient supine, forcefully dorsiflex the foot and squeeze the
posterior calf muscles.
Many patients, but not all, with thrombophlebitis will experience
significant pain in the calf muscles.
APPLICATION OF BLOOD PRESSURE CUFF
Inflate the cuff until the patient experience pain in the calf.
Patient with acute thrombophlebitis usually cannot tolerate
pressures above 40 mmHg.
IMPEDANCE PLETHYSMOGRAPHY
Assesses volume changes at rest produced by a proximal,
pneumatic, veno-occlusive cuff.
EXERCISE VENOUS PLETHYSMOGRAPHY
Lower limb venous function is tested by performing a
plethysmographic evaluation of limb volume before, during, and
after exercise.
DUPLEX SCANNING
Used to diagnose deep or superficial venous thrombosis, assess
venous incompetence, and map the superficial veins before
surgical harvest for bypass operation.

ARTERIOVENOUS FISTULAS AND MALFORMATION


Vascular malformations are classified as either:
1. CONGENITAL ARTERIOVENOUS MALFORMATION
Related to the stage of embryonic maturity at the time of
development arrest.
2. ACQUIRED ARTERIOVENOUS MALFORMATION
Results from surgical construction of angioaccess for dialysis,
penetrating injury, infection neoplasm and aneurysmal erosion.
CLINICAL FINDINGS:
Pulsating hematoma
Palpable thrill
Bruits
Ischemia pain paresthesia
Muscular weakness
Swelling
Discoloration
Dermatitis
Ulceration
TREATMENT

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Early recognition and management of an acquired


arteriovenous fistula are preferred.
Elastic support is beneficial
Appropriate footwear
Maintain mobility of the joint and soft tissue
Preserve normal gait pattern

LYMPHATIC SYSTEM
ANATOMY
The three components of the lymphatic system:
Lymphatic Capillaries and peripheral plexuses
Are the most peripheral structures in the system and anastomose
to form what are termed as peripheral plexuses.
These plexuses, consisting solely of a layer of endothelial cells, lie
in direct contact with the tissues and give rise to short channels that
lead to collecting ducts.
Collecting ducts
The main difference in the ducts are the number of muscular layers
present. The range in complexity from those with single muscular
layer, to those with two, and finally three layers of muscles.
These vessels are more plentiful than veins and tend to accompany
the veins as they course through the body. Their thin walls make
them susceptible to trauma.
Any injury significant enough to affect venous return most likely
inflicts damage to the lymphatics. The ramifications for edema
becomes apparent.
Lymph nodes
Consist of small accumulation of lymphocytes housed in an
encapsulated network of connective tissue.
FUNCTIONS:
Filtering and phagocytosis system
Nodes work to rid the body of unwanted substances that
have been deposited into their dense network.
Production of lymphocytes
The lymphatic and venous systems work in harmony to absorb the arterial
capillary filtrate. It is estimated that approximately 10 percent of this
filtrate, and almost all protein molecules, are handled via the lymphatic
system.

LYMPHATIC DISORDERS

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LYMPHEDEMA
Manifested by an excessive accumulation of tissue fluid due to
disruption of the lymph channels.
It is caused by a disturbance of the water and protein balance
across the capillary membrane. It is characterized by
overaccumulation of fluid in the interstitial tissues and fibrotic
changes in the soft tissue. These changes start in the
subcutaneous fatty tissue and generally extend superficially to
involve the skin and deep to involve the fascial sheets of the
muscle.
The overall incidence is uncertain. A female:male ration of 10:1 has
been described. The peak incidence of onset is in the first decade
after menarche.
PATHOPHYSIOLOGY
The lymphatic system is specifically designed to remove plasma
proteins that filter into tissue spaces. Obstruction or removal of
lymphatic vessels causes retention of proteins in tissue spaces.
The increase protein concentration draws greater amounts of water
into the interstitial space, leading to lymphedema.
There are three structural defects in lymphedema from or cause
overaccumulation of protein-enriched interstitial fluid.
1. Obstruction of superficial and deep lymphatic with fibrosis of
regional lymph node
2. Increase in subcutaneous fatty tissue with fibrosis of
interlobar septa
3. Thickening of deep fascia
CLASSIFICATIONS
CONGENITAL LYMPHEDEMA
Have a faulty lymphatic system due to a complete failure of lymph
vessel to develop (AGENESIS) or poorly developed vessels
(APLASIA)
a. MILROYS DISEASE (HEREDITARY FORM)
Transmitted as autosomal dominant trait.
The clinical characteristics are predominantly an
enlargement of an extremity at birth with firm, nonpitting
edema.
The childs development and activities are not impaired.
b. LYMPHEDEMA PRAECOX
This group is composed primarily of females in the second
and third decades of life.
It presents spontaneously without an apparent etiology.
The edema is initially soft and pitting but becomes firm and
nonpitting over time.
There is no pain or ulceration, but recurrent infection can
occur
c. LYMPHEDEMA TARDA

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Patient who develop lymphedema after the age of 35 years.


This occur without obvious etiology
The edema is nonpitting and firm
Pain and ulceration do not occur, but recurrent infections are
common
SECONDARY LYMPHEDEMA
Due to another pathology or disease process (infectious, malignant,
traumatic, iatrogenic)

SIGNS AND SYPMTOMS


1. Edema
Painless swelling of the distal extremity most often seen over
the dorsum of the hand or foot.
PITTING EDEMA
Indicates short-duration swelling
BRAWNY EDEMA (hard edema)
Associated with long-term venous insufficiency
There are four causes of edema:
1. Increased capillary permeability
2. Decreased osmotic pressure of plasma proteins
3. Increased pressure in venules and capillaries
4. Obstruction to lymphatic flow
2. Increase weight or heaviness of the extremity
3. Sensory disturbances (paresthesia) of the hand or foot
4. Stiffness of the fingers or toes
5. Tautness of skin
6. Susceptibility to skin breakdown
7. Decreased resistance to infection, causing frequent episode of
cellulitis
EVALUATION OF LYMPHATIC DISORDERS
1. Girth measurements of the extremity
2. Volumetric measurements
The involved extremity is immersed in the tank of water
The amount of water displaced as the extremity is lowered into
the water is measured
3. Palpation of the dependent limb to different pitting edema from brawny
edema with subcutaneous fibrosis.
MANAGEMENT
The general aim of treatment:
1. Mobilization of fluid
2. Reduction of girth
3. Prevention of complications
Etiology should be determined before starting the treatment.
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The majority of patients in the clinical setting have lymphedema secondary


to obstruction of the lymphatic system from trauma, infection, radiation, or
surgery. If the patient is at risk for developing lymphedema, PREVENTION
is the best goal.
To increase lymphatic drainage, the HYDROSTATIC pressure of the
tissues must be increased. This is accomplished by external compression
of the skin.
Lymphatic and venous return can also be increased by elevation of the
limb.
Lymphedema caused by lymphatic disorders, such as lymphagitis and
cellulitis, does not diminish as readily with elevation as does edema
secondary to venous disorders.
CONSERVATIVE TREATMENT
Intermittent compression
80-120 mmHg as tolerated is applied preferably twice a day for
40 to 45 minutes each time and should be used with the
extremity elevated.
Manual Massage
Pressure garment
Isometric exercises
Skin and nail care
Range of motion exercises
Weight reduction
Generalized conditioning program
Patient education
GUIDELINES FOR LYMPHEDEMA CARE
Define etiology
History and physical examination
Laboratory
Treatment in hospital
Pneumatic compression
Gradient elastic compression stocking
Education of patient and family
Antibiotics
Diuretics
Discharge
Extremity compression prescribed for 2 to 4 hours/day
Use of gradient elastic stocking
Skin care
Observation for signs and symptoms of infection
Note:
Please include to study REHABILITATION OF DIABETIC FOOT PROBLEMS of
Rehabilitation Medicine by Joel A. De Lisa. This is included in the PRELIM
EXAMINATION.

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