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PERIPHERAL VASCULAR

DISORDER

IV.

CLINICAL MANIFESTATIONS

GENERAL MEDICAL BACKGROUND


I.

DEFINITON
conditions that may affect the circulatory
system external to the heart that involves
arterial, venous, lymphatic circulatory system.
a)

b)

c)

d)

Arteries
these are vessels through which the
blood passes away from the heart to
various parts of the body
they convey highly oxygenated blood
from the left side of the heart to the
tissues
Capillaries
thin walled vessels through which
nutrients and waste products pass
allow the exchange of fluid and nutrients
between the blood and the interstitial
spaces
Veins
transport deoxygenated blood from the
tissues back to the heart and lungs for
oxygenation
Lymphatic System
transport fluids that have escaped from
the blood vascular system to the blood

V.

DIAGNOSTIC EXAMS
- specific to the body system affected

arteriography of the involved area


CT scan
MRI
Non-invasive testing of the vascular
system:
a) Duplex studies
b) Sequential Doppler studies
c) Ankle brachial index

Interpretation:

above 0.90 = normal

0.71 - 0.90 = mild obstruction

0.41 0.70 = moderate obstruction

0.00 0.40 = severe obstruction


VI.

MEDICAL & PHARMACOLOGIC


MANAGEMENT
- modification of risk factors
- prescriptive management

Anticoagulants

antiplatelet therapy

lipid -lowering agents

antihypertensives

vascular rehabilitation and exercise

ARTERIAL DISORDERS
1)

intermittent claudication
rest pain
tissue loss
embolic events
decreased or absent pulses; bruits

ARTERIOSCLEROSIS & ATHEROSCLEROSIS

I.

DEFINITION
- arteriosclerosis: is an arterial disease
manifested by a loss of elasticity and a
hardening of the vessel wall
- atherosclerosis: is the most common type
of arteriosclerosis, manifested by the
formation of atheromas

II.

VII.
1.

Endovascular procedures:
a) Percutaneous transluminal angioplasty
be done with or without placement of
intraluminal stent
done to relieve arterial stenosis when
lesions are accessible through the
use of special inflatable balloon
catheters and metal stents
superficial femoral and iliac arteries
b) Endovascular grafting
placement of prosthetic graft via a
transluminal approach
c) Rotational atherectomy
high-speed cutter that removes
lesions by abrading plaque
d) Laser angioplasty
amplified light waves are transmitted
by fiberoptic catheters
laser beam heats the tip of a
percutaneous catheter and vaporizes
the atherosclerotic plaque
a) Revascularization of the affected vessels:
a. Embolectomy
b. Thromboectomy
c. Bypass

ETIOLOGY/RISK FACTORS:
Modifiable

nicotine use

diet

hypertension

diabetes

stress

sedentary lifestyle
Non-modifiable

age

gender

genetic predisposition

HFD

III.

PATHOPHYSIOLOGY:
most common theory: reaction to injury
Two types of atherosclerotic lesions:
a)

b)

fatty streaks
are yellow and smooth, protrude slightly
into the lumen of the artery and are
composed of lipids and elongated
smooth muscle cells
fibrous plaque
composed of smooth muscle cells,
collagen fibers, plasma components and
lipids
can develop at any point in the body, but
certain sites are more vulnerable,
typically bifurcation or branch areas

SURGICAL MANAGEMENT

2)

ARTERIAL OCCLUSION /INSUFFICIENCY

a.

ACUTE

I.

DEFINITION
is a sudden decrease in the arterial supply
to an extremity

II.

EPIDEMIOLOGY
Acute embolic occlusion
common in those who have had a recent
myocardial infarction, atrial fibrillation or
other source of possible embolus.

III.

III. PATHOPHYSIOLOGY

Progressive narrowing causes by


atherosclerosis

Progressive occlusion leads to hypoperfusion


and ischemia

The arms and legs are the most vulnerable to


ischemia

Acute thrombotic occlusion


common in those who have had
experienced previous symptoms of
claudication without cardiac dysfunction
ETIOLOGY / RISK FACTORS

MC cause: embolization

consist of thrombus, atheromatous debris


and tumor

originate in the heart, occur after invasive


procedures

arteriosclerosis may cause roughening or


ulceration of the atheromatous plaques

may also be associated with immobility,


anemia and dehydration

emboli tend to lodge at bifurcations and


atherosclerotic narrowings

other causes include: trauma, thrombus,


venous outflow obstruction

IV. CLINICAL MANIFESTATIONS

Intermittent claudication

Ischemic rest pain

Edema of affected extremity

Sensory changes: numbness of foot or toes,


parasthesia
V.

DIAGNOSTIC EXAMS

Doppler ultrasonography

Plethysmography

VI. MEDICAL MANAGEMENT


IV.

PATHOPHYSIOLOGY

once dislodged, an embolus may travel and


lodge in an arterial branch

formation of a soft coagulum near the area


of stagnant blood flow secondary
thrombus

no adequate circulation, the distal tissues


are deprived of oxygen ischemia, pain
and paresthesia in the affected area
muscle necrosis

V.

Medications

Anticoagulants, vasodilators and antiplatelets

Pentoxifylline (Trental) ---- decreased blood


viscosity
Surgery

Percutaneous transluminal angioplasty

Arterial revascularization, reconstruction


VII. EVALUATION

Arterial Pulses
o Palpation: slightly reduced or absent
o Auscultation: presence of bruits at rest
and after exercise

Skin, Nails and Hair


o Ulcerations; glossy, cold, smooth skin;
pallor
o Atrophic nails; delayed capillary refill
o Hair loss

CLINICAL MANIFESTATIONS

acute pain
paralysis
paresthesia of part
pallor
poikilothermia (coldness)
pulselessness
edema
rigidity of extremity

VIII. DIAGNOSES AND INTERVENTIONS


VI.

DIAGNOSTIC EXAMS

Neurovascular assessment of affected area

Doppler ultrasonography, segmental limb


pressure and pulse volume recordings
may indicate decreased blood flow

Radionuclide scan
may identify clot

Arteriography
determines location of obstruction and
character of arterial circulation
proximal and distal to
obstruction

VII.

1.

2.

MEDICAL MANAGEMENT
Medications

Anticoagulants: Heparin

Thrombolytics: Streptokinase, urokinase

3.

Surgery

embolectomy: must be performed w/in 6 to


10 hrs
amputation of limb
b.

CHRONIC

I.

DEFINITION
condition where there is inadequate blood
flow in arteries

II.

ETIOLOGY / RISK FACTORS

length and size


3)
I.

primary cause: atherosclerosis obliterans


thromboangitis obliterans
cystic degeneration of the popliteal artery
some connective tissue disorders

Altered peripheral tissue perfusion (chronic)


related to interruption of arterial flow

Assess arterial pulses

Observe skin color changes and venous


filling

Avoid procedures or bed positions that


interfere with gravitational blood flow

Protect the affected extremity

Instruct patient to avoid nicotine


Pain related to peripheral ischemia

Assess quality and degree of pain

Provide position of most comfort

Frequent, small position changes may be


helpful

Instruct the patient on methods to relieve pain

Begin a slow, progressive exercise program


Impaired skin integrity (actual and high risk for)
related to impaired circulation

Assess skin, temperature and integrity

Provide daily skin care

Ensure skin is thoroughly dried

Treat ulcerations as they occur

Medications and dressings as ordered

Avoid using adhesive tape directly on skin


Avoid use of tight constricting socks/hose;
use cotton/wool socks that have proper

ARTERIOSCLEROSIS OBLITERANS
DEFINITION
is a form of arteriosclerosis in which the
peripheral arteries are blocked
Most common form of chronic occlusive
vascular disease affecting the lower
exrtremities.
Slowly developing, degenerative process and
manifestations occur insidiously.

II.

III.

This begins with monocyte adherence to


endothelial wall following physical damage
such as trauma, hypertension, or
biomechanical process.
A fatty streak develops and results in
production of an atheromatuos plaque in the
intima of the artery. As the plaques increases
in size, the lumen is narrowed and linear
blood flow is impaired.
Atherosclerosis affects most segments of the
arterial system with a focal distribution of
lesions. Lesions tend to develop at major
arterial bifurcations and sites of acute vessel
angulation

I.
-

EPIDEMIOLOGY

Common in geriatric population

in men ages 50-70.

Most common sites of ASVD:


a. the superior femoral artery,
b. aortoiliac segment,
c. popliteal artery and
d. abdominal aorta (1/6 of cases).

Major risk factors are DM, obesity, cigarette


smoking, hyperlipidemia and HTN.

Non modifiable:

Age

Gender

Familial predisposition
CLINICAL MANIFESTATIONS

Sensation of coldness or numbness

Intermittent claudication

Pale

Ruddy or cyanotic

Skin and nail changes

Ulcerations

Gangrene

Muscle atrophy

Bruits

Unequal pulses between extremities

Absence of a normally palpable pulse

EPIDEMIOLOGY

Predominant in young male smokers


between the ages of 20-40.

III.

ETIOLOGY / RISK FACTORS

Cause is unknown but believed to be an


immune vasculitis.

Occurs most often in men between 20 and


35 years old

Heavy smoking or chewing of tobacco

IV.

PATHOPHYSIOLOGY

Recurring inflammation ---- thrombus


formation and occlusion of blood vessels

V.

CLINICAL MANIFESTATIONS

Intermittent claudication

Rest pain

Dependent rubor

Numbness / tingling of feet or toes

Iatrophic changes associated with


tissue malnutrition

Tissue loss / non healing ulcers

VI.

DIAGNOSTIC EXAMS

Segmental limb pressure

Duplex ultrasonography

Contrast angiography

VII.
V.

VI.

DIAGNOSTIC EXAMS

Doppler

Ankle-Brachial indices

Treadmill tesing

Duplex ultrasonography

MEDICAL MANAGEMENT
Essentially same as that for Arteriosclerosis
Obliterans
Goals:

Reestablish blood flow

Preserve the extremity

Relieve pain

Provide sufficient blood flow for wound


healing

Conservative treatment; modification of risk


factors : walking, weight reduction, smoking
cessation, control of other conditions

Pharmacologic treatment with antiplatelet and


anticoagulant agents

MEDICAL MANAGEMENT
- Exercise program
- Weight reduction and cessation of tobacco use
Medications

pentoxifylline (Trental)

cilostazol (Pletal)

Antiplatelet aggregating agents


Surgery

Vascular grafting

Bypass graft

DEFINITION
Inflammatory process of arterial wall, which is
followed by thrombosis.
An occlusive disease of the median and small
arteries and veins.
Commonly affects the distal upper and lower
limbs
Second most common form of chronic
occlusive arterial disease.
This disease process is similar to that of
arteriosclerosis obliterans but tends to occur
predominantly in young men smokers.
Manifested initially in the distal aspects of the
extremities and progress proximally.
The clinical symptom of decreased tissue
temperature and tissue necrosis is due to
inflammatory process in the veins and arteries
that appears to be related to tobacco use.
Nicotine is very potent vasoconstrictor and is
responsible for immediate decrease in skin
temperature seen in smokers.

II.
ETIOLOGY / RISK FACTORS
Modifiable:

Nicotine use

Hypertension

Diet

Obesity

Sedentary lifestyle

Stress

Diabetes Mellitus

IV.

BUERGERS DISEASE (THROMBOANGITIS


OBLITERANS)

4)

VIII.
1.

2.

DIAGNOSES AND INTERVENTIONS


Altered Tissue Perfusion (peripheral) related to
decrease arterial blood flow

Perform neurovascular checks frequently

Inspect lower extremity or feet for new areas


of ulcerations

Encourage well-balanced diet

Encourage walking or performance of ROM


exercises

Administer pain medications as ordered


Sensory / Perceptual Alteration (tactile) of lower
extremity

Avoid tight-fitting socks/shoes


Avoid sitting with legs crossed
Avoid using adhesive tape and harsh soaps
on affected skin

Instruct patient to check temperature or bath


water

Perform and teach how to do foot care


3. Risk for infection related to decreased arterial flow

Apply lanolin or petrolatum to intact skin of


lower extremities

Encourage to wear clean hose / socks daily

Teach patient to:

Trim toenails straight across after


soaking

Place wisps of cotton under corner of


great toenail

Teach patient signs to report:

Redness, swelling, irritation, blistering,


foul odor

Itching, burning, rashes

Bruises, cuts, unusual appearance of


skin

New areas of ulceration


5)

I.

II.

DIAGNOSTIC EXAMS

Digital plethysmography

Peripheral arteriography

Clinical symptoms must last at least 2 years

Tests may be conducted to rule out secondary


disease processes
Note: Raynauds phenomenon - Fingers become
white due to lack of blood flow, then blue as
vessels dilate to keep the blood in tissues, finally
red as blood flow returns

VII.

MEDICAL/SURGICAL MANAGEMENT

Avoidance of trigger and aggravating factors

Calcium channel blockers

Nitroglycerin or sympatholytics such as:

Reserpine ( Serpasil)
guanithidine (Ismelin)
prasozin ( Minipress)

Anti- platelet agents

Symphatectomy- removal of sympathetic


ganglia or division of their branches

Assist patient in avoiding exposure to cold

Encourage patient to stop smoking

Let patient understand the need to avoid


stressful situations

Stress management

Instruct regarding drug therapy

Advise patient that episode may be terminated


by soaking hands/feet in warm water

Pain related to hyperemic stage:

Explain to the patient when to expect the


occurrence of pain

Teach about self- administration of analgesics

Reassure patient that pain is temporary

VASOSPASTIC DISORDER (RAYNAUDS


DISEASE) FUNCTIONAL ARTERIAL
DISORDER
DEFINITION
Disorder of small cutaneous arteries
Vasospasm of the arterioles and arteries of the
upper and lower extremities that is brought on
by an unusual sensitivity to cold or emotional
stress
Commonly referred as Raynauds
Phenomenon.
This is caused by vasospasm, most often
affecting the arterioles and small arteries of the
fingers.
It is characterized by skin color and
temperature changes.
This disorder is usually seen in young adults
and this can be precipitated by exposure to
cold or by emotional stress.

6)

II.

III.

PATHOPHYSIOLOGY

Occurrence of vasoconstriction due to the


release of catecholamines

CLINICAL MANIFESTATIONS

Coldness, pain, pallor

Fingers- asymmetric; thumbs are less often


involved

Characteristic color changes : White Blue Red

Ulceration of the fingertips

Fingers become white due to lack of blood flow,


then turn blue as vessels dilate to keep the
blood in tissues, finally red as blood flow returns

DEFINITION
Distention of an artery brought about by a
weakening / destruction of the arterial wall.

ETIOLOGY / RISK FACTORS


Atherosclerosis
Trauma
Infection
Heredity
Immunologic conditions

False aneurysms are associated with


trauma to the arterial wall.
Contributing factors:

Hypertension

Arteriosclerosis

Three phases:
a. Severe constriction
Results in blanching of the fingers
Followed by dilatation of the vessels
b. Ischemic Phase
Fingers turn white and the cyanotic, numb
and cold
c. Hyperemic Phase
Fingers turn red and patient experiences
throbbing pain
V.

ANEURYSMS

I.

EPIDEMIOLOGY

F>M, usually in young adults

usually begins in early decades of life,


st
nd
predominantly in the 1 and 2 decades

III. ETIOLOGY / RISK FACTORS


o

Unknown cause but may be 2 to connective


tissue and other immunologic disorders

May be triggered by emotional factors or


unusual sensitivity to cold

Common in F ages 16- 40

Seen most frequently in cold climates and


during winter months
IV.

VI.

IV.

PATHOPHYSIOLOGY
Localized weakness and stretching in the
medial layer or wall of an artery
High pressure causes the aneurysms to
enlarge compressing surrounding
structures.
Intralumenal thrombus may cause further
damage
Most common sites: ascending aorta and
aortic arch
Morphologically, aneurysms are classified
as:
> Saccular
> Fusiform
> Dissecting

DIAGNOSTIC EXAMS
Abdominal or chest X-ray.
CT scanning and ultrasonography.
MRI / MRA
Arteriography

V.

CLINICAL MANIFESTATIONS

VI.

1.

Thoracoabdominal Aorta

Pulse and blood pressure difference

Pain and pressure symptoms

Constant, boring pain

Intermittent and neuralgic pain

Dyspnea

Cough

Hoarseness,
voice
weakness
or
complete aphonia

Dysphagia

Edema of chest wall

Dilated superficial veins on chest

Cyanosis

Ipsilateral dilation of pupil

Abnormal pulsation apparent on chest

2.

Abdominal Aneurysm

Most are asymptomatic

Abdominal pain

Low back pain

Feeling of an abdominal pulsating mass

Hypertension

Distal variability of BP

Ruptured --- hypotension or hypovolemic


shock

Surgery:

surgical revascularization

Surgical bypass
b. SYPHILITIC AORTITIS
I.

DEFINITION
the late manifestation of leutic infection that
usually affects the proximal ascending aorta,
particularly the aortic root, resulting in aortic
dilation and aneurysm formation.

II.

III.
VI.

Follow small aneurysms (4cm or less) with


CT scan or ultrasound every 6 months
Control BP

Surgery:

Resection of the aneurysm

Endovascular grafting

7)

MEDICAL MANAGEMENT
-

MEDICAL MANAGEMENT:
Glucocorticoids and immunosuppressive
agents: acute stage
Anticoagulation agents

IV.

CLINICAL MANIFESTATIONS
May result from aortic regurgitation, from
narrowing of coronary ostia and also due to
the compression of adjacent structures
Sensations of substernal heaviness, viselike
feelings of constriction of the chest, attacks of
agonizing pain
DIAGNOSTIC EXAMS:

AORTITIS

PATHOPHYSIOLOGY
Obliterative endarteritis of the vasa vasorum
(adventitia) --- caused by the invasion of
spirochetes
Destruction of the aortic media (via the
lymphatics) --- destruction of collagen and
elastic tissue --- dilatation of the aorta, scar
formation and calcification

Positive serologic test


VDRL
Fluorescent treponemal antibody en & short
attacks of dyspnea.

a. TAKAYASUS DISEASE
VENOUS DISORDERS
I.
-

II.

III.

IV.

DEFINITION
Inflammatory diseases of the aortic arch
resulting in the obstruction of the aorta and its
major arteries

A.

OBSTRUCTIVE

1)

Thrombosis and Embolus

ETIOLOGY / RISK FACTORS


Prevalent in young females and is more
common in those of Asian descent.

I.

PATHOPHYSIOLOGY
Exact pathologic mechanism is unknown but
thought to be immune complex mediated.
Systemic inflammation end organ ischemia
CLINICAL MANIFESTATIONS
Acute stage:

Fever

Malaise

Weight loss

Elevation of the ESR


Chronic Stage:

Upper extremity claudication

Cerebral ischemia

Syncope

V.

DIAGNOSTIC EXAMS

Magnetic resonance angiography

CT

Duplex ultrasonography

Arteriography

II.

DEFINITION

Thrombus
A clot composed of platelets, fibrin,
clotting factors, and cellular debris
attached to the interior wall of an
artery or vein.

Embolus
A clot or solid particle carried by the
bloodstream, which may interfere
with tissue perfusion in an artery or
vein.

Superficial Thrombophlebitis
A condition in which a clot forms in
a vein secondary to phlebitis.

Phlebothrombosis
Formation of a thrombus in a vein

Deep Vein Thrombosis


Thrombosis of deep veins.
ETIOLOGY / RISK FACTORS
Endothelial damage
Trauma
Surgery
Pacing wires
Central venous catheters
Local vein damage
Repetitive motion injury
Venous stasis
Bed rest or immobilization
Obesity Hx. Varicosities
Age (over 65 y/o)
Coagulopathy
Cancer

Pregnancy
Oral contraceptives
Polycythemia
Septicemia

III.

PATHOPHYSIOLOGY
Three antecedent factors are believed to
play a significant role in the development
of venous thromboses: Virchows Triad
> Stasis of blood
> Injury to the vessel wall
> Altered blood coagulation

Usually two of the three factors occurs


before thrombosis develops

II.

IV.

III.

IV.

V.

Clinical manifestations vary with site and


length of affected vein.
DVT may occur asymptomatically or may
produce severe pain, fever, chills, malaise
and swelling and cyanosis of affected arm or
leg.
Superficial thrombophlebitis produces visible
and palpable signs such as heat, pain,
swelling, erythema, tenderness, and
induration along the length of the affected
vein.

V.

MEDICAL MANAGEMENT
Goals: To prevent propagation of the thrombus,
prevent recurrent thrombus formation, prevent
pulmonary emboli, and limit venous valvular
damage.
Medications

Anticoagulation

For documented cases of DVT

Heparin is given IV initially, followed by 3 to 6


months of oral anticoagulant therapy

Heparin and enoxaparin also be given


subcutaneously

Thrombolytic Therapy

May be used in life or limb-threatening


situations

Non-pharmacologic Therapies
1. Bed rest

Recommended for 5 days

Prevents muscle contraction with walking,


which may dislodge clot.
2. Elevation of affected extremity

At least 10 to 20 degrees above the level of the


heart

Enhance venous drainage and decrease


swelling
3. Compression

Promotes venous return and reduces swelling


4. Dry heat
5. Moist heat
Surgery

placement of a filter into the inferior vena


cava

thromboectomy

1)

PATHOPHYSIOLOGY
Postphlebitic syndrome and stasis
Inadequate exchange of oxygen and other
nutrients in the tissue
Secondary bacterial infection occurs because
of decreased circulation

CLINICAL MANIFESTATIONS

B.

ETIOLOGY / RISK FACTORS


Venous stasis
Deep venous obstruction from abdominal
tumor or pregnancy
Valvular incompetency in the ileofemoral vein
Major burn
Sickle cell disease
Neurogenic disorders
Hereditary factors

VI.

CLINICAL MANIFESTATIONS
Severity of symptoms depends on the extent
and duration of vascular insufficiency.
Open sore
Drainage may be present or the area may be
covered by a dark crust
Swelling, heaviness, aching and fatigue
Edema and pigmentation around ulcer
DIAGNOSTIC EXAMS
Non-invasive tests: plethysmography and
venous Doppler.
Wound cultures will identify microorganisms if
infected.
MEDICAL MANAGEMENT

1. Removing devitalized tissue.

Necrotic material is flushed out with cleansing


agents to dissolve slough.

Surgical excision of slough


2. Stimulating formation of Granulation Tissue

Dressing of choice

Application of compression over dressings

Bed rest with leg elevation

Systemic drug therapy

Application of skin grafts


3. Preventing recurrence.

Ligation
of
the
saphenofemoral
or
saphenopopliteal vessels with stripping.

Ligation of the lower leg communicating veins.


2)

CHRONIC VENOUS INSUFFICIENCY

I.
II.

DEFINITION
Also called postphlebitic syndrome
Is a form chronic venous stasis; it may be a
residual effect of phlebitis
Inadequate venous return over a long period
of time
ETIOLOGY / RISK FACTORS

Follows most severe cases of deep vein thrombosis,


although it may also occur as a result of:

Leg trauma

Varicose veins

Neoplastic obstruction of the pelvic veins


Valvular incompetence
Long term sequelae may be chronic leg ulcers

VENOUS INSUFFICIENCY / STASIS


VENOUS STASIS ULCERS OR LEG ULCERS

I.
-

DEFINITION
is an excavation of the skin surface produced
by sloughing of inflammatory necrotic tissue,
usually caused by vascular insufficiency in
the lower extremity.

Risk factors

Poor nutrition

Immobility

Local trauma

Previous history of burns


III.
-

PATHOPHYSIOLOGY
Dilation of veins valvular incompetence can
no longer prevent back flow thereby chronic
venous stasis swelling and edema superficial
varicose veins

Damaged/destroyed valves in veins Decreased


venous return Increased venous pressure
Venous stasis inadequate valve function and
absence of calf muscle pump Blood flows in
veins bidirectionally High ambulatory venous
pressures in the calf veins Dilation of
superficial veins and capillaries RBCs,
proteins, fluids leak out of the capillaries into
interstitial spaces Edema and reddish brown
pigmentation
Commonly involves iliac and femoral veins and
occasionally saphenous vein

IV.

CLINICAL MANIFESTATIONS

V.

VI.

V.

chronic edema, worse while legs are in


dependent position or Progressive edema of
the leg
- intractable induration, discoloration, pain,
ulceration
Thickening, coarsening and brownish
pigmentation of the skin around the ankles
Venous stasis ulceration
Skin of involved extremity is usually thin,
shiny, dry and cyanotic
Dermatitis and cellulitis may develop later in
the condition
DIAGNOSTIC EXAMS
Doppler ultrasonography
Plethysmography
MEDICAL MANAGEMENT

Directed at reducing venous stasis and


preventing ulcerations.
Avoid complications that can occur with
vascular ulceration and chronic wounds
Plan of care essentials:
Formulating and exercise prescription
Collaborating with a nutritionist
Gold standard for treatment of venous
insufficiency especially with (+) venous leg
ulcers: Compression therapy
Goal is to promote venous return to
central circulation

3)

VARICOSE VEINS

I.

DEFINITION
An abnormal dilation of veins leading to
tortuosity of the vessel, incompetence of the
valves and a propensity of thrombosis

II.

IV. PATHOPHYSIOLOGY
Weakened vein walls cannot withstand
normal pressure and dilate with pooling of
blood.
Incompetent valve Unable to withstand
normal pressure Pooling of blood Veins
dilate and lose their elasticity More blood
collects in the veins Veins become more
swollen and dilated
Vein dilation prevents the valve cusps from
meeting --- increased backup pressure in
lower vein segments.
The combination of vein dilation and valve
incompetence produces the varicosity.

touch
VI.

VII.

Congenital valve or vein wall defects


Valve damage
Chronic venous distention
Systemic condition that interfere with venous
return
Loss of vein elasticity with aging

Risk factors:

Heavy lifting

Prolonged sitting or standing

Hormonal changes (pregnancy, menopause,


hormonal therapy)

Relaxes vein walls

Pressure associated with:

Pregnancy

Obesity

Heart failure

Hemorrhoids

Constipation

Esophageal varices

Hepatic cirrhosis

Trendelenburg test
Walking tourniquet test
Photoplethysmography
Doppler ultrasound
Venous outflow and reflux plethysmography
Ascending and descending venography

MEDICAL MANAGEMENT
Conservative therapies

Periodic daily rest periods

Elevate feet above the level of the heart

Client education of promoting circulation

Frequent changes in posture

Daily exercise program

Appropriate use of properly fitting elastic


stockings

III. ETIOLOGY / RISK FACTORS

DIAGNOSTIC EXAMS

EPIDEMIOLOGY

Women > Men (Secondary to pregnancy)


until 70 years old: Men = Women

Develops between the ages of 30-50 years

CLINICAL MANIFESTATIONS

Dilated, twisting, discolored veins

Mild leg aching after prolonged standing

Easy leg fatigue

Cramping and a feeling of heaviness in the


legs

Ankle edema

Bleeding with abrasion of a vein surface

May be asymptomatic

Development of varicosities is usually gradual

Most common symptom: dull, aching


heaviness, tension or fatigue brought on by
periods of standing

Cramps of lower legs may occur especially at


night; elevation often provides relief

Visible signs: Dilated, tortuous, elongated


veins beneath the skin readily visible when
standing

Secondary tissue changes: Thinning of


skin above the ankle, swelling around the
ankles
Untreated veins become thick and hard to

Surgery:

May be considered for ulceration, bleeding,


and cosmetic purposes

sclerosing injection

multiple vein ligation

ligation and stripping of the greater and lesser


sapphenous vein

venous reconstruction or venous valvular


transplant

Laser therapy (non-invasive use of near


infrared wavelengths)
VIII.

PROGNOSIS

Early conservative care during initial stages


may help condition from worsening

Advanced disease may not be prevented


from recurring

Surgery can improve appearance but may not


reduce physical discomfort

High mortality associated with ruptured,


bleeding esophageal varices

CHARACTERISTICS
Pain

ARTERIAL
Severely
ischemic
(intermittent
claudication)

VENOUS
Crampy
(Homans)

Skin changes

Loss of hair,
foot and toes,
nails are
thickened and
ridged

Brown pigment
around ankles

Temperature

Cool

Normal to cool

Color

Pale on
elevation; dusky
red on
dependency

Normal or
cyanotic on
dependency

Peripheral pulse

Diminished or
absent

Normal

Edema

Absent or mild

Present

Ulcers

Toes

Ankles

Gangrene

May develop

Does not develop

DIFFERENTIAL DIAGNOSIS FOR PERIPHERAL VASCULAR DISEASES

Etiology

ARTERIAL
Arteriosclerosis Obliterans
Atheroembolism

VENOUS
Thrombophlebitis
Trauma, vein obstruction

Risk Factors

Smoking
Diabetes mellitus
Hyperlipoproteinemia
Hypertension

Venous hypertension
Varicose veins
Inherited trait

Severely ischemic (intermittent claudication)


Rest pain = severe involvement
Muscle fatigue, cramping, numbness
Paresthesias over time

Minimal to moderate steady pain


Aching pain in lower leg with
prolonged standing or sitting
(dependency)
Superficial pain along course of
vein

Signs and Symptoms


Pain

Muscle compartment tenderness

Brown pigment around ankles

Temperature

Calf

lower leg or dorsum of foot

thigh

hip or buttock

Loss of hair

foot and toes

nails are thickened and ridged


Cool

Color

Pale on elevation; dusky red on dependency

Normal or cyanotic on dependency

Peripheral pulse

Diminished or absent

Normal

Edema
Ulcers

Absent or mild
Toes or feet or areas of trauma

Present
Sides of ankles, especially on medial
malleolus

Gangrene

May develop

Absent

Location of Pain

Skin changes

Normal to cool

LYMPHATIC DISORDERS
1)

LYMPHANGITIS

I.

DEFINITION
Is an acute inflammation of lymphatic channels
Arises most commonly from infection in an
extremity

II.

CLINICAL MANIFESTATIONS

Characteristic red streaks

High fever, chills

Local pain, tenderness, swelling

Enlarged, red, render lymph nodes


(lymphadenitis)

Produces and abscess

VI.

MEDICAL MANAGEMENT

Bed rest with leg elevation

Active and passive exercises

Decongestive therapy

External compression devices

Elastic stockings

Diuretics

Surgical debulking

Excision: Transfer of superficial lymphatics to


deep lymphatic system by buried dermal flap

VII.

PROGNOSIS
Without treatment, the protein-rich interstitial fluid is
replaced by fibrinoid material. Inflammatory cells
accumulate and progressive fibrosis, sclerosis and
elephantiasis develops

III. CLINICAL MANAGEMENT

Administration of antibiotics

Treat affected part by rest, elevation

Incise and drain


2)
I.
-

II.

b.

Stage 0
(Latent
Lymphedema)

Stage I

Stage II

Stage III
(Lymphostatic
Elephantiasis)

Lymph

Transport
reduced

Accumulation
of protein-rich
lymph

Accumulation
of protein-rich
lymph

Edema

(-)

Reversibil
ity of
Edema

N/A

Pitting edema
Increases with
activity, heat
and humidity
With elevation,
may be normal
in the morning

Skin
Changes

N/A

Non-pitting
with
connective
scar tissue
Does not
resolve
overnight,
increasingly
more difficult
to pit
Present in
severe case

Accumulation of
protein-rich
lymph with
significant
increase in
connective and
scar tissue
Severe nonpitting fibrotic
edema

LYMPHEDEMA
DEFINITION
Swelling of the soft tissues that results
from the accumulation of protein-rich
fluid in the extracellular spaces
Caused by decreased lymphatic
transport capacity and/or increased
lymphatic load
Seen in the extremities but can occur
in the head, neck abdomen and
genitalia
Obstruction may be in both the lymph
nodes and the lymphatic vessels
CLASSIFICATION

a.

STAGES OF LYMPHEDEMA

Primary - Idiopathic or may be present


from birth
Secondary Acquired

III.

EPIDEMIOLOGY
700,000 people in the Americas
30% of breast cancer survivors
Females > Males, 4:1
Incidence increases after surgery and radiation

IV.

ETIOLOGY
Primary Lymphedema:

Unknown

Hereditary

Developmental abnormality
Secondary Lymph Edema:

Trauma

Surgical Dissection of Lymph Node(Radical


Mastectomy, femoro-popliteal by-pass)

Radiation

Disease Infection and Inflammation

Chronic Venous Insufficiency

Tumor

Filariasis

V.

CLINICAL MANIFESTATION
Location: Distal extremities particularly dorsum of
the foot
Severity:
a. Pitting edema- Pressure on the edematous
area causes an indentation of the skin that
persists for several seconds after pressure is
removed.
b. Brawny edema- Pressure on edema feels hard
with palpation
c. Weeping edema- Fluid leaks from cuts and
sores
Increase Size of the limb
Sensory Disturbances: feeling of heaviness of the
limb and sometimes paresthesia
Stiffness and Limited Range of Motion
Decreased resistance to infection

N/A

VIII.

Irreversible

Atrophic
(hardening of
dermal tissue,
skin folds, skin
papillomas,
hyperkeratosis)

PT EXAMINATION

A.

ARTERIAL
Palpation of pulses

Basis of any evaluation of the intensity of


integrity of the arterial system is the detection
of pulses in the distal portion of the
extremities

(+) pulselessness is a sign of severe arterial


insufficiency
Skin Integrity and pigmentation

Diminished arterial blood flow causes tropic


changes in the skin peripherally characterized
by dryness, diminished color (pallor), hair loss,
shiny or waxy appearance of skin and
ulcerations
Test for rubor/reactive hyperemia

Patient is supine, noting the color of the soles


of the feet

Legs are then elevated 45 degrees

Pallor or blanching of the skin will occur in the


feet within 1 minute or less if arterial circulation
is poor

Pinkish flush appears in the feet after several


seconds

Color changes may occur more than 30


seconds to occur and will be bright red or
rubor.

Claudication time
Objective is to determine the amount of time a
patient can exercise before experiencing
cramping and pain in the distal musculature

Common test is to have patient walk on a level


treadmill (1-2mph). Period walk, before
claudication prohibits further activity is
recorded

B.

VENOUS

C.

LYMPHATIC

IX.

Girth measurement
Volumetric of extremity
Palpation to distinguish between pitting or nonpitting edema
PROBLEM LIST

X.

Girth measurements of the extremity


Brodie-Trendelenburg test determine the
competency of the valves in the deep and
superficial veins of the legs in patients with
varicose veins
Percussion test (competence of greater
saphenous vein) for patients with varicose
veins
Homans sign test for DVT
Application of blood pressure cuff @ calf muscle

Detects/tests DVT

Impaired range of motion of involved extremities


Edema
Presence of or risk of skin breakdown
Impaired mobility
Impaired endurance
Impaired respiratory status
Impaired balance
Impaired strength
Knowledge deficit regarding precautions, activity
progression, healing process
Pain
Sensation deficits
INTERVENTIONS WITH RATIONALE

ARTERIAL

Putting the extremity on dependent position to


promote gravity assisted arterial blood flow

Avoid wearing compressive garments to prevent


obstruction of blood flow

Wound care for ulcerations and skin breakage to


prevent infections
VENOUS AND LYMPHEDEMA

IPC with pneumatic pump and sleeve or bag (for


several hours daily to assist in edema drainage)

Elevation of extremities above heart level (30-45


degrees) while sleeping or as often as possible
during the day to assist in edema drainage and
venous return

Manual Lymphatic Drainage

Massage from distal to proximal along the length of


the extremity to assist edema drainage and venous
return

Isometric and isotonic pumping to prevent


development of thrombi

Wear support stockings or sleeves to assist in


edema drainage and venous return

Avoid putting extremity on dependent position to


decrease load on lymphatics

Environmental assessments and patient education


to avoid untoward incidents that may worsen
condition

Proper skin care and wound care techniques