DISORDER
IV.
CLINICAL MANIFESTATIONS
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
Interpretation:
Anticoagulants
antiplatelet therapy
antihypertensives
ARTERIAL DISORDERS
1)
intermittent claudication
rest pain
tissue loss
embolic events
decreased or absent pulses; bruits
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)
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
MC cause: embolization
Intermittent claudication
DIAGNOSTIC EXAMS
Doppler ultrasonography
Plethysmography
PATHOPHYSIOLOGY
V.
Medications
Arterial Pulses
o Palpation: slightly reduced or absent
o Auscultation: presence of bruits at rest
and after exercise
CLINICAL MANIFESTATIONS
acute pain
paralysis
paresthesia of part
pallor
poikilothermia (coldness)
pulselessness
edema
rigidity of extremity
DIAGNOSTIC EXAMS
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
3.
Surgery
CHRONIC
I.
DEFINITION
condition where there is inadequate blood
flow in arteries
II.
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.
I.
-
EPIDEMIOLOGY
Non modifiable:
Age
Gender
Familial predisposition
CLINICAL MANIFESTATIONS
Intermittent claudication
Pale
Ruddy or cyanotic
Ulcerations
Gangrene
Muscle atrophy
Bruits
EPIDEMIOLOGY
III.
IV.
PATHOPHYSIOLOGY
V.
CLINICAL MANIFESTATIONS
Intermittent claudication
Rest pain
Dependent rubor
VI.
DIAGNOSTIC EXAMS
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:
Relieve pain
MEDICAL MANAGEMENT
- Exercise program
- Weight reduction and cessation of tobacco use
Medications
pentoxifylline (Trental)
cilostazol (Pletal)
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.
4)
VIII.
1.
2.
I.
II.
DIAGNOSTIC EXAMS
Digital plethysmography
Peripheral arteriography
VII.
MEDICAL/SURGICAL MANAGEMENT
Reserpine ( Serpasil)
guanithidine (Ismelin)
prasozin ( Minipress)
Stress management
6)
II.
III.
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS
DEFINITION
Distention of an artery brought about by a
weakening / destruction of the arterial wall.
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
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
Dyspnea
Cough
Hoarseness,
voice
weakness
or
complete aphonia
Dysphagia
Cyanosis
2.
Abdominal Aneurysm
Abdominal pain
Hypertension
Distal variability of BP
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.
Surgery:
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
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)
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
Cerebral ischemia
Syncope
V.
DIAGNOSTIC EXAMS
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
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
II.
IV.
III.
IV.
V.
V.
MEDICAL MANAGEMENT
Goals: To prevent propagation of the thrombus,
prevent recurrent thrombus formation, prevent
pulmonary emboli, and limit venous valvular
damage.
Medications
Anticoagulation
Thrombolytic Therapy
Non-pharmacologic Therapies
1. Bed rest
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.
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
Dressing of choice
Ligation
of
the
saphenofemoral
or
saphenopopliteal vessels with stripping.
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
Leg trauma
Varicose veins
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
PATHOPHYSIOLOGY
Dilation of veins valvular incompetence can
no longer prevent back flow thereby chronic
venous stasis swelling and edema superficial
varicose veins
IV.
CLINICAL MANIFESTATIONS
V.
VI.
V.
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.
Risk factors:
Heavy lifting
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
DIAGNOSTIC EXAMS
EPIDEMIOLOGY
CLINICAL MANIFESTATIONS
Ankle edema
May be asymptomatic
Surgery:
sclerosing injection
PROGNOSIS
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
Etiology
ARTERIAL
Arteriosclerosis Obliterans
Atheroembolism
VENOUS
Thrombophlebitis
Trauma, vein obstruction
Risk Factors
Smoking
Diabetes mellitus
Hyperlipoproteinemia
Hypertension
Venous hypertension
Varicose veins
Inherited trait
Temperature
Calf
thigh
hip or buttock
Loss of hair
Color
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
VI.
MEDICAL MANAGEMENT
Decongestive therapy
Elastic stockings
Diuretics
Surgical debulking
VII.
PROGNOSIS
Without treatment, the protein-rich interstitial fluid is
replaced by fibrinoid material. Inflammatory cells
accumulate and progressive fibrosis, sclerosis and
elephantiasis develops
Administration of antibiotics
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
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
Radiation
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
Claudication time
Objective is to determine the amount of time a
patient can exercise before experiencing
cramping and pain in the distal musculature
B.
VENOUS
C.
LYMPHATIC
IX.
Girth measurement
Volumetric of extremity
Palpation to distinguish between pitting or nonpitting edema
PROBLEM LIST
X.
Detects/tests DVT
ARTERIAL