VASCULAR DISORDERS
AORTIC
DISSECTION
PIYALI BISWAS
MSC NURSING 2ND YEAR
DEFINITION
Aortic dissection often
misnamed "dissecting
aneurysm" is not a type of
aneurysm.
Aortic dissection occuring
most commonly in the
thoracic aorta is the result of
the tear in the intimal
(innermost) lining of the
arterial wall.
INCIDENCE
aortic dissection most commonly occurs in men
and occurs most frequently between the fourth
and the seventh decades of life.
This process usually is acute and life
[Link] it may also be self limiting
and result in a chronic and stable process for a
period of time.
if patients have an acute aortic dissection and are
not surgically treated the mortality rate is 90%.
PATHOPHYSIOLOGY
The tear in the intimal lining of the artery allows blood to track
between the intima and media and creates a false lumen of blood
flow.
As the heart contracts each systolic pulsation causes increased
pressure in the damaged area,which further increases the
dissection.
As it extends proximally or distally it may occlude major branches
of the aorta cutting off blood supply to the areas such as the
brain,abdominal organs,kidneys,spinal cord and extremities.
occassionally a small tear develops distally and the blood flow
reenters the true vessel lumen.
ETIOLOGY AND RISK FACTORS
The exact cause of dissection is uncertain although many experts attribute
dissection to the destruction of the medial layers elastic fibers.
most people with dissection is older and have chronic hypertension.
Persons with marfan's syndrome( a premature degeneration of vascular
elastic tissue) have a high incidence of aortic dissection.
Pregnancy promotes increased vascular stress because of increased total
blood volume,decreased peripheral vascular resistance and increased
aortic compliance.
Blunt trauma also is a precipitating factor associated with aortic
dissection.
areas that undergo the greatest amount of stress are most prone to
dissection and include the ascending aorta,the aortic arch and the
descending aorta beyond the origin of the left subclavian artery
CLINICAL MANIFESTATIONS
The typical patient with acute aortic
dissection usually has sudden,severe pain
in the anterior part of the chest or
intrascapular pain radiating down the
spine into the abdomen and legs.
The pain is described as tearing or
[Link] severre pain may mimic that
of an [Link] the dissection progresses pain
may be located both above and below the
diaphragm.
Pregnant women may experience
epigastric discomfort or heartburn like
[Link],neurologic and
respiratory signs also may be present.
If the aortic arch is involved the patient may exhibit neurologic deficiencies
including an altered level of consciousness,dizziness and weakened or absent
carotid and temporal pulses.
An ascending aortic dissection usually produces some degree of disruption in
coronary artery blood flow and aortic valvular [Link] patient may
develop angina,MI and a new high pitched diastolic cardiac murmur.
if severe enough these complications can result in left ventricular failure with
the development of dyspnea and orthopnea caused by heart failure and
pulmonary edema.
when either subclavian artery is involved radial,ulnar and brachial pulse
quality and BP readings may be significantly different between the left and the
right [Link] the dissection progresses down the aorta,the abdominal organs
and lower extremities demonstrate evidence of altered tissue perfusion.
COMPLICATIONS
severe and life threatening complication of
aortic dissection of the ascending aorta arch is
cardiac tamponade which occurs when blood
escapes from the dissection into the pericardial
sac.
Clinical manifestations of cardiac tamponade
includes hypotension,narrowed pulse
pressure,distended neck veins,muffled heart
sounds and pulsus paradoxus.
hemorrhage may occur into the mediastinal,pleural or
abdominal cavities.
Rupture of a dissected aorta typically results in exsanguition
and death.
Dissection can lead to occlusion of the arterial supply to vital
organs such as spinal cord,kidneys and abdominal organs.
ischemia of the spinal cord produces symptoms varying from
weakness and decreased pain sensation to complete paralysis of
the lower extremities.
Renal ischemia include abdominal pain,decreased bowel
sounds and altered bowel elimination.
DIAGNOSTIC STUDIES
left ventricular hypertrophy is a common finding
on an echocardiogram and may be related to
changes caused by systemic hypertension.
A chest x-ray may show a widening of the
mediastinal silhouette and left pleural effusion.
A transesophageal echocardiogram can identify
dissections that are closest to the aortic root.
An MRI or multidetector row CT (MDRCT)
scan are the emergency diagnostic procedures of
choice.
angiography may be neccessary to assess the
extent of the dissection.
COLLABORATIVE CARE
The initial goal of therapy for aortic dissection without
complications is to lower the BP and myocardial contractility to
diminish the pulsatile forces within the aorta.
An IV beta adrenergic blocker,such as esmolol,typically is used
to decrease the BP and the force of myocardial contractility.
Esmolol is particularly useful since it has rapid onset and a
short halflife.
Other antihypertensive agents such as sodium
nitroprusside,calcium channel blockers nd angiotensin
converting enzymes inhibitors may also be used.
CONSERVATIVE THERAPY
supportive treatment includes pain relief,blood
transfusion (if required) and management of
heart failure( if indicated).
If the dissection is limited to the descending
aorta,conservative therapy may be adequate.
success of the treatment is judged by relief of
pain,which is an indication of stabilization of
the dissection.
SURGICAL THERAPY
Surgery is indicated when drug therapy is
ineffective or when complications of aortic
dissection(eg:heart failure,leaking
dissection,occlusion of an artery) are present.
The aorta is fragile following the
[Link] surgery is delayed for as
long as possible to allow time for edema in the
area of the dissection to decrease and to permit
clotting of the blood in the false lumen.
Surgery for aortic dissection involves resection of the
aortic segment containing the intimal tear and
replacement with synthetic graft material.
The extent of aortic replacement depends on the extent
of the dissection.
Even with prompt surgical intervention,30 DAY
MORTALITY OF ACUTE AORTIC DISSECTION
REMAINS HIGH (10-28%) WITH CAUSES OF
DEATH RELATED TO MI,cerebral ischemia,sepsis
and multiorgan failure.
NURSING MANAGEMENT
Preoperatively nursing management includes keeping
the patient in bed in a semi fowlers position and
maintaining a quiet environment.
These measures assist in keeping the systolic BP (SBP)
at the lowest possible level that maintains vital organ
perfusion.
Opioids and tranquilizers should be administered as
[Link] and anxiety must be managed for patient
comfort especially since they may cause elevations in
the SBP.
Continuous IV administration of antihypertensive
agents requires close nursing supervision.
continuous ECG and intraarterial pressure
monitoring are required .
The nurse should observe for changes in the quality of
peripheral pulses and signs of increasing
pain,restlessness and anxiety.
Vital signs are taken frequently sometimes as often as
every 2 to 3 minutes while obtaining control of the BP.
If the blood vessels branching off the aortic arch is
involved,decresed cerebral blood flow may alter the sensorium
and the level of consciousness.
In preparation of the discharge the nurse should focus on
patient and family [Link] therapeutic regimen includes
antihypertensives drugs.
The patient needs to understand that these drugs must be
taken to control [Link] ADRENERGIC BLOCKERS can be
taken orally to continue to decrease myocardial contractility.
The patient should be told to discuss any side effects with the
health care provider before discontinuing the drug.
VARICOSE VEINS
Varicose veins or
varicosities are
dilated,tortuous
subcutaneous veins
most frequently found in
the saphenous system.
They may be small or
inocuous or large and
buldging.
TYPES
Primary varicose veins(idiopathic) which are more
common in women and patients with a strong family
history, are probably caused by congenital weakness of
the veins.
Secondary varicose veins typically result from a
previous DVT or another identifiable obstruction.
Secondary varicose veins may also occur in the
esophagus (esophageal varices),in the anorectal region(
hemmorrhoids) and as abnormal arteriovenous
connections(AV fistulas and malformations).
Reticular veins are smaller
varicose veins that appear
flat,less tortuous and blue
green in colour.
Telangiectasis (often referred
as spider veins) are very small
visible vessels (generally
<1mm in diameter) that
appear bluish black,purple or
red.
ETIOLOGY AND
PATHOPHYSIOLOGY
The etiology of varicose
veins is
[Link]
veins in the lower
extremities become
dilated and tortuous with
increased venous
pressure.
Risk factors for varicose veins
includes congenital weakness of
the vein structure,female
gender,use of hormones(oral
contraceptives or
HRT),increasing
age,obesity,pregnancy,venous
obstruction resulting from
thrombosis or extrinsic pressure
by tumours or occupations that
require prolonged standing.
As the veins enlarge the valves are stretched and
become incompetent allowing venous blood flow
to be reversed.
As back pressure increases and the calf muscle
pump muscle movement (that squeezes venous
blood back towards the heart) further venous
distension results.
The increased venous pressure is transmitted to
the capillary bed and edema develops.
CLINICAL MANIFESTATIONS
Discomfort from varicose veins varies
dramatically among people and tends
to be worsened by superficial
[Link] addition many
patients voice concern about cosmetic
disfigurement.
The most common symptom of
varicose veins is an ache or pain after
prolonged standing which is relieved
by walking or by elevating the limb.
Some patients feel
pressure or a cramp like
sensation in the legs.
Swelling may
accompany the
discomfort.
Nocturnal leg cramps in
the calf may occur.
COMPLICATIONS
Superficial thrombophlebitis is
the most frequent complication
of varicose veins and may occur
either spontaneously or after
trauma,surgical procedures or
pregnancy.
Rare complications includes
rupture of the varicose veins
from weakening of the vessel
wall and ulceration of the skin.
DIAGNOSTIC STUDIES
Superficial varicose veins can
be diagnosed by appearance.
A duplex ultrasound can
detect obstruction and reflux
in the venous system with
considerable accuracy.
It is the most widely used test
to diagnose deep varicose
veins.
COLLABORATIVE CARE
Treatment usually is not indicated
if the varicose veins are only a
cosmetic problem.
If incompetency of the venous
system develops collaborative care
involves rest with the affected limb
elevated,compression stockings
and exercise such as walking.
An herbal therapy used for the
treatment of varicose veins is
horse chestnut seed extract.
Sclerotherapy involves the injection
of a substance that obliterates
venous telengiectasis,reticular
veins and small superficial varicose
veins.
Two sclerotherapy techniques are
available:injection of a sclerosing
agent alone or a mixture
containing a sclerosing and
foaming agent.
Commonly used sclerosing agents
includes hypertonic saline,saline
plus hypertonic dextrose,morrhuate
sodium and ethanolamine oxalate.
Direct IV injection of a
sclerosing agent induces
inflammation and results in
eventual thrombosis of he vein.
This procedure can be
performed safely in an office
setting and causes minimal
discomfort.
Potential complications includes
itching,pain,blistering ,edema,h
yperpigmentation,necrosis,super
ficial thrombophlebitis and
DVT.
After injection the leg is wrapped with an elastic
bandage for 24 to 72 hours to maintain pressure
over the vein.
After removal of the elastic bandage,compression
stockings are recommended for 2 to 3 weeks to
minimize complications.
Long term compression therapy is advised to help
prevent the development of further varicosities.
never more costly but noninvasive options for the treatment of
venous telangiectasias include laser therapy and high
intensity pulsed light therapy.
laser or light therapy is indicated for isolated small
telengiectasis or for patients in whom slerotherapy is
contraindicated or has been previously ineffective
laser treatment typically requires more than one session
scheduled at 6 to 12 weeks intervals.
vascular laser works by heating the hemoglobin in the vessels
which injures the endothelium resulting in vessel sclerosis.
Pulsed light therapy is similar to laser therapy but
uses a spectrum of light rather than a single
wavelenght.
Potential complications associated with both these
therapies includes pain,blistering,hyperpigmentation
and superficial erosions.
Surgical intervention is indicated for recurrent
thrombophlebitis or when CVI cannot be controlled
with conservative therapy.
The traditional surgical intervention involves ligation of the
entire vein and dissection and removal of the incompetent
tributaries.
An alternative but time consuming technique is ambulatory
phlebectomy which involves pulling the varicosities through
a stab incision followed by excision of the vein.
Newer less invasive procedures includes endovenous
occlusion using radiofrequency closureor laser or
transilluminated powered phlebectomy
Both methods of endovenous occlusion may also be done in
combination with saphenofemoral ligation.
Transilluminated powered
phlebectomy involves the
use of a powered tissue
resector to destroy the
varices and removes the
pieces via aspiration.
Surgical treatment for
varicose veins typically is
done as an outpatient
procedure.
NURSING MANAGEMENT
Prevention is a key factor related to
varicose veins.
The nurse should instruct the patient to
avoid sitting or standing for long periods of
time,maintain ideal body weight,take
precautions against injury to the
extremities,
avoid wearing constrictive clothing and
participate in a daily walking program.
After vein ligation surgery the nurse
should encourage deep breathing which
helps to promote venous return to the right
side of the heart.
The extremities should be checked regularly for
color,movement sensation,temperature,presence
of edema and pedal pulses.
Bruising and discolouration are considered
[Link] operatively the legs are elevated at 15
degree angle to prevent edema.
Compression stockings are applied and removed
every 8 hours for short periods and then
reapplied.
Long term management of varicose veins is directed towards
improving circulation,relieving discomfort,improving the
cosmetic appearance and avoiding complications such as
superficial thrombophlebitis and ulceration.
Varicose veins can recur in other veins after vein ligation
The patient should be taught proper care of the lower
extremities including cleanliness and the use of individually
fitted compression stockings.
The patient should be taught to put on the stockings while
still lying down before rising in the morning.
The importance of periodic positioning of the
legs above the heart should be stressed.
The overweight patient may need assistance
with weight reduction.
The patient with an occupation that requires
prolonged periods of standing or sitting needs to
change position frequently.
CHRONIC VENOUS INSUFFICIENCY AND VENOUS LEG
ULCERS
DEFINITION
It is a common medical problem in the elderly,is a condition
in which the valves in the veins are damaged which results in
retrograde venous blood flow,pooling of blood in the legs and
swelling.
CVI also occurs as a result of previous episodes of DVT can
lead to venous leg ulcers (formerly called venous stasis
ulcers or varicose ulcers).
Although CVI and venous ulceration are not life threatening
diseases,they are painful,debilitating and costly chronic
conditions that can adversely affect the quality of the patients
lives.
ETIOLOGY AND PATHOPHYSIOLOGY
The causes of CVI includes vein incompetence,deep vein
obstruction,congenital venous malformation,AV fistula and
calf muscle failure.
The basic dysfunction is incompetent valves of the deep veins.
As a result the hydrostatic pressure in the veins increases and
serous fluid and RBC'S leak from the capillaries and venules
into the tissues resulting in edema.
Enzymes in the tissues eventually break down the RBC'S
causing the release of hemosiderin which causes a brownish
skin discolouration
Over time the skin and
subcutaneous tissue around the
ankle are replaced by fibrous
tissue resulting in thick,hardened
contracted skin.
Although the causes of
CVI are known,the exact
pathophysiology of venous ulcers
remain unknown.
It is known that decreased
fibrinolysis,pericapillary fibrin
cuffs and WBC trapping occur in
venous ulcers.
CLINICAL MANIFESTATIONS AND COMPLICATIONS
In individuals with CVI the skin of the
lowerleg is leathery with a characteristic
brownish or BRAWNY APPEARANCE
FROM THE HEMOSEDERIN
DEPOSITION.
edema usually has beenpersistent for a
prolonged period.
Eczema or stasis dermatitis is often present
and pruritus is a common complaint.
Patients with CVI also have a higher skin
temperature in the ankle area compared to
healthy adults.
Venous ulcers classically are
located above the medial
[Link] they can occur
near the lateral malleolus.
The wound margins are irregularly
shaped and the tissue is typically a
ruddy colour.
Venous ulcers are typically partial
thickness wounds that extend
through the epidermis and portions
of the dermis.
Ulcer drainage may be extensive especially when the
leg is [Link] ulcer is often quite painful
particularly when edema or infection is present.
Pain may be worse when the leg is in the dependent
position.
If the venous ulcer is untreated the lesion becomes
more extensive eroding wider and deeper and
increasing the likelihood of wound infection and
cellulitis.
Recurrent episodes of
cellulitis may lead to
destruction of the superficial
lymphatics causing a
secondary lymphedema to
develop.
On very rare occasions severe
CVI with long standing
nonhealing venous ulceration
may result in need for
amputation.
COLLABORATIVE CARE
Compression is essential to the management of
CVI,venous ulcer healing and prevention of
ulcer recurrence.
A variety of options are available to achieve
compression,including elastic wraps,custom
fitted compression stockings,elastic tubular
support bandages,a velcro wrap,ICD a paste
bandage with an elastic wrap and multilayer
bandage systems.
There are benefits to each type of compression
therapy and the nurse must evaluate each
patient individually whwn choosing an extrinsic
compression method.
Before instituting compression therapy assessment of the arterial
status is neccessary to make sure that co-existing arterial disease is
not [Link] ABI of <0.9 suggests that the patient also has PAD
and should not have high levels of compression.
Moist environment dressings are the mainstay of wound care.
A variety of these dressings are available and includes transparent
films dressings,hydrocolloids,hydrogels,foams,calcium
allginates,impregnated gauze,gauze moistened with saline and
combination dressings.
When used in conjunction with extrinsic compression moist
environment dressings have proven to be more effective in hastening
the healing of venous leg ulcers than dry dressings.
Nutritional status and intake should be evaluated in a
patient with a venous leg ulcers.
A balanced diet with adequate protein,calories and
micronutrients is essential for healing.
Nutrients most importantly for healing includes
proteins,vitamin A and C and [Link] high in
protein (eg: meat,beans,cheese,tofu), vitamin A(green
leafy vegetables),vitamin C (citrus fruits,tomatoes and
cantaloupe) and zinc must be provided.
For patients with coexisting diabetes mellitus,maintaining
normal blood glucose levelsfacilitates the healing process.
For overweight individuals with CVI AND NO ACTIVE
VENOUS ULCERS, a weight reduction diet may be prescribed.
Routine prophylactic antibiotic theray typically is not indicated.
Clinical signs of infection in a venous ulcer includes change in
quantity,color and odor of the drainage,presence of
pus,erythema of the wound edges,change insensation around
the wound,increased local pain,edema or both,dark coloured
granulation tissue,induration around the wound,delayed heaing
and cellulitis.
However if signs of infection are present a culture
should be obtained and appropriate antibiotic therapy is
then instituted.
The usual treatment of infection is sharp
debridement,wound excision and systemic antibiotics.
Nanocrystalline silvercoated dressings are an additional
antimicrobial option for infected chronic wounds such
as venous ulcers.
if the ulcer fails to respond to conservative
therapy,alternative treatments may be indicated.
Patients at greatest risk for delayed healing are
those with long standing ulcers.
Alternative treatments includes use of a radiant
heat bandage,vacumm assisted closure therapy
and coverage with split thickness skin
graft,cultured epithelial autografts,allografts or
bioengineered skin such as apligraft or
dermagraft.
Typically when a split thickness skin graft is
used the ulcer is debrided,varicosities in the area
of the lesion are removed and veins are ligated
before the tissue from a donor site is applied.
hyperbaric oxygen another alternative therapy
has not been shown to improve venous ulcer
healing.
An herbal therapy used for the treatment of CVI
is horse chestnut seed extract.
Escins the active ingredient are thought to act
as antiexudative and antiinflammatory agents.
Effects includes the vascular permeability and
thus a prevention of edema.
minor side effects includes dizziness,GI
compliants,headache and pruritus.
NURSING MANAGEMENT
Long term mangement of venous leg ulcers should focus on
teaching of the patient about self care measures because the
incidence of reccurence is high.
This is particularly important because research indicates that
patients with CVI lack understanding of appropriate
treatments.
Patients and family teaching should include avoidance of
trauma to the limbs,
proper skin care measures,application and regular
replacements of prescribed compression stockings and
appropriate activity and limb positioning.
Proper foot and leg care is essential to avoid additional
trauma to the skin.
PATIENTS with CVI have dry and,flaky and itchy
[Link] moisturizing of the skin decreases the itching
and prevents [Link] products may
includes antibacterial agents,additives in
bandages,ointments containing
lanonin,parabens,alcohol,benzocaine.
The wound should be assessed for signs and symptoms
of infection during each dressing change.
The patient with CVI with or without a venous ulcer is
instructed to avoid standing or sitting with the feet dependent
for long periods.
It also decreases the periulcer skin blood perfusion and
oxygen [Link] ulcers patients are also instructed to
elevate their legs above the level of the heart to reduce
edema.
Once an ulcer is healed,a daily walking program is
[Link] compression stockings should be
worn daily and repalced every 4 to 6 months to reduce the
occurrence of CVI.
BIBLIOGRAPHY
