TINJAUAN PUSTAKA

KEPANITERAAN KLINIK BEDAH

BEDAH THORAX DAN KARDIOVASKULAR
ARTERIAL DISEASES

Disusun oleh:
Ivanna Octaviani
0712010021

TABLE OF CONTENTS

Abdominal Aorta Aneurysm

Aortic Dissection

Peripheral Artery Disease

11

Diabetic Foot

13

Buergers Disease

16

Lower Extrimity Ulcer

20

Arterial Thrombosis

23

Arterial Embolism

27

Raynauds Syndrome

29

Claudication

31

ABDOMINAL AORTA ANEURYSM

Definition
An aneurysm is a bulge in a blood vessel caused by a weakness in the blood vessel wall. As blood
passes through the weakened blood vessel, the blood pressure causes it to bulge outwards like a
balloon. So, when aneurysm happens in the abdominal aorta, it is call abdominal aortic aneurysm.
Aneurysms can occur anywhere in the body, but the two most common places for them to form are
in the abdominal aorta and the brain. Exactly what causes the blood vessel wall to weaken is
unclear, though hardening of the arteries, smoking and high blood pressure are thought to increase
the risk of an aneurysm.
Epidemiology
Abdominal aortic aneurysms are most common in men aged over 65, Men are six times more likely
to have an aneurysm than women with around in 1 in 25 men being affected. On average, a ruptured
aortic aneurysm occurs 10 years later in women than in men.
Anatomy of Abdominal Aorta
The abdominal aorta is the largest blood vessel in the body. It is roughly the width of a garden hose.
It transports oxygen-rich blood away from the heart to the rest of the body. It runs in a straight line
down from the heart, through the chest and abdomen before branching off into a network of smaller
blood vessels. In most cases, an abdominal aortic aneurysm causes no noticeable symptoms and does
not pose a serious threat to health. However, theres a risk that a larger aneurysm could burst open
(rupture). A ruptured abdominal aortic aneurysm can cause massive internal bleeding, which is
usually fatal. Four out of five people with a ruptured aortic aneurysm will die as a result.

Picture 1. Aorta Abdominal

Etiology and Pathophysiology

Physicians and researchers are not quite sure what actually causes an AAA to form in some people.
The leading thought is that the aneurysm may be caused by inflammation in the aorta, which may
cause its wall to weaken or break down. Some researchers believe that this inflammation can be

associated with atherosclerosis (also called hardening of the arteries) or risk factors that contribute to
atherosclerosis, such as high blood pressure (hypertension) and smoking. In atherosclerosis fatty
deposits, called plaque, build up in an artery. Over time, this buildup causes the artery to narrow,
stiffen and possibly weaken.

Picture 2. Pathophysiology of Aortic Aneurysm

Besides atherosclerosis, other factors that can increase your risk of AAA include:

Being a man older than 60 years

Having an immediate relative, such as a mother or brother, who has had AAA

Having high blood pressure

Smoking

Clinical Manifestation
AAA is often called a "silent killer" because there are usually no obvious symptoms of the disease.
Three out of four aneurysms show no symptoms at the time they are diagnosed. When symptoms are
present, they may include:

Abdominal pain (that may be constant or come and go)

Pain in the lower back that may radiate to the buttocks, groin or legs

The feeling of a "heartbeat" or pulse in the abdomen

Once the aneurysm bursts, symptoms include:

Severe back or abdominal pain that begins suddenly

Paleness

Dry mouth/skin and excessive thirst

Nausea and vomiting

Signs of shock, such as shaking, dizziness, fainting, sweating, rapid heartbeat and sudden
weakness

Further examinations
No specific laboratory studies can be used to diagnose AAA. The following imaging studies,
however, can be employed diagnostically:

Ultrasonography: Standard imaging technique for AAA

Computed tomography scanning: Offers certain advantages over ultrasonography in defining

aortic size, rostral-caudal extent, involvement of visceral arteries, and extension into the
suprarenal aorta

Magnetic resonance imaging: MRI permits imaging of the aorta comparable to that obtained
with CT scanning and ultrasonography, without subjecting the patient to dye load or ionizing
radiation

Angiography: Helpful in determining aortic anatomy and has been advocated for
preoperative use in certain cases

Treatment
Currently, there are three treatment options for AAA:
Watchful Waiting - Small AAAs (less than 5 centimeters or about 2 inches), which are not rapidly
growing or causing symptoms, have a low incidence of rupture and often require no treatment other
than watchful waiting under the guidance of a vascular disease specialist. This typically includes
follow-up ultrasound exams at regular intervals to determine if the aneurysm has grown.
Surgical Repair - The most common treatment for a large, unruptured aneurysm is open surgical
repair by a vascular surgeon. This procedure involves an incision from just below the breastbone to
the top of the pubic bone. The surgeon then clamps off the aorta, cuts open the aneurysm and sews in
a graft to act as a bridge for the blood flow. The blood flow then goes through the plastic graft and
no longer allows the direct pulsation pressure of the blood to further expand the weak aorta wall.

Picture 3. Open Surgical Repair

Interventional Repair - This minimally invasive technique is performed by an interventional

radiologist using imaging to guide the catheter and graft inside the patient's artery. For the procedure,
an incision is made in the skin at the groin through which a catheter is passed into the femoral artery
and directed to the aortic aneurysm. Through the catheter, the physician passes a stent graft that is
compressed into a small diameter within the catheter. The stent graft is advanced to the aneurysm,
then opened, creating new walls in the blood vessel through which blood flows. This is a less
invasive method of placing a graft within the aneurysm to redirect blood flow and stop direct
pressure from being exerted on the weak aortic wall. This relatively new method eliminates the need
for a large abdominal incision. It also eliminates the need to clamp the aorta during the procedure.
Clamping the aorta creates significant stress on the heart, and people with severe heart disease may
not be able to tolerate this major surgery. Stent grafts are most commonly considered for patients at
increased surgical risk due to age or other medical conditions. The stent graft procedure is not for
everyone, though. It is still a new technology and we don't yet have data to show that this will be a
durable repair for long years. Thus, people with a life expectancy of 20 or more years may be
counseled against this therapy. It is also a technology that is limited by size. The stent grafts are
made in certain sizes, and the patient's anatomy must fit the graft, since grafts are not custom built
for each patient's anatomy.

Picture 4. Aortic Stent Grafts

AORTIC DISSECTION

Introduction
The aorta is the largest artery in the body. It carries the blood from the heart to the branch arteries
that supply the rest of the body. The aorta has the same dimensions as a garden hose and curves up
from the heart before extending down to the waist.
The aorta is identified by 3 major sections: the ascending aorta, the descending aorta, and the
abdominal aorta. The aortic wall has 3 layers (from inside to outside): the intima, media, and
adventitia. These layers are made up of connective tissue and elastic fibers, which allow the aorta to
stretch from pressure produced by the flow of blood. Abnormalities of the aortic wall may lead to
enlargement of the aorta (aneurysm) and tearing (dissection) of the lining of the aorta.
Definition
In an aortic dissection, a small tear occurs in the tunica intima (the inside layer of the aortic wall in
contact with blood). Blood can enter this tear and cause the intima layer to strip away from the media
layer, in effect dividing the muscle layers of the aortic wall and forming a false channel, or lumen.
This channel may be short or may extend the full length of the aorta. Another tear more distal
(further along the course of the aorta than the initial tear) in the intima layer can let blood re-enter the
true lumen of the aorta. Blood flow into the false lumen can cause several problems: It can rob
crucial blood from the rest of the body, it can cause the dissection to spread and affect other arteries,
and it can block blood flow in the true aortic channel (true lumen). These problems may cause
decreased blood flow to vital organs. Aortic dissection also weakens the aortic wall and may lead to
rupture, which may be fatal, or to formation of a balloon-like expansion of the aorta, known as an
aneurysm.
In some cases, the dissection will cross all three layers of the aortic wall and cause immediate
rupture and almost certain death. In most other cases, the blood is contained between the wall layers,
usually causing pain felt in the back or flanks.
Epidemiology
Aortic dissections are uncommon, yet they are highly lethal. If untreated, an aortic dissection can be
fatal within the first 24 to 48 hours. Several risk factors are associated with aortic dissections, such as
high blood pressure (hypertension), genetic disorders affecting the blood vessel wall, atherosclerosis,
cocaine use, and trauma. Data show that the average age for dissection to occur is in the 60s and that
two thirds of dissections occur in men. However, dissections can occur in young patients, especially
those with genetic disorders that affect the aorta and aortic valve.

Etiology
Congenital and acquired factors, alone or in combination, can lead to aortic dissection. Aortic
dissection is more common in patients with hypertension, connective tissue disorders, congenital
aortic stenosis, or a bicuspid aortic valve, as well as in those with first-degree relatives with a history
of thoracic dissection. These diseases affect the media of the aorta and predispose it to dissection.

Acquired conditions
Arterial hypertension is an important predisposing factor for aortic dissection.[6] Of patients with
aortic dissection, 70% have elevated blood pressure. Hypertension or pulsatile blood flow can
propagate the dissection.
Pregnancy can be a risk factor for aortic dissection, particularly in patients with an underlying
anomaly such as Marfan syndrome. An estimated 50% of all cases of aortic dissection that occur in
women younger than 40 years are associated with pregnancy. Most cases occur in the third trimester
or early postpartum period.
Other acquired causes of aortic dissection include the following:

Syphilitic aortitis

Deceleration injury possibly with related chest trauma

Cocaine use

Cystic medial necrosis

The normal aorta contains collagen, elastin, and smooth muscle cells that contribute the intima,
media, and adventitia, which are the layers of the aorta. With aging, degenerative changes lead to
breakdown of the collagen, elastin, and smooth muscle and an increase in basophilic ground
substance. This condition is termed cystic medial necrosis. Atherosclerosis that causes occlusion of
the vasa vasorum also produces this disorder. Cystic medial necrosis is the hallmark histologic
change associated with dissection in those with Marfan syndrome.
Early on, cystic medial necrosis described an accumulation of basophilic ground substance in the
media with the formation of cystlike pools. The media in these focal areas may show loss of cells (ie,
necrosis). This term still is used commonly to describe the histopathologic changes that occur.

Iatrogenic causes
Iatrogenic aortic dissection can result from cardiologic procedures such as the following:

Aortic and mitral valve replacements

Coronary artery bypass graft surgery

Percutaneous catheter placement (eg, cardiac catheterization, percutaneous transluminal

coronary angioplasty)

Aortic dissection occurs when the layers are split in the process of cannulation or aortotomy.
Pathophysiology
The aortic wall is exposed to high pulsatile pressure and shear stress (the steep slope of the pressure
curve; ie, the water hammer effect), making the aorta particularly prone to injury and disease from
mechanical trauma. The aorta is more prone to rupture than any other vessel, especially with the
development of aneurysmal dilatation, because its wall tension, as governed by the Laplace law
(proportional to the product of pressure and radius), is intrinsically high.
An aortic dissection is a split or partition in the media of the aorta; this split is frequently horizontal
or diagonal. An intimal tear connects the media with the aortic lumen, and an exit tear creates a true
lumen and a false lumen, resulting in a double-barreled aorta.
The true lumen is lined by intima, and the false lumen is within the media. Although the false lumen
is within the media, suggesting that it is "lined" with media is misleading; if the aortic dissection
becomes chronic, the lining becomes a serosal pseudointima.
The true lumen is frequently smaller than the false lumen, but not invariably. Typically, flow in the
false lumen is slower than in the true lumen, and the false lumen often becomes aneurysmal when
subjected to systemic pressure. The dissection usually stops at an aortic branch vessel or at the level
of an atherosclerotic plaque.
Most classic aortic dissections begin at one of the following 3 distinct anatomic locations:

Approximately 2.2 cm above the aortic root

Distal to the left subclavian artery

The aortic arch

The most common site of dissection is the first few centimeters of the ascending aorta, with 90%
occurring within 10 cm of the aortic valve. The second most common site is just distal to the left
subclavian artery. Between 5 and 10% of dissections do not have an obvious intimal tear. These
often are attributed to rupture of the aortic vasa vasorum as first described by Krukenberg in 1920.
Keeping the descending aorta in mind is important. The descending aorta is the location of most late
clinical events after any dissection of the aorta.

Ascending aortic involvement may result in death from wall rupture, hemopericardium and
tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency.
The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the
production of pain.
Clinical Manifestation
The symptoms usually begin suddenly, and include severe chest pain. The pain may feel like a heart
attack, and can be:

Described as sharp, stabbing, tearing, or ripping

Felt below the chest bone, then move under the shoulder blades or to the back

Move to the shoulder, neck, arm, jaw, abdomen, or hips

Change position -- pain typically moves to the arms and legs as the aortic dissection gets
worse

Symptoms are caused by a decrease of blood flowing to the rest of the body, and can include:

Anxiety and a feeling of doom

Fainting or dizziness

Heavy sweating (clammy skin)

Nausea and vomiting

Pale skin (pallor)

Rapid, weak pulse

Shortness of breath -- trouble breathing when lying flat (orthopnea)

Other symptoms may include:

Pain in the abdomen

Stroke symptoms

Swallowing difficulties from pressure on the esophagus

Investigations
Physical Examinations

A "blowing" murmur over the aorta, heart murmur, or other abnormal sound

A difference in blood pressure between the right and left arms, or between the arms and legs

Low blood pressure

Signs resembling a heart attack

Signs of shock, but with normal blood pressure

An electrocardiogram (ECG) may show complications of dissection, including a heart attack. The
chest x-ray may show an enlarged aorta. However, both the ECG and chest x-ray may be completely
normal in aortic dissection and cannot diagnose or exclude aortic dissection.
The most frequently performed tests to diagnose aortic dissection and its complications include
computed tomography (CT) scan, transesophageal echocardiogram, and magnetic resonance imaging

(MRI). All 3 tests are highly accurate in diagnosing aortic dissections. The specific test performed
often depends on the availability and expertise of the particular hospital, as well as individual patient
characteristics. CT scans require the use of intravenous dye (contrast) to visualize the true and false
lumen of the aorta and branch vessel involvement. A transesophageal echocardiogram may be done
at the patients bedside and involves placing an ultrasound probe into the patients esophagus to
image the heart and aorta. Although highly accurate in diagnosing acute aortic dissection, an MRI
scan takes longer than the other tests and usually is not the first test of choice.
Of note, sometimes aortic dissection may be diagnosed by a transthoracic echocardiogram, an
ultrasound performed on the chest wall. Some patients require multiple different tests to confirm
aortic dissection and its complications. At present, no blood tests are available to diagnose acute
aortic dissection.
Treatments
Aortic dissection is a life-threatening condition and needs to be treated right away.

Dissections that occur in the part of the aorta that is leaving the heart (ascending) are treated
with surgery.

Dissections that occur in other parts of the aorta (descending) may be managed with surgery
or medications.

Two different techniques may be used for surgery:

Standard, open surgery -- requires a Dacron graft (a synthetic material) to replace part of the
aorta to prevent blood flow into the false lumen.

Endovascular aortic repair -- the aorta is repaired by placing stent grafts through a leg artery
into the aorta.

Drugs that lower blood pressure may be prescribed. These drugs may be given through a vein
(intravenously). Beta-blockers are the first drugs of choice. Strong pain relievers are usually needed.
If the aortic valve is damaged, valve replacement is needed. If the heart arteries are involved, a
coronary bypass is also performed.
After a dissection, patients will usually be required to stay in the intensive care unit so that they can
be continuously monitored. Recovery from surgery usually requires 7 to 10 days.

10

PERIPHERAL ARTERY DISEASE

Introductions
Peripheral arterial disease (P.A.D.) is a disease in which plaque builds up in the arteries that carry
blood to your head, organs, and limbs. Plaque is made up of fat, cholesterol, calcium, fibrous tissue,
and other substances in the blood. When plaque builds up in the body's arteries, the condition is
called atherosclerosis. Over time, plaque can harden and narrow the arteries. This limits the flow of
oxygen-rich blood to your organs and other parts of your body.
P.A.D usually affects the arteries in the legs, but it also can affect the arteries that carry blood from
your heart to your head, arms, kidneys, and stomach. This article focuses on P.A.D. that affects
blood flow to the legs. Blocked blood flow to your legs can cause pain and numbness. Patients may
have leg pain when they walk or climb stairs. It also can raise your risk of getting an infection in the
affected limbs. The body may have a hard time fighting the infection. If severe enough, blocked
blood flow can cause gangrene (tissue death). In very serious cases, this can lead to leg amputation.
Smoking is the main risk factor for P.A.D. it increases up to four times. Other factors, such as age
and having certain diseases or conditions, also increase the risk of P.A.D.

Picture1. Comparison of a normal artery and artery with plaque

Etiology and Pathophysiology
The most common cause of peripheral arterial disease (P.A.D.) is atherosclerosis. Atherosclerosis is
a disease in which plaque builds up in your arteries. The exact cause of atherosclerosis isn't known.
The disease may start if certain factors damage the inner layers of the arteries. These factors include:

Smoking

High amounts of certain fats and cholesterol in the blood

High blood pressure

High amounts of sugar in the blood due to insulin resistance or diabetes

11

When damage occurs, your body starts a healing process. The healing may cause plaque to build up
where the arteries are damaged.
Eventually, a section of plaque can rupture (break open), causing a blood clot to form at the site. The
buildup of plaque or blood clots can severely narrow or block the arteries and limit the flow of
oxygen-rich blood to your body.
There are some diseases that are included in a peripheral artery disease, such as:

Diabetic foot

Buergers disease

Raynauds syndrome

Arterial thrombosis

Arterial embolism

Claudication

Lower extremity ulcer

And will be explained deeper in the next pages.

12

DIABETIC FOOT

Introduction
People with diabetes are at increased risk of peripheral vascular disease and neuropathy, as well as
having a higher risk of developing infections and decreased ability to clear infections. Therefore,
people with diabetes are prone to frequent and often severe foot problems and a relatively high risk
of infection, gangrene and amputation.
Epidemiology
The results of cross-sectional community surveys in the UK showed that 5.3% (type 2) and 7.4%
(types 1 and 2 combined) of people with diabetes had a history of active or previous foot ulcer. An
annual incidence of 2.2% was found in a large community survey in the UK, and up to 7.2% in
patients with neuropathy. The incidence of major amputation is between 0.5 and 5.0 per 1,000 people
with diabetes.
Etiology
People with diabetes develop foot ulcers because of neuropathy, ischaemia or both.
The initiating injury may be from acute mechanical or thermal trauma or from repetitively or
continuously applied mechanical stress.

Peripheral neuropathy in people with diabetes results in abnormal forces being applied to
the foot, which diabetic ischaemia renders the skin less able to withstand.

Other complications contributing to the onset of ulceration include poor vision, limited
joint mobility, and the consequences of cardiovascular and cerebrovascular disease.

However, the most common precipitant is accidental trauma, especially from ill-fitting
footwear.

Once the skin is broken, many processes contribute to defective healing, including bacterial
infection, tissue ischaemia, continuing trauma, and poor management.
Infection can be divided into superficial and local, soft tissue and spreading (cellulitis), and
osteomyelitis. Typically, more than one organism is involved, including Gram-positive, Gramnegative, aerobic, and anaerobic species. Staphylococcus aureus is the most common pathogen in
osteomyelitis.
Pathophysiology
Motor, sensory and autonomic fibers may all be affected in people with diabetes mellitus.

Because of sensory deficits, there are no protective symptoms guarding against pressure and
heat and so trauma can initiate the development of a leg ulcer.

Absence of pain contributes to the development of Charcot foot, which further impairs the
ability to sustain pressure.

Motor fiber abnormalities lead to undue physical stress, the development of further

13

anatomical deformities (arched foot, clawing of toes), and contribute to the development of
infection.

When infection complicates a foot ulcer, the combination can be limb-threatening or lifethreatening.

Detection and surveillance of diabetic neuropathy are an essential routine part of a diabetic
annual review.

Presentation
Diabetic foot ulcers are usually painless, punched-out ulcers in areas of thick callus superadded
infection, pus, oedema, erythema, crepitus, malodour. Neuro-ischaemic ulcers tend to occur on the
margins of the foot, and neuropathic ulcers tend to occur on the plantar surface of the foot.

Neuropathic foot tends to be warm with dry skin, bounding pulses, distended veins, reduced
sensation and callus around the ulcer.

Neuro-ischaemic foot tends to be cool, pink with atrophic skin and absent pulses; the foot
may be painful and there is little callus.

Treatment and Management

When treating diabetic foot ulcers it is important to be aware of the natural history of the diabetic
foot, which can be divided into five stages: stage 1, a normal foot; stage 2, a high risk foot; stage 3,
an ulcerated foot; stage 4, an infected foot; and stage 5, a necrotic foot. This covers the entire
spectrum of foot disease but emphasises the development of the foot ulcer as a pivotal event in stage
3, which demands urgent and aggressive management.
Diabetic foot care in all stages needs multidisciplinary management to control mechanical, wound,
microbiological, vascular, metabolic and educational aspects. Achieving good metabolic control of
blood glucose, lipids and blood pressure is important in each stage, as is education to teach proper
foot care appropriate for each stage. Ideally, it is important to prevent the development of ulcers in
stages 1 and 2.

In stage 1, the normal foot, it is important to encourage the use of suitable footwear, and to
educate the patient to promote healthy foot care and footwear habits.

In stage 2, the foot has developed one or more of the following risk factors for ulceration:
neuropathy, ischaemia, deformity, swelling and callus. The majority of deformities can be
accommodated in special footwear and as callus is an important precursor of ulceration it
should be treated aggressively, especially in the neuropathic foot.

In stage 3, ulcers can be divided into two distinct entities: those in the neuropathic foot and
those in the neuroischaemic foot. In the neuropathic foot, ulcers commonly develop on the
plantar surface of the foot and the toes, and are associated with neglected callus and high
plantar pressures. In the neuroischaemic foot, ulcers are commonly seen around the edges of
the foot, including the apices of the toes and back of the heel, and are associated with trauma
or wearing unsuitable shoes. Ulcers in stage 3 need relief of pressure (mechanical control),

14

sharp debridement and dressings (wound control), and neuroischaemic foot ulcers may need
vascular intervention (vascular control).

In stage 4, microbiological control is crucial and severe infections need intravenous

antibacterial therapy, and urgent assessment of the need for surgical drainage and
debridement. Without urgent treatment, severe infections will progress to necrosis.

In stage 5, necrosis can be divided into wet and dry necrosis. Wet necrosis in neuropathic
feet requires intravenous antibacterials and surgical debridement, and wet necrosis in
neuroischaemic feet also needs vascular reconstruction.

Table1. Wagner Ulcer classification system

Table2. University of Texas classification wound

Aggressive management of diabetic foot ulceration will reduce the number of feet proceeding to
infection and necrosis, and thus reduce the number of major amputations in diabetic patients.

15

BUERGERS DIZEASE

Definitions
Thromboangiitis obliterans or Buerger's disease is a segmental occlusive inflammatory condition of
arteries and veins, characterized by thrombosis and recanalization of the affected vessels. It is a nonatherosclerotic inflammatory disease affecting small and medium sized arteries and veins of upper
and lower extremities.
Etiology
Although the cause of Buerger's disease remains unknown, a strong association with tobacco use has
been established. Use or exposure to tobacco plays central role in the initiation and progression of
the disease. By using an antigen-sensitive thymidine-incorporation assay, showed that patients with
TAO have an increased cellular sensitivity to type I and III collagen, compared to that in patients
with arteriosclerosis obliterans or healthy males. Similarly to other autoimmune diseases, TAO may
have a genetic predisposition without a direct "causative" gene mutation. Most investigators feel that
Buerger's disease is an immune-mediated endarteritis. Recent immunocytochemical studies have
demonstrated a linear deposition of immunoglobulins and complement factors along the elastic
lamina. he inciting antigen has not been discovered. The role of hyperhomocysteinemia in the
pathogenesis of Buerger's disease is controversial. An association between thrombophilic conditions
such as antiphospholipid syndrome and Buerger's disease has also been suggested.
Pathophysiology

Picture 1. Pathophysiology of Burgers disease

16

Presentation

Since the specificity of Buerger's disease is characterized by peripheral ischemia of inflammatory

nature with a self-limiting course, diagnostic criteria should be discussed from clinical point of view.
Several different criteria have been proposed for the diagnosis of thromboangiitis obliterans.
Diagnostic criteria of Shionoya

smoking history;

onset before the age of 50 years;

infrapopliteal arterial occlusions;

either arm involvement or phlebitis migrans;

absence of atherosclerotic risk factors other than smoking.

Diagnostic criteria of Olin

age under 45 years;

current or recent history of tobacco use;

the presence of distal-extremity ischemia indicated by claudication, pain at rest, ischemic

ulcers or gangrenes and documented by non-invasive vascular testing;

exclusion of autoimmune diseases, hypercoagulable states and diabetes mellitus;

exclusion of a proximal source of emboli by echocardiography or arteriography;

consistent arteriographic findings in the clinically involved and non-involved limbs.

Investigations
Recommended tests to rule out other causes of vasculitis include a complete blood cell count; liver
function tests; determination of serum creatinine concentrations, fasting blood sugar levels and
sedimentation rate; tests for antinuclear antibody, rheumatoid factor, serologic markers for CREST
(calcinosis cutis, Raynaud phenomenon, sclerodactyly and telangiectasia) syndrome and
scleroderma, and screening for hypercoagulability. Screening for hypercoagulopathy, including
antiphosolipid antibodies and homocystein in patients with Buerger's disease, is recommended.
If a proximal source of embolization is suspected, transthoracic or transesophageal echocardiography
and arteriography should be performed. Angiographic findings include severe distal segmental
occlusive lesions. The more proximal arteries are normal. The role of modern imaging methods, such
as computerised tomography (CT) and magnetic resonance imaging (MRI) in diagnosis and
differential diagnosis of Buerger's disease still remains unsettled. In patients with leg ulceration
suspected of having TAO, the Allen test should be performed to assess the circulation in the hands
and fingers.
The histopatologic findings are most likely to be diagnostic in the acute phase of the disease, most
commonly at biopsy of a segment of a vessel with superficial thrombophlebitis. histopathological
phases, such as intermediate (subacute) and end-state (chronic) phases, have been described. The
acute-phase lesions include an occlusive, highly cellular, inflammatory thrombus with less

17

inflammation in the walls of the blood vessels. Polymorphonuclear leukocytes, microabscesses and
multinucleated giant cells may exist. When TAO occurs in unusual locations, the diagnosis should be
made only when histopathological examination identifies the acute-phase lesion. In the intermediate
phase of disease there is progressive organization of the thrombus in the arteries and veins.When
only organized thrombus and fibrosis are found in the blood vessels, the phase is considered to be
end-stage
Management and Treatment
The most effective treatment for Buerger's disease is smoking cessation. It is therefore essential that
patients diagnosed with Buerger's disease stop smoking immediately and completely in order to
prevent progression of the disease and avoid amputation. Early treatment is also important, because
Buerger's disease may provoke social problems that influence quality of life. Even smoking one or
two cigarettes per day or using smokeless tobacco (chewing tobacco or using nicotine-containing
patches) may keep the disease active. If there is no gangrene when the patient discontinues smoking,
amputation is avoided. Patients who continue smoking are at risk of amputation of fingers and toes.
Physicians must educate and counsel their patients repeatedly about the importance of discontinuing
the use of all tobacco products. Despite the very strong correlation between smoking cessation and
the decline of clinical manifestations of TAO, patients may continue to have claudication or
Raynaud's phenomenon after complete cessation of tobacco usage.
Supportive care should be directed towards maximizing blood supply to the affected limbs. Care
should be taken to avoid thermal, chemical or mechanical injury, especially from poorly fitting
footwear or minor surgery of digits, as well as fungal infection. Vasoconstriction provoked by coldexposure or drugs should be avoided.
Despite the clear role of inflammation in the pathogenesis of TAO, anti-inflammatory agents, such as
steroids, have not been shown to be of real benefit. The results of intravenous therapy with Iloprost
(a prostaglandin analogue) show that this drug is superior to aspirin in providing total pain relief at
rest and complete healing of all trophic changes. It diminishes the risk of amputation. Although
acetylsalicylic acid (aspirin) is often prescribed to patients with Buerger's disease, the benefit of this
or other orally administered anti-clotting agents has not been confirmed by controlled studies. Intraarterial thrombolytic therapy with streptokinase has been tested in some patients with gangrene or
pregangrenous lesions of the toes or feet, with some success in avoiding amputation.
For patients with TAO, arterial revascularization is usually not possible due to the diffuse segmental
involvement and distal nature of the disease. The benefit of bypass surgery to distal arteries also
remains controversial because of the high incidence of graft failure. However, if the patient has
severe ischemia and there is a distal target vessel, bypass surgery with the use of an autologous vein
should be considered.

18

Sympathectomy may be performed to decrease arterial spasm in patients with Buerger's disease. A
lapraroscopic method for sympathectomy has also been used. ympathectomy has been shown to
provide short-term pain relief and to promote ulcer healing in some patients with Buerger's disease,
but no long-term benefit has been confirmed. Spinal cord stimulator and vascular endothelial growth
factor gene therapy have been used experimentally in patients with Buerger's disease with promising
results.

19

LOWER EXTERIMITY ULCERS

Definition
Lower extremity Ulcers are wounds or open sores that will not heal or keep returning that may or
may not be painful in the lower extremity. The patient generally will has a swollen leg and may feel
burning, itching, rash, redness, brown discoloration or dry, scaly skin.
There are three most common types of leg and foot ulcers:

Venous statis ulcers

Neurotrophic (diabetic)

Arterial (ischemic ulcers)

They are typically defined by the appearance, location, and the way the borders and surrounding skin
of the ulcer look.
Etilogy

Poor circulation, often caused by arteriosclerosis

Venous insufficiency (a failure of the valves in the veins of the leg that causes congestion
and slowing of blood circulation in the veins)
Other disorders of clotting and circulation that may or may not be related to atherosclerosis
Diabetes
Renal (kidney) failure
Hypertension (treated or untreated)
Lymphedema (a buildup of fluid that causes swelling in the legs or feet)
Inflammatory diseases including vasculitis, lupus, scleroderma or other rheumatological
conditions
Other medical conditions such as high cholesterol, heart disease, high blood pressure, sickle
cell anemia, bowel disorders
History of smoking (either current or past)
Pressure caused by lying in one position for too long
Genetics (ulcers may be hereditary)
A malignancy (tumor or cancerous mass)
Infections
Certain medications

Pathophysiology
Endothelial cell dysfunction and smooth cell abnormalities develop in peripheral arteries as a
consequence of the persistent hyperglycemic state. There is a resultant decrease in endotheliumderived vasodilators leading to constriction. Further, the hyperglycemia in diabetes is associated with
an increase in thromboxane A2, a vasoconstrictor and platelet aggregation agonist, which leads to an
increased risk for plasma hypercoagulability. There is also the potential for alterations in the vascular
extracellular matrix leading to stenosis of the arterial lumen. Moreover, smoking, hypertension, and

20

hyperlipidemia are other factors that are common in diabetic patients and contribute to the
development of PAD. Cumulatively, this leads to occlusive arterial disease that results in ischemia in
the lower extremity and an increased risk of ulceration in diabetic patients.
Clinical Manifestations
History:
Claudicating pain
Rest pain, night pain
Non-healing, painful ulceration
Findings:
Cold limb or feet
Shiny, atrophic skin
Hairless
Painfull
Dependent rubor
Elevation pallor
Dry gangrene, punched-out ulcer of toes or over bony prominence

Table1. Clinical manifestation of arterial ulcers

Picture1. Example of an arterial ulcer

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Arterial Insufficiency
Diagnosis Non-Invasive Studies:
Ankle brachial index (ABI)
o

0.5 0.8: peripheral arterial occlusive disease

>1.2 suggests noncompressibility, need TBIs

<0.4: severe ischemia

Toe brachial index (TBI)

o

<30 mmHg systolic pressure: severe ischemia

Treatment
Diagnose level of arterial insufficiency:
o

Segmental pressures, pulse volume recordings

Arteriography +/- endovascular treatment

Open surgical bypass
Medication Management
Wound Care: surgical debridement, amputation;
o

Dry dressing or open to air

No ointments or creams

Minimal to no debridement

Pressure relief

Infection control

Post-Intervention:
o

Keep dry until eschar gone, may trim edges

For pink wound base, keep moist

Accommodate wound

Smoking cessation

ASA and statin therapy

Exercise

Vascular surveillance after procedures

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ARTERIAL THROMBOSIS

Introduction
Thrombosis is the formation of a blood clot inside a blood vessel, obstructing the flow of blood
through the circulatory system. When a blood vessel is injured, the body uses platelets
(thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not
injured, blood clots may form in the body under certain conditions. A clot that breaks free and begins
to travel around the body is known as an embolus.
Definition
Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial
thrombosis follows rupture of atheroma, and is therefore referred to as atherothrombosis.
Etiology

Table1. Inherited, acquired and mixed coagulation or metabolic risk factors

Pathophysiology
Our blood contains cells called platelets and proteins, known as clotting factors. Together they make
up the blood-clotting mechanism. When a blood vessel is cut, the platelets and clotting factors in
your blood mesh together to form a solid clot at the site of the wound. This clot acts as a plug to stop
the wound from bleeding.

Picture1. Thrombus formation

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Normally, the blood-clotting mechanism is only triggered when a blood vessel is damaged and
bleeds, such as when you cut yourself. However, the blood may sometimes begin to clot even when a
blood vessel has not been damaged. If this happens, a blood clot can form within a vein or artery
(thrombosis).
Clinical Manifestation
The symptoms of a thrombosis is depending on where the clot lies in your body, and it can cause:

Heart disease, atherosclerosis and angina

Heart attack

Stroke

Peripheral vascular disease (blood clots in the arteries of your legs)

Each of the above conditions has its own set of symptoms. For example, the symptoms of angina
may include:
o

Pain in your chest when you are physically active or stressed

Breathlessness or a choking feeling

Feeling sick or exhausted

Heart attack
A heart attack can occur when a blood clot completely blocks an artery that pumps blood to your
heart. If this occurs, you may experience:
o

A crushing central chest pain or mild chest discomfort

Shortness of breath

A clammy, sweaty and grey complexion

Dizziness

Nausea and vomiting

Stroke
Arterial thrombosis can cause a stroke if a blood clot is blocking an artery that supplies blood to your
brain. The symptoms of a stroke usually come on suddenly and may include:
o

Numbness or weakness down one side, ranging in severity from weakness in your hand to
complete paralysis of the whole side of your body

Weakness in your face, which can make you drool saliva

Dizziness

Difficulty talking and understanding what others are saying

Problems with balance and co-ordination

Difficulty swallowing

Peripheral vascular disease

If you have a blood clot in an artery in one of your legs (peripheral vascular disease) you may have:
o

Pain when exercising, usually in the lower half of your legs

Pain that may affect both legs, but develops in one leg before the other

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Pale, cold skin and numbness in one of your legs

Further Investigations
The tests used to diagnose blood clots in the arteries (arterial thrombosis) will depend on what
medical condition the blood clot has triggered.
Suspected cases of unstable angina and heart attacks are diagnosed using an

electrocardiograph (ECG)
Blood may also be taken to measure levels of a protein called troponin, which is released

when the heart muscle is damaged by a heart attack.

Suspected cases of stroke are diagnosed using CT scans or magnetic resonance imaging

(MRI) scans to scan the brain.

Treatment
Medication
In some cases, a type of medication called a thrombolytic can be used to dissolve blood clots and
restore the flow of blood in an artery. Examples of thrombolytic medicines include alteplase and
reteplase.
These medicines are most effective if they are used as soon as possible after a heart attack or stroke
starts.
Surgery
Surgery for arterial thrombosis involves unblocking the affected artery or re-routing blood flow
around the blockage. The type of surgery used will depend on the location and severity of your
condition.
For example, you may need heart surgery if the blood clot is in an artery that supplies blood to your
heart. Operations used to treat this include:

Coronary stent placement where a balloon is inflated in a blocked artery (angioplasty)

to allow a hollow metal tube called a stent to be placed so it can widen the artery and stop
it from becoming blocked again

Coronary artery bypass graft where a blood vessel taken from another part of the body
is used to bypass the point of the blockage

Carotid endarterectomy - a cut is made in your neck to open up the artery and remove the
fatty deposits.

Preventions
Medication

Statins to lower the blood cholesterol levels

Anticoagulant medicines (such as warfarin) or antiplatelet medicines (such as low-dose

aspirin or clopidogrel) to thin the blood and reduce the risk of clotting

Antihypertensive medicines to reduce high blood pressure, such as angiotensin-

25

converting enzyme (ACE) inhibitors

Lifestyle
You can also reduce your risk of developing arterial thrombosis and heart disease by:

Not smoking

Reducing the amount of salt you eat

Cutting down on fat (particularly saturated fat)

Eating at least five portions of fruit and vegetables a day

Doing a minimum of 150 minutes of moderate exercise a week, such as walking, cycling or
energetic housework

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ARTERIAL EMBOLISM

Definitions
An arterial embolism is a blood clot that has traveled through arteries and become stuck. This can
block or restrict blood flow. Clots generally affect the arms, legs, or feet. An embolism is anything
that obstructs blood flow. The plural of embolism is emboli. A blood clot is also known as a
thrombus.
A single clot can cause more than one embolism. Pieces may break free and get stuck in other parts
of the body. Some emboli travel to the brain, heart, and kidneys. When an artery is blocked, it can
cause tissue damage or death in the affected area. Because of this, an arterial embolism is a medical
emergency. It requires immediate treatment to prevent permanent injury.
Etiology
A number of things may cause an arterial embolism. Damage to the arteries by disease or other
health conditions is one major cause. High blood pressure may also increase the risk of an embolism.
It weakens the arterial walls. Blood may accumulate in the weakened artery and form clots.
Other common causes of blood clots include:

Smoking

Hardening of the arteries, from high cholesterol

Surgery that affects blood circulation

Injuries to the arteries

Heart disease

Atrial fibrillation

Clinical Manifestation
Symptoms may begin quickly or slowly depending on the size of the embolus and how much it
blocks the blood flow.
Symptoms of an arterial embolism in the arms or legs may include:

Cold arm or leg

Decreased or no pulse in an arm or leg

Fingers or hands feel cool

Lack of movement in the arm or leg

Muscle pain in the affected area

Muscle spasm in the affected area

Numbness and tingling in the arm or leg

Pale color of the arm or leg (pallor)

Weakness of an arm or leg

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Late symptoms:

Blisters of the skin fed by the affected artery

Shedding (sloughing) of skin

Skin erosion (ulcer)

Tissue death (necrosis; skin is dark and damaged)

Symptoms of a clot in an organ vary with the organ involved but may include:

Pain in the part of the body that is involved

Temporarily decreased organ function

Further Investigations
Physical examination
Check for a decrease in your pulse or heart rate. The lack of a local pulse may indicate tissue death.
Imaging tests:

Angiogram examines the blood vessels for abnormalities

Doppler ultrasound watches blood flow

MRI takes images of the body to locate blood clots

Laboratory tests:

Euglobulin lysis time (ELT)

Factor VIII assay

Isotope study of the affected organ

Plasminogen activator inhibitor-1 (PAI-1) activity

Platelet aggregation test

Tissue-type plasminogen activator (t-PA) levels

Treatment
The goals of treatment are to control symptoms and to improve the interrupted blood flow to the
affected area of the body. The cause of the clot, if found, should be treated to prevent further
problems.
Medications include:

Anticoagulants (such as warfarin or heparin) can prevent new clots from forming

Antiplatelet medications (such as aspirin or clopidogrel) can prevent new clots from forming

Painkillers given through a vein (by IV)

Thrombolytics (such as streptokinase) can dissolve clots

Surgical procedures include:

Bypass of the artery (arterial bypass) to create a second source of blood supply

Clot removal through a balloon catheter placed into the affected artery or through open
surgery on the artery (embolectomy)

Opening of the artery with a balloon catheter (angioplasty) with or without a stent

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RAYNAUDS SYNDROME

Definition
Raynaud's phenomenon is a condition in which cold temperatures or strong emotions cause blood
vessel spasms. This blocks blood flow to the fingers, toes, ears, and nose.
Etiology
There are two types of Raynaud's. These are:

Primary when the condition develops by itself (this is the most common type)

Secondary when it develops in association with another health condition

Most cases of secondary Raynauds are associated with conditions such as:

Diseases of the arteries (such as atherosclerosis and Buerger's disease)

Drugs that cause narrowing of arteries (such as amphetamines, certain types of betablockers, some cancer drugs, certain drugs used for migraine headaches)

Arthritis and autoimmune conditions (such as scleroderma, Sjogren syndrome, rheumatoid

arthritis, and systemic lupus erythematosus)

Repeated injury or usage (such as from typing, playing the piano, or heavy use of hand tools)

Smoking

Frostbite

Thoracic outlet syndrome

Pathophysiology
The condition occurs because your blood vessels go into a temporary spasm which blocks the flow
of blood. This causes the affected area to change colour to white, then blue and then red as the blood
flow returns.
Clinical Manifestations
Strong emotions or exposure to the cold bring on the changes.

First, the fingers, toes, ears, or nose to become white, then turn blue.

When blood flow returns, the area becomes red and then later returns to normal color.

The attacks may last from minutes to hours.

People with primary Raynaud's phenomenon have problems in the same fingers on both sides. Most
people do not have much pain.
People with Raynaud's phenomenon that is due to other medical conditions are more likely to have
pain or tingling in the fingers. The pain is rarely severe. Ulcers may form on the affected fingers if
the attacks are very bad.

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Picture1. Hands of a Reynauds syndrome patient

Further Investigations
Tests that may be done to confirm the diagnosis include:

Vascular ultrasound

Cold stimulation test for Raynaud's phenomenon

Blood tests may be done to diagnose arthritic and autoimmune conditions that may cause Raynaud's
phenomenon.
Treatment
Taking these steps may help control Raynaud's phenomenon:

Stop smoking. Smoking causes blood vessels to narrow even more.

Avoid caffeine.

Avoid taking medicines that cause blood vessels to tighten or spasm.

Keep the body warm. Avoid exposure to cold in any form. Wear mittens or gloves outdoors
and when handling ice or frozen food. Avoid getting chilled, which may happen after any
active recreational sport.

Wear comfortable, roomy shoes and wool socks. When outside, always wear shoes.

Medicines to relax the walls of the blood vessels including topical nitroglycerin cream that you rub
on your skin, calcium channel blockers, sildenafil (Viagra), and ACE inhibitors may be prescribed.

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CLAUDICATION

Definition
Claudication refers to the pain, aching or fatigue of the muscles of the buttocks, thigh and/or calf that
occurs with exertion. This pain or cramping is caused by poor circulation due to blockage of the
arteries of the lower extremity. It may occur in one or both legs, depending on where the blockage
occurs. The pain is brought on by walking or exercise and disappears with rest. Claudication can
range from being a mild nuisance to a disabling limitation.
Epidemiology
Nearly nine million people, or 12 percent of the U.S. population, experience occasional claudication.
This increases to 20 percent in people over the age of 70.
Pathophysiology
Claudication is caused by atherosclerosis in the lower extremities that is known as peripheral arterial
disease (PAD). Atherosclerosis is the hardening and narrowing of the arteries over time through the
build up of fatty deposits, called plaque, along the artery walls. As plaques grow, they increasingly
block the flow of blood through the arteries. Artery blockages that cause claudication may be in the
abdomen, pelvis, groin, thigh and/or the calf.
Risk Factors
Risk factors for claudication are the same as those for atherosclerosis, hardening and narrowing of
the arteries due to the buildup of fatty deposits called plaque:

Age

Smoking

Diabetes

Overweight or obesity

Sedentary lifestyle

High cholesterol

High blood pressure

Family history of atherosclerosis or claudication

Clinical Manifestation

Pain in the buttocks, thigh and/or calf, occurring with walking

Tired or burning sensation in the buttocks, thigh and/or calf with walking

Diagnosis

Auscultation: The presence of a bruit, or whooshing sound, in the arteries of the legs is
confirmed using a stethoscope.

Ankle-brachial index (ABI): The systolic blood pressure in the ankle is divided by the

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systolic pressure at the arm.

Doppler ultrasound: This form of ultrasound can measure the direction and velocity of blood
flow through the vessels.

CT angiography

Magnetic resonance angiography (MR angiography

Angiogram

Treatment
Reducing risk factors
Treatment for claudication usually focuses on the reduction of risk factors associated with
atherosclerosis.

Smoking cessation

Walking, usually 30 minutes a day

Medication and lifestyle changes aimed at reducing cholesterol, blood pressure and bloodsugar levels

Medication, such as aspirin, to prevent heart attack and stroke

Medication to improve walking distance, such as cilostazol (Pletal)

Diet low in saturated fats

Endovascular treatments
Minimally invasive endovascular treatments may be recommended if claudication interferes with a
patient's work or lifestyle, and if the diseased arteries are likely to improve with such treatment. The
Vascular Center has the full complement of endovascular options available. The option
recommended depends on the location and severity of the arterial blockages. In general, insertion of
a catheter through a needle puncture, under local anesthesia, into the arteries of the groin will allow
access to the diseased portion of the artery. Some of the endovascular procedures used to treat
claudication include:

Angioplasty: A tiny balloon is inserted through a puncture in the groin. The balloon is
inflated using a saline solution one or more times to expand the narrowed or occluded artery.
o

Cutting balloon: A balloon imbedded with micro-blades is used to dilate the

diseased area. The blades cut the surface of the plaque, reducing the force necessary
to dilate the vessel.

Cold balloon (CryoPlasty): Instead of using saline, the balloon is inflated using
nitrous oxide. The gas freezes the plaque during the dilatation. The procedure is
easier on the artery; the growth of the plaque is halted; and little scar tissue is
generated.

Stents: Metal mesh tubes are expanded and left in place to provide scaffolding for an
artery that has been opened using a balloon angioplasty.
o

Balloon-expanded: A balloon is used to expand the stent. These stents are stronger,

32

but less flexible.

o

Self-expanding: Compressed stents are delivered to the diseased site. They expand
upon release and are left in place to hold open the artery. These stents are more
flexible.

Laser atherectomy: Small bits of plaque are vaporized by the tip of a laser probe.

Directional atherectomy: A catheter with a rotating cutting blade is used to physically

remove plaque from the artery, opening the flow channel.

Recovery from these procedures takes one or two days, and most of these procedures are done on an
outpatient basis.
Surgical treatments Patients who are severely limited by their claudication, but are not good
candidates for minimally invasive endovascular procedures, may be given the option of surgical
treatment. This treatment often involves bypass around the diseased segment with either a vein
from the patient or a synthetic graft. Hospitalization after a bypass operation varies from a few
days to more than a week. Recovery from surgery may take several weeks.

33