Study Guide 7

1. Describe the structure of capillaries:

 Describe how they differ from arteries and veins in structure
Capillaries, the smallest of blood vessels, have diameters of 5– 10 μm, and form the U-turns that connect the
arterial outflow to the venous return. Since red blood cells have a diameter of 8 μm, they must often fold on
themselves in order to pass single file through the lumens of these vessels. This network forms an enormous
surface area to make contact with the body’s cells. The flow of blood from a metarteriole through capillaries
and into a postcapillary venule (venule that receives blood from a capillary) is called the microcirculation of the
body. The structure of capillaries is well suited to their function as exchange vessels because they lack both a
tunica media and externa. Because capillary walls are composed of only a single layer of endothelial cells and a
basement membrane, a substance in the blood must pass through just one cell layer to reach the interstitial
fluid and tissue cells. Exchange of materials occurs only through the walls of capillaries and the beginning of
venules; the walls of arteries, arterioles, most venules, and veins present too thick a barrier.
  Describe the functions of capillaries
The primary function of capillaries is the exchange of substances between the blood and interstitial fluid.
Because of this, these thin-walled vessels are referred to as exchange vessels. Capillaries are found near almost
every cell in the body, but their number varies with the metabolic activity of the tissue they serve. Body tissues
with high metabolic requirements, such as muscles, the brain, the liver, the kidneys, and the nervous system,
use more O2 and nutrients and thus have extensive capillary networks. Tissues with lower metabolic
requirements, such as tendons and ligaments, contain fewer capillaries. Capillaries are absent in a few tissues,
such as all covering and lining epithelia, the cornea and lens of the eye, and cartilage.

 Describe how their structure reflects their function

Capillaries form extensive branching networks that increase the surface area available for rapid exchange of
materials. In most tissues, blood flows through only a small part of the capillary network when metabolic needs
are low. However, when a tissue is active, such as contracting muscle, the entire capillary network fills with
blood. Capillary walls are composed of only a single layer of endothelial cells and a basement membrane,
hence substance in the blood must pass through just one cell layer to reach the interstitial fluid and tissue cells.

 Describe the structures within capillaries that allow substances to pass from capillary lumen to interstitial
space, and from interstitial space into capillary. Tortora-page 746
Diffusion, the most widely-used mechanism, allows the flow of small molecules across capillaries such as glucose
and oxygen from the blood into the tissues and carbon dioxide from the tissue into the blood. The process
depends on the difference of gradients between the interstitium and blood, with molecules moving to low-
concentrated spaces from high-concentrated ones. In sinusoids, however, the intercellular clefts are so large
that they allow even proteins and blood cells to pass through their walls. In red bone marrow, blood cells are
formed (hemopoiesis) and then enter the bloodstream through sinusoids. In contrast to sinusoids, the capillaries
of the brain allow only a few substances to move across their walls. Most areas of the brain contain continuous
capillaries; however, these capillaries are very “tight.” The endothelial cells of most brain capillaries are sealed
together by tight junctions. The resulting blockade to movement of materials into and out of brain capillaries is
known as the blood–brain barrier. In brain areas that lack the blood–brain barrier, for example, the
hypothalamus, pineal gland, and pituitary gland, materials undergo capillary exchange more freely.
Transcytosis is the mechanism whereby large, lipid-insoluble substances cross the capillary membranes. The
substance to be transported is endocytosed by the endothelial cell into a lipid vesicle which moves through the
cell and is then exocytosed to the other side. For example, the hormone insulin (a small protein) enters the
bloodstream by transcytosis, and certain antibodies (also proteins) pass from the maternal circulation into the
fetal circulation by transcytosis.
Bulk flow is used by small, lipid-insoluble solutes in water to cross the capillary wall. The movement of materials
across the wall is dependent on pressure and is bi-directional depending on the net filtration pressure derived
from the four Starling forces that modulate capillary dynamics. Pressure-driven movement of fluid and solutes
from blood capillaries into interstitial fluid is called filtration. Pressure-driven movement from interstitial fluid
into blood capillaries is called reabsorption. Two pressures promote filtration: blood hydrostatic pressure (BHP),
the pressure generated by the pumping action of the heart, and interstitial fluid osmotic pressure. The main
pressure promoting reabsorption of fluid is blood colloid osmotic pressure. The balance of these pressures,
called net filtration pressure (NFP), determines whether the volumes of blood and interstitial fluid remain
steady or change. Overall, the volume of fluid and solutes reabsorbed normally is almost as large as the volume
filtered. This near equilibrium is known as Starling’s law of the capillaries. Within vessels, the hydrostatic
pressure is due to the pressure that water in blood plasma exerts against blood vessel walls. The blood
hydrostatic pressure (BHP) is about 35 millimeters of mercury (mmHg) at the arterial end of a capillary, and
about 16 mmHg at the venous end. BHP “pushes” fluid out of capillaries into interstitial fluid. The opposing
pressure of the interstitial fluid, called interstitial fluid hydrostatic pressure (IFHP), “pushes” fluid from
interstitial spaces back into capillaries. However, IFHP is close to zero. For discussion we assume that IFHP equals
0 mmHg all along the capillaries. The difference in osmotic pressure across a capillary wall is due almost entirely
to the presence in blood of plasma
proteins, which are too large to
pass through either fenestrations
or gaps between endothelial cells.
Blood colloid osmotic pressure
(BCOP) is a force caused by the
colloidal suspension of these large
proteins in plasma that averages
26 mmHg in most capillaries. The
effect of BCOP is to “pull” fluid
from interstitial spaces into
capillaries. Opposing BCOP is
interstitial fluid osmotic pressure
(IFOP), which “pulls” fluid out of
capillaries into interstitial fluid.
Normally, IFOP is very small—0.1–
5 mmHg—because only tiny
amounts of protein are present in
interstitial fluid. The small amount
of protein that leaks from blood
plasma into interstitial fluid does
not accumulate there because it
passes into lymph in lymphatic
capillaries and is eventually
returned to the blood. For
discussion, we can use a value of 1
mmHg for IFOP.

2. Explain the regulation of blood flow through capillaries, via the precapillary sphincter.
Throughout the body, capillaries function as part of a capillary bed, a network of 10–100 capillaries that arises
from a single metarteriole. In most parts of the body, blood can flow through a capillary network from an
arteriole into a venule as follows:
Capillaries. In this route, blood flows from an arteriole into capillaries and then into venules (postcapillary
venules). As noted earlier, at the junctions between the metarteriole and the capillaries are rings of smooth
muscle fibers called precapillary sphincters that control the flow of blood through the capillaries. When the
precapillary sphincters are relaxed (open), blood flows into the capillaries; when precapillary sphincters contract
(close or partially close), blood flow through the capillaries ceases or decreases. Typically, blood flows
intermittently through capillaries due to alternating contraction and relaxation of the smooth muscle of
metarterioles and the precapillary sphincters. This intermittent contraction and relaxation, which may occur 5 to
10 times per minute, is called vasomotion. In part, vasomotion is due to chemicals released by the endothelial
cells; nitric oxide is one example. At any given time, blood flows through only about 25% of the capillaries.
Thoroughfare channel. The proximal end of a metarteriole is surrounded by scattered smooth muscle fibers
whose contraction and relaxation help regulate blood flow. The distal end of the vessel has no smooth muscle; it
resembles a capillary and is called a thoroughfare channel. Such a channel provides a direct route for blood from
an arteriole to a venule, thus bypassing capillaries.

3. Describe the types of capillaries:

 Continuous
The body contains three different types of capillaries: continuous capillaries, fenestrated capillaries, and
sinusoids. Most capillaries are continuous capillaries, in which the plasma membranes of endothelial cells form
a continuous tube that is interrupted only by intercellular clefts, gaps between neighboring endothelial cells.
Continuous capillaries are found in the central nervous system, lungs, muscle tissue, and the skin.
 Fenestrated
Other capillaries of the body are fenestrated capillaries (fenestr- = window). The plasma membranes of the
endothelial cells in these capillaries have many fenestrations, small pores (holes) ranging from 70 to 100 nm in
diameter. Fenestrated capillaries are found in the kidneys, villi of the small intestine, choroid plexuses of the
ventricles in the brain, ciliary processes of the eyes, and most endocrine glands.
 Sinusoidal
Sinusoids (sinus = curve) are wider and more winding than other capillaries. Their endothelial cells may have
unusually large fenestrations. In addition to having an incomplete or absent basement membrane, sinusoids
have very large intercellular clefts that allow proteins and in some cases even blood cells to pass from a tissue
into the bloodstream. For example, newly formed blood cells enter the bloodstream through the sinusoids of
red bone marrow. In addition, sinusoids contain specialized lining cells that are adapted to the function of the
tissue. Sinusoids in the liver, for example, contain phagocytic cells that remove bacteria and other debris from
the blood. The spleen, anterior pituitary, and parathyroid and adrenal glands also have sinusoids.
Study Guide 8
1. Explain the Dynamics of Capillary Exchange (using diagram):

 Net Filtration Pressure

Two pressures promote filtration: blood hydrostatic pressure (BHP), the pressure generated by the pumping
action of the heart, and interstitial fluid osmotic pressure. The main pressure promoting reabsorption of fluid is
blood colloid osmotic pressure. The balance of these pressures, called net filtration pressure (NFP), determines
whether the volumes of blood and interstitial fluid remain steady or change. Overall, the volume of fluid and
solutes reabsorbed normally is almost as large as the volume filtered. This near equilibrium is known as
Starling’s law of the capillaries.

 Blood Hydrostatic Pressure

The hydrostatic pressure in the capillaries tends to force fluid and its dissolved substances through the capillary
pores into the interstitial spaces. Conversely, osmotic pressure caused by the plasma proteins (called colloid
osmotic pressure) tends to cause fluid movement by osmosis from the interstitial spaces into the blood.
Blood hydrostatic pressure (BHP), the pressure generated by the pumping action of the heart. Within vessels,
the hydrostatic pressure is due to the pressure that water in blood plasma exerts against blood vessel walls. The
blood hydrostatic pressure (BHP) is about 35 millimeters of mercury (mmHg) at the arterial end of a capillary,
and about 16 mmHg at the capillary’s venous end. BHP “pushes” fluid out of capillaries into interstitial fluid.
 Interstitial Hydrostatic Pressure
The opposing pressure of the interstitial fluid, called interstitial fluid hydrostatic pressure (IFHP), “pushes” fluid
from interstitial spaces back into capillaries. However, IFHP is close to zero.
 Blood Colloid Oncotic Pressure
The capillary plasma colloid osmotic pressure, which tends to cause osmosis of fluid inward through the capillary
membrane. The main pressure promoting reabsorption of fluid is blood colloid osmotic pressure.
The difference in osmotic pressure across a capillary wall is due almost entirely to the presence in blood of
plasma proteins, which are too large to pass through either fenestrations or gaps between endothelial cells.
Blood colloid osmotic pressure (BCOP) is a force caused by the colloidal suspension of these large proteins in
plasma that averages 26 mmHg in most capillaries. The effect of BCOP is to “pull” fluid from interstitial spaces
into capillaries.
 Interstitial Colloid Osmotic Pressure
The interstitial fluid colloid osmotic pressure, which tends to cause osmosis of fluid outward through the
capillary membrane.
Opposing BCOP is interstitial fluid osmotic pressure (IFOP), which “pulls” fluid out of capillaries into interstitial
fluid. Normally, IFOP is very small—0.1–5 mmHg—because only tiny amounts of protein are present in
interstitial fluid.
2. Explain:
 The factors that determine all of these pressures
Capillary Hydrostatic Pressure (PC)
This pressure drives fluid out of the capillary (i.e., filtration), and is highest at the arteriolar end of the capillary
and lowest at the venular end. Depending upon the organ, the pressure may drop along the length of the
capillary by 15-30 mmHg (axial or longitudinal pressure gradient). The axial gradient favors filtration at the
arteriolar end (where PC is greatest) and reabsorption at the venular end of the capillary (where P C is the lowest).
The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the
ratio of post-to-precapillary resistances (R V/RA). An increase in either arterial or venous pressure will increase
capillary pressure; however, a given change in PA is only about one-fifth as effective in changing P C as the same
absolute change in PV. Because venous resistance is relatively low, changes in P V are readily transmitted back to
the capillary, and conversely, because arterial resistance is relatively high, changes in P A are poorly transmitted
downstream to the capillary. Therefore, PC is much more influenced by changes in PV than by changes in PA.
Furthermore, PC is increased by precapillary vasodilation (particularly by arteriolar dilation), whereas precapillary
vasoconstriction decreases PC.  Venous constriction increases PC, whereas venous dilation decreases PC.
Tissue (Interstitial) Pressure (Pi)
This hydrostatic pressure is determined by the interstitial fluid
volume and the compliance of the tissue interstitium, which is
defined as the change in volume divided by the change in
pressure. The more fluid that filters into the interstitium, the
greater the volume of the interstitial space (Vi) and the
hydrostatic pressure within that space(Pi). In some organs, the
interstitial compliance is low, which means that small increases in
interstitial volume lead to large increases in pressure. Examples of
this include the brain and kidney, which are encased by rigid bone
(brain) or by a capsule (kidney). In contrast, soft tissues such as skin, muscle and lung have a high compliance
and therefore the interstitial space can undergo a large expansion with a relatively small increase in pressure. As
interstitial volume increases, interstitial pressure increases, which can limit the amount of filtration into the
interstitium because this pressure opposes the capillary hydrostatic pressure. In other words, as the hydrostatic
pressure gradient (PC - Pi) decreases owing to the rise in interstitial pressure, fluid filtration will be attenuated.
However, large increases in tissue interstitial pressure can lead to tissue damage and cellular death. Normally,
Pi is near 0.
Capillary Plasma Oncotic Pressure (ΠC)
Because the capillary barrier is readily permeable to ions, the osmotic pressure within the capillary is principally
determined by plasma proteins that are relatively impermeable. Therefore, instead of speaking of "osmotic"
pressure, this pressure is referred to as the "oncotic" pressure or "colloid osmotic" pressure because it is
generated by colloids. Albumin generates about 70% of the oncotic pressure. This pressure is typically 25-30
mmHg. The oncotic pressure increases along the length of the capillary, particularly in capillaries having high
net filtration (e.g., in renal glomerular capillaries), because the filtering fluid leaves behind proteins leading to an
increase in protein concentration.
Tissue (interstitial) Oncotic Pressure (Πi)
The oncotic pressure of the interstitial fluid depends on the interstitial protein concentration and the reflection
coefficient of the capillary wall. The more permeable the capillary barrier is to proteins, the higher the
interstitial oncotic pressure. This pressure is also determined by the amount of fluid filtration into the
interstitium. For example, increased capillary filtration decreases interstitial protein concentration and reduces
the oncotic pressure. A reduction in the interstitial oncotic pressure increases the net oncotic pressure across
the capillary endothelium (πC - πi), which opposes filtration and promotes reabsorption thereby serving as a
mechanism to limit capillary filtration. In a "typical" tissue, tissue oncotic pressure is about 5 mmHg (i.e., much
lower than capillary plasma oncotic pressure).
 How the balance of these pressures results in a net filtration pressure
The net filtration pressure (NFP) represents the interaction of the hydrostatic and osmotic pressures, driving
fluid out of the capillary. It is equal to the difference between the CHP and the BCOP. Since filtration is, by
definition, the movement of fluid out of the capillary, when reabsorption is occurring, the NFP is a negative
number. Filtration, the movement of fluid out of the capillaries, is driven by the CHP. Reabsorption, the influx of
tissue fluid into the capillaries, is driven by the BCOP. Filtration predominates in the arterial end of the capillary;
in the middle section, the opposing pressures are virtually identical so there is no net exchange, whereas
reabsorption predominates at the venule end of the capillary.
  Why oedema does not occur in tissues normally
The Role of Lymphatic Capillaries
Since overall CHP is higher than BCOP, it is inevitable that more net fluid will exit the capillary through filtration
at the arterial end than enters through reabsorption at the venous end. Considering all capillaries over the
course of a day, this can be quite a substantial amount of fluid: Approximately 24 liters per day are filtered,
whereas 20.4 liters are reabsorbed. This excess fluid is picked up by capillaries of the lymphatic system. These
extremely thin-walled vessels have copious numbers of valves that ensure unidirectional flow through ever-
larger lymphatic vessels that eventually drain into the subclavian veins in the neck. An important function of the
lymphatic system is to return the fluid (lymph) to the blood. Lymph may be thought of as recycled blood plasma.

3. Explain the mechanisms that lead to oedema (with examples):

 Increase hydrostatic pressure within capillaries
Increased capillary blood pressure causes more fluid to be filtered from capillaries. Hence leading to increased
filtration causing oedema.

 Increased intravascular fluid volume

The intravascular compartment contains fluid (i.e., blood) within the cardiac chambers and vascular system of
the body. In some cases, total fluid volume increases in the body so that both intravascular and extravascular
compartments increase in volume. This can occur, for example, when the kidneys fail to excrete sufficient
amounts of sodium and water.
As fluid shifts into the interstitial space, intravascular volume is depleted. Intravascular volume depletion
activates the renin-angiotensin-aldosterone- vasopressin (ADH) system, resulting in renal sodium retention. By
increasing osmolality, renal sodium retention triggers water retention by the kidneys and helps maintain plasma
volume. Increased renal sodium retention also may be a primary cause of fluid overload and hence edema.
Excessive exogenous sodium intake may also contribute.
  Decreased plasma oncotic pressure
Decreased concentration of plasma proteins lowers the blood colloid osmotic pressure. Inadequate synthesis or
dietary intake or loss of plasma proteins is associated with liver disease, burns, malnutrition.
Less often, edema results from decreased movement of fluid out of the interstitial space into the capillaries due
to lack of adequate plasma oncotic pressure as in nephrotic syndrome, protein-losing enteropathy, liver failure,
or starvation.

 Increased capillary permeability

Increased permeability of capillaries raises interstitial fluid osmotic pressure by allowing some plasma proteins
to escape. Such leakiness may be caused by the destructive effects of chemical, bacterial, thermal, or mechanical
agents on capillary walls. Increased capillary permeability occurs in infections or as the result of toxin or
inflammatory damage to the capillary walls.
  Lymphatic blockage
Because lymphatic drainage represents the major route for removal of interstitial fluid (and macromolecules)
formed by capillary filtration, dysfunction of lymphatic vessels causes the development of edema and can
exacerbate edema induced by other causes. Lymphedema occurs with physical obstruction of the lymphatic
vessel lumen (either by extramural forces exerted by tumors or intraluminal obstruction by metastasizing tumor
cells), destruction or regression of existing lymphatics, incompetence of the valves between lymphangions,
paralysis of lymphatic muscle, reduced tissue motion, diminished arterial pulsations or venomotion, or by
elevated venous pressure at the drainage points where lymphatics empty into the systemic blood circulation.

4. Describe and differentiate local and systemic oedema.

Systemic oedema: the causes of this edema are generalized to the whole body, can cause edema in multiple
organs and peripherally. It can be caused by either systemic disease that affect the various organ systems of the
body. Generalized edema is most commonly caused by
 Heart failure
 Liver failure
 Kidney disorders (especially nephrotic syndrome)
Local edema is the edema that will occur in specific areas. Certain places develop edema through specific
mechanisms. The most common local conditions that cause oedema are varicose veins and thrombophlebitis
(inflammation of the veins) of the deep veins of the leg. These conditions can cause inadequate pumping of the
blood by the veins (venous insufficiency). The resulting increased back-in pressure the veins forces fluid to stay
in the extremities (especially in the ankles and feet). The excess fluid then leaks into the interstitial tissue spaces,
causing oedema. Localized edema is most commonly caused by
  DVT or another venous disorder or venous obstruction (e.g., by tumor)
 Infection
 Angioedema
 Lymphatic obstruction
Chronic venous insufficiency may involve one or both legs.

5. Describe and differentiate congestion from hyperaemia.

Study Guide 9
1. Explain the pathogenesis of varicose veins:
 Aetiology
The veins have one-way valves so that the blood can travel in only one direction. If the walls of the vein become
stretched and less flexible (elastic), the valves may get weaker. A weakened valve can allow blood to leak
backward and eventually flow in the opposite direction. When this occurs, blood can accumulate in the vein(s),
which then become enlarged and swollen.
 Figure A  shows a normal vein with a
properly working valve.  In Figure B,
the varicose vein has a faulty valve, the
walls of the vein are thin and
stretched.
Image credit: National Heart Lung and
Blood Institute.
The veins furthest from the heart are
most often affected, such as those in
the legs. This is because gravity makes
it harder for blood to flow back to the
heart. Any condition that puts pressure
on the abdomen has the potential to
cause varicose veins; for instance,
pregnancy, constipation and, in rare
cases, tumors.

 Predisposing/ risk factors

Risk factors
Experts are not sure why the walls of veins stretch or why the valves become faulty. In many cases, it occurs for
no clear reason. However, some potential risk factors include:
 menopause
 pregnancy
 being over 50 years
 standing for long periods
 family history of varicose veins
 obesity
The following risk factors are linked to a higher risk of having varicose veins:
 Gender: Varicose veins affect women more often than males. It may be that female hormones relax
veins. If so, taking birth control pills or hormone therapy (HT) might contribute.
 Genetics: Varicose veins often run in families.
 Obesity: Being overweight or obese increases the risk of varicose veins.
 Age: The risk increases with age, due to wear and tear on vein valves.
 Some jobs: An individual who has to spend a long time standing at work may have a higher chance of
varicose veins.

 Common sites for varicose veins

This topic focuses primarily on varicose veins in the legs, but sometimes varicose veins form in other parts of the
body. Hemorrhoids are a type of varicose vein that develops in the rectum. Varicoceles occur in the testicles and
may be linked to infertility in men. Varicose veins can also develop in the esophagus, stomach, or liver. Other
vein problems that affect smaller blood vessels are telangiectasia and spider veins. Veins close to the surface of
the legs, especially the saphenous vein, are highly susceptible to varicosities; deeper veins are not as vulnerable
because surrounding skeletal muscles prevent their walls from stretching excessively. Varicose veins in the anal
canal are referred to as hemorrhoids. Esophageal varices result from dilated veins in the walls of the lower part
of the esophagus and sometimes the upper part of the stomach. Bleeding esophageal varices are life-
threatening and are usually a result of chronic liver disease.

 Mechanism of formation
Veins have one-way valves inside them that open and close to keep blood flowing toward the heart. However,
weakened or damaged valves or walls in the veins can cause blood to pool and even flow backwards. This is
called reflux. The veins may grow larger and become distorted, resulting in varicose veins.
Leaky venous valves can cause veins to become dilated and twisted in appearance, a condition called varicose
veins or varices (singular-varix). The condition may occur in the veins of almost any body part, but it is most
common in the esophagus, anal canal, and superficial veins of the lower limbs. Those in the lower limbs can
range from cosmetic problems to serious medical conditions. The valvular defect may be congenital or may
result from mechanical stress (prolonged standing or pregnancy) or aging. The leaking venous valves allow the
backflow of blood from the deep veins to the less efficient superficial veins, where the blood pools. This creates
pressure that distends the vein and allows fluid to leak into surrounding tissue. As a result, the affected vein and
the tissue around it may become inflamed and painfully tender. Veins close to the surface of the legs, especially
the saphenous vein, are highly susceptible to varicosities; deeper veins are not as vulnerable because
surrounding skeletal muscles prevent their walls from stretching excessively. Bleeding esophageal varices are
life-threatening and are usually a result of chronic liver disease.

 Complications
Any condition in which proper blood flow is undermined has a risk of complications. However, in the majority of
cases, varicose veins have no complications. If complications do occur, they may include:
 Bleeding.
 Thrombophlebitis: Blood clots in the vein of the leg cause inflammation of the vein.
 Chronic venous insufficiency – the skin does not exchange oxygen, nutrients, and waste products with
the blood properly because the blood flow is weak. Chronic venous insufficiency is not caused by
varicose veins, but the two entities are closely related.
People with chronic venous insufficiency may develop varicose eczema, lipodermatosclerosis (hard and tight
skin), and venous ulcers. Venous ulcers classically form around ankles and are often preceded by a discolored
area. It is important to get medical evaluation for chronic venous insufficiency.
Several treatment options are available for varicose veins in the lower limbs. Elastic stockings (support hose)
may be used for individuals with mild symptoms or for whom other options are not recommended.
Sclerotherapy involves injection of a solution into varicose veins that damages the tunica interna by producing a
harmless superficial thrombophlebitis (inflammation involving a blood clot). Healing of the damaged part leads
to scar formation that occludes the vein. Radiofrequency endovenous occlusion involves the application of
radiofrequency energy to heat up and close off varicose veins. Laser occlusion uses laser therapy to shut down
veins. In a surgical procedure called stripping, veins may be removed. In this procedure, a flexible wire is
threaded through the vein and then pulled out to strip (remove) it from the body.
Surgery
If varicose veins are large, they may need to be removed surgically. This is usually done under general
anesthetic. In most cases, the patient can go home the same day – if surgery is required on both legs, they may
need to spend one night in hospital.
Laser treatments are often used to close off smaller veins, and also spider veins. Strong bursts of light are
applied to the vein, which gradually fades and disappears.
Ligation and stripping
Two incisions are made, one near the patient’s groin at the top of the target vein, and the other is made further
down the leg, either at the ankle or knee. The top of the vein is tied up and sealed. A thin, flexible wire is
threaded through the bottom of the vein and then pulled out, taking the vein with it. Ligation and stripping can
sometimes result in bruising, bleeding, and pain. In extremely rare occasions, there may be deep vein
thrombosis. After surgery, most patients will need 1-3 weeks to recover before going back to work and other
normal duties. During recovery time, compression stockings are worn.
Sclerotherapy
A chemical is injected into small and medium-sized varicose veins, which scars and closes them. A few weeks
later, they should fade. A vein may need to be injected more than once.
Radiofrequency ablation
A small incision is made either above or below the knee, and with the help of an ultrasound scan; a narrow tube
(catheter) is threaded into the vein.
The doctor inserts a probe into the catheter, which emits radiofrequency energy. The radiofrequency energy
heats up the vein, causing its walls to collapse, effectively closing it and sealing it shut. This procedure is
preferred for larger varicose veins. Radiofrequency ablation is usually done with a local anesthetic.
Endovenous laser treatment
A catheter is inserted into the patient’s vein. A small laser is threaded through the catheter and positioned at
the top of the target vein; it delivers short energy bursts that heat up the vein, sealing it shut.
With the aid of an ultrasound scan, the doctor threads the laser all the way up the vein, gradually burning and
sealing all of it. This procedure is done under local anesthetic. There may be some nerve injury, it is usually brief.
Transilluminated powered phlebectomy
An endoscopic transilluminator (special light) is threaded through an incision under the skin so that the doctor
can see which veins need to be taken out. The target veins are cut and removed with a suction device through
the incision. A general or local anesthetic may be used for this procedure.

2. Explain the pathogenesis of thrombophlebitis:

 Aetiology
Thrombophlebitis is an inflammatory process that causes a blood clot to form and block one or more veins,
usually in your legs. The affected vein might be near the surface of your skin (superficial thrombophlebitis) or
deep within a muscle (deep vein thrombosis). Causes include trauma; an injury to a vein, surgery or being
immobile for long periods, such as during an injury or a hospital stay (prolonged inactivity), an inherited blood-
clotting disorder.
 Predisposing/ risk factors
Your risk of thrombophlebitis increases if you:
 Are inactive for a prolonged period, either you're confined to bed or traveling by car/plane for a long period
 Have varicose veins, which are a common cause of superficial thrombophlebitis
 Have a pacemaker or a thin, flexible tube (catheter) in a central vein, for treatment of a medical condition,
which may irritate the blood vessel wall and decrease blood flow. Internal trauma to a vein due to an
indwelling catheter or a difficult phlebotomy procedure can also cause venous injury and inflammation.
 Are pregnant or have just given birth
 Use birth control pills or hormone replacement therapy, which can make your blood more likely to clot; Both
estrogens and progestogens are implicated in promoting thrombosis, even with low-dose therapy.
 Have a family history of a blood-clotting disorder or a tendency to form blood clots
 Have had previous episodes of thrombophlebitis
 Are older than 60
 Are overweight or obese
 Have cancer
 Smoke
If you have one or more risk factors, discuss prevention strategies with your doctor before taking long flights or
road trips or if you're planning to have elective surgery, recovery from which will require you not to move much.
 Mechanism of formation
Thrombophlebitis, inflammation of a vein coupled with formation of a blood clot (thrombus) that adheres to the
wall of the vessel. The inflammation may precede or follow formation of the clot. Because movement of the
blood through veins depends upon contractions of the muscles, prolonged inactivity (such as bed rest after a
surgical procedure or during convalescence from a serious illness) may lead to insufficient movement of the
blood through the veins, with resultant formation of clots and inflammation. The condition most often affects
the legs. There may be pain at the site of the blockage or throbbing pain throughout the leg. If the affected vein
is near the surface, it feels like a cord to the touch.
 Complications
Pulmonary embolism
Complications from superficial thrombophlebitis are rare.
However, if you develop DVT, the risk of serious
complications increases. Complications might include:
 Pulmonary embolism. If part of a deep vein clot
becomes dislodged, it can travel to your lungs,
where it can block an artery (embolism) and
become potentially life-threatening.
 Post-phlebetic syndrome. This condition, also
known as post-thrombotic syndrome, can
develop months or even years after you've
had DVT. Post-phlebetic syndrome can cause
lasting and possibly disabling pain, swelling, and a
feeling of heaviness in the affected leg.
Laboratory Studies (Plasma D-Dimers):  Plasma D-dimers are the most recent addition to the noninvasive tests
for VTE (Venous Thromboembolism). They are a product of fibrin degradation, detectable in the blood after a
blood clot is degraded by fibrinolysis. D-dimer assays are fast, accurate, and readily available but vary in their
sensitivity and specificity. While D-dimer assays have a high negative predictive value of around 94%, a positive
result is not diagnostic since a number of conditions, such as impaired renal function, ongoing blood loss,
pregnancy, and atrial fibrillation, can cause D-dimer levels to rise. In addition, an electrocardiography may be
performed to rule out a myocardial infarction and an echocardiography done to detect any signs of right-sided heart
strain.
3. Explain phlebothrombosis (Deep vein thrombosis):
 Virchow’s Triad
Rudolf Virchow described 3 factors that are critically important in the development of venous thrombosis: (1)
venous stasis, (2) activation of blood coagulation, and (3) vein damage. These factors have come to be known
as the Virchow triad.
Venous stasis can occur as a result of anything that slows or obstructs the flow of venous blood. This results in
an increase in viscosity and the formation of microthrombi, which are not washed away by fluid movement; the
thrombus that forms may then grow and propagate. Endothelial (intimal) damage in the blood vessel may be
intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult. A
hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result
from an increase in circulating tissue activation factor, combined with a decrease in circulating
plasma antithrombin and fibrinolysins.

 Predisposing/ risk factors

Many factors can increase your risk of developing deep vein thrombosis (DVT). The more you have, the greater
your risk of DVT. Risk factors include:
 Inheriting a blood-clotting disorder. Some people inherit a disorder that makes their blood clot more easily.
This condition on its own might not cause blood clots unless combined with one or more other risk factors.
 Prolonged bed rest, such as during a long hospital stay, or paralysis. When your legs remain still for long
periods, your calf muscles don't contract to help blood circulate, which can increase the risk of blood clots.
 Injury or surgery. Injury to your veins or surgery can increase the risk of blood clots.
 Pregnancy. Pregnancy increases the pressure in the veins in your pelvis and legs. Women with an inherited
clotting disorder are especially at risk. The risk of blood clots from pregnancy can continue for up to six
weeks after you have your baby.
 Birth control pills (oral contraceptives) or hormone replacement therapy. Both can increase your blood's
ability to clot.
 Being overweight or obese. Being overweight increases the pressure in the veins in your pelvis and legs.
 Smoking. Smoking affects blood clotting and circulation, which can increase your risk of DVT.
 Cancer. Some forms of cancer increase substances in your blood that cause your blood to clot. Some forms
of cancer treatment also increase the risk of blood clots.
 Heart failure. This increases your risk of DVT and pulmonary embolism. Because people with heart failure
have limited heart & lung function, the symptoms caused by even a small pulmonary embolism are more
noticeable.
 Inflammatory bowel disease. Bowel diseases, e.g. Crohn's disease or ulcerative colitis, increases risk of DVT.
 A personal or family history of deep vein thrombosis or pulmonary embolism. If you or someone in your
family has had one or both of these, you might be at greater risk of developing a DVT.
 Age. Being older than 60 increases your risk of DVT, though it can occur at any age.
 Sitting for long periods of time, such as when driving or flying. When your legs remain still for hours, your
calf muscles don't contract, which normally helps blood circulate. Blood clots can form in the calves of your
legs if your calf muscles don't move for long periods.

 Mechanism of formation
Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in your
body, usually in your legs. Deep vein thrombosis can cause leg pain or swelling, but also can occur with no
symptoms. Deep vein thrombosis can develop if you have certain medical conditions that affect how your blood
clots. It can also happen if you don't move for a long time, such as after surgery or an accident, or when you're
confined to bed.
Deep vein thrombosis can be very serious because blood clots in your veins can break loose, travel through your
bloodstream and lodge in your lungs, blocking blood flow (pulmonary embolism).
The blood clots of deep vein thrombosis can be caused by anything that prevents your blood from circulating or
clotting normally, such as injury to a vein, surgery, certain medications and limited movement.
 Complications

Pulmonary embolism
A serious complication associated with deep
vein thrombosis is pulmonary embolism.
Pulmonary embolism
A pulmonary embolism occurs when a blood
vessel in your lung becomes blocked by a
blood clot (thrombus) that travels to your
lung from another part of your body, usually
your leg.
A pulmonary embolism can be life-
threatening. It's important to watch for signs
and symptoms of a pulmonary embolism
and seek medical attention if they occur.
Signs and symptoms of a pulmonary embolism include:
 Sudden shortness of breath
 Chest pain or discomfort that worsens when you take a deep breath or when you cough
 Feeling lightheaded or dizzy, or fainting
 Rapid pulse
 Coughing up blood
Postphlebitic syndrome
A common complication that can occur after deep vein thrombosis is known as postphlebitic syndrome, also
called post-thrombotic syndrome. Damage to your veins from the blood clot reduces blood flow in the affected
areas, which can cause: persistent swelling of your legs (edema), leg pain, skin discoloration, skin sores.

Study Guide 10
1. Describe the symptoms and signs of varicose veins and leg vein thrombosis.
Varicose veins may not cause any pain. Signs you may have varicose veins include:
 Veins that are dark purple or blue in color
 Veins that appear twisted and bulging; they are often like cords on your legs
When painful signs and symptoms occur, they may include:
 An achy or heavy feeling in your legs
 Burning, throbbing, muscle cramping and swelling in your lower legs
 Worsened pain after sitting or standing for a long time
 Itching around one or more of your veins
 Skin discoloration around a varicose vein
Spider veins are similar to varicose veins, but they're smaller. Spider veins are found closer to the skin's surface
and are often red or blue. Spider veins occur on the legs, but can also be found on the face. They vary in size &
often look like a spider's web.
Deep vein thrombosis signs and symptoms can include:
Swelling in the affected leg. Rarely, there's swelling in both legs.
 Pain in your leg. The pain often starts in your calf and can feel like cramping or soreness.
 Red or discolored skin on the leg.
 A feeling of warmth in the affected leg.
Deep vein thrombosis can occur without noticeable symptoms.
When to see a doctor
If you develop signs or symptoms of deep vein thrombosis, contact your doctor.
If you develop signs or symptoms of a pulmonary embolism — a life-threatening complication of deep vein
thrombosis — seek immediate medical attention.
The warning signs and symptoms of a pulmonary embolism include:
 Sudden shortness of breath
 Chest pain or discomfort that worsens when you take a deep breath or when you cough
 Feeling lightheaded or dizzy, or fainting

2. Discuss assessment of venous circulation in the lower limb. ****

General Evaluation of Lower Extremity Circulation
Inspect the legs from the groin to the feet noting any asymmetry, skin changes, hair distribution, varicosities, or
edema. Signs of vascular insufficiency include pallor, coolness, cyanosis, atrophy, loss of hair, pigmentation along
the shin or ankles, or ulcers. Check the capillary refill by pinching the great toes and noting the time that it takes
for the color of the nail beds to return to normal (should be less than 3 seconds).
Deep Venous Obstruction
With the patient supine, check the veins over the tibial plateau. Dilated veins that do not collapse with leg
elevation suggest deep venous obstruction (Pratt's sign). If the skin on 1 leg is warm and stiff to a pinch
(secondary to edema), then deep venous thrombosis is also indicated (Rose's sign). Measure the difference in
 circumference between the normal and distended leg -- both thighs and calves. Greater than 2.5 cm difference
between the calves and greater than 2 cm between the thighs suggest deep venous thrombosis.
 Asymmetric tenderness to blood pressure cuff inflation at less than half the pressure of the opposite side
(Löwenberg's sign). The Lowenberg cuff test is another helpful clinical maneuver for detection of calf vein
thrombosis. Wrap a blood pressure cuff around the thigh just above the knee, taking care not to pinch the
skin behind the knee. Close the valve and inflate the cuff gradually to 180 mm Hg. Ask the patient to tell you
of any unusual discomfort. Minimal discomfort immediately under the cuff is common. Spontaneous
complaint of calf pain at 20 to 80 mm Hg (that is, above venous pressure) is highly suggestive of local
venous disease, particularly if 150 to 180 mm Hg contralateral thigh pressure is well tolerated.
 Skin erythema or warmth may be noted in active phlebitis. A thrombosed segment of vein (i.e., a cord) may
be palpable, especially in the superficial veins of the lower extremity.
 Pain is a prominent feature of muscular, synovial, or vascular leg disease and various tests have been
suggested to help identify the specific etiology. Homan's test (dorsiflexion sign) is most popularly used to
detect irritability of the posterior leg muscles through which inflamed or thrombosed veins course. A
popular clinical misconception is that calf pain is the endpoint of the test; however, Homan clearly stated
that "discomfort need have no part in this reaction." A positive sign is when dorsiflexion of the foot on the
affected side is less complete or is met with more resistance than on the unaffected side. Resistance to
dorsiflexion may also be manifested by involuntary flexion of the knee.
Varicose Veins
Varicose veins with pulsations suggest tricuspid insufficiency. Hearing a murmur over the veins suggests
tricuspid insufficiency. Dark purple discoloration of the skin with varicose veins suggests arteriovenous fistula.
Inspect the saphenous system for varicosities that will appear as large wormlike, tortuous vessels. Perform the
manual compression test by having the patient stand and placing your right hand over the distal lower part of
the varicose vein and your left hand over the proximal vein. Your hands will be about 15-20 cm apart. Compress
the proximal portion of the varicose vein. If you feel a palpable pulsation in your distal hand, the test is positive.
Now perform Trendelenburg's test. Have the supine patient elevate the leg to 90° until the venous blood has
drained from the great saphenous vein. Now place a tourniquet around the upper thigh of the patient's leg
tightly enough to occlude the great saphenous vein but not the arterial pressure. Help the patient stand and
look for venous filling. Slow filling (over 30 seconds) below the superficial veins while the tourniquet is applied is
normal. Rapid filling of the superficial veins while the tourniquet is applied is abnormal, as is sudden additional
filling of the superficial veins after the tourniquet has been released.
CLINICAL CLASSIFICATION
C0 No visible or palpable signs of venous disease
C1 Telangiectasia or reticular veins
C2 Varicose veins
C3 Edema
C4a Pigmentation or eczema
C4b Lipodermatosclerosis or atrophie blanche
C5/C6 Healed venous ulcer, Active venous ulcer, respectively
S Symptomatic, including ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and
other complaints attributable to venous dysfunction
Doppler Ultrasonography:  Doppler ultrasonography indicates the presence of a thrombus in a vein whereby the
presence of internal echoes and a compressible vein are indicative of DVT. A negative Doppler ultrasonography
result is not sufficient on its own to exclude the diagnosis of DVT. It is recommended that the patient’s D-dimer
levels be checked and, if elevated, that the ultrasonography be repeated in another week. Ultrasonography
unfortunately does not differentiate between old and new clots and has a lower sensitivity and specificity for
venous thrombosis of the calf and upper extremity.
Impedance  Plethysmography: This technique measures the change in blood volume in the calf while a thigh cuff
is inflated. Venous emptying of the leg is assessed by the rapidity of volume decrease whereby the slower the
rate of emptying, the greater the obstruction. The sensitivity and specificity of this technique for DVT lie at 91%
and 96%, respectively. Other conditions that restrict forward blood flow or result in hypotension or venous
compression, such as preexisting venous disease, heart failure, or peripheral artery disease, may give false-
positive results. Impedance plethysmography is of limited value when DVT is asymptomatic or distal.

3. Explain the management of Deep Vein Thrombosis:

 Anticoagulation Therapy
Anticoagulant Therapy:  Anticoagulant therapy prevents the deposition of further clots and allows an existing
clot to disintegrate. Anticoagulants exert their effects through their action on the coagulation cascade.
Anticoagulants, particularly warfarin, should be used with caution since they have a narrow therapeutic index
and a high number of drug interactions.
Other anticoagulants that may be used
in the acute management of DVT
include enoxaparin,  dalteparin,
and  rivaroxaban. Enoxaparin
and dalteparin work by enhancing the
inhibition of factor Xa and thrombin by
increasing antithrombin III activity. They
are both administered for 7 to 14 days,
followed by maintenance therapy with
warfarin. Rivaroxaban is an oral
factor Xa inhibitor that inhibits platelet
activation by selectively blocking the
active site of factor Xa without requiring
a cofactor for its activity. More recently
the direct thrombin
inhibitor dabigatran and the
factor Xa inhibitor fondaparinux have
been approved by the FDA for the
treatment and reduction in the risk of
recurrence of DVT and PE.

 Heparin
 Heparin is an acid glycosaminoglycan that is prescribed as first-line anticoagulant therapy. Since it works by
augmenting the activity of antithrombin III and preventing the conversion of fibrinogen to fibrin, it cannot lyse
an existing clot but can prevent further thrombogenesis. An initial bolus dose of 80 mg/kg is followed by a
continuous infusion of 18 mg/kg/h. The aim of therapy is to achieve an activated partial thromboplastin time
(aPTT) of 1.5 to 2 times baseline. Heparin therapy is followed by a longer course of warfarin sodium.
 Warfarin
Warfarin exerts its effect by blocking the synthesis of vitamin K–dependent coagulation factors in the liver. The
dose of warfarin should be tailored to maintain an international normalized ratio (INR) of 2.0 to 3.0. It is
recommended that warfarin therapy be administered for a minimum of 3 months.

 Direct Oral Anti-Coagulants

Direct oral anticoagulants (DOACs) is the generic term for a group of anticoagulating substances that act directly
against certain coagulation factors and can be taken orally.
 Warfarin continues to be the most widely used oral anticoagulant but the use of the newer oral
anticoagulants (dabigatran etexilate, rivaroxaban and apixaban) is increasing.
 Warfarin antagonizes Vit K (needed for synthesis of clotting factors) & takes 2-3 days to exert its full effect.
 In some situations, heparin needs to be given for immediate anticoagulation, whilst waiting for the INR to
get into the required range.
 Dabigatran etexilate, rivaroxaban and apixaban are relatively newer oral anticoagulants. Dabigatran
etexilate is a direct thrombin inhibitor, whilst rivaroxaban and apixaban inhibit activated factor Xa.
Anticoagulation recommendations
Which anticoagulant to use and the
Indication Duration
international normalised ratio (INR)
Warfarin - 2.5 (3.5 for pulmonary
embolus sustained whilst already on
Pulmonary embolus.
warfarin with INR above 2). At least three months if risk factors are temporary but at
Proximal deep vein
Rivaroxaban is an option for the least six months if they are permanent or cause unknown.
thrombosis (DVT).
treatment of DVT and pulmonary
embolism in adults.
Warfarin not indicated. Dabigatran - start within 1-4 hours of surgery and
Dabigatran etexilate and rivaroxaban continued for 10 days after knee replacement and for 28-35
are both licensed for use in adults after days after hip replacement.
Prophylaxis of venous total hip replacement or total knee Rivaroxaban - start 6-10 hours after surgery, continue for
thromboembolism replacement surgery. five weeks for patients having major hip surgery, and two
Rivaroxaban is an option for the weeks for patients having major knee surgery.
prevention of recurrent DVT and Apixaban - start 12-24 hours after surgery and continue for
pulmonary embolism in adults. 32-38 days (hip surgery) or 10-14 days (knee surgery).
At least six months if temporary risk factors. Long-term
Calf DVT. Warfarin - 2.5.
anticoagulation may be appropriate.
Recurrence of DVT
Warfarin - 3.5. Long-term.
(whilst on warfarin).
Recurrence of DVT Warfarin - 2.5. At least six months if temporary risk factors. Long-term
(when not on Dabigatran etexilate is recommended anticoagulation may be appropriate.
Anticoagulation recommendations
as an option for treating and for
warfarin). preventing recurrent DVT and
pulmonary embolism in adults.

 Mechanism of actions of each of these drugs

 Potential side effects
Direct Oral Anticoagulants
Rivaroxaban was the first approved factor Xa inhibitor. FXa is a clotting factor at a crucial turn in the
coagulation pathway leading to thrombin generation and clot formation.
Rivaroxaban rapidly, reversibly and highly selectively binds human factor Xa, for which it has a >1000-fold
greater selectivity than for other biologically relevant serine proteases.
The mechanism of action of rivaroxaban and all other factor Xa inhibitors is the inhibition of prothrombinase
complex-bound and clot-associated factor Xa, resulting in a reduction of the thrombin burst during the
propagation phase of the coagulation cascade. They do not directly affect platelet aggregation induced by
collagen, adenosine diphosphate or thrombin, but by inhibiting factor Xa, they indirectly decrease clot formation
induced by thrombin. It is eliminated in active form by the kidneys to an extent of 33%.
Apixaban is another highly selective & reversible inhibitor of free and clot-bound factor Xa. After oral
administration it is absorbed rapidly and reaches steady state plasma concentrations in three days (taken twice
daily) with only mild accumulation. Most of the administered dose is eliminated in the feces, and about 25% is
recovered in the urine.
Edoxaban is a once-daily oral anticoagulant that rapidly & selectively inhibits factor Xa in a concentration-
dependent manner. Edoxaban is eliminated in feces and urine, and a lower proportion of the administered dose
is eliminated by the kidneys (50%) in comparison to dabigatran (80%), apixaban (27%) and rivaroxaban (33%) 

Side Effects of Direct Oral Anticoagulant Medications

 Uncontrolled bleeding (most serious side effect)
Animal studies of some DOACs suggest the potential for fetal harm, so pregnant women and those planning a
pregnancy should discuss LMWH as the preferred therapy with their doctor.
Action of WARFARIN
Warfarin decreases blood clotting by blocking an enzyme called vitamin K epoxide reductase that reactivates
vitamin K1. Without sufficient active vitamin K1, clotting factors II, VII, IX, and X have decreased clotting
ability. The anticlotting protein C and protein S are also inhibited, but to a lesser degree. A few days are required
for full effect to occur, and these effects can last for up to five days.
The common side effect is bleeding. Less common side effects may include areas of tissue damage and purple
toes syndrome. Use is not recommended during pregnancy.
Action and side effect of Heparin
Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its
activation through an increase in the flexibility of its reactive site loop. The activated AT then
inactivates thrombin, factor Xa and other proteases. The rate of inactivation of these proteases by AT can
increase by up to 1000-fold due to the binding of heparin. Common side effects include bleeding, pain at the
injection site, and low blood platelets. Serious side effects include heparin-induced thrombocytopenia.

4. Explain the management of varicose veins.

Treatment
Self-care — such as exercising, losing weight, not wearing tight clothes, elevating your legs, and avoiding long
periods of standing or sitting — can ease pain and prevent varicose veins from getting worse.
Compression stockings
Wearing compression stockings all day is often the first approach to try before moving on to other treatments.
They steadily squeeze your legs, helping veins and leg muscles move blood more efficiently. The amount of
compression varies by type and brand.
You can buy compression stockings at most pharmacies and medical supply stores. Prescription-strength
stockings also are available, and are likely covered by insurance if your varicose veins are causing symptoms.
Additional treatments for more-severe varicose veins
If you don't respond to self-care or compression stockings, or if your condition is more severe, your doctor may
suggest one of these varicose vein treatments:
 Sclerotherapy. In this procedure, your doctor injects small- and medium-sized varicose veins with a solution
or foam that scars and closes those veins. In a few weeks, treated varicose veins should fade.
Although the same vein may need to be injected more than once, sclerotherapy is effective if done correctly.
Sclerotherapy doesn't require anesthesia and can be done in your doctor's office.
 Foam sclerotherapy of large veins. Injection of a large vein with a foam solution is also a possible treatment
to close a vein and seal it.
 Laser treatment. Doctors are using new technology in laser treatments to close off smaller varicose veins
and spider veins. Laser treatment works by sending strong bursts of light onto the vein, which makes the
vein slowly fade and disappear. No incisions or needles are used.
 Catheter-assisted procedures using radiofrequency or laser energy. In one of these treatments, your doctor
inserts a thin tube (catheter) into an enlarged vein and heats the tip of the catheter using either
radiofrequency or laser energy. As the catheter is pulled out, the heat destroys the vein by causing it to
collapse and seal shut. This procedure is the preferred treatment for larger varicose veins.
 High ligation and vein stripping. This procedure involves tying off a vein before it joins a deep vein and
removing the vein through small incisions. This is an outpatient procedure for most people. Removing the
vein won't adversely affect circulation in your leg because veins deeper in the leg take care of the larger
volumes of blood.
 Ambulatory phlebectomy. Your doctor removes smaller varicose veins through a series of tiny skin
punctures. Only the parts of your leg that are being pricked are numbed in this outpatient procedure.
Scarring is generally minimal.
 Endoscopic vein surgery. You might need this operation only in an advanced case involving leg ulcers if
other techniques fail. Your surgeon uses a thin video camera inserted in your leg to visualize and close
varicose veins and then removes the veins through small incisions. This procedure is performed on an
outpatient basis.