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Ulceration, bleeding, airway block and visual disturbances
are common complications.
A definitive even though rare, but important life-threatening
complication is platelet trapping and severe thrombocytopenia presenting as ecchymosis, petechiae, intracranial
haemorrhage massive GI bleed.
Raised angiogenic (fibroblastic) growth factor which is
secreted in patient’s urine is useful lab investigation to differentiate it from vascular malformations.
It is actually a capillary malformation even though
considered under haemangioma. It results from defect
in maturation of sympathetic innervation of skin causing
localised vasodilatation of intradermal capillaries.
¾
It is often associated with Sturge-Weber syndrome,
Klippel-Trenaunay-Weber syndrome and Proteus
syndrome.
¾
It needs treatment—laser (pulsed dye/diode); excision
and grafting; cosmetic coverage. Expected result by
treatment is not possible many times.
HAEMANGIOMA CLASSIFICATION (OLD)
B
x Capillary
SRB’s Manual of Surgery
– Strawberry haemangioma
x Cavernous haemangioma
Note:
Salmon patch and port-wine stain are actually capillary vascular
malformations even though they were earlier classified under capillary
haemangioma.
Note:
Presently word ‘capillary haemangioma’ is restricted to strawberry type
only; salmon patch and port-wine stain are actually classified under
vascular malformations.
Capillary Vascular Malformations
Salmon patch (stork bite):
¾
It is actually capillary vascular malformation also called
as naevus simplex; it is very commonly seen in 40% of
newborns.
¾
It presents at birth. It commonly occurs in nape of the
neck (50%), face, scalp and limbs. It usually involves
wide area of skin. It is caused by an area of persistent
fetal dermal circulation. With age, it goes for spontaneous
regression and disappears completely (usually in one
year). Hence masterly inactivity is the treatment.
Fig. 1.373: Port-wine stain (Naevus flammeus).
Fig. 1.372: Salmon patch.
Port-wine stain (Naevus flammeus):
¾
It presents at birth and persists throughout life without
any change. Spontaneous regression will not occur. It
presents as smooth, flat, reddish blue/intensely purple
area; common in head, neck and face; often with maxillary and mandibular dermatomes of 5th cranial nerve.
Eventually surface becomes nodular and keratotic.
¾
It persists throughout life. It is less common; seen in
0.3% of all newborns. It is also a capillary vascular
malformation.
Capillary Haemangioma
Strawberry haemangioma:
¾
It may start at birth or child is normal at birth; between
one to three weeks it appears as red mark which rapidly
increases in size in 3 months to form strawberry/raspberry haemangioma. It contains immature vasoformative
tissues. There will be eventually intravascular thrombosis,
fibrosis and mast cell infiltration.
Fig. 1.374: Strawberry haemangioma.
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It is a true capillary haemangioma.
¾
It is 20 times more common than port wine stain.
¾
It is common in white girls. Male to female ratio is 1 : 3.
¾
It is common in head and neck region.
¾
It is clinically compressible, warm with bluish surface.
¾
Bleeding can occur after minor trauma and also ulceration.
¾
It involves skin, subcutaneous tissues and often muscles
also.
¾
After 1 year of age, it slowly begins to disappear, and
completely in 7–8 years (70% in 7 years).
¾
It is the most common haemangioma.
x Haemangioma in periorbital region obstructs the vision in
newborn with amblyopia and if it persists for 7 days causes
permanent visual damage. Astigmatism also can occur
x Haemangioma in nasal area in newborn may obstruct nasal airway
seriously (as newborn cannot breathe through mouth—obligatory
nasal breathing)
x Skin ulceration may cause haemorrhage
x Infection can occur which may lead into sepsis, necrosis or rarely
septicaemia
x Systemic steroid for 3 weeks induces involution
x Usually there is no role for surgery. Surgery is done only for
retained tissue after involution
INDICATIONS FOR SURGERY OR INTERVENTION
B
x Uncontrolled growth; Accidental haemorrhage
x Functional impairment like vision or hearing
ASSOCIATED SYNDROMES
B
x Klippel-Trenaunay-Weber syndrome: Naevus flammeus + osteo-
hypertrophy of extremities (soft tissue and bone hypertrophy)
+ varicose veins of lower limbs. If there is an association of
arteriovenous fistula (AV fistula), it is called as Parkes-Weber
syndrome
x Kasabach Merritt syndrome: Capillary haemangioma + DIC
(Disseminated intravascular coagulation) with thrombocytopenia
x Sturge-Weber syndrome: Haemangiomas (Naevus flammeus) +
hemiplegia and Jacksonian epilepsy (calcified vascular cerebral
and meningeal deposits) + glaucoma
x Maffucci syndrome: Cavernous haemangioma + dyschondro-
plasia
x Proteus syndrome: Naevus flammeus + regional gigantism with
lymphaticovenous malformation (asymmetrical hypertrophy)
x Osler-Rendu-Weber syndrome: Haemangioma of skin and lip
with gastrointestinal tract haemangioma (hereditary haemorrhagic
telangiectasia), (autosomal dominant)
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CHAPTER 1M General Surgery: Vascular Lesions
Treatment
They are treated by wait and watch policy commonly—
allowed for spontaneous regression.
Pulsed dye laser (diode laser), surgical excision and recon-
struction. Feeding vessels may need to be ligated after wide
exposure before achieving complete extirpation. Sclerotherapy/cryotherapy/CO2 snow therapy cause unpleasant
scarring.
Preoperative embolisation facilitates surgical excision and
reduces the operative blood loss. When once embolisation
done, surgery should be done as early as possible otherwise
recurrence occurs and much more worried formation of
enlarged collaterals can occur. Materials used are—foam,
plastic spheres, stainless/platinum steel coils, ethanol,
polyvinyl alcohol foam of 1000 µ meters size, and rapidly
polymerizing acrylic. Problems are tissue necrosis, reaction,
normal tissue embolisation. Procedure is done with
interventional radiology under image intensifier guidance.
Rapidly growing haemangioma may need systemic/oral and
intralesional steroid therapy.
Antiangiogenic interferon 2a may be useful.
Life-threatening platelet trapping may be controlled by cyclo-
phosphamide chemotherapy.
Haemangioma with drug resistant CCF can be treated with
radiotherapy.
Cavernous Haemangioma
It is present at birth and consists of a multiple venous
channels.
Its size increases gradually and may cause problems.
It often contains feeding vessels which is of surgical
importance.
Sites: Head, neck, face, limbs, tongue, liver and other internal
organs.
Large or multiple cavernous haemangiomas can cause
congestive heart failure (hyperdynamic) due to shunting of
large quantity of blood.
Cavernous haemangioma with dyschondroplasia is called as
Maffucci syndrome.
Cavernous haemangioma is often mixed with lymphatic
component also (mixed vascular and lymphatic).
A
Figs. 1.375A and B: Cavernous haemangioma in
B
(A) tongue and (B) knee.
When I was young, I observed that nine out of ten things I did were failures. So I did ten times more work.
—George Bernard Shaw
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Features
¾
It is smooth, soft, well-localised, warm, fluctuant,
compressible, nonpulsatile swelling with bluish surface
occurring in skin and subcutaneous tissue (often in
mucosa like oral cavity) without any transillumination.
¾
Compressibility and bluish surface is diagnostic. When
swelling is pressed it reduces partially/often completely
but when pressure is released it slowly attains its original
size and shape. Vascular and lymphatic malformations
are compressible.
¾
It is usually nontender unless it gets infected or undergoes thrombosis or causes haemorrhage.
SRB’s Manual of Surgery
Differential Diagnosis
¾
Lymphangioma: It is brilliantly transilluminant unless it
is infected or fibrosed.
¾
Lipoma, cold abscess, lymph cyst—clinically it is easier
to differentiate.
Fig. 1.377: Laparoscopic view of cavernous haemangioma of liver. It
is the most common benign tumour of the liver.
Complications: Haemorrhage; DIC; Thrombosis; Infection,
ulceration and septicaemia; Erosion into the adjacent bone;
High output cardiac failure.
Investigations: Ultrasound, Doppler; CT angiogram to find
out feeding vessel; Platelet count; MRI/MR angiogram to see
feeding vessels and deeper extension.
Treatment
¾
Sclerosant therapy: It is the initial first line of therapy. It
causes aseptic thrombosis and fibrosis of the cavernous
haemangioma with less vascularity and smaller size. It
is directly injected into the lesion. Sodium tetradecyl
A
sulphate/hypertonic saline are used. Often multiple injections are needed to achieve complete required effect.
Later excision of the lesion is done.
¾
Ligation of feeding artery and often at later stage excision
is done once haemangioma shrinks.
¾
Therapeutic embolisation.
¾
If small and located in accessible area, excision is the
initial therapy.
¾
Laser ablation—diode pulsed laser is becoming popular
because of good control of bleeding. CO
/Nd:YAG laser
2
is also equally effective.
B
Figs. 1.376A and B: Cavernous haemangioma in the cheek near angle
of the mouth and in the tip of the tongue. Haemangioma tongue is one
of the causes of macroglossia.
VASCULAR MALFORMATIONS
Secondary to defect in development of vascular components,
in 8th week of intrauterine period.
Single layer endothelium lined spaces derived from arterial,
capillary, venous or lymphatic system showing ectasia.
There is no growth in tissue culture. Raise in mast cells is
not seen.
Associated with many syndromes.
Can be located in skin or in deeper planes.
Present at birth and grows in proportion to child’s growth.
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Pale skin which later darkens over the age or faint blue mass
is the presentation.
Spontaneous involution is not common.
Capillary malformation (CM) type is due to lack of sympa-
thetic control.
Venous malformation (VM) type is most common vascular
malformation which shows hypoplasia, hyperplasia or aplasia
of superficial or deeper system. It is seen in subcutaneous
plane as faint blue compressible mass with morning pain and
stiffness of the area.
Lymphatic malformation (LM) type can be microcystic
(lymphangioma) or macrocystic (cystic hygroma). It can
cause lymphoedema, soft tissue and bony hypertrophy,
asymmetry (face), macrochelia, macroglossia, macrotia,
cellulitis.
Low/slow flow malformations can cause skeletal hypoplasia;
high/fast flow malformations can cause hypertrophy. AVM
is high flow type.
Consumption coagulopathy (DIC) can occur.
It is equal in both sexes (1:1).
Doppler is commonly used investigation; but MRI (MR
angiogram is ideal) with contrast is ideal to identify and to
differentiate low and high flow types.
Treatment—conservative with compression garments and
sclerotherapy. Laser photocoagulation is the choice for
superficial malformations; multiple sittings may be needed;
complete clearance may not be achieved. Surgical excision
can be done. Preoperative embolisation may be needed.
Vin rose patch:
It is a congenital intradermal pale pink vascular malformation
with dilatation of vessels in subpapillary dermal plexus. It may
be associated with haemangiomas; AV malformations in limbs;
congenital lymphoedema.
CIRSOID ANEURYSM
It is actually a rare arteriovenous fistula / malformation of the
scalp usually of congenital origin (80%) but occasionally can
be traumatic. 90% occur in relation to superficial temporal
artery but few occur additionally also in relation to occipital
arteries. It should be differentiated from the true aneurysm of
the superficial temporal artery. Cirsoid means varix.
It is a rare variant of capillary haemangioma occurring in
skin, beneath which abnormal artery communicates with the
distended veins.
Commonly seen in superficial temporal artery and its
branches.
Often the underlying bone gets thinned out due to pressure.
Occasionally extends into the cranial cavity.
Ulceration is the eventual problem which will lead to uncon-
trollable haemorrhage.
Fig. 1.378: Typical cirsoid aneurysm involving superficial temporal
artery region; it is commonly congenital.
Features
Pulsatile swelling in relation to superficial temporal artery,
which is warm, compressible, with arteria lisation of adjacent
veins and with bone thinning (due to erosion). It feels like a
‘pulsating bag of worms’.
Investigations: Doppler study, CT scan; Angiogram, X-ray
of the part.
Treatment
¾
Ligation of feeding artery and excision of lesion, often
requires preliminary ligation of external carotid artery.
¾
Intracranial extension requires formal neuro surgical
approach.
¾
Endovascular therapy is also useful.
¾
Percutaneous direct puncture embolisation often with
transarterial embolisation is also said to be effective
method of treatment currently.
ARTERIOVENOUS FISTULA (AVF)
It is an abnormal communication between an artery and vein.
Types of AVF
T
Congenital: AV malformation
Acquired: Traumatic
High flow: >800 mL/minute
Normal flow: 400-800 mL/minute
Low flow: <400 mL/minute
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CHAPTER 1M General Surgery: Vascular Lesions
When stethoscope is applied aneurysm is either silent or a systolic bruit can be heard, but an arteriovenous stula emits a
continuous murmur throughout the systole and diastole. —Charle G Rob
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A
SRB’s Manual of Surgery
B
Fig. 1.379: MR angiogram of AV malformation in cranial cavity.
Fig. 1.380: MRI picture of AV malformation.
A
Figs. 1.381A and B: Hypertrophic changes due to AV malformation.
B
C
E
Figs. 1.382A to E: Congenital arteriovenous malformation involving right
upper limb, axillary region and part of right half of neck and face. Note
the limb lengthening and widened girth. Limb is warmer. Limb should
be measured at each level. Auscultation reveals continuous bruit over the
limb. Note the dilated tortuous veins due to hyperdynamic circulation.
D
Congenital Arteriovenous Malformation
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(
Fistula)—AVM (AVF)
During developmental period AV communications occur.
It is high flow type of vascular malformation. It is 30% of all
vascular malformation. 90% of AVM contains both arterial and
venous components. Shuting of blood with thrill and bruit with
hyperdynamic circulation is common.
SITES
B
Limbs, either part or whole of the limb is involved. It may be localised
to toes or fingers.
Lungs.
Brain—in circle of Willis.
Other organs like bowel, liver.
Features
Structural changes in the limb:
Limb is lengthened due to increase in blood flow since
developmental period.
Limb girth is also increased.
Limb is warm.
Continuous thrill and continuous machinery murmur all
over the lesion.
Dilated arterialised varicose veins are seen due to increased
blood flow and also due to valvular incompetence.
Often there is bone erosion or extension of AVF into the
bone as such.
Physiological changes
Because of the hyperdynamic circulation, there is increased
cardiac output and so often congestive cardiac failure.
Complications
Haemorrhage; Thrombosis; Cardiac failure (CCF)
Investigations
Angiogram—MR angiogram is ideal.
Doppler study; X-ray of the part; ECG, echocardiography.
Treatment
Conservative—sclerotherapy, compression, avoiding injury.
Indications for intervention
¾
Absolute: Haemorrhage, ischaemia, CCF.
¾
Relative: Pain, functional disability, cosmesis, limb
asymmetry.
¾
Emergency: Torrential bleeding usually after trauma
(example—road traffic accidents).
Interventions
¾
Surgical ligation of feeding vessels and complete excision of the lesion. Often if lesion is extending into deeper
planes it is technically difficult; but with usage of tour-
niquet, careful meticulous dissection and ligation of all
vessels will lead into successful excision of entire lesion.
¾
Therapeutic embolisation/preoperative embolisation
hasten the proper surgical excision.
¾
In emergency bleeding, adequate transfusion of blood,
tourniquet usage, intraoperative embolisation and then
excision of entire lesion is done. Occasionally when extensive AVM is present often involving the entire limb, amputation is the final option left as a life-saving procedure.
Acquired Arteriovenous Fistula (AVF)
Fig. 1.383: AV fistula.
Causes
Trauma in (most common cause): Femoral region; Popliteal
region; Brachial region; Wrist; Aorta—vena caval; Abdomen.
It may be following road traffic accidents, penetrating
wounds, cock-fight injury (common in South India).
After surgical intervention of major vessels.
Therapeutic: For renal dialysis, AVF is created (Cimino fistula)
to achieve arterialisation of veins and also to have hyperdynamic circulation. It is done to have easy and adequate
venous access for long time haemodialysis.
Common sites are wrist, brachial, and femoral region.
Pathophysiology
Physiological changes: Cardiac failure due to hyper-dynamic
circulation.
Structural changes:
Changes at the Level of Fistula
Blood flows from high pressure artery to low pressure vein
causing diversion of most of the blood. Between the artery and
vein, at the site of fistula, dilatation develops with formation of
fibrous sac called as aneurysmal sac. This presents as warm,
pulsatile, smooth, soft, compressible swelling at the site with
continuous thrill and continuous machinery murmur.
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CHAPTER 1M General Surgery: Vascular Lesions
Honesty breeds respect and respect breeds trust.
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A
SRB’s Manual of Surgery
B
Figs. 1.384A and B: Acquired arteriovenous fistula in the wrist over
radial vessels. It should be palpated for compressibility and thrill. It
should be auscultated for bruit.
Management
Investigations: Doppler, CT angiogram; ECG, echocardiog-
raphy.
Excision of fistula and reconstruction of artery and vein with
graft.
Done in early stages—larger vessels. Venous or Dacron
graft is used.
Fig. 1.386: Reconstruction of AV fistula using graft.
Fig. 1.385: AV fistula created for treating chronic renal failure has
formed an aneurysm. It may rupture to cause severe haemorrhage.
Thrombosis or sepsis also can occur in this.
Changes Below the Level of the Fistula
Because of diversion of arterial blood distal part becomes
ischaemic. Because of high pressure arterialisation of veins and
valvular incompetence occurs causing varicose veins.
Changes Proximal to the Fistula
Hyperdynamic circulation causes cardiac failure. Cardiac
failure may be very severe in traumatic AVF (often resistant
to drug therapy).
If pressure is applied to the artery proximal to the fistula,
swelling will reduce in size, thrill and bruit will disappear,
pulse rate and pulse pressure becomes normal. This is called
as Nicoladoni’s sign or Branham’s sign.
In emergency situation, quadruple ligation, i.e. both artery
and vein above and below are ligated without touching the
fistula and sac. Patient recovers well from cardiac failure.
Therapeutic embolisation may be tried.
Hunter’s ligation should be avoided. It is used as life-saving
measure because it invariably causes limb ischaemia and
gangrene even though patient recovers from cardiac failure. It
is ligation of artery proximally so as to make cardiac function
normal. But it invariably steals the blood from the limb leading
to gangrene.
A
Figs. 1.387A and B: (A) Quadruple ligation of AV fistula. (B) Hunter’s
ligation is ligation of artery proximal to AV fistula. It should not be done
as it causes diversion of all blood from periphery leading to gangrene
of distal part.
B
Note:
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Other rare conditions
Campbell de Morgan spots: It is usually smaller (0.2 to 6 mm)
in size, circular, elevated and bright red swelling. It is common
in trunk; common in elderly; also called as cherry angiomas. It
usually does not require treatment; when needed, excision or
electrodesiccation or laser removal is done.
Parry-Romberg disease: It is hemifacial atrophy of skin, soft
tissue and bone; common in females; usually begins at twenties.
Atrophy of skin, fat, muscle, cartilage and bone causing coupe
de sabre deformity – are the features.It is a self-limiting disease.
Aesthetic reconstruction is offered when severe deformity
develops.
Hamartomata: Hamartano/hamartia means ‘I miss’ (Greek);
or ‘fault’ or ‘misfire’ or ‘error’— (missing the mark in spear
throwing). Presently this terminology is not very much in use.
It is a benign lesion with aberrant differentiation producing a
mass of disorganised but mature specialised cells or tissue
indigenous to the particular site. It is tumour like overgrowth of
tissue or tissues proper to that part. It may be single lesion or
multiple lesions; haemangiomas, lymphangiomas, AV malformations, neural malformations are the examples. It is commonly
observed in lungs, heart, brain (hypothalamus), skin, stomach,
spleen, etc. It can be vascular, bone forming, cartilage forming,
bronchial, neurofibromatosis, nevi, etc. Problems with hamartomas are—pressure symptoms, bleeding, infection, gigantism,
cosmetic problem. Treatment: Depends on site, type, extent;
cryotherapy, ligation of feeding vessels, sclerotherapy, excision
or laser therapy are options.
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CHAPTER 1M General Surgery: Vascular Lesions
Attitudes are more important than facts.
C hapter Outline
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N. Venous Diseases
·
Anatomy of Veins of
Lower Limb
·
Physiology of Venous
Blood Flow in Lower
Limb
·
Deep Vein Thrombosis
·
Varicose Veins
·
Venous Ulcer
·
Compression Therapy
for Varicose Veins
·
Thrombophlebitis
·
Klippel-Trenaunay
Syndrome
·
Anticoagulants
·
Oral Anticoagulants
·
Pulmonary Embolism
ANATOMY OF VEINS OF LOWER LIMB
Deep Veins
Tibial, popliteal, femoral veins are called as “veins of
conduits” which drain blood into iliac veins and then to IVC.
Pumping veins: They are venous sinuses existing in the calf
muscles which pump blood towards major veins. They are
better termed as musculo venous pumps. They are also called
as the peripheral heart.
Paired veins of anterior tibial, posterior tibial and peroneal
with soleal and gastrocnemius veins join together to form
popliteal vein which at subsartorial canal (Hunter’s) continue
as femoral vein where it is joined by profunda (deep) femoral
vein. Later femoral vein continues as external iliac vein
beyond above the inguinal ligament.
Fig. 1.388: Bilateral varicosity of great saphenous veins.
Supercial Veins
Long (Great) saphenous vein (LSV / GSV): It begins from
the medial part of the dorsal venous arch of the foot
runs in front of the medial malleolus ascends up to the
posteromedial aspect of the knee joint, and then ascends
upwards in the thigh towards the saphenous opening.
Saphenous opening lies 3.75 cm below and lateral to the
pubic tubercle. It pierces the cribriform fascia to enter the
femoral vein. LSV contains 12–20 valves. It is the longest
vein in the body. In the lower part of the leg LSV is closely
associated with saphenous nerve which can get damaged
during surgeries to LSV varicosity. Tributaries of GSV
are— posterior arch vein, anterior vein of the leg, anterolateral vein, posteromedial vein and sometimes accessory
saphenous vein.
Short (Small) saphenous vein (SSV): Lateral marginal
vein of the foot behind the lateral malleolus continues as
SSV ascending upwards along the lateral margin of the
tendoachilles. It runs along the middle of the back of the leg
between two heads of the gastrocnemius into the lower part
Fig. 1.389: Great saphenous vein–anatomy and tributaries.
of the popliteal fossa and ends into the popliteal vein. It has
got 6–12 valves. Sural nerve runs closely along the SSV which
may get injured during surgery. Saphenopopliteal junction is
variable, but usually located at popliteal fossa; it can be above
or below the actual site.
Posterior arch vein of Leonardo from medial ankle to the
LSV below.
Anterior arch veins to popliteal veins.
Note:
• Superficial veins have got multiple valves; blood always drains from
superficial veins towards deep veins. Inferior vena cava (IVC) and iliac
veins do not have valves. Superficial veins of lower limb drains skin and
subcutaneous tissues (10% of blood). Veins can accommodate large
quantity of blood hence called as capacitance vessels.
A B
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Figs. 1.390A and B: Short saphenous vein varicosity.
• Spider veins (pin veins/dermal veins/telangictasia/hyphen webs)→
reticular vein (feeder vein/subdermal veins) → superficial vein → deep
vein. Malleolar flare (ankle flare/corona phlebectatica) is a fan shaped
venous flare is an early sign of advanced venous disease.
Perforator Veins
Communicating Veins
They are veins in the subcutaneous plane communicating
between different superficial veins of the leg. They usually do
not perforate the deep fascia. Long intersaphenous communicating vein often exists between cranial extension of SSV to
join GSV and can be varicose and pathological and is called as
communicating vein of Giacomini-Cruveilhier. Anterior accessory
great saphenous vein (AAGSV, Anterolateral vein of thigh) is
communicating vein into the GSV anteriorly and laterally. AAGSV
communicates into GSV usually just proximal to preterminal
valve (60%); often at confluence (39%); rarely onto femoral vein
(1%). In many patients with varicose veins it is this vein which is
diseased than GSV. It often receives superficial circumflex vein
before joining the GSV. Communicating veins are often called
as anastomotic veins.
215
CHAPTER 1N General Surgery: Venous Diseases
They are the veins which connect superficial to deep veins at
various levels. They travel from superficial fascia through an
opening in the deep fascia before entering the deep veins. The
direction of blood flow here is from superficial to deep veins.
These perforators are also guarded by valves so that the blood
flow is unidirectional, i.e. towards deep veins. Reversal of flow
occurs due to incompetence of perforators which will lead to
varicose veins.
TYPES
B
x Ankle perforators (May or Kuster)
x Bassi’s paraAchillean (5 cm above calcaneum) perforator
x Lower leg perforators: I, II, III (of Cockett)
x Gastrocnemius perforators (of Boyd)—below knee
x Mid-thigh perforators (Dodd)
x Hunter’s perforator in the thigh
A
B
Figs. 1.392A and B: Communicating and perforator veins in the leg.
PHYSIOLOGY OF VENOUS BLOOD
FLOW IN LOWER LIMB
Veins are thin-walled collapsible vessels, that assume an
elliptical configuration in collapsed state and circular configu-
ration in the filled state.
Venous valves are abundant in the distal lower extremity and
the number of valves decreases proximally, with no valves in
superior and inferior vena cava.
Fig. 1.391: Perforator veins and different compartments in the leg.
Factors Affecting the Venous Return
Arterial pressure across the capillary increases the pumping
action of vein.
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