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Examination in Venous Diseases
https://t.me/med1917
Fig. 6.27: Diagram showing different perforators.
V is-a –tergo of adjoining muscle; Nonrefluxing valves
in course of veins.
Venous Pathology
Venous pathology develops when venous return is
impaired. It can be of deep, superficial or mixed types.
It can be due to primary muscle pump failure, venous
obstruction, and venous valvular incompetence. It may
be segmental or affecting the entire leg. Here venous
wall shows increase in collagen and reduction in elastin.
Causes of primary muscle pump failure ar e—muscle
wasting, neuromuscular disease, deep fasciotomies,
local vein valve failure. It leads to nonreduction of
postambulatory pressure; causes increased hydrostatic
pressure and thus decreased arterial inflow. Present
concept is inflammatory pathology of the venous wall
and valve. Bottom to top theory is newly changed
present concept with segmental pathophysiology. So
VHM (venous mapping) is essential prior to surgical
intervention. Incompetence can be of three types—
perforator; superficial and deep.
161
Perforator incompetence is reversal of normal
flow across the perforators. Normal flow is from
superficial veins to deep veins. Perforator valve failure
causes deep to superficial reflux causing congestion
and venous hypertension. It causes transmission of
extreme high pressure (150-200 mm Hg) generated
at the deep veins into the superficial veins. This high
pressure reflux (hydrodynamic reflux) causes distal
valvular incompetence of the superficial venous system
causing varicosity and its problems. Problems here
are more rapid and progressive than just superficial
vein incompetence.
Superficial vein incompetence is the most
common form of the venous disease. It shows retrograde flow (hydrostatic r eflux) due to malfunctioning
valves. It is the tributaries which become commonly
incompetent and diseased as it is in subcutaneous plane
with less support and also has got thin muscle in the
wall. Here effects are slow and gradual.
Deep incompetence may be isolated incompetence
of deep veins or may be associated with incompetence
of superficial venous system. Here blood pumped out
in normal volumes but extremity refill includes normal
arterial inflow and also pathological reflux. Venous
refill is rapid with normal or elevated ambulatory
venous pressure (Fig. 6.28).
Varicose Veins
Definition of the Varicose Veins
It is dilated, tortuous and elongated superficial vein
with reversal of blood flow due to incompetence of
valves. It is seen only in human beings due to erect
posture. It is not seen in animals. A varicose vein is one
which has permanently lost its valvular efficiency . As
a result of continuous dilatation under pressure in
course of time, varicose vein becomes elongated,
tortuous, pouched, thickened, inelastic and friable
structure. Incidence of varicose veins is 5% in general
population.
Presentations of Varicose Veins
It is more common in females (10:1). It is much more
common in females with a family history. Often it
is familial. Familial varicose veins begin in younger
age group and are seen bilaterally, involve all veins
including deep veins. Presents with visible dilated veins
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SRB’s Clinical Surgery
Fig. 6.28: Great saphenous vein anatomy at its saphenofemoral junction showing reflux.
in the leg with pain, distress, nocturnal cramps, feeling
of heaviness, muscle fatigue, throbbing heavy legs,
(restless legs), soreness, burning, pruritus. Often
there is pedal oedema, pigmentation, dermatitis,
ulceration, tenderness, restricted ankle joint movement,
bleeding, and positive cough impulse at the saphenofemoral junction. Thickening of tibia occurs due to
Figs 6.29A and B: Saphena varix in the groin—near the saphenous opening.
periostitis. It may present with DVT, especially in
pregnancy. Local gigantism may be the presentation
in varicose veins due to congenital A V malformation
(Figs 6.29A and B).
Note: Extent of valvular incompetence is not related
to the presence and severity of the symptoms.
Examination in Venous Diseases
https://t.me/med1917
Symptoms in varicose veins
Dilated tortuous vein – asymptomatic but cosmetic
Dragging pain
Heaviness/tiredness in the legs
Night time cramps – usually late night - typical
Oedema feet/itching/thickening feet/eczema feet and leg
Discolouration/ulceration in the feet/painful walk
Bleeding blow outs
Signs
All different positive tests
Blow outs – localised dilated vein segment suggests
incompetent perforator – Fegan’s test
Superficial thrombophlebitis
Ankle flare (Fig. 6.30)
Dermal flare (thread veins) < 1 mm– it is within the skin
Reticular veins (1-3 mm) in the subcutaneous tissue
Saphena varix – A large varicosity in the groin (of GSV;
often of anterolateral thigh vein)
Talipes equino varus
Champagne bottle sign (inverted beer bottle look) –
contraction of ankle skin and subcutaneous tissue with
prominent oedematous calf.
Causes of pain/cramps in varicose veins/venous
diseases
Increased venous wall tension – chronic venous
hypertension
Hypoxia of tunica media of the venous wall due to altered
function of vasa vasorum
Increased capillary pressure
Hyperviscosity of red cells
Platelet hyperaggregation
Reduction in capillary permeability causing capillary
functional disorder
Altered cutaneous microcirculation due to leucocyte
adhesion and accumulation into the venous wall; release
of free radicals cause microvascular lesional disease.
163
Fig. 6.30: Typical ankle flare. Thread veins are dermal and
are < 1 mm in size. Reticular veins are subcutaneous and
are between 1-3 mm in size.
Oedema in venous diseases
Can be localised or generalised
Localised oedema is due to ankle flare or dilatation of
medial marginal vein
Cellulitis and lymphangitis association causes oedema,
scarring and thickening of dermal and subdermal tissues
– lipodermatosclerosis (brawny induration)
Ankle becomes narrower due to contraction of skin and
subcutaneous tissues but calf remains prominent –
champagne bottle appearance (Fig. 6.31)
Pale atrophic skin with white patches surrounded by dilated
capillaries and pigmentation – atrophic blanche.
Aetiologies for Varicose Veins
V aricosities are more common in lower limb. Because
of erect posture long column of blood has to be
supported which can lead to weakness and incompetence of valves leading to varicosities.
Fig. 6.31 Champagne bottle sign/inverted beer bottle sign
is seen in lipodermatosclerosis due to prominent calf with
narrow ankle contracted skin and subcutaneous tissue. Sign
is often observed in DVT also.
Primary varicosities are due to—
Congenital incompetence or absence of valves;
weakness of valves; weakness or wasting of muscles;
stretching of deep fascia. It is precipitated by prolonged
standing and recurrent thrombophlebitis.
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SRB’s Clinical Surgery
Secondary varicosities are due to—
Recurrent thrombophlebitis; occupational—standing
for long hours; obstruction to venous return like
abdominal tumour, retroperitoneal fibrosis, pelvic
mass; ascites; lymphadenopathy; pregnancy (due to
progesterone hormone); acquired AV fistula (due to
surgery/trauma). It may be due to previous deep venous
thrombosis.
Congenital
Congenital A-V malformations; Klippel-Trenaunay
syndrome; A valvulia.
Sites where varicosities can occur
Lower limb
Pampiniform plexus of veins—varicocele
Vulval/ovarian varices
Sites of portosystemic anastomosis (Piles/oesophageal
varices/gastric varices)
Types of Varicose Veins
1. Long saphenous vein varicosity.
2. Short saphenous vein varicosity.
3. Varicose veins due to perforator incompetence.
4. Thread veins (dermal flares): Are small varices in
the skin usually around ankle which look like
dilated, red or purple network of veins of < 1 mm
in size.
5. Reticular varices: Are slightly larger than thread
veins located in subcutaneous region 1-3 mm in
size.
6. Combinations of any of above.
Venous segmental disease score (venous clinical
scoring system) is done based on different symptoms/
signs/ulcer activity/compression therapy with 10
parameters with each having 3 scores as mild/moderate/
severe (Figs 6.32A and B).
Complications of varicose veins
Haemorrhage: Venous haemorrhage can occur from the
ruptured varicose veins or sloughed varicose veins, often
torrential, but can be controlled very well by elevation
and pressure bandage
Eczema and dermatitis
Periostitis causing thickening of periosteum
Venous ulcer
Marjolin’s ulcer – due to unstable scar of long duration—
very well differentiated squamous cell carcinoma
Lipodermatosclerosis
Ankylosis of the ankle joint
Talipes equino varus
Deep venous thrombosis
Calcification
A
It can be—Primary varicose veins; Secondary varicose
veins; Reticular veins (V enulectasia); T elangiectasias
(Spider veins, Hyphen webs, Thread veins). Corona
phlebectatica are blue telangiectasias on the medial
aspect of the foot below the malleolus around ankle
level. More than 5 such lesions are the best independent
predictor of the skin changes.
Venous disability scoring system
Score 0 Asymptomatic
Score 1 Symptomatic but able to carry out activities
without any therapy
Score 2 Symptomatic – can do activities only with
compression/limb elevation
Score 3 Symptomatic – unable to do daily activities
even with compression or limb elevation
B
Figs 6.32A and B: Crepe bandage or stockings are used
in varicose veins or in DVT. After any intervention for
varicose veins, crepe bandages/stockings should be applied
for 6 months. It should be worn from toes to knee joint.
Examination in Venous Diseases
https://t.me/med1917
Lipodermatosclerosis and development of different
problems in varicose veins
Fibrin deposition, scarring and tissue hypoxia due to
chronic venous hypertension around ankle joint is
called as lipodermatosclerosis. It is irreversible change
in the soft tissue which eventually leads into ulceration
(Fig. 6.33).
T wo theories: Fibrin cuff theory; White cell trapping
theory
Incompetence of venous valves → stasis of blood →
chronic ambulatory venous hypertension (Pressure
up to 80-100 mm Hg) → defective microcirculation
→ RBC’s diffuses into tissue planes → lysis of RBC’s
→ release of haemosiderin, pigmentation → dermatitis
→ capillary endothelial damage → prevention of
diffusion and exchange of nutrients → severe anoxia
→ chronic venous ulceration (Fibrin cuff theory).
Inappropriate activation of trapped leucocytes
release proteolytic enzymes which cause cell destruction and ulceration—White cell trapping theory.
Venous Ulcer
It is the complication of varicose veins or deep vein
thrombosis.
Pathogenesis of Venous Ulcer
Varicose veins or DVT which are recanalised, eventually causes chronic venous hypertension around ankle
→ causes hemosiderin deposition in the subcutaneous
plane from lysed RBC’s, Eczema → dermatitis and
lipodermatosclerosis → fibrosis →anoxia → ulcera-
tion. Ar ea where venous ulcer commonly develops is
around and above the medial malleoli because of
presence of large number of perforators which transmit
pressure changes directly into superficial system. This
area is called as Gaiter’s zone (Fig. 6.34). It can be seen
on both malleoli. Ulcer is often large, nonhealing,
tender, recurrent with secondary infection. Vertical
group of inguinal lymph nodes are usually enlarged and
tender . Often it leads to scarring, ankylosis, Marjolin’s
ulcer formation. Sloughing from the ulcer bed may give
way causing venous haemorrhage. Periostitis is
common which also prevents ulcer from healing. Due
to regular walking on toes to get relief from pain, causes
contraction and extra articular fibrosis of Achilles
tendon– talipes equino varus (Figs 6.35A to C).
165
Fig. 6.33: Lipodermatosclerosis left leg.
CEAP Classification (Advanced 2004)
It is the classification used for lower extremity venous
diseases.
CEAP Classification
C— Clinical signs (grade 0-6); (A) for asymptomatic or
(S) for symptomatic presentation
E— Aetiological classification (congenital, primary,
secondary, no venous aetiology)
A— Anatomic distribution (Superficial (As), deep (Ad)
or perforator (Ap))
P— Pathophysiologic dysfunction (reflux or obstructive
or both or no pathophysiologic dysfunction)
Grading of clinical signs (C)
0— No visible or palpable signs of venous diseases
1— Telangiectases, reticular veins or malleolar flare
2— Varicose veins
3— Oedema without skin changes
4— Skin changes due to venous diseases like
pigmentation, eczema or lipodermatosclerosis 4a—
pigmentation; 4b—lipodermatosis, atrophia blanche
5— Skin changes as above with healed ulceration
6— Skin changes as above with active ulceration
Anatomical distribution (A)
As—superficial system
1. Telangiectases, reticular veins
2. Great saphenous vein above the knee—ostial and
preterminal
3. Great saphenous vein below the knee
4. Small saphenous vein
5. Nonsaphenous—43%
Ad—deep system
From 6 to 15
Ap—perforator system
17—Perforator vein (PV) of the thigh
18—Perforator vein (PV) of the calf and leg
An—no anatomical lesion identified
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Fig. 6.34: Gaiter’s zone is the handbreadth
area around ankle where problems/
complications/ulceration of venous disease
occur.
SRB’s Clinical Surgery
Note:
50% of venous ulcer occurs as a result of recanalisation
of DVT, and the leg is commonly called as post-
phlebitic limb (leg). It presents with all complications
of venous diseases like eczema, ulceration, lipodermatosclerosis, and venous ulcers. Here surgery for
superficial varicose veins is contraindicated. Most of
the venous ulcers have surrounding lipodermatosclerosis. Lipodermatosclerosis is due to pigmentation,
thickening, chronic inflammation and induration of
the skin in calf and around ankle. 70-80% of leg ulcers
are venous ulcers.
A
B
Complications of venous ulcers
Haemorrhage
Marjolin‘s ulcer
Infection
Talipes equino varus
Periostitis is common over the tibia/calcaneum/other
Foot bones
Disability
Calcification
DVT
Deep Vein Thrombosis (DVT)
It is thrombosis of the deep venous system. It can
be acute or recurrent. It can be occlusive or non-
occlusive. It can be free thrombus or fixed thrombus.
C
Figs 6.35A to C: Typical site of venous ulcer. Often
venous ulcer can be bilateral.
It can be propagative which propagates proximally
and has higher chance of formation of embolism or
nonpropagative. Factors— Virchow’s triad (1856):
Stasis; Hypercoagulability; Vein wall injury.
Causes
Following childbirth; trauma; muscular violence;
prolonged immobility; debilitating illness, obesity, bed
rest, pregnancy, puerperium, oral contraceptives, and
oestrogens.
Examination in Venous Diseases
https://t.me/med1917
Postoperative thrombosis: Common after the age of
40 years. Incidence following surgeries is 30%. In
30% of cases both legs are affected. Usually it is seen
after prostate surgery, hip surgery, major abdominal
surgeries, gynaecological surgeries, cancer surgeries.
Bedridden for more than 3 days in the postoperative
period increases the risk of DVT.
Spontaneous thrombosis is common in visceral
neoplasm like carcinoma pancreas or carcinoma
stomach. It is often migrating type.
Thrombus may start in a venous tributary which
may eventually extend into the main vein causing DVT.
167
Fig. 6.36: Venous gangrene right leg.
Axillary vein thrombosis : Upper limb DVT (5% of total
DVT) can occur spontaneously , following compression
by cervical rib, by various causes of thoracic inlet
syndrome, or arm being in the hyperabduction state for
prolonged period (e.g painting the ceiling, athletes,
swimmers) , after axillary lymph node block dissection,
after radiotherapy to axilla, occasionally as a complication of venous cannulation. Idiopathic upper limb
DVT may be due to some occult malignancy in the body .
Even though upper limb DVT is less common chances
of pulmonary embolism is more—33% of upper limb
DVT can lead into pulmonary embolism.
Polycythaemia vera, thrombocytosis; deficiencies
of antithrombin III, protein C, protein S; factor V of
Leiden, antiphospholipid syndrome, thrombophilia,
recent myocardial infarction, heart failure, nephrotic
syndrome, thrombosis (in people who sit on computer
for long time) are other causes.
Sites: (1) Pelvic veins—Common. (2) Leg veins—
Common in femoral and popliteal veins (Common
on left side). (3) Upper limb veins—Not uncommon
(Axillary vein thrombosis).
Phlegmasia alba dolens: It is DVT of femoral vein
(deep femoral vein commonly) causing painful
congestion and oedema of leg, with lymphangitis,
which further increases the oedema and worsens the
situation (White leg). Phlegmasia cerulea dolens: It
is extensive DVT of iliac and pelvic veins causing
blue leg with either venous gangrene or areas of
infarction (Fig. 6.36).
Clinical Features
Fever is the earliest and common symptom. Pain and
swelling in the calf and thigh, commonly associated
with fever. Pain is often so severe that the patient finds
difficult to flex or move the leg. Leg is tense, tender,
warm, pale or bluish with stretched and shiny skin
(Fig. 6.37).
Fig. 6.37: DVT both legs.
Positive Homan’s sign: Passive forceful dorsiflexion
of the foot with extended knee will cause tenderness
in the calf. Positive Homan’s sign is confirmative sign
of DVT; but absence of Homan’ s sign is not a reliable
indicator of absence of DVT.
Mose’s sign: Gentle squeezing of lower part of the
calf from side-to-side is painful. Gentleness is very
important otherwise it may dislodge a thrombus to
form an embolus.
Neuhof ’s sign: Thickening and deep tenderness is
elicited while palpating deep in calf muscles.
Linton’ s test: After applying proximal tourniquet: with
elevation after walk; superficial veins are still prominent. Most often, DVT is asymptomatic (60%) and
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SRB’s Clinical Surgery
presents suddenly with features of pulmonar y embolism like chest pain, breathlessness and haemoptysis.
Investigations
Venous Doppler; Duplex scanning (Fig. 6.38).
Venogram—It is invasive method. It is good test to
find out occlusive and nonocclusive thrombus, but
has got 10% interpretation error. Ascending functional
venogram is better.
Fig. 6.38: Duplex scan showing DVT in leg. Deep vein
thrombosis is contraindicated for varicose vein surgery.
Radioactive I
125
fibrinogen study; haemogram with
platelet count.
Impedance plethysmography is not commonly done
procedure. When applied cuff in the upper thigh is
deflated, there is normally rapid outflow and reduction
of volume. In venous thrombosis, outflow wave is
prolonged.
Fibrin/fibrinogen assays: It is the measurement of
degradation of intravascular fibrin. In D-dimer test
cross linked degradation products are measured.
Negative D-dimer test has high negative predictive
value (98%) which is more reliable than positive
D-dimer test.
MR venography is useful in imaging iliac veins
and IVC.
bandage, early ambulation, maintaining hydration are
essential measures. Low dose heparin is given in
suspected cases, in major surgeries and continued
during postoperative period till the patient is
ambulated. 5000 units is given subcutaneously 2 hours
before surgery . V arious measures like graduated static
compression, elastic stockings, electrical stimulation
of calf muscles, pneumatic compression are used to
prevent sluggish flow of blood. Intravenous 500 ml
dextran-70 during surgery and another 500 ml in postoperative period in 24 hours can also be used to prevent
DVT.
Effects and sequelae of DVT
Pulmonary embolism—15%
Infection
Venous gangrene
Partial recanalisation, chronic venous hypertension
around the ankle region causing venous ulcers—chronic
venous insufficiency (CVI)
Recurrent DVT
Propagation of thrombus proximally
Superficial Thrombophlebitis
It is thrombosis with inflammation of superficial veins
(Figs 6.39A and B). It can be acute—due to IV cannulation, trauma, minor injury/infection, hypercoagulability; spontaneous—due to polycythaemia, polyarteritis nodosa, TAO; migratory thrombophlebitis
(Trousseau’s sign—1876—Trousseau himself had
migratory thrombophlebitis due to advanced carcinoma) is due to underlying gastrointestinal malignancy
commonly carcinoma pancreas. Mondor’ s disease is
superficial thrombophlebitis of subcutaneous veins of
breast and chest wall. Clinical features are pain, occasionally fever, redness, tenderness, and cord-like
thickening of veins. Complications are—DVT , venous
valve destruction and incompetence, infection like
cellulitis, embolism. It is managed by anti-inflammatory drugs, pressure bandage, antibiotics.
Prevention of DVT
Care has to be taken to see for proper positioning
of legs with no pressure on the calf muscles. Pressure
bandage/stockings to the legs have to be applied during
major surgeries, and laparoscopic surgeries. During
postoperative period, elevation, massaging, pressure
Figs 6.39A and B: Superficial thrombophlebitis forearm
and arm.
Examination of Lymphatic System
https://t.me/med1917
Examination of
169
7
Lymphatic System
Surgical Anatomy
Primordial lymphatic system begins to develop during
6th week of development adjacent to jugular vein as
lymph sacs. Peripheral lymphatic systems develop
from these primordial lymph sacs. Lymphatic system
has three components. Terminal lymphatic capilla-
ries,which have high porosity absorb lymph, macromolecules, cells and microbes from tissues into the
system; lymphatic vessels which collect and transport
lymph; lymph nodes which are interposed in the lymp-
hatic pathway filters lymph and maintain immunity of
the body . Lymphatic vessels run adjacent to main blood
vessels reaching the major lymphatic channels.
Cisterna chyli is formed in the abdomen, continues as
thoracic duct (formed at 9th week of gestation) in the
thorax which has got initial main course towards right
side of the mediastinum; but later migrates towards left
side entering the internal jugular vein at its joining point
of the subclavian vein. In the periphery there is hardly
any lymphovenous communications. Lymphovenous
communications occur at lymph node level; iliac, subclavian and jugular levels. Lymphatics are absent in
epidermis, cornea, CNS, cartilage, tendon and muscle.
Great lymph ducts are the thoracic duct—single;
right lymph duct—single; subclavian, bronchomediastinal and jugular trunks on both sides. These ducts
contain valves to prevent backflow.
Cisterna chyli is formed by joining of right and
left lumbar lymphatic trunks and intestinal lymphatic
duct. Lumbar trunks are short lymph vessels arising
from para-aortic lymph glands. It receives lymph from
lower limb, pelvis and pelvic viscera, kidney , adrenal
and abdominal wall deep lymphatics. Left lumbar trunk
is behind the aorta. Intestinal lymph duct arises from
preaortic nodes. It joins the cisterna chyli from front.
It receives lymph from stomach, intestines, liver
(except most convex surface which drains into right
lymph duct), spleen and pancreas. Cisterna chyli is
a lymph sac lying in front of the L
between aorta and crus of the diaphragm. From its
upper end it continues as thoracic duct. Thoracic duct
passes through the aortic orifice of the diaphragm,
runs medial to azygos vein and right of the aorta in
posterior mediastinum. In front it is related to
oesophagus, diaphragm and pericardium; behind right
intercostals arteries, hemiazygos and accessory
hemiazygos vein. At the level of 7th thoracic vertebra
it crosses towards left side behind the oesophagus
obliquely reaching left side at 5th thoracic vertebral
level. It runs upwards between left margin of
oesophagus, medial part of left pleura, and behind
left subclavian artery. In the neck it passes in front
of vertebral system (vertebral vessels and sympathetic
chain) and behind carotid system (Common carotid
artery, internal jugular vein, vagus nerve), crossing
scalenus anterior, phrenic nerve and transverse cervical
and suprascapular arteries ending as a single vessel
at the junction of internal jugular vein and subclavian
vein with a valve. Tributaries of thoracic duct aretrunk from lateral intercostals nodes from lower six
spaces; efferents from posterior mediastinal nodes,
lateral intercostal nodes of upper six spaces, left
jugular lymph trunk from head and neck region, left
subclavian lymph trunk from left upper limb, left
bronchomediastinal trunk from left side of the thorax
(Fig. 7.1). Single termination of duct is common (77%);
but double/triple/quadruple terminations are known
to occur. Occasionally it may end in left subclavian
vein, left vertebral vein, right internal jugular vein,
right subclavian vein. Thoracic duct is 45 cm in length
and 5 mm wide (wider at both ends; narrow in the
middle).
and L2 vertebrae
1
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Fig. 7.1: Anatomy of thoracic duct; cisterna chyli;
tributaries of thoracic duct.
SRB’s Clinical Surgery
Right lymph duct is 2.5 cm in length, formed by
right jugular, right subclavian and right bronchomediastinal trunks; runs on the scalenus anterior joining
the junction of right internal jugular vein and subclavian
vein.
There are about total 450-600 lymph nodes in the
body . Around 200 in the neck; around 100 in the thorax;
around 50 - 60 in the axilla; around 250 in the abdomen
and pelvis; around 50 in the groin area.
Lymphatic Watersheds of Skin
Lymph from the dermis and appendages drain into
a plexus in deep fascia which in turn drains into
respective lymph nodes. There are six watershed areas
in the body for lymphatic drainage. One vertical midline
divides into right and left. Two horizontal lines on
each side divide the area into three zones. First lies
above the line of clavicle; second between line of
clavicle and line at umbilical level; third below the
level of umbilical line. First drains into head and neck
lymph nodes; second drains into axillary nodes; third
drains into inguinal/groin nodes. Malignancy drains
to their respective nodes which depends on the location.
Lesion on the line can spread to both territory lymph
nodes. In skin and appendageal cancers, deep fascia
also should be cleared (Fig. 7.2).
Fig. 7.2: Watershed zones/areas of
lymphatic drainage. Vertical sagittal
midline; clavicular horizontal line;
umbilical line-are used to divide
areas into three zones on each side.
Above clavicular line drainage occurs
to cervical nodes; between clavicular
line and umbilical line drainage
occurs into axillary nodes; below
umbilical line drainage occurs to
inguinal lymph nodes. At the line,
drainage can occur to lymph nodes
on either side.
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