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fondaparinux) or oral (dicumarol, warfarin, rivaroxaban); in
vitro—heparin, sodium citrate, sodium oxalate and EDTA
(Ethylene diamine tetra acetic acid).
Contraindications for anticoagulant therapy: Ongoing bleeding;
recent surgery/invasive procedure; severe trauma; bleeding
tendency (clotting factor deficiency); intracranial haemorrhage;
pericarditis/pericardial effusion; patient prone to fall.
Heparin (Unfractionated/UFH)
It is a natural anticoagulant, a mucopolysaccharide. It
activates plasma antithrombin III and so blocks extrinsic
SRB’s Manual of Surgery
pathway. It has got antiplatelet action. It prevents clotting of
blood both in vivo and in vitro by acting on all three stages of
coagulation. It prolongs clotting time and activated thromboplastin time in specific (by 1.5–2.0 times the control).
Heparin also causes hyperkalaemia, thrombocytopenia and
osteoporosis.
Commercial heparin is derived from lung and intestinal
mucosa of pigs and cattle. The onset of action is immediate
after administration lasting for 4 hours. It is metabolised in
the liver by heparinase.
It does not cross placental barrier and is not secreted in
breast milk.
Indications: As prophylaxis in major surgeries, postoperative
period, puerperium; as therapy in DVT; in vascular diseases.
Dose: For prophylaxis - 5,000 units/subcutaneously 8th
hourly. For therapy - 10,000 units/IV 6th or 8th hourly; later
changed to subcutaneous dose. In severe cases, 5,000 units
to 20,000 units is given daily through IV infusion at a rate of
1,000 units per hour. Daily dose should not exceed 25,000
units.
Heparin should not be given intramuscularly and it is better
not to combine with penicillins, hydrocortisone. Heparin is
not given orally. Heparin administration should always be
monitored with APTT.
Complications: Allergy, bleeding, thrombocytopenia, alopecia,
osteoporosis.
Contraindications: Bleeding disorders, severe hyperten-
sion, GIT ulcer, piles, malignancy, ocular and neurosurgery,
chronic alcoholism, cirrhosis, etc.
Note:
• Danaparoid is an antifactor Xa, heparinoid is an anticoagulant used in
patients where heparin is contraindicated.
• Heparin antagonist: 50 mg of 1% protamine sulphate solution is given
slow intravenous. 1 g reverses 100 units of heparin. It is given only after
doing activated thromboplastin time. Overdosing or infusion without
indication may itself precipitate bleeding.
Low Molecular Weight Heparin (LMWH)
It is a commercially prepared heparin with a molecular weight
of 4,000 to 6,500.
It acts by inhibiting factor Xa. It shows lesser antiplatelet
action and lower incidence of haemorrhagic complications.
It has got better bioavailability on subcutaneous administration (once daily).
Drugs are – Enoxaparin; Dalteparin; Parnaparin; Reviparin;
Fraxiparine. It is used as subcutaneous injection.
Uses: (1) Prophylaxis of DVT and Pulmonary embolism in
surgery, stroke and immobilized patients (2) DVT (3) myocardial infarction (4) Rheumatic heart disease (5) Haemodialysis
patients.
Advantages: It has got longer duration of action once a day;
has better anticoagulant effect; less interaction with platelets;
less antigenic; usage is easier and more acceptable; monitoring is not necessary.
Disadvantages: They are expensive; only partially reversible
by protamine sulphate; it is monitored by anti-Xa assay which
is not freely available.
Fondaparinux
It is a synthetic pentasaccharide factor Xa inhibitor. It acts
by binding antithrombin III.
Fondaparinux (Arixtra) is injected subcutaneously into the
abdominal wall as once daily dose (2.5 to 10 mg).
It is used for initial treatment of deep vein thrombosis (DVT)
and pulmonary embolism (PE) and for prevention of venous
thromboembolism in patients undergoing surgery for hip
fracture or hip/knee replacement.
ORAL ANTICOAGULANTS
They are given orally and are slow-acting.
Types
Coumarin derivatives: Bishydroxycoumarin (Dicou marol):
First coumarin drug derived from sweet clover.
Warfarin sodium: Most common oral anticoagulant used.
Indandione derivative: Phenindione, anisindione.
Mode of Action of Oral Anticoagulant Therapy
By suppressing synthesis of prothrombin, factors VII, IX
and X.
By inhibiting vitamin K mediated carboxylation of glutamic
acid.
Oral anticoagulant does not have in vitro action.
They are slow-acting, and long-acting.
Control of oral anticoagulant therapy is by monitoring
prothrombin time.
PT comes to normal only 7 days after cessation of the drug.
They cross placental barrier and are known to cause terato-
genicity when given in 1st trimester.
They are secreted in breast milk.
Indications
In DVT after cessation of heparin for maintenance therapy.
After valve replacement surgery.
To achieve adequate anticoagulant effect and to prevent
thromboembolic episodes the INR has to be maintained
within 2–3.
Side Effects
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Bleeding—it may require blood transfusion/FFP or vitamin K
injection intramuscular or oral to control.
Cutaneous gangrene.
Fetal haemorrhage and teratogenicity.
Alopecia, urticaria, dermatitis.
Drug interactions: with NSAIDs, cimetidine, omeprazole,
metronidazole, cotrimoxazole, ery thromycins, barbiturates,
rifampicin, griseofulvin.
WARFARIN
WARFARIN (Wisconsin Alumni Research Foundation +
coumARIN) derivative) SODIUM is the most common drug used.
It has got lesser side effects. It has got cumulative action and
so given in tapering dose.
Dose is 5 mg, once a day.
It should be discontinued 7 days before any surgery like tooth
extraction and prothrombin time should return to normal level.
During surgery, if excess bleeding occurs, fresh frozen plasma
may be given.
The effects of warfarin sodium is reversed by injection vitamin
K; the dose depends on INR and emergency of reversal (takes
24 times to reverse).
THROMBOLYTIC AGENTS
B
x Streptokinase; urokinase; anistreplase
x Altepase - Recombinant tissue plasminogen activator (rtPA);
half life is 5 minutes; given as 10 mg IV bolus followed by 90 mg
infusion in 90 minutes.
x Tenecteplase: genetically engineered, higher fibrin selectivity.
Differences between oral anticoagulants and heparin
T
Oral anticoagulant Heparin
Slow-acting Immediate
Long-acting Short-acting
Only in vivo action Both in vitro and in vivo action
Monitored by Prothrombin time Partial thromboplastin time
Crosses the
placental barrier
Secreted in milk Not secreted in milk
Administration Orally Intravenously/subcutaneously
Does not cross the placenta
Non-vitamin K antagonist oral anticoagulants
(NOACs)
Direct thrombin inhibitors
¾
Recombinant hirudin and hirudin analogues—derived
from leeches, are direct inhibitors of thrombin.
¾
Synthetic direct thrombin inhibitors (factor IIa) -Argatroban, dabigatran etixilate (Pradaxa 110 mg).
Direct factor Xa inhibitors
¾
Rivaroxaban—It is given orally once or twice daily as
15–20 mg dose per day. It is given initially 15 mg twice
daily, later 20 mg once daily. It shows rapid bioavailability;
shows rapid onset of action; coagulation monitoring is
not required. Apixaban (2.5 mg) and edoxaban are other
drugs.
Contraindications for NOACs: Renal impairment; disorders
of haemostasis; active bleeding; prosthetic heart valve; liver
disease; pregnant and breastfeeding women; children less than
18 years.
Note:
Idarucizumab (Praxbind) is used to reverse the anticoagulant effects of
dabigatran.
Reversal agents for apixaban and rivaroxaban are currently not available.
Antiplatelet Drugs
Small dose aspirin—inhibits platelet synthesis of thrombaxane
A2.
Ticlopidine (125 mg BD)—alters platelet membrane, thereby
platelet aggregation.
Clopidogrel—action similar to ticlopidine.
Dextran—decreases platelet aggregation.
Abciximab—glycoprotein IIb/IIIa inhibitors, block platelet aggregation, and platelet adhesion to fibrin.
Dipyridamole—xanthine oxidase inhibitor.
PULMONARY EMBOLISM
It is commonly due to lower limb DVT (15% of lower limb
DVT). It can also occur after pelvic vein DVT or upper limb
DVT (30% of upper limb DVT).
Chest pain, cough, haemoptysis, dyspnoea are the features.
Often site of DVT may be asymptomatic. When symptomatic,
fever, pain, tense, tender calf, with positive Homan’s sign
may be evident.
Massive embolism causes sudden cardiac arrest and death
due to pulmonary artery block. Moderate embolism causes
pyramidal wedge-shaped infarcts in lungs.
Duplex scan of limb, CT angiogram of thorax, pulmonary
angiogram (gold standard), X-ray chest, ventilation perfusion scan, ECG, echocardiography are useful investigations.
Treatment is thrombolysis, heparin/LMWH, compression
bandage.
Occasionally surgical removal of clot from pulmonary artery
is done if possible.
IVC filter placement is essential in recurrent DVT with anti-
coagulation, DVT with contraindication for anticoagulation,
pulmonary hypertension. Greenfield IVC filter is ideal with
95% patency rate. Complications are—bleeding, haematoma,
migration of filter into pulmonary artery, thrombosis at filter
level, IVC perforation.
Retrievable IVC filters are newer method used to prevent long-
term filter complications. It is used in young patients who
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CHAPTER 1N General Surgery: Venous Diseases
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are at risk of DVT and embolism, for short specified period
only like—high-risk trauma with orthopaedic injuries, extensive iliofemoral thrombosis, during thrombolytic therapy.
Recovery filter, Gunthur-Tulip filter, Opt
Ease filters are
used. They are deployed through IJV or femoral vein under
Gunthur-Tulip types are recovered through right IJV. OptEase
is recovered from right femoral vein. Complications are same
as nonretrievable IVC filters. Retrieval failure, retrieval site
thrombosis and embolism are specific complications.
DVT prophylaxis is a must in all these patients.
angiographic or intravascular US guidance. Recovery and
VENOUS THROMBO EMBOLISM (VTE)
B
x VTE can be provoked (with identifiable causes) or unprovoked (no identifiable causes)
x Acute dyspnoea, chest pain, haemoptysis, later haemodynamic instability, shock, RV dysfunction are the features. High, moderate and low
risk groups are identified. Wells and modified Geneva criteria are used.
SRB’s Manual of Surgery
x CT angiogram is diagnostic. D dimer/duplex Doppler US of leg, MRI pelvis, coagulation profile, chest X-ray are other needed investigations
x Treatment modalities—anticoagulants, thrombolysis, percutaneous interventions, surgery
– Anticoagulants (Heparin) are used in pulmonary embolism without haemodynamic instability or without right ventricular dysfunction
– Thrombolysis—Indications: Pulmonary embolism with haemodynamic instability with right ventricular dysfunction or instability in spite
of heparin therapy or with intracavitary right heart thrombi/massive embolism. Thrombolysis dissolves the thrombus obstructing the
pulmonary artery; prevents the release of neurohumoral factors and serotonin which causes pulmonary arterial hypertension (PAH);
reverses right heart failure; dissolves venous thrombus in periphery. Thrombolysins used are—streptokinase (loading dose is 2,50,000
units IV; continuous infusion of 1, 00,000 units/hour for 24 hours), urokinase (loading dose 2000 units/lb infused IV in 10 minutes,
continuous infusion IV 2000 units/lb/hour for 24 hours), tissue plasminogen activator (tPA is ideal)—alteplase continuous infusion 100
mg/2 hours, reteplase bolus IV 10 units in every 30 minutes, tenectplase, desmoteplase. Contraindications for thrombolysis—stroke,
brain tumour, bleeding disorders, major trauma/surgery, recent GI bleed, pregnancy, endocarditis, advanced liver disease
– Percutaneous catheter fragmentation of clots and thrombolysis using pigtail catheter/clot buster/angio jet
– Retrievable IVC filters are used commonly now. Permanent filters are used only in—high risk group, risk of recurrent embolism, life
expectancy less than 6 months
x Venous thrombosis/VTE in pregnancy is more common with 2/1000 pregnancies with 5 times more in postnatal period. It is 90% left
side mainly proximal. Left calf asymmetry with >2 cm in 1st trimester with features of embolism. Calf and thigh US for leg DVT and MRI
for pelvic DVT should be done. Echocardiography should be done to check embolism; chest X-ray with abdominal shield may be needed.
LMWH should be given. Warfarin (crosses placenta), rivaroxaban are avoided. TPA crosses the placenta but is used in massive pulmonary embolism with haemodynamic instability as life-saving often along with embolectomy. LMWH is given throughout the pregnancy;
stopped peridelivery period; continued postnatal period for 1 month with 75% of earlier dose; later compression stockings and warfarin
for 6 months. Compression stockings, hydration, ambulation, left lateral position are preventive measures in pregnancy often along with
LMWH if needed/indicated.
x ACCP guidelines 2012 for VTE therapy:
– Initial phase up to 7 days—UFH/LMWH/Fondaparinux/rivaroxaban;
– Long-term up to 3 months—LMWH/rivaroxaban/dabigatran/VKA with INR 2–3 range (optimum 2.5);
– Extended is beyond 3 moths—VKA/rivaroxaban/dabigatran/LMWH if needed
VENOUS TUMOURS
B
x Venous tumours are rare.
x Venous malformations usually considered under this which includes arteriovenus malformations, haemangomas also. It can occur anywhere
in the body from skin to deeper structures.
x Leiomyoma and leiomyosarcoma of the venous wall can occur. It is slow growing lesion presenting as mass with pain with venous obstruc-
tion features with oedema distally. Dilated veins are often obvious. MRI and FNAC confirm the diagnosis. Treatment is wide excision with
the involved vein. If vein is major one, then resected vein should be reconstructed with prosthetic graft (example—IVC).
O. Lymphatics
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C hapter Outline
·
Surgical Anatomy
·
Lymphangiography
·
Isotope
Lymphoscintigraphy
·
Acute Lymphangitis and
Lymphadenitis
·
Lymphoedema
·
Lymphomas
x Hodgkin’s
Lymphoma
x
Non-Hodgkin’s
Lymphoma
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 capillaries, 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 lymphatic pathway
filter 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 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 deep lymphatics of abdominal wall. Left
lumbar trunk is behind the aorta. Intestinal lymph duct arises
from preaortic nodes. It joins the cisterna chyli from front. It
·
Mantle Cell Lymphoma
·
Malt Lymphoma
(Maltoma)
·
Burkitt’s Lymphoma
·
Cutaneous T Cell
Lymphoma
·
Chylous Ascites
·
Chylothorax
·
Chyluria
·
Sarcoidosis
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
and L2 vertebrae between aorta and crus of the diaphragm.
the L
1
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 intercostal 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, 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 are—trunk from lateral
intercostal nodes from lower six spaces; efferents from posterior
Fig. 1.4 31: Thoracic duct anatomy; cisterna chyli; tributaries of
thoracic duct.
In very early oedema, during pinching, there is a resistance that is not present on normal site,
owing to thickening of dermis and subcutaneous tissue. —Sidney S Rose
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SRB’s Manual of Surgery
Fig. 1.4 32: 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 level of (lines) drainage can
occur to lymph nodes on either side.
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. 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).
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.
cytic aggregations of primary follicles or lymphocytic aggregation
with germinal centres of secondary follicles due to antigenic stimulation. It contains B lymphocytes, macrophages, dendritic reticulum
cells. Germinal centre is surrounded by small B lymphocytes. Both
cortex and medulla are associated with humoral immunity. Proliferation of germinal centres suggests active humoral immunity with
antibody production. Central medulla contains mainly lymphatic
sinuses, arteries and veins, plasma cell and B lymphocytes. Paracortex is located in a zone between cortex and medulla. It contains
T lymphocytes, related to cell mediated immunity. Post-capillary
venules with high endothelial cells and lymphocytes in the wall are
typical. In cell mediated immunity, paracortex expansion occurs.
Afferent lymph vessels enter the node through the capsule. It enters
the marginal sinus, communicates with intranodal sinus, merging
as efferent lymph vessels which enter the hilum. Intranodal sinus
lining is highly phagocytic containing littoral cells and sinus lining
histiocytes. Main artery and veins pass through the hilum to enter
the medulla, paracortex and inner part of cortex. Superficial cortex
is supplied by direct capsular vessels.
Function of Lymphatics
Most of the intravascular proteins are daily filtered through
lymphatics and returned to the circulation again. Macromol-
ecules (albumin, globulin and fibrinogen) and microbes are also
filtered at the nodal level as first immune system. From GIT fat is
absorbed directly through lymphatics. Lymph shows centripetal
flow. Cholesterol, long chain fatty acids, fat soluble vitamins are
transferred through lymphatics into cistern chyli directly from GIT
bypassing the liver. Transport is mainly due to intrinsic contractility
of the lymphatic vessels which contain valves for effective forward
flow. To a lesser extent other factors like muscle contraction, arterial pressure, thoracic pressure, respiratory movements play role.
8 litres of lymph is produced daily; once it reaches to lymph nodes
it is concentrated to 4 litres which enters the venous circulation.
Protein concentration in lymph is very high (25 grams/litre).
Note:
Lymph drains protein rich fluid; there are no communicating/perforator
lymphatics; lymphatics will not regenerate
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
into their respective nodes depending 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.
Microanatomy of Lymph Node
Lymph node contains three regions—cortex; paracortex and
medulla. Cortex contains mainly follicles. It may be rounded lympho-
LYMPHANGIOGRAPHY
Indications
Congenital lymphoedema like aplasia, hypoplasia, hyper-
plasia.
Lymphomas show reticular pattern. It is also useful to assess
the response to treatment.
Secondaries in lymph nodes, especially iliac and para-aortic
lymph nodes.
Technique
Patent blue dye or 1 ml isosulphan blue is injected subcuta-
neously between toes. Dye is taken up by lymphatics which
will be visualised clearly. After making incision, one of the
lymphatic vessels is dissected and 30 G needle is passed.
Ultra-fluid lipiodol which is an oily contrast medium is
injected slowly using pressure pump at a rate of 1 ml in 8
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minutes (total quantity is 7 ml). Slowly in 24 hours, it passes
through the lymphatics and reaches the iliac and para-aortic
lymph nodes. Radiographs taken will help to visualise both
lymphatic vessels as well as lymph nodes.
Secondaries in lymph nodes causes filling defects.
Lymphomas shows enlarged nodes which have foamy or
reticular appearance.
Disadvantages: Technically difficult; Extravasation of dye can
occur; Dye may not reach the required area; Time consuming
and invasive procedure.
Lymphangiographic classification of lymphoedema (Browse classification): (Norman Browse)
Congenital hyperplasia (10%): Congenital; common in males;
entire leg is involved; one or both sides; with often family history;
progressive; involves increased number of lymphatics and lymph
nodes associated with chylous ascites, chylothorax and protein
losing enteropathy
Distal obliteration (80%): Common in females; starts at puberty;
calf and ankle are involved; often bilateral; with often family
history; slow progression; aplasia/hypoplasia of lymphatics
Proximal obliteration (10%): Occurs at any age; equal in both
sexes; leg and thigh involved; unilateral; rapid progression;
proximal aortoiliac nodal block
ISOTOPE LYMPHOSCINTIGRAPHY
This test gives a qualitative assessment of the lymphatic
function. Quantitative measure is done to assess lymphatic
transfer by dynamic component to static part.
Radioactive technetium labelled sulphide colloid particles,
or radioiodinated human albumin are injected into the web
space using fine needle. These particles are specifically taken
up by lymphatics.
Using gamma camera, limb and inguinal region is exposed to
visualise the lymphatics and inguinal lymph nodes.
Radioactivity in inguinal nodes is measured at 30 and 60
minutes. Normal uptake is 0.6–1.6%; if it is <0.3% in 30
minutes it is diagnostic of lymphoedema. If it is >2% it
suggests rapid abnormal clearance due to oedema as the
result of venous disease.
In 3 hours, it reaches the para-aortic lymph nodes, other
abdominal lymph nodes and liver.
Later thoracic duct also can be visualised. It can be compared
to the take up on the other limb.
Advantages:
¾
It is more sensitive.
¾
Technically easier and faster compared to lymphangiography.
¾
Thoracic duct, other lymph nodes and liver can be visualised.
¾
It is the test of choice. It is simple and safe.
¾
It has 90% sensitivity; 100% specificity.
ACUTE LYMPHANGITIS AND LYMPHADENITIS
Acute inflammation of the lymphatics occurs after bacterial
infection like Streptococcus pyogenes and Staphylococcus
aureus. It is common infective condition especially in limbs.
Condition is often associated with cellulitis.
Fig. 1.4 33: Acute lymphangitis leg. Usually regional lymph
nodes are enlarged and tender.
Diffuse swelling in the skin with redness which blanches on pres-
sure is typical. Fever, chills, pain and tenderness are common.
Regional lymph nodes often get infected causing palpable
tender lymph nodes as acute lymphadenitis; abscess in the
area can occur which may require often incision and drainage.
Minor trauma, lymphoedema are precipitating factors.
Infection spreads faster especially in diabetics and immuno-
suppressed people often leading into septicaemia.
Deep vein thrombosis, cellulitis are differential diagnosis.
Total count will be raised; blood sugar should be assessed.
Ultrasound with venous Doppler is done.
Treatment: Antibiotics oral or intravenous; limb elevation;
glycerine magnesium sulphate local application; anti-inflammatory drugs are needed to treat. If suppuration occurs then
incision and drainage or fasciotomy with wound debridement
is required. Large raw area if develops may require split skin
grafting to cover. If septicaemia develops critical care treatment is required after admission.
Recurrent infection; development lymphoedema; septicaemia;
lymphadenitis – are complications.
LYMPHOEDEMA
It is accumulation of fluid (lymph) in extracellular and extravascular fluid compartment, commonly in subcutaneous tissue. It
is primarily due to defective lymphatic drainage.
It is increased protein rich interstitial fluid.
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CHAPTER 1O General Surgery: Lymphatics
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Classication
Kinmonth classified lymphoedema as:
Primary without any identifiable lymphatic disease.
Secondary is acquired due to definitive cause. Most common
form.
PRIMARY TYPE
B
It affects commonly females.
It is common in lower limb and left side.
It can be:
Familial
Syndromic (Turner’s/Klinefelter’s/Down’s/Klipple Trenauny
SRB’s Manual of Surgery
Weber)
It can be:
Lymphoedema — Present at birth—<2 years
congenital (10%) — Familial type is called as
Nonne-Milroy’s disease. It is type I
Lymphoedema — Present at puberty—up to 2–35 years (80%).
praecox
— Familial type is called as Letessier-Meige’s
Lymphoedema — Present in adult life—after 35 years
tarda
It can be radiologically (lymphangiography):
Hypoplasia 70%
Aplasia 15%
Hyperplasia (varicose lymphatics) 15%
Fig. 1.4 34: Right side congenital limphoedema in a girl.
familial, autosomal dominant—chromosome 5 related; bilateral upper and lower
limbs, genitalia and face may be involved.
Incidence is 1:6000 of live births.
syndrome. It is type II familial. It occurs
between puberty and middle age.
Fig. 1.4 35: Early lymphoedema left side—pitting type.
Pathophysiology of Lymphoedema
Decreased lymphatic contractility, lymphatic valvular insufficiency, lymphatic obliteration by infection, tumour or surgery
causes all effects and pathology of lymphoedema. This leads
to lymphatic hypertension and dilatation causing lymph stasis,
accumulation of proteins, glycosamines, growth factors, and
bacteria. There is more collagen formation, deposition of
proteins, fibroblasts, ground substance causing fibrosis in
subcutaneous and outside deep fascia. Muscles are normal
without any oedema but may get hypertrophied.
CAUSES OF SECONDARY LYMPHOEDEMA
B
Trauma
Surgery—inguinal block or axillary block dissection/post-
mastectomy with axillary clearance
Filarial lymphoedema due to Wuchereria bancrofti—common
cause in coastal region
Tuberculosis, Syphilis, Fungal and Bacterial infection
Advanced malignancy—hard, fixed lymph nodes in axilla or in
inguinal region
Postradiotherapy lymphoedema
Rare causes: Rheumatoid arthritis, snake and insect bites, DVT,
chronic venous insufficiency
Note:
Secondary lymphoedema develops rapidly.
Fig. 1.4 36: Late lymphoedema—grade 2.
Filariasis
It is caused by a parasite Wuchereria (Brazil) Bancrofti
(Australia). It was also called as Malabar leg in 1709, by Clarke,
Cochin. Female adult worm is longer 7–10 cm than male worm
(4 cm). Microfilaria is colourless, translucent, 300 µ length and
10 µ thick. It has head, body and tail. Microfilaria circulates in
blood. In India, Asian countries and China, they show nocturnal
periodicity (from 10 PM to 4 AM). It is related to night biting
habits of the vector, Culex fatigans mosquito and sleeping habits
of the host.
Man is the definitive host; animal or reservoir host is not
known. Female mosquito is intermediate host (in India and
China—Culex fatigans). Development or multiplication of micro-
filaria will never occur in human blood. Life span of microfilaria
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in human blood is 3
months. Microfilaria is infective to female
mosquito. A density of 15 microfilaria/drop of blood are needed
to make it infective.
Fig. 1.4 37: Lymphoedema leg extending into the thigh with
lymphangitis.
A
stage larva in one week → elongated actively motile third stage
infective larva in one more week (one microfilaria forms one
infective larva; microfilaria never multiplies in mosquito nor
in human) → enters the proboscis of mosquito to become
infective to human during the mosquito bite; it takes 20 days
for microfilaria to develop into infective 3rd stage larva in
mosquito [extrinsic incubation period]→ enters human skin
while biting → many larvae get destroyed in human skin by
immunity, few enters lymphatics → enters regional lymph
nodes in inguinal or axillary or abdominal nodes → develop
into adult worm in lymph nodes → mating of female and
male worms takes place → gravid female worm releases up
to 50,000 microfilariae/day into lymph circulation → thoracic
duct → subclavian vein → microfilaria in human circulation
→ infective to female mosquito. Time from 3rd stage infective
larva entering human skin and forming adult worm and later
releasing microfilaria into blood is called as biological incuba-
tion period (12 months); time from 3rd stage infective larva
entering human skin to appearance of first clinical feature is
called as clinical incubation period (16 months).
Effects of Wuchereria Bancrofti Infection
Carrier stage having circulating microfilaria but asympto-
matic.
Immune and allergic reactions by adult worm causing
macrophage and lymphocyte infiltration, endothelial
hyperplasia, lymphatic vessel wall thickening, lymph stasis,
dilatation, further reaction, fibrosis, further blockage,
calcification, recurrent streptococcal infection, filarial
lymphoedema.
Filarial fever, utricaria, pruritus, epididymo-orchitis as acute
presentation.
Occult filariasis where microfilaria is not demonstrable in
blood but identified in lungs (by biopsy confirmation) causing
eosinophilia, bronchospasm, nocturnal cough, fever, wheeze,
weight loss, arthritis, thrombophlebitis, tenosynovitis.
Lymphadenitis, lymphangitis.
Lymphangiovarix, lymphorrhagia, lymph scrotum,
lymphocele, chyluria, chylous diarrhoea, retroperitoneal
lymphangitis, chylous ascites, chylothorax.
Blood smear—night time (thick and thin), lymph node biopsy,
skin test, eosinophilia, serological tests, DEC provocation test
(by giving 100 mg DEC) are different investigations.
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CHAPTER 1O General Surgery: Lymphatics
B
Figs. 1.438A to C: Lymphoedema foot in different patients—severe
with vesicles/oedema/skin changes/fissures.
Life Cycle
Microfilaria from carrier human blood → enters the stomach
of female Culex mosquito when it bites human carrying the
parasite in blood → ex-sheathing of microfilaria in stomach of
mosquito in 6 hours → penetrate the stomach wall → migrate
to thoracic muscles of mosquito in 12 hours → metamorphosis
into sausage shaped first stage larva in 48 hours → second
C
PATHOLOGY (COMMONLY IN FILARIAL LYMPHOEDEMA)
B
Recurrent lymphangitis causes obliteration of lymph vessels
↓
Dermal lymphatic backflow
↓
Retrograde obliteration (or die back of lymphatics)
↓
Oedema, initially pitting but later nonpitting
↓
Recurrent cellulitis—thickening of skin
↓
Contd...
Knowledge speaks, but wisdom listens.
244
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Contd...
Accumulation of proteins, growth factor, glycosaminoglycans
↓
Activation of collagens and keratinocytes
↓
Protein rich lymphoedematous tissue formation
↓
Deposition of ground substance, subdermal fibrosis
↓
Dermal thickening and dermal proliferation, Fissuring → Cracks—
Ulceration—Abscess formation
↓
SRB’s Manual of Surgery
Stout leg with unbearable weight
↓
Elephantiasis.
Rarely it causes protein losing diarrhoea, chylous ascites,
chylothorax, chyluria, lymphorrhoea. Recurrent lymphadenitis
occurs in the region which aggravate the condition.
Disease in the limb is confined to skin and subcutaneous
tissue, i.e. often, only superficial lymphatics are involved by
the disease, deep lymphatics are not. Superficial and deep
lymphatics are not communicating with each other (Unlike the
veins in the limb where superficial and deep veins are freely
communicating with each other).
SITES OF LYMPHOEDEMA
B
Lower limb—most common
Upper limb, Scrotum, penis (Ram’s horn penis)
Breast—requires reduction mammoplasty
Labia, Eyelid
Localised lymphoedema
A
B
Figs. 1.439A and B: Different lymphoedema pictures. Note the oedema,
fissuring, cracks. All these make it more vulnerable for infection.
Clinical Features
Swelling in the foot, extending progressively in the leg—tree
trunk pattern leg.
Loss of normal perimalleolar shape—tree trunk pattern leg.
Buffalo hump in the dorsum of the foot; Squaring of toes.
Skin over the dorsum of foot cannot be pinched because of
subcutaneous fibrosis—Stemmer’s sign.
Initially pitting oedema occurs, which later becomes nonpit-
ting.
Dull ache/severe pain/burning/bursting/cramps; 50% patients
will have pain.
Debility/immobility/obesity/muscle wasting.
Athlete’s foot with joint pain and disability.
Eczema, fissuring, papillae formation, ulceration, lymph ooze,
elephantiasis are other features.
Fever, malaise, headache; Recurrent abscess formation.
Psychological and social discomfort causing severe morbidity.
Endemic elephantiasis/podoconiosis is common in Africa;
seen in barefoot workers; due to destruction of lymphatics
by silica derived from soil containing alkaline volcanic
rocks.
Fig. 1.4 40: Lymphoedema of lower limb developed after ilioinguinal
block dissection for nodal secondaries from melanoma.
Fig. 1.4 41: Recurrent filarial leg with nodules and ulceration.
Fig. 1.4 42: Extensive scrotal lymphoedema of filarial origin. Patient
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underwent scrotal reduction.
245
CHAPTER 1O General Surgery: Lymphatics
B
Figs. 1.444B
Figs. 1.444A and B: Lymphoedema of penis. It needs reduction and
reconstruction otherwise it may cause urinary problem and sexual
dysfunction.
Fig. 1.4 4 3: Lymphoedema right forearm. Common causes for upper
limb lymphoedema are filarial and post-mastectomy with axillary nodal
clearance.
A
Fig. 1.444A
Indecisive people are like a blind man looking in a dark room for a black cat that isn’t there.
Fig. 1.4 4 5: Severe lymphoedema foot with vesicles and thickening.
BRUNNER’S GRADING OF LYMPHOEDEMA
B
Latent—subclinical: No clinically apparent lymphoedema.
Grade I
Pitting oedema which more or less disappears on elevation
of the limb—is due to excess deposition of interstitial fluid
Nonpitting oedema occurs which does not reduce on
Grade II
elevation
Grade III
B
Oedema with irreversible skin changes like fibrosis,
papillae, fissuring
LYMPHOEDEMA CAN BE
Mild lymphoedema—<20% of excess limb volume.
Moderate lymphoedema—20—40%.
Severe lymphoedema—>40%.
Differential Diagnosis
Cardiac causes, hypoproteinaemia, malnutrition, nephrotic
syndrome, liver failure.
Myxoedema, Trauma, Venous diseases like DVT.
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