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- •Preface to the Sixth Edition
- •Preface to the First Edition
- •Acknowledgements
- •Competencies
- •Contents
- •1. Doctor–Patient Relationship
- •2. Communication and Counselling
- •3. Ethics in General Surgery
- •6. Perioperative Care
- •7. Pain Management
- •4. Surgical Audit
- •9. Investigation and Interpretation
- •10. Asepsis, Sterilization and Disinfection
- •11. Nutrition in Surgical Patients
- •Perioperative Nutritional Support
- •Route of Administration of Nutrition
- •13. Day Case/Care Surgery
- •14. Principles of Safe General Surgery
- •15. Metabolic Response to Injury
- •17. Shock and Haemorrhage
- •Haemorrhage
- •Indicators of Fluid Responsiveness
- •18. Blood Transfusion
- •Complications of Blood Transfusion
- •Autologous Transfusion
- •Hyperbaric Oxygen
- •19. Acid–Base Balance
- •Basic Definitions
- •Regulation of Acid–Base Balance
- •Acid–Base Disorders
- •Rapid Interpretation of an ABG Report
- •20. Fluids and Electrolytes
- •Normal Physiology
- •Water Regulation (Regulation of Volume)
- •Disturbances of Volume
- •Regulation of Sodium Concentration
- •Disturbances in Concentration
- •Disturbances in Composition of Body Fluids
- •Perioperative Fluid Therapy
- •Abscess
- •Other Special Types of Pyogenic Infections
- •Surgical Site Infections (SSIs)
- •Transmissible Viral Infections
- •23. Tetanus and Gas Gangrene
- •24. Hand, Foot Infections and Tendon Transfer
- •Superficial Infections
- •Deep Infections
- •Other Hand Infections
- •Foot Infections
- •Tendon Transfer
- •25. Chronic Infectious Disease
- •Actinomycosis
- •Leprosy (Hansen’s Disease)
- •Syphilis: French Disease, Great Pox
- •AIDS and the General Surgeon
- •Clinical Examination of an Ulcer
- •Traumatic Ulcer
- •Venous Ulcer
- •Arterial/ischaemic Ulcer
- •Tropical Ulcer
- •Post-Thrombotic Ulcer
- •Rare Ulcers
- •Bazin’s Ulcer
- •Diabetic Foot
- •Pressure Sores
- •Acute Arterial Occlusion
- •Peripheral Aneurysms
- •Miscellaneous
- •Intensive Care Unit (ICU) Gangrene
- •Thoracic Outlet Syndrome
- •Axillary Vein Thrombosis
- •Vasculitis Syndromes
- •Gangrene
- •Various Types of Gangrene
- •Cancrum Oris
- •Acrocyanosis
- •Drug Abuse and Gangrene
- •Lymphoedema
- •Primary (Congenital) Lymphoedema
- •Secondary Lymphoedema (Acquired)
- •Lymphangiography
- •Hodgkin’s Lymphoma (HL)
- •Non-Hodgkin’s Lymphoma (NHL)
- •Different Sites of Lymph Nodes in NHL
- •Sézary’s Syndrome
- •Chyluria
- •Deep Vein Thrombosis (DVT)
- •More Details of Anticoagulation and DVT
- •Miscellaneous
- •31. Skin Tumours
- •Squamous Cell Carcinoma (SCC)/Epithelioma
- •Melanocytic Tumours
- •Malignant Melanoma (Melanocarcinoma)
- •Stagewise Treatment (more Details) and Recent Advances
- •Other Malignant Skin Tumours
- •32. Burns and Skin Grafting
- •Free Skin Grafting
- •Neural Tumours
- •33. Tumours and Soft Tissue Sarcoma
- •Benign Tumours
- •Malignant Tumours
- •Paraneoplastic Syndromes (PNS)
- •Soft Tissue Sarcomas (STS)
- •Cystic Swellings
- •Transilluminant Swellings in the Body
- •Swellings in Submandibular Triangle
- •Carotid Body Tumour (Chemodectoma)
- •Neck Dissections
- •Metastasis in Cervical Lymph Nodes—Various Levels
- •Pancoast’s Tumour
- •Oral Cancer
- •Carcinoma of Buccal Mucosa
- •Carcinoma of Tongue
- •Carcinoma of Lip
- •Carcinoma Maxillary Antrum
- •Benign Lesions in the Oral Cavity
- •Odontomes
- •Median Mental Sinus
- •Vincent’s Angina
- •Cleft Lip and Cleft Palate
- •Miscellaneous
- •Mucous Cysts
- •36. Salivary Glands
- •Surgical Anatomy of the Parotid Gland
- •Acute Parotitis
- •Chronic Submandibular Sialoadenitis
- •Salivary Gland Tumours
- •Mucoepidermoid Tumour
- •Other Tumours
- •Malignant Parotid Tumours
- •Frey’s Syndrome—Gustatory Sweating
- •Parotid Fistula
- •Minor Salivary Gland Tumour
- •Surgery for Facial Nerve Palsy
- •Peripheral Nerve Repair and Transfers
- •37. Thyroid Gland
- •Surgical Anatomy of Thyroid Gland
- •Physiology
- •Thyroid Function Tests
- •Clinical Examination of Thyroid Swelling
- •Goitre
- •Multinodular Goitre
- •Retrosternal Goitre
- •Toxic Goitre—Thyrotoxicosis
- •Graves’ Disease
- •Malignant Tumours
- •Papillary Carcinoma Thyroid (PCT)
- •Follicular Carcinoma
- •Anaplastic Carcinoma
- •Medullary Carcinoma of the Thyroid (MCT)
- •Solitary Nodule of the Thyroid Gland
- •Thyroiditis
- •Complications of Hashimoto’s Thyroiditis
- •Complications of Thyroidectomy
- •Miscellaneous
- •Ectopic Thyroid
- •38. Parathyroid and Adrenals
- •Parathyroid Glands
- •Adrenal Glands/Suprarenal Glands
- •Disorders of Adrenal Cortex
- •Incidentalomas
- •39. Breast
- •Congenital Anomalies of Breast
- •Surgical Anatomy of Breast
- •Cystic Swellings of Breast
- •Other Types of Breast Abscesses
- •Cyclical Mastalgia with Nodularity
- •Idiopathic Granulomatous Mastitis (IGM)
- •Macrocysts
- •Galactocele
- •Discharge per Nipple
- •Galactorrhoea
- •Duct Papilloma
- •Axillary Tail Hypertrophy
- •Traumatic Fat Necrosis
- •Gynaecomastia
- •Phyllodes Tumours
- •Carcinoma Breast

224
Manipal Manual of Surgery
2. Splenectomy: Spleen is required for immunological
functions.
3. Gallium scan: Detection of lymph nodes is done by
scintigraphy, if required.
4. Bipedal lymphangiogram: Same reasons as men-
tioned above.
5. Intravenous pyelography: Renal function can be
easily assessed by CT scan.
6. MOPP regimen: Not favoured—because of toxicity
7. Pelvic RT (responsible for infertility): Not favoured.
8. Classification: Ryle’s classification is no longer used.
NON-HODGKIN’S LYMPHOMA (NHL)
Aetiology
1. Age and sex
• Small lymphocytic lymphoma: Elderly patients
• Lymphoblastic lymphoma: Male adolescents and
young adults
• Follicular lymphoma: Middle-aged adults
• Burkitt’s lymphoma: Children, young adults
2. Viruses
• RNA viruses: Human immunodeficiency virus
(HIV) produces AIDS. These patients may develop
high grade B cell lymphoma.
• DNA viruses: Epstein-Barr viruses (EBV) may
produce Burkitt’s lymphoma.
3. Bacteria: H. pylori: Gastric extranodal marginal zone
B cell lymphomas of MALT type.
4. Immunodeficiency states and immune disorders:
AIDS and organ transplantation treated with immunosuppression. Sjögren’s syndrome, rheumatoid
arthritis, systemic lupus erythematosus.
5. Genetic syndromes: Down syndrome and Klinefelter’s
syndrome.
6. Inflammatory bowel disease in particular Crohn’s
disease and its treatment.
7. Radiation exposure, to atomic bombs and nuclear
reactor accidents are at an increased risk of
developing NHL after 10–20 years.
Classification of Non-Hodgkin’s Lymphoma
. Low grade
I
• Small lymphocytic
• Follicular, predominantly small cleaved cell
II. Intermediate grade
• Follicular, predominantly large cell
• Diffuse, small cleaved cell
• Diffuse mixed small and large cell
Section II • General Surgery
• Diffuse large cell
III. High grade
• Large cell immunoblastic
• Lymphoblastic
• Burkitt’s or non-Burkitt’s lymphoma
Pathological Classification
I
. B cell NHL: Small lymphocytic lymphoma, follicular
lymphoma, Burkitt’s lymphoma (Key Box 29.11).
II. T cell NHL: Cutaneous T cell lymphoma, mycosis
fungoides and Sézary syndrome, lymphoblastic
lymphoma.
Key Box 29.11
Follicular Lymphomas (FL) or
Small Lymphocytic Lymphoma (SLL)
Called indolent lymphomas
Can be of many years’ duration
Present as painless lymphadenopathy
Spontaneous regression in 20% of patients
Also called waxing and waning adenopathy
‘B’ symptoms are unusual
Uncommon before the age of 50
Good prognosis
Remission duration and survival improvement with
‘rituximab’ (anti-CD20 antibody specific for B lymphocytes)
Clinical Features
• Outer horizontal group of lymph nodes are commonly
enlarged. Refer to Table 29.7.
Investigations
• Complete blood count
• Liver function tests including LDH: Increase LDH
represents tumour burden
• Creatinine, calcium
• Ultrasound, CT scan
• Core needle biopsy, lymph node biopsy, bone
marrow biopsy
• Immunohistochemistry is required for subclassifica-
tion. Examples: Small lymphatic lymphoma (CD5+,
CD23+), Mantle cell (CD5+, CD23–), etc.
If Waldeyer’s ring is involved, an upper GI scopy should be
considered since the incidence of gastric involvement in such
cases is increased.

Lymphatics, Lymph Vessels and Lymphoma
Table 29.7 Comparison of Hodgkin’s and non-Hodgkin’s lymphomas
Hodgkin’s lymphoma Non-Hodgkin’s lymphoma
Age Bimodal age More than 50 years
Involvement of lymph nodes Left supraclavicular, axillary, External Waldeyer’s ring, submental, submandibular,
inguinal preauricular, postauricular, occipital nodes
Retroperitoneal nodes Uncommon Common
Tonsil enlargement Not enlarged Tonsils may be enlarged
Epitrochlear node Not enlarged Can be enlarged
Hepatomegaly Uncommon Common in low grade
Involvement of bone Uncommon (10%) In 40% of cases, iliac crest is involved by the time of diagnosis
Alcohol-induced pain Characteristic Absent
Fluctuating fever Present Absent
Prognosis Better prognosis Poor prognosis
Common presentation Lymphatic organ Extralymphatic
Mediastinal nodes Common Very few patients with DLC (diffuse large B cell lymphoma)
225
DIFFERENT SITES OF LYMPH NODES IN NHL (Figs 29.18 to 29.23)
A B
Fig. 29.18: Large occipital lymph
node
Fig. 29.21: Bilateral lymph nodes in
the upper neck
Figs 29.19A and B: Massive axillary lymphadenopathy
and enlargement of submandibular, upper deep cervical
and preauricular lymph nodes
Fig. 29.22: Preauricular, post-
auricular and facial lymph nodes
Management of Non-Hodgkin’s Lymphoma
Depends on the Grade of the tumour, Stage of the disease.
• Stages I and II: Low grade—radiotherapy/chemo-
therapy with CHOP—Cyclophosphamide, Doxorubcin, Oncovin and Prednisone in cases of indolent
or low-grade lymphoma. If relapses another regimen
is added.
• Stages I and II: Intermediate and high grade—CHOP-
chemotherapy.
Fig. 29.20: Advanced case of non-
Hodgkin’s lymphoma with involvement of groin nodes, testicle and
skin deposits in the thigh
Fig. 29.23: Epitrochlear lymph
node enlargement
• Stages III and IV and high-grade Rituximab is added.
R-CHOP.
• Those who relapse can be treated with Rituximab
monotherapy.
Aggressive large B cell lymphomas with CD20
positive cases are treated with R-CHOP.
Gastric MALT lymphomas may completely regress
with therapy against H. pylori with appropriate antibiotics and proton pump inhibitors.
Section II • General Surgery

226
Manipal Manual of Surgery
Anaplastic large cell lymphoma (ALCL): It is treated
with immunotoxins: They act as homing devices to
deliver the toxins directly to the cancer cells. An example
of this is brentuximab vedotin, which contains an
antibody to CD30 attached to a cell poison. This has
been shown to help treat patients who are unresponsive
to chemotherapy
MISCELLANEOUS
BURKITT’S LYMPHOMA
(SMALL NONCLEAVED LYMPHOMA)
• It is a type of high grade non-Hodgkin’s lymphoma,
first described by Burkitt, affecting the jaw bone
(maxilla, mandible).
• It is rare everywhere except in a few places where
malarial infestation is heavy.
• It is caused by Epstein-Barr virus (EBV), which multi-
plies in the presence of heavy malarial infestation.
Types
• Endemic: Parts of Africa and other tropical locations.
It is associated with EBV. It affects the jaw and orbit
and has a good prognosis.
• Sporadic: Throughout the world. It is not associated
with EBV. It affects the abdomen and GI tract, rather
than bones, and has a poor prognosis.
Diagnosis
• Biopsy will reveal typical ‘starry sky’ appearance
with primitive lymphoid cells and large clear histiocytes.
Treatment
• Endemic cases respond well to cyclophosphamide.
• Sporadic cases need to be treated with combination
chemotherapy.
SÉZARY’S SYNDROME
It is also a type of cutaneous T cell lymphomas. Here,
skin involvement is manifested clinically as a
generalised exfoliative erythroderma along with an
associated leukaemia of Sézary cells.
These cells are characterised by a cerebriform nucleus.
They are indolent tumours so patients have a good
survival time.
CHYLURIA
• It is the most common manifestation of ruptured
lymph vessels due to filariasis (others being chylocoele, chylous ascites, and chylothrax).
• It occurs when intestinal lymphatics are obstructed
by filarial fibrosis and the lymphatics are diverted to
renal lymphatics.
• The dilated and tortuous lymphatics, due to high
pressure, rupture into the renal pelvis and ureter,
leading to chyluria. Passage of a large amount of
chyle leads to a loss of protein and fat, resulting in
malnutrition. Such patients are also debilitated with
loss of immunity.
• Oral ingestion of fat labelled with Sudan red III turns
the urine pink in these cases.
• It is treated by diethylcarbamazine, bed rest, foot-
end elevation of the bed, and administration of a high
protein diet.
Section II • General Surgery

Lymphatics, Lymph Vessels and Lymphoma
227
1. Which of the following is false regarding functions
of the lymphatic system?
A. Lymph circulation occurs through lymphatico-
venous junctions
. Lymphatic fluid contains macromolecules
B
C. The right lymphatic duct drains into the internal
jugular vein
D. The lymphatic fluid from the intestines pass
through the liver
2. The following are true for lymph trunks except:
A. They are lined by a single layer of endothelial cells
. Pulsations of the vessels help in lymph circulation
B
C. The thoracic duct drains into the right internal
jugular vein
D. They do not accompany neurovascular bundles
in the central nervous system
3. The following are risk factors for lower limb
lymphoedema except:
A. Inguinal block dissection
. Pelvic radiotherapy
B
C. Obesity
D. Alcohol abuse
4. Stemmer’s sign refers to:
A. Gross thickening of the subcutaneous tissue in a
lymphoedematous leg
B
. Deep muscle of the leg is not involved
C. Skin on the dorsum of the toes cannot be pinched
D. Buffalo hump on the dorsum of the foot
5. The following are true for filarial elephantiasis of
the leg except:
A. It is caused by Wuchereria bancrofti
. It is transmitted by Culex fatigans
B
C. Microfilariae do not produce any lesion
D. Significant changes occur deep to the deep fascia
6. The majority of primary lymphoedema is due to:
A. Congenital hyperplasia of lymphatics
. Distal obliteration of lymphatics
B
C. Proximal obliteration of lymphatics
D. Central obliteration of lymphatics
7. Oxerutins used in lymphoedema act by the following
mechanisms except:
A. Decrease capillary permeability
. Improve microcirculatory perfusion
B
C. Stimulate interstitial macrophage proteolysis
D. Increase platelet aggregation
8. Which of the following is true regarding lymphoedema?
A. Dermal lymphatics are never involved in filariasis
. Oxerutins are not used in lymphoedema
B
C. Lymphoedema pressure bandage requires 0 mmHg
pressure in the leg
D. Lymphoedema does not predispose to malig-
nancies
9. Contiguous and centripetal spread occur in:
A. Hodgkin’s lymphoma
. Non-Hodgkin’s lymphoma
B
C. Burkitt’s lymphoma
D. Sézary’s syndrome
10. The following are true for lymphocytic predominance nodular lymphoma except:
A. It has large atypical cells
B
. It expresses CD20+
C. It is indolent
D. It has a favourable prognosis
11. The following are true about classical Hodgkin’s
lymphoma except:
A. Spread is contiguous
B. Large atypical cells are seen
C. B symptoms are characteristic
D. CD15 and CD30 are expressed
12. The following are the features of a Reed-Sternberg
cell except:
A. It is a giant cell
. It contains mirror-image nuclei
B
C. It is a large multinucleated cell
D. It is not derived from B lymphocytes
13. The following are true for mediastinal lymphoma
except:
A. It is the most common malignancy in the media-
stinum
. Its response to chemotherapy is dramatic
B
C. It is Hodgkin’s lymphoma
D. The posterior compartment is commonly involved
Section II • General Surgery

228
Manipal Manual of Surgery
14. The following are no longer followed in lymphomas
except:
A. Pelvic radiotherapy
. Splenectomy as a staging procedure
B
C. Rye’s classification
D. ABVD regimen is commonly given
15. The following are causes of epitrochlear node
enlargement except:
A. Hodgkin’s lymphoma
. Non-Hodgkin’s lymphoma
B
C. Secondary syphilis
D. Cat-scratch fever
16. The following are true for Rituximab except:
A. It is a monoclonal antibody against protein CD20
. It is used to treat leukaemia
B
C. It can also be used to treat follicular lymphomas
D. It has no role in transplant rejections
17. The following are true for Burkitt’s lymphoma
except:
A. It is associated with Epstein-Barr virus
. It is not associated with heavy malarial infestation
B
C. It affects the jaw and orbital bones
D. It gives a starry sky appearance on histopathology
Answers
1. D 2. C 3. D 4. C 5. D 6. B 7. D 8. A 9. A 10. A
11. C 12. D 13. D 14. D 15. A 16. D 17. B
Section II • General Surgery

30
Varicose Veins and
Deep Vein Thrombosis
Primary varicose veins
Secondary varicose veins
Surgical anatomy of venous system of legs
Anatomy of the long saphenous vein
Clinical examination
Treatment
INTRODUCTION
Varicosity is the penalty for verticality against gravity.
This is the common statement made in lecture classes.
The blood has to flow from the lower limbs into the
heart against gravity because of the upright posture of
human beings. In many cases, varicose veins are
asymptomatic. Raised intra-abdominal pressure may
also precipitate varicose veins, which is more common
in females due to repeated pregnancy. The complications of varicose veins lead to hospitalisation.
Examples of varicosity: Long saphenous varicosity,
short saphenous varicosity, oesophageal varices, fundal
varices, haemorrhoids, etc. In this chapter, varicosity
of the leg is discussed.
DEFINITION
Complications
Short saphenous varicosity
Recurrent varicose veins
Deep vein thrombosis
Pelvic congestion syndrome
Pulmonary thromboembolism
• Factors that predispose to varicose veins are given
in Key Box 30.1.
• Very often, the valve at the saphenofemoral (SF)
junction is incompetent/absent. The valves may also
be absent at the junction of superficial veins joining
the deep veins.
• Klippel-Trénaunay syndrome is a congenital venous
abnormality wherein superficial and deep veins
do not have any valves. It is also called valveless
syndrome (Key Box 30.2). It is not a hereditary
condition.
• Primary varicosity may also be genetic. Some patients
inherit abnormalities in the FOXC2 gene. These
factors, in addition to prolonged standing (agriculturists, traffic police, hotel workers), contribute to the
development of varicose veins.
Dilated, tortuous, and elongated superficial veins of the
limb due to reflux are called varicose veins. They are
about 3 mm in diameter.
PRIMARY VARICOSE VEINS
• Primary varicose veins occur as a result of congenital
weakness in the vein wall due to defective connective
tissue and smooth muscle.
• They may also result from muscular weakness or
congenital absence of valves.
Key Box 30.1
Factors which Predispose to Varicose Veins
Height: Tall individuals suffer more
Weight: Obesity may weaken vein wall
Occupation: Hotel workers, policemen, shopkeepers,
tailors
Side: Left is affected more than the right
Age and sex: Not very clear
229

230
Manipal Manual of Surgery
Key Box 30.2
Klippel-Trénaunay Syndrome
Incidence 1 in 1,00,000 population.
Also called angio-osteohypertrophy syndrome
Characterised by nevus flammeus (port-wine stain),
venous malformations, lymphatic malformations and
soft tissue hypertrophy of the affected limb.
Can also have large arteriovenous malformations.
Patients can complain of pain heaviness in the limbs,
difficulty in walking due to abnormal length of the limb.
Excision of veins, sclerotherapy, laser treatment for
port-wine stain are a few methods to treat the veins.
SECONDARY VARICOSE VEINS
• Women are more prone to varicose veins because of
the following reasons:
– Pregnancy and pelvic tumours cause proximal
obstruction to the blood flow.
– Pills (oral contraceptive pills) alter the viscosity of
blood.
– Progesterones dilate the vessel wall.
• Congenital arteriovenous (AV) fistula increases
blood flow and increases venous pressure.
• Deep vein thrombosis may occur postoperatively, as
a result of road traffic accidents, etc. These may lead
to the destruction of valves, resulting in varicose veins.
Key Box 30.3
Superficial System—Salient Features
As the name suggests, they are in the superficial fascia
and are often visible (saphenous means easily seen).
They are low pressure and poorly supported system.
They are provided with numerous valves.
The middle coat of these veins consists mostly of
smooth muscle.
The middle coat is also thicker than that of other veins.
Normal blood flow is from superficial to deep system
of veins.
SU27.5: Describe the applied anatomy of venous system
of lower limb.
SURGICAL ANATOMY OF THE VENOUS SYSTEM OF LEG
It may be discussed under the following headings:
1. Superficial venous system—long and short
saphenous veins and their tributaries
2. Perforators
3. Deep venous system
SUPERFICIAL VENOUS SYSTEM
Anatomy of the L
ong Saphenous Vein (LSV)
LSV starts in the foot from the tributaries of the dorsal
venous arch which runs in front of metatarsal heads in
the subcutaneous tissue in the dorsal aspect of foot. It
ascends in front of the medial malleolus, and runs along
the medial side of the leg. It then ascends in the thigh
and ends at the saphenofemoral (SF) junction by joining
the femoral vein, which is 1.5 inches (4 cm) below and
lateral to the pubic tubercle. SF junction can be variable,
more superiorly located sometimes. Today the junction
Section II • General Surgery
is marked before surgery during venous ultrasound
Fig. 30.1: Long saphenous vein, tributaries, communicating veins
which helps in placing the incision accordingly. It has
15–20 valves. Absence of valves results in varicose veins
(Key Box 30.3 and Fig. 30.1).
Tributaries: These tributaries connect the long
saphenous with the short saphenous vein (SSV). They
are also known as communicators. They are as follows.
Tributaries Near its Termination
1. Superficial circumflex iliac vein
. Superficial epigastric vein
2
3. Superficial external pudendal vein
Tributaries in the Lower Thigh
1. Lateral superficial femoral vein
2
. Medial superficial femoral vein
3. Transverse suprapatellar vein
4. Transverse infrapatellar vein
Tributaries in the Leg
1. Anterior vein of the leg—also called anterior
(accessory) saphenous vein (ASV).

Varicose Veins and Deep Vein Thrombosis
231
2. Posterior arch vein—lies parallel to and behind the
main trunk of long saphenous vein. It anastomoses
with small venous arches connecting the medial
perforating veins.
PERFORATORS (Fig. 30.2)
These are the veins which connect long saphenous vein
with the deep system of veins. Since they perforate the
deep fascia, they are called perforators. There are
5 constant perforators in the lower limb on the medial
side.
• Leg perforators: They are 3 in number. The lowest
perforator is below and behind the medial malleolus,
the middle perforator is 10 cm above the tip of the
medial malleolus, and the upper perforator is 15 cm
above the medial malleolus.
• Knee perforator: It is just below the knee.
• Thigh perforator: It is a palm-breadth above the knee.
A knowledge of perforators forms the basis of the
multiple tourniquet test. Most of the perforators
contain valves. Weakness of or damage to these valves
results in varicosity.
DEEP VENOUS SYSTEM
This comprises the femoral and the popliteal veins, veins
or 3 pairs of venae comitantes accompanying the
anterior tibial, posterior tibial, and peroneal arteries, and
the valveless veins draining the calf muscles (soleal
venous sinus).
• Formation of popliteal vein: It is formed by these
6 venae comitantes which unite and form popliteal
vein in the popliteal fossa. Short saphenous vein (SSV)
as the name implies is short and ascends behind the
lateral malleolus joins popliteal vein at saphenopopliteal junction (SP junction). Termination point
can be variable often it is inferior. Near the
termination it pierces popliteal fascia. Popliteal vein
also receives Giacomini vein and gastrocnemius
veins.
• Formation of femoral vein: Popliteal vein continues
upwards in the sub-sartorial canal as femoral vein
and receives long saphenous vein at SF junction. All
tributaries mentioned above would have joined the
vein and before it pierces it not only receives named
3 tributaries but also receives deep profunda vein.
Femoral vein continues as external iliac vein above
the inguinal ligament.
• Soleal plexus of veins: These are called deep veins
of the calf region or also called calf muscle pump.
Blind ended soleal sinusoids join them and help in
pumping the blood. These veins are also called
capacitance vessels. This is because they have the
capacity to accumulate large volume (60%) of blood
inside. Using this principle, simple elevation of both
legs is done in hypovolaemic shock patients as initial
step to resuscitate.
Salient Features of the Deep Venous System
• It is a high pressure system, well-supported by powerful
muscles.
• They are connected to the superficial veins through
perforators.
• The powerful calf muscle contraction returns blood to
the heart.
• The deep veins also contain valves (Fig. 30.3).
Fig. 30.2: Perforators
Venous pathophysiology: Pressure at the capillary side
of venule is very low, around 10 to 12 mmHg. Pressure
Fig. 30.3: Deep venous system
Section II • General Surgery

232
Manipal Manual of Surgery
becomes less and less as the vein is traced upwards.
For example: In inferior vena cava it is about 5 mmHg.
Blood is returned to the heart from the lower limbs
through the following mechanisms:
• Calf muscle pump: In standing position blood
pressure at the venule is about 100 mmHg. It refers
to the alternate contraction and relaxation of the
muscles of the leg (the major factor). The pressure
within the calf compartment rises to 200–300 mmHg
during walking.
• Negative intrathoracic pressure during inspiration
resulting in increase in intrathoracic volume.
• Competent valves (unidirectional) in the leg (Key
Box 30.4): When these valves are absent or weak,
perforator incompetence develops, which results in
varicose veins.
• Vis-a-tergo of the circulation: The pressure trans-
mitted from the arterial tree passes the capillary bed
to the venous side, which helps return blood to the
heart at rest.
• Venae comitantes.
Key Box 30.4
Distribution of Valves
Inferior vena cava : No valve
Common iliac vein : No valve
Long saphenous vein : 10–14 valves
Short saphenous vein : 1 valve
A Few Terminologies for Dilated Veins
1. Telangiectasia: Confluence of dilated intradermal
venules of <1 mm diameter.
2. Reticular veins: Dilated subdermal veins of 1–3 mm
diameter.
3. Ankle flare: Dilated group of reticular (corona
phlebectasia) veins near the medial malleolus.
4. Blowout: A localised dilatation of the vein which is
‘dome’ like/ballooned out.
5. Saphena varix: A dilated long saphenous vein near
the termination (SF junction) in the groin which is
soft and reducible on lying down and elevating the
leg.
6. Atrophic blanche: Atrophic skin with pigmentation
and reticular veins—seen in the ankle region.
Before we start the clinical examination of the varicose
veins study Tables 30.1 and 30.2.
Table 30.1 Classification
venous disease
Classification Definition
CClinical signs (grades 0–6): A for
asymptomatic or S for symptomatic
EEtiologic classification (congenital,
primary or secondary)
AAnatomic distribution (superficial, deep
or perforator, alone or in combination)
PPathophysiologic dysfunction (reflux or
obstruction, alone or in combination)
Table 30.2 Clinical (C) (Figs 30.4 to 30.10)
Grade Characteristics
C0 No visible or palpable signs of venous disease
C1 Telangiectases, reticular veins
C2 Varicose veins
C2r Recurrent varicose veins
C3 Oedema without skin changes
C4 Skin and subcutaneous changes
C4a Pigmentation, eczema
C4b Lipodermatosclerosis or atrophic blanche
C4c Corona phlebectasia
C5 Healed ulceration
C6 Active ulceration
C6r Recurrent active ulceration
Etiological classification (E)
Ep: Primary
Es: Secondary: Esi Secondary intravenous, Ese Secondary
extravenous
Ec: Congenital
En: No cause identified
Anatomical
As Superficial: example: As- Ret: reticular veins, As-SSV
means short saphenous vein.
Ad Deep veins—example Ad IVC means inferior vena
cava Involvement.
Ap Perforator involvement—example: TPV means thigh
perforator involvement.
An No venous anatomic location identified.
Pathological
Pr Reflux
Po Obstruction
Pr,o Reflux and obstruction
Pn No pathophysiology identified
1
of chronic lower extremity
SU27.6: Describe the pathophysiology, clinical features,
investigations and principles of management of DVT and
varicose veins.
1
The 2020 revision of CEAP: Summary of clinical (C) classifications. Ref: Lurie et al, Journal of Vascular Surgery: Venous and Lymphatic Disorders,
2020.
Section II • General Surgery

Varicose Veins and Deep Vein Thrombosis
233
CLINICAL EXAMINATION OF A CASE OF LEG VARICOSITY
Symptoms
• The patient often complains of swelling of the legs. It
is due to an increased volume of fluid in skin and
subcutaneous tissues, increased interstitial fluid,
impaired lymphatic drainage, and increased
hydrostatic pressure. Most patients present with
dilated veins in the leg. They are minimal at the start
of the day and are sufficiently large by the end of the
day due to venous engorgement.
• Dragging pain in the leg or a dull ache due to
heaviness. Night cramps occur due to change in the
diameter of veins. Aching pain is relieved at night
by taking rest or elevating the limbs. Night cramps
also occur due to the prevention of nutrients and
oxygen from reaching the muscles due to pooling of
deoxygenated blood, which results in lactic acid
accumulation. Night cramps are more common in
women.
• Sudden pain in the calf region with fever and oedema
of the ankle region suggests deep vein thrombosis
(DVT). Some patients with DVT may be asymptomatic.
• Patients may present with ulceration, eczema,
dermatitis, and bleeding.
• Symptoms of pruritus/itching and skin thickening.
Interestingly, pain due to varicose veins is relieved with exercise
in contrast to pain due to arterial diseases, which worsen with
exercise.
Signs
Inspection (should be done in standing position)
• Dilated veins are present in the medial aspect of leg
and the knee. Sometimes they are visible in the thigh
(Figs 30.4 to 30.10).
• A single dilated varix at the SF junction is called
saphena varix. It is due to saccular dilatation of
the upper end of the long saphenous vein at the
saphenous opening (Tables 30.1 and 30.2).
• Veins are tortuous and dilated.
• A localised, dilated segment of the vein, if present, is
an indication of a blowout. It signifies an underlying
perforator (Fig. 30.11).
Fig. 30.4: Grade 0
Fig. 30.5: Grade 1 Fig. 30.6: Grade 2 Fig. 30.7: Grade 3
See Table 30.2
for description
of various
grades of
chronic lower
extremity
venous disease
Fig. 30.10: Grade 6Fig. 30.9: Grade 5Fig. 30.8: Grade 4
Section II • General Surgery
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