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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

244
Manipal Manual of Surgery
monitored with prothrombin time and international
normalized ratio (INR). INR should be 2.0–3.0.
3. Low molecular weight heparin (LMWH) is given
once or twice a day, in the form of injection. No blood
monitoring is required. Incidence of bleeding is less
with LMWH. More details are given at the end of
this chapter.
4. Inferior vena caval filters indicated if thrombus is
extensive and recurrent. They can be inserted
percutaneously via the femoral vein in patients who
have contraindications for lytic therapy.
5. Compression stockings.
IVC filters are more commonly indicated in patients with
recurrent DVT and symptomatic pulmonary embolism.
CHRONIC DEEP VEIN THROMBOSIS
• DVT lasting for >4 weeks is defined as ‘Chronic DVT’.
Signs and symptoms include pain, oedema, telangiectasia, hyperpigmentation, lipodermatosclerosis,
ulceration, and venous
claudication.
• The clinical manifestations
are secondary to postthrombotic sequelae (PTS)
and occur after an episode
of DVT, as thrombosis leads
to venous hypertension
from venous obstruction
and reflux. Classically, the
limb is described as having
an inverted beer bottle or
champagne bottle appearance (Fig. 30.39).
Fig. 30.39: Patient with
DVT. (Courtesy: Dr Siddesh,
senior consultant, Mysore,
Karnataka.)
Investigations
. Doppler study: It is ideal for femoral vein thrombosis
1
or if the thrombus extends into the popliteal vein.
Normal femoral vein gives a wind storm sound
which completely disappears at the end of inspiration. No sound is heard if there is femoral thrombosis
(Key Box 30.15).
Key Box 30.15
Duplex Scanning in Deep Vein Thrombosis (B-Mode)
Vein is larger than normal because of occlusion
Not completely compressible
Lacks respiratory variation
Does not show flow augmentation with calf compression
May have collateral flow
Section II • General Surgery
• Chronic thrombosis is diagnosed by luminal filling
defect on gray-scale images, noncompressible vein,
narrow vein, absence of color Doppler, and loss of
augmentation.
2. Contrast venography: It is done by injecting a radio-
opaque dye into the dorsal venous arch with an
inflatable cuff both above the ankle and above the
knee. The clot appears as a filling defect. However,
venography is not routinely done because it is
expensive and invasive.
Treatment
Chronic DVT
• Graded compression stockings and anticoagulation
therapy. Compression stockings (30–40 mmHg) should
be worn daily for 2 years from the onset of DVT.
• Parenteral anticoagulation initially, followed by oral
anticoagulation titrated to the INR. Vitamin K antagonist (warfarin 5–10 mg/day) is given and INR is
monitored (INR should remain between 2.0 and 3.0).
• Patients with proximal DVT (iliofemoral), recurrent
episodes, or DVT secondary to malignancy should
be treated for 6 months–1 year. Indefinite therapy is
recommended for patients with recurrent episodes
of venous thrombosis, regardless of the cause.
• Post-phlebitis limb with ulcers may heal with aspirin
and pentoxifylline.
• Chronic thrombosed veins are treated by balloon
dilatation—venoplasty, thrombolysis. Venous
stenting is frequently needed of the IVC and iliac
veins to maintain flow and venous patency.
• Surgery is not done routinely. However, in chronic
cases, venous bypass has been attempted with moderate success. Palma operation is performed for
iliofemoral thrombosis wherein the common femoral
vein below the block is anastomosed to the opposite
femoral vein using the long saphenous vein from the
opposite side. May-Husni operation, wherein the popliteal vein is anastomosed to long saphenous vein above.
Complications
1. Permanent oedema of the limb. The limb has an
inverted beer bottle appearance.
. Pulmonary embolism because the thrombus is not
2
attached to the vessel wall.
3. Secondary varicosity and nonhealing ulcer.
PROPHYLAXIS OF DVT (Key Box 30.16)
• Decrease obesity and advise exercises before surgery.
• Low dose heparin 5,000 units subcutaneously,
2 hours before surgery and 24 hours after surgery,
then 12 hourly for 5 days in cases of major surgeries

Varicose Veins and Deep Vein Thrombosis
245
Key Box 30.16
Prophylaxis: Risk Groups
Low risk : >40 years
Minor illness
Operation <30 minutes
Moderate : >40 years
risk Debilitating illness
Major surgery <30 minutes
High risk : >50 years, medical conditions—MI, stroke,
recent thromboembolism, orthopaedic
surgeries, major surgery, malignancy, obesity.
like cholecystectomy, abdominoperineal resection,
etc. Low molecular weight heparin decreases chances
of bleeding.
• Intermittent pneumatic compression of the calf
throughout the operation maintains blood flow in the
lower limbs. Inflation pressure is around 30–50 mmHg.
• Dextran 40 inhibits sludging of red blood cells and
platelet aggregation.
• Aspirin with dipyridamole has been used
(antiplatelet agents).
• Early mobilisation, walking, and adequate hydration.
MORE DETAILS OF ANTICOAGULATION AND DVT
Treatment should be initiated at the earliest. The main
aims are to reduce the morbidity and risk of pulmonary
thromboembolism (PTE) and to decrease postthrombotic sequelae.
Treatment Modalities
. Anti-thrombotic therapy:
1
A. Heparin: It is a natural anti-coagulant. It is also un-
fractionated heparin (UFH). Initial IV/SC heparin
therapy is continued for a minimum of 5 days.
Heparin acts by binding to antithrombin, which in
turn inhibits factors IIa, Xa, XIa, and XIIa. It also
binds to tissue factor pathway inhibitor, which
inhibits the conversion of X to Xa and IX to XIa. It
also catalyses inhibition of thrombin by cofactor
II, independent of the antithrombin mechanism.
Dose of heparin: 80 U/kg IV bolus infusion at
18 U/kg/hour or 10000 units IV 8th hourly. The
route is later changed to subcutaneous.
Complications of heparin:
• Haemorrhage, which may be reversed by protamine
sulphate (up to 50 mg IV over 10 mins)
• HIT (heparin-induced thrombocytopaenia) due to
heparin-associated antiplatelet antibodies directed
against platelet factor IV
• Osteopenia
• Rarely—skin necrosis/hypersensitivity
• Hypoaldosteronism and osteoporosis
Contraindications to heparin therapy:
• Eye surgery, neurosurgery
• Bleeding disorders
• Uncontrolled, severe hypertension
• Cirrhosis, renal failure
B. Low molecular weight heparin (LMWH): They are
safe and efficacious. They may be administered
easily once or twice daily subcutaneously.
Enoxaparin and dalteparin are a few drugs.
Enoxaparin 0.5 mg/kg is given for prophylactic
dosing. The therapeutic dose is 100 U/kg twice
daily. They act by selectively inhibiting factor Xa.
They do not require laboratory monitoring.
Compared to heparin, they have a very low chance
of resulting in thrombocytopaenia. Since they have
lesser anti-platelet action, there are less chances of
haemorrhage.
C. Fondaparinux: It is a synthetic pentasaccharide
factor Xa inhibitor. The dose depends on the weight
of the patient—5 mg OD (once daily) for 50 kg,
7.5 mg OD for 50–100 kg, 10 mg OD for ≥100 kg
given as subcutaneous injections.
D. Direct thrombin inhibitors: Examples include
hirudin, agatroban, and bivalirudin. They are
indicated in patients with HIT. They are usually
given for 7 days till platelet counts normalize and
then heparin is re-introduced. Dosing is as follows.
Hirudin 4 mg/kg IV bolus f/b infusion T½—
30–60 min with APTT at 1.5 to 2.5 times. Agatroban
2 µg/kg/min infusion, T½—40–50 min with APTT
at 1.5 to 3 times.
E. Warfarin (Wisconsin Alumni Research Foundation
coumARIN): It is given orally, 2–10 mg/day. It
interferes with hepatic synthesis of vitamin Kdependent soluble anticoagulation factors. An
advantage of warfarin is that it is given orally. Its
disadvantage is that it requires more frequent
monitoring than heparin. Bleeding may occur, if
the INR ratio is high.
F. Acitrom (Acenocoumarol) is another anticoagulant
used in the treatment and prevention of abnormal
blood clots. It is similar to warfarin but has a longer
half-life and less interactions. It does not dissolve
formed blood clots but may prevent them from
becoming larger and leading to more serious
problems like embolism.
2. Thrombolysis: It is popularly called catheter-directed
thrombolysis. Streptokinase, urokinase, etc. are used.
They convert plasminogen to plasmin which in turn
degrades fibrin, thereby dissolving the clots.
Section II • General Surgery

246
Manipal Manual of Surgery
Advantages of thrombolysis include early recovery
of symptoms and signs, early prevention of
pulmonary thromboembolism, and prevention of
post-phlebitis syndrome. However, clot propagation
and re-thrombosis cannot be prevented.
Alteplase: Recombinant tissue plasminogen activator
(rtPA). It is given as a 10 mg IV bolus, followed by a
90 mg infusion over 90 minutes.
3. IVC (inferior vena cava) filters: Patients with
recurrent embolism, pelvic vein thrombosis, or large
calf venous thrombosis may be treated with IVC
filters. The IVC filter is placed through a small incision
in a vein in the groin or neck. A thin, flexible tube
(catheter) is inserted inside the vein. The catheter is
then gently guided into the IVC. An IVC filter is
introduced into the vein in a collapsed state. The filter
is left in place, and the catheter is removed. The filter
then expands and attaches itself to the walls of the
IVC. In a few cases of recurrent thromboembolism, it
may be left in place permanently. In some cases, it
may be removed after a period of time.
4. Operative thrombectomy: It is definitely indicated
for pulmonary embolism but is rarely performed for
leg veins.
PULMONARY THROMBOEMBOLISM
• Mostly thrombus originates in the leg veins—from
deep veins and cause pulmonary embolism.
Prolonged immobilisation, postoperative patients,
major fracture long bones are a few important causes.
Patients present with the following features. Recently
COVID
-19 infections have been associated with many
cases of thrombosis.
• Tachypnoea and tachycardia
• Chest pain cough with or without streaks of blood
• Breathlessness
• ECG may show an S1Q3T3 pattern (S wave in lead I,
Q and inverted T waves in lead III).
Investigations
• Ventilation perfusion scan (V/Q)
• CT angiography of the thorax
Treatment
• Rest, compression bandage, elevation
• Anti-DVT treatment
MISCELLANEOUS
PELVIC CONGESTION SYNDROME
A few premenopausal patients complain of dull aching/
severe pain in the pelvis. Clinical examination may
reveal tenderness in the hypogastrium. A few salient
features are given below.
Premenopausal patients
Excessive micturition, excessive bleeding during
menstruation
Leg varicosity in atypical sites, such as the thigh
Varicosity of the ovary, vulva, pelvic veins
Increased on standing
Chronic, noncyclical pelvic pain
Remember as PELVIC
Management
• Ultrasound, CT, and MRI may be necessary to rule
out a pelvic pathology.
• Psychotherapy and nonsteroidal anti-inflammatory
drugs are of some help.
Heparin was started on the 5th day for 5 days. He was
advised 4 mg of warfarin postoperatively for 6 months,
with frequent monitoring of APTT and INR. The dose of
warfarin was adjusted after 1 month. He was also advised
to wear elastic compression stockings. At the end of
6 months, his DVT was completely cured.
Section II • General Surgery

Varicose Veins and Deep Vein Thrombosis
247
1. Which of the following statements is false regarding
long saphenous vein anatomy?
A. It starts from the dorsal venous arch
It ascends in front of the medial malleolus
B.
C. It has 15–20 valves
D. The posterior arch vein is not a tributary of long
saphenous vein
2. The following are true for the short saphenous vein
except:
A. It has 6 valves
B.
It ascends behind the lateral malleolus
C. Its termination is often not constant
D. Incompetency results in an ulcer on the lateral
side of the leg
3. The following are features of the deep venous system
except:
A. High pressure system
Has valves
B.
C. Present in the soleal group of muscles
D. Connected to the superficial veins
4. The following are true for perforators except:
A. They communicate between the superficial and
deep veins
B.
They are present in the leg
C. They do not have valves
D. SEPS is the endoscopic surgery performed for
perforators
5. Trendelenburg test is performed to determine:
A. Saphenopopliteal incompetence
B.
Saphenofemoral incompetence
C. Deep vein thrombosis
D. Site of perforators
6. Perthes’ test is done to determine:
A. Saphenopopliteal incompetence
B.
Saphenofemoral incompetence
C. Deep vein thrombosis
D. Site of perforators
7. The characteristic feature of a venous ulcer in the leg is:
A. Deep, painful ulcer
B.
Superficial ulcer with surrounding pigmentation
C. Penetrating ulcer with visible bone
D. Ulcers on the dorsum of the foot
8. Plethysmography is based on the measurement of
which of the following?
A. Volume changes B. Pressure changes
C.
Sound changes D. Velocity
9. The following are true for Doppler ultrasound
except:
A. It can detect patency of veins
B.
It can detect arterial pulses
C. It acts by the Doppler principle
D. It is used to visualise movement of blood within a
vessel
10. The following are true about injection sclerotherapy
for treating varicose veins except:
A. The vein has to be full during injection
Below-knee varicosity may be treated with sclero-
B.
therapy
C. Recurrent varicosity may be treated with sclero-
therapy
D. It is useful in veins with <3 mm diameter
11. Which of the following is true about radiofrequency
ablation?
A. Long saphenous varicosity may be treated
B.
Hepatoma >6 cm is often an indication for treatment
C. May be used for Barrett’s oesophagus
D. Nerves and cardiac muscles are not stimulated
during the treatment
12. The following are true for venous ulcer formation
except:
A. Ambulatory venous hypertension
B.
Free radical release
C. Fibrin, fibronectin, collagen IV
D. Haem deposition
13. The earliest sign of DVT is:
A. Calf tenderness
B
Rise in temperature
.
C. Swelling of calf muscles
D. Homan’s sign
14. The following are seen in DVT except:
A. High fever
B.
Increased local temperature
C. Pain
D. Tenderness
Answers
1. D 2. C 3. C 4. C 5. B 6. C 7. B 8. A 9. D 10. A
11. B 12. D 13. A 14. A
Section II • General Surgery

31
Skin Tumours
Classification of skin tumours
Premalignant lesions
Basal cell carcinoma
Squamous cell carcinoma
Melanocytic tumours
INTRODUCTION
The skin, the outermost coat of the human body,
functions as a protective cover against various insulting
agents, such as ultraviolet radiation, excessive heat, and
various chemical agents.
• Hence, it is one of the commonest cancers in elderly
patients. However, more than 90% of skin tumours
are curable because they are diagnosed early and
easily (unlike intra-abdominal malignancies). Many
of them are low-grade cancers. Among skin cancers,
about 70% are basal cell carcinomas, 20% are
squamous cell carcinomas, and 5% are melanocarcinomas.
• Other rare skin cancers are sebaceous carcinomas,
dermatofibrosarcomas, etc. In this chapter, only
common malignant skin tumours and some
common skin lesions, such as corn and wart, are
discussed.
Malignant melanoma
RECIST criteria
Other malignant skin tumours
Other skin lesions
II. Melanocytic Tumours
A. Benign
• Junctional naevus
• Compound naevus
• Intradermal naevus
• Hutchinson’s freckle
• Hairy and blue naevus
B. Malignant
• Superficial spreading melanoma
• Nodular melanoma
• Lentigo maligna melanoma
• Amelanotic melanoma
• Acral lentiginous melanoma
• Desmoplastic melanoma
CLASSIFICATION OF SKIN TUMOURS
I. Epider
A. Benign
• Papilloma
• Seborrhoeic keratosis
• Verrucous naevus
B. Malignant
• Basal cell carcinoma
• Epithelioma and Marjolin ulcer
mal Tumours
III. Sweat Gland Tumours (Malignant)
• Hidradenocarcinoma
• Adenoid cystic carcinoma
IV. Sebaceous Gland Tumours
• Sebaceous adenoma
• Sebaceous carcinoma
V. Other Tumours
• Dermatofibrosarcoma protuberans
• Trichofolliculoma (hair follicle tumour)
248

Skin Tumours
PREMALIGNANT LESIONS OF
THE SKIN AND RISK FACTORS
1. Chronic irritation to the skin may occur due to
various carcinogenic chemicals, such as dyes, tar and
inorganic arsenic. Coal tar contains polycyclic
aromatic hydrocarbons, such as benzopyrenes which
are carcinogenic, arsenic, soot, mineral oil.
• Chimney Sweeps’ carcinoma, is a scrotal skin
cancer caused by an environmental carcinogensoot. This was observed and brought to the notice
of the British Parliament, and the Chimney
Sweepers Act was introduced due to the work of
Sir Percivall Pott.
2. Solar keratosis (actinic keratosis): Prolonged
exposure to sun rays may cause hyperkeratosis of the
skin (solar keratosis). Skin changes occur due to the
accumulated effect of ultraviolet rays over a period
of many years. Ultraviolet rays are also present in
phototherapy used to treat psoriasis (PUVA
therapy—Psoralen Ultra Violet-A).
Common sites: Back of hands, face, rim of ears.
• Age group: Middle age, more than 50 years.
• Clinically, the lesion is an irregular, firm, and
irritating patch which is flat or raised, and is better
felt than seen.
• Malignancy should be suspected when the lesion
becomes indurated, when a nonhealing ulcer
develops, when the central crust sheds, or when
regional lymph nodes are palpable.
3. Chronic scar: Squamous cell carcinoma that develops
in scar tissue is called Marjolin ulcer (Fig. 31.1). Burns
scar is the most common cause, followed by a varicose
ulcer scar, snakebite scar, chronic osteomyelitis scar,
and lupus vulgaris (tuberculosis of face) scar.
• Marjolin ulcer differs from squamous cell carcinoma
by the characteristics in Table 31.1.
Once Marjolin ulcer infiltrates the normal skin, it behaves like
squamous cell carcinoma.
249
Fig. 31.1: Marjolin ulcer arising in a burns scar
4. Radiodermatitis: An increased incidence of skin
cancer was initially found in persons who worked in
the radiology department. Now, the incidence is less
due to the usage of protective gear. Radiation changes
in the skin may vary from simple erythema to atrophy
or hyperpigmentation. Later, this lesion develops into
squamous cell carcinoma.
5. Bowen’s disease is an intraepidermal carcinoma.
Chronic solar damage, inorganic compounds, and
human papillomavirus (HPV)-16 are possible aetiological factors. It is rare, and occurs in middle-aged
patients. It occurs on the skin of the trunk as scaly,
erythematous plaques, which are often multiple.
They are brownish patches with raised margins.
Microscopically, large clear cells are found (these cells
are also found in Paget’s disease of the nipple).
Topical application of 5-FU and/or imiquimod is an
effective treatment (Figs 31.2 and 31.3).
6. Leukoplakia (see page 350).
7. Autosomal recessive disorders: In this group, one
or more of the DNA repair enzymes are defective or
deficient. As a result, sites exposed to the sun are
vulnerable to the development of various skin cancers.
Xeroderma pigmentosum and albinism increase the
risk of skin cancer (Fig. 31.4). Muir-Torre syndrome,
dystrophic epidermolysis bullosa, Werner syndrome,
nevoid basal cell carcinoma, Li-Fraumeni syndrome
are the other genetic syndromes with skin cancers.
Table 31.1 Comparison of Marjolin ulcer and squamous cell carcinoma
Marjolin ulcer Squamous cell carcinoma
Grows very slowly because of scar tissue Grows slowly
It is painless as scar does not contain nerves It can be painful if it infiltrates the nerve fibres
Lymphatic metastasis does not occur because Lymphatic metastasis is the chief method of spread
lymphatics are destroyed or occluded
It is less malignant Comparatively more malignant
Surgery cures the disease, radiotherapy is not very useful Both surgery and radiotherapy are used
Section II • General Surgery

250
Fig. 31.2: Bowen’s disease—premalignant condition
Fig. 31.3: Albinism with squamous cell carcinoma of the right
elbow region—patient also has photophobia (Courtesy: Dr Satish
Deshmukh and Dr Murtaza Akhtar, NKP Salve Medical College
and Research Center, Nagpur)
Manipal Manual of Surgery
White race is a definite risk factor for skin cancer. Previous
diagnosis of cutaneous carcinoma—increases the risk to 35%
at 3 years and 50% at 5 years.
BASAL CELL CARCINOMA (BCC)/RODENT ULCER
It is the most common malignant skin tumour. It arises
from basal cells of the pilosebaceous adnexa and occurs
only on the skin. Generally, it is a slow-growing
neoplasm which may present as an ulcer of a chronic
(many years) duration. Metastasis and death from this
disease is extremely rare. In some cases, it may present
as a locally penetrating, ulcerative, and destructive
lesion. The majority of lesions are found on the face,
above a line from lobule of the ear to the angle of mouth.
Common Sites (Figs 31.5 to 31.8)
• Inner canthus of the eye, outer
canthus of the eye, eyelids,
bridge of the nose.
• Around the nasolabial fold.
These sites are the areas where
tears roll down. Hence,
also known as tear cancer cell
carcinoma (Figs 31.6–31.8).
BCC is
Fig. 31.5: Sites of basal
cell carcinoma (BCC)
• Naevoid basal cell carcinoma syndrome (NBCCS) :
Gorlin syndrome is an inherited medical condition
with multiple body systems which are defective, such
as the skin, nervous system, endocrine system, eyes,
and bones. Inborn kyphoscoliosis and anomalies in
the ribs may be present. Other lesions are ovarian
fibroma and odontogenic tumours.
Fig. 31.4: Bowen’s disease with ulcerated squamous cell
carcinoma
8. Immunosuppression:
• Squamous cell carcinoma develops in 50% of
patients within 20 years of organ transplantation
due to immunosuppression. Skin cancer is the most
common neoplasm after solid organ transplantation.
• Patients with lymphoma, leukaemia, and auto-
immune diseases on treatment may also develop
skin cancers.
Section II • General Surgery
• 30% may be aggressive
Fig. 31.6: Basal cell carcinoma
involving the right ear
A brother and sister with xeroderma pigmentosum developed
33 and 26 skin malignancies respectively which included basal
cell carcinoma, squamous cell carcinoma and malignant
melanoma, since the age of 5 till 22 years. Eventually the boy
died at 22 years of age (Fig. 31.6). This is the sad part of this
distressing and frustrating disease. I have not seen this girl since
20 years now
Fig. 31.7: Basal cell carcinoma
involving nasolabial fold skin

Skin Tumours
structures, like muscle or bone, depending on the
level of invasion.
• When the lesion is big, it is called a rodent ulcer
(Figs 31.10 and 31.11).
Scabbing typically occurs only in benign ulcers. Basal cell
carcinoma is the only malignant ulcer which shows scabbing.
251
Fig. 31.8: Basal cell carcinoma—typical site
Basal cell carcinoma cannot occur in mucosal surfaces that do
not have pilosebaceous adnexa (e.g. cervix, lips, tongue).
Precipitating Factors
• Ultraviolet (UV) rays: Broad-spectrum short-
wavelength UVB radiation (290–320 nm) also called
as sunburn rays are probably responsible for basal
cell carcinoma.
Australia
1
Basal cell carcinoma is common in
and New Zealand because of this reason.
Latent peroid between skin damage to development
of BCC is about 20 years.
• Fair skin is vulnerable to the development of basal
cell carcinoma.
• Arsenic, which was once used in skin ointments, also
increases the risk of basal cell carcinoma.
Clinical Features
• The most common clinical presentation is an ulcer
that never heals (Fig. 31.9). Sometimes, healing takes
place with scabbing, which later breaks down and
forms an ulcer again. The ulcer has a raised and
beaded edge, may be indurated, and bleeds on touch.
The base may be subcutaneous fat or deeper
• It may also present as a painless, firm, nodule, which
is pigmented with fine blood vessels on its surface
(Key Box 31.1).
• It may be present in a noduloulcerative form
(Fig. 31.8).
• Rarely, it may be a nodulocystic variety, which does
not show fluctuation.
• Field fire rodent ulcer is a rapidly growing rodent
ulcer, with destruction and disfigurement of the facial
skin. It has an advancing edge with a healed, central
scar.
• The more aggressive, infiltrative form is morphea-
form, and the more common form is the noduloulcerative form. Less aggressive: Nodular, superficial
and micronodular, basosquamous
Key Box 31.1
Basal Cell Carcinoma: Types
Nodular: Nodulocystic or noduloulcerative—70%
Pigmented
Superficial: Occur on the trunk
Cystic
Infiltrative
Basosquamous: Rare
Fig. 31.9: Nonhealing ulcer of 3 years
duration—lesion that does not heal and
grows slowly—classical history of BCC
1
This may be the reason why Australian and New Zealand cricket players apply some protective cream to the potentially risky sites while playing
the match.
Fig. 31.10: Pigmented large destructive
BCC (Courtesy: Dr Vidyadhar Kinhal, HOD,
Surgery, VIMS, Bellary, Karnataka)
Fig. 31.11: Lateral view of the same
patient showing elevated edge, a few
areas of scab and slough
Section II • General Surgery

252
Manipal Manual of Surgery
Differential Diagnosis
• Keratoacanthoma: It occurs only over the face. The
edge may be raised with ulceration, resembling basal
cell carcinoma.
• Sclerosing angioma
• Malignant melanoma: Pigmented basal cell carci-
noma may be mistaken for malignant melanoma.
• Squamous cell carcinoma
Spread
• It spreads by local invasion. Even though it is slow-
growing, it slowly penetrates and destroys the deeper
underlying tissues, such as bone, cartilage, or even
the eyeball (hence, the name rodent ulcer). It does
not spread by lymphatics because of its large tumour
emboli. Blood spread is extremely rare.
• Morpheaform BCC synthesises type IV collagenase
and, therefore, spreads rapidly. White scar-like
growth pattern is seen in the morpheaform variety.
TNM Staging
TNM STAGING Skin cancer other than melanoma
T1 Tumour <2 cm in greatest dimension with less than
2 high-risk features
T2 Tumour >2 cm in greatest dimension (or) tumour of
any size with 2 or more high-risk features.
T3 Tumour invasion of maxilla, mandible orbit or
temporal bone.
T4 Tumour with invasion of skeleton or perineural
invasion of skull base
N0 No regional lymph nodes
N1 Metastasis in a single ipsilateral lymph node <3 cm
N2 Metastasis in a single ipsilateral lymph node >3 cm
but <6 cm; or B/L or contralateral lymph nodes
none >6 cm in greatest dimension
N3 Metastasis to lymph node >6 cm in greatest dimension
M0 No metastases
M1 Distant metastases
Key Box 31.2
Microscopic Picture
Central mass of polyhedral cells
Cells are darkly stained
With peripheral palisade layer of columnar cells. Cell
nests, keratinisation and mitotic figures are absent.
Fig. 31.12: Palisading islands of basaloid cells seen in BCC (Courtesy:
Dr Laxmi Rao, Head, Department of Pathology, KMC, Manipal)
reatment
T
Surgery followed by reconstruction is the main line of
treatment.
I. Surgery is indicated when the lesion is very close to
the eye, adherent to cartilage or bone, in easily accessible
sites, such as the neck or hand and in radiation failure
cases. Wide excision is done in all cases: This means
excision of the growth with at least 3–4 mm of healthy
margin all around, including at the base. The resulting
defect is closed by:
.
Primary suturing of the defect if the lesion is small.
a
b. Skin grafting if defect is big, as in the neck or the
dorsum of the hand.
c. Rotation flaps in the face for a better cosmetic effect
(Figs 31.13–31.20).
Investigations
Wedge biopsy from the edge of the ulcer. The edge is
selected because of the following reasons:
• The edge is the growing part, so malignant cells are
numerous
• The centre has slough or scabs, which may not reveal
malignancy
• Comparison with normal skin is possible
Histology (Key Box 31.2, Fig. 31.12)
Types: 1. Basosquamous, 2. Morpheaform, 3. Adenoid,
Section II • General Surgery
4. Infiltrative.
Fig. 31.13: Reconstruction with nasolabial flap following excision

Skin Tumours
Fig. 31.14: BCC excision and reconstruction by using bilobed
flap
Fig. 31.18: Pigmented, elevated
lesion—5 years duration
253
Fig. 31.19: Wide excision
in progress
Figs 31.15 and 31.16: BCC reconstruction
Fig. 31.20: Wide exersion and suturing
Mohs’ micrographic surgery: It is a special surgical
technique which involves excision of skin cancer under
microscopic control. It minimises the chance of recurrence
and maximises conservation of the surrounding
normal tissue. The technique offers complete evaluation of the lateral and deep margins of the tumour site.
This procedure gives better cosmetic results, since only
a minimal amount of normal tissue is removed.
Indications for Mohs’ procedure are:
• Centrofacially located tumours
• Large tumours, poorly defined tumour margins
• Lesions with perineural/perivascular involvement
• Tumours at the site of prior radiation therapy
• Tumours in the setting of immunosuppression
• High-risk histological subtype of BCC
• Recurrent lesions
II. Radiation is indicated in elderly patients who have
an extensive lesion requiring a complicated plastic
reconstruction. Dosage: 4000–6000 cGy units. Radiation
chondritis and osteitis are the complications.
Fig. 31.17: Treatment of BCC
III. Other forms of treatment
• Small and superficial: Curettage with electro-
desiccation.
• Liquid nitrogen for tumours <1 cm in diameter.
• CO
laser (Key Box 31.3).
2
Section II • General Surgery
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