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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 occlusionNot completely compressibleLacks respiratory variationDoes not show flow augmentation with calf compressionMay 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 tumoursPremalignant lesionsBasal cell carcinomaSquamous cell carcinomaMelanocytic 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 melanomaRECIST criteriaOther malignant skin tumoursOther 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%PigmentedSuperficial: Occur on the trunkCysticInfiltrativeBasosquamous: 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 cellsCells are darkly stainedWith 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