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Posts Tagged ‘Sabiston MCQs’

Surgery MCQs (Grafts)

Posted by Dr KAMAL DEEP on May 27, 2011

Grafts:-

 Skin grafting dates back >3000 years to India, where forms of the technique were used to resurface nasal defects in thieves who were punished for their crimes with nose amputation.

 

Full thickness skin graft can be taken from the following sites except – (AIIMS 87)  ?
a) Elbow b) Back to neck
c) Supraclavicular area d) Upper eyelids

Free skin graft is rejected on – (AIMS 89)  ?
a) Muscle b) Fat
c) Deep fascia d) Dermis

Skin graft for facial wounds is taken from – (AIIMS 92)
a) Medial aspect of thigh b) Cubital fossia
c) Groin d) Post auricular region

The best skin graft for open wounds is – (A193)
a) Isograft b) Homograft
c) Allograft d) Autograft

The organism causing destruction of skin grafts is – (PGI 95)
a) Streptococcus b) Staphylococcus
c) Pseudomonas d) Clostridium

For on open wound of leg with exposure of bone, treatmen of choice – (AIIMS 96)
a) Partial skin graft b) Complete skin graft
c) Pedicle graft d) Reverdin graft

(Reverdin is credited with performing the first "fresh skin" allograft, and in 1869 while working in Paris, introduced the "pinch graft", which is a procedure for removing tiny pieces of skin from a healthy area of the body and seeding them in a location that needs to be covered. This procedure is sometimes referred to as a "Reverdin graft". His name is also associated with the "Reverdin suture needle", which is a specialized surgical needle.)

Graft is not taken up on the following-(AIIMS 96)
a) Fat b) Muscle
c) Deep fascia d) Skull bone

Man sustained an injury with loss of skin cover exposing bone of 10×10 cms. The best treatment is –
a)Full thickness graft (AIIMS 99)
b)Pedicle graft
c)Amnion
d)Split thickness skin graft

Skin graft survival in the first 48 hrs is dependent on – (AIIMS 99)
a)Random connection between
host & donor capillaries
b)Plasmatic imbibition
c)Saline in dressing
d)Development of new blood vessels

Skin grafting is not done in infection with-(MP 2K)
a)Pseudonmonas aeroginosa
b)Staph. Aureus
c)Beta hemolytic streptococci
d)E. coli

Split skin graft can be applied over – (PGI 99)
a) Muscle b) Bone
c) Cartilage d) Eyelid

Best procedure to be done after an injury to leg associated with exposure of underlying bone and skin loss – (MAHA 05)
a) Pedicle flap b) Split skin grafting
c) Full thickness grafting d) Skin flap

Dacron vascular graft is – (Al 06)
a) Nontextile synthetic b) Textile synthetic
c) Nontextile biologic d) Textile biologic

Which one of the following statements about Mesh Skin Grafts is not correct? – (UPSC 06)
a)They permit coverage of large areas -True
b)They allow egrees of fluid collections under the graft) -True
c)They contract to the same degree as a grafted sheet of skin
d)They "take" satisfactorily on a granulating bed

Split skin grafts in young children should be harvested from – (UPSC 07)
a) Buttocks b) Thigh
c) Trunk d) Upper limb

Wolfe grafts is – (UP 07)
a)Full thickness -skin grafts
b)Partial thickness skin grafts
c)Split-skin grafts
d)Pedicled flap

Deep skin burns is treated with – (AIIMS 91)
a)Split thickness graft
b)Full thickness graft
c)Amniotic membrane
d)Synthetic skin derivatives

For aortic graft the best material available is – (JIPMER 81, Delhi 79, 92)
a) Dacron b) Artery
c) Vein d) None

A knitted Dacron artery graft (PGI 99, AIIMS 84)
a)Is not porous
b)Is eventually dissolived by tissue reaction
c)Never gets infected
d)Can be easily incised and the opening resutured

Not used as graft material in peripheral vascular disease – (PGI 97)
a) Dacron graft b) Vein
c) PTFE d) PVC

Graft used in infra inguinal by pass is 4Jipmer 2K)
a) PTFE b) Dacron
c) Autologous vein d) Autologous artery

Most common artery used for coronary artery bypass graft is – (Rohtak 97)
a) Int. Mammary artery b) Intercostal artery
c) Radial artery d) Dorsalis pedisartery
e)Brachial artery

 

Skin Grafts and Skin Substitutes

Discussion of skin grafting requires a basic review of skin anatomy. Skin is comprised of 5% epidermis and 95% dermis. The dermis contains sebaceous glands, whereas sweat glands and hair follicles are located in the subcutaneous tissue. The dermal thickness and concentration of skin appendages vary widely from one location to another on the body. The skin vasculature is superficial to the superficial fascial system and parallels the skin surface. The cutaneous vessels branch at right angles to penetrate subcutaneous tissue and arborize in the dermis, finally forming capillary tufts between dermal papillae.4

Each technique has advantages and disadvantages. Selection of a particular technique depends on the requirements of the defect to be reconstructed, the quality of the recipient bed, and the availability of donor site tissue.


Type Description Thickness (in)
Split thickness Thin (Thiersch-Ollier) 0.006–0.012
  Intermediate (Blair-Brown) 0.012–0.018
  Thick (Padgett) 0.018–0.024
Full thickness Entire dermis (Wolfe-Krause) Variable
Composite tissue Full-thickness skin with additional tissue (subcutaneous fat, cartilage, muscle) Variable

Split-Thickness Grafts

Split-thickness skin grafting represents the simplest method of superficial reconstruction in plastic surgery. Many of the characteristics of a split-thickness graft are determined by the amount of dermis present. Less dermis translates into less primary contraction (the degree to which a graft shrinks in dimensions after harvesting and before grafting), more secondary contraction (the degree to which a graft contracts during healing), and better chance of graft survival. Thin-split grafts have low primary contraction, high secondary contraction, and high reliability of graft take, often even in imperfect recipient beds. Thin grafts, however, tend to heal with abnormal pigmentation and poor durability compared with thick-split grafts and full-thickness grafts. Thick-split grafts have more primary contraction, show less secondary contraction, and may take less hardily. Split grafts may be meshed to expand the surface area that can be covered. This technique is particularly useful when a large area must be resurfaced, as in major burns. Meshed grafts usually also have enhanced reliability of engraftment, because the fenestrations allow for egress of wound fluid and excellent contour matching of the wound bed by the graft. The fenestrations in meshed grafts re-epithelialize by secondary intention from the surrounding graft skin. The major drawbacks of meshed grafts are poor cosmetic appearance and high secondary contraction. Meshing ratios used usually range from 1:1.5 to 1:6, with higher ratios associated with magnified drawbacks.

Full-Thickness Grafts

By definition full-thickness skin grafts include the epidermis and the complete layer of dermis from the donor skin. The subcutaneous tissue is carefully removed from the deep surface of the dermis to maximize the potential for engraftment. Full-thickness grafts are associated with the least secondary contraction upon healing, the best cosmetic appearance, and the highest durability. Because of this, they are frequently used in reconstructing superficial wounds of the face and the hands. These grafts require pristine, well-vascularized recipient beds without bacterial colonization, previous irradiation, or atrophic wound tissue.

Graft Take:- Differences in Schwartz and Sabiston

Graft Take

Schwartz:- Skin graft take occurs in three phases, imbibition, inosculation, and revascularization. Plasmatic imbibition refers to the first 24 to 48 hours after skin grafting, during which time a thin film of fibrin and plasma separates the graft from the underlying wound bed. It remains controversial whether this film provides nutrients and oxygen to the graft or merely a moist environment to maintain the ischemic cells temporarily until a vascular supply is re-established. After 48 hours a fine vascular network begins to form within the fibrin layer. These new capillary buds interface with the deep surface of the dermis and allow for transfer of some nutrients and oxygen. This phase, called inosculation, transitions into revascularization, the process by which new blood vessels either directly invade the graft or anastomose to open dermal vascular channels and restore the pink hue of skin. These phases are generally complete by 4 to 5 days after graft placement. During these initial few days the graft is most susceptible to deleterious factors such as infection, mechanical shear forces, and hematoma or seroma

Special considerations in choosing a skin graft donor site include skin quality and color from the donor region that will best match the recipient site. For example, skin harvested from the blush zone above the clavicles is best suited for facial grafting. Skin grafts harvested from areas caudal to the waist will result in tallow discoloration and possible unwanted hair growth. Because split-thickness donor sites will permanently scar, it is wise to choose a donor site that can be concealed. When a large amount of graft is needed, the thighs and buttocks are areas that can be hidden with everyday clothes. The inner arm and groin crease are each fine sources for full-thickness grafts because both areas offer relatively glabrous skin sources, the donor sites of which can be easily hidden with clothes. One often overlooked split-thickness donor site is the scalp, taking extreme care to avoid taking the graft below the level of the hair follicle; this donor site heals quickly, painlessly, and with imperceptible scar consequences.

 

Sabiston :- The skin graft must be applied to a well-vascularized recipient wound bed. It will not adhere to exposed bone, cartilage, or tendon devoid of periosteum, perichondrium, or peritenon, respectively, or devoid of its vascularized perimembranous envelope.There are three steps in the “take” of a skin graft: imbibition, inosculation, and revascularization. Imbibition occurs up to 48 hours after graft placement and involves the free absorption of nutrients into the graft. Inosculation designates the time period when donor and recipient capillaries become aligned. There remains a debate as to whether new channels are formed or if preexisting channels reconnect. Finally, after about 5 days, revascularization occurs, and the graft demonstrates both arterial inflow and venous outflow.

Time period and Graft take not well explained in bailey .

Sabiston:- By examining the skin graft before the fourth postoperative day, a hematoma or seroma can be evacuated, and the mechanical obstruction to revascularization of the graft is thus removed. Some surgeons make stab incisions in the graft preemptively to create small outlets for fluid to drain from beneath the graft, a technique know as pie crusting. Others might use a mesh expander device, which creates a chain-link fence pattern in the graft. Although these methods may provide egress portals for serous fluid or blood, an unsightly meshed pattern results, making this technique unsuitable for aesthetic reconstruction.

Because split-thickness donor sites can be reharvested after re-epithelialization, this method of wound closure is the workhorse for burn injuries

Split grafts may be meshed to expand the surface area that can be covered. This technique is particularly useful when a large area must be resurfaced, as in major burns. Meshed grafts usually also have enhanced reliability of engraftment, because the fenestrations allow for egress of wound fluid and excellent contour matching of the wound bed by the graft. The fenestrations in meshed grafts re-epithelialize by secondary intention from the surrounding graft skin. The major drawbacks of meshed grafts are poor cosmetic appearance and high secondary contraction. Meshing ratios used usually range from 1:1.5 to 1:6, with higher ratios associated with magnified drawbacks.

Technical aspects
Graft take is only possible at well-vascularised recipient sites. Grafts will not take on bare bone, bare tendon or cartilage, but can survive on periosteum, paratenon and perichondrium. The graft must remain adherent to the bed until it revascularises; shearing forces must be eliminated. Meti­culous care with suturing and dressings is essential. Where grafts are applied over mobile areas appropriate splintage must be used. Limbs that have been grafted should be elevated to reduce venous pressure during the process of revascularisation. Haemostasis at the recipient site must be good to prevent bleeding beneath the graft resulting in its elevation by clot and failure of take. Skin grafts can be stored in a refrigerator at 40C for 2 weeks for delayed application. Grafts take well on granulation tissue, but excessive conta­mination with bacteria will prevent take. Streptococci at levels above 105 microorganisms per gram of tissue will result in graft loss. Preparation of the bed with dressings may help; it may be necessary to excise the granulation tissue.

FLAPS

Skin flap is used in all except – (AIIMS 89)
a) Bone b) Tendon
c) Burn wound d) Cartilage

The subdermal plexus forms the vascular basis for –
a)Randomised flaps (JIPMER 2002)
b)Axial flaps
c)Mucocutaneous flaps
d)Vasciocutaneous flaps

full thickness loss of middle one third of the upper lip is best reconstruted by – (AIIMS 84)
a) Naso labial flap b) Cheek flap
c) Abbey flap d) Estlander’s flap

In the reconstruction following excision of previously irradiated cheek cancer, the flap will be – (AIIMS 85)
a)Local tongue
b)Cervical
c)Forehead
d)Pectoralis major myocutaneous

Reconstruction of the breast following total mastectomy for cancer is done ideally by using –
a)Distant tube pedicvle (AIIMS 84)
b)Opposite breast
c)Trapezius myocutaneous flap
d)Latissmus dorsi myocunaneous flap

Flap commonly used in breast reconstruction is -a) Serratus anterior b) TRAM (TN 03)
c) Flap from arm d) Delto pectoral flap

Best flap for eosphagus repair – (CMC Vellore)
a) Colon b) Stomach
c) Jejunum d) Latismus dorsi

imageimage imageimage

                                                                                                                                                                                                                                                                                               Vascular patterns of random pattern (A) and axial pattern (B) skin flaps    Graphic representation of the bilobed flap commonly used for nasal reconstruction. P, primary flap; S, secondary flap

A flap is defined as a partially or completely isolated segment of tissue perfused with its own blood supply. Flaps are the reconstructive option of choice when a padded and durable cover is needed to reconstruct an integumentary defect over vital structures, tissues devoid of perivascular membrane, or implants. Flaps vary greatly in terms of complexity from simple skin flaps with a random blood supply to microvascular free flaps containing composite tissue. Numerous schemes exist to classify flaps. Flaps may be classified based on the type of tissue contained in the flap: fasciocutaneous, musculocutaneous, or osteocutaneous flaps. Flaps are also described based on their design and method of transfer: advancement, rotation, transposition, interpolation, or pedicled flaps. Flaps may be further defined by the source of their blood supply: random, axial, or free. Random flaps rely on the low perfusion pressures found in the subdermal plexus to sustain the flap and not a named blood vessel. Nevertheless, random flaps are used widely in reconstruction of cutaneous defects, including those resulting from Mohs excision of cutaneous malignancies. These local flaps recruit adjacent tissue based on geometric design patterns.

Advancement and rotation flaps represent commonly used random-pattern skin flaps. The Z-plasty, bilobed flap, rhomboid, and V-Y (or Y-V) advancement flaps are commonly used random flaps. Z-plasty involves transposing two adjacent triangular flaps to redirect and lengthen an existing scar (the central limb).The angles of the Z-plasty can be increased to provide greater length. Typically a 60-degree angle is used that lengthens the central limb by 75%.The bilobed flap is commonly used for nasal reconstruction; here, a larger primary and smaller secondary flap are transposed into adjacent defects borrowing the loose adjacent tissue to close the defect . The rhomboid flap described by Limberg uses a 60- and 120-degree parallelogram to transpose tissue into a diamond-shaped defect. It is an extremely versatile flap option and the workhorse for most plastic surgeons. Finally, the V-Y (or Y-V) advancement flaps are commonly used to lengthen scars around the nose and mouth. A backcut at the base of a flap may decrease tension at a flap’s tip, creating a greater arc of rotation; overzealous back cut or tension at flap inset can each cause ischemia to the flap and threaten its survival.

An axial flap is based on a named blood vessel and can provide a reproducible and stable skin or skin-muscle (myocutaneous) flap. Flaps can also be raised with the underlying fascia (fasciocutaneous), which recruits the fascial blood supply, thereby increasing the predictable vascularity to the flap. Because of its reliable blood supply, the axial flap can be used to provide much needed length and bulk, which the random flap cannot. An axial flap that remains attached to its proximal blood supply and is transposed to a defect is known as a pedicled flap. Alternately, the vascular pedicle can be completely transected and the paddle of tissue transferred and reanastomosed to recipient vessels in a remote location. This technique requires the use of an operating microscope and is known as microsurgery

Keratoacanthoma is- (AIIMS 85)
a)A type of basal cell carcinoma
b)Infected sebaceous cyst
c)Self healing nodular lesion with central ulceration
d)Pre-malignant disease

True about keratoacanthoma – (PGI 2000)
a)Benign tumor
b)Malignant skin tumor like squamous cell carcinoma
c)Treatment same as for squamous cell carcinoma
d)Easy to differentiate from squamous cell Ca. histologically
e)Treatment is masterly inactivity (
Watchful Waiting:-A hands-off management philosophy in which certain conditions are closely monitored, but treatment withheld until symptoms either appear or some measurable parameter changes. Active management is begun once the patients become symptomatic)

Keratoacanthoma
Keratoacanthoma (molluscum sebaceum) arises as a rapid proliferation of squamous epidermal cells. The nodule grows rapidly for 6—8 weeks at which time it usually begins to resolve spontaneously. Keratoacanthoma must be distinguished from SCC. Usually rapid evolution to relatively large size, irregular crater shape and keratotic plug, and the undamaged surrounding skin make a distinction possible. Spontaneous healing further confirms the diagnosis. Histologically, it is difficult to differentiate between a keratoacanthoma and SCC. There is also a possibility of a highly anaplastic SCC behaving like a keratoacanthoma. Excision biopsy is mandatory if the diagnosis is in doubt as curetted specimens yield poor sections.

Which of the following is a regressing
tumour- (AI 91)
a) Portwine stain b) Strawberry angioma
c) Venous angioma d) Plexiform angioma

Spontaneous regression is seen in all except –
a)Salmon patch (Al 93)
b)Small Cavernous hemangioma
c)Portwine stain
d)Strawberry angioma

All are features of pesudopancreatic cyst, except
a)Follows acute pancreatitis (AI 97)
b)Lined by false epithelium
c)May regress spontaneously
d)Treatment of choice is percutaneous aspiration

Least likely to regress spontaneously is(AIIMS 96)
a) Osteosarcoma b) Retinoblasoma
c) Choriocarcinoma d) Malignant melanoma

Spontaneous Regresssion is seen in all except –
a) Retinoblasoma b) Malignant melanoma (AI 98)
c) Osteosarcoma d) Choriocarcinoma

Cystic hygroma – (SCTIMS 98)
a)Should be left alone
b)Excision of cyst at an early age
c)Spontaneous regression
d)Manifests in 2nd – 3rd decade

[Ref Bailey & Love 240/e p. 771 & 23"/e p. 701] Spontaneous regression may occur in cystic hygroma

Spontaneous regression of malignant tumour is seen in – (JIPMER 80, AIIMS 81)
a) Burkits lymphoma
b) Neuroblasoma
c) Wilm’s tumour d) Renal cell carcinoma

Salmon patch usually disappears by age- (PGI 80, 81, a) One mouth b) One year UPSC 89)
c) Puberty d) None of the above

Regarding hemangiomas following are true –
a)Salmon patch disappears after the age of one
b)Port wine stain present throughout life
c)Salmon patch-on forehead midline and over occiput
d)all are correct

Eleven month old child presents with erythematous lesion with central clearing which has been decreasing in size – (Al 97)
a)Strawberry angioma
b)Nevus
c)Portwine stain
d)Cavernous haemangioma

The best cosmetic results for large capillary (port wine) hemangiomas are achieved by – (UPSC 05)
a)Excision and split-thickness skin
b)Laser ablation
c)Cryosurgery
d)Tattooing

True about Hemangioma of head & neck -(PGI 01)
a) Are very common b) Sturge Weber synd
c) High output failure
d) Thrombocytopenia

Hemangioma of the rectum – (PGI June 07)
a)Common tumour
b)Fatal haemorrhage seen
c)Ulcerative colitis like symptoms seen

True about lymphangioma – (PGI 03)
a)It is a malignant tumour
b)It is a congenital sequestration of lymphatic
c)Cystic hygroma is a lymphangioma

d)Laser excision is done
e)Sclerotherapy is commonly done’

Which is the commonest incidentaloma detected in the liver – (Karn. 94)
a)Focal nodular hyperplasia
b)Haemangioma
c)Hepatocellular adenoma
d)Hydatid cyst

"Crumbled egg appearance" in liver seen in –
a) Hepatic adenoma (UP 07)
b) Chronic amoebic liver abscess
c)Hydatid liver disease
d)Haemangioma

Earliest tumour to appear after bith is-(JIPMER 87)
a) Sternomastoid tumour
b) Cystic hygroma
c) Branchial cyst d) Lymphoma

Ans. is ‘b’ i.e., Cystic hygroma [Ref Bailey & Love 24th/e p. 771 & 23'/e p. 700] 50% to 65% of Cystic hygroma prasent of birth

Cystic compressible, translucent swelling in the posterior triangle of neck- (Al 89) a) Cystic hygroma
c) Thyroglossal cyst
b) Branchial cyst
d) Dermoid cyst

Treatment of cystic hygroma is – (JIPMER 88)
a)Surgical excision
b)Injection of sclerosants
c)Irradiation
d)Masterly inactivity

The brilliantly transilluminant tumour in the neck may be- (AI 91)
a) Branchial cyst b) Thyroglossal cyst
c) Sternomastoid tumour d) Cystic hygroma

All are true about cystic hygroma except –
a)Pulsatile (AMU 95)
b)May cause respiratory obstruction
c)Common in neck
d)Present at birth

All are true about cystic hygroma except -(PG1 99)
a)Aspiration is diagnostic
b)50% present at birth
c)Presents as posterior cervical swelling
d)Sequstration of lymphatic tissue

True about cystic hygroma – (PGI 2000)
a)Congenital sequestration of lymphatics
b)Resolves spontaneouly by 5 year of age
c)Common in upper 1/3rd of lateral neck
d)Surgery is the treatment of choice

Calcifying epithelioma is seen in – (JIPMER 95)
a) Dermato fibroma b) Adenoma sebaceum
c) Pyogenic granuloma d) Nevo cellular nevus

none?

Margins of squamous cells carcinoma is -(JIPMER a) Inverted b) Everted 81,Delhi 86)
c) Rolled d) Undermined

Calcifying epithelioma is also known as —
a)Pilomatrixoma (AIMS 86)
b)Myoblastoma
c)Calcinosis cutis
d)Dermatofibroma lenticulare

VASCULAR MALFORMATION.

Vascular malformations are developmental errors in blood vessel formation. Malformations do not regress and slowly enlarge. They should be named after the predominant blood vessel forming the lesion .Table helps differentiate vascular malformations from true hemangiomas.


Vascular Malformations
TYPE EXAMPLES
Capillary Port-wine stain
Venous Venous malformation
  Angiokeratoma circumscriptum (hyperkeratotic venule)
  Cutis marmorata telangiectasia congenital (congenital phlebectasia)
Arterial Arteriovenous malformation
Lymphatic Small vessel lymphatic malformation (lymphangioma circumscriptum)
Large vessel lymphatic malformation (cystic hygroma)
 

Major Differences Between Hemangiomas and Vascular Malformations
HEMANGIOMAS VASCULAR MALFORMATIONS (CAPILLARY, VENOUS, LYMPHATIC, ARTERIAL, AND ARTERIOVENOUS, PURE OR COMPLEX-COMBINED)
Clinical Variably visible at birth Usually visible at birth (AVMs may be quiescent)
  Subsequent rapid growth Growth proportionate to the skin’s growth (or slow progression); present lifelong
  Slow, spontaneous involution  
Sex ratio F: M 3 : 1 to 5 : 1 and 7 : 1 in severe cases 1 : 1
Pathology Proliferating stage: hyperplasia of endothelial cells and SMC-actin+ cells Flat endothelium
  Multilaminated basement membrane Thin basement membrane
  Higher mast cell content in involution Often irregularly attenuated walls (VM, LM)
Radiology Fast-flow lesion on Doppler sonography Slow flow (CM, LM, VM) or fast flow (AVM) on Doppler ultrasonography
  Tumoral mass with flow voids on MRI MRI: Hypersignal on T2 when slow flow (LM, VM); flow voids on T1 and T2 when fast flow (AVM)
  Lobular tumor on arteriogram Arteriography of AVM demonstrates AV shunting
Bone changes Rarely mass effect with distortion but no invasion Slow-flow VM: distortion of bones, thinning, underdevelopment
    Slow-flow CM: hypertrophy
    Slow-flow LM: distortion, hypertrophy, and invasion of bones
    High-flow AVM: destruction, rarely extensive lytic lesions
    Combined malformations (e.g., slow-flow [CVLM, Klippel-Trenaunay syndrome] or fast-flow [CAVM, Parkes-Weber syndrome]): overgrowth of limb bones, gigantism
   
Immunohistochemistry on tissue samples Proliferating hemangioma: high expression of PCNA, type IV collagenase, VEGF, urokinase, and bFGF Lack expression of PCNA, type IV collagenase, urokinase, VEGF, and bFGF
One familial (rare) form of VM linked to a mutated gene on 9p (VMCM1)
Involuting hemangioma: high TIMP-1, high bFGF  
Hematology No coagulopathy (Kasabach-Merritt syndrome is a complication of other vascular tumors of infancy, e.g., Kaposiform hemangioendothelioma and tufted angioma, with a LM component) Slow-flow VM or LM or LVM may have an associated LIC with risk of bleeding (DIC)
From Eichenfield LF, Frieden IJ, Esterly NB: Textbook of Neonatal Dermatology. Philadelphia, WB Saunders, 2001, p 337.

AVM, Arteriovenous malformation; bFGF, basic fibroblast growth factor; CAVM, capillary arteriovenous malformation; CLVM, capillary lymphatic venous malformation; CM, capillary malformation/port-wine stain; DIC, disseminated intravascular coagulation; LIC, local-ized intravascular coagulopathy; LM, lymphatic malformation; MRI, magnetic resonance imaging; PCNA, proliferating cell nuclear antigen; SMC, smooth muscle cell; TIMP, tissue inhibitor of metalloproteinase; VEGF, vascular endothelial growth factor; VM, venous malformation

CAPILLARY MALFORMATION (PORT-WINE STAIN/CAPILLARY NEVUS

Port-wine stains are present at birth. These vascular malformations consist of mature dilated dermal capillaries. The lesions are macular, sharply circumscribed, pink to purple, and tremendously varied in size .The head and neck region is the most common site of predilection; most lesions are unilateral. The mucous membranes can be involved. As a child matures into adulthood, the port-wine stain may become darker in color and pebbly in consistency; it may occasionally develop elevated areas that bleed spontaneously.

True port-wine stains should be distinguished from the most common vascular malformation, the salmon patch of neonates, which, in contrast, is a relatively transient lesion .When a port-wine stain is localized to the trigeminal area of the face, specifically around the eyelids, the diagnosis of Sturge-Weber syndrome (glaucoma, leptomeningeal venous angioma, seizures, hemiparesis contralateral to the facial lesion, intracranial calcification) must be considered .Early screening for glaucoma is important to prevent additional damage to the eye. Port-wine stains also occur as a component of Klippel-Trenaunay syndrome and with moderate frequency in other syndromes, including the Cobb (spinal arteriovenous malformation, port-wine stain), Proteus, Beckwith-Wiedemann, and Bonnet-Dechaume-Blanc syndromes. In the absence of associated anomalies, morbidity from these lesions may include a poor self-image, hypertrophy of underlying structures, and traumatic bleeding.

The most effective treatment for port-wine stains is the pulsed dye laser (PDL). This therapy is targeted to hemoglobin within the lesion and avoids thermal injury to the surrounding normal tissue. After such treatment, the texture and pigmentation of the skin are generally normal without scarring. Therapy can begin in infancy when the surface area of involvement is smaller; there may be advantages to treating within the 1st year of life. Masking cosmetics may also be used.

SALMON PATCH (NEVUS SIMPLEX:- Salmon patches are small, pale pink, ill-defined, vascular macules that occur most commonly on the glabella, eyelids, upper lip, and nuchal area of 30–40% of normal newborn infants. These lesions, which represent localized vascular ectasia, persist for several months and may become more visible during crying or changes in environmental temperature. Most lesions on the face eventually fade and disappear completely, although lesions occupying the entire central forehead often do not. Those on the posterior neck and occipital areas usually persist. The facial lesions should not be confused with a port-wine stain, which is a permanent lesion. The salmon patch is usually symmetric, with lesions on both eyelids or on both sides of midline. Port-wine stains are often larger and unilateral, and they usually end along the midline

Boil can occur at all sites except – (TN 95)
a) Pinna b) Skin
c) Scalp d) Palm

Excision of the hyoid bone is done in – (PGI 88)
a) Branchial cyst b) Branchial fistula
c) Thyroglossal cyst d) Sublingual dermoids

Cystic Hygroma

Nelson:- Lymphangioma (cystic hygroma) is a mass of dilated lymphatics. Some of these lesions also have a hemangiomatous component .Surgical treatment is complicated by a high incidence of recurrence. Intralesional sclerosing with OK-432, a streptococcal derivative, has been used successfully in selected patients. Macrocystic lesions appear to respond better than microcystic lymphangiomas to sclerotherapy. Lymphatic dysplasia may cause multisystem problems. These include lymphedema, chylous ascites, chylothorax, and lymphangiomas of the bone, lung, or other sites.

Bailey:- Cystic hygroma:-Cystic hygroma is an abnormal lymph-filled, often multilocular, space which usually presents in childhood as a soft, brilliantly transluminable swelling in the base of the neck. It is also found in the head and inguinal regions as they develop from primitive lymph cisterns. It behaves like a benign tumour and grows gradually in size, leading to cosmetic problems and compression of surrounding structures. Recurrence is common after simple aspiration and injection of sclerosant. Excision is technically challenging due to the large number of vital structures in the vicinity.

Sabiston:-A cystic hygroma is a lymphatic malformation that occurs as a result of a maldeveloped localized lymphatic network, which fails to connect or drain into the venous system. Most (75%) involve the lymphatic jugular sacs and present in the posterior neck region .Another 20% occur in the axilla, and the remainder are found throughout the body, including the retroperitoneum, mediastinum, pelvis, and inguinal area. Roughly 50% to 65% of hygromas present at birth, and most become apparent by the second year of life.

Because hygromas are multiloculated cystic spaces lined by endothelial cells, they usually present as soft, cystic masses that distort the surrounding anatomy. The indications for therapy are obviously cosmetic. In addition, the hygroma may expand to compress the airway, resulting in acute airway obstruction. Prenatal recognition of a large cystic mass of the neck is associated with significant risk to the airway, greater association with chromosomal abnormalities, and higher mortality rates. Improved fetal imaging modalities may allow for intervention at the time of delivery based on principles of pharmacologic maintenance of placental circulation until endotracheal intubation is achieved. This technique is referred to as the ex utero intrapartum therapy (EXIT) procedure.and is discussed later in this chapter. In addition to accumulating lymph fluid, hygromas are prone to infection and hemorrhage within the mass. Thus, rapid changes in the size of the hygroma may necessitate more urgent intervention.

Complete surgical excision is the preferred treatment; however, this may be impossible because of the hygroma infiltrating within and around important neurovascular structures. Careful preoperative magnetic resonance imaging (MRI) to define the extent of the hygroma is crucial. Operations are routinely performed with the aid of loupe magnification and a nerve stimulator. Because hygromas are not neoplastic tumors, radical resection with removal of major blood vessels and nerves is not indicated. Postoperative morbidity includes recurrence, lymphatic leak, infection, and neurovascular injury.

Injection of sclerosing agents such as bleomycin or the derivative of Streptococcus pyogenes OK-432 have also been reported to be effective in the management of cystic hygromas. Intracystic injection of sclerosants appears to be most effective for macrocystic hygromas, as opposed to the microcystic variety.

Ex Utero Intrapartum Therapy Procedure  (Schwartz)

The ex utero intrapartum therapy (EXIT) procedure is used in circumstances in which airway obstruction is predicted at the time of delivery due to the presence of a large neck mass, such as a cystic hygroma or teratoma .or to congenital tracheal stenosis. The success of the procedure depends on the maintenance of uteroplacental perfusion for a sufficient duration to secure the airway. To achieve this, deep uterine relaxation is obtained during a cesarian section under general anesthesia. Uterine perfusion with warmed saline also promotes relaxation and blood flow to the placenta. On average, between 20 and 30 minutes of placental perfusion can be achieved. The fetal airway is secured either by placement of an orotracheal tube or performance of a tracheostomy. Once the airway is secured, the cord is cut, and a definitive procedure may be performed to relieve the obstruction in the postnatal period. In general, infants with cystic neck masses such as lymphangiomas have a more favorable response to an EXIT procedure than infants with solid tumors such as teratomas; this is particularly true for premature infants

Marjolin ulcer – (PGI June 07)
a)Ca in marjolin’s is squamous cell ca
b)Chronic venous insufficiency
c)Basal cell carcinoma
d)arise from base of the ulcer

Wounds that are chronically inflamed and do not proceed to closure are susceptible to the development of squamous cell carcinoma .Originally reported in chronic burn scars by Marjolin,other conditions have also been associated with this problem, including osteomyelitis, pressure sores, venous stasis ulcers, and hidradenitis. The wound appears irregular, raised above the surface, and has a white, pearly discoloration. The premalignant state is pseudoepitheliomatous hyperplasia. If this report is obtained on a biopsy specimen, the biopsy is repeated because squamous cell carcinoma may be present in other areas.

True about Marjolins ulcer – (PGI 03)
a)Develops in long standing scar
b)Sq cell Ca develops
c)Slow growing lesion
d)Also know as Baghdad sore
e)Common in Black races

True about marjolins ulcer is – (PGI 97)
a) Ulcer over scar b) Rapid growth
c) Rodent ulcer d) Painful

Chronically lymphoedematous limb is predisposed to all of the following except – (Al 04)
a)Thickening of the skin
b)Recurrent soft tissue infections
c)Marjolin’s ulcer
d)Sarcoma

Chronic lymphedema predisposes to all except – (PGI 89)
a) Lymphangiosarcoma b) Marjolins ulcer
c) Recurrent infections d) Thickening of skin

Not a premalignant ulcer – (Kerala 94)
a)Bazin’s ulcer
b)Pagets disease of nipple
c)Marjolins ulcer
d)Lupur vulgaris

Commonest cancer in burn scar is – (PGI 97)
a) Sq. cell Ca b) Fibrosarcoma
c) Adenoa Ca d) Adeno-squamous Ca

Oriental sore (syn. Delhi boil, Baghdad sore, etc.):-This disease is due to infection by a protozoal parasite, Leishmania tro pica, and is a common condition in Eastern countries which is occasionally imported to Western zones.

Malignancies of Skin

Margins of squamous cells carcinoma is -(JIPMER a) Inverted b) Everted 81,Delhi 86)
c) Rolled d) Undermined

In pigmented basal cell carcinoma, treatment of choice is – (PGI 98)
a) Chemotherapy b) Radiotherapy
c) Cryosurgery d) Excision

Diagnostic procedure for basal cell Ca – (PGI 98)
a) Wedge biopsy b) Shave
c) Incisional biopsy d) Punch bio

Moh’s Micrographic excision for basal cell carcinoma is used for all of the following except –
a)Recurrent Tumour (Karnataka 06)
b)Tumor less than 2 cm in diameter
c)Tumors with aggressive histology
d)Tumors with perineural invasion

Basal cell carcinoma spread by – (MAHE 07)
a) Lymphatics b) Haematogenous
c) Direct spread d) None of the above

The commonest clinical pattern of basal cell carcinoma is – (Corned 08)
a) Nodular b) Morpheaform
c) Superficial d) Keratotic

A 48-year-old sports photographer has noticed a small nodule over the upper lip from four months. The nodule is pearly white with central necrosis, telangiectasia. The most likely diagnosis would be –
a)Basal cell carcinoma (AIIMS 06)—Telangiectasia uncommon in SCC
b)Squamous cell carcinoma
c)Atypical melanoma
d)Kaposis sarcoma

Match list I with list II and select the correct answer using the code given below the lists – (UPSC 07)
List I List II
(Carcinoma) (Characteristic)
A.Seminoma testis 1. Hormone dependent
B.Carcinoma prostate 2. Does not spread by
C.Basal cell carcinoma lymphatics
D.Malignant melanoma 3. Prognosis depends on thickness
4. Highly radiosensitive
Code :
a)
A B C D
4 1 2 3
b)A B C D
4 2 1 3
c)A B C D
3 1 2 4
d)A B C D
3 2 1 4

Ans. is ‘a’ i.e., Basal cell carcinoma [Ref: Sabiston 17"/e p. 796; Harrison 166/e p. 497;
S.Das text book of Surgery Pile 101-103]

 

Basal Cell Carcinoma BCC is a malignancy arising from epidermal basal cells. The least invasive of BCC subtypes, superficial BCC, classically consists of truncal erythematous, scaling plaques that slowly enlarge. This BCC subtype may be confused with benign inflammatory dermatoses, especially nummular eczema and psoriasis. BCC can also present as a small, slow-growing pearly nodule, often with small telangiectatic vessels on its surface (nodular BCC). The occasional presence of melanin in this variant of nodular BCC (pigmented BCC) may lead to confusion clinically with melanoma. Morpheaform (fibrosing) BCC and micronodular BCC, the most invasive subtypes, manifest as solitary, flat or slightly depressed, indurated, whitish or yellowish plaques. Borders are typically indistinct, a feature associated with a greater potential for extensive subclinical spread.

Rx:- The most frequently employed treatment modalities for BCC include electrodesiccation and curettage (ED&C), excision, cryosurgery, radiation therapy, laser therapy, Mohs micrographic surgery (MMS), topical 5-fluorouracil, and topical immunomodulators. The mode of therapy chosen depends on tumor characteristics, patient age, medical status, preferences of the patient, and other factors. ED&C remains the method most commonly employed by dermatologists. This method is selected for low-risk tumors (e.g., a small primary tumor of a less aggressive subtype in a favorable location). Excision, which offers the advantage of histologic control, is usually selected for more aggressive tumors or those in high-risk locations or, in many instances, for aesthetic reasons. Cryosurgery employing liquid nitrogen may be used for certain low-risk tumors but requires specialized equipment (cryoprobes) to be effective for advanced neoplasms. Radiation therapy, while not used as often, offers an excellent chance for cure in many cases of BCC. It is useful in patients not considered surgical candidates and as a surgical adjunct in high-risk tumors. Younger patients may not be good candidates for radiation therapy because of the risks of long-term carcinogenesis and radioderma

Squamous Cell Carcinoma Primary cutaneous SCC is a malignant neoplasm of keratinizing epidermal cells. SCC can grow rapidly and metastasize. The clinical features of SCC vary widely. Commonly, SCC appears as an ulcerated erythematous nodule or superficial erosion on the skin or lower lip, but it may present as a verrucous papule or plaque. Overlying telangiectasias are uncommon. The margins of this tumor may be ill-defined, and fixation to underlying structures may occur. Cutaneous SCC may develop anywhere on the body but usually arises on sun-damaged skin. A related neoplasm, keratoacanthoma, typically appears as a dome-shaped papule with a central keratotic cra-ter, expands rapidly, and commonly regresses without therapy. This lesion can be difficult to differentiate from SCC. Actinic keratoses and cheilitis, both premalignant forms of SCC, present as hyperkeratotic papules on sun-exposed areas. The potential for malignant degeneration in untreated lesions ranges from 0.25 to 20%. Bowen’s disease, an in situ form of SCC, presents as a scaling, erythematous plaque. Treatment of premalignant and in situ lesions reduces the subsequent risk of invasive disease.

Rx:- SQUAMOUS CELL CARCINOMA The therapy of cutaneous SCC should be based on an analysis of risk factors influencing the biologic behavior of the tumor. These include the size, location, and degree of histologic differentiation of the tumor as well as the age and physical condition of the patient. Surgical excision, MMS, and radiation therapy are standard methods of treatment. Cryosurgery and ED&C have been used successfully for premalignant lesions and small primary tumors. Metastases are treated with lymph node dissection, irradiation, or both. 13-cis-retinoic acid (1 mg orally every day) plus INF-α (3 million units subcutaneously or intramuscularly every day) may produce a partial response in most patients. Systemic chemotherapy combinations that include cisplatin may also be palliative in some patients.

 

image

This basal cell
carcinoma shows central ulceration and a pearly, rolled, telangiectatic
tumor border.

image

Squamous cell carcinoma is seen here as a hyperkeratotic crusted
and somewhat eroded plaque on the lower lip
. Sun-exposed skin such
as the head, neck, hands, and arms are other typical sites of involvement.

image

Keratoacanthoma
is a low-grade squamous cell carcinoma that presents as
an exophytic nodule with central keratinous debris

Keratoacanthoma
Keratoacanthoma (molluscum sebaceum) arises as a rapid proliferation of squamous epidermal cells. The nodule grows rapidly for 6—8 weeks at which time it usually begins to resolve spontaneously. Keratoacanthoma must be distinguished from SCC. Usually rapid evolution to relatively large size, irregular crater shape and keratotic plug, and the undamaged surrounding skin make a distinction possible. Spontaneous healing further confirms the diagnosis. Histologically, it is difficult to differentiate between a keratoacanthoma and SCC. There is also a possibility of a highly anaplastic SCC behaving like a keratoacanthoma. Excision biopsy is mandatory if the diagnosis is in doubt as curetted specimens yield poor sections.

image

Malignant pustule occurs in – (PGI 88) a) Melanoma b) Gas gangrene ) Ovarian tumour d) Anthrax

All are true statement about malignant melanoma except- (A197)
a)Clark’s classification used for prognosis
b)Women have better prognosis
c)Acral lentigenous have better prognosis
d)Limb perfusion is used for local treatment

Prognosis of malignant melanoma depends on – (JIPMER 98)
a) Grade of tumor b) Spread of tumor
c) Depth of invasion d) Metastasis

Worst prognosis in Melanoma is seen in the subtype-
a)Superficial spreading (Kerala 2001)
b)Nodular Melanoma
c)Lentigo Maligna Melanoma
d)Amelanotic Melanoma

Least malignant melanoma is- (Kerala 2001)
a) Lentigo maligna b) Superifcial spreading
c) Nodular d) Amelanotic

Prognosis of melanoma depends on – (PGI 98)
a
)Stage
b)Depth of melanoma on biopsy

c)Duration of growth
d)Site

Which one of the following is not included in the treatment of malignant melanoma – (UPSC 05)
a) Radiation b) Surgical excision
c) Chemotherapy d) Immunotherapy

In the Clatke’s level of tumor invasion for malignant melanoma level 3 refers to – (COMED 06)
a)All tumar cells above basement membrane
b)Invasion into reticular dermis
c)Invasion into loose connective tissue of papillary dermis
d)Tumor cells at junction of papillary and reticular dermis

True about melanoma of the anal canal is -(PGI 99)
a)Present usually as anal bleeding
b)AP resection gives better result than local excision
c)Local recurrence at the same site after resection
d)Radiosensitive

Most common site of Ientigo maligna melanoma is -a) Face b) Legs (PGI 01)
c) Trunks d) Soles

Most common origin of melanoma is from –
a)Junctional melanocytes (AMU 01)
b)Epidermal cells
c)Basal cells
d)Follicular cells

Melanomas originate from neural crest-derived melanocytes; pigment
cells present normally in the epidermis and sometimes in the dermis.

The back is the
most common site for melanoma in men. In women, the back and the
lower leg (from knee to ankle) are common sites.

The most important prognostic factor is the stage at the time of presentation. Fortunately, most melanomas are diagnosed in clinical stages I and II. The revised American Joint Committee on Cancer (AJCC) staging system for melanoma is based on microscopic primary tumor depth (Breslow’s thickness), presence of ulceration, evidence of nodal involvement, and presence of metastatic disease to internal sites

An alternative prognostic scheme for clinical stages I and II melanoma, proposed by Clark, is based on the anatomic level of invasion in the skin. Level I is intraepidermal (in situ); level II penetrates the papillary dermis; level III spans the papillary dermis; level IV penetrates the reticular dermis; and level V penetrates into the subcutaneous fat. The 5-year survival for these stages averages 100, 95, 82, 71, and 49%, respectively.

Any pigmented cutaneous lesion that has changed in size or shape or has other features suggestive of malignant melanoma is a candidate for biopsy. The recommended technique is an excisional biopsy, as that facilitates pathologic assessment of the lesion, permits accurate measurement of thickness if the lesion is melanoma, and constitutes treatment if the lesion is benign. For large lesions or lesions on anatomic sites where excisional biopsy may not be feasible (such as the face, hands, or feet), an incisional biopsy through the most nodular or darkest area of the lesion is acceptable; this should include the vertical growth phase of the primary tumor, if present. Incisional biopsy does not appear to facilitate the spread of melanoma.

The following margins can be recommended for primary melanoma: in situ: 0.5 cm; invasive up to 1 mm thick: 1.0 cm; >1 mm: 2.0 cm. For lesions on the face, hands, and feet, strict adherence to these margins must give way to individual considerations about the constraints of surgery and minimization of morbidity. In all instances, however, inclusion of subcutaneous fat in the surgical specimen facilitates adequate thickness measurement and assessment of surgical margins by the pathologist.

Patients who have advanced regional disease limited to a limb may benefit from hyperthermic limb perfusion with melphalan. High complete response rates have been reported, and responses are associated with significant palliation of symptoms

wedge biopsy:- An excisional biopsy in which a lesion identified at the time of a surgical procedure is removed, with a wedge of normal surrounding tissue

Trophic ulcers are caused by – (PGI 02)
a) Leprosy b) Buerger’s disease
c) Syringomyelia d) DVT
e) Varicose veins

Trophic ulcers [trophe (Greek) = nutrition] are due to an impairment of the nutrition of the tissues, which depends upon an adequate blood supply and a properly functioning nerve supply. Ischaemia and anaesthesia therefore will cause these ulcers. Thus, in the arm, chronic vasospasm and syringomyelia will cause ulceration of the tips of the fingers (respectively painful and painless). In the leg, painful ischaemic ulcers occur around the ankle or on the dorsum of the foot. Neuropathic ulcers due to anaesthesia (diabetic neuritis, spina bifida, tabes dorsalis, leprosy or a peripheral nerve injury) are often called perforating ulcers .Starting in a corn or bunion, they penetrate the foot, and the suppuration may involve the bones and joints and spread along fascial planes upwards, even involving the calf.

Nonspecific ulcers are due to infection of wounds, or physical or chemical agents. Local irritation, as in the case of a dental ulcer, or interference with the circulation, e.g. varicose veins, are predisposing causes.

A healing, nonspecific ulcer has a shelving edge. It is pearly, rolled or rampant if a rodent ulcer, and raised and everted if an epithelioma, under­mined and often bluish if tuberculous, vertically punched out if syphilitic.

Treatment for pyoderma gangrenosum is –
a)Steroids (Jharkand 03)
b)I.V. antibiotics
c)Surgery + antibiotics
d)Surgery alone

Which of the following materials for implants will
evoke least inflammatory tissue response –
a)Polypropylene (SGPGI 04)
b)Bovine collagen
c)Polygiactin
d)Cotton

Chronic Burrowing ulcer is caused by – (.AI07)
a)Microaerophilic streptococci
b)Peptostreptococcus
c)Streptococcus viridans
d)Streptococcus pyogenes

Schwartz:- Pyoderma gangrenosum is a relatively uncommon destructive cutaneous lesion. Clinically, a rapidly enlarging, necrotic lesion with undermined border and surrounding erythema characterize this disease. Linked to underlying systemic disease in 50% of cases, these lesions are commonly associated with inflammatory bowel disease, rheumatoid arthritis, hematologic malignancy, and monoclonal immunoglobulin A gammapathy.Recognition of the underlying disease is of paramount importance. Management of pyoderma gangrenosum ulcerations without correction of underlying systemic disorders is fraught with complication. A majority of patients receive systemic steroids or cyclosporine.Although medical management alone may slowly result in wound healing, many physicians advocate chemotherapy with aggressive wound care and skin graft coverage.

Sabiston:- Extraintestinal manifestations of ulcerative colitis include arthritis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, and primary sclerosing cholangitis. Arthritis, particularly of the knees, ankles, hips, and shoulders, occurs in about 20% of patients, typically in association with increased activity of the intestinal disease. Ankylosing spondylitis occurs in 3% to 5% of patients and is most prevalent in patients who are HLA-B27 positive or have a family history of ankylosing spondylitis. Erythema nodosum arises in 10% to 15% of patients with ulcerative colitis and often occurs in conjunction with peripheral arthropathy. Pyoderma gangrenosum typically presents on the pretibial region as an erythematous plaque that progresses into an ulcerated, painful wound. Most patients who develop this condition have underlying active inflammatory bowel disease. Arthritis, ankylosing spondylitis, erythema nodosum, and pyoderma gangrenosum typically improve or completely resolve after colectomy.

Colectomy has no effect on the course of PSC.

According to Harrison:- Pyoderma gangrenosum (PG) is seen in 1–12% of UC patients and less commonly in Crohn’s colitis. Although it usually presents after the diagnosis of IBD, PG may occur years before the onset of bowel symptoms, run a course independent of the bowel disease, respond poorly to colectomy, and even develop years after proctocolectomy. It is usually associated with severe disease. Lesions are commonly found on the dorsal surface of the feet and legs but may occur on the arms, chest, stoma, and even the face. PG usually begins as a pustule and then spreads concentrically to rapidly undermine healthy skin. Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema. Centrally, they contain necrotic tissue with blood and exudates. Lesions may be single or multiple and grow as large as 30 cm. They are sometimes very difficult to treat and often require intravenous antibiotics, intravenous glucocorticoids, dapsone, azathioprine, thalidomide, intravenous cyclosporine, or infliximab.

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