Plastic Surgery for Undergraduates

8/3/2019 Plastic Surgery for Undergraduates

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PLASTIC SURGERY DEPARTMENT

AIN-S HAMS UNIVERSITY

2005- 2006


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Chapter 1

Burn Trauma

A burn is necrosis of tissues by physical or chemical agents.

Types and incidence

I) Physical burns:

Thermal burns.

Electric burns.Radiation burns.

II) Chemical:

Acid burns.

Alkali burns.

N.B. 75 % of all burns are due to thermal agents, 25% are induced by the other agents.

Thermal BurnsThey are caused by direct flames or by direct contact with hotfluids or objects. They are further divided into:

1-Flame burns: Either directly from the fire or by the ignition of clothes.

2-Scalds: Due to contact of the skin with hot fluids.

3-Contact burns: It results from direct contact with hot objects (irons).

4-Steam burns: Due to the high carrying capacity of steam .Also steam inhalation

can cause thermal injury to the airway.

Electric BurnsThey are caused by low orhigh voltage electric currents. Low voltage currents (less

than 1000 volts) usually cause local tissue damage (e.g. household currents), whereas

high voltage (more than 1000 volts) currents tend to cause severe tissue damage.

Mechanism of damage:

Thermal effects: Due to the heat generated at the point of contact.

Interference with the electric activity of body organs (CNS, CVS)

Non thermal effects: Due to:

Endothelial damage and thrombosis.

Disruption of cell membrane and cell homeostasis.

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High voltage currents have entry and exit sites, and the amount of damage to

internal organs depends on the route between the two sites. Current passes through

tissues without significant damage if the tissue resistance is low e.g. fat, however

damage is more apparent in tissues with greater resistance e.g. bone.

High voltage electricity can arc in the air for distance up to 2 - 3 feet. Temperatures

in the arc can reach 2000 4000 C.

Effects of electric burns:

1. Muscular damage

2. Renal injury in the form of acute renal failure due to myoglobin pigments

liberated from damaged muscles.

3. Cardiac muscle injury which appears in the form of arrhythmias e.g. AF,

VF

4. Pulmonary complications.

5. CNS injury

6. Cataract formation7. Fractures of bones due to tetanic muscle contractions or from associated

trauma

Chemical BurnsThey are caused by contact with acids or alkalis. Both acids and alkalis can be defined

as caustics.

Mechanism of damage:

1. Acids cause coagulative necrosis and denature proteins, leading toformation of a crust which stops further penetration of the acid

2. Alkalis cause liquefactive necrosis with saponification of fats, which does

not limit the progression of the alkali

Chemical burns must be promptly irrigated by water for at least half an hour in

order to dilute their effect (Neutralization of the substance is better avoided to protect

the tissues from the heat liberated during the neutralization reaction).

Radiation burns

Injuries following exposure to radiation depend on; doses, wave length and wavefrequency.

-Long wave length radiation (e.g. radio-waves, micro-waves, and infrared light)penetrates the skin to very little extent or not at all. They do not ionize matter and the

tissue damage is by heat only.

- Short wave length radiation (e.g. x-ray, Gamma-rays) cause very severe tissue

damage due to its ionizing effect with the production of free radicals. The non

ionizing radiation may cause superficial skin burn. The skin changes are seen within

24 hours. These changes either return to normal or progress vessel thrombosis,

necrosis, and ulceration. The healing is slow, and the scar is avascular and liable to

ulceration.

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Classification of Burns

1. According to extent

Total Body Surface Area (TBSA) affected is calculated by:

Rule of Nines (for adults) The palm of the patients hand: It is considered roughly to be 1% of the body

surface area.

Lund-Browder chart (for children)

A- The rule of nines:

It is more accurate.

It is used in adults.

The body is divided into areas corresponding to 9% or multiples.

C-Lund-Browder chart (for children):

It is used in children.

It makes the allowance for the changing proportion of the body surface area

from infancy to adult life.

The differences are mainly in the head, thighs, and the legs.

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2. According to depth

1st degree burns: no or minor epithelial damage e.g. sunburns.

2nd degree (partial thickness) burns: damage extends to the dermis and is

further divided into

Superficial dermal burns which are characterized by formation of

bullae and extends to the outer dermis. They usually heal within 15

days.

Deep dermal burns which reach deeper into the dermis, but the skin

appendages are spared. Healing usually takes 3 4 weeks.

3rd degree burns: damage to all layers of the skin and the skin appendages,

therefore there is no 1ry healing, and grafts are needed for coverage.

Pathophysiology of Burns

A) Local:The burn wound is divided into three zones due resistance of tissues and heat transfer.

1. Zone of coagulation: This is in the centre, with cessation of circulation and

vessel thrombosis.

2. Zone of stasis: Surrounds the first zone, and is characterized by a pronounced

inflammatory reaction.

3. Zone of hyperemia: Outermost zone, with minimal tissue damage and early

spontaneous recovery.

B) General:There is loss of various skin functions as insulation and anti-bacterial protective

barrier.

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The body responds to the burn with the release of inflammatory mediators into the

circulation e.g. histamine, serotonin, prostaglandins, Tumor Necrosis Factor (TNF-),

interleukins (IL-1&2) etc. These mediators start a systemic response affecting various

organ systems.

1. Circulatory changes:Local response as previously discussed. Systemic response is in the form ofhypovolemia. This is due to sequestration of plasma from the intravascular space

into the interstitial space.

2. Blood changes: Increased haematocrite value and viscosity

Decrease in platelet count

Anemia and decrease in RBC life span.

Leucocytosis

3. Metabolic changes:Patients with major burns develop a hyper-catabolic state leading to utilization of

the glycogen, fat, and muscle stores for the production of energy. This state can be

reversed by high nutrition of the burned patient. This hyper-catabolic is due to

obligatory energy expenditure with the increase of the evaporative water loss from

the burn surface.

This hyper-catabolic state is responsible for:

A- Increase in the loss of proteins (urinary nitrogen excretion increases up to

300%).

B- Rapid loss of weight.

4. Immunological changes:Patients develop a generalized state of immunosuppression due to:

Inflammatory mediators and burn toxins.

Iatrogenic causes as in repeated blood transfusion.

Management of Burns

At burn scene (first aids):

1. Remove victim from the fire, and extinguish flames, remove clothes

and wrap the patient in a clean blanket.

2. Check air way and ensure that it is patent.

3. Quick assessment for associated trauma.

4. Transport to the near by burn unit for definitive management.

Management in the Emergency Room:

1. Secure a patent airway, and obtain vital data for patient (pulse, blood

pressure, temperature).

2. Exclude associated trauma.

3. Start to estimate the depth and the extent of the burn.

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4. Secure a reliable intra-venous line (may need more than one) and start

fluid therapy.

5. Insert a naso-gastric tube for fear of aspiration.

6. Insert a Foleys self retaining urinary catheter for monitoring of urinary

output.

7. Medications: Tetanus vaccine or immunoglobulin

Antibiotics: better to use broad spectrum antibiotics

Analgesics: IV morphine to avoid neurogenic shock

Anti-ulcer measures

8. Escharotomy and/or fasciotomy

Escharotomy is done to relieve the tourniquet like effect ofcircumferential deep burns, which cause vascular and/or respiratory

compromise.

Fasciotomy is done in electric burns where the deep muscular

compartments are affected leading to vascular compromise.

9. Chemical burns:

Prolonged irrigation with water to dilute the caustic substance. This is

continued for at least hour.

No attempt at neutralization of the acid or alkali because this can

generate heat that increases the tissue damage.

10. Electric burns:

Forced diuresis with mannitol to avoid tubular necrosis.

Fasciotomy if needed.

DC shock if a patient develops ventricular arrhythmia.

Fluid therapy:

In burns < 20% TBSA (adults) or < 10% TBSA (children), fluid

therapy can be given by the oral route.

In burns that are 20 30% TBSA, the oral route is supplemented by IV

fluids.

In burns > 30% TBSA, fluid therapy is given via the IV route.

Calculation:

o Parkland formula = 4 cc x BW (Kg) x TBSA (%) given as ringer lactate. Half the

quantity given over 8 hours, then the other half given over 16 hours. In the next

day half the original quantity is given.o Evans formula = 1 cc x BW (Kg) x TBSA (%) in colloid + 1 cc x BW (Kg) x

TBSA (%) in normal saline + 2000 cc 5% Dextrose as maintenance. One half in

the first 8 hours, and the other half over 16 hours. In the nest day give half the

previous amount with the same maintenance.

N.B. Monitoring fluid therapy:

o Adequate urine output, 1 1.5 cc/Kg/hr.

o Normal blood pressure and pulse.

o CVP around 10 cmH2O.

Burn Wound Management

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Initial management

1. Remove all clothing at the time of admission.

2. Loose skin should be gently snipped.

3. Vesicles should be opened and debrided.

4. Escharotomy and/or fasciotomy may be needed.

Daily care

1. Topical antimicrobial agents

Silver sulfadiazine

Mafenide acetate

Betadine ointment

Silver nitrate aqueous solution

2. Wound dressing

Open method: wound is cleansed, covered by a layer of antimicrobialagent and the patient is left exposed in a special sterile room with

control of temperature and humidity. The patient is daily washed in aspecial tank, and other layer of antimicrobial agent added.

Closed method: applying topical agents and covering it with sterile

compression/absorption dressing. The dressings are changed every 3-5

days. Wet to wet dressings is suitable for areas requiring moderate non

surgical debridement .These dressings are changed every 4-8 hours.

Other types of dressings:

Synthetic dressings (silicone and opsite).

Semi-synthetic dressings: Two layers, the outer one is

semipermeable , the inner is bovine collagen , e.g. Integra.

Biological dressings: human cutaneous allografts ,amniotic membranes, and porcine xenografts.

Cultured keratinocytes.

Burn Wound Surgery:

1. Escharotomy: Done as an emergency procedure to relieve the tourniquet

like effect of a circumferential deep burn. The eschar is incised till the

underlying subcutaneous fat bulges.

2. Escharectomy: excision of the whole eschar till subcutaneous fat is reached.

Tangential excision: removal of successive layers of the eschar till punctuate dermal

bleeding appears, denoting viable dermis.

Excision to fascia: done is 3rd degree burns, where the whole eschar and

subcutaneous fat is removed till investing fascia is reached.

Complications of Major Burns

A- Early complications:

Cardiovascular

1. Acute heart failure occasionally seen with burns exceeding 70%.

2. Congestive heart failure due to over hydration during the resuscitationperiod, or due to pre-existing heart disease.

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3. Arrhythmias which occur more commonly with electric buns.

4. Endocarditis and myocarditis which are complications of severe sepsis.

Renal

1. Acute tubular necrosis resulting from severe hypovolemia.

2. Myoglobinuria which is associated with severe electric burns.

Pulmonary

1. Inhalation injury which can be due to:

Inhalation of super heated air

Inhalation of noxious burn fumes

Inhalation of carbon monoxide

N.B.Inhalation injury is suspected when:

- Fire is in a closed space. - Presence of facial burns.

- Hoarseness of voice. - Presence of carbonaceous sputum or soot.- Presence of singed facial hairs and nostrils.

Management:

Immediate endotracheal intubation.

100% O2 which is gradually decreased till arterial PO2 reaches normal

level.

2. Pulmonary embolism due to prolonged immobilization and

hypercoagulable state of the patient.

3. Pneumothorax is rare but fatal complication.

Infection1. Burn wound sepsis, occurring mainly in 2nd and 3rd degree burns and the

most common pathogens arePseudomonas auroginosa, Staphylococcusaureus, and Streptococcus pyogenes

2. Urinary tract infection, usually due to prolonged catheterization

3. Pneumonia

4. Septic shock

5. Suppurative thrombophlebitis

GIT

1. Paralytic ileus can occur in burns exceeding 30% TBSA.2. Curlings ulcer seen in major burns.

B-Late complications:

1- Presence of raw skin areas due to 3rd degree burns.

2- Pigmentary skin changes in the form of hypo/hyper pigmentation

3- Scarring and loss of quality of skin

4- Hypertrophic scarring and keloids

5- Wound contracture

6- Disfigurement and loss of digits

7- Malignant change (Marjolin ulcer)

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Chapter 2

Wounds and Wound Management

A wound by definition is any breakdown in the continuity of any tissue or

organ. The causative factor may be internal or external.

Classification of wounds

I. According to the causative factor

Abrasions: These wounds are caused by blunt objects that hit the body

surface tangentially. This leads to removal of layers of the skin and

underlying structures.

Contusions: These wounds occur when blunt objects hit the body in a

perpendicular way; this causes damage of the underlying tissues that

can reach the bones causing fractures. These wounds are characterized

by haematoma formation and bruising of the skin.

Lacerations: These wounds are caused when a sharp object hits the

body tangentially leading to elevation of layers of the body. They are

further divided into:

Simple: do not need application of skin grafts or flaps.

Lacerations with skin loss.

Stab wounds: These wounds occur when a sharp object hits the bodyperpendicularly leading to penetrating wounds. In this situation, the

external wound is small, but there is damage to the deeper structures

according to the location of the injury.

II. According to wound circumstances

Accidental.

Homicidal.

Suicidal.

Self inflicted.

III. According to duration

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Acute wounds

They are usually expected to heal within a predictable time , e.g.

surgical incision, animal bites, burns.

Chronic wounds

They are long lasting, recurrent, and difficult to heal e.g. bed sores,malignant ulcers, leg ulcers.

IV. According to wound environment

InfectedBad odor, wound exudates and discharge, painful, edema,

Not infected

Wound HealingWound healing can take place in a dry or wet environment.

Dry Wound Healing

It is termed dry because fibrin clots dehydrate and form a scab. This scab

allows desiccation of underlying tissues.

Disadvantages:

Cells cannot move so the wound is hard to epithelialise.

No nutrients or growth factors.

Dead tissues are a good media for anaerobic bacteria.

Scabs delay healing.

More painful.

Moist Wound Healing

Healing takes place in a moist environment, under occlusive or semi-occlusive

dressings.

Advantages:

Allow wound nutrition.

Temperature regulation.

Allow granulation through cell migration.

Moist wound prevents scab formation.

Epithelialisation is fast.

Stages of Wound Healing

Inflammatory Phase

This is the initial response of all tissues to injuries. The aim is to establish

haemostasis, and mobilize the immune system. This phase is composed of a

vascular response and a cellular response.

Vascular response

Haemostasis Occurs in 5-10 minutes

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Causes initial vasoconstriction

There is activation of the clotting cascade

Vasodilatation

Occurs during 1st 72 hours.

Responsible for the signs of inflammation; redness, hotness, tenderness

Vascular response is precipitated by:

Serotonin and histamine release

Activation of kallekrin from kinins

Platelet activation factor (PAF)

Complement factor C5a

Cellular response

The cells responsible for the cellular response are:

Leucocytes:

Migrate through the vessel wall by diapedesis stimulated by chemotacticfactors.

Liberate enzymes that facilitate the breakdown of debris and bacteria.

Macrophages:

The main cell in wound healing.

Release chemotactic and growth factors that activate and stimulate the

division of fibroblasts and new blood vessels.

They are dominant 3 4 days after injury.

Mast cells:

Release histamine, heparin.

Maybe involved in the breakdown of debris and removal of collagen.

Lag or Substrate Phase

After 3 5 days from the original insult.

Removal of debris and migration of capillary fibroblasts and endothelial cells.

Muco-polysaccharides provide the environment for collagen deposition and

fiber formation.

There is no increase in tensile strength.

Proliferative Phase

From 5 21 days. Epithelial regeneration:

Loosening of epithelial cells from their dermal attachment as well as

mitosis of the existing cells.

Healing by 1ry intention occurs in clean cut wounds closed by sutures that

require small amount of new tissue.

Healing by 2ry intention occurs where there is tissue loss and a defect that

needs to be covered by tissues. It can take weeks to months.

Affected by moisture, temperature, pH, infection, foreign bodies.

Granulation tissue:

Starts 5 days after injury. Beefy red in color.

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Smooth with no offensive discharge.

Formed of a network of new blood vessels in a collagen network.

Unhealthy granulation tissue is less vascular, edematous, hemorrhagic, has

sloughs.

Connective tissue repair:

Fibroblasts produce collagen and ground substance (muco-polysaccharides

and glycosaminoglycans).

Collagen fibers are deposited.

Vitamin C acts as a co-enzyme for the hydroxylation of proline to

hydroxy-proline.

Hydroxy-proline is essential for the cross linkage of collagen fibers.

Wound contraction:

Gradual wound shrinkage is an attempt to decrease the area to be covered

by epithelium.

In the healing wound the advancing epithelium forms a marginal zone of

smooth tissue. Wound contracture must be differentiated from wound contraction. The

former is decrease in the size of the scar itself, whereas contraction is

decrease in the size of the wound itself.

Remodeling Phase

Type III collagen formed during the proliferation phase is converted to type I,

and undergo extensive reorganization, the fibers become lined up along the

stress lines of the wound.

Scar tissue becomes softer, flat, and its color fades.

This stage may last for a year or more.

Factors Affecting Wound Healing

Local:

Dry environment

Infection

Edema

Necrotic tissue

Local blood supply

Systemic:

Age: wounds in the young heal more rapidly than those in the elderly.

Nutrition: Proteins and vitamins (C-A-E), are essential for wound healing.

Chronic diseases e.g. Diabetes mellitus, cancer

Vascular insufficiency

Radiation

Immunosuppression e.g. AIDS, chemotherapy

Smoking

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Complications of Wound Healing

Early

Infection

HaematomaWound dehiscence and disruption

Late

Ugly scars.

Hypertrophic scars.

Keloids.

Wound contracture.

Malignant transformation (Marjolin ulcer)

Management of woundsThe management of wounds passes in stages, each following the other. The final

goal of wound management is to obtain a good quality healing with a nice scar.

These stages are:

i- Primary wound care

ii- Wound dressings

iii-Surgical wound management

Primary wound care:

Wound cleansing: using liberal amount of antiseptics and normal saline.Wound debridement: where the foreign material implanted in the wound is

removed.

Wound excision: where the apparently dead parts of tissues are excised.

Bleeding points are secured by electrocautry or ligatures.

Wound Dressing:

This is an important step in obtaining a nice and smooth wound. Wound dressings

have changed markedly due to continuous research. The ideal wound dressing should

have the following properties:

Maintain a moist environment for healing.

Remove excess exudates.

Allow gaseous exchange.

Impermeable to bacteria.

Atraumatic on removal.

Non-allergic.

Comfortable and conformable.

Protect against further trauma.

Provide thermal insulation.

Cost effective with a long shelf life.

Carrier for medications.

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Comes in a wide array of sizes and shapes.

Surgical wound management:

1-Direct skin closure.

This technique is used when there is minor skin defect.2-Skin grafts and skin flaps:

These are used when there is extensive skin

loss and/or other soft tissue or skeletal loss.

A skin graft is a segment of dermis and

epidermis separated completely from its blood

supply at the donor site before it is transferred

to the recipient site. Skin grafts are either split

thickness or full thickness skin grafts.

A- Thin split thickness skin graft.

B- Medium thickness skin graft.C- Thick split thickness skin graft.

D- Whole (full) thickness skin graft.

A- Split Thickness Skin Grafts (Thiersch):

Composed of epidermis and a portion of dermis. According to the amount of

dermis in the harvested graft, it can be classified as thin, intermediate, or thick

split thickness graft. Thickness of the graft varies from 10 25/1000 inch.

Donor sites of split thickness skin graft:

Thigh specially the medial aspect.

Arm.

Back of trunk.

Scalp.

Indications of split thickness skin graft:

Extensive skin loss with healthy granulation tissue.

After malignant tumor resection.

Coverage after deep burns.

Advantages:

Easy harvesting and application.

Can cover a wide area.

Early detection of recurrence of malignancy.

Chances of take are high.

Disadvantages:

Liable to contracture.

Poor texture and color mismatch.

Cannot be use in weight bearing areas.

B-Full Thickness Skin Grafts (Wolf):

Composed of epidermis and the entire thickness of the dermis.

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Indications:

Facial wounds that cannot be closed directly with sutures.

Palmar aspect of hands and feet.

Donor sites:

Post-auricular area

Supraclavicular area

Flexural skin

Thigh and abdomen

3- Flaps

A flap is a portion of tissue that depends on its

survival on a well maintained or surgicallyestablished circulation.

Classification of Flaps: According to blood supply

Random pattern flaps: no dominant blood supply.

Axial flaps: dominant source vessel.

Reverse flow flaps: flap survives on an intact distal feeding vessel.

According to proximity of defect

Local: flap shares a border with the defect. Regional: flap is near but not adjacent to the defect.

Distant: flap is not near the defect.

Free flap: flap is raised with its blood vessels and anastomsed in therecipient site with a suitable

blood vessel.

According to method of

transfer

Advancement.

Transposition.

Rotation. Interpolation.

According to the type of

tissues:

Cutaneous.

Fasciocutaneous.

Musculocutaneous.

Osteocutaneous.

Osteomusculocutaneous.

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Advantages:

Good color and texture match.

Can allow future operations through the area.

Provide extra vascularity.

Disadvantages:

May require many stages.

May hide recurrence after excision of malignant tumors.

Are sometimes bulky.

Central part of the flap remains almost insensitive.

Chapter 3

Cleft Lip & Cleft Palate.

Embryology Upper lip is formed by the fusion of the fronto-nasal process with the two

maxillary processes.

The lower lip is formed by the fusion of the two mandibular processes.

The fronto-nasal process also forms the central alveolar segment, and thetriangular anterior palate.

The maxillary process forms the remaining part of the upper alveolus, and theposterior part of the palate.

Fusion in the oral region takes place at the 8 th week.

Anatomy of the Lip:

Morphologically the lip is divided into:

Vermilion borderwhich is also called the white roll, it is the junction

between the white and red portions of the lip

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Philtral ridges which are the two vertical ridges that extends from the

vermilion borderer to the nose.

Cupids bow is a V shaped definition in the vermilion border between thetwo philtral ridges.

The lip is formed of three layers; skin, muscle, and mucous membrane.

The main muscle of the lip is the orbicularis oris. It is divided into:

Superficial part: inserted in the anterior nasal spine.

Deep part: occupies the red margin and acts as a sphincter.

Blood supply: Facial artery.

Ophthalmic artery.

Maxillary artery.

Anatomy of the Palate: The palate is the anatomical barrier between the oral cavity and the nasal cavity. It

also controls and separates the oropharynx from the nasopharynx.

The orifice or aperture between the nasopharynx and the oropharynx is called the

velo-pharengeal valve.

Important landmarks in the palatine bone: Y-shaped suture between the three segments of the palate.

Incisive foramen in the junction between the anterior and posteriorparts of the palate.

Posterior nasal spine.

Pterygoid plates and thepterygoidhammulus arising from the

medial plate.

The soft palate is a fibromuscular layer composed of the following muscles:

Tensor palati muscle (nerve supply from the trigeminal nerve).

Levator palati.

Palatoglossus. Palatopharengeous.Uvulae muscle

The last four muscles receive their nerve supply from the pharyngeal plexus(IX, X, XI nerves).

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The combined action of the soft palate is to be pulled upward and backward to

make surface contact between the posterior third of the soft palate and the

posterior pharyngeal wall.

Blood supply:

Greater and lesser palatine vessels are the main blood supply of the hard

palate.

Ascending pharyngeal branch of the external carotid artery is the main

blood supply of the soft palate.

Incidence of cleft lip and cleft palate:

Cleft lip and cleft palate are the second most common congenital deformity (hand

deformities are the first). They occur in 1 from each 750-1000 of the population.

Etiology of Cleft lip and cleft Palate:

Is twice as common in females as in males.

Environmental rather than familial factors.

Up to 60% of cases are associated with other syndromes e.g. Treacher Collins

syndrome, Crouzons and Aperts syndrome.

Types of Cleft Lip & Cleft Palate

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I-clefts of the primary palate (lip-alveolus and anterior palate):

Unilateral cleft lip (complete or incomplete) Bilateral cleft lip (complete or incomplete)

II-Clefts of the secondary palate (posterior hard palate):

Unilateral cleft palate (soft and/or hard)

Bilateral cleft palate (soft and/or hard)

III- Combined clefts of the primary and secondary palate

Clinical Presentation:

Cosmetic deformity (more common in cleft lip than cleft palate)

Nasal deformity

Defective suckling and regurgitation of milk

Nasality and speech problems

Facial skeleton deformities and teeth deformities

Ear troubles e.g. otitis media, and conductive deafness

Upper and lower respiratory tract infections

Management of Cleft Lip

Timing:

Best results are obtained when the treatment is completed as early aspossible.

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With isolated primary or secondary clefts, the treatment is done between

six weeks and six months.

With combined primary and secondary clefts, we usually start by the cleft

lip between six weeks and three months, and then palatal repair is done at

six months.

Alveolar repair can be done with the lip repair or at another stage.

Cleft lip/nasal deformity is corrected at the age of 3-5 years.

Orthodontic work to correct teeth deformities must start as early as

possible.

Secondary skeletal work for the facial skeleton is done after full growth

(between 13 -15 years)

Goals of lip repair: Cosmetic lip repair, where all the lip anatomical deficits are corrected.

Repair of the anterior palate, because it is difficult to be repaired during

palatal repair.

Functional repair of the orbicularis oris muscle to restore its functional andfacial expression components.

Repair of the alveolus in the same setting, if possible.

Commonly Used Surgical Techniques Le Mesurier technique (quadrangular flap technique)

Tennisons technique (triangular flap technique)

Millards technique (rotation advancement flap technique)

Le mesuriers technique. Tennisons technique Millards technique.

Management of Cleft Palate

Goals of repair:

Anatomical closure of the palate to restore the barrier between the oral and

nasal cavities.

Functional closure of the soft palate to restore the control of the Velo-

pharyngeal sphincter (valve that controls & separates the oropharynx

from the naso-pharynx).

Commonly Used Surgical Techniques

Wardill-Kilner V-Y push-back technique

Primary veloplasty.

Furlow technique.

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Primary pharyngeal flap.

Wardill-Kilner V-Y pushback technique

Chapter 4

Hypospadias:Hypospadias is an abnormality where the external urethral meatus opens on the

ventral surface of the penis.

Embryology The external genitalia are formed between the 4th 12th week intra-uterine life.

The differentiation between male and female starts at the 8th week.

Male external genitalia are formed from:

Genital tubercle (d)

Genital folds (fuse to form male urethra) (b)

Genital swellings (from scrotum) (a)

Urethral plate (c)

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Hypospadias results from failure of fusion of the genital folds. According to the point

of fusion arrest, the degree of hypospadias will be.

Types of Hypospadias:

Glanular

Coronal

Penile

(proximal, mid penile, distal penile)

Penoscrotal

Perineal

Clinical Picture:

Abnormal external urethral opening

Incomplete prepuce opened ventrally.

Ventral curvature of the penis (chordee)

Abnormal urinary stream

Downward direction Bifid stream

Narrow stream

Difficulty in micturition

Difficulty in sex differentiation

Management

Treatment of hypospadias is mainly surgical, even with the mild cases like

glandular or coronal hypospadias.

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The main reason is to prevent psychological trauma to the patient who feels that

his organ is abnormal.

Timing: Must be as early as possible.

Surgery must be completed before school age.

Stages of Repair

Straightening of the penis by excising the chordee.

Urinary diversion for a period of 10 15 days post-operatively, this

can be done using the following techniques:

Perineal urethrotomy.

Suprapubic cystostomy.

Transurethral diversion by stent or self retaining urinary catheter.

The third stage is urethral reconstruction.

Surgical Techniques

Meatal Advancement and Galanuloplasty (MAGPI) for glandular and

coronal hypospadias.

Meatal based flap technique (flip-flap) for distal penile hypospadias.

Transverse preputal flap technique for more severe degrees.

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Chapter 5

Epispadias and Extrophy.This is a condition where the external urethral opening is present on the dorsal surface

of the penis. This is sometimes associated with a defect in the anterior abdominal wall

and non closure of the urinary bladder and its sphincters.

Embryology Epispadias and extrophy occur at an earlier age than hypospadias.

The cause of this deformity is most probably related to the

development of the genital tubercle in a position distal to the urogenital sinus,

thus the urethra is cephalad to the penis.

The development of the penis in this position interferes with the

development of the urethra, bladder, symphysis pubis, and anterior abdominal

wall.

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Clinical Picture Urethral opening on the dorsum of the penis.

Glans penis is spade like.

The penis is short.

The symphysis pubis is opened. In most cases there is bladder extrophy.

In severe cases there is urinary incontinence of the bladder sphincters.

Management Epispadias alone is corrected by techniques similar to hypospadias with the

addition of:

Penile lengthening.

Transposition of the urethral opening to the ventral surface.

Correction of glandular deformity.

Severe cases with bladder extrophy need:

Osteotomy of the pelvis to close the symphysis pubis.

Closure of the bladder in layers.

Closure of the anterior abdominal wall.

Chapter 6

Hamartomas.A hamartoma is descriptive of histologic clustering of cells into nests that shareembryologic origin but in an ectopic location. Examples include:

1- Congenital vascular diseases

2- Neurofibromas

3- Pigmented skin lesions

4- Lung hamartomas

5- Bony hamartomas

1-Congenital Vascular Diseases Old Classifications: (Descriptive classification)

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Port-wine stain

Salmon pink patch

Cavernous haemangioma

Cersoid aneurysm

Classification based on cell origin:

Capillary malformations: Port-wine stain

Venous malformations: Cavernous haemangioma

Arterial malformations: AV fistulae, cersoid aneurysm

Lymphatic malformations:

Capillary lymphatic malformations: Linear nevu.

Cavernous lesions: Cavernous lymphangioma, cystic hygroma

Recent classification (based on endothelial cell characteristics):

Haemangiomas

Vascular malformations

Haemangiomas 70% of these lesions are present at birth and 30% appear within the 1st year of life.

They are vascular tumours with increased endothelial cells.

The lesion passes in three phases:

Proliferative phase: This lasts for a few months, and usually starts

as an erythematous patch that enlarges in the surrounding skin.

Stationary phase: This lasts for a few years and the lesion doesnt

increase in size.

Involution phase: this usually starts between 5 7 years, andeventually the lesion disappears completely.

TreatmentIn hidden areas and in deep lesions we can depend on spontaneous involution.

Indications for interference are:

Lesions in the field of vision.

Ulcerating lesions.

Rapidly growing lesions.

Therapeutic measures:

Corticosteroid injection: Systemic or intra-lesional.

Laser surgery: Intra-lesional Nd- YAG laser.

Surgical excision.

Complications of Haemangiomas

Haemangiomas in the nose can cause squint if not treated early.

Ulceration is a common complication which can lead to involution of the

lesion and is not associated with bleeding.

Infection; and this also lead to fibrosis and involution of the lesion.

Vascular Malformations

Vascular malformations by definition are always present at birth. There is no

evidence that they grow by cellular hyperplasia to invade surrounding tissues. The

do not involute and the do not disappear spontaneously.

Classification

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Low flow malformations:

Capillary vascular malformations (port-wine stain).

Lymphatic malformations.

Venous malformations.

High flow malformations:

Arterial malformations.

AV malformations.

Investigations:

Arteriography: indicated in most cases to define the nature of the lesion, its

feeding arteries and its draining veins.

CT scan: to define the lesion and to show the relation to surrounding

structures.

Selective and super-selective angiography: this is not a routine investigation.

Treatment:

Laser: they can be completely cured by pulsed dye or Nd YAG lasers. Surgery: most definite therapeutic line.

Embolization: this is done as a preoperative procedure to minimizebleeding during the surgery.

Conservative management: until now some vascular malformations

still have no definite treatment.

2-Neurofibroma A neurofibroma is a hamartoma of the nervous system. There is tumour like

masses from the nerve sheaths, either the neurelemmal sheath or Schwan cells

Clinical types:

Solitary neurofibroma.

Generalized neurofibromatosis (Von ricleng Hausens disease).

Diffuse neurofibromatosis.

Localised gigantism.

Oribito-temporal type.

Elephantiasisneurofibromatosis.

Neuro-fibro sarcoma.

Treatment:

Surgery is the treatment of choice for neurofibromatosis but with the

following considerations:

Usually there is recurrence after excision before the age of puberty, but

this doesnt prevent debulking of the lesion.

In the orbito-temporal type, treatment should be started very early

because the lesion can cause blindness.

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Patients with generalized neurofibromatosis might have cerbelo-

pontine angle tumor, acoustic neuroma, or intra-thecal tumor. Thus these

patients need to be followed closely by neurosurgeons.

3-Pigmented Skin Lesions:Tumours of the melanocyte system are present in two distinct forms:

Naevus cell tumours:

Small nevi: they are less than 1.5 cm in diameter

Medium sized: lesions between 1.5 and 20 cm

Large or giant nevi: lesions larger than 20 cm

Melanocytic tumours

Naevus Cell Tumors:o Tumors arising from the naevus cells are called naevi.

o Naevi are the most common tumors in humans. At birth2.5% of children have pigmented skin lesions.

o Naevi in younger in patients are junctional, and most of

them turn intradermal by adulthood.

o There are three varieties of naevi:

Junctional.

Dermal

Compound.

Malignant Transformation in Naevi: There is controversy about malignant transformation in congenital naevi.

However there is no doubt that giant hairy naevi carry high possibility ofmalignant transformation.

Malignant transformation is suspected by:

Spontaneous ulceration and bleeding.

Enlargement of the lesion.

Darkening of the lesion.

Pigmented satellite lesion.

Inflammation without trauma.

Pain and itching.

Lymph node swelling in the drainage area.

Treatment Majority of lesions require no treatment.

Surgery is indicated in suspicious lesions, or if the patient asks to

have it removed for cosmetic causes.

Giant hairy naevi must be excised as soon as possible.

Melanocyte Tumors Lesions with increased activity:

Freckles. Lesions with increased number of melanocytes:

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Lentigo simplex.

Lentigo maligna.

Lesions with dermal melanocytes:

Mongolian spot.

Naevus of Ito.

Naevus of Ota.

Blue naevus.

Cellular blue naevus.

N.B. Precancerous Pigmented Skin Lesions:

Solar or actinic keratosis.

o Xeroderma pigmentosum.

Treatment

Medical treatment:

Quinolones have proved effective in management of most of these

lesions.

Laser (Q-switched).

Surgical excision.

Chapter7

LymphedemaThis is a condition where excess protein and extracellular fluid accumulate in the

interstitial subcutaneous space. It can occur due to:

i- Increased lymph production e.g. in congestive heart failure.

ii- Decreased absorption due to lymphatic obstruction.

iii- Lymhpedema affects mainly the extremities and to a lesser extent the

genitalia.

Physiology: Lymph drainage is controlled against gravity by:

Skeletal muscle contraction.

Adjacent arterial pulsations.

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Intra-abdominal and intra-thoracic pressure fluctuations.

Intrinsic contraction of larger lymphatic.

Anatomy : In the lower extremity there are two sets of lymphatics:

The superficial lymphatics which accompany the long and shortsaphenous venous systems. They drain in to the superficial inguinal lymph

nodes.

The deep lymphatics which are found around the bones. They draininto the deep inguinal lymph nodes.

There is no connection between the superficial and deep systems in the lower

limb.

Etiology:

1ry Lymphedema

Lymphedema congenital.

Lymphedema precox. Lymphedema tarda.

Meiges disease.

2ry Lymphedema

Inflammatory: acute non specific inflammation, parasitic.

Traumatic: surgical, direct trauma, irradiation, or malignancy.

Diagnosis

1. Non-invasive studies:

Limb measurements.

Isotopes of gold (Au 198). Blood film for micro-filaria.

Immune studies for filaria.

2. Invasive studies:

Lymphangiography.

Lymphocintography.

Treatment:

o Medical treatment for acute lymphedema and early stages of congenital

lymphedema.

Rest in bed with foot elevation.

Antibiotics in case of infection.

Antifilarial treatment.

Diuretics.

Elastic bandage.

o Surgical treatment:

Physiological operations to attempt to reconstruct lymphatic

drainage by microvascular techniques, local flaps, or distant

pedicled tissues.

Excisional operations which remove various amounts of

lymphedematous subcutaneous tissue and skin.

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Chapter8

CongenitalHandAnomalies:The incidence of congenital hand anomalies is 1.14 per 1000 live births, 5% have

other syndromes.

Etiology

i- Genetic/hereditary.

ii- Environmental.

iii- Sporadic.

Classification of Congenital Hand Anomalies Arrest of development

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Transverse deficiencies e.g. amputation.

Longitudinal deficiencies e.g. phocomelia, club hand, cleft hand.

Failure of differentiation

Syndactyly.

Synostosis.

Duplication

Thumb polydactyly.

Finger polydactyly.

Mirror hand.

Over growth.

Under growth.

Congenital constriction ring.

N.B. Commonest anomalies

- Syndactyly - Polydactyly

- Camptodactyly - Clinodactyly

- Radial club hand - Amputation.

Goals of Treatment

To produce a functional limb

Powerful grip.

Adequate sensation.

Improve hand abilities in space.

To improve the cosmetic shape of the hand.

Timing of Surgery If growth is increasing the deficiency: at 1 year of age.

If developmental pattern necessitates: at 2 years of age.

If patient cooperation is necessary: at 4 5 years of age.

Treatment:

o Conservative

Physiotherapy

Prosthetics

o Surgery e.g.

Syndactyly: division and closure by Z flaps and/or skin grafts.

Radial club hand: centralization of the radius and lengthening ofthe radius.

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Constriction ring: Z-plasty for the distal deformity.

Chapter 9

Hand Trauma Examination

General: evaluate the patient to identify any associated trauma

elsewhere in the body e.g. concussion.

Local:

Circulation.

Bones and joints.

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Tendons.

Nerves.

Wound (clean/infected).

Finger Tip Injuries

Most common hand injuries.

May lead to significant disability.

Goals of Treatment:

Adequate sensation.

Minimal tenderness.

Maximum length.

Satisfactory appearance.

Full joint motion.

Methods of Treatment:

Healing by secondary intention.

Composite graft.

Skin grafts (split or full thickness).

Bone shortening and direct closure.

V Y advancement flaps.

Regional flaps e.g. cross finger flaps, thenar flaps.

Distant flaps.

Flexor Tendon Injuries:

Examination

Start by a brief history from the patient

Time of injury.

Mechanism of trauma.

Observe the posture of the digits.

Check the function to evaluate which tendon is injured

Repair Options Primary repair (within the 1st 24 hours).

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Delayed primary repair.

Secondary repair.

Tendon graft.

Principles of Tendon Repair

Zig zag skin incisions. Atraumatic handling of the tendon with magnification.

Preserve annular pulleys.

Gentle tendon retrieval.

Use of strong non absorbable suture material e.g. prolene.

Fractures of Metacarpals and Phalanges

Commonly occurring fractures.

They can cause stiffness and deformities if neglected.

Treatment: Reduction.

Open.

Closed.

Fixation.

Internal fixation using:

K Wires.

Interosseous wire.

Intermedullary fixation.

Interfragmentary compression screw.

Plate and screw fixation. External fixation in unstable fractures with/without bone loss.

Immobilization.

Chapter 10

Malignant Skin Tumors Etiology:

Exposure to UV radiation

Exposure to chemical carcinogens e.g. tar, arsenic. Exposure to viral carcinogens e.g. Human papilloma virus.

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Chronic inflammation.

Exposure to radiation therapy.

Premalignant Lesions

Keratoacanthoma: fleshy, elevated, central hyperkeratosis, rapid growth and

involution. Actinic keratosis: most common, sun exposed areas, multiple, well

circumscribed.

Bowens disease: more common in elderly men, solitary, erythematous, scaly

plaque.

Xeroderma pigmentosa: extreme sensitivity to sun light, progressive drynessof the skin, and malignant changes to BCC and SCC.

Leukoplakia: chronic inflammation of oral mucosa, it usually occurs in oldermen, who are smokers.

1-Basal Cell Carcinoma (BCC):

The most common type of malignant skin tumors. It is a locally malignant disease.

The cell of origin is the prickle cell layer of the skin.

Incidence

More in males than females.

90% occurs in exposed sites.

85% in head and neck.

More common in fair skinned patients.

More in those with outdoor occupations.

Clinical types

i- Nodulo-ulcerative BCC

o Most common type.

o Mostly in head and neck.

o Smooth, raised, waxy.

o Thin epithelium and pearly edges.

o Slowly growing.

ii- Pigmented BCC

o Can be confused with malignant melanoma.

o Extremely slow in progression.

iii- Sclerosing BCCo Waxy, flat and indurated.

o Shiny smooth surface.

o Telangiactasis is present.

iv- Cicatricial BCC

o Cicatricial surface with nests of active lesions.

o No tendency to infiltrate.

v- Cystic BCC

o A variant of the nodulo-ulcertive type.

o Pale, pearly pink to blue grey in colour.

vi- Infiltrating BCCo Commonly seen in recurrent cases.

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vii- Aggressive in nature.

viii- Ulcerated BCC

o Any of the previous types can be ulcerated.

o Ulcer is painless, none irritating, fails to heal.

o Edges are beaded, raised, rolled in.

Histopathological Types

a) Differentiated: shows slight degree of differentiation towards the

cutaneous appendages.

b) Undifferentiated: solid BCC.c) Basi-squamous: (squamous cell carcinoma contagious to BCC).

Metastatic potential of BCC

It has marked tendency to invade locally.

Three dimensional spread.

It doesnt usually metastasize.

Treatment

Excision with an adequate safety margin.

Closure of the defect by:

o Direct closure.

o Skin graft.

o Local or distant skin flaps.

Other treatment modalities:

o 5-Fluorouracil (5-FU).

o Cryotherapy:

o

Radiotherapy.

2-Squamous Cell Carcinoma

The second most common type of skin cancer. It originates from the Malpigian

cell layer of the epithelium. Occurs in older patients and in males more than

females.

Clinical types

i- Non invasive

o Slowly growing.

o Verrucous in nature.

o Exophytic.

o Less like to metastasize.

ii- Highly invasive

o More nodular.

o Indurated.

o Greater tendency to metastasize.

Potential to Metastasize

Local metastasis. >> Blood. >> Lymphatic.

Treatment

Primary without lymph node enlargement:

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o Excision with safety margin and follow up.

Primary with lymph node enlargement:

o Surgical excision with safety margin.

o Block lymph node dissection.

o Radiotherapy.

3-Malignant Melanoma (MM):

i- Benign Pigmented Lesions:

ii- Intradermal naevus.

iii- Junctional naevus.

iv- Compound naevus.

v- Freckles.

vi- Hutchinson freckles.

Phases of Tumour Development

Radial growth phaseo Proliferation of neoplastic melanocytes within the epidermis.

o Single cell invasion of papillary dermis.

Vertical growth phase

o Proliferation of neoplastic melanocytes to invade the papillary dermis and

to invade the reticular dermis.

Classification

Clarks classification

I. Melanocytic hyperplasia.

Papillary dermis. Junction of reticular dermis.

Reticular dermis.

II. Subcutaneous tissue.

Breslows classification

More than 1.7 mm: very high incidence of metastasis.

From 0.7 1.5 mm: lesser incidence of metastasis.

Less than 0.7 mm: very low incidence of metastasis.

Types of Malignant Melanoma:

Lentigo MM

o Occurs in sun exposed areas.

o More common in old females than males.

o Non invasive type: tan brown, irregular border.

o Invasive type: dark brown, raised.

Superficial spreading MM

o 50 70%

o No sex predilection.

o No site predilection.

o In females: back and legs.

o In males: mainly in the trunk.

Nodular MM

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o 10 20%

o Affects any age group.

o Common in trunk, head, and neck.

o Very aggressive.

o Vertical growth without radial growth phase.

Acral lentigo

o 2 8%.

o More than 60 years of age.

o Dark skinned patients.

o Affects palms and soles.

Subangual.

Treatment

Stage I and IA

o Wide excision: periphery 5 cm..

o

Closure with skin graft.Stage II and IIB

o Surgical excision

o Regional lymph node dissection

o Adjuvant therapy: chemotherapy or immunotherapy

Stage III

o Primary excision

o Lymph node dissection

o Adjuvant therapy

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Chapter 11

Management of Facial Injuries

In the initial management of facial injuries the surgical priorities have to be taken in toconsideration. So the management passes in the following sequence:

1. Maintenance of the air way

2. Control of hemorrhage

3. Control of shock

4. Checking for cervical spine injury

5. anagement of abdominal or thoracic associated injuries

6. Lastly, the management of facial injuries

Clinical Examination Palpation

o Bimanual

o Tenderness

o Crepitus

o Dental occlusion

Diplopia.

Depressed zygoma

Asymmetry

CSF rhinorrhea

o Occur in high maxillary fractures, naso-ethmoidal fractures.

o Occur as a result of dural lacerations.

Soft tissue lacerations

o Facial nerve.

o Salivary gland duct.

o Lacrimal canaliculi.

o Canthal ligament.

Radiographic Examination Plain X ray

o Waters view.

o Submento-vertical view (base view).

Panorama.

CT facial boneso Axial cuts.

o Coronal cuts

1-Fracture Zygoma

Diplopia

Enophthalmos

Ocular dystopia.

Numbness and anaesthesia

Restriction of mouth opening Peri-orbital ecchymosis

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Subconjuctival haemorrhage

Depressed cheek

Palpable stepping

Epistaxis (unilateral/bilateral)

2- Fracture Maxilla

Eye ecchymosis

Facial oedema

Elongated mid face

Retruded mid face

Mobility of the maxilla

Malocclusion.

Types of Maxillary Fractures

Le Forte I fracture

Le Forte II fracture

Le forte III fracture

3-Fractures of the Orbit

Periorbital ecchymosis

Subconjuctival haemorrhage

Hypothesia and numbness

Diplopia Dystopia

4-Fractures of the mandible

Swelling of the lower face

Pain and tenderness over the mandible

Malocclusion of teeth

Inability to open the mouth and to chew

Movement of the fractured segments

Types of mandibular fractures:

Parasymphyseal fractures.

Mandibular body fractures.

Mandibular angle fractures.

Subcondylar fractures.

Condylar fractures.

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Management of Facial Fractures: Reduction and fixation

Within 2 weeks in adults

Within 5 7 days in children.

Surgical exposure

Through traumatic lacerated wounds.

Subciliary incision (for zygomatic fractures).

Gingival-buccal sulcus incision (for maxillary and mandibular fractures).

Coronal incision (for frnto-orbital and pan-facial fractures).

Fixation

o Plates and screws.

o Interosseous wires.

Bone defects can be managed by:

o Salvaged bone fragments.o Bone grafts.

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Chapter 12

Tumours of the Jaws and Oral Cavity

Intra-oral tumours

Benign

o Hemangioma.

o Lymphangioma.

o Papiloma.

Premalignant

o Leukoplakia.

o Xero derma pigmentosa.

o Behsets disease.

Malignanto SCC of lips, tongue, palate, and gums.

Malignant salivary gland tumours.

o Melanoma.

o Lymphoma.

Swellings of the Jaws

Dental origin

o Inflammatory: dental cyst, dentigerous cyst

Neoplastic: amyloblastoma, odontomes. Bony swellings

o Congenital: congenital bone cyst.

Trauma: traumatic bone cysts.

o Reactive: giant cell reparative granuloma.

o Neoplasms: fibroma, osteoma, chondroma, haemangioma, osteoclastoma,

chondrosarcoma.

Common Clinical Picture of Jaw Swellings

Toothache.

Loose teeth. Hard swelling on the bone.

Ulceration of the mucous membrane.

Loss of sensation in the lower lip.

Diagnosis:

Radiological :

o Plain X ray.

o Panorama.

o CT scan and MRI.

Angiography. Fine needle aspiration and cytology

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Biopsy

o Incisional.

o Excisional.

Dental Cyst:

Decayed tooth

There is chronic inflammation and granulation tissue with exudation.

Diagnosed by X ray showing radiolucent area.

Treatment

o Tooth extraction

o Curettage of the cyst.

Dentigerous Cyst

Cyst formed around a missing 3rd molar.

Cystic enlargement with bone expansion and thinning.

Diagnosed by X ray showing radiolucent area and the crown of the molar.

Amyloblastoma

Originates from the remnants of the dental epithelium.

Occurs between 20 40 years of age.

Affects the mandible more than the maxilla.

There is soft tissue growth inside the bone causing bone expansion and pressureon the roots of the teeth, which eventually fall.

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Locally invasive lesion.

Treatment

o Excision with safety margin.

o Reconstruction of the defect by bone graft.

Giant Cell Lesions

These lesions have the same clinical picture as amyloblastoma and are

differentiated only by biopsy.

Treatment

o Excision.o Mandibular reconstruction.

Osteogenic Sarcoma

Affects ages 20 30.

Bone swelling and bone destruction.

Loose teeth and intra-oral mucosal ulceration.

X Ray shows bone destruction or new bone formation Sun ray appearance.

Biopsy is diagnostic.

Treatment

o Pre-operative radiotherapyo Wide excision.

Squamous Cell Carcinoma

Ulcerated lesion with indurated edges.

Can be exophytic or endophytic.

Lymphatic spread.

Cancer Tongue

Most common intra-oral tumor

Usually affects the anterior 2/3 on the lateral border or ventral surface.

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Presented as a painless swelling or ulcer

Later on there is induration and fixation of the tongue to the mandible.

30% of cases are associated with lymph node at first presentation.

Treatment

o T1 lesion: excision or irradiation.

o T2 lesion: partial glossectomy with/without excision of part of the

mandible, and neck dissection or irradiation.

o T4 lesion: excision and post operative irradiation with chemotherapy.

Cancer of the Floor of the Mouth:

The second most common site for intra-oral tumours.

Associated with alcohol and smoking.

Affects the anterior and midline parts of the floor of the mouth.

Clinically presented by

o Lymph node enlargement.

o Infiltration of the tongue.

o Submandibular gland swelling.

Treatment

o Excision of the lesion with safety margin and/or irradiation.

o Excision of a part of the mandible in large lesions.

Documents

Plastic Surgery for Undergraduates