Introduction,ulcers And Wounds

Question 1

What is surgery
What is it’s history
State the main surgical specialties

Answer 1

Surgery; Hand work.
•A branch of medicine where treatment of injuries, or disorders of the body is by incisions or manipulation with instrumments.
•History of surgery; started in the stone age where holes were cut in the skulls of patients to drain blood.
•EgyptgreeksRomans. Barbers.
•Modern surgery became possible with the discovery of anaesthesia, the germ theory and blood transfusion in the 19th century.
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Surgical specialties
•12 main specialties in surgery.
•General, pediatric, gynaecology and obstetrics, urology, orthopaedic, plastic, cardiothoracic, neurological , otorhinolaryngology, ophthalmic, oral and maxillofacial, anaesthesia.

Question 2

What do the main type of surgical specialties involve(specifically general surgery and trauma and orthopedics)(their scope)
Give four main operations in trauma and orthopedics

Answer 2

GENERAL SURGERY.
•The foundation(mother) of all surgeries. All specialties are break away from the general surgery.
•Scope: endocrine organs: thyroid gland, breast, adrenal gland
•Hepatobiliary; esophagus, stomach, liver, gallbladder, pancreas.
•Colorectal: small bowel, large bowel, rectum.
Vascular: peripheral artery disease, DVT, vascular surgeries.
•Laparoscopic surgery: appendix, gallbladder, hernia, upper GI and lower GI endoscopies,diagnostic laparoscopy.
•Others: cutanous lesions, lumps, bumps.

Trauma and Orthopaedic
•Specialty that deals with bones, joints and their associated soft tissues ie ligaments, nerves and muscles.
•Scope; upper and lower limb fractures. Joint reconstruction, spine surgeries, bone tumors, paediatric orthopaedics, sports and exercise surgery.

MAIN OPERATIONS
•Some main operations;
•Joint arthroscopy- a minimally invasive technique which involves inserting probes into the joints to diagnose and repair damaged joint tissue.
•Fracture repair- with pins and plates, immobilization with external fixators.
•Arthrosplasty- replacement of whole joints, esp Hip and knee replacement.
•General repair procedures on damaged muscle or tendon.
•Corrective surgery; procedures aimed at correcting problems of anatomical alignment.

Question 3

What does urology deal with
What are the common pathologies in urology
What are the common procedures in urology
What is plastics as a surgical specialty and what are its sub specialties
What are the sub specialties in neurosurgery

Answer 3

UROLOGY
•Deals with the urogenital system. Kidney,bladder, urinary problems, men’s sexual and reproductive health.
•Common pathology: renal failure, urinary tract stones, prostate and bladder cancer, incontinence, erectile dysfunction.
•Subspecialties; complex pelvic surgery, uro-gynaeclogy, andrology, paediatric urology.

Common Procedures.
•Circumcision
•Vasectomy.
•Hydrocelectomy.
•Removal of prostate, kidney or bladder for cancer.
•Removal of kidney for stone or infection.
•Diversion of urine into a stoma( ileal conduit)
•Reconstruction of bladder, urethra( urethroplasty)

Plastics
•Involves the restoration of normal form and function. 80% of all plastic surgery is reconstructive.
•Scope: hand trauma, burns and scalds, soft tissue injuries involving face, trunk or limbs. Reconstuctive surgery for congenital and acquired abnormalities, breast reconstruction etc.

Subspecialties.
•Congenital; treatment of conditions like cleft lip and palate, facial and ear deformities, craniofacial defects, hypospadias, upper limb anomalies, congenital skin conditions.
•Breast surgery; reconstruction following cancer, congenital anomalies, cosmetic.
•Trauma; reconstructive repair of facial truama, burn injury etc.
•Cancer; reconstruction after extensive cancer surgery.

NEUROSURGERY.
•Involves the brain, central nervous system and spinal cord.
•Subspecialties; paediatric, neuro-oncology, functional neurosurgery, neuro-vascular surgery, traumatology, skull-base surgery and spinal surgery

Question 4

Explain cardiothoracic and paediatric specialties in surgery
What are the common surgeries in cardio and what are the sub specialties in paediatric surgery

Answer 4

CARDIOTHORACIC
•This deals with disease of the heart, lungs, oesophagus and chest.
•Common surgeries; coronary artery bypass, grafting, valve operation, lobectomy, pnrumonectomy, heart transplant etc.

PAEDIATRIC
•The surgical treatment of diseases, trauma and malformations of childhood years( foetal-teenage years.)
•Subspecialties;
•Neonatal surgery,; gastroschisis, diaphragmatic hernia.
•Paediatric oncology; leukemia etc
•Paediatric urology;

Question 5

What is the importance of radiology in surgery and when was X ray discovered
What is the use of ultrasound,CT scan,
What is MRI
Give two uses of MRI
Explain radiotherapy
What is the future of surgery

Answer 5

IMPORTANCE OF RADIOLOGY IN SURGERY.
•The discovery of x-ray by German Wilhelm Conrad Rontgen in 1895 unfolded a vast new world in investigative medicine and surgery which has aided precision in diagnosis.

•Initially used in the diagnosis of fractures and location of foreign bodies in tissues, it is now useful in all the systems of the body.

OTHER IMAGES
•Ultrasound; excellent is assessing fluid containing tissues and soft tissues.

•Computerized tomography(CT) scan. Uses computer to reconstruct mathematically a cross-sectional image of the body. It gives a detailed images of deep seated tissues and tumors.

MAGNETIC RESONANCE IMAGING(MRI)
•MR is a technique that produces tomographic images by means of magnetic fields and radio waves. It gives better results in soft tissues.

•ENDOSCOPY; Has transducers which are passed into hollow viscus. Eg oesophagus, stomach, bladder, uterus.
•Laparoscopic surgery;

RADIOTHERAPY
•Radiotherapy is the clinical discipline involving the treatment of disease with x-rays and other radioactive substances which emit gamma and beta radiation.

•Radiotherapy is key in the treatment of cancers.

FUTURE OF SURGERY.
•MINIMALLY INVASIVE PROCEDURES

•ROBOTICS; The use of Robots in surgery.

Question 6

State the causes of wounds
Types of wounds
What happens in a contusion
What is a wound,ulcer,fracture
What’s the difference between a wound and an injury
In ulcer there is a demarcation between the normal tissue and abnormal true or false?
Vascular ulcers tend to bleed a lot true or false
Examination of the ulcer will help you know if it’s acute or chronic
Every ulcer has a peculiar edge and the floor shows if the ulcer is acute or chronic and the floor of the ulcer is the innermost part of the wound
True ir false

Withthe exception of surgical wounds, all open wounds mustberegardedas contaminated.Suchwoundsdo notbecome infecteduntil after the space of a few hours when bacterial invasionwouldhaveoccurredandtheinflammatory responses initiated.Thelikelihood of infection therefore increases with theperiodof exposure of an open wound.
True or false

Answer 6

CAUSES OF WOUNDS.
•Mechanical agents. Eg RTA, home accidents, assault, occupational accidents. ofassault.Thetvoundssoproducedareofvarious types but generally they are either closed, when they are described as contusions, or open when the term lacerations is use

•Chemical Agents. Egs strong Acids, Alkalis,corrosive chemicals

Epithelial tissuestaketbe brunt ofthis, forexamplethecutaneous wounds
fromacid burns, skin necrosis accompanying snake or insect biles; the oesophageal stricture that follows swallowing of caustics is another example of such tissue injury.

•Radiant Energy, egs X-rays,radium,high voltage electricity,heat and intense cold

• produces extensive wounds
  notable for the degree of tissue necrosis entailed; healing is Lacerated Wound is produced. These wounds may be necessarily delayed in these wounds

•heat,; hot water, hot soup etc.

TYPES OF WOUNDS.
•Contusion; bruise results from injury of tissues subjacent to the surface epithelia. Usually caused by blunt trauma. There is disruption of the connective tissue with extravasatiouof blood, hence the bruise or ecchymosis. The epithelium, if it remains intact, protects the damaged tissue from microbial insult. If this is successful then resolution, thoughoften slow, can beexpected
•Open wounds; mere loss of the superficial layers of the epithelium.
•Subtypes of open wounds:
Abrasion: Mere loss of the superficial layers of the epithelium is the simplest f orm of open wound. This is called an Abrasion. Secondary bacterial invasion is the problem in all open wounds;

puncture wound: he open wound may be much deeper and penetratethe full thickness of the skin. If the wound of entry is small as occurs when the causative agent is a pointed instrument, a nail or narrow bladed knife, a Puncture Wound results
lacerations:when the wound of entry is relatively wider as compared to that of a puncture wound it is a laceration. These wounds may be produced by sharp knives or blunt force.
Penetrating or perforating wounds:
In the former, the wounds enter a body cavity such as the chest or alxlomen;inthelatter, theyentirelypassthrough anorganor ravityandarecharacteristic offirearm missileinjuries.

avulsion: Occasionallyportionsof the bodymaybetomorwrenched away.These Avulsion wounds, usually irregular withjagged edges.occuronthescalpandtheextremities.Theavulsioa may reComplete where there is no connectionbetween the injured mil its original site or Partial where tenuous and strained 1trands of tissue connect the tissue to the site. Other subtypes crushed , degloving.

Wounds refer to tissue injury from various agents or any trauma to the tissue
•Ulcer is the loss of continuity of epithelial tissue,break in the continuity of a tissue
•Fracture is loss of continuity of bone tissue.

necrosis). Is there a difference between the terms “wounds: and “injuries”? The difference is marginal.: while Injury implies a wider range of damage from the most trivial 10 the severest involving deeper tissues and body cavities, wound refers 10 lighter and more superficial tissuedefeci.

Question 7

State the classification of ulcers
Give examples under each class
State the subtypes under non specific ulcers
Know how the class of ulcers look like

Answer 7

CLASSIFICATION OF ULCERS.
• Ulcers are classified in connection to a pathogen.
•Specific ulcers.:specific ulcers are caused by specific organisms or those organisms are known

Specific ulcers:
I. Tuberculous ulcers.
2. Buruli ulcers.
3. Syphilitic ulcers.
4. Yaws Trepomema pertenueulcers.
5. Mycobacterium Leprae ulcers

•Non-specific ulcers.:not caused by specific organisms but caused by other things such as trauma

Non-specific ulcers:
1. Traumatic ulcers.
2. Pyogenic ulcers.
3. Ulcers of vascular origin:
(i) Venous (gravitational) ulcers.
(ii) Arterial ulcers. (iii) Decubitusulcers. (iv) Pressuresores.
4. Neurotropic (trophic) ulcers(Ulceration is caused by unrecognized and oft-repeated traumato.orprolongedpressure on,ananaestheticskin. The lossofpainandothersensationistheresultofdiseaseorinjury ofperipheralnerves or spinal cord. Commoncausesareleprous neuropathy,diabeticneuropathy. syringomyeliaand peripheral nerve injury. Others are spinal cord lesions due to trauma, tabes dorsalis. tumours and congenital disease such as spina bifidaandVil B12 deficiency)
(i) Leprosy.
(ii) Diabetic neuropathy. (iii) Cord lesions.
(iv) Peripheral neuropathies. (v) Syringomyelia.
5. Ulcers associated with metabolic or systemicdisease:
(i) Diabetic ulcers.
(ii) Haernoglobinopathic ulcers.
(iii) Ulcersofspherocytosis.
(iv) Ulcers of ulcerative colitis.

•Neoplastic ulcers.

Neoplastic ulcers:
l. Squamous cell carcinoma.
2. Rodent ulcer.

Malignant melanoma. Kaposi’s sarcoma. Penetrating malignant tumour.

Question 8

State and define the characteristics of an ulcer
What kind of edges are seen jn each class of ulcers?

Examine an ulcer like a lump.
True or false
What is the floor of an ulcer used to determine?

Answer 8

Characteristics of an ulcer
An ulcer has the following features:
Edge: It is where the healthy skin (epithelium) begins. Structurally this is the margin of the ulcer in profile or cross section. The edge of the ulcer. where the ulcer ends.
That is,is sloping in a non-specific ulcer, undermined(ulcer goes under the normal skin) in a tuberculous ulcer, raised or above the skin (it is raised because of rapid proliferation of malignant cells causing it to be so big that it is raised) in a malignant ulcer and punched out inasyphilitic ulcer (Fig 6-1).
Floor:Itiswhatisseen.Itmaybesloughing withaprofuse, offensive, yellowish discharge, or consist of pinkish red granulation with a thin serous discharge suggestive of healing. Itmaybenodular suggestive of malignancy.
The floor is used to determine the stage/phase of healing of the ulcer.

Base: It is what is palpated. It may be indurated or hard (malignantorlongstanding callous ulcer). It may be darkened, oedematous or tender.

Clinically ulcers fall into 3 broad groups:
I. Specific ulcers: They are caused by specific organisms e.g. mycobacterium ulcerans bacilli, treponema pallidum or pertenue. The edge is characteristic for each tYJ><:.
2. Non-specific ulcers: They have essentially the same feature of a sloping edge, but the underlying aetiologies are varied. They are the commonest ulcers.
3. Malignant ulcers: They are neoplastic inorigin. Some- rimesachroniculcercan become neoplastic eg. chronic buruli ulcer, chronic burns wound. Such an ulcer is called Marjolin’ s ulcer. The edge is raised, the floor may be nodular and the base indurated.

Question 9

Explain the phases non specific ulcers go through

Answer 9

The ulcer goes through the following phases.
l. Acute or infective phase: In this the initial phase, the ulcer is painful and the histology is similar to that of an abscess. The sloughing floor is covered with purulent discharge inwhichdifferent typesof bacteria maybe identified. Theedge issharp andsurrounded bydamagedcells.Thesurrounding skin is oedematous, warm and tender.
2. Transition phase: The slough separates, the pus drains, infection subsides, granulation tissue grows and the floor becomes clean and pinkish-red. The edge, which is
sloping, has a thin bluish-white layer of young epithelium growing inwards. Thesurroundingskin lssttgbtlyhyperaemic or normal.
3. Reparatlve or healing phase: The ulcer is now painless. The healthy granulation tissue fills the floor and the epithelium grows fromtheedgeat the rateof Imm/day tocover the floor.
4. Chronic, indolent or callous phase: Some ulcers may enter a chronic phase a nd remain unhealthy for a long time because of secondary infection, defective circulation, poor general condition, lack of rest, presence of foreign bodies or malignantchange.The edgesarethenragged, thefloor greyish or creamy pink and bathed with profuse offensive, yellow dischargeandthesurroundingskinwarmandoedematous. Ina long-standing ulcer -indolent or callous ulcer - fibrosis or the floor causes induration of the base, the floor has unhealthy greyish fibrotic granulation, the borders are rigid and hard and the epitl1elium of the edge does not grow inwards. The surrounding skin may be atrophic and hyper-pigmented. The ulcer rarely heals and when it does, the scar is unstable and minimal trauma causes further breakdown

Question 10

How are lumps examined?
What is a gangrene?
What is Doppler scan used to sche j for concerning blood vessels and why

A wound brought to the hospital after eight hours is considered contaminated or a dirty wound true or false
Do biopsy if a wound is suspected to be chronic true or false
FBS is diagnostic of diabetes true or false

Answer 10

OBSERVATION: site, size, shape.

•PALPATION: differential warmth, tenderness. Surface, consistency(soft or firm)edge

•PERCUSSION; Mobility, attachment to skin, muscles, associated lymph nodes/blood vessels.

•AUSCULTATION: vascular swellings.(know the big common vessels in the body especially the foot to see if the vessels are proper or not. Use anatomic terms to describe the position of the ulcer)
Doppler scan can check the condition of blood vessels which help in ulcer healing cuz if the vessel is damaged,blood flow will be poor thus slowing wound healing

Question 11

Explain how ulcers are graded and staged
What is a wound contraction

Answer 11

This looks at the pathological progress of an ulcer.
•Wagner classification of ulcer.
•1) stage 1-superficial ulcer; epithelial tissue
•2) stage 2-subcutanous tissue: vessels, nerves.
For stage 1 and 2,wound dressing will be enough
•3) stage 3-muscles, tendons, bones.
•4) stage 4-limited gangrene.
•5) stage 5-massive gangrene

For three and four,surgery or debridement is required
For stage five the affected part of the limb is likely to be cut off

WOU~ CONTRACTION
Thelossof skinina woundisapermanentdefectmadegood onlythroughstretchingofthesurroundingskintocover the exposed subcutaneoustissue. T his phenomenoncalled wound contraction,shouldbe distinguishedfrom contracture which implies some deformityof scar from shrinkage of excessive fibrosis.

Question 12

What is wound healing
What is regeneration
What is resolution
When there is significant tissue destruction how does the body heal?
What is described as the hallmark of wound repair?
When there is tissue loss,how does the body heal?
What processes affect wound healing

Answer 12

WOUND HEALING
In its broadest sense, this implies the replacement of damaged tissue by living tissue which in man is essentially fibrous rissue.

rissue. In the lower ordersof animals, replacementof lost tissues is more completeand the newtissue is morphologi- cally and histologically similar to the destroyed entity. This phenomenon is referred to as Regeneration; if the tissue so restored is indistinguishable from the original then regeneration is perfect and this happens in lesser animals such as earthworms

Wherethetissuedamage is minimal, recoveryoccursand the end result is essentially the same type of tissue as the original; no new tissue is formed in the process. This is Resolution, and isexemplified by the natural history ofa blind boil or lobar pneumonia. A blind boil starts and rapidly rises toaheadburthenecrorising agentsaresoonneutralizedandthe skin returns to normal. Similarly in lobar pneumonia, exudate fillsthealveolibutthere isnodestructionofthealveolarwall. Theexudate isremovedbycoughingupor byabsorptionthrough lymphatics and blood vessel

Where thereissignificanttissue destruction,thecompound structuresofthehumanbodycanonlyhealthroughthesealing ofthewoundby(1) epltheliallzatton and (2) thesynthesisor fibroustissue by the organizationofstimulated granulation tissue. Fibrous tissuemaywellbedescrihedasthehallmarkof woundrepairand isresponsibleforstructuralstrength.When there is tissue loss, an additional process· (3) wound contr ac- tion - ensures the inward movement of viable tissue margins into closer approximation

ever thetypeofwound,theprocessofhealingandthe factors affectingthe process are basically the same and depend
on:
I. Adequateenergyforcellproliferationandmovementand
also for protein synthesis.
2. Adequate proteins amino acids and peptides for the
synthesis of proteins requiredand
3. Adequate stimuli (growth factors) and hormones to
complete the process.

Question 13

What are the stages of wound healing
Explain Em

Techniques of studying Wound Healing
Microscopy: Light microscopy permitted the original observations on cellular and vascular changes which occur during wound healing. Recently, electron microscopy has amplifiedthisinformation andinparticularexpandedknowl- edge of the origin and structure of the collagen fibre.
Planlmetryhasbeenusedextensively tomeasuretherate ofhealingofsuperficialwoundsandagreat dealof information hasbeen collected ontherole ofcontractioninthese wounds.
Tenstometryappeals tothesurgeonbecauseitprovidesan index of the ability of wounds to resist disrupuon. It is also a useful experimental tool as it is simple, quantitative and capable of precise control. In effect, it evaluates the progress of fibroplasia in the wound.
Biochemistry: Biochemical techniques have provided extensiveinformationon the numerous processesoccurringin the ground substance of the healing wound

What cytokines stimulate wound healing
What is scab formation

Answer 13

INFLAMMATION.:
DEMOLITION
PROLIFERATION
MATURATION

Traumatic Inflammation: Immediately after the
infliction of a deep incised wound, the edges become sealed together first with platelet clot and then fibrin clot. The adjacent capillaries constrict and are plugged with clot, but withinafewhours theydilatefollowingreleaseofvasodilators such as serotonin, histamine, bradykinin and prostaglandins. The platelets release also (i) growth factors, PDGF, TGF-B, IGF-1, adhesive glycoproteins-fibronecun, thromboplasrin,
laminin, (ii) serotonin which increases vascular permeability and (iii) other chemoattractants and lysosomes containing hydrolases and proteases (leucocyte-elastate, cathepsin G protease-3,μPM, μMP-8andμMP-9, (IV) and pro-inflamma- torycytokines(IL-Ia), IL-1b, TNF-a) whichactivate additional mediator systems (KGF, IL-6, IL-8, μCP-1).
The aggregation and activation of platelets and release of chemotactic factors are initiated and promoted by exposure of blood to fibrillar collagen of the injured tissues.
Following the vasodilation and increased permeability of the vascular endothelium, plasma, plasma proteins, C5a and C3a are poured into the wound site causing the turgid wound. Neutrophils, activated by the platelets, and later monocytes migrate through thecapillary wall andenter thewoundsitetoo. The response is similar in principle to that seen in the early stages of bacterial inflammation and as in that condition also, the body temperature is raised usually to 37.5-38.5° C.
The process probably serves to raise the metabolic rate of the wound preparatory to its repair. It also brings together the materials necessary for the subsequent stages of repair, i.e. plasma, fibrin, polymorphonuclear leucocytes. The ground substance ofthe connective tissue undergoes depolymerization and granules disappear from most cells.
2. Destructive Phase (Demolition): This immediately follows the inflammatory phase and is concerned with r emoval ofdeadand dying tissues fromthe wound. The neutrophils and monoeytesmigrateintothewound, k.iJJanybacteriaaroundand ingest dead bacteria and tissues. Monocytesconvert to mac- rophages but some macrophages are local in origin. The macrophages secrete b-FGF, other growth factors and other
cytokines.
The first two phases described represent the lag period in
wound healing during which the wound has no tensile strength. Preparation phase would bemore appropriate, for the founda- tions for repair are being laid down at this time. The period varies from 4-6 days and is rather constant from one animal to another. It is prolonged by the development of bacterial inflammation.
3. Proliferation Phase: This isthe stageof granulation tissue formation. As congestionof the wound subsides collagen formation becomes evident. The growth factors, secreted by the macrophages, platelets and fibroblasts, activate local endothelial cells, fibroblasts and epithelial cells to start the process ofrepair.
The endothelial cells divide and migrate to form a new capillary network in the wound. The fibroblasts from cells surrounding the wound are also activated and migrate into the wound. The endothelial cells and fibroblasts use fibronectin, hyalurooicacid,lamininandotherglucosaminoglycans(GAC).
in the extracellular space in the wound as the scaffolding matrix. Fibroblasts now deposit collagen on the fibronectinand GAC scaffolding. Matrix degradation is blocked; synthesis of proteases is decreased but synthesis of protease inhibitors is increased at the same time. Fibrin derived from the provisional . fibrinclotisanimportantpartoftheextracellularmatrix. Thus the damage is repaired. The ground substance now shows striking metachromasia indicating depolymerization and increasing quantities of mucopolysacchar ides. The process ~·~rebycapillary loops, fibroblasts and collagenreplace the initialfibrinclot is known as Organisation. At first, the collagenfibrils are fine and few in relation to the cells but as healing proceeds, the fibre-cell ratio increases until in the adultscartissueonlyafewelongated fibroblastsarevisible. The initial fine fibrils of collagen have been called Tropocollagen.Ithasbeenmuchstudied structurallyunderthe electronmicroscope. tisduringmephase offibroplasia that the tensile strength ofthewoundrapidly increases; it increases rapidly from 1 to 6weeksandslowly up to a year. Wound sutures can be dispensedwithfromthe7thtothe 10thday withminimumrisk ofdehlscencc.
4. Maturation Phase: The peak of fibroplasia is soon followedbygradualshrinkage andmaturationofconnective tissueinthewound.Thescar,whichup10 thistimehas remainedelevated and congested, over a period of weeks or monthsthinsout and flattens and becomes progressively less conspicuous. Histologically the blood vessels gradually disap- pear (Endarteritis obliterans), the number of fibroblasts in relation10 collagen fibres rapidly falls so that eventually few celscanbe seen. At the same time there is progressive increaseintensilestrengthwhich inthefasciaeofthebodygoes onformany months. The entire process is sometimes called Cicatrization.

Wound healing is initiated and regulated by the release of IIA , growth factor peptides - transforming growth factor-beta (TGF-B), platelet-derivedgrowth factor (PDGF), basic fibroblast growth factor (b-FGF), epidermal growth factor (EGF) - cytokines secreted by plareletsandmacrophages- insulin-likegrowthfactor 1(IGF- 1) and vascular endothelialgrowth factor (VEGF)

Scab formation: The scab is the clot exposed to air. The processofepithelializationasdiscussedabovestarts within24h under the stimulus of the cwidemJal growth factor and by 48h, sheets of migrating epidermal keratinocytes have bridged and covered the wound, separating it from the overlying clot or scab. The new epithelium deposits keratin on its surface beneath the dried clot after which the scab separates spontane- ously usually about the fifth day.

Question 14

What are the two major factors tha affect wound healing and give types under each

Answer 14

Systemic or general: Age-Age:Oddlyenough woundsheal well inold people. If there iidelayitisprobablyduetoadeficiencystate, starvationor deficientbloodsupply,andthisisnotinitselfattributableto age

Chronic illnes. Egs diabetes, hypertension, cancer, TB. Etc.

Nutrition.: Ascorbic Acid· It is firmly established that the wounds of people deficient in this vitamin heal poor

Protein Deficiency: Starvarion of animals delays heal- ingandthis presentsaconundrumbecausewhen woundhealing is observed in human beings who are undernourished, the wounds often appear toheal moderately but significantlywell.

ApartfromvitaminC, vitaminAhasbeenshowntoenhance the early inflammator y response, stimulate fibroblast proliferation and increase wound tensile strength. Deficiency delays wound healing, increasing the risk of wound infection a ndimpairscollagen synthesis.
Trace Elements Deficiencies: Zincdeficiency, uncommon exceptinchildrenintheMiddle East,isknowntoretardwound healing by preventing cellular mitosis and disturbance of fibroblast function and collagen synthesis.

Local: Oxygen

Blood supply.

Foreign bodies.

Local Factors
Oxygen: It has-become evident that oxygen is the most important woundnutrient. Itsdelivery tothehealing woundis impairedbyanumberoflocal factorssuchastissuetraumaand tight suturing techniques. More serious problems arise when woundcapillary perfusionis impaired by systemicdisordersas occurs in shock.
Blood Supply: Trivial wounds on the ischaemic legs of atherosclerotic patients heal very slowly. In contrast, wounds in vascular areas heal very quickly; sutures may be safely removed from scalp and facial wounds after three days in the knowledge that healing is already well advanced. Venous ulcers also heal poorly because of impairment of the local circulation.

Residual Infection: Invasion of a healing wound by pathogenic bacteria is invariably followed by a delay in healing, the duration of which depends in part upon the destructive powers of the organisms. In very severe infections, especially with anaerobes, tissue destruction may be great and healingdelayed for weeks or months. Infection also impairs bloodflowand raises local need for oxygen in the wound. Adhesionstobonysurfaces resulting from infection may, by anchoringthewoundedges, prevent contraction.John Hunter
longagonotedthisinulcers over thetibia. ImmobilizationandTrauma: Inadequate immobilization
may lead to separation of wound edges with subsequent infection.Repeatedmovement hastheeffectofdisruptingthe newlyregenerated capillaries and collagen laid down during thephaseof fibroplasia. One of the most frequentcauses of delayedhealingof an abdominal wound is the development of apersistentcoughearlyinthepost-operativeperiod. Eventhe changingofdressings, ifnot carefullycarriedout, mayleadto destructionoftheadvancingmarginofepithelialtissue. Inthe absenceof infection, it is desirable to keep wounds covered umil !he healing process is well established.
Foreign Bodies: Any kind of foreign material retained in awoundwill delay healingif infection is present. The wound remainsunhealed until the foreign body, usually a stitch, is extrudedorremoved. In this respect,dead bodytissues-bone, teeth, nails· behave as foreign bodies. On the other hand, a cleanobjectsuchasapieceofglass. maybeburiedinawound whichwill heal without significant complication; in due time
localpainand tenderness may necessitate removal.
Surgical Technique: If wound edges are not correctly opposed, adead space forms which soon becomes filled with
tissuefluidor blood and subsequently replaced by granulation tissue.Healingis thenineffectbysecondary intention.

Question 15

How are ulcers or wounds managed(history,exam,investigations,ddx of ulcers ,complications)
State six special lab investigations for ulcers
In picture 1 of the slide it’s a sloping ulcer,pic 2 is an undermined ulcer,pic 3 raised ulcer
True or false

Answer 15

PRINCIPLES;
History-Swelling.
Pain, fever.
Polyuria, polydipsia, hyperglycemia
Chronic cough, night sweats.
Intermitant claudication, rest pain.
Dizziness, palpitations
Weight loss, bleeding.

Examination-General
Chest; cardiorespiratory
Abdomen
Status localis.

Investigation-Classication; diagnostic and supportive.
Diagnostic; Fbs, chest x-ray, sputum culture, doppler scan. Wound biopsy, x-ray of the affected limb.

Diagnosis/differential diagnosis-
Post cellutic ulcer,
Diabetic foot ulcer.
Peripheral arterial disease.
Tuberculosis ulcer
Malignant ulcer

Conservation/ Radical
Complication-Septicaemia
Acute lymphangitis
Gangrene
Wasting of the involved muscles.
Osteomyelitis
Joint deformities.
Malignant change.
Fascitis, pyomyocitis.
Tetanus
6. Lymphoedema:- Recurrent lymphangitis may lead to
below-knee lymphoedema of varying degrees.
7. Periostitis:- When the ulcer is close to bone, periostitis
occurs and if persistent may lead to new bone formation at the base of the ulcer.
8. Malignant change:- Long-standing ulcers and unstable scars may undergo squamous carcinornatous change.
9. Deformities of the foot or ankle may occur if deep tissues are involved in the fibrosis.

Prognosis/prevention

Special Investigations for Ulcer s L Urine - for sugar and albumin.
2.Blood:
(i) V.D.R.L. for syphilis.
(ii) Sugar level for diabetes mellitus.
(iii) Haemoglobin genotype for baemoglobinopathy. (iv) Haemoglobin level to exclude anaemia.
(v) Plasma protein levels
(vi) Mantoux test.
(vii) E.S.R.
3. Bacteriology of the ulcer - for special organisms, Mycobacteria, Fusobacteria, Borrelia
4. Radiology:
(i) Plain films of ulcer to see any bony changes or
calcification.
(ii) Duplex Doppler scanning, arteriography or venography for vascular disorders.
(iii) Plain films of the chest should be done also if ruberculosis or malignancy is suspected.
5. Biopsy of ulcer - may be the final step in definitive diagnosis.
6. Other tests may be done as indicated by the probable cause of the ulcer e.g. Lepromin test in suspected leprosy.

Question 16

How is debridement or sloughectomy done

Answer 16

Regular saline dressing.
Surgically using scalpel.
Biological method; use of sterile maggots.
Enzymatic method; mashed fresh pawpaw.
Osmotic method; sugar and honey.
Negative pressure therapy.

Question 17

State and define the types of amputation
State the levels of amputation from the waist to the leg downward

Answer 17

Amputation
Local Amputation may be a simple extension of debridement

Transphalangeal amputation is indicated when the disease process affects the deep tissues of the toe such as tendon, bone or joint

Ray amputation taking the metatarsal head is an extension of this for more proximal disease often excising the originating ulcer on the plantar surface

Major Amputation
May be required to control sepsis or excise gangrene when minor amputations will not suffice or where revascularization is unavailable or unsuccessful

BKA is preferred to ABK considering rehabilitation

Hemipelvectomy
Hip disarticulation
Very short above knee
Short above knee
Medium above knee
Long above knee
Knee disarticulation
Short below knee
Standard below knee
Symes
Hind foot such as Boyd
Chopart
Lisfranc
Transmetatarsal
Toe disarticulation or amputation

Question 18

Under non specific ulcers,explain the causes of the types ,clinical features ,investigations and treatment

Answer 18

TYPES OF NON-SPECIFIC ULCERS 1. TRAUMATIC ULCER
Skin loss of varying severity follows direct, mechanical trauma and irradiation. Suchwounds may become infectedand result in a non- specific ulcer.
Diagnosis is based on the history and sloping edge of the ulcer.

2.
PYOGENIC OR INFECTIVE ULCER
An acuteinfectivediseasesuchasacarbuncle,abscessor cellulirisleadstodevitalization, necrosisandJossofskinand ulcer formation.Theulcermayfollowruptureorincisionof an abscess. After the acute phase the ulcer has a sloping edge. Treatment: As for non-specific ulcer.

3.
ULCERS OF VASCULAR ORIGIN
(i) Venous (gravitational} Ulcer (See also Ch. 50) lt occurs in the lower limb usually just above the medial malleolus, but at times on the lateral side. Venous ulcers usually follow many years of venous disease such as varicose
veins and deep venous thrombosis. It is thought to result from poor venousdrainagecommonly associated with deepvenous thrombosisorvaricoseveins. Thevalvesoftheperforatingand deep veins are destroyed when the veins are recanalized after thrombosis. This, as in varicose veins with incompetent valves, causes backpressure and high venous pressure leading to stasis. The high venous pressure causes leakage of plasma from the capillaries into the tissue spaces leading to oedema formation.Thisresultsinpoor oxygenationandnutritionofthe affected pan and the least trauma or infection leads to ulceration. The subcutaneous veins are dilated and the skin may later become atrophic because of poor nutrition. lt is postulated that chronic venous hypertension and consequent dilatationofthecapillaries increasesleakageoffibrinogenand macromolecules into the interstitial space of the skin. The fibrinogen is convened to fibrin which is not broken down because of deficient plasminogen activator. A pericapillary fibrinformsaroundthecapillariesandactsasa diffusion barrier for oxygen and nutrients with resultant lipodermatosclerosis (pigmentation, inflammation and induration ) first and later to ulceration.
Diminished diffusion of oxygen and nutrients may be due
alsotothe increased interstitial fluid from the high venous pressure.
Theaffectedskin is often pigmented from breakdown ofred ceUsreleased into the tissues when the high venous pressure causesrupture of the capillaries. The subcutaneous veins are dilatedandtheskinmaylater become atrophic because ofpoor mnrition.

Clinical features
I. ThereisahistoryofD.
V.T. perhaps after child birth or
operation.
2. Thelegor ankle may be swollen and varicose veins are
ofteoprominent.
3. Theulcer which may be painful is irregularly circular,
afewmillimetres to several centimetres in diameter, and situated just above the medial malleolus or at times nearly eocircling the leg. It has a shallow floor and sloping edges.
4. Thesurrounding skin is often pigmented and small distendedveins are evident in the subcutaneous tissue.
Diagnosis: The presence of varicose veins and/or oedema of tbelegorankle, orahistoryofD.V.T. inapatientwithanulcer jostabovethemedial malleolus helps toestablish thediagnosis.
Treatment
I. The prime aim is to improve venous drainage andsoimprove oxygenation and nutrition of the affected tislues. This is achieved by:
(i) Bed rest with the foot of the bed elevated.
(ii)Below knee supportive occlusive, multi layer elastic, compression bandage from the toes t o the tibial lllberclewhich, by compressing the muscles and veins, helps to reduceoedema. It also helps the muscles to massage the veins, lrlps toreduce oedema. It also helps the muscles to massage dieveinsduring walking.
(iv)Regularwound dressing using saline. Most ulcers will ~ under under above treatment.
(v)Ifconservative measures do not succeed, sclerotherapy orsurgeryisresorted to.
(vOLigation anddivision of incompetent perforating veins andstrippingofvaricose veins ifconservative measures donot !llCCeed.
(vii)lftbeu!cer still does not heal, it isexcised and grafted 1reothefloor fills up with healthy granulation tissue.
2.Following healing by either of these methods, the legs tlRISlbesupported by a firm crepe bandage for a period of not lessthanthree months to allow proper consolidation of the ~ed wound; otherwise breakdown of the wound quickly i:ilows.

Question 19

Continuation of ulcers of vascular origin features,investigations,etc (arterial ulcers,pressure sores,stages of pressure sores )

Answer 19

Arterial Ulcer
lscbaemia of the skin by occlusive arterial disease may lead milsnecrosis either spontaneously or following trauma. The ulcer may start as a gangrenous patch.
Clinical features
I. The patient isusually elderly, 50orover, and there may be a history of intermittent claudication.
2. The ulcer is usually on the toe or distal part of the foot andexquisitely painful. Thefloorisnecrotic andthesurround- ing skin erythematous.
3. The skin of the foot is shiny, often hairless, hypoaestbetic and may be cold and even cyanotic. The nails are brittle and there may be loss of nail pulp.
4. The dorsalis pedisand posterior tibial pulses are usually absent.
Investigation
Duplex doppler scanning may show narrowing or blockage
of the femoral, popliteal or tibial artery. Treatment
The ulcer may heal with rest. The blood supply may be improved by transluminal angioplasty, endarterectomy or arterial grafting.
(iii) Pressure Ulcer (Decubitus Ulcer)
It usually results from excessively Jong compression of the soft tissues between a bony prominence and the bed or chair upon which the paitent is resting. Prolonged local pressure induces ischaemia leading to thrombosis in the small blood vessels within the compressed soft tissues. The ischaemia may persist after relief of the pressure because of the reduced and incomplete circulation when the tissues rather need increased blood flow. The time limit betweenreversible and irreverisble
changes depend on the local temperature and the patients’s general condition and other factors such as whether the patient is lying on a mattress or a bare metal trolley.
It is usually seen in those who are unaware of the warning signals of discomfort or pain to change their position, e.g. unconscious or paraplegic patients, or those too weak to change their position or call for help. Poornutritional status, anaemia, maceration of skin by sweat, faeces or urine, and infection predispose to the early development of pressure ulcer. This ulcer is therefore a reflection of inadequate nursing care.

Prevention
Prevention depends on turning the patient two hourly to prevent prolonged pressure on bony points.adequate skin care by massage to encourage blood circulation and powdering to help absorb sweat, application of barrier cream and an adequate care of the bladder, if necessary by catheterization, and of the bowel. T he skin is inspected frequently for areas of rednessor blackness and at the first sign, all pressuremust be takenoff. The bed must be clean and bed sheets must not be creased. Cradles may be used to take the weigh! of bed clothes awayfromthe patient.
Special soft beds, pans of which can be periodically removed10 preventprolongedpressure,ripplebeds, circular bedsandStryker bedswith mechanical devices 10 help nurses changethe position of patients, are useful aids in the manage- ment of these patients. Air levitation bed is useful when pressureis impossible.
Apart from avoidance of pressure and skin care, early ambulation whenever possible, by the use of crutches, braces orparallelbars,ishelpfulingeuing thepatientupandthereby relieving the pressure.
Treatment
Information should be sought on the following: diabetes, hypercension,sickle cell disease and medications eg. soluble aspirin.
Localdressings of saline are applied to aid early separation of slough; desloughing may have to be done with scissors. Platelet-derived growth factor-B promoteshealing. Whenthe wound becomes clean, it is covered with skin graft or if ii is deepbya myocutaneous flap. Nutrition mustbe improved.

Stages of pressure sores
Stage 1 Blanch ing; non-blanching hyperaemia
Stage II Blistering
Stage III (i) With necrosis (ii) Without necr osis
Stage IV Deep ulceration
Stage V (i) With necrosis (ii) Without necrosis Chronic ulcer.

Question 20

Continuation of ulcers of neurotrophic origin and non specific ulcers associated eith metabolic or systemic diseases clinical features,investigations,diagnosis,treatment etc
Why do diabetics get ulcers?
Why do Sickle cell patients get ulcers ?

Answer 20

NEUROTROPHIC (TROPHIC) ULCERS
Ulceration is caused by unrecognized and oft-repeated traumato.orprolongedpressure on,ananaestheticskin. The lossofpainandothersensationistheresultofdiseaseorinjury ofperipheralnerves or spinal cord. Commoncausesareleprous neuropathy,diabeticneuropathy. syringomyeliaand peripheral nerve injury. Others are spinal cord lesions due to trauma, tabes dorsalis. tumours and congenital disease such as spina bifidaandVil B12 deficiency.
Clinical features
The sole of the foot, usually over a bony prominence, is affected. The ulcer is deep and penetrating and is usually of long-standing.Thebonesorjointsmaybesecondarily infected.
Treatment
To prevent such ulcers, patients with lesions causing anaesthesiaof the foot should wearprotective footwear.
Theulcer isdresseddaily with hydrogenperoxide, saline orsugarpasteuntilitbecomes clean.Itisthencoveredwith vaselinegauze and a viscopasteor ichthyopastcapplied. Dead bonesareremoved.
S. NON-SPECIFIC ULCERS ASSOCIATED WITH METABOLIC OR SYSTEMIC DISEASE
(i) Diabetic ulcer.
(ii) Haemog)obinopathiculcer.
(iii) Patients with spherocytosis may, for unexplained
reasons, develop chronic ulcers of the legs. The ulcer heals on
after splenectomy which controls the underlying disease.
(iv) Chronic ulcerarion is also a complication of ulcerative
colitis.
(v) Ulcers of self-inflicted trauma.

(i) Diabetic Ulcer
Itisanulcer indiabeticsfrominfection,traumaorpressure necrosis. The predisposing factors are hypoaesthesia from peripheral neuropathy and iscbaemia due to atherosclerosis. The ulcer is on the foot, especiallyover the head of the first metatarsal or big toe. It is deep and punched out with hyperkeratinisation aroundtheedge.
The infectionmayspreadandevenprecipitategangreneof thefoot.Organismscommonlyisolated arcStaph.aureus,E. coli, Proteus, Strep. pyogenesand pseudomonas.
Diagnosis: There is glycosuria and the fasting blood sugar is elevated. Absenceofvibration senseandjointposition sensein thefootconfirms neuropathy.Peripheralpulsesmaybeabsent
Treatment
1. The diabetcs must be controlled.
2. Antibioucsare administered co control infection.
3. Localsaline or sugar dressing helps to remove sloughs
and clean up the ulcer. Slough and dead bone if present are excised.
(ii) Haemoglobinopathiculcer (See also Cll. 51)
It is found in patients with the homozygoussickle cell(SS) disease.Theulceroccursasaresultofhaemolytic episodes with thrombosis of small peripheral skin vessels and conse- quentanoxia ofthe affectedskin. Theulcer is most often seen inthelowerlimbsclosetothemedialmallcolus(Fig.51-3). h is associated with fibrosis, atrophic skin and hyperpigmcnta- tion. The ulcer is difficult to treat because of the lowered oxygen tension, fibrosis around the ulcer, recurrences of haemolytic crisis and of the low haemoglobin level.
Treatmentconsistsofgeneralmeasures,bedrest, admin- istration of iron, folic acid and anti-malarial drugs and, if necessary,ofskingrafting after adequaieexcision.Thehealed ulcer often breaks down again.

Question 21

Continuation of non specific ulcers tropical ulcers clinical features,investigations,diagnosis,etc (

Answer 21

Thisulcerhasforlongbeendesignated”Tropicalulcer” for the simple reason that it is seen predominantlyin tropical and subtropical regionsbutperhapspathologicallyrepresents nothing more than a post cellulitic ulcer, but for which the causative infectiveorganismsare the an-aerobicFusobacteria (Bacteriodes fusiformis) and the aerobic Borrelia vincenti.
It istrue theulcerisseenpredominantlyinthetropicaland subtropical regions and is seen more commonly in males but clinically its natural history is indistiguistiable from a trau- matic pyogenic non-specific ulcer and should be treated as such.

Clinical features
1. The lesion starts as a painful septic blister or vesicle aboutl-I.5cmindiameter, containingsero-sanguinous fluid andsurrounded by oedematous inflamed skin. The acute inflammatoryprocess is accompanied by pain, heat, redness a.OOswelling.Sometimesthere isinabilitytomove theaffected part.Thereare also constitutional symptoms which include pyrexia,generalmalaise and tachycardia.
Withtimeandespecially if the infectionis not treated or ispoorlytreated, it spreadsby the lymphaticsintothe regional lymphnodescausinglymphangitis andlymphadenitis.
Jtmayspreadthrough thebloodstreamcausingbacteraemia andsepticaemia. Where the patient is seen early i.e., at or beforetheonsetofblistersandadequatelytreated, itispossible toabortthewholeinflammatory processbygivingappropriate antibiotic.
2. Ifuntreatedorpoorlytreated,theblisterrupturesafter afewdaystoexposeafoul-smelling, ragged,yellowish-brown, greyorblacksloughoftheskinandsubcutaneoustissues. The infectioncanalsoaffectdeeperstructures such as muscles and tendonscausingthemtoslough off.
Blood vessels may also be affected causing them to thrombose. Where the affected vessels are end-arteries or veins,gangrenemayresulte.g. gangreneofthetoes. Bones mayalsobeaffectedresulting in periostitis. The slough with timeliquefies, discharges offensive pus and separates. A circular ulcer about 4-IOcm in diameter then forms.
3. The ulcer in the acute stage has a heaped up edge liecauseofthe inflammatory oedema of the surroundingskin andsubcutaoeoustissues. The floor is covered with unhealthy granulationtissue. The granulation tissue is pale, avascular, heapedup, slimy, oedematous and does not bleed easily when touched.(Fig. 6-4).
4. Iftreated, theinflammationsubsides, theslough sepa- rates, the discharge gets less and the granulation tissue becomeshea!thyi.e. firm,flat,brightredanddoesnotbleeds readilywhentouched. The epitheliumfromtheslopingedgeof theulcergradually grows to cover the granulation tissue. Untreated, the ulcer becomes chronic after 4-6 weeks with a densefibroustissue at its base. The granulation tissue then becomesavascular andpale.
Theulcerat this stage assumes the features of an indolent non-specificulcer.
Diagnosis . FBC and differential, ESR, sickling and urine analysis are done. Intheacutephase the causative organisms can bestained usingGRAMstainingandalsoculturedfromthedischarge. At the chronic phase, the ulcer assumes the features of a non- specific ulcer and there are no specific organisms; the diagnosis can only be suspected from the mode of onset. Anx-rayoftheaffectedlimbisdonewhereindicated torule out bony involvement.
Complications
1. Acute lymphangitis and lymphadenitis. 2. Septicaemia.
3. Sympathetic effusion into adjacent joints e.g. knee joint.
4. Wastingoftheinvolvedandadjacentmuscles.
5. Gangrene formation e.g. of the toes when the foot and toesare involved.
6. Periostitis or osteomyelitisof the underlying bone. 7. Tetanus.
8. Constricting scars or obliterative lymphangitis may
lead to lymphoedema.
9. Constricting scars may cause deformities e.g. equinus
deformity of the ankle if the tendo Achilles is affected.
10. Malignant change may occur in a long-standingulcer.

”

Question 22

Continuation of non specific ulcers specifically neoplastic ulcers clinical features. How is History and exam of ulcers done

Answer 22

NEOPLASTIC ULCERS
Primary malignant lesions of the skin - squamous cell carcinoma, rodent ulcer, Kaposi’s sarcoma, malignant mela- noma - present as ulcers. These ulcers have a raised evened edge,aninduratedbaseandanangrynodular floor;theedgeof a rodent ulcer is rolled.
Fig. 6-5 Squamous car cinoma of the leg showing raised cverted edge.
DIFFERENTIAL DIAGNOSIS OF AN ULCER
The diagnosis is arrived at after: 1. Carefulhistory.
2. Clinical examination and 3. Investigations.
1. History
(i) The mode of onseti-Ai: ulcer starting as a painful blister and rupturing is most likely tropical; one after an abscessorcellulitis,’ infectiveorpyogenic;oneafteraninjury, traumatic; one with intennittent claudication and a black patch, arterial; and one after deep venousthrombosis, venous or gravitational

(ii)Duraiioni-A long history may suggest an indolent or callous non-specific ulcer, malignant change in a simple ulcer orachronicspecific ulcer such as tuberculosis. A sborthistory suggestsatraumaticorpyogenic ulcer.
(iii)Pain:Ifpainful tropical, pyogenic, arterial or venous ulcer is suspected. Absence of pain suggests a neuropathic lesion.
(iv)Progressoftheulcer:-Anactively spreading ulcer may beduetoinfection, poor blood supply or malignancy.
(ix)The surrounding skin - whether it is inflamed or pigmented.
(x) The state of local circulation - presence of
(v) Painful regional lymph nodes:- This suggests inflammatory ulcer.

Symptoms or past history suggestive of the following diseases are sought:
(a) Diabetes - polydipsia, frequency, weight loss. (b) Tuberculosis-night sweats, weight loss, anorexia,
cough.
(c) Deep venous thrombosis - painful swelling of a
leg after child-birth or operation.
(d) Varicose veins - distended veins on the leg.
(e) Arterial disease - intermittent claudication,
paraesthesia,
(f) Haemoglobinopathy- attacks ofjoint and muscle
pain especially during the cold or rainy season,
weakness.
(g) Neuropathy - loss of pain sensation in the limb;
history of leprosy, nerve or spinal injury.
(h) Yaws - history of previous granulornatouslesions
of the skin.
(i) Syphilis - history of a previous chancre and second-
aryrash.
2. Clinical examination
(a) Ulcer:
(i) Number:- Multiple ulcers may be due to Kaposi’s sarcoma, yaws, spherocytosis, ulcerative colitis or self-in- flicted injuries.
(ii)Anatomical site.- An ulcer near the medial malleo- lusmaybevenous,traumaticorduetoS.S.disease. Anulcer onthetoes or dorsum of tbe foot may be arterial or diabetic in origin. One in the sole is most probably neuropathic or malignant melanoma, one around the knee joint probably !)philitic and one in thegroin or neck probably tuberculous. An ulceronthefacemay bearodent ulcer.
(ii) The size.
(lv)Tlzeshape - whether round, oval irregular or serpigi- nous(syphilitic).
(v) Edge:-This is the most important part of the ulcer. Sloping edge - non-specific ulcer. Raised and evened - lltllignantulcer. Raised androlled -rodentulcer. Undermined -tuberculousorBuruliulcer. Punchedout-syphilitic oryaws.
(vi)Floor - whether sloughy and-discharging, clean and pink(healing) or nodular (malignant). The type of discharge is al.mooted.
(vii) Base - whether slightly indurated as in chronic non- !p:!Cific ulcer or indurated and fixed as in carcinoma or callous oon-specific ulcer.
(viii)The discharge - pus, serous or serosanguinous, o:lour, profuse or scanty.

(ix)The surrounding skin - whether it is inflamed or pigmented.
(x) The state of local circulation - presence of
(v) Painful regional lymph nodes:- This suggests inflammatory ulcer.
an
(xi)State of arterial pulses of the limb -aortic, femoral, popliteal, dorsalis pedis and posterior tibial.
(xii) State of innervation - any loss of sensation or motor power.
(xiii) Regional lymph nodes - this is important espe- cially in carcinomatous ulcer. If enlarged, tenderness and mobility should bedetermined.
(b) General examination-Colour of conjunctivae, hepato- splenomegaly, andalherosclerosis should be particularly looked for.

Question 23

How are ulcers and wounds managed
And what advice will you give to affected patients in discharge

Answer 23

Treatment plan
a) resuscitation b) optimization

Admission and bed Rest, elevation of foot.
RESUSCITATION; A, B, C, D
Samples taken for investigation.
Antibiotics and Anagesics started.
Classify the wound. EG Wagner’s classification.
Conserve/ surgical procedure debridement.

Treatment
1. Thereshould beadmission, bedrestandelevationofthe
foot end of the bed in patients with acute infection.
2. Parenteral antibiotics are started. Benzyl penicillin 6 hourlywithmetronidazole 8hourlyisveryeffectiveagainstthe infecting organisms and results in rapid resolution of the inflammation. Whenthetemperaturebecomesnormal, treat- ment is continued with penicillin V and oral metronidazcle. Erythromycinisgiven tothosewhoaresensitivetopenicillin. Intravenous fluid therapy is given to those who are too ill to drink.
Treatmentshould bereviewedassoonasthewoundculture result becomes available. Where treatment is effective, favourablesignsappear in24-48h. Theoedemaandpainbegin to subside and the temperature falls.
3. Adequate analgesia e.g. diclofenac is given to relieve pain.
4. Aboosterdoseoftetanustoxoidisgiven.
5. The ulcer is cleansed with a non-irritant solution such as normal saline. The dressing is changed as often as is necessary depending ontheamountofdischarge.
6. Theulcerisgraftedwithsplitskingraftassoonasthe granulation tissuebecomes healthy.
7. Where thereisaninfectedslough,itisnecessarytoput thepatient onappropriateantibiotics.
Thesloughcanberemoved usingthefollowingmethods: a) Regularsalinedressing.
b) Sloughectomy using a sterile scalpel or a pair of
scissors. If properlydone, it should_bepainless. Small sloughs can beremovedinthewardbutextensive onesmustbedonein the theatre under general anaesthesia.

c) Lessorthodoxmethodsofremoving sloughs include
i) Biological method: Use of maggots. Sterile larvae (maggots) of the greenbottle Luciga Seriata can be used to removeslough and necrotic tissue from wounds.
Indications: These larvae can be used in any wound containing slough or necrotic tissue eg. leg ulcers (specific, non-specific), venous and arterial ulcers, pressure sores, burns, diabetic ulcers etc.
Contra-indications.Theuseoflarvae iscontra-indicatedin wounds that have a tendencyto bleed or that communicate with bodycavity or internal organ.
Method ofuse: It should be used in a dressing system that retains the larvae within the area of the wound and allows the larvae toobtainadequatesupply of oxygen. The larvae produce proteolytic enzymes that degrade and liquefy necrotic tissue which they ingest as a source of nutrient. They are also able tocombat odour and infection by ingestingand killing bacteria present inthewound.
Side-effects: I. On rare occasions the use of larvae has caused wound bleeding. 2. Some patients are allergic to the secretions of these larvae. 3. Some patients fear maggots and would not allow them to be used on their wounds.
Change of dressing: Larvae should be left on the wound foraminimumof3 days.
ii) E nzymatic method: Mashed fresh pawpaw (papaya), sandwiched between layers of gauze, can be applied to the ulcer. Itiseffectiveinremovingsloughandproducinghealthy granulation tissue.
iii) Osmotic method: Sugar and honey act by osmosis and absorb water from tissues and organisms. They are therefore antimicrobial. They also promote proliferation of localmacrophagesandenhancegrowthoffibroblasts. Filling the ulcer cavity with granulated sugar or dripping honey into it is effective in getting rid of the slough and odour and promoting growth of healthy granulation tissue. This is done once or twice a day depending on the discharge.
iv)Negative p ressur e therapy: With this method, the wound is cleansed with normal saline and a suction tube introducedintothewoundcavity. Thewoundiscoveredwith a foam and sealed with opsite. The suction tube is then connected to a low pressure suction machine cg. Robert’s suctionmachine. Thenegativepressuresocreatedcontinu- ouslysucksanyfluidthatisformedinthewoundcavity. Italso exerts negative pressure on the floor of the wound thus sucking fluid andorganisms from the floor, and intheprocess the blood supplytothefloorisimproved. Thispromotestheproduction of healthy granulation tissue and helps the wound to heal rapidly. This method is very effective for treating extensive ulcers with unhealthy granulation tissue especially cavity
wounds.
8. Theulceristhengrafted.
9. The affected limb is splinted in the position of function toprevent thedevelopment ofcontractures.
10. Physiotherapy: As soon as the patient is admitted. physiotherapyisstarted. Earlyphysiotherapyhelpstoprevent muscle wasting and development of contractures.
IL General measures: Other measures include adequate nutrition, correction of anaemia, etc.
12. Nursing care: Attention should be paid to pressure areas to prevent the development of pressure sores.
13. Medical stockings should be worn or crepe bandage applied from the toes to the knee to enhance blood and lymphatic flow.
14. Obeseandelderlypatientsshouldbeputonsubcutane- ous heparin.
After discharge
I. the patient is advised to protect the legs and feet by
wearing a comfortable pair of socks and shoes.
2. farmers are advised to wear protective clothing and boots.
3. the patient is advised about proper foot hygiene.
4. where there is extensive scarring, the patient is advised
to continue wearing medical stocking or crepe bandage.
5. to seek prompt attention for any abrasion or laceration
to the affected limb

Treatment of Non-specific Ulcers A. Acute ulcer
L Intheacutephase,thepatientisadmittedforbedrest and the footend of the bed elevated.
2. Wound swab is done for gram staining, culture and sensitivity ofanyorganismscultured.
3. Broad-spectrum antibiotics are started white awaiting the results of the culture and sensitivity tests.
4. Tetanus booster dose is given to prevent tetanus infec- tion.
5. The wound is cleansed regularly with normal saline. Aceticacid iseffectiveforcleansingwoundssuspectedtobe infectedwithpseudomonas.
6. Crepe bandage is applied firmly from the toes to the knee to promote lymphatic and venous drainage.
7. Theaffectedlimbissplintedinthepositionoffunction to prevent formation of contracture.
8. Physiotherapy is started early to prevent wastage of muscle and contractures.
9. Oncetheulcerbecomeshealthy,itisgraftedwithsplit skin graft.
10. Where there is an infected slough, appropriate antibi- otics are started and the slough removed either with saline soaks or by sloughectomy i.e. surgical excision of the slough.
The wound is then cleansed regularly until healthy granu- lation tissue is formed.
A wound swab is then taken for culture to rule out streptococcal infection before grafting with split skin.
B. Chronic or Indolent Ulcers
These ulcers may be excised and then grafted with split- skin graft or covered with a flap.
78
C.
thekneetopromote lymphandvenousdrainage wheretheres
Advice After Discharge
L Thepatientisadvisedonfoothygiene.
2. He is advised to use pressure dressing from the toesto excessive scarring.
3. Farmersareadvisedtowearprotectiveclothingand boots.
4. The patient should seek prompt treatment for any abrasion to the affected limb.

Question 24

State the clinical features,investigations and treatment for specific ulcers (buruli ulcer and tuberculous ulcers)

Answer 24

TUBERCULOUS ULCER (See Ch. 2)2.
I. It is seen in skin over discharging tuberculous abscess especially in the neck and groin.
2. The outline is irregular and the edges are thin, blue and undennined (Fig. 6-1) so that a probe
canbepassed underneath them. The floor is covered with palegranulations and the discharge is thin and watery. The base ~soft.
3. There may be satellite sinuses and enlarged lymph IXX!es.
The bacillus produces a heat -Iabile toxin called mycolacton which has both cytotoxic and immunosuppressive properties. It also has an affinity for fat cells. This toxin is thought to be responsible for the necrosis ofthe dermis and subcutaneous tissues seen in typical lesions. It is also thought to be responsible for the lack of fever, pain, general malaise etc, which is usually associated with other bacterial infection. It has a low mortality, but high morbidity and disability rate.
Epidemiology
Buruli ulcers have been reported from many tropical and subtropical areas. Cases have been in more than 30 countries in Africa, Asia, Latin America, The Western Pacific and Australia. But West Africa is by far the worst affected area. Insome African countries Buru Iiulcer has become the second most prevalent mycobacterial disease after tuberculosis. A few cases have been reported in North America and Europe possibly due to international travel.
Sir Albert Cook first described ulcers consistent with M. ulcerans infections in 1897 in Uganda. Maccallum first published detailed descriptions of it and established the aetiol- ogy of the disease in Australia in 1948 where it is called Baimsdale ulcer. The disease, howerver, takes its current name from a riverine village in the Mengo District of Uganda, Buruli, where extensive studies were done on the disease by Clancey and the Buruli group in 1961.
Most of the patients (70%) are children, under 15 years, who live near rivers, lakes or wetlands. Presently there is no evidence to indicate transmission from person to person.
Human immunodeficiency virus (HIV) infected persons do notappear tobeatincreasedriskformycobacteriumulcerans infection.
Currently the mode of transmission is not known. It is, however, thought that the organism enters the body through abrasions, puncture wounds etc. It has also been suggested that bites from aquatic insects (naucoris and dyplonychus species) which harbour the mycobacterium ulcerans bacilli in their salivary glands can transmit the organism during a bite.
Sites
The commonest sites affected in order of frequency are the lower limbs, upper limbs and the trunk,but any partofthe body may be affected.
The lesion
Once the organisms enter the body, they produce toxins - mycolactone - which cause extensive destruction of the subcu- taneous tissues and to some extent adjacent structures such as skin, muscles, tendons, blood vessels, nerves, bones etc within reach of the toxins. With time, thedestructive properties of the toxins cease and healing starts. The exact mechanism is not known but it appears either the toxins are neutralized or the organisms stop to proliferate or produce toxins.
4. There may be a tuberculous Investigations
focus in the lung or bone.
I. Acid-fast bacilli may be found in or cultured from the discharge.
2. Abiopsy specimen of the ulcer edge shows a typical ruberculous histology.
Treatment: Anti-tuberculous measures are adopted

BURULI ULCER
Buruli ulcer is a devastating skin disease caused by Mycobacterium ulcerans. It is an. acid-fast bacillus and therefore belongs to the same family of organisms that cause ruberculosis and leprosy. It is the third most common mycobacterial infection after tuberculosis and leprosy. It stains well with Ziehl-Neelsen stains and grows optimally at temperatures lower than central body temperature i.e. at 30- 32’C.ltcanbe grownonLowenstein-Jensenmediumat30-32”C raking6-12 weeks or longer to grow.

The bacillus produces a heat -Iabile toxin called mycolacton which has both cytotoxic and immunosuppressive properties. It also has an affinity for fat cells. This toxin is thought to be responsible for the necrosis ofthe dermis and subcutaneous tissues seen in typical lesions. It is also thought to be responsible for the lack of fever, pain, general malaise etc, which is usually associated with other bacterial infection. It has a low mortality, but high morbidity and disability rate.

ection.
Currently the mode of transmission is not known. It is, however, thought that the organism enters the body through abrasions, puncture wounds etc. It has also been suggested that bites from aquatic insects (naucoris and dyplonychus species) which harbour the mycobacterium ulcerans bacilli in their salivary glands can transmit the organism during a bite.
Sites
The commonest sites affected in order of frequency are the lower limbs, upper limbs and the trunk,but any partofthe body may be affected.
The lesion
Once the organisms enter the body, they produce toxins - mycolactone - which cause extensive destruction of the subcu- taneous tissues and to some extent adjacent structures such as skin, muscles, tendons, blood vessels, nerves, bones etc within reach of the toxins. With time, thedestructive properties of the toxins cease and healing starts. The exact mechanism is not known but it appears either the toxins are neutralized or the organisms stop to proliferate or produce toxins.

Question 25

State the clinical features,investigations and treatment for specific ulcers (classification of diseases caused by M ulcerans)
State the stages the buruli ulcer goes through
What is a characteristic feature of the ulcer
What is recurrent buruli ulcer
State the ddx of a pre ulcerative buruli nodule
State the complications of M ulcerans disease

Answer 25

Clinical classification of disease caused by ulcer eventually heals leaving characteristic stellate scars.
Mycobacterium Ulcerans
The disease can be classified into two broad clinical types:
A. Pre-ulcerativedisease and
B. Ulcerative disease.

A. Pre-ulcerative M. ulcerans disease
This can be divided into:
I. A papule (Fig 6-2a): This is an intradermal pre-
ulcerative lesion, commonly seen in Australian patients who probably presentearly.
leis not commonly seen in West African patientsprobably becausetheypresentlate. It is notpainfulnortender,butmay cause itching. It is a raised palpable lesion in the skin.
2. A nodule (Fig 6-2b): It is a circumscrbed lesion attached to the skin but not to thesubcutaneoustissue. Itisless than 3cm in diameter. II is painless, firm and may cause itching. It is easily palpable.
3. A plaque Fig 6-2c): It is a well- demarcated lesion. II is painless, dry, firm, pigmented, indurated and slightly elevated. Itisusuallymorethan3cmindiameter.
4. Oedematous lesions (Fig 6-2d): These are exten- sive, diffuse, usually painfuland tender. non-pittingswellings that are undermined to varying degree.
B. Ulcerative M. ulcerans disease (Fig 6-2 e, r, g)
The pre-ulcerative disease can break down into an ulcer which, unless interfered with byapplicationof herbal medi- cine,basatypicalwhiteceotral plugofnecroticfat.Thislater forms a necrotic slough. The acid-fast bacilli are confined almost exclusively to the necrotic slough in the bed of the ulcer and the surrounding necrotic fat.
The buruli ulcer lesion goes through the following stages:
The necrotic stage: This is the early stage of the disease during which there is necrosis of the subcutaneous tissues and surroundingstructures. The destroyed subcutaneous tissues are pale yellow unlike the normal subcutaneousfat. lo the initial stage the whole lesion feels indurated and there is very little or no cellular immune response and the buruli skin test is negative.
The organising stage: During this stage the necrotictissues becomeliquefied intoslough. Thehost developscell-mediated immunity and the buruli skin test may become positive. The bacilliare found in thesloughandsurroundingnecroticfac. The slough starts to separate leaving an ulcer with oedematous base, undermined edges and a floor covered with unhealthy granulationtissue.
The healing stage: Inthis stage the ulcer is fairly clean and healingstarts. Theedgesoftheulcerareunderminedtovarying extent. The indur ation of the base starts t o resolve and healthy granulation tissue Stans appearing. The undermined skin becomes adherent to the underlyinggranulation tissue. The
During the necrotising andorganisingstages,thereareno prodr ornal symptoms such as fever or general malaise and the patient remains relatively well unless the lesion becomes secondarily infectede.g. throughapplicationof herbal medi- cine.
A characteristic feature of the ulcer is the fact that it is painless and odourless compared with other bacterial ulcers such as tropical ulcer.

Recurrent buruli ulcer
It is the development of a further mycobacteriumulcerans lesion at the same or different site within one year. While a recurrent buruli ulcer lesion at the same site may be due to inadequate excision. one at a different site may be due to a haernatogenous or lympathic spread.

Differential diagnosis of a pre-ulcerative Buruli nodule
1. Foreign body granuloma: llere there may be a history of trauma and on excision, the foreign body itself may be found.
2. Nodular rasciitis or fibroma: These lesions are usually deep-seatedandonlyoccasionallyattachedtotheskin.
3. Phycomycosis: The definitive diagnosis can only be
made histologically.
4. A boil:There is throbbing pain with associated fever
and general malaise at times.
5. Sebaceous cyst: It may have a puncrum,
6. Onchocercoma: It is located on a bony prominence.
Skin changes may be present.
For these reasons, every skin lesion excised must be
histologically examined for proper documentationand proper treatment given where necessary.

Complications of M. ulcerans disease
I . Anaemia is common and is due to extensive tissue damage caused by mycolactone, repeated blood loss fromthe woundduringdressingsand inadequate proteinintake.
2. Malnutrition occurs in patients with extensive lesions.
3. Ostcomyelitis from haematogenous or direct spread into the underlying bone.
4. Gross deformities from the resulting scarring.
5. Joiruconrracruresandsubluxationofjointsfromfailure to splint adjacentjoints inpositionof function.
6. Distal lymphoedemaduetoscarring
7. Loss of a part of the eye wher e the sock etor the eyeball is affected. Lagophtbalmos results when the eyelids are also affected.
8. Tetanusmayfollowapplicationofherbalmedicineor scarrification marks.
9. Marjolin’sulcer: lfanextensiveulcerisallowedtoheal without grafting, the resulting scar or ulcer becomes unstable. This may lead to the development of squamous carcinoma.
10.Gangrene of pan or whole of a limb may result.
lI. Deathfromoverwhelminginfection has been reported

Question 26

State the clinical features of pre-ulcerative and ulcer- ativemycobacteriumulcerans disease and how it can be diagnosed
How can it be treated (with drugs and with surgery) and prevented

Answer 26

Diagnosis
I. Theclinical features of the pre-ulcerative and ulcer- ativemycobacteriumulcerans disease are characteristic espe- ciallyintheendemicareasandshouldbeeasytodiagnose. The diagnosis can usually be made by the patients themselves and bytrainednon-medical personnel.
2. AFB can easily be seen in Ziehl-Neelsen stained sections. ·
3. Swabs can be cultured using Lowenstein-Jensen me- dium.
4. Biopsyestablishesthediagnosis.
5. Polymerasechainreaction(PCR)issuitablefordetect- ingmycobacteriumulcerans intheenvironment. PCRtesting ispresentlyavailable in reference laboratoriesonly.
6. FBC,sickling,urineR/E and stoolR/E are done.

Management
Prevention
I. Althoughthemodeoftransmissionofthediseaseisnot emirelyknown,itisbelievedthatdirectinoculation intothe skinseems the most likely route. Wearing of protective ck>lhingandfootwear such as Wellington boots may reduce the riskofinoculation.
2. A better environmental and personal hygiene e.g. preventing patients with ulcers on their legs from walking in rivers,lakes,damsinorder tofetchdrinkingwatershouldhelp.

BCG Vaccination
Itappearstooffershort termprotection fromthedisease andreducesthe nunberof new cases. It is not clear, however, towhatextent it can control the disease.

Medical Treatment
Aclinical trial ofa combination of rifampicin and strepto- mycinin treating early buruli ulcer appears encouraging. A trial of rifarnpicin lOmg/kg body weight and streptomycin/ amikacin 15mg/kg for 4weeks, and not more than 12weeks, underdirect obervation is taking place under WHO supervi- sion.
If it proves effective, medical treatment will prevent recurrence, minimize the extent of surgical excision in ad- vancedlesions and avoid the needof sur gical treatment in early lesions.

Surgical Treatment
Jcdepends on the clinical stage of the disease. For fear of disseminating the bacilli, it is recommended that Esmach tourniqet.sshouldnot be used. Affected limbs can, however, be elevatedhighfor about 2min. and atouniquetappliedproximal tothelesionwithoutexsanguinating the limb and the lesion. This will help to control the bleeding since some of these lesionsare very extensive and bleed profusely.

1. Papule
   It is excised under local anaesthesia or destroyed using cryotherapy.
   2.
   Nodular disease
   i. The nodule is excised widely to include disease-free margin(nodulectomy), Localanaesthesiaisinfiltratedaway from the lesion.
   ii. Adequatehaemostasisissecuredtopreventhaematoma formation and other complications.
   iii. Primary closure of the wound is done. iv. Adequateanalgesiaforpainisgiven.
   v , The specimen is sent for histological confirmation.
   vi. The District Director for Health is notified.

Non-ulcerative plaque
Correction of anaemia if any.
iii) Wide excision to include disease-free margin is done. Split skin grafting of the defect is done immediately or when it is filled with granulation tissue i.e. in 2 to 3 weeks. The specimen is sent for histology.
iv) The limb is splinted in the position of function and physiotherapy started to prevent coruractures.
v) The District Director of Health is notified.
3.non ulcerative plaque
i.correction of anemia if any
ii.Administrationofa combinationofrifampicinlOmg/kg
ii)
and strepromycln/amikacin l 5mg/kg for 4 weeks and not more than 12 weeks under direct supervision. This results in partial resolutionof the lesion and allows demarcation of the necrotic tissue ensuring limited excision.
iii. i) Wide excision to include disease-free margin is done. Split skin grafting of the defect is done immediately or when it is filled with granulation tissue i.e. in 2 to 3 weeks. The specimen is sent for histology.
iv) The limb is splinted in the position of function and physiotherapy started to prevent coruractures.
v) The District Director of Health is notified.
iv.

4. Oedematous disease
   Same as in non-ulcerative plaque.
5. Ulcerative disease
   i) Extensive lesions such as ulcerated plaque and ulcer- ated oedematous disease should be admitted.
   ii) Where indicated, tetanus toxoid is given.
   iii) Appropriateantibiotics should be given where there is secondary bacterialinfection.
   iv) The wound is cleansed with normal saline but if it is infected with Ps. aeroginosa, with l % acetic acid. Slough is removed with normal saline or cut in the ward with scissors or excised in the theatre under general anaesthesia.
   v) Anaemiaiscorrectedandadequatenutritionprovided. Transfusion is given ifnecessary.
   vi) Theaffectedlimbissplintedinthepositionoffunction. Physiotherapy isstarted.
   vii)Split skin-grafting of the ulcer is done when the granulation tissue becomes healthy.

Someofthecomplicationsincludecontractures andsublux- ation of joints, loss of limbs e.t.c. These patients should be managed by a team made up of physiotherapists, a clinical psychologist, the District Director of Health Services, the Plastic Surgeon, the Orthopaedic Surgeon and a team from the Rehabilitation Department. Apart from the release of oontractures, tendon transfers, arthrodesisofjointsetc., these patientsmayalsoneedartificial limbs,trainingfornewjobs, l)S)thological support and support from the social welfare department and their own families.
Social problems
1. Extensiveulcersmayaffectschooling.
2. Affectedadultsmaybeunabletogoabouttheirnormal workwithresultantloss of income.
3. Severely affeced individuals may be marginalized in lhesocieiy.
4. Social integration of affected pauents is usually diffi- cult.
S. PatientsadmirtedtohospitaIoftenspendlongperiodsin M!pital. Affected children should have access to teachers.
6. Surgical treatment is expensive and not all pauents can afford it. This compels some to seek herbal treatment.

Question 27

State the diagnosis and treatment of syphilitic ulcers,yaws,mycobacterium leprae

Answer 27

SYPIDLITC (GUMMATOUS) ULCER
ltisnowuncommon. rtfollowsbreakdownofasubcutaneous gwnmaespeciallyaroundtheknee. hhasaserpiginous outline ~use asithealsinsomepartsitspreadsinothers.Theedge bpunchedout (Fig. 6-1). Thefloor iscoveredwithyellowish slooghandthedischarge is thick and foul-smelling.
llilgnosis:Apartfromthecharacteristiclesion,V.D.R.L. is stronglypositive. A biopsy specimen shows the typical histol- cgy.
Treatment: A course of penicillin. 4.YAWS(SeeCh. 2)
Yawswereeradicated bytheW.H.O. adecadeorsoago. llutlheyarereappearing. Thedisease iscaused byTreponema penenue. The primary lesion starts as a small erythematous maculcwhichbecomes an enlarging papule up to 5cm wide. Theskinoften ulcerates and exudes a serous fluid. It heals l!l(mleOUSly.
Inthe second stage single or multiple heaped up ulcers ippcareither around the primary lesion or all over the body. Ulctrationand secondary infection may occur. Resembling l)’philitic ulcers, they are punched out with sloughing base. Theyhealspontaneously after a fewweeks, theskin over them oftenbecoming depigmented. The regional Iymph nodes are marged.
Diagnosis: Thelesionsarecharacteristic. Treponemapertenue arefoundinthesmear indark ground illumination. TheKahn
Tratment: Penicillin (PAM) is very effective.
5. MYCOBACTERIUM LEPRAE ULCERS
Theseulcers take the form of chronic skin lesions, usually 1tOwiththedeformities caused byneurological lesions of
tubereuloid leprosy in peripheral nerves e.g. the claw hands (ulnar nerve) foot drop (common peroneal nerve). There is usually sensory impairment, so these arc functionally neuropathic ulcers. The ulcers, apart from c hroniciry and indolence, do not show particular features associated with specific ulcers.

Question 28

State and explain five complications of wound healing

Answer 28

Complications of Wound Healing
Infection: This enters via the primary wound and inter- feres with the healing process. A wound that is exposed to bacterial invasion goes through the phase of contamination, colonization,criticalcolonizationand infection,dependingon the risk of infectionand host resistance.In the first two phases thereis apostivebacterialbalancewhile thebalancebecomes negative in the last two.
Discharge becomes profuse, no clot forms and epithelial migrationis hindered.Tissuedeath occursandsloughsaccumu- late. Onlywhen this is shedwould adequategranulation tissue form. In effectinfectionconvenshealingbyprimarytohealing secondaryintention. Itmayspreadand becomesystemicifnot promptlytreated.
Keloidandhypertrophicscarformation:
(Fig. 16-1) These are due to excessive fibroblasticactivity withmarked granulationtissue formationresultingin a mark-
edlyraisedscar.Theexactcauseisunknown.Negroesordark skinned people are predisposed to this and there may be a genetic basis. Keloid are particularlyliable to occur in the scarsofburns. Ageisimportant,theconditionoccurringmore often in younger people. T he ear, beard area, neckand chest areas are frequent sites for such lesions (See Chapte r 16)

Cicatrization : Continued thickening and shortening of collagen may on occasionproduce contractureswhich later embarrassfunction. The deformity so produced is frequently gross withuntowardeffectsonfunctione.g. distortionoflimbs, or stricture formation in important organs - oesophagus, intestine, and urethra.

Lymphoedema: may occur from recurrent bacterial lymphangitisand Iymphadenitisandensuingchronicblockage of the lymphatic drainage pathway. This causes initially pitting oedema which becomes “organized” with attendant nodular and cicatrial disfigurement.

Hyperpigmentation: It frequently occurs at sites of chronicscars. Depositionof degradationproductsofhaemoglo- bin probably contributesbut the exact cause is uncertain.
Implantation cysts: These are the result of epithelial elementspenetratingthe woundand proliferatinginsitu to form epidermoidcysts. Such mayoccur along stitchtracts.
Neoplasia:Theintensecellular proliferationandmigration that characterizeshealing tissues is reminiscentof embryonic activityor the uncontrolled growthof a neoplasm. The impor- tantdifferenceis thefactorofcontrol.Inahealingwound,the embryonicstatusistemporary,a restingstate is sooninduced presumablyby contactinhibition and remodellingensues

Question 29

State and explain advances in wound healing

Answer 29

ADVANCES IN WOUND HEALING
Woundfailureornon-healingistheresultofan impairment
in one or more of the biological processesdiscussed under the
widerangeoflocal andgeneralfactors.Inviewofthemulti-
factorial nature of this, management must perforce be
interdisciplinary, Thus at the very onset of therapy the
vascular(varicoseveins andvenous insufficiency,ischaemia),
metabolic (diabetes mellitus), nutritional, neurological and
baemotological contribution to the chronicity should be
determined.

i) Debridement:
As a first stepchronicwoundsshouldbe cleanedof necrotic or fibrinousdebriswhichactasbarrier toformationofhealthy granulationtissue. Debridementcan be carriedoutmechnically, enzymatically,autolyticallyor surgically. Criticallycolonized wounds needtobetreatedwithantisepticsinorder to prevent or limitdevelopmentof infection;usefulagents includeiodine,
in form ofpovidone iodin eor iodophors and silver in formof sulpbadiazineor nanocrystallinesliver.These are not without side-effects,sotheir usemustnotbe prolonged. Hydrogels, ie non-adhesiveabsorbentsheet-likegels, as wellashydrocolloids are frequently used. In autolytic debridementthe naturalself clearance of debrisin the wound bed byphagocyticcells and endogenousproteolyticenzymesisenhanced.Thisprocesscan be promotedandenhancedby maintainingamoistenvironment using occlusive dressings

tissue.
(ii) Induction of granulation tissue
Oncethewoundisclean, awide variety of wounddressings whichareclaimed to stimulate granulation tissue formation canbe applied. They act as a barrier between wound and environmentpreventingtissuedryingand infection,maintaining qitimally moist environment using occlusive dressings. H)’drocolloids, alginates, microporous polyurethane foam dressingsandhyaluronicacidbasedblomaterials areproving usefulagents.
(ill) Induction of re-epithelializatlon
Themost clean wound environment is ideal for efficient epithelialization.Recentabsorbentpolymers (Tendawet)that areablecobind the wound exudate in exchange for Ringer’s solutionareproving effective.
Furlherstrategiesto healchronic wounds have emerged, notablygrowth factor therapy and use of biological skin subslilutes. Growth factor topical preparations eg. keraJinocytegrowth factor 2 (KGF2), have been used to atcelerate the healing process co

Question 30

State how wound healing occurs in some special tissues such as skeletal,gastrointestinal,sutured blood vessels

Answer 30

HEALING IN SPECIAL TISSUES
The general principles so far discussed in connection with skin, subcutaneoustissuesandfasciaeapplytoallbodytissues but there are modifications relating to specific tissues.
In skeletal muscle tissue, fibroplasia is prominent but some attempt at replacement is indicated by budding and outgrowth of the living ends of the divided muscle fibres. Regeneration isimperfectfortheorientation ofthefibresis disturbed and much of the replacement is by fibrous tissue.

In sutured blood vessels, fibroblastsform the basis upon whichthe sproutingendothelialcells advance iJ1the wound.

The gastro-intcstinal mucosa, particularly stomach and intestine, heals by regenerationof theepithelial cellsand even the specializedsecretorycellsare restored.The muscular andserosalcoatshealbyfibrous tissuewhichisresponsiblefor the resulting surfacedeformity and strictures.
In the repair of bone, rhe phenomena of haematoma formation,absorptionofdebrisandstructuraltissueproduction proceed with the modification that specialized cells, namely osteoblasts, rake the place of the fibroblasts and lay down matrix which is subsequently converted to bone.
The essential element of the proliferative phase is the building of callus formed by the pluripotential cells fromthe periosteumandevidentfromthethirdandfourthdayofhealing (radiological)aftertwoweeks.

fibrocartilage.
Tendon healsbypassingthroughallthestagesmentioned earlier. Theinflammatoryphasecontinuesforupto10days-, Fibroblasts arise from the tendon itself or from surrounding connective tissue.

Question 31

The ideal suture material has what features?
Why are monofilament sutures better than multifilament sutures
State three absorbable and four non absorbable sutures and explain how they work
State the advantages of metallic sutures

Answer 31

Suture materials and wound healing
The ideal suture material has the following features:- (i) Itiscompletelyinert,itspresenceexcitinglittleorno
reaction in the tissues of the wound

ii) It does not affect the tensile strength of the wound

There are several gauge sizes of suture material but the finest are preferred as they cause least tissue reaction. Monofilament sutures are also better than multifilament or twistedonesastheydonotharbourbacteria anddonotexert a capillary or wick-like action.

Absorbable sutures
Catgut is made from the submucosa of the small intestine of sheep or from the serosal layer of cattle intestine. It may be twisted, dried and sterilized - plain.catgur - or tanned with chromicacid beforesterilization-chromiccatgut. Plaincat- gut produces intense inflammatory reaction in the tissuesand sodelayswoundhealing.Italsoimpairswoundtensilestrength. It is digested in 5-6 days; its tensile strengthis indeed zero in 3-6 days. Chromic catgut excites tissue reactionwhich is not assevereasthatofplaincatgutbutsufficienttodepress wound tensile strength. It loses its tensile strength by 21 days about

which time it is usually absorbed.
Reconstituted collagen is another naturally occurring
absorbablesuturematerialderivingfromsheepmucosaorthe tendons of caule with features similar to those of catgut. Althoughit ismorepredictable inthe patternofweakeningof itstensilestrength,itisnotsofrequentlyused.Ithasbeenused as a fine suture for the eye.
Alsoavailableare severalsyntheticabsorbablesuturesof which polyglycolicacid (PGA, Dexon), polygJactin 910 (Vicryl)andpolydioxanone(PDS)arenotablefortheirtensile strengthandductilenature.Thesehave thepotentialadvan tagesofpredictablelossoftensilestrength, (halflostin28-56 days),good handlingabilityand lesspotentiation ofsepsisthan
catgut.Theinflammatoryreactionislessseverethantheother biodegradablesutures because the synthetic materialunder· goes hydrolysisrather than proteolytic digestion. In a sense, theseobservationsrendercatgutanobsolescentsuturethough theessentialconservatismofsurgeonsmayresultonlyinaslow move from the traditional material. Recent experienceof disease has led to virtual precipitate withdrawal of catgut in Europeand North America.

Non-absorbable sutur es
Thesegenerallyhavenoeffectonwoundtensilestrength. Silkand cottonare naturalproductswhilenylon,polypropylene and dacron are syntheticproducts.
Silk is an animal protein and excites moderate tissue reaction.It may fragmentand be slowlyabsorbedandextruded. Its tensile strength is thus progressively lost. Its other disadvantagestems from its multifilament nature; it may harbourbacteriaandithasawick-Iikeactionwhenusedasskin suture.
Cotton causes a greater tissue reaction than silk. Its tensilestrengthdiminishes more rapidly than silk reaching about50 per cent at 2 years.

Nylon
Monofilamentnyloncausesonly a slight inflammatory reaction. It remains intact and maintains its tensile strength almostindefinitely.ItSmaindisadvantageisthepoorhandling ability; the knots tend to slip. Braiding in the form of multifilamentnylonmaymarginallyimprove this. M ultifila- mentnylonontheotherhandcausesseveretissuereactionand loses its tensilestrength rapidly. It may also harbour bacteria.

Polypropylene:There is little tissue reaction to this suture but it may occasionallyfragment. Its tensile strength is on the whole retained much longer than obtains with nyIon.
Dacron, Teflon and Orlon cause very little tissue reactionholdingontotheirtensilestrengthoverlongperiods. Dacronor Teflonis oftenpreferredto nylon in theserespects.

Metallic sutures
Stainless steel wire is remarkably inert and maintainsits tensile strength for a long period. It eventually fragments
however and may cause undue pain
It’s main diss advantage is difficulty in knotting

Aluminiumwire is equally inert and has been found to maintain its tensile strength for much longer. The tensile streogthofwoundssuturedwith aluminium rises more rapidly alremainsoonsistentlyhigher longafter the sutures have been removed.Thisisbelievedtobeanelectrochemicaleffect of the metal on the tissue fluids

Clips and Staples
Clipsandstaplesarerapidlyreplacing ligatures andsutures in!Olllecircumstances.Mostligature clips aremade of metal, aresuitableonlyfortheocclusion ofsmallstructuresandcan mwhateasilybedislodgedwhen caught upinaswabduring subsequent dissection. New absorbable clips made of poljl!ioxanoneandwithalockingdevice are nowon the market. Theyareparticularlyuseful where non-absorbable material shouldbeavoidedasinthebiliary andrenal tracts.
Funhermore,devicestoapplyindividual staples forbowel closureandvascular anastomosis are gaining popularity. StJples are particularly suitable for closing skin wounds, peoetralingnofurtherthanthedermisandtherefore lesslikely toieal’epermanentmarksacross a wound. The high cost of lhesesutures,however, relatively limits their application in diedevelopingworld.

Skin tape
Thisisanon-suturemethodof closing woundedges.
The tape is microporous and adhesiveand isappliedtotheskinafter adequatesubcuticular closure of the deeper layers of the wound.
lnfectionisminimalasthereisnoburiedsuturethrough theskintoexcitetissue reaction. The tendency to epithelial
dov.ngrowthsalongneedletracks isalsoavoided.

Skin adhesives
Thesearesuperglues made often from cyanoacrylates. Theynoconlyactassubstitutes forskinclosurebuttheyalso assistinholdinggraftsonthe bed.

Question 32

QUESTION 1) A 71year old man , known diabetic and hypertensive presented to the clinic with 6x6cm ulcer at the medial aspect of the right foot. Examination of the ulcer by the surgeon in charge revealed a chronic ulcer with malignant changes and bone exposure.
a) Outline with explanation the causes of leg ulcer.
b) Outline with explanation the investigation you would request for this man.
c) Discuss the management of the ulcer