The document provides an overview of the etiopathology and management of chronic leg ulcers. It begins with an introduction and classifications of chronic leg ulcers. It then discusses the pathophysiology and pathology of various types of ulcers including venous, arterial, diabetic foot and neoplastic ulcers. The management involves taking a thorough history, examination, investigations to determine the cause, and multimodal treatment including wound care, debridement, offloading, antibiotics and addressing any underlying conditions or complications. The document concludes with a discussion of prognosis and future trends in chronic leg ulcer management.

1. AETIOPATHOLOGY
AND CURRENT TREND
IN THE
MANAGEMENT OF CHRONIC
LEG ULCERS
PRESENTER:
EZEAKU CHIZOWA
1

2. • INTRODUCTION
• CLASSIFICATION
• PATHOPHYSIOLOGY/PATHOLOGY
• MANAGEMENT
• COMPLICATIONS
• PROGNOSIS
• FUTURE TRENDS
• CONCLUSION
• REFERENCE
2

3. INTRODUCTION
• Chronic leg ulcer is defined as a defect in the skin below the level of
knee persisting for more than six weeks and shows no tendency to
heal after three or more months.
• Chronicity results from prolonged inflammatory phase which leads to
overgrowth of granulation tissue.
• CLU is reported to have impact on virtually every aspect of daily life:
pain is common, sleep is often impaired, mobility and work capacity
tend to be restricted, and personal finances are often adversely
affected.
3

4. EPIDERMIOLOGY
• Chronic leg ulcers affect 0.6–3% of those aged over 60 years,
increasing to over 5% of those aged over 80.
• It is thought that the incidence of ulceration is rising as a result of
aging population and increased risk factors for atherosclerotic
occlusion such as smoking, obesity, and diabetes.
• It has been reported that ulcers related to venous insufficiency
constitute 70%, arterial disease 10%, and ulcers of mixed etiology
15% of leg ulcer presentations.
4

5. Factors leading to chronicity
• Recurrent infection
• Foreign body
• Trauma
• Absence of rest
• Poor blood supply
• Oedema of the area
• Loss of sensation
• Malignancy
• Specific etiology with chronic course eg Tuberculosis
• Fibroses, chronic inflammation
• Periosteitis , osteomyelitis
5

6. Characteristics of an ulcer
• An ulcer has the following features:
• Edge: It is where the healthy skin (epithelium) begins. Area between
the margin and floor.
• Floor: It is what is seen.
• Base: Area on which the ulcer rests. It is what is palpated.
• Margin : Junction between normal epithelium and ulcer. It may be
regular or irregular. Rounded or oval
6

7. Classification of ulcers
• A . Specific ulcers:
• I. Tuberculous ulcers.
• 2. Buruli ulcers.
• 3. Syphilitic ulcers.
• 4. Yaws ulcers.
• 5. Mycobacterium Leprae ulcers
7

8. • B. Non-specific ulcers:
• 1. Traumatic ulcers.
• 2. Pyogenic ulcers.
• 3. Ulcers of vascular origin:
• (i) Venous (gravitational) ulcers. (ii) Arterial ulcers. (iii) Decubitus ulcers. (iv) Pressure
sores.
• 4. Neurotropic (trophic) ulcers:
• (i) Leprosy. (ii) Diabetic neuropathy. (iii) Cord lesions. (iv) Peripheral neuropathies.
• (v) Syringomyelia.
• 5. Ulcers associated with metabolic or systemic disease:
• (i) Diabetic ulcers.
• (ii) Haemoglobinopathic ulcers.
• (iii) Ulcers of spherocytosis.
• (iv) Ulcers of ulcerative colitis.
8

9. • C. Neoplastic ulcers:
• l. Squamous cell carcinoma.
• 2. Rodent ulcer.
• 3. Malignant melanoma.
• 4. Kaposi's sarcoma.
• 5. Penetrating malignant tumour
• 6.Marjolins ulcer
9

10. PATHOPHYSIOLOGY/PATHOLOGY
• Specific ulcers are due to specific causative organism.
• Neoplastic ulcers are usually seen in the context of genetic mutation
and predisposing risk factors
• Non specific ulcers:
• There are several causes. The distinctive feature is a sloping edge. The ulcer
goes through the following phases.
10

11. PATHOPHYSIOLOGY/PATHOLOGY
• 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 in which different types of bacteria may be identified. The
edge is sharp and surrounded by damaged cells. The surrounding skin
• is oedematous, warm and tender.
11

12. PATHOPHYSIOLOGY/PATHOLOGY
• 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. The surrounding skin slightly hyperaemic or normal.
12

13. PATHOPHYSIOLOGY/PATHOLOGY
• Reparative or healing phase:
• The ulcer is now painless. The healthy granulation tissue fills the floor
and the epithelium grows from the edge at the rate of Imm/day to
cover the floor.
13

14. PATHOPHYSIOLOGY/PATHOLOGY
• Chronic, indolent or callous phase:
• Some ulcers may enter a chronic phase and remain unhealthy for a long
time because of factors leading to chronicity. The edges are then ragged,
the floor greyish or creamy pink and bathed with profuse offensive,
yellow discharge and the surrounding skin warm and oedematous.
• In a long-standing ulcer -indolent or callous ulcer - fibrosis of the floor
causes induration of the base, the floor has unhealthy greyish fibrotic
granulation, the borders are rigid and hard and the epithelium 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.
14

15. PATHOPHYSIOLOGY/PATHOLOGY
• Venous ulcers:
• Seen in the setting of chronic venous hypertension and valvular
incompetence.
• There are three major theories of how ulceration develops.
• (1) Fibrin cuff theory: Fibrinogen leaks from dilated capillaries of the
epidermis forming a pericapillary fibrin cuff. This is then responsible for a
reduced diffusion of oxygenated blood to the tissues resulting in ulceration.
• (2) Microangiopathy theory: it has been demonstrated that some of the
capillaries in patients with venous leg ulcers are occluded by microthrombi
or exhibit long intracapillary stasis. This in turn can reduce nutrition and
oxygenation of the skin, predisposing to ulceration.
15

16. PATHOPHYSIOLOGY/PATHOLOGY
• Venous ulcers:
• (3)Leukocyte entrapment theory: Venous hypertension reduces the
pressure gradient between the arteriolar and venular end of the
capillaries. This results in sluggish movement of the blood within
these capillaries and increases the adherence of blood cells to the
endothelium. Inflammatory mediators (ICAM-1, VCAM-1) and
reactive oxygen species are then released resulting in the obliteration
of functioning capillary loops aggravating ischemia and result in
ulceration
16

17. PATHOPHYSIOLOGY/PATHOLOGY
• Arterial ulcers:
• Arterial leg ulcers occur as a result of reduced arterial blood flow and
subsequent tissue perfusion.
• There are three mechanisms involved in the pathophysiology :
• (1) extramural strangulation
• (2) mural thickening or accretion, and
• (3) intramural restriction of blood flow
• . There is often considerable overlap, and the exact pathogenesis cannot be
always well defined. Most acute forms of vasculitis and some subacute and
chronic forms are likely to cause leg ulceration due to tissue hypoxia and
exudation of fibrin-like substances.
17

18. PATHOPHYSIOLOGY/PATHOLOGY
• Diabetic foot ulcer:
• The diabetic foot is characterized by infection, ulceration and/or
destruction of deep tissue in the foot, and is usually associated with
neurological abnormalities and varying degrees of peripheral vascular
disease in the lower limb
18

19. PATHOPHYSIOLOGY/PATHOLOGY
• Diabetic foot ulcer:
• Peripheral neuropathy
• Vascular occlusion of vasa nervorum
• Endothelial dysfunction
• Effects of increased sorbitol and fructose
• Deficiency of myoinositol –altering myelin synthesis
• Diminished Na-K-ATPase
• Peripheral vascular disease
• Atherosclerosis and ischemic changes, glycosylated Hb
• Infection
• Rich culture media(sugar and dead tissue),reduced leucocyte function, polymicrobial
19

20. Triad of sin…….
20

21. PATHOLOGY
• Macroscopy:
• Hyperpigmentation
• Hyper keratosis
• Dyschromia
• Contractures
• Fibrotic ulcer margins
• Induration
• Woody hard swelling of the leg
21

22. PATHOLOGY
• Microscopy
• Features of chronic inflammations(macrophages,lymphocyte,plasma
cells, angiogenesis and fibrosis)
• Features of malignancy..pleomorphism, cellular atypia,
hyperchromatic nuclei,etc
22

23. Management
• Adequate and elaborate history
• Detailed examination
• Differential diagnosis
• Proper investigations and,
• Multimodal treatment
23

24. History
• Biodata (Age, occupation)
• Complaints: sore or ulcer of at least 6 weeks duration.
• Site :gaiters area(venous),bony prominence (pressure),
• The mode of onset- painful blister and rupturing is most likely
tropical; one after an abscess or cellulitis,' infective or pyogenic; one
after an injury, traumatic; one with intermittent claudication and a
black patch, arterial; and one after deep venous thrombosis, venous
arising from mole, scar tissue,recurrence, malignant.
24

25. History
• Progression :-An actively spreading ulcer may be due to infection, poor blood
supply or malignancy.
• Pain: If painful tropical, pyogenic, arterial or venous ulcer is suspected. Absence
of pain suggests a neuropathic lesion.
• Discharge :
• a. Serous: In healing ulcer.
• b. Purulent: In infected ulcer.
• Staphylococci: Yellowish and creamy, Streptococci: Bloody and opalescent
• Pseudomonas: Greenish colour due to pseudocyanin
• c. Bloody: Malignant ulcer, healing ulcer from healthy granulation tissue.
• d. Seropurulent
• e. Serosanguinous: Serous and blood
• f. Serous with sulphur granules: Actinomycosis
• g. Yellowish: Tuberculous ulcer
25

26. History (Aetiology)
• (a) Diabetes - polydipsia, frequency, weight loss.
• (b) Tuberculosis-night sweats, weight loss, anorexia, chronic cough.
• (c) Venous ulcers - painful swelling of a leg after child-birth or
operation(DVT), varicose veins(dilated, tortuous, elongated ,palpable)
• (e) Arterial disease - intermittent claudication, claudication distance, rest
pain paraesthesia, loss of skin appendage, cold extremities.
• (f) Haemoglobinopathy- attacks of joint and muscle pain especially during
the cold or rainy season, weakness, yellowness of the eyes
• (g) Neuropathy - loss of pain sensation in the limb, history of leprosy, nerve
or spinal injury.
• (h) Yaws - history of previous granulomatous lesions of the skin.
• (i) Syphilis - history of a previous chancre and secondary rash.
• (J)malignancy-weight loss, anorexia, low back pain, recurrence, scar tissues
26

27. History (complication)
• Fever(infective process, septicaemia)
• Weightloss.,recent cough(malignancy)
• Peripheral swelling(lymphedema)
• Inability to use the limb
• Deformity of foot and ankle(Contractures)
• Discharging pus, bony spicules(Osteomyelitis)
• Painful red streaks(lymphangitis)
• Groin swelling(lympadenitis,>>>>mestatasis)
27

28. Other relevant history(conditions leading to chronicity)
• PMH
• : DM, malnutrition, malignancy, RVD, SCA, PVD,CKD, Htn(Martorell ulcers)
• Drug history:
• Steroids,Cytotoxic drugs,beta-blockers
• FSH:
• Cigarette(nicotine retards wound healing)
28

29. PHYSICAL EXAMINATION
• General examination: chronic ill looking, pallor, fever, jaundice,
peripheral lymphadenopathy,
29

30. Examination of ulcer
• Inspection:
• Number:- Multiple ulcers may be due to Kaposi's sarcoma, yaws,
spherocytosis, ulcerative colitis or self inflicted injuries.
• Anatomical site.- An ulcer near the medial malleolus may be venous,
traumatic or due to S.S. disease. An ulcer on the toes or dorsum of the
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 syphilitic and one in the groin or neck probably
tuberculous.
30

31. Examination of ulcer
• Size :
• Venous ulcers(flat, shallow, usually do not penetrate deep fascia)
• Arterial ulcer , diabetic ulcers ,penetrate deep fascia and expose underlying
structure
• Shape :
• Whether round, oval irregular or serpiginous(syphilitic).
• Floor :
• Whether sloughy and-discharging, granulation tissue- clean, pink,
flattened, minimal bleeding-(healthy) or nodular (malignant).
• The type of discharge is also noted.
31

32. Examination of ulcer
• Edge :
• Sloppy-healing, traumatic and venous
ulcers.
• Punched out- syphilitic, yaws, trophic
ulcers.
• Raised and everted-squamous cell
carcinoma.
• Raised and rolled –basal cell carcinoma
• .
• Undermined –Mycobacterial, eg
tuberculous ulcers.
32

33. Examination of ulcer
• Surrounding skin
• Features of inflammation and chronicity.
• Blow out veins, atrophie blanche, stasis dermatitis, lipodermatosclerosis
suggests venous ulcer.
• Skin with loss of hair on the leg, thin shiny skin, brittle nails with transverse
ridges suggest arterial ulcer.
33

34. Examination of ulcer
• Palpation :
• Differential warmth(cold-arterial)
• Tenderness(neuropathic ulcers usually painless)
• Base :induration, mobility or attachment of the ulcer
• Slightly indurated in chronic non specific ulcers, indurated and fixed as in carcinoma or callous
non specific ulcer
• Peripheral pulses-dorsalis pedis and posterior tibial..etc
• Sensation of the dermatomes of limb
• Joint –range of motion
• Regional lymphnodes
• Check for gait
• EXAMINATION OF OTHER SYSTEMS
34

35. Arterial ulcer
35
Venous ulcer

36. DIFFERENTIAL DIAGNOSIS
• SEE CLASSIFICATION
36

37. INVESTIGATIONS
• LOCAL DIAGNOSTIC INVESTIGATIONS
• Wound biopsy M/C/S, Cytology and AFB.
• Wound biopsy and histology(wedge).
• INVESTIGATIONS TO ASSESS EXTENT OF THE DISEASE
• Plain radiograph of the affected limb
• FNAC of enlarged lymphnode
• INVESTIGATIONS OF SPECIFIC ETIOLOGY
• Chest xray- TB
• Mantoux test –TB
• Fasting blood sugar, urinalysis- DM
37

38. INVESTIGATIONS
• Arterial or venous Doppler/duplex scan
• Angiogram-vascular ulcers
• HB genotype-sickle cell disease
• VDRL-syphilitic ulcers
• BASELINE INVESTIGATION
• FBC +ESR, EUCr, ECG
38

39. TREATMENT
• Treatment is multi disciplinary and depends on the etiology of the
ulcer.
• It involves plastic and reconstructive surgeon, vascular surgeon,
orthopedic surgeon, wound care specialist, hematologist,
rheumatologist, endocrinologist ,podiatrist , physiotherapist etc
39

40. General Principles of treatment
• Establish the cause and treat it
• Care for the ulcer
• Rest affected part (offloading)
• Debridement
• Wound care and dressing
• Wound closure
• General measures
• Correct anaemia, transfuse where necessary
• Correct deficiencies like protein,vitamins
• Control pain
• Antiobiotics(iv or oral)…control infection
40

41. Relief of pressure
• Off-loading: is the avoidance of all mechanical stress on the
wound
• Techniques:
• total contact casts (TCC) ……”gold standard”
• Instant TCC
• Removable contact walkers (RCW)
• surgical shoes
• walkers
• healing sandals/ half shoes
• felted foam dressings
• bed rest.
• Crutches
• Wheel chairs
• The method of choice is determined by the location of the
wound and by the patient's level of activity.
41

42. Debridement
• Surgical
• Enzymatic
• Autolytic
• Mechanical
• Biologic
42

43. Removal of necrotic tissues - debridement
• Surgical sharp debridement.
43

44. Removal of necrotic tissues - debridement
• Enzymatic
• Relies on the addition of proteolytic and other exogenous enzymes to the
wound surface.
• Can be effectively combined with moist wound dressing.
• Enzymes are inactivated by heavy metals (silver, zinc), which may be
introduced from some wound care products, such as antimicrobial
dressings (e.g. Acticoat, silvadene). Detergents present in skin cleansing
agents may also inactivate enzymes.
• Examples – 2 common ones
• papain-urea based combinations (Accuzyme[R], Panafil®) - Papain breaks down any
protein with cysteine residues, rendering it a non-selective debriding agent.
• collagenases (Santyl®).
44

45. Removal of necrotic tissues - debridement
• Autolytic:
• This process relies on enhancing the natural process of selective
liquefaction, separation and digestion of necrotic tissue and eschar
from healthy tissue that occurs in wounds because of macrophage
and endogenous proteolytic activity.
• Requires provision of a moist wound environment and, as such, is
likely to be integral to wound care management. The use of occlusive,
semi-occlusive or moist interactive dressings can both promote
phagocytic activity and the formation of granulation tissue. Autolytic
debridement is recognized to be effective in the maintenance phase
of debridement.
45

46. Removal of necrotic tissues - debridement
• Mechanical:
• This is the use of non-discriminatory physical force to remove necrotic
tissue and debris from the wound surface. In its simplest form,
mechanical debridement involves the use of wet-to-dry dressings which
unselectively remove tissue, both healthy and necrotic, at dressing
changes.
• It is painful, can damage healthy tissue and may lead to wound
desiccation.
• Alternative methods:
• wound irrigation, ranging from cleansing to pressure irrigation, whirlpool therapy,
ultrasonic therapy and laser therapy
46

47. BIOLOGIC
Removal of necrotic tissues – application of larval (maggot)
therapy
• Biosurgery uses the larvae of the green bottle fly (Lucilia sericata) to debride selectively
any sloughy tissue without attacking healthy granulation tissue. Larvae are bred under
sterile conditions and the maggots don’t digest healthy tissue or burrow into the skin.
• Disinfect by secreting ammonia which increases Ph and substances inhibitory to bacteria
• The healthy skin surrounding the ulcer is covered with a hydrocolloid dressing to protect
it from the proteolytic enzymes produced by the larvae. The larvae are secured in the
wound under a fine mesh net to prevent escape. Moist gauze swabs are placed over the
net and changed on a daily basis to prevent the larvae from drying out.
• A fresh application of larvae is used twice a week after the old larvae have been removed
with forceps or flushed out of the wound with sterile saline. Larval therapy is used until
healthy granulation tissue has formed and conventional dressings can then be applied as
appropriate.
• Contraindicated in wounds with bleeding tendency, communicating with body cavity 47

48. Wound care (dressing)
• THE IMPORTANT CRITERIA FOR OPTIMAL WOUND DRESSINGS
• Remove excess exudate and toxic components.
• Maintain high humidity at the wound/dressing interface.
• Allow gaseous exchange.
• Provide thermal insulation.
• Protect from secondary infection.
• Free of particulate or toxic contaminants.
• Allow removal without trauma at dressing change.
• Antimicrobial properties.
• Should maintain optimum pH of wound environment (acidic).
• Should meet the person's needs i.e., suit their lifestyle, aesthetic
sensibilities.
48

49. Classification of dressings
• Films (opsite,tegaderm)
• Foams(lyofoam,Allevyn)
• Hydrogels (intrasite, duoderm)
• Hydrocolloids(granuflex, comfeel)
• Alginates(kaltostat, algistat)
• Medicated dressings.
49

50. • Tissue involved
• State of healing
• Aetiology of wound
• Environment and care giver
• Healthcare system.
Selection of wound dressings
50

51. 51

52. Wound care
• Antiseptics
• Honey
• Growth factors
• Bioengineered tissues / living skin equivalents
• Hyperbaric oxygen therapy (HOT)
• Negative pressure / vacuum assisted closure (VAC)
52

53. Wound care
• ANTISEPTICS
• Antiseptics are chemical agents that slow or stop the growth of micro-
organisms (germs) on external surfaces of the body and help prevent
infections. Antiseptics should be distinguished from
• Antibiotics that destroy micro-organisms inside the body, and from
• Disinfectants, which destroy micro-organisms found on inanimate
(non-living) objects. However, antiseptics are often referred to as skin
disinfectants.
• Common examples – EUSOL, H2O2 (cytotoxic to fibroblasts).
• Generally reduce bacterial burden and removes slough.
53

54. Wound care
•Honey
• c.50 AD,
Dioscorides
described honey as
being "good for all
rotten and hollow
ulcers
• antibacterial
property of honey
was first
recognised in 1892
by van Ketel
• potency rating called a UMF (Unique Manuka Factor). UMF graded honey is
also sterilised by gamma irradiation without loss of any antibacterial activity.
• High osmolality: The lack of ‘free’ water inhibits the growth of
microorganisms.
• Antinflammatory activity
• Hydrogen peroxide: When honey is diluted by wound exudates,
hydrogen peroxide is produced via a glucose oxidase enzyme
reaction. This is released slowly to provide antibacterial activity
but does not damage tissue.
• Antibacterial phytochemicals..
• In addition to its antimicrobial properties, honey also appears to
stimulate lymphocytic and phagocytic activity (0.1%).
At 1% ,monocytes are stimulated to produce cytokines, TNF-α,
IL-1 & 6.These are key body immune responses in the battle
against infection.
• Deodorizing agent
• Hygroscopic agent
54

55. Wound care
• Growth factors
• Recombinant human PDGF
• Chemotactic
• Mitogenic
• Angiogenic
• Stimulatory
• E.g Becaplermin gel (repagrinex ®)
• Requires removal of necrotic and fibrotic tissues
55

56. Wound care
• Bioengineered tissues / living skin equivalents
• Apligraft
• Cultured living epidermis and dermis from neonatal foreskin
• Dermis
• Allogenic living-dermis equivalent derived from human fibroblast.
• e.g. - Dermagraft
56

57. Wound care
• Hyperbaric oxygen therapy (HOT)
• Useful in well vascularized wounds.
• HOT increases oxygen tension, promotes angiogenesis , collagen
synthesis and re-epithelialization thus leading to improved wound
healing.
57

58. Wound care
• Negative pressure / vacuum assisted closure (-125mmHg)
• Used in extensive wounds with unhealthy granulation, cavity wounds
• Benefits
• Helps promote granulation tissue formation
• Decrease bacterial burden
• Reduces local / interstitial oedema
• Increases local blood flow
• Reduces dressing frequency
• Contraindications
• Malignancy, necrotic tissue, active bleeding, potential for post op. haemorrhage,
devitalised,fibrotic and dessicated wound
58

59. Negative pressure / vacuum assisted closure
59

60. Wound closure
• Surgical treatment is only indicated
• If defect >5cm
• Failure of non operative treatment
• Involves secondary suturing, skin graft/ flap
• Meshed grafts are more successful than sheet graft
60

61. Role of antibiotics
DEPENDS ON SENSITIVITY PATTERN OF CULTURED ORGANISMS
Oral Vs. IV Antibiotics
• Choice is dependent on a host of factors:
• severity of infection,
• spectrum of activity of antibiotic
• patient's overall health status and
• bioavailability of the antibiotic.
• Oral antibiotics are indicated for
• outpatient treatment
• treatment of early infections
• uncomplicated skin and soft tissue infections.
• Mild infections with minimal amount of cellulitis
• Intravenous antibiotics are indicated for the
• treatment of limb-threatening infections
• a failed course of oral therapy
• many antibiotic resistant bacteria .
• The use of topical antibiotics can assists to decrease the bacterial burden (bioburden) of
wounds. 61

62. Venous ulcers(Specific)
• The prime aim is to improve venous drainage and so improve
oxygenation and nutrition of the affected tissues.
• In addition to general principles
• Limb elevation
• Graded Compression bandaging (40mmhg at ankle, 14mmhg at calf)
• Containdicated in ABI<0.8
• Regular wound dressing with saline and honey.
• If failure,
• Varicose vein surgeries(ligation ,stripping,foam sclerotherapy,laser ablation etc)
• Venous valve surgery
62

63. Arterial ulcers(Specific)
• In addition to general principles
• Risk factor modifications(stop smoking, control
hyperlipidemia,hypertension etc)
• Regular graded exercise within limits of pain and tolerance.
• Blood supply may be improved by transluminal angioplasty,
endarterectomy or arterial grafting.
63

64. Diabetic ulcers(Specific)
• Restoration of skin perfusion
• Graded compression bandaging
• Improve metabolic control(glycaemic control)
• Treatment of co-morbidities
• Psycho-social support
• Education
64

65. COMPLICATIONS
• 1. Septicaemia
• 2. Lymphangitis
• 3. Lymphadenitis
• 4. Wasting
• 5. Tetanus
• 6. Lymphoedema
• 7. Periostitis
• 8. Malignant change
• 9. Deformities of the foot or ankle may occur if deep tissues are involved in
the fibrosis
65

66. PROGNOSIS
• Generally prognosis depends on aetiology.
• Specific and non specific ulcers have favourable outcomes, when
aetiology-specific treatments are instituted.
• The outcome of neoplastic ulcers usually are unfavourable due to
late presentation.
66

67. FUTURE TREND
• (1)The discovery of miRNAs has opened up vast therapeutic opportunities.
Knowledge of miRNA function in the regulation of wound healing and
developing improved miRNA modulation techniques in the skin will help in
translating this knowledge into more effective therapies.
• (2) Chronic wounds are characterized by changes in cell receptors (integrins).
The activation or inhibition of integrin receptors by various agents may
provide an excellent means of influencing wound healing.
• (3)Venous leg ulcers can be healed with a spray formulation of allogeneic
neonatal keratinocytes and fibroblasts without the need for tissue
engineering, at an optimum dose every 14 days.
• (4)Stem cell-based therapies.
• (5) Electrical stimulation has been demonstrated to enhance wound healing.
67

68. Conclusion
• As many factors lead to chronic leg ulceration, an interdisciplinary
approach to the systematic assessment of the patient is required, in
order to ascertain the pathogenesis, definitive diagnosis, and optimal
treatment.
• A correct diagnosis is essential to avoid inappropriate treatment that may
cause deterioration of the wound, delay wound healing, or harm the
patient.
68

69. REFERENCE
• Kahle B.O,etal: “Evidence-based treatment of chronic leg ulcers,”
Deutsches Ärzteblatt International, vol.108, no. 14, pp. 231–237, 2011.
• Archampong E.Q., etal: Cutaneous Ulcers, Sinuses and Fistula. Baja’s
Principles and Practice of Surgery including Pathology of the Tropics, 5th
edition, 2015: pg 72 – 83
• Omoigiade E.U. :Clinical Surgery Manual, 2nd edition,2016: pg 148-155
• emedicine.medscape.com/article/diabeticulcers
69

70. THANKS FOR LISTENING
70