Date post: | 16-Dec-2015 |
Category: |
Documents |
Upload: | martina-nelson |
View: | 249 times |
Download: | 2 times |
Wound◦Breach in the continuity of skin or mucous membrane
Ulcer◦Persistent breach in the continuity of skin or mucous membrane associated with cell death
Wounds
Acute Wounds
Cuts, Abrasions, LacerationsContusionsPuntureSkin flaps and BitesBenbow ( 2005) Any wound >
3/12 considered a chronic woundThey passes through the
normal healing process readily
Fail to pass through normal healing process
Chronic Wounds
Time
Hemostasis
Platelet Aggregation Neutrophil
ImmigrationMonocyte ImmigrationGranulation
Re-epithelialization
Wound Closure
Scar FormationRemodeling
Minutes Hours Days Weeks Months Years
The wound healing cascade impairs and arrests at different stages
Chronic wounds
CHRONIC WOUND
They are poly peptides, stimulate wound healing, promote chemotaxis, miotgenesis of fibroblasts and smooth muscle cells
Platelet derived growth factor Insulin like growth factor epidermal growth factor fibroblast growth factor transforming growth factor 1
Normal healing process impaired
Arrest at different levels
Remains at same stage without progressing
to wound healing
Often an underlying cause remains and
undetected
Inadequate blood supply ** Increased skin tension Poor surgical apposition Wound dehiscence Poor venous drainage ** Presence of foreign body and foreign body reactions Continued presence of micro-organisms & Infection ** Excess local mobility, such as over a joint
Systemic factors Advancing age and General immobility ** Obesity *** Smoking Malnutrition *** Deficiency of vitamins and trace elements ***
Systemic malignancy and terminal illness
Chemotherapy and radiotherapy
Immunosuppressant drugs, corticosteroids, anticoagulants
Inherited neutrophil disorders, such as leucocyte adhesion deficiency
Diabetes and CRF***
approach has been criticised for being too simplistic as wound healing is a continuum and wounds often contain a mixture of tissue types.
Wound Healing Continuum (Gray et al. 2005) havebeen developed. This tool incorporates intermediate colour combinations between the four key colours
The presence of multiplying organisms within a wound that overwhelm the host immune response with associated clinical signs and symptoms. (Kingsley 2001)
Organism Density
1. The quantity of micro-organisms2.quality –Virulence and antibiotic resistance
3. The patients resistance to the level of bacteria in the wound( immune response)
Microbial bio-burden within wounds can range from contamination, colonisation, critical colonisation and infection.
Wound Surface
2.Organisms from GIT and GUTGram Negatives such as E.coli,
Klebsiella, Enterobacter, Anerobes
1.Organims from surrounding skin- Regional flora-
Deptheroids, Anerobes
3.Organisms from External environment- through direct or
indirectly – Pseudomonas, Multiresistant organisims etc
Wound Contamination
Wound Colonization
Critical Colonization
Wound Infection
Advance Wound Infection
Fecal and urinary management systems
Hand hygeine
Classical Signs
1. Increased pain
2. Copious amounts of exudate
3. Malodour
4. Cellulitis
5. Pyrexia
6. Abscess Formation
◦Increase in size of wound
◦Delayed wound healing
◦General unwellness
◦Dark discoloured granulation tissue
◦Increased friability
◦Pocketing at base of wound. (Cutting and
Harding 1994).
Crushing of Muscles>Extravasation of
blood>Myoglobin release
Earthquakes, Industrial accidents, Air crashes
Renal failure, Toxemia, Septicemia, Gas
gangrene
Rx- Multiple deep incisions, Mannitol,
NaHCO3, Hemodialysis
Tropical ulcersTuberculosisBuruli ulcers- myco ulceransSyphilis- trp pallidiumYaws- treponema pertenueActinomycosis
Traumatic Ulcers of Vascular origin
VenousArterialPressure sores Neurotropic (trophic) ulcers
LeprosyDiabetic neuropathies
Cord lesions
• Ulcers with metabolic or systemic disease
• Diabetic ulcers• Haemoglobinopathies
• Infective (pyogenic)
Cryopathic
Grade 0- Preulcerative/HealedGrade 1- SuperficialGrade 2- Deeper to subcutaneousGrade 3- Abscess formationGrade 4- Gangrene of part of tissue
Grade 5- Gangrene of entire limb
EdgeSloping – non specificUndermined – tuberculous/ decubitus
Punched out – syphilitic/neuropathic
Floor – what is seen
Base – what is palpated
Granulation◦Red◦Pale & Smooth◦Pink, Punctate,
◦Nodular – suggestive of malignancy
• Discharge• Serous• Purulent• Sero-purulent
• Bloody• Sero-sanguinous
• Sulpher granules
Tropical UlcersCaused by synergy of F fusiformis / Borrelia vincenti
Starts as septic blistersTropical Countries – poor hygeine,malnutrition, walking barefooted
In the chronic phase the ulcer becomes non specific
Bursting of Caseous LNSlightly painfulNeck, Axilla, GroinUndermined thin reddish-blue edge, Sero-sanguinous discharge & induration
Enlarged LNLupus Vulgaris- Cutaneous TB- Face & Hands
Check the lungs- CXR
Treponema PallidumHard Chancre- Ext GenitalsPunched out edgesPainless, indurated base(button Like)
Nipple, lip, tongue, anal canalSecondary- Mucus patches, Condylomas
Tertiary – Gummatous (Subcut bones)
VDRL/ biopsy
Causes are many Sloping edgePhases1.Acute or infective phase2.Transition phase3.Reparative or healing phase4.Chronic, indolent or callous phase 5.-secondary infection, poor circulation, fB
Anywhere on bodyDiagnosis is based on history & sloping edge
Limbs-Shin, Malleoli, JointsChronic- StaphEg◦Plaster Sores, Skin burns, Caustic ulcers
Occurs in theMedial lower 3rd legDue to venous stasis- poor oxygenation/nutrition
Leg oedema ,Surrounding skinPigmentation
varicositiesCauses◦Varicose veins-Perforator incompetence, Stasis
◦DVT-Valveless Recanalisation after DVT
Inadequate skin circulationLimbs- Repeated pressure/traumaCausees◦Atherosclerosis- Ant & lat legs, Dorsum, Heels
◦Buerger’s disease- Painf, Claudication, Punched out ulcers
◦Raynaud’s disease◦The skin is shiny, hairless & hypoaesthetic
◦Dorsalis pedis/ post tibial pulses are absent
Neurologic deficit, Impaired blood supply & nutrition
Sites - trochanter◦Sacrum, Heel, Buttocks, Occiput
Bedsores, Perforating Ulcers CausesCauses◦Diabetic Neuropathy, Paraplegia, Leprosy, Spinal injury, Peripheral injury, Peripheral neuritis
Ischemia from prolonged pressure bw
Bed and body prominences those unaware of warning signals of discomfort eg unconscious patient,
Maceration of skin from sweat, urinePoor nutritional statusReflection of nursing care
Marjolin’s ulcer◦SCC from chronic scar
Malignant◦Lips, cheeks, penis, vulva, mouth, oesophagus
◦40 yrs+◦SCC, BCC, Melanoma
Soft Chancre- Ducreys◦Painful, Ext genitals, with Bubo
Meleney’s Ulcer◦Post-op- Perforated viscus, ◦Empyema Thoracis◦Strepto & Staph, Abdomen
Martorell ◦Hypertensive, Old age◦Post calf
Bazin’s
Wound Care Plan (WCP)
Patient Centered – dealing with person with a
chronic wound
Holistic –Total care -Not only wound itself- need to address pts other needs, diseases, and psychosocial wellbeing
Inter-diciplinaryNeeds Participation of
multitude of disciplines
Mode of onsetDurationPainful or painlessDischargePMH suggestive of systemic illnessDM, TB, SCD, Neuropathy, Peripheral ischaemic symptomsarterial disease – intermittent claudication
◦ Previous interventions◦ Treatment
Venous◦Varicose veins◦DVT/thrombophlebitis◦Sclerotic changes◦Oedema
Vasculitis◦History of autoimmune disease◦Painful◦Lack chronic arterial occlusive symptoms
◦Systemic symptoms of autoimmune disease
InspectionSize & ShapeNumberPosition ( anatomical site)
Edge, Margin, Floor
DischargeSurrounding area
• Palpation• Tenderness• Edge & margin• Base• Depth• Bleeding• Surrounding skin
Specific◦VDRL,◦X-ray of part/ CXR◦Edge biopsy◦FNAC of LN◦Colour Doppler
Connective disease profile Angiography
Dressings◦ Encourage healing
Moist Reduce oedema Remove pathogens Protect healing tissue
Debridement Necrotic tissue Slough Foreign bodies amputation
Vascularise Angioplasty Bypass Optimise cardiac circulation
Eliminate venous hypertension Varicose vein surgery Venous valve replacement Sclerotherapy Venous bypass
Wound closure Secondary intention SSG V.A.C. Plastic surgery flaps
Systemic treatment Steroids Diet Trace elements Avoid cross contamination
Healing without complications such as infection and disfiguring
Wound care ◦ Remove FB◦ Dry or wet to dry dressing to cover the wounds◦ Suturing if acute◦ Bites - Prophylaxis
Incised◦Primary Suturing
Lacerated◦Excision & Primary Suturing
Crushed◦Debridement, excision◦Delayed Primary Suturing
Deep devitalised◦Debridement◦Secondary Suturing/ Grafting
Treatment of causeCorrection of DeficienciesBlood transfusionsPain MangementDebridement, Cleaning, DressingAntibioticsSuturing, Grafts, Flaps
Cleansing agents◦ Flowing Water –Requesting pt to bath before dressing
change◦ Normal Saline***◦ Commercial Cleansers◦ Hydrogen Peroxide◦ Povidone iodine◦ Hypochlorite solution◦ Sterile vinegar solution◦ Mechanical Cleansers –Whirl pools◦ Salt dips◦ Honey
Protect from bacterial invasion
maintain optimum humidity
absorb serum from wound site
protect granulation tissue
reduce pain
Debridement – Mechanical / surgical /
biological / enzymatic
Off loading foot wear .
Antibiotics
Appropriate wound care .
No role for
◦ Hydrogen peroxide
◦ Boric acid
◦ EUSOL
◦ Dakin solution (hypochlorite )
◦ Iodine
As they are toxic to the tissues
Poly urethane films ◦ transmit water vapour , oxygen , carbon dioxide ◦ non absorbent ◦ useful for healing wounds with minimal drainage
Foams and Hydrocolloids
◦ Permeable , easy to apply , minimum re injury when removing the dressings
◦ 60-95% water content maintains the moist atmosphere
Alginates
◦Sea weed preparation
◦ absorb exudates
◦ useful for exudative wounds
Cultured keratinocytes
◦Cells are cultured and transferred to
petroleum gauze
◦ labour intense and expensive
Nutrition-proteins , zinc , vitamin c
Pain management
Change of dressings
Removal of slough- hydrogels , varidase
decrease the bacterial load – iodoflex Reduction of exudates- alginates Odour – iodoflex, silver , metronidazole Eczema- steroids
Bacteria can secondarily colonize the wound and general tendency is to over treat .
Not necessarily indicate infection
wound bacteria may be transient and may not be detected on random swabs
Fever /erythema /swelling / increased pain / leucocytosis
Only indicated if contaminated or evidence of infection is demonstrated
Evidence of infection (local)◦ Redness◦ Warmth◦ Swelling◦ Tenderness◦ Local Lymphadenopathy
For spreading infection and or evidence of
systemic infection
Take blood cultures
Treated with Broad Spectrum antibiotics
intravenously.
Topical antimicrobials - used to reduce
wound bio burden (EWMA 2006).
Granulation enhancers
Minimal Dressing changes to reduce disturbances to the granulation
Avoid usage of substances which impede granulation tissues
1. For those with Diabetes for wound healing and further prevention: A - Check A1c - greater than 9% will affect wound
healing. Recommended is less than 7%. B – Blood Pressure C - Cholesterol D - Diet E - Exercise F - Foot care - Check both feet at each
appointment, shoes should be professionally fitted, consider chiropody.
S- Smoking
2. For those with Venous Ulcer Disease - Compression bandaging is for treatment, stockings are for prevention.
◦ (Exudate/creams will damage the integrity of the stockings).
◦ COMPRESSION IS FOR LIFE! The right compression is the one the patient will wear
3. For those with any distal neuropathy - Shoes should be professionally fitted.
4. Smoking Cessation -IMPORTANT FOR ALL! - each cigarette decreases leg circulation for 30% for an hour or increase sympathetic tone for 8 hours
5. If wounds not decreased by 30% in size by week 4, unlikely to heal by week 12. Consider biopsy or a comprehensive re-assessment
6.Query Infection? Culture using the Levine technique (Compress wound with normal saline for 10 minutes, press swab into a clean granulated area to express fluid and rotate 360 degrees
7. Treat the cause! Consider all the possible contributors to non-healing: Drugs, Occult malgnancySystemic Disease (diabetes anemia, vascular disease), smoking, non-adherence
Definition
Problem – How big is it ?
Types
Pathophysiology of venous , arterial ,
diabetic ulcers
Assessment / Evaluations
Treatment options – Dressing agents ,
surgical options
Chronic ulcers results when sequel of repair is disturbed at one or more stages of inflammation
proliferation , re epithelialization ,remodelling
common organisms colonizing the ulcers
Staph aureus , Strep pyogens , Strep fecalis , E coli