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CPTA Annual Conference 9/20/2013
Rose Hamm, PT 1
ACUTE CARE WOUND CARE:UNDERSTANDING WOUND HEALING IN THE ACUTE CARE SETTING
Rose Hamm, PT, DPT, CWS, FACCWS
Assistant Professor of Clinical Physical Therapy
Division of Biokinesiology and Physical Therapy
University of Southern California, Los Angeles
Objectives
• At the end of this presentation the participant will be able to:• Perform a chart review, subjective, and objective assessment of a
patient with a wound.
• Recognize the factors that are impeding wound healing using the common lab values available in the acute setting.
• Diagnose a wound by etiology.
• Stage a pressure ulcer using the NPUAP classification.
• Develop a plan of care for a patient with a wound in the acute care setting.
• Select the appropriate adjunct therapy to facilitate wound healing for a patient in the acute care setting.
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 2
Review of healing response to injuryDermalTendon/ligmt. Muscle Bone
(Bone phases)
Hemostasis
PlateletsEndothelial cells
Platelets and leukocytes; hematoma formation
Inflammation
LeukocytesMonocytesMacrophages
Phagocytes destroy the hematoma
Platelets release fibronectin, PDGF, TGF
(Hematoma formation)
a p agLymphocytes
Proliferation
FibroblastsMacrophagesEndothelial cellsKeratinocytesEpithelial cells
Matrix formation –fibroblasts, myoblasts, endothelial cells
Soft callus formation, angiogenesisHard callus formation/osteoblasts
(Reparative)
(Modeling)
Remodeling
FibroblastsEpithelial cellsMacrophagesLeukocytes
Maturation and contraction of the scar tissue;
Osteoclasts and osteoblasts
(Remodel-ing)
TIME OF NORMAL HEALING PHASES
Phase 1 Phase 2 Phase 3 Phase 4Hemostasis Inflammation Proliferation Remodelinga a a a d g
0---------------------------------REPAIR-----------------------------2 Years
Injury30mins 3-7days------ 21 days---------- 2 Years
Cellular activity levels in wound healing
Out of control cellular activity• No inhibition of cellular response in place• Increased cellular necrosis, increased cellular by-products,
unable to progress healing phases, increased opportunity for infection
U l t d ll l ti itUp-regulated cellular activity• Normal cellular response to injury or bacteria with cells
attracted to area by chemotaxis• Normal sequence of events for wound healing to occur
Baseline• Normal surveillance occurring for injury or bacteria• Normal cell reproduction in response to apoptosis
Cellular activity levels in wound healing
Baseline• Normal surveillance occurring for injury or
bacteria• Normal cell reproduction in response to
apoptosisapoptosis
Senescent• Non-responsive cells, unable to initiate healing response• Altered cell receptor display• Secretion of cell products/gene expression• Metabolic drain- senescent cells consume energy with no
contribution to local cell/tissue health• Resistant to apoptosis• Normal tissue differentiation disrupted Tammy Luttrell, PT,
PhD
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 3
Patient evaluation•Answers two questions:
• Why does this patient have the wound?
• Why is the wound not healing?Why is the wound not healing?
WHY???WHY???
Diagnostic process
• Chart review
• Subjective history
• Objective medical history
• Wound history
• Wound observation
• Wound assessment
• Tests and measures
Diagnostic process
Chart review
Wound assessment
Tests and measures-vascular
Subjective history
Medical history
Wound history
Wound observation Laboratory
tests
Diagnosis
Common diagnoses seen in acute care
• Arterial
• Venous
• Pressure
• Neuropathic
• Burn
• Surgical incision/dehsicence
Wound evaluation by etiologyLocation Tissue Pain Skin Exudate
Arterial Distal digits
Toes or fingers
Dry, necrotic or slough, little or no granulation
Yes!!! May have dependent leg syndrome
Dry, hairless, shiny, thin
None unless infected
Venous Lower 1/3 of the leg (called the gaitor area)
Red or pink, bark texture, yellow slough
Poor granulation
Generally not unless vasculitic
Hemosiderous(dark, brawny appearance)
Atrophie blanche
Varies, may have copious serous drainage
Pressure Over bony prominences
Varies from dark red to eschar
Varies depending on the structures involved
Macerated, wet, erythematous
Varies
Neuro-pathic
Weight bearing surface of the foot or dorsal digits
Callus or blister, slough, may probe to bone, necrotic with PAD
None!!! Until infected, then deep throb
Dry, thick, scaly, hyperkeratotic
Varies, depending on infection
Common causes of non-healing wounds in acute care setting• Infection• Protein energy malnutrition• Diabetes with poorly control blood sugars• Edema• Arterial insufficiency
Medications• Medications• Age• Co-morbidities• History of radiation/chemotherapy• Stress • Obesity• Stress• Social behaviors (smoking, alcohol)• Improper positioning
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 4
Levels of contamination• Normal flora• Contaminated – presence of microbes on the wound bed• Colonized – the microbes are reproducing• Critically colonized – the number of microbes is sufficient
to impede the healing processto impede the healing process• Infected – the number of microbes is more than the host
can deal with; with or without clinical signs of infection (105
organisms/gram of tissue)• Septic – the infection is throughout the body and life-
threatening
Biofilm
• A biofilm is an aggregate of microorganisms in which cells adhere to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm EPS, which is also referred to as slime(although not everything described as slime is a biofilm), is a ( g y g ),polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides. Biofilms may form on living or non-living surfaces and can be prevalent in natural, industrial and hospital settings. The microbial cells growing in a biofilm are physiologically distinct from planktonic cells of the same organism, which, by contrast, are single-cells that may float or swim in a liquid medium.
Diabetes
• <100mg/dL = normal fasting blood glucose• 100-125mg/dL = prediabetic• >126mg/dL = diagnosis of diabetesg g• <200mg/dL = min. level for protein synthesis
• <150mg/dL = recommended for wound healing
• HbA1c = now the gold standard for diagnosing and
Criteria For Diagnosis of Diabetes & Pre-Diabetes in Adults
Stage Fasting Plasma Glucose Test*
Casual Glucose Test†
Oral Glucose Tolerance Test
Normal <100 mg/dL 2-hr PPG <140 mg/dl
Increased risk -AKA Pre-diabetes
100-125 mg/dL A1C 5 7 6 4%
2-h PPG 140-199 mg/dlAKA Pre diabetes
(impaired glucose tolerace)
5.7-6.4% 199 mg/dl
Diabetes >126 mg/dl >200 mg/dl (plus symptoms)
2-h PPG >200 mg/dl
Diabetes A1C >6.5%
22Diabetes Care January 2011 vol. 34 no. Supplement 1 S11-S61 available at: http://care.diabetesjournals.org/content/34/Supplement_1/S11.full
* Fasting means no calorie intake for 8 hours† Casual means testing any time of day without regard to time since last meal; symptoms are the classic ones of polyuria, polydipsia, and unexplained weight loss.
Poor nutrition
• Protein energy malnutrition• Fewer protein substrates available for new tissue formation• Less energy available for anabolic activity• Decrease in lean body mass
• >10% - wound healing is impaired• >20% - wound healing ceases
• Usually measured by • Albumin (3.5-5.5 g/dL = normal)• Pre-albumin (20-40mg/dL = normal)
Medications
• Steroids• Prednisone• Methotrexate
• NSAIDsh• Cox-2 inhibitors
• Ibuprofen• Naprocin• Aspirin
• Immunosuppressive agents• Anti-rejection medications (Cellcept)• Anticoagulants
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 5
Social factors
• Stress• Hypermetabolism• Increased catabolic activity• Decreased resources for healing and fighting infection
• Smoking/alcohol• Smoking/alcohol• Peripheral vasoconstriction => hypoxia• Decreased fibroblasts, macrophages, cytokines
• Obesity• Decreased vascularity in adipose, poor granulation• Higher frequency of dehisced wounds, infections• Frequently protein energy malnourished• Higher risk for pressure ulcers
Inappropriate dressings• Hydrogen peroxide
• Dakin’s solution (unless infected necrotic tissue)
• Acetic acid (pseudomonas only)
• Betadine
Why is this wound not healing?Time of eval After 2 weeks
After 6 weeks
What is the etiology?
• Arterial
• Neuropathic
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathicp
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathicp
• Pressure
• Venous
• Atypical
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 6
What is the etiology?
• Arterial
Neuropathic• Neuropathic
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathicp
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathic
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathic
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathic
• Pressure
• Venous
• Atypical
What is the etiology?
• Arterial
• Neuropathic
• Pressure
• Venous
• Atypical
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 7
Pathophysiology of pressure ulcers
Shear Pressure FrictionShear Pressure Friction
Moisture
Causative factors
Pressure
• Force that is perpendicular to the bony prominence
• Occurs most frequently over areas with little subcutaneous tissuesubcutaneous tissue
• Occurs with bony prominence pushing or resting on a hard surface
Pressure
Pressure against hard surface with
increased interstitial fluid pressure
Capillary collapse, fluid loss, tissue
edema → ischemia
Inflammatory response and
autolysis of dead cells
Decreased nutrients and oxygen to the
tissue
Necrosis and ulceration
Shear
Result is wound with undermining and tracking
i
Tissue anoxia,
inflammatory response,
tissue
Parallel forces break and distort capillaries sinusestissue
necrosiscapillaries
Note discoloration ofSkin that indicates undermining
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 8
Friction
Two surfaces rub against each
other
Abrades the epidermis
Initiates an inflammatory
response
Creates a blister between the
epidermis and dermis
Occurs most frequently at
elbows and heels
Moisture
Decreases the strength and
thickness of the skin
Increases the skin pH,
destroys the acid mantle
Decreases resistance to
bacterai
Increases risk of dermatitis
Creates portal for bacteria to enter the skin
Types of moisture
• Urinary incontinence
• Fecal incontinence
• Wound drainage
• Perspiration
Location, location, location!!!
scapula
elbow
occiput
greater trochanter
ischial tuberosity
medial knee
heel
sacrum, coccyx
Achilles tendon
medial/lateral malleoli
How long does it take???• Intensity versus duration
• Prolonged exposure to mild to moderate increase in forces• Short exposure to moderate to severe increase in forces
Time for pressure ulcer to develop is not the same for every patient!
NPUAP Staging System
• Adopted in 1989 and revised in 2007
• Used ONLY for describing tissue involvement of pressure ulcers
• Required documentation if POA or present on admission; signed by MD within 48 hours of admissiong y
• Is not always easy!!!
• Recommend “two eyes on” policy or
“master stager” consulting
policy within facility
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 9
Stage I
• Intact skin with non-blanchable redness of localized area, usually over bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.
• Further description: The area may be painful firm softFurther description: The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk).
Stage II
• Partial-thickness loss of dermis presenting as shallow open ulcer with a red-pink wound bed, without slough. May present as an intact or open/ruptured serum-filledblister
• Further description: Presents as a shiny or dry shallowFurther description: Presents as a shiny or dry shallow ulcer without slough or bruising. (Bruising indicates suspected deep tissue injury.) Stage II should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or denudement.
Stage III
• Full-thickness tissue loss. Subcutaneous fat may be visible; bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.
• Further description: Depth of Stage III pressure ulcer i b t i l l ti Th b id f thvaries by anatomical location. The bridge of the nose,
ear, occiput, and malleolus do not have subcutaneous tissue, and Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Areas with no subcutaneous fat may be shallow; areas with significant adiposity can be deep. Bone and tendons are not visible or directly palpable.
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 10
Stage IV
• Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often includes undermining and tunneling.
• Further description: The depth of Stage IV pressure ulcerFurther description: The depth of Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and Stage III ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (eg, fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone and tendons are visible or directly palpable.
Suspected deep tissue injury
• Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, and warmer or cooler compared to adjacent tissue.p j
• Further description: Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with treatment.
Unstageable
• Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Undermining and sinus tracts also may be associated with Stage IV pressure ulcers.
• Further description: Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or flutuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 11
Prevention
• Risk assessment
• Skin care (hydrate, protect)
• Optimize nutrition
• Reposition
• Support surfaces
• Heel protectors (float the heels)
• MOBILIZE!!!
Interventions for the foot
Correct positioning of the foot in a positioner is necessary to prevent ulceration of the metatarsal heads and the Achilles tendon.
Supine positioning
• Weight evenly distributed throughout entire body
• Bed flat as possible
• Head of bed less than 30 degreesg
• Knees elevated slightly to prevent sliding
• Heels off-loaded with pillows
Fowler’s position
30-degree side-lying
150-degree side-lying Prone position
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 12
Treatment of pressure ulcers• Support surfaces• Limit use of linen and bed pads• Reposition with 30-degree side-lying• Avoid donuts and rings• Avoid heat on the pressure ulcer• Avoid head elevation > 30 degrees• Avoid head elevation > 30 degrees• Stage I and II – use protective dressing• Stage III and IV
• Treat infection• Debride moist wound dressings• Electrical stimulation• Ultrasound• Negative pressure wound therapy• Pulsed lavage with suction
Treatment of ICU patients
• Reposition more frequently
• Map pressure for effective pressure redistribution
• Monitor shear when using rotational beds
• Monitor pre-albumin levels carefully
• Float heels at all times
• Use hand-relief of vulnerable areas for reperfusion
Arterial wounds - diagnosisCritical phases of PAD1. Collateral circulation insufficient for metabolic needs => shunting of
blood to muscles where there is less resistance => delayed healing of traumatic wounds
2. Claudication - pain with activity – most effectively treated with exercise
a. thigh and buttock claudication = aortoiliac or iliac involvement
b. calf claudication = femoral or popliteal involvement
3. Rest pain – requires revascularization surgery• Characterized by “dependent leg syndrome”• May be accompanied by signs of ischemia at distal digits
Treatment of claudication
• Differential diagnosis• Arterial insufficiency
• Spinal stenosis
• Progressive exercise program• Establish baseline on treadmill• Establish baseline on treadmill
• Monitor vital signs, pain levels, and rest time for pain to abate
• Perform 3 tasks for each treatment session
• Stress increase in grade rather than speed
• Takes about 3 weeks to have increased function
• Takes about 3 months to have decreased pain levels
Guidelines for establishing plan of care
• Transcutaneous oxygen tension (TcPO2)• Provides information on amount of oxygen available to the tissue
via microcirculation• Used to predict healing potential• Interpretation of readings• Interpretation of readings
• <20 mmHg- healing unlikely• <30 mmHg – delayed healing• <30 mmHg – debridement contraindicated• >40 mmHg – normal
Patients with diabetes may have higher TcPO 2 readings than patients without diabetes, leading to poorer healing results.
Guidelines for establishingplan of care
• Ankle-brachial index• 1.0– 1.2 – Normal
• 0.8-1.0 – Compression for edema control is safe to use.
• 0 5-0 8 – Compression therapy is contraindicated if <0 6; modified• 0.5-0.8 – Compression therapy is contraindicated if <0.6; modified compression is indicated if 0.6-0.8.
• <0.5 – Compression therapy is (almost) always contraindicated.
• <0.2 – Tissue death will occur.
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 13
Prevention of wounds with PAD
• Control blood sugars
• Cease smoking
• Control hypertension, hyperlipidemia, hypercholesterolemiahypercholesterolemia
• Provide proper foot care including shoes that fit and provide pressure relief
• Exercise to build collateral circulation
Treatment before surgery
• Do not debride
• Keep area dry; protect toes with cotton or sterile gauze between toes
• Use foot cradle
• Off-load heels with pillows
• Discourage limb elevation
• Elevate head of bed 5-7 degrees
• Keep extremity warm
• Avoid excessive exercise
Protector
Positioner
Treatment after surgery
• Debride wound of necrotic tissue when granulation tissue is visible at the edges (D. Armstrong)
• Provide moist wound environment with the appropriate advanced dressing
Protect foot with pillows under calves• Protect foot with pillows under calves
• Off-load wound with orthotic, special shoes, assistive device
• Control post-op edema to prevent incisional dehiscence• Cover incision with dry sterile gauze
• Apply short stretch elastic bandage in spiral wrap
• AVOID ELASTIC WRAPS!!!
Dressings
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 14
Shoes/orthotics for arterial wounds
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Venous wounds – treatment
• Venous wounds• Antibiotics if indicated• Debridement• Absorbent wound dressings• Biological dressings
C i• Compression • Pentoxifylline• Exercise
• Activate the venous pump• Increase ankle range of
motion• Gait training to emphasize
heel/toe sequence
Antibiotics• Systemic
• For overt infection (usually with erythema and warmth 2 cm or more beyond wound margin
• For cellulitis, osteomyelitis
• Topical • For colonization/critical
colonization• For wounds that show no
improvement after 2 wks• For patients with impaired
• Based on culture• Wounds < 1 month
duration: usually gram+• Wounds > 1 month
duration or immunosuppressed pts: broad spectrum Sibbald 2007
p pperfusion with poor delivery of systemic antibiotics (PVD, edema)
• Recommendations:• Low tissue toxicity• Avoid sensitizers that lead
to resistant organisms• Neomycin, bacitracin
Machet 2004
Suggested topical antimicrobials• Purpose
• To restore a balance between bioburden and local immune system• Types of topical antimicrobials that are considered “best practice”
• Ionic silver dressings• Available in a variety of dressings
• Cadexomer iodine• Cadexomer iodine• Iodosorb, Iodoflex
• Polyhexamethylene biguanide compound (PHMB)• XCell antimicrobial
• Acetic acid soaks• For pseudomonads only
Debridement• Types of debridement recommended for venous wounds
• Selective/sharp if pain levels are low• Enzymatic
• Collagenase
• Ultrasound• Ultrasound• Low frequency
• Non-contact: MIST – 40 kHz• Contact – 25-26 kHz
• Soring Sonoca-180 • Arabello
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 15
Absorbent wound dressing
• Purpose• Achieve optimal moisture balance for the wound to heal
• Types• Foams
• Cellulose fiber fillers• Cellulose fiber fillers
• Calcium alginate
• Hydrocolloids
Compression
• Purpose • Augment venous return to central circulation
• Increase interstitial tissue pressures by compressing superficial tissues
• Provide external support (static or dynamic) to the venous• Provide external support (static or dynamic) to the venous pump
• Types• Elastic – multilayered, single layer long stretch, elastic
stockings
• Inelastic – paste, short stretch, orthotic (Circaid)
Traditional Current
Compression for venous wounds
• Unna boot• Semi-rigid
• Requires active gastrocsoleus, ambulation to be
• Multi-layer compression• Is not rigid, conforms to
extremity size and shape
• Effective on an extremity with hypomobile anklea bu a o o be
effective
• Does not shrink as extremity girth decreases
ypo ob e a e
• Provide higher sub-bandage resting pressure
• Shrinks as the extremity girth decreases
Application of multi-layer compression
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 16
Compression Vascular parameters for multilayer compression
• ABI >0.8 – full compression (30-40 mmHg pressure)
• ABI 0.6-0.8 – modified compression (23-27 mmHg pressure)• Examples: short stretch bandages or layers 1,2,4
from the multilayer systems
• ABI <0.5 – static compression contraindicated, may use short stretch bandages.
Exercise!!!• Ankle mobilization
• Joint mobilization• Gastroc stretches
• Exercises to activate the gastrocsoleus musclesA kl• Ankle pumps
• Rocker board• Heel-toe raises in sitting/standing
• Gait training• Progress to heel/toe sequence
during stance phase• Treadmill or bicycle activities
Post-healing• Compression needs to be continued to prevent recurrence. Samson
(1996) reported 79% recurrence in patients who were non-compliant with compression after healing; 4% in those who were compliant.
• Types
• Elastic stockingsElastic stockings• Circaid• Farrow bandages
Post-healing compression
Circaid Farrow bandages
Components of Gait Cycle
Stance 60%
Reference foot is in contact with floor
Swing 40%
Reference foot is not in contact with floor
Single limb support
40%1 limb on ground
Terminal double limb support
10%Both feet on ground
Loading response
10%
Mid-stance
20%Foot flat
Terminal stance20%
Heel off ground
Pre-swing
10%
Initial
13.3%
Mid
13.3%
Terminal13.3%
ROM NEEDED FOR NORMAL GAIT CYCLE
• Ankle
• 0-10 degrees dorsiflexion in stance phase, 0 degrees in swing phase
• 0-20 degrees plantarflexion in stance phase to allow for push offpush-off
• 0-5 degrees eversion at subtalar joint in stance phase
• Metatarsophalangeal joint
• 50-60 degrees of dorsiflexion at the 1st
metatarsalphalangeal joint during push off (deficiency is cause of shear stress in deep tissue)
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 17
GAIT CHANGES IN PATIENTS WITH DIABETES
• Slow speed - Secondary to peripheral effect of DM on other body systems (Brach)
• Prolonged stance phase (associated with slower speed)
• Short stride• Increased step width - May be related to
peripheral nerve motor function or to central influences of the disease (Brach)
• I
central influences of the disease (Brach)• Decreased push off (related to hallux
ROM)• Wider base of support• Greater step time variability on uneven
surfaces (Brach)• Significantly longer activation delays in
the tibialis anterior and vastas lateralis(Sacco and Amadio)
• Increased shear forces between bone and deep tissue OR between shoe material and skin
WALKING FACTS!!!
• Patients with DM take an average of 4548 steps/day, 52% of these steps are in the home!!! Home is not a safe zone! (Armstrong)
• Reaction times are 2x as long in patients with diabetes vs.Reaction times are 2x as long in patients with diabetes vs. age-matched controls (Petrofsky)
ROAD TO NEUROPATHIC WOUNDS
Neuropathy• Sensory• Motor• Autonomic
Foot deformity• Loss of fat pad• Callus
formation
diabetic foot ulcer
NEUROPATHIC ULCERS
• Develop calluses from repeated friction that results in over‐development of the upper most layer of the edipermisp
• Occur under calluses that lead to high pressure points
• Develop due to altered musculoskeletal biomechanics and atrophy of underlying fat pads
100
And the patient does not feel it becauseof the sensory neuropathy!
NEUROPATHIC ULCER APPEARANCE
• Located on weight‐bearing surfaces of the foot or the dorsal toe joints
• Have a pale pink or red wound bed
• Have periwound callus/ hyperkeratotic tissue
• Have slight to minimal drainage
• May be round in shape, especially
101
May be round in shape, especially with arterial component
• Have variable pain pattern based on presence of infection or arterial component
• May have either bounding or diminished pulses
FORCES THAT ARE MEASURED BY FORCE PLATFORM DURING THE STANCE PHASE OF GAIT
• Vertical forces
• Anteroposterior shear
• Mediolateral shear
Shear – what is its effect on deep tissue???
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 18
SHEAR
Is this the same as deep tissue injury???
COMMON CAUSE OF MECHANICAL TRAUMA
Poorly fitting shoes
COMMON CAUSE OF TRAUMA
Walking barefoot
Burns!!
PURPOSE OF FOOTWEAR AND ORTHOTICS
• To reinforce the elements of best practice for each wound type• Neuropathic – off-loading
• Arterial – protection from trauma
• Venous – activate the venous pump and accommodate compression b dbandages
• Pressure – redistribute pressure away from involved area
SHOES FOR ARTERIAL WOUNDS
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CPTA Annual Conference 9/20/2013
Rose Hamm, PT 19
Shoe to accommodate compression bandages
TYPES OF FOOTWEAR USED TO OFF-L0ADDIABETIC FOOT ULCERS
• The gold-standard – the Total Contact Cast
ALTERNATIVES TO TCC
• Wound healing shoe
• Accommodative dressing
• Football dressing
• Post-op shoe with plastazote inserts
• Non-weight bearing with assistive device
• Wheelchair ambulation only
D’Arco Co.
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 20
Wound bed preparation
• Removal of the barriers to healing so that the wound can progress to the next stage of healing• Static -> inflammatory
• Inflammatory -> proliferation
• Proliferation -> epithelialization
Barriers can be intrinsic,
local, or extrinsic…
Wound bed preparation
D/T debride necrotic tissue
I address inflammation/infection
M maintain moist wound environmentM maintain moist wound environment
E facilitate epithelial migration at the edges
(Sibbald/Falanga)
Debridement
Removal of devitalized tissue
Changes wound into a healthy, positive environment
D th b t i l l dDecreases the bacterial load
Facilitates healing by secondary intention
Changes a chronic wound to an acute wound
Types of debridement• Surgical – non-selective, performed in OR• Sharp – selective, uses sharp instruments or high
powered pulsed irrigation• Autolytic – uses body fluid enzymes to break down
devitalized tissueEnzymatic uses pharmaceutical proteolytic enzymes in• Enzymatic – uses pharmaceutical proteolytic enzymes in a topical dressing
• Mechanical – non-selective, uses physical force to remove necrotic tissue and debris
• Biosurgery – uses sterile maggots, selective.• Hydrosurgical – uses high-powered waterjet (Versajet)• Low-frequency contact ultrasound – uses 40,000 kH
sound waves with built-in saline lavage
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 21
Moist wound dressings• Primary dressing
• Facilitate wound healing• Debridement• Antimicrobial• Maintain moisture balance
Secondary dressing• Secondary dressing• Anchor primary dressing• Protect the wound from mechanical forces• Manage edema
Select the primary dressing based on the wound bed. Select the secondary dressing based on patient’sactivity level.
Dressing SelectionBased on Wound Healing Phase
Inflammatory phaseAntimicrobials
Debriding agentsAbsorbent fillers
Proliferative phase
Remodeling phase
Fillers, foamsHydroactive dressingsHydrogels, biologicals
Silicone-backed foamScar therapy
DIME paradigm for dressing selectionDebridementGels, films Enzymes
Inflammation/infectionAntimicrobialsAlginatesAlginates
Moisture balanceAbsorbent fillersHydroactive dressingsHydrogels
EdgesCollagen Xeroform
(Sibbald)
Dressing selection based on moistureAmount of drainageModerate to copious Cellulose Foams Alginates
Minimal to moderate Cellulose Foams Alginates Hydrocolloids Hydroactive dressings
Scant to minimal Thin foams Hydrocolloids Hydroactive dressings Hydrogels
Maintain moisture balance of wound bed without causing periwound skin maceration.
Biophysical technologies
Pulsed lavage with suction• Post-amputation for removal of coagulum,
bacteria, and exudate
Negative pressure wound therapy• Post-amputation for wound contraction, removal ofPost amputation for wound contraction, removal of
bacteria, stimulation of angiogenesis
Non-contact, non-thermal ultrasound• Superficial wounds for maintenance debridement,
antimicrobial, pain control
Electrical stimulation• Post-amputation for facilitation of
angiogenesis, epithelial migration
NPWT precautions
• Achieve hemostasis before application
• <30% necrotic tissue
• Wound bed moist to wet, not drynot dry
• Intermittent suction preferred for faster granulation
• Protect tendons, bone, muscle with interface
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 22
Tips for NPWT
• Protect edges with Xeroform.
• Cut foam to fit inside wound, not overlapping edges.
• Adjust pressure to manage pain, especially in abdominal wounds.
C b t d l ith dh t h t• Cover bone, tendon, muscle with non-adherent mesh to prevent dessication of the tissue.
• Use thrombin over areas that tend to bleed or produce lymphatic fluids.
• Use topical Lidocaine gel at the edges to reduce pain when removing the dressings.
Case study
Cellulose/saline dressingModified compression
Six days later 4 months later
CPTA Annual Conference 9/20/2013
Rose Hamm, PT 23
References • National Pressure Ulcer Advisory Panel. Pressure Ulcer Prevention and
Treatment. 2010. Available at www.npuap.org.• Holtman D, Gahtan V. Peripheral arterial perfusion: Is it adequate for
wound healing? Wounds. 2008;20(8):230-235.• Bowker JH, Pfeifer JH. Levin and O’Neal’s The Diabetic Foot.
Philadelphia, PA: Elsevier. 2008.• Brach, JS, Talkowski JB, Strotmeyer ES, Newman AB. Diabetes Mellitus y
and gait dysfunction: possible explanatory causes. Physical Therapy 2008;88(11):1365-1374.
• McCulloch JM. Venous insufficiency and ulceration. In McCullocah JM, Kloth LC (Eds.). Wound Healing, 4th edition. Philadelphia, PA: FA Davis, 2010. Pp. 248-255.
• McGuire J. Transitional off-loading: an evidence-based approach to pressure redistribution in the diabetic foot. Advances in Skin and Wound Care 2010;23:175-188.
• Panuncialman J, Falanga V. The science of wound bed preparation. Surgical Clinics of North America. 2009;89(3):611-626.
• Wrobel JS, Najafi B. Diabetic foot biomechanics and gait dysfunction. Journal of Diabetes Science and Technology 2010;4(4):833-845.
Laboratory Values that Indicate Healing Impairments Laboratory Test Normal Range Values Affecting
Wound Healing Clinical
Presentation CBC WBC 4.5 – 11 x 103/mm3 Increased
Decreased
Signs of infection, inflammation, necrosis, trauma or stress Failure to initiate immune response against bacteria
RBC M 4.5-5.5 x 106
/mm3
F 4.1-4.9 x 106/mm3
Decreased Pale or anemic granulation or failure to progress
Hemoglobin M 13.5-18 g/dL F 12-15 g/dL
Decreased Increased
Pale or anemic granulation or failure to progress Failure to progress (patient may show signs of congestive heart failure or COPD)
Hematocrit M 37-50% F 36-46%
Decreased Increased
Pale or anemic granulation or failure to progress Signs of thrombi or emboli
Platelet count 150-400 x 103/mm3 Decreased Increased
Bleeds easily, fatigue Signs of infection or inflammation
Automated Differential
Neutrophil Rel 57-67% of leukocyte count
Increased Bacterial infection Chronic inflammation
Lymphocyte Rel 25-33% of leukocyte count
Increased Decreased
Signs of bacterial infection Opportunistic infections
Monocyte Rel 3-7% of leukocyte Increased Tissue injury
count Early healing response
Eosinophil Rel 1-4% of leukocyte count
Increased Decreased (with corticosteroid use)
Allergic reaction Parasitic infection Delayed inflammatory response
Basophil Rel 0-0.75% of leukocyte count
Increased Allergic reaction
Neutrophil Abs 4,300-10,000 cells/mm3
Increased Signs of infection
Lymphocyte Abs 2500-3300 cells/mm3
2000-2500/µL
Increased Decreased
Signs of bacterial infection Opportunistic infections
Monocyte Abs Eosinophil Abs Basophil Abs 0-1,000 cells/mm3 Increased Allergic reaction Coagulation Studies PT (prothrombin time)
12.3-14.2 sec Increased (>2.5 x reference range)
Bleeds easily
PTT (partial thromboplastin time)
25-34 sec
INR Normal 0.9-1.1 Therapeutic range 2-3 Mechanical heart valves 2.5-3.5
Elevated Bleeds easily Skin bruising
Routine Chemistry Sodium 135-145 mEq/L
Potassium 3.5-5.3 mEq/L Chloride 95-105 mEq/L CO2 22-29 mEq/L
35-45 mmHg (arterial)
Glucose 70-115 mg/dL Decreased (<70) Increased (>200)
Headache, dizziness, altered mental status, malaise Arrested healing processed Signs of infection Increased risk of abscess formation
Calcium 8.8-10.5 mg/dL Phosphate 2.5-5.0 mg/dL BUN 7-18 mg/dL Increased (renal
failure) Decreased (liver failure)
Edema Poor healing Jaundiced skin Yellow fluids
Creatinine 0.1-1.2 mg/dL Increased (renal failure) Decreased
Edema Decreased lean body mass
Albumin 3.5-5.5 g/dL Decreased Increased
Lack of granulation tissue Bilateral edema Muscle wasting Signs of dehydration
Pre-albumin level 15-36 mg/dL Decreased Poor wound healing Lack of granulation formation
Globulin 2.5-3.5 g/dL Fibrinogen 200-400 mg/dL A/G Ratio 1.5:1—2.5:1 Decreased (liver
damage) Increased (iron deficiency)
Bilirubin Total 0.1-1.0 mg/dL Increased Yellow wound fluids Jaundiced skin
Alkaline Phosphate 30-85 U/L Others Hb1AC 4-6% Increased Delayed healing C-reactive protein (CRP)
0-1.0 mg/dL or <10 mg/L
Increased Inflammation Infection
Retinal binding protein
10 mg/L 0.002 g/kg body wt.
Increased Delayed healing due to protein deficits
Magnesium 1.5-2.5 mEq/L Phosphorus Iron Decreased
Increased
Lack of granulation Hemachromotosis
Ferritin Decreased Increased
Anemic granulation Lack of granulation Hemosiderosis
Transferrin 204-360 µg/dL <0.1 g/kg body wt.
Decreased Increased
Delayed wound healing due to protein deficits Iron deficiency
Zinc Decreased Delayed wound healing Lack of epithelialization
Microbology Wound culture Negative Positive Poor wound healing
Wound degradation Blood culture Negative Positive Systemic signs of
infection 1. Goodman CC, Fuller KS, Boissonnault WG. Pathology: Implications for the Physical
Therapist, 2nd Edition. Philadelphia, PA: Saunders. 2003.
2. Huether SE, McCance KL. Understanding Pathophysiology, 4th Edition. St. Louis, MO: Mosby. 2008.
Copyright: Rose L. Hamm, PT, DPT, CWS, FACCWS