Diagnosis and evaluation of chronic ulcers

Diagnosis and evaluation of chronic ulcers
Which Ulcers are Which? Diagnosis and evaluation of chronic ulcers Thomas M. Bozzuto, DO, FACEP, UHM Medical Director Phoebe Wound Care and Hyperbaric Center Albany, GA Past President, American College of Hyperbaric Medicine

Course Outline How to differentiate different types of ulcers
Tips in diagnosing Arterial ulcers Venous ulcers Pressure ulcers Dehisced surgical ulcers Treatment suggestions Resources

The Burden of Chronic Wounds
Affect 6.5 million people Medicare spending in was $35.3 billion Infections = $16.7 billion Chronic ulcers = $9.4 billion Surgical wounds = $6.5 billion

Acute wounds Definition: Short duration (<6 weeks)
Normal Healing Process Normal inflammatory phase Normal granulation Normal tensile strength No local / systemic compromise No underlying etiology Cause: Usually trauma / surgery As we indicated in the normal healing process, acute wounds are usually healed by about six weeks. The normal inflammatory phase generates adequate granulation and ultimately heal with sufficient strength to avoid reopening. Under normal conditions there is no local or systemic compromise, and consequently also no underlying disease process. They are usually the result of trauma or surgery.

Chronic Wounds Definition: Long duration (>6 weeks)
Abnormal Healing Process Prolonged inflammatory phase Poor / absent granulation Poor tensile strength / dehiscence Local / systemic compromise (ischemia, corticosteroids) Underlying etiology (DM; RA; SLE: etc.) Causes: Local Systemic In contrast, a chronic wound takes longer to heal than we would expect. In other words the process is usually longer than six weeks. Chronic wounds are characterised by a prolonged inflammatory phase, the absence or poor quality of granulation tissues, and in adequate tensile strength to remain healed with either failure to close or dehiscence. There is usually local or systemic compromise, such as vascular insufficiency or the prolonged use of cortisone. Their maybe underlying problems such as diabetes, rheumatoid arthritis, lupus and other autoimmune diseases, etc. The causes are also frequently related to local or systemic conditions and diseases.

Distribution of Wound Types

5-Year Mortality Armstrong DG, Wrobel J, Robbins JM: Are diabetic-related wounds and Amputations worse than cancer? Int Wound Journal, 2009; 4(4): 286-7

Systemic Illness Soft Tissue Infection Nutrition Oxygen Osteomyelitis
WOUND Oxygen Osteomyelitis Perfusion Pressure Systemic Healing Ability They are large number of potential barriers. The slide lists only a few. During the discussion on the ABCDE of wounds we will cover the barriers to healing in greater detail. Edema Compliance

The Ideal Wound Approach
From diagnosis to follow up: Evidence based Recognition of wound characteristics Criteria for assessment Labs and imaging Wound bed preparation Appropriate treatment Proactive follow-up

Approach Wound etiology must be accurately identified
Clear treatment plan Offloading DFU Compressing VLU Appropriate dressings

Stages of wound healing
Vascular response (immediate – 5 days) Inflammatory response (3 – 7 days) Proliferation (3 – 25 days) Maturation (25 days – 1 year) Wound healing occurs in a series of overlapping physiological and biochemical events. Depending on the size and complexity of the wound, as well as the state of the normal healing response, wounds may heal in as little as one-day or become lifelong afflictions. Immediately following wounding there is a vascular and haematological response. If this does not occur the story ends there are. This vascular response may last up to five days. From the third day there is an inflammatory response. Under normal conditions this is usually concluded within about 7 to 14 days. Chronic wounds all become trapped in the inflammatory phase. From the third day to about a month there is a proliferative phase. This is the time in which granulation tissues forms and the body actively starts replacing the damaged tissue. Finally from about a month to a year or more there is a maturation phase, whether scar tissue is gradually remodelled and the tissue reshaped. 100 50 % … … 365 Days

Metabolic Syndrome - Type 2 Diabetes

Diabetic Foot Ulcers Ulceration below the ankle – commonly on plantar surface Associated with neuropathy, PAD or both Having an ulcer doubles the 5 year mortality in diabetics 1 and 5 year survival rates for LEA in diabetics are 69% and 34% respectively.

Major Contributing Causes and Risk Factors for DFU
DFU Type Major Contributing Cause Risk Factors Neuropathic Hyperglycemia Peripheral Sensory Neuropathy Repetitive mechanical forces of gait, which can lead to thick callus that causes ulceration Deformity High Plantar Pressures PAD Advanced Age Obesity Hypertension Previous Amputation Ischemic Ischemia from PAD Coronary Artery Disease Cerebrovascular Disease Longer disease duration Poor glycemic control PVD Presence of Retinopathy Smoking Neuropathic/Ischemic Occlusive vascular disease is the main factor; peripheral sensory neuropathy is present Trauma Unsuitable Shoes Neuroischemic foot Presence of retinopathy Smoking and other evidence of atherosclerotic vascular disease Absence of vibratory sensation

Ulcers Any leg ulcer, regardless of etiology may have associated arterial insufficiency Must mitigate the trauma and treat the arterial insufficiency as well as treating the wound Ruling out associated arterial disease in leg ulcers is critical for wound healing Pain with elevation Arterial disease Pain when dangling Venous disease

Smoking Smokers are 16 times more likely than non-smokers to have PAD
Smokers are more likely to have amputations Smokers are more likely to have proximal amputations Higher pack-years = more likely to have proximal amputation Neither the amputation level nor the amputation itself was enough motivation for the patients to participate in smoking cessation. Anderson JJ, et al. A comparison of diabetic smokers and non-smokers who undergo lower extremity amputation: a retrospective review of 112 patients. Diabet Foot Ankle. 2012; 3: /dfa.v3i

Diagnostic and Laboratory Tests
Toe pressures and wave forms are considered first line The ABI is known to be unreliable in patients with vascular stiffness and fails to detect the early phase of arteriosclerotic development. The toe vessels are less susceptible to vessel stiffness, which makes the TBI useful1 TcpO2 or fluorescein/indocyanine green angiography may provide better information about perfusion at site of ulceration ABI (absent of feeble pulses with ABI <.7 confirms ischemia. May be inaccurate with numbers > 1.2 because of calcification (non-compressible) Pulse-volume recordings Medicare does not consider palpation of pulses to be adequate vascular testing When to consult vascular ABI < 0.8 TcpO2 <40 mmHg Toe pressure < 45 mmHg Ankle systolic pressure <50 mmHg 1. Høyer C, Sanderman J, Petersen L. The toe-brachial index in the diagnosis of peripheral arterial disease. J Vasc Surg. 58:1, July 2013

Neuropathic Testing

Diagnostic and Laboratory Tests
Imaging If able to probe to bone – x-ray or MRI should be done MRI is most accurate imaging in diagnosing osteomyelitis or soft tissue infection If lower extremity ischemia is suspected – doppler or angiography Tc99 bone scan in patients with kidney disease who cannot get MRI (or can use gadolinium as contrast for MRI) Labs CBC (leukocytosis and anemia) Glucose (HgbA1c) CRP & ESR Prealbumin Comprehensive Metabolic Panel

The Ulcerated Foot and Off-Loading
The most reliable way to maintain off-loading in a patient with a diabetic plantar foot ulcer is with a device that the patient cannot interfere with, even inadvertently, because the device cannot be removed from the foot.

Plantar pressures and diabetes
Plantar pressures with various footwear.

Efficacy of Various Treatments in Healing Ulcers
Percent Healed TCC Dermagraft Apligraf Regranex “Usual Care” 20 12 Weeks

Beware the great masquerader
Any patient with a warm swollen neuropathic foot (with or without pain) is Acute Charcot foot until proven otherwise. Many are painful despite LOPS. Distended dorsal foot veins, evidence of AV shunting of autonomic neuropathy.

Mortality from Charcot foot is 45% in 3.7 years

Venous and Arterial Leg Ulcers
Venous Leg Ulcers Open lesion between knee and ankle that occurs in the presence of venous disease Venous disease is the MOST COMMON cause of leg ulcers (60- 80%) Arterial Leg Ulcers Can occur anywhere in lower extremity Account for 5-10% of leg ulcers

Primary Characteristics of Venous and Arterial Ulcers
VLU Arterial Insufficiency Ulcer Sensation Throbbing, aching , heavy feeling in legs Improves with elevation and rest Usually very painful while exercising ,at rest or during night Improves with dependency Typical location Lower leg (mid calf or below) Characteristically adjacent to or above the malleoli Between or on the tips of toes, outer ankle, or lateral foot over pressure points Exposure of deep structures None Often extends to underlying tendon or bone Wound appearance Covered with fibrinous layer mixed with granulation Shallow, superficial Varying depths within ulcer Small to large May be discrete or circumferential Base of wound typically does not bleed and is yellow, brown, grey or black Characteristically deep Punched out, usually round, with well-defined, even wound margins Periwound Hemosiderin staining Lipodermatosclerosis in long standing ulcers Variable pigmentation Dermatitis, erythema, weeping, itching Skin and nails appear atrophic Skin is pale, shiny, taut and thin Minimal hair May turn red with dependency and pale with elevation Foot/leg temperatures Higher temperature consistent with chronic venous insufficiency Lower limb cool of cold to touch Exudate and edema Heavy exudate Pitting edema (may predate ulcer) Minimal exudate Limited edema

Arterial vs Venous Ulcers
Labs CBC CRP, ESR Diagnostics ABI, TCOM, Doppler Monofilament testing Imaging MRA Angiogram Venous doppler

Scope of the Problem –Venous Ulcers
Comprises 70% of LE ulcers in the U.S. 500,000-1,000,000 people Over 40% report first ulcer by age 50 13% report first ulcer by age 30 Recurrence rate – 72% at one year US annual healthcare expenditure $ billion Each case > $40,000 2 million annual workdays lost

Scope of the Problem Median duration 9 months
20% have not healed in one year 66% had episodes of ulceration lasting 5 years 2-3% of total US healthcare budget

Etiology Over 50% caused by previous DVT Sedentary lifestyle Obesity
Women Standing Men who smoke

Etiology Primary cause: Reflux through incompetent valves
Venous outflow obstruction (DVT) Superficial reflux – 45% Deep reflux 12% Mixed – 43%

Action of the Musculovenous Pump in Lowering Venous Pressure in the Leg
After prolonged standing, venous pressure in the foot is approximately 90 mm Hg in both a patient with incompetent venous valves and a person with a normal leg. During walking, the musculovenous pump rapidly lowers the venous pressure in the normal leg but is ineffective in the leg with valvular incompetence.

Treatment Underlying pathophysiology is failure of muscle pump
If this is corrected, 93% of all VU’s will heal at a mean of 5.3 months (requires at least 80% compliance with wear) Physical modalities Exercise Compression

Treatment Key Points Compression is the mainstay of therapy
Always precede compression with arterial evaluation of leg 40-50 mmHg is required (30-40 is adequate) Sustained compression is required

Elastic vs. Inelastic Bandages
Unna’s Boot Low resting pressure and high pressure on ambulation Impregnated with Zinc oxide Calamine Glycerin Sorbitol Mg silicate Ace wrap or Coban over boot

Multi-layer compression
Elastic bandages produce sustained compression with minor variations in walking Layer one Soft padding Layer two Ace bandage Layer three Coban

Arterial Ulcers Risk factors Diabetes mellitus
Foot deformity and callus formation resulting in focal areas of high pressure Poor footwear that inadequately protects against high pressure and shear Obesity Absence of protective sensation due to peripheral neuropathy Limited joint mobility

Arterial Ulcers Etiology
Restrictions to blood vessels due to peripheral vascular disease Chronic vascular insufficiency Vasculitis (inflammatory damage of blood vessels) Diabetes mellitus Renal failure High blood pressure Arteriosclerosis (hardening of the arteries) Atherosclerosis (thickening of the arteries, due to the buildup of fatty materials) Trauma Limited joint mobility Increased age

Arterial Ulcers Treatment
Examine feet (especially between the toes) and legs daily for any unusual changes in color or the development of sores. Quit smoking. Smoking can harden or clog the arteries, leading to improper perfusion to the extremities. Manage blood pressure, cholesterol, triglyceride and glucose levels. Ensure that footwear is properly fitted to avoid points of rubbing or pressure. Avoid wearing constrictive socks. Avoid crossing legs while sitting. Avoid sitting or standing for extended periods. Avoid cold temperature. Protect legs and feet from injury and infection. Exercise as frequently as is comfortable.

Pressure Ulcers A pressure ulcer is defined as a localized injury to the skin or underlying tissue usually over a bony prominence as a result of pressure in combination with shear and/or friction

Pressure Ulcers

Capillary Closing Pressures
Capillary closure Local ischemia Impaired cellular nutrition Accumulation of metabolic wastes Cellular death Ulceration Once the capillaries close, cells are deprived of oxygen and the tissue becomes ischemic. Capillary closure also causes interference with cellular nutrition and an accumulation of metabolic waste products. These effects in combination with the prolonged local ischemia ultimately lead to cellular death and ulceration. * Could also result from friction or shear forces

Shear and Friction Skin sticks to surface
Muscle Skin sticks to surface Deeper tissues move in opposite direction Capillaries kink Local ischemia Bone Subcutaneous tissue Dermis Epidermis Shear Friction in combination with gravity can produce shear forces. Gravity pulls down on the body and deeper tissues, while resistance or friction from the bed surface tends to hold the skin in place. This causes angulation, stretching, twisting, or even tearing of capillaries in the affected area, which leads to disruption of blood flow, ischemia, and cellular death. Shear forces can result in ischemia even more quickly than pressure. Think of how easy it is to stop the flow of water through your garden hose by kinking it as opposed to standing on it… Shearing forces most commonly occur when the head of the bed is elevated greater than 30 degrees and the patient slides down. Additional shearing and friction damage can be inflicted if caregivers use improper lifting techniques and drag the bedridden patient up to the head of the bed or across the surface of the bed. SURFACE

Prevention is Key Heel protectors Support surfaces (mattresses/beds)
Paraplegic/quadriplegic Post hip arthroplasty Support surfaces (mattresses/beds) Same as above Altered mental status Dehydrated or malnourished

Common Locations for Pressure Ulcers

Stage 1 - non-blanching erythema of skin
Stage 2 - partial thickness skin loss (epidermis, dermis or both) Stage 3 - full thickness, damage or necrosis to SQ extending to, but not through underlying fascia Stage 4 - Full thickness involving bone, muscle, tendon, joint with sinus tracts and undermining

The Deadly Sins of Staging
The Unstageable Wound The Deep Tissue Injury (infarction of skin) Reverse Staging Shearing Sepsis The whole concept of Reverse Staging is invalid and physiologically inaccurate because it suggests that severe ulcers heal back to normal in terms of anatomically functioning tissue, and this is incorrect. Scar tissue had very different properties than uninjured normal tissue. The most common cause of Stage II ulcers is actual shearing or friction, NOT pressure. Of over 114,000 people whose cause of death was ascribed to pressure ulcers between , almost 40% had septicemia

Pressure ulcer prevention
AHCPR Clinical Practice Guideline Number 3. Pressure Ulcers in Adults: Prediction and Prevention. (AHCPR # , May, 1992) 12,000 abstracts collected (included duplicates from various data sources) 800 manuscripts selected (27% were research based) 26 specific recommendations Class A recommendations: 1 Class B recommendations: 4 Class C recommendations: 21 Class A recommendations: good research-based evidence Class B recommendations: is fair research-based evidence Class C recommendations: expert opinion and panel consensus

Pressure ulcer treatment
AHCPR Clinical Practice Guideline Number 15: Treatment of Pressure Ulcers. (AHCPR # , Dec 1994) 45,000 abstracts collected (included duplicates from various data sources) 17,000 manuscripts selected (40% were research based) 81 specific recommendations Class A recommendations: 2 Class B recommendations: 9 Class C recommendations: 70 Class A recommendations: good research-based evidence Class B recommendations: fair research-based evidence Class C recommendations: expert opinion and panel consensus

Development of Pressure Ulcers
Inside out OR Outside in Moisture and friction DO should not be grouped with pressure ulcers, but often are. Friction produces specific types of tissue damage Strain is the tissue deformation which happens in response to pressure Shear forces are produced with contiguous tissues slide relative to each other in a direction parallel to their plane of contact (may be primary cause of all pressure ulcers For many years the standard explanation was that PU occurred when tissues trapped between a bony prominence and a hard surface were exposed to tensions in excess of mean capillary pressure (32mmHg) resulting in tissue ischemia and necrosis The first evidence of damage is in tissues with highest oxygen demands Epidermal cells are able to withstand prolonged absence of oxygen whereas more metabolically active muscle cells can be more vulnerable to injury

More Resistant to Damage
Tissue Damage More Resistant to Damage More Oxygen Sensitive Tissues near bony prominences experience the most pressure Pressure

Pressure Ulcer Sensation Moderate, constant pain
Increased pain with greater severity of ulcer Typical location Skin overlying bony prominences Exposure of deep structures Exposed or directly palpable fascia, muscle, bone, ligament, cartilage Wound appearance Slough and/or eschar in wound bed Undermining or tunneling Rolled wound edges often present Base color depends on Staging Periwound Indurated, erythematous, macerated or healthy Foot/leg temperature and pulses Localized areas of warmth or coolness Exudate and edema Exudate volume related to size of wound Edema may be indication of Stage I pressure ulcer

Pressure Ulcer Labs Imaging CBC ESR, CRP HgbA1c Tissue culture
Nutritional parameters (albumin, prealbumin, transferrin, total protein) Imaging Plain films or bone scan or MRI to diagnose osteomyelitis

What ARE Risk Factors Low serum albumin Low total lymphocyte count
Fecal incontinence Fractures Increased age Length of paralysis Social state of patient Smoking

Basic Wound Care Principles
Surgical Closure 61% ulcer and 69% patient recurrence in 9.3 months 31% long term success

Guidelines Repositioning schedule Avoid elevation of HOB
Support surface Static Dynamic Avoid prolonged sitting Use seat cushion Exact turning interval is not known Limit amount of time the HOB is elevated and elevate only when there is a compelling medical indication (1-2 hrs. after tube feeding, severe respiratory or cardiac compromise)

Guidelines Nutritional assessment Labs Treat distant infections
Arginine Oxandrolone Labs Albumin, pre-albumin, transferrin, CRP Treat distant infections UTI, Cardiac valves, sinuses Remove ALL devitalized tissue Arginine – necessary for collagen, but no evidence in wound healing when used alone. No acceleration of wound healing has been shown with Vitamin A, C or zinc Oxandrolone – facilitate weight gain, but no evidence of impact on wound healing outcome

Guidelines Determine presence of infection and treat appropriately
Topical Systemic If bone exposed, 90% likelihood of osteomyelitis – biopsy for culture Wound cleansing Moisture balance Systemically administered antibiotics do not effectively decrease bacterial levels in granulating wounds Once confirmed, osteomyelitis underlying a pressure ulcer should be adequately debrided and covered with a myofascial flap

Guidelines 14. Negative Pressure Wound Therapy
Increases wound perfusion and formation of granulation tissue and reduces bacterial load.

Dehisced Surgical Wounds
A complication where a wound breaks open along a surgical incision

Risk Factors Age Diabetes Obesity Trauma to wound postoperatively Smoking Radiation exposure Liver, kidney or heart disease Chronic steroid or immunotherapy use Emergency surgery Malnutrition Immunocompromised Major contributing causes Subacute infection Excessive tension on wound edges Poor surgical technique Poorly perfused wound edges

Appearance Redness Induration Warmth around suture line Suture line separation Sensation Fever Increased, sustained localized pain Location Any closed incision Exudate Frothy or pus Surgical wound entry points that continue to bleed Temperature Localized warmth may precede dehiscence Edema Swelling

Wound Bed Preparation Moist - Optimal absorption / hydration
Warm - Coverage Non toxic - No antiseptics Uninfected - Monitor & manage bacterial loading Clean - Mechanical / chemical debridement

The Ideal Wound Healing Environment
Moist Warm Non toxic Uninfected Clean of debris / devitalized tissue  Granulation  Contraction  Epithelialization Healing is a preferred physiological process – if impairments are removed, healing occurs

Why Moist Healing Chronic Wounds: Acute Wounds: Increased: Decreased:
Leukocyte activity Healing Decreased: Inflammation Infection Scarring (Fibrosis) Chronic Wounds: Increased: Autolytic debridement Growth Factors Granulation Epithelial migration & Healing Decreased: Pain Michie ‘94 Eaglestein ’91; Phillips ‘93

The Ideal Dressing High moisture permeability Non-adherence
High absorbency Good adhesion to surrounding skin Non allergenic Comfortable Cost-effective Scales 1956

Pointers Evaluate wounds in terms of their ability to heal
Elderly, demented, hospice patients may no longer be responsive to curative treatment Best interest and welfare of the patient Diabetes management Usually not the responsibility of the wound care physician Impacts wound healing of all types Obesity and nutrition management Binge diets and poor food choices Just because a patient is obese, doesn’t mean their nutrition is good Nicotine use Inform patients of relationship Nicotine patches should not be used as a substitute for smoking

Pointers Circulation Incontinence Pain Cultures
Consider the likelihood of healing BEFORE creating a wound in a patient who is not a surgical candidate Incontinence Pressure ulcer periwound areas should be treated with skin barriers Pain Pain can relate in vasoconstriction and decreased perfusion, but narcotics can delay wound healing, cause androgen deficiency and increase likelihood of infection Cultures This study demonstrates that swabs and biopsies tend to yield the same culture results when taken from the same location. For frequently occurring microorganisms, agreement between the two methods was even higher. Therefore, there seems to be no direct need for invasive biopsy in clinical practice. Haalboom M, et al. Wound swab and wound biopsy yield similar culture results. Wound Repair and Regeneration. March

Pointers Consider Patient’s potential function Life expectancy
What is the ambulation potential? Life expectancy How will this change the patient’s independence? Risk assessment What risks are involved in aggressive vs. conservative care Remember: WHO reports that average patient nonadherence rate is 50% among those with chronic illness.

Relationship between Opioid Treatment and Rate of Healing in Chronic Wounds
After controlling for co-morbidities and pain score, opioid exposure was associated with delayed wound healing Opioid exposure may impact keratinocyte biology and wound healing Opioid exposure in the post-op period was associated with wound dehiscence Opioid exposure may impact ultimate wound healing and increase time to healing

Why? There are functionally active μ-opiate receptors on human keratinocytes. Activation of these receptors by the μ-opiate agonist β-endorphin results upregulation of TGF-β and cytokeratin 16 Shown that CK 16 response can be blocked by incubation together with the μ- opiate receptor antagonist naltrexone Biligardi PL, Sumanovski LT, Büchner S, et al. Different Expression of μ-Opiate Receptor in Chronic and Acute Wounds and the Effect of β-Endorphin on Transforming Growth Factor β Type II Receptor and Cytokeratin 16 Expression. J Invest Derm. 120:1, Jan

Non-healing stratified by opiate exposure

Non healing stratified by opiate dose
Shanmugam VK, Couch KS, McNish S, Amdur RL. Relationship between Opioid Treatment and Rate of Healing in Chronic Wounds. Accepted Article doi:10.111/wrr

The neuroendrocrine inhibitory effects of opioids on gonadal function were first reported over 30 years ago. Effect can occur within hours with testosterone concentrations reaching castration levels in 86% of men.

Opioid-induced adrenal insufficiency occurs because of suppression of hypothalamic pituitary-adrenal communication and may be challenging to diagnose but has been reported in 9% to 29% of patients receiving long-term opiate therapy.

Advances in Skin & Wound Care – March 2017

https://onlinelibrary.wiley.com/doi/epdf/10.1111/wrr.12396

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Diagnosis and evaluation of chronic ulcers

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