Presented by Frances L Wilson CNS MSN CWOCN amp CFCN May 14 2016 Objectives Upon completion of this presentation Participants will be able to Discuss the epidemiology etiology and pathology of LEND lower extremity neuropathic disease ID: 784633 Download
Sharon D. White, BSN,RN,CWOCN. University of Alabama - Birmingham. Objectives. Identify different types of lower leg ulcers. Describe at least 3 major risk factors that may contribute to arterial, venous and diabetic ulcers.
brPage 2br You have recently had an amputation due to trauma lack of blood supply or infection This booklet will provide helpful information and tips For the first few days you may remain in bed to prevent swelling of your stump Discomfort of the St
Please provide an answer for eac h activity Today do you or would you have any difficulty at all with Activities Extreme Difficulty or unable to perform activity Quite a bit of difficulty Moderate difficulty A little bit of difficulty No difficulty
Presented by Frances L Wilson CNS, MSN, CWOCN & CFCN. May 14, 2016. Objectives. Upon completion of this presentation Participants will . . be able to:. Discuss the . epidemiology, etiology . and pathology of LEND (lower extremity neuropathic disease).
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Lower Extremity Neuropathic Disease
Presentation on theme: "Lower Extremity Neuropathic Disease"— Presentation transcript:
Lower Extremity Neuropathic Disease
Presented by Frances L Wilson CNS, MSN, CWOCN & CFCN
May 14, 2016
Upon completion of this presentation Participants will
be able to:
and pathology of LEND (lower extremity neuropathic disease)
Identify how diabetes and disease management interventions affect wound
Identify concepts of basic wound healing and optimal wound healing environment
Discuss basic treatment interventions for prevention and care of neuropathic wounds
Improved understanding of the pathway to foot amputation in diabetes
evidence based tools for Diabetic Foot Screening
Scope of Public Health Challenge with
Nearly 7 million people with chronic wounds in the USA
Over 20 billion dollars of health care is spent on chronic wound management
Situation is intensifying and worsening with the aging population
(Friedman, 2011:Sen et al, 2012)
trained health care providers
amputations in adults 20 years or older
60% of these amputations occurred in patients with diabetes, making diabetes the MOST common cause of non –traumatic amputation in the U.S.
One diabetes-related primary lower extremity amputation occurs every 30 seconds worldwide, resulting in over 2,500 limbs lost per day
In 2012 the total healthcare costs related to diabetes were $245 billion, accounting for
25 % of all Medicare expenditures
The direct medical costs related to diabetes, $176 billion, were more than twice the direct medical costs of treating people without diabetes.
The remaining $69 billion are the indirect costs of diabetes due to disability, lost time at work and premature death.
Healthcare costs related to diabetic lower extremity ulcerations flow from the requirement for hospital admission and inpatient costs that increase further when one must address poor vascular status via endovascular or open surgical procedures.
Whether payment occurs via Medicare or private payer insurance, inpatient expenditures account for 73 to 80 percent of the total healthcare costs of treatment.
Contrast this with routine outpatient wound care, which accounts for less than 25 % of healthcare costs related to wound care.
True Cost of Primary Amputation
Loss of function and independence
Reduced quality of life
Increased mortality rate
Some researchers claim that primary amputation will lead to shorter recovery time and ambulation with prosthesis, only 47 to 67 percent of patients with ischemia and/or ulceration who undergo primary amputation successfully rehabilitate to this level
30% increased incidence of depression
Self reported diminished physical and mental scores on various health questionnaires
Currently, the majority of non traumatic primary amputations
related to Diabetes Mellitus occur
fashion or after a prolonged course of non-integrated medical management and wound care.
Mortality rates following primary amputation reach 40% at one year postoperative and 80% at five years.
The FDA has only approved two drugs for the treatment of diabetic neuropathy :
1. pregabalin (Lyrica) an anticonvulsant
2. duloxetine (Cymbalta) a serotonin-norepinephrine reuptake inhibitor
Complications from neuropathy account for more hospitalizations than ALL other diabetic complications combined!
Even more important is the fact that at least 50% of all amputations due to neuropathy
are preventable with early
Pathology, and Manifestations of Peripheral Neuropathy
There are more than 100 specific types of peripheral neuropathy, and each has a characteristic pattern of development, symptomatology, and prognosis.
However, the type and severity of functional impairment and symptoms
type and severity of nerve damage and can be broadly categorized as
Sensory nerves transmit messages related to touch, position, pressure, temperature, and pain such as the feeling of light touch or the pain caused by stepping on a sharp object.
Sensory nerve damage causes a complex array of symptoms because sensory nerves have a diverse and highly specialized range of functions.
Patients with sensory nerve damage are typically unable to coordinate complex movements like walking or maintaining balance when their eyes are shut and are at increased risk of falling.
More significantly, individuals with progressive sensory neuropathy lose the ability to recognize minor (eventually major) trauma to the feet.
Motor nerves control movement and tone of the muscles of the foot and affect foot contours, weight bearing and gait.
Damage to these nerves alters the contours of the foot, resulting in foot deformities, abnormal weight bearing patters and altered gait.
Abnormal rigidity of the toes and ankles due to atrophy of the intrinsic muscles is a common manifestation of motor neuropathy and cause increased plantar foot pressure when walking.
Soft tissue glycosylation can result in shortening of the Achilles tendon, which causes deformities such as abnormally prominent metatarsal heads and claw toes.
Musculoskeletal AbnormalitiesHammer (Claw) Toes
Autonomic nerves regulate biologic activities that are not under conscious control, such as thermal regulation and sweating, and blood vessel tone and diameter.
Loss of autonomic control of the sweat glands commonly manifests in severely dry skin (anhidrosis)that may result in partial-thickness or full thickness fissures; these wound then permit invasion of pathogens that can cause serious soft tissue infections.
Autonomic neuropathy can also cause persistent vasodilation of the arterial vessels in the foot, due to loss of sympathetic innervation, which normally provides for partial constriction when the foot is at rest.
Persistent high volume blood flow is thought to contribute to the demineralization of the bones in the foot over time, eventually producing thin fragile bones (osteopenia) that are vulnerable to fracture.
Autonomic involvement may also compromise the function of other body systems, causing complications such as urinary retention due to loss of detrusor contractility, gastroparesis and persistent vomiting due to the loss of gastric motility, or lower extremity edema due to cardiovascular compromise.
Care and Treatment
Need to be followed by podiatrist for preventive foot care
Vinegar-water soaks for 10 minutes 2-3 times /
followed by light buffing to remove dry skin (good drying between toes!!)
Emollients to soften tissue (never between toes)
No bathroom surgery
**Medicare covers 1 pair of extra depth shoes and 3 pairs of molded inserts/year. Must have RX, should be sent to orthoptist/
to assure shoes are fitted correctly and have appropriate insoles.
Increased risk of infection due to poor vascular supply
Slowed recruitment of neutrophils. Persistent inflammation, slowed macrophage activity
Reduced tensile strength of collagen and collagen deposition. Reduced fibroblast activity
Reduced tensile strength f collagen. Reduced risk of ulcer recurrence due to scaring.
Why Diabetics have healing challenges
Lack of comprehensive management
Lack of understanding of about the seriousness of wounds,
both the patient and health care providers
I’ve healed this before
Pathology of Neuropathic Ulcers
Breakdown most commonly occurs in areas exposed to painless, repetitive trauma from friction or pressure:
Where shoes rub on the back or side of the heels or the tops of the toes
On the plantar aspect of the foot, beneath the metatarsal heads where the fat pads have thinned (1
metatarsal head is the most common location)
Plantar aspect of the foot where calluses have formed from toe or foot deformities or altered gat
Between toes from excess pressure or friction or in the presence of excess moisture.
Repetitive stress results in inflammatory changes in tissues—the patient with LOPS (Loss
Sensation) is unaware/does not modify gait or footwear as a person with intact sensation would do, therefore get additional trauma and damage, and eventual ulceration.
Patients can have both neuropathy and PAD, so must always assess for coexisting compromise in perfusion; however, neuropathy is frequently seen in patients with warm feet and good pulses (approximately 60% of “diabetic foot ulcers” are due to neuropathy with NO ischemic component).
Characteristics of Neuropathic Ulcers
- Usually rounded or oblong and found over a bony prominence. May initially be covered with callus tissue, may resemble laceration, puncture, or blister if from direct trauma, shearing, or heat.
May be necrotic, pink, or pale. Depth varies from partial thickness to deep bone involvement.
- Callus formation around the wound is common, continued development of callus after serial debridement may indicate inadequate offloading. Also may have maceration, erythema and induration.
-Drainage usually small to moderate (unless infected!)
- Majority are located at pressure points and bony deformities on the plantar surface of the forefoot. Most common sites are the interphalangeal joint of the great toe and 1
Management of neuropathic ulcers
Reduce or eliminate pressure and trauma: Offloading
Evaluate perfusion and initiate vascular consult if indicated. Please remember this is don’t remember anything else!! If wound is ischemic and covered with dry eschar and there are no s/sx of infection:
DO NOT DEBRIDE
Control glucose levels as close to normal as possible, 100 to 140. MUST keep glucose under 180 to maintain adequate leukocyte function. Hyperglycemia may affect growth factor/cytokine production as well.
Wound Bed Preparation
The process of identifying common impediments to healing chronic wounds and implementing corrective management strategies to promote closure.
The process is orderly and based upon well demonstrated scientific evidence, using the
TIME Mode (Tissue integrity, inflammation/Infection, Moisture balance, Edge progression).
Necrotic tissue is a known risk factor for wound infection and for delayed healing; thus prompt and complete debridement of ALL necrotic debris, both visible and non visible is essential to the establishment of a clean wound bed that supports repair.
Periwound callus is a common complication of plantar surface neuropathic wounds and is indicative of continued repetitive pressure and shear on the wound.
Callus actually increases soft tissue trauma from pressure and shear if the patient continue to walk, and calloused wound edges prevent epithelial resurfacing.
Thus callus should be routinely removed by means of paring.
Inflammation and Infection
High bacterial counts and/or prolonged inflammation leads to high levels of inflammatory cytokines and protease activity and decreased growth factor activity, all of which impair wound healing.
Removal of infected debris and use of topical antimicrobials and systemic antibiotics are frequently required to reverse inflammation, balance wound bacterial loads, reduce cytokine and protease activity and restore wound healing potential.
****TIGHT glycemic control is also essential, since hyperglycemia interferes with normal white blood cell function****
Moisture balance is essential to promote granulation tissue formation and epithelial migration across the wound surface.
Excessive wound moisture creates edematous hypergranulation tissue and macerates wound edges, which delays wound healing.
Inadequate wound moisture, desiccation, removes the fluids that support wound healing and cell migration and causes cell death.
Effective wound management must include exudate management and maintenance of a moist wound surface.
Epithelial Edge Advancement
An open epithelial wound edge is essential for keratinocyte migration, epithelial resurfacing, and wound closure.
Effective healing requires the reestablishment of an intact epithelium and restoration of skin function.
Wounds with extensive undermining of the wound edge may require surgical debridement, and surface wounds that fail to epithelialize may require skin grafts, or skin substitutes.
If we know the right way to care for these wounds why aren’t we???
Wounds are usually advanced when discovered
Patients are rarely provided optimal therapy initially (once the wound is infected, things finally get ramped up!!)
Most practitioners are not familiar with evidence based wound care
Many patients do not realize the seriousness of this situation
Lack good standards on how we deal with wounds
Wound care is big business, that is poorly monitored….lot’s of players…Home Care, Acute Rehab, Wound Care Centers, Podiatrist, Vascular Surgeons, Primary Care Physicians, Plastic Surgeons, Orthopedic Surgeons, Acute Care Hospitals, the VA, the Local Drug Store (CVS, Walgreens, RiteAid)===everyone is doing something different!!
Osteomyelitis is an infectious complication of importance in the management of diabetic foot ulcers because there are multiple bones in each foot and very little soft tissue: thus, surface infection can rapidly progress to deep soft tissue and bone infection.
In addition, diabetes is associated with three comorbid conditions that increase the risk of bone infection: immunocompromised, neuropathy, and arterial disease.
Osteomyelitis should be suspected with any tunneling wound and any wound with exposed bone and must be ruled out when there is evidence of Charcot osteoarthropathy.
MRI has demonstrated the highest sensitivity and specificity for evaluating soft tissue and bone pathology in patients with diabetes and foot ulcers.
When osteomyelitis is determined to be present, bone biopsy with culture is recognized as the gold standard for determining the specific pathogen and its sensitivities.
Limited evidence suggest that oral agents may be as effective as
Wound WILL NOT heal until infection is resolved, if it does heal it will reopen
Need to be followed by a podiatrist for preventive foot care
A TCC minimizes ground reactive pressure and shear (friction) stresses through intimate total contact with the forefoot, arch, heel, Achilles tendon, and cone of the lower leg. A TCC will eliminate the propulsive phase of gait, shorten stride length, allow for healing while ambulating, and force patient compliance.
Who needs TCC?
Patients being treated for (1) neuropathic foot ulcers
(2) Charcot neuroarthopathy
(3) post operative surgical site protection.
What are the indications for TCC
>adequate blood supply to heal (ABI grater than or equal to 0.7) and ulcer must be Wagner grade I or II
Prevention for Patients
Routine Self Care (never going barefoot, inspecting feet daily, breaking in new shoes gradually)
Early recognition and prompt reporting of potential foot problems
Routine foot surveillance by health care providers
Individual footwear requirements
Tight glycemic control
Keeping weight WNL…
Starting to sound familiar???
Evidence Based Screening Tool
The goal in management of the diabetic patient with neuropathy is prevention of ulceration and amputation, which requires appropriate footwear, daily foot care, and daily foot inspection.
Effective management of neuropathic ulcers requires attention to off-loading, glycemic control, aggressive debridement to eliminate necrotic tissue, and systemic and topical therapies to control bacterial loads.
Caring for these patients truly calls for a interprofessional (multidisciplinary), integrated approach.
Patients have to understand the seriousness of their situation and be involved with their care.
We should employ the motto:
toe before foot, foot before leg and leg before life” in every instance of patients presenting with diabetic lower extremity amputation
ReferencesBeitz, Janice-WOCN 2012 National Conference Presentation, The Impact of Chronic Disease on Wound Healing/Wound Causation.
Karam J. Shepard A, Rubinfeld I. Predictors of operative mortality following major lower extremity amputations using the National Surgical Quality Improvement Program Public use date. J Vasc Surg. 2013: 58 (5):1276-82.
Ponticello, M. Andersen, A. Marmolejo, V. (2016).
Limb Salvage Versus Amputation: A Closer Look At The Evidence, Costs And Long-Term