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Lower Extremity Neuropathic Disease

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:

Slide1

Lower Extremity Neuropathic Disease

Presented by Frances L Wilson CNS, MSN, CWOCN & CFCN

May 14, 2016

Slide2

Objectives

Upon completion of this presentation Participants will

 

be able to:

Discuss the

epidemiology, etiology

and pathology of LEND (lower extremity neuropathic disease)

Identify how diabetes and disease management interventions affect wound

healing

Identify concepts of basic wound healing and optimal wound healing environment

issues

Discuss basic treatment interventions for prevention and care of neuropathic wounds

Improved understanding of the pathway to foot amputation in diabetes

 

Discuss

evidence based tools for Diabetic Foot Screening

Slide3

Scope of Public Health Challenge with

Wounds

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)

Not enough

specialty

trained health care providers

Slide4

CDC

2014 Statistics/Epidemiology

73,000

non traumatic

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.

Slide5

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.

Slide6

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

Slide7

Currently, the majority of non traumatic primary amputations

related to Diabetes Mellitus occur

in an

emergent

fashion or after a prolonged course of non-integrated medical management and wound care.

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Mortality rates following primary amputation reach 40% at one year postoperative and 80% at five years.

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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

Slide12

Complications from neuropathy account for more hospitalizations than ALL other diabetic complications combined!

Slide13

Even more important is the fact that at least 50% of all amputations due to neuropathy

are preventable with early

intervention.

CDC 2014

NIH 2014

WOCN 2012

Slide14

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.

Slide15

However, the type and severity of functional impairment and symptoms

depend

on

the

type and severity of nerve damage and can be broadly categorized as

:

SENSORY

MOTOR

AUTONOMIC

MIXED

Slide16

Sensory

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.

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Motor

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.

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Musculoskeletal AbnormalitiesHammer (Claw) Toes

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Autonomic

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.

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Autonomic

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.

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Care and Treatment

Need to be followed by podiatrist for preventive foot care

Pumice stone

Vinegar-water soaks for 10 minutes 2-3 times /

wk

followed by light buffing to remove dry skin (good drying between toes!!)

Emollients to soften tissue (never between toes)

No bathroom surgery

Proper footwear

**Medicare covers 1 pair of extra depth shoes and 3 pairs of molded inserts/year. Must have RX, should be sent to orthoptist/

pedorthist

to assure shoes are fitted correctly and have appropriate insoles.

Slide36

Charcot Arthropathy

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The Human Body “wired” to Heal

Slide45

Normal

Wound Healing

Four phases overlapping/special cells (keratinocytes, fibroblasts, endothelial cells, macrophages, platelets)

Hemostasis-platelets, growth factors (immediate)

Inflammation-macrophages, leucocytes, mast cells (day 1-4)

Proliferation-fibroblasts, myofribroblasts, endothelial cells

Remodeling (maturation) (Day 21 – 2 years)

Slide46

Factors Known to Impair Wound Healing

Systemic

Nutrition deficiencies Collagen Disorders

Aging Stress

Alcoholism Medications

Uremia Diabetes

AIDS/HIV

Slide47

Diabetes and Wound Healing

Has major hemorrheological alteration

Affects RBCs- decreases RBC deformability, increases aggregability

Increased blood viscosity

DM causes decreased nitric oxide and increased cytokines leading to functional vasoconstriction and possible thrombosis

Increase in Reactive Oxygen Species (ROS) cased by hyperglycemia, hyperinsulinemia, and insulin resistance

Diminished tissue perfusion

Chronic inflammation

Decreased platelet plasticity/increase in platelet aggregation

DM causes vascular membrane thickening, intravascular fibrosis slowing of oxygen and nutrient transit, endothelial dysfunction and peripheral occlusive arterial disease

Slide48

DM and Risk for DFU

Intrinsic: Neuropathy, PVD, Diabetes Severity

Extrinsic: Wound Infection, Callus formation, Trauma

Slide49

DM and DFU Current Therapies

(Tecilazich et al, 2011)

Debridement

Off loading

Growth factors

Revascularization

Treating Infection

Local Wound Care (Basic and Advanced)

Slide50

Normal Healing Versus DM

NORMAL

Hemostasis

Inflammation

Proliferation

Maturation

Impairment in DM

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.

Slide51

Why Diabetics have healing challenges

Blood Sugars

Vascular challenges

Lack of comprehensive management

Poor compliance

Lack of understanding of about the seriousness of wounds,

both the patient and health care providers

Slide52

I’ve healed this before

Slide53

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

st

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.

Slide54

Repetitive stress results in inflammatory changes in tissues—the patient with LOPS (Loss

of Protective

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.

Slide55

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).

Slide56

Characteristics of Neuropathic Ulcers

Shape

- 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.

Wound base-

May be necrotic, pink, or pale. Depth varies from partial thickness to deep bone involvement.

Periwound

- 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.

Exudate

-Drainage usually small to moderate (unless infected!)

Location

- 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

st

and 5

th

metatarsal heads

Slide57

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.

Slide58

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).

Slide59

Tissue Integrity

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.

Slide60

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****

Slide61

Moisture Balance

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.

Slide62

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.

Slide63

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!!

Slide64

Osteomyelitis

Slide65

Osteomyelitis

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.

Slide66

Osteomyelitis

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

systemic

antibiotics (WOCN, 2012)

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Care and Treatment

Ensuring patient is on the correct antibiotic

Absorb drainage

Protect the skin around the wound

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

BS controlled

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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.

Slide81

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

>non infected

>adequate blood supply to heal (ABI grater than or equal to 0.7) and ulcer must be Wagner grade I or II

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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

Smoking cessation

Keeping weight WNL…

Starting to sound familiar???

Slide85

Evidence Based Screening Tool

Slide86

Conclusion

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.

Slide87

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

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ReferencesBeitz, Janice-WOCN 2012 National Conference Presentation, The Impact of Chronic Disease on Wound Healing/Wound Causation.

Blair, M. (2016). Diabetes mellitus review. Urologic Nursing 36 (1), 27-36.

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

Outcomes. Podiatry Today Volume 29-Issue 3.

Wound Management, WOCN Core Curriculum, edited by Dorothy Doughty & Laurie McNicol

(2016). Wolters Kluwer. Pages 466-507.

Available at

http://www.ecd.gov/diabetes/pdfs/data/2014-report-estimates-of-diabetes

. Last accessed May 7, 2016.