wound care in the post acute, rehabilitative setting care in the post acute, rehabilitative setting...

Wound Care in the Post Acute, Rehabilitative Setting

By: Phillip Zingale PAC

Objectives

• Identify the physiologic phases of wound healing

• Identify the appropriate diagnostic modalities involved in differentiating wound etiology

• Identify the varieties of modalities of wound treatments

Wound Care - A Burden to Society

A rough estimate is 2% prevalence rate of the general population suffers from chronic non-healing wounds

Costs

• Estimates of exceeding 50 Billion Dollars a Year in overall costs

• The annual Venous Leg Ulcer costs in the US are between 14.9 and 1.9 Billion Dollars

• The annual Diabetic Foot Ulcer (DFU) treatment costs are between 9.1 and 13.2 Billion Dollars

• The annual Pressure Sore treatment costs are between 9.1 and 11.6 Billion Dollars

Definition of a Wound

• A wound by true definition is a breakdown in the protective function of the skin

The loss of continuity of epithelium, with or without loss of underlying connective tissue (i.e. muscle, bone, nerves) following injury to the skin or underlying tissues/organs caused by surgery, a blow, a cut, chemicals, heat/cold, friction/shear force, pressure or as a result of disease

Wound Care – Anatomy and Physiology

• SkinLargest organ of the body

Dermis

Epidermis

Sub-dermis (Subcutaneous)

http://www.webmd.com/skin-problems-and-treatments/picture-of-the-skin#1


• Skin Main Functions:Protection

Regulation: controls variations in temperature

Sensation: allows interpretation through impact and pressure


• Phases of Wound HealingInflammatory Phase

Proliferative Phase

Maturation Phase

http://www.maximisesportstherapy.com/blog/what-happens-when-an-injury-occurs-a-simple-guide-to-the-stages-of-healing


• Inflammatory PhaseNatural response to injury

Hemostasis

Antibodies, White Blood Cells,

Growth Factors, Enzymes & Nutrients

Rise in Exudates (Maceration)

Erythema, Heat, Edema, & Pain(The predominant function of phagocytic cells mounting a host response with neutrophils and macrophages autolyzing any devitalized necrotic/sloughy tissue)


• ProliferationWound Rebuilding ProcessNew Granulation Tissue

CollagenExtracellular Matrix

Angiogenesis: formation of new blood vesselsFibroblast: action maintaining healthy granulation dependent on sufficient oxygen & nutrients supplied by new blood vessels via angiogenesisIndicators of Wound Healing Progress:

Color of granulationFriabilityEpithelialization


• Maturation PhaseFinal phase occurs once the wound has closed

Re-modelling - Transition of collagen type III to collagen type I

Cellular activity reduces, and the number of blood vessels in the wounded area regress and decrease

Most Common Wounds Encountered in Rehabilitation• Surgical Wounds

• Pressure Sores

• Wounds Attributed to Vascular Diseasel: Venous Stasis Disease

ll: Arterial Insufficiency

• Diabetic Wounds – Diabetic Foot Ulcers (DFU)

• Traumatic Wounds

Most Common Wounds Encountered in Rehabilitation• Surgical Wounds

A cut or an incision made by a scalpel during surgery

Drain placement during surgery

Most common causes of surgical wounds not healing are:

Infection

Ischemia

Malnutrition

Various disease entities including immunocompromised states

https://pblinsurgery.wordpress.com/2014/01/19/abdominal-wound-dehiscense/

Most Common Wounds Encountered in Rehabilitation• Pressure Injury (formerly known as

pressure sores)A pressure injury is localized damage to the skin and underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and maybe painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and condition of the soft tissue.

http://www.webmd.com/skin-problems-and-treatments/four-stages-of-pressure-sores

Most Common Wounds Encountered in Rehabilitation• Pressure Injury

• Stages:Stage l: Non Blanching Erythema of Intact SkinIntact skin with a localized area of non blanching erythema which may appear differentlyIn darkly pigmented skin. Presence of blanching erythema or changes in sensation, temperature or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury.

http://decubitusulcervictims.com/info/stages-of-decubitus-ulcers/ http://www.msktc.org/sci/factsheets/skincare/Recognizing-and-Treating-Pressure-Sores#stageone

http://www.msktc.org/sci/factsheets/skincare/Recognizing-and-Treating-Pressure-Sores#stageone


• Stages:Stage ll: Partial thickness skin loss with exposed dermis

The wound bed is viable, pink or red, moist and may also present as an intact or ruptured serum-filled blister Adipose and deeper tissues are not visible. Granulation tissue, slough and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture associated skin damage (MASD) including incontinence dermatitis(IAD), intertriginous dermatitis(ITD), medical adhesive related skin injury(MARSI), or traumatic wounds (skin tears, burns, abrasions).

http://bedsore.com/pictures-of-pressure-sores/


• Stages:Stage lll Full thickness skin loss

Adipose is visible in the ulcer and granulation tissue and epibole ( rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament cartilage and bone are not exposed.

http://www.npuap.org/online-store/product.php?productid=17534


• Stages: Stage lV: Full Thickness Skin and Tissue Loss

Full thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location.

sci.washington.edu/info/forums/reports/pressure_ulcers_2012.asp#4


• Stages: Unstageable InjuryFull thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a Stage lll or Stage lV pressure injury will be revealed. Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be removed.

http://www.npuap.org/online-store/product.php?productid=17531 http://sci.washington.edu/info/forums/reports/pressure_ulcers_2012.asp


• Deep Tissue Pressure Injury: Persistent non-blanching deep red, maroon or purple discoloration.

lntact or non-tact skin with localized area of persistent non-blanching deep red, maroon, purple discoloration or bed epidermal separation revealing a dark wound or blood filled blister. Pain and temperature change often precede skin color interface. The wound may evolve rapidly to reveal the actual extent of tissue injury or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures are visible, this indicates a full pressure injury. Do not use DPTI to describe vascular, traumatic, neuropathic, or dermatologic conditions.

www.msktc.org/sci/factsheets/skincare/Recognizing-and-Treating-Pressure-Sores#stagedeeptissueinjury

Most Common Wounds Encountered in Rehabilitation• Wounds attributed to vascular

disease• Venous stasis disease

• Arterial insufficiency

http://www.yourveinexpert.com/chicago-il-vein-doctor-explains-difference-vein-disease-arterial-disease/

Most Common Wounds Encountered in Rehabilitation• Wounds attributed to vascular disease

• Venous stasis diseaseVenous stasis disease causes venous ulcers (also known as stasis, insufficiency or varicose ulcers). They are caused by malfunctioning venous valves, which results in increased pressure in the veins. This increased pressure in the veins causes blood to pool and the walls of the veins to stretch. Blood products then infiltrate into the subcutaneous tissues causing edema and tissue destruction due to reduced oxygen and other nutrients.

Fibrin Cuff Theory: The protein fibrin coats arterioles, which inhibits the diffusion of oxygen and other nutrients.

Common causes of venous stasis disease are varicose veins, deep venous thrombosis or even congestive heart failure.

Most Common Wounds Encountered in Rehabilitation• Wounds attributed to vascular

disease• Venous stasis disease

Stasis dermatitis: scaling and erythema of the skin in the lower extremities.

Skin may appear brown or yellow due to hemosiderin deposits.

Lipodermatosclerosis, skin induration (thickening) frequently occurs

hardinmd.lib.uiowa.edu/dermnet/dermatitisstasis10.html


• Venous stasis diseaseVenous ulcers: These wounds typically occur on the lower aspect of the legs. They are usually shallow with irregular margins. Wound beds are erythematous and will weep. With infection, which is a common complication, considerable drainage may occur.

Conditions that may increase risk for venous stasis disease are:

Diabetes mellitusCongestive heart failure

Peripheral vascular disease

Deep vein thrombosisPregnancy

Obesity

www.aafp.org/afp/2010/0415/p989.html


• Arterial insufficiencyInsufficient delivery of nutrient-rich blood to peripheral extremities, predominantly lower extremities, can commonly lead to ischemia and subsequent breakdown of skin. An at-risk extremity will have diminished or absent peripheral pulses, may be cool to the touch and have decreased capillary refill. Skin may appear atrophic and demonstrate hair loss.

These wounds typically are described as being “punched out” or “scooped out.” They are round, have sharply defined edges and may be very painful. Commonly these wounds are deep, extending to underlying tissues. They will not bleed and tend to be covered with brown or gray slough or black necrotic tissue or eschar.

dermaamin.com/site/atlas-of-dermatology/1-a/118-arterial-ulcer-.html

Most Common Wounds Encountered in Rehabilitation• Diabetic wounds (Diabetic foot ulcers)

• Diminished sensation in the periphery (notably the foot) can result in microinjuryand subsequent breakdown and ulceration of the overlying tissue. The impairment of peripheral nerves leads to diminished sensation (temperature or pain) in the feet. Thus, minor trauma (scrapes, cuts, burns, etc) can progress to significant ulcerated wounds because the wounds go unnoticed.

• Motor deficits as a result of neuropathy can lead to atrophy of muscles, impacting balance. Further, deformities may develop due to flexor and extensor muscle damage (claw toes, prominent metatarsal heads, Charcot deformity), putting unnatural stress on tissues. This stress lends itself to further microinjury and potential for ulcerative lesions.

http://cottonwoodpodiatry.com/diabetic-wound-care

Most Common Wounds Encountered in Rehabilitation• Diabetic wounds (Diabetic foot

ulcers)Wounds are typically undermined, can be macerated. Commonly they demonstrate surrounding heavy callous and the depth of the lesion is dependent upon the extent and duration injury.

http://www.balanceorthofoot.com/diabetic-foot-care-avoiding-amputation/


Wagner Grading System

Grade 1: Superficial Diabetic Ulcer

Grade 2: Ulcer extension

Involves ligament, tendon, joint capsule or fascia

No abscess or osteomyelitis

Grade 3: Deep ulcer with abscess or osteomyelitis

Grade 4: Gangrene to portion of forefoot

Grade 5: Extensive gangrene of foot

Most Common Wounds Encountered in Rehabilitation

https://mobile.twitter.com/Doctor_Yousif/status/669088359747346432


• InfectionA very common complication of diabetic wounds is infection, which may progress to osteomyelitis. This is largely in part due to the mixture of both ischemia from micro-arterial insufficiency, neuropathy and delayed wound healing. Without aggressive treatment, these wounds will progress significantly, frequently leading to extensive complications (sepsis, amputation).

Most Common Wounds Encountered in Rehabilitation• Traumatic Wounds

Lacerations, hematomas, burns, other injuries that occur in a hospital setting

http://www.podiatrytoday.com/how-treat-traumatic-wounds-lower-extremity

Diagnostics in Wound Care

• Laboratory

• Imaging

• Diagnostic Procedures


• LaboratoryCBC: leukocytosis, anemia, thrombocytopenia

BMP: electrolytes renal function

Albumin (prealbumin, transferrin)

Coagulation Studies

Tissue Cultures: Deep vs Superficial


• ImagingPlain Radiography

CT Scan

MRI/MRA

Ultrasound

Vascular Ultrasound/Limb Plethysmography

Technetium Tc 99m-labeled WBC scanning (Bone Scan)


• Diagnostic ProceduresTissue Biopsy

Transcutaneous Oximetry

Wound Care Treatment

• History & Physical ExamAssess Systemic Disorders as they relate to wound etiology

Endocrine: Diabetes, Thyroid

Cardio-Pulmonary

Hematologic

Vascular

Nutritional Status


• Key Factors in Wound TreatmentDebridement

Infection Control

Moisture Balance


• DebridementThe procedure or action which eliminates non-viable devitalized, infected tissue and/or foreign material from a wound, which helps minimize antimicrobials, toxins and any other substances that restrict healing.

Material such as soft necrotic tissue, nonviable tendon, muscle and bone have demonstrated inhibition to host defense response and prone tissues to active infection.


• Debridement Autolytic

Mechanical

Enzymatic

Sharp


• Autolytic DebridementNatural response to injury at various levels

WBC’s produce endogenous enzymes: elastase, collagenase, myeloperoxidase, acid hydrolase & lysosomal enzymes

Autolytic Debridement is enhanced by the use of occlusive dressings

Typically is painless, maintains a moist wound bed and promotes healthy granulation

Products to Enhance Autolytic DebridementHydrogels

Honey: anti bacterial action, acts as a deodorant and possesses anti-inflammatory properties


• MechanicalA method of using mechanical force to remove tissue from a wound.

Wet-to-dry wet gauze is placed into a wound and allowed to dry. When removed devitalized tissue is stuck or trapped within the gauze and forcibly removed.

Hydro-Therapies:Pressurized Irrigations

Whirlpool

Negative Pressure Wound Therapy (NPWT)


• Enzymatic DebridementIs a highly selective technique of debridement that incorporates naturally produced proteolytic enzymes bioengineered by pharmaceutical companies for the purpose of wound debridement.

Collagenase Derived from Clostridium histolyticum

Digest Triple Helical Collagen

Avoids degrading proteins that do not possess a triple helix. Thus making collagenase a selective debriding agent.

Papain/Urea fruit derived (no longer available in the US)


• Sharp Debridement Quickest method to rid devitalized tissue and prepare a wound bed

Often requires the use of an anesthetic agent topical or injectable and on occasion general anesthesia for extensive procedures done in the OR.

Looked upon as a selective method; viable tissue may be damaged, however this may be beneficial as this delivers growth factors and cytokines to the wound bed which potentiates the healing process.


• Infection Control Chronic wounds all contain bacteria (wounds may still heal)

What is important is the interaction with the host that determines the course of wound healing

Contamination: non-replicating microorganisms

Colonization: adherent microorganisms that replicate but do not cause cellular damage

Localized Infection: increased bioburden which can be indistinguishable between colonization and infection

Characteristics: delayed healing, pain, friable wound bed (bleeds easily), odor

Spreading Infection: replicating microorganisms within a wound with a host response of delayed wound healing

Characteristics: erythema, warmth, pain, foul odor, often purulent drainage, sepsis


• AntibioticsUseful in treating infected wounds, but most important in eradicating spreading infections (cellulitis, ascending lymphangitis). Should not be considered first line treatment.

OralIntravenousTopical

• Slow Release AntisepticsUnlike Antibiotics; Slow Release Antiseptics mode of action is on several levels, attacking bacteria at the cell membrane, cytoplasmic organelle and nucleic acid level (bacterial resistance is rare)

Silver topicalsCadexomer iodine


• Moisture BalanceMoist Wound Treatment

The “Cardinal Rule: the Wound stays wet; the Skin stays dry.”In 1962 George Winter PhD, University of London conducted a study by creating multiple small partial thickness wounds on the backs of pigs. Portions of the wounds were allowed to dry and form scabs, while the remainders were covered with a polymer film.

The results showed the wounds that were covered by the film epithelialized twice as quickly as those wounds exposed to air.


• Wound applications to keep wounds moist:Normal Saline Solution

Isotonic Sodium Chloride Gel

Hydro-active Paste (hydrocolloids)

Occlusive Dressings (Polyvinyl film dressings)


• Application for wet wounds (exudative wounds)Calcium Alginate Products

Hydro-fiber dressings

Polyurethane or Silicone foams


• Collagen in wound treatmentCollagen is the primary protein of the Extra-Cellular Matrix(ECM)

Matrix Metalloproteinases typically form in abundance in chronic wounds and degrade viable collagen thus inhibiting formation of the ECM.

Collagen Based Products added to the wound deactivates the mode of action of MMP’s


• Other Treatment Modalities• Compression wraps & bandages (Venous Disease)

Single Layer

Multi-Layer

Unna paste boot (zinc-oxide)

• Total Contact Cast (DFU)


• Negative Pressure Wound Therapy (NPWT)

• HyperBaric Oxygen Therapy

• Biologic Applications

• Nutrition

Thank you!

• Questions?

References

1. Berger MM. Enzyme debriding preparations. Ost Wound Manag 1993; 39: 61-2, 66-69.

2. Boulton AJM, Kirsner RS, Vileikyte L. “Neuropathic Diabetic Foot Ulcers.” N Engl J Med 2004. 351: 48-55. doi: 10.1056/NEJMcp032966.

3. Brett D. A review of collagen and collagen-based wound dressings. Wounds. 2008; 20(12):347-56.

4. Cleveland Clinic. Lower Extremity (Leg and Foot) Ulcers. Cleveland Clinic. http://my.clevelandclinic.org/heart/disorders/vascular/legfootulcer.aspx. Updated

November 2010. Accessed August 8, 2012.

5. Cutting KF, Harding KG. Criteria for identifying wound infection. J Wound Care 1994; 3(4): 198-201.

6. Daly BJ, Panthaki ZJ. Wound Care Workup. Medscape.com. Updated 11Mar2016. http://emedicine.medscape.com/article/194018-workup Accessed 02Oct16.

7. DeFranzo AJ, Argenta LC, Marks MW, et al. The use of vacuum-assisted closure therapy for the treatment of lower-extremity wounds with exposed bone. Plast

Reconstr Surg 2001; 108 (5): 1184-91.

8. De Haan B, Elllis H, Wilks M. The role of infection in wound healing. Surg Gynecol Obstet 1974; 138:693-700.

9. DePietro M. What is a surgical wound? Health-line. Reviewed by Krucik G. 07Jan2014. http://www.healthline.com/health/surgical-wound. Accessed 01Oct2016.

10. Dow G, Browne A, Sibbald RG. Infection in chronic wounds: Controversies in diagnosis and treatment. Ost Wound Manag. 1999; 45: 23-40.

11. Driver VR, Fabbi M, Lavery LA, Gibbons G. The costs of diabetic foot: the economic case for the limb salvage team. J Am Podiatr Med Assoc. 2010;100(5):335–341.

12. Eaglstein WH, Falanga V. Chronic wounds. Surg Clin North Am 1997; 77:689-700.

13. Edlich RF, Panek PH, Rodeheaver GT, et al. Physical and chemical configuration of sutures in the development of surgical infection. Ann Surg 1973; 177: 679-88.

14. Elek S. Experimental staphylococcal infections in the skin of man. Ann NY Acd Sci 1956; 69:56.

15. Filius PM, Gyssens IC. Impact of increasing antimicrobial resistance on wound management. Am J Clin Dermatol 2002; 3 (1):1-7.

16. Fowler E. Instrument/sharp debridement on non-viable tissue in wounds. Ost Wound Manag 1992; 38:26, 28-30, 32-3.

17. Fowler E, van Rijswijk L. Using wound debridement to help achieve the goals of care. Ost Wound Manag 1995; 41 (7A Suppl): 23S-35S.

http://my.clevelandclinic.org/heart/disorders/vascular/legfootulcer.aspx

http://emedicine.medscape.com/article/194018-workup

http://www.healthline.com/health/surgical-wound Accessed 01Oct2016

References

18. Gabriel A. Vascular Ulcers. Medscape Reference. http://emedicine.medscape.com/article/1298345-overview. Updated July 11, 2012. Accessed August 8, 2012.

19. Gardner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized wound infection. Wound Repair Regen 2001; 9(3):

178-86.

20. Gordon MD, Gottschlich MM, Helvig EI, Marvin JA, Richard RL. Review of evidence-based practice for the prevention of pressure sores in burn patients. J Burn Care

Rehabil. 2004;25(5):388–410.

21. Healthwise, Inc. Skin Problems & Treatments Health Center. WebMD. http://www.webmd.com/skin-problems-and-treatments/tc/venous-skin-ulcer-t.... Updated

September 3, 2009. Accessed August 8, 2012.

22. Hess CT. Putting the squeeze on venous ulcers. Nursing. 2004;34(Suppl Travel):8–13.

23. Hutchinson J. (1992) The Wound Programme. Centre for Medical Education: Dundee.

24. Hulten L. Dressings for surgical wounds. Am J Surg 1994; 167(1A): 42S-44S.

25. Kerstein MD. Wound infection: Assessment and management. WOUNDS 1996; 8:141-144.

26. Kuhn BA, Coulter SJ. Balancing ulcer cost and quality equation. Nurs Econ. 1992;10(5):353–359.

27. Leaper DJ and Harding KG. (1998) Wounds: Biology nd Management. Oxford University Press.

28. London Health Sciences Centre. Diabetic/Neuropathic Ulcer. London Health Sciences Centre.

http://www.lhsc.on.ca/Health_Professionals/Wound_Care/diabetic.htm. Accessed September 26, 2016.

29. London Health Sciences Centre. Venous Stasis & Arterial Ulcer Comparison. London Health Sciences Centre.

http://www.lhsc.on.ca/Health_Professionals/Wound_Care/venous.htm. Updated February 1, 2009. Accessed August 8, 2012.

30. Marks J, Harding KG, Hughes LE. Staphlococcal infection of open granulation wounds. Br J Surg 1987; 74(2):95-7.

31. Madsen SM, Westh, H, Danielsen L, Rosdahl VT. Bacterial colonization and healing of venous leg ulcers. APMIS 1996; 104: 895-9.

http://emedicine.medscape.com/article/1298345-overview

http://www.webmd.com/skin-problems-and-treatments/tc/venous-skin-ulcer-topic-overview

http://www.lhsc.on.ca/Health_Professionals/Wound_Care/diabetic.htm

http://www.lhsc.on.ca/Health_Professionals/Wound_Care/venous.htm

References

32. Mayo Foundation for Medical Education and Research. Diabetic neuropathy. Mayo Clinic. www.mayoclinic.com/health/diabetic-neuropathy/DS01045. Published

March 6, 2012. Accessed September 26, 2016.

33. McGuire J. Transitional off-loading: an evidence-based approach to pressure redistribution in the diabetic foot. Advances Skin Wound care. 2010; 23(4): 175-8.

34. Molan PC. Re-introducing honey in the management of wounds and ulcers – theory and practice. Ost Wound Manag 2002; 48 (11): 28-40.

35. Mosquera D. Chronic venous insufficiency and leg ulcers. Vascular.co.nz. http://www.vascular.co.nz/chronic_venous_insufficiency and leg ulceration.htm. Accessed

August 8, 2012.

36. Sen CK, Gordillo GM, Roy S, et al. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen. 2009;17(6):763–

771.

37. Sibbald RG, Williamson D, Orsted HL et al. Preparing the wound bed – debridement, bacterial balance and moisture balance. Ost Wound Manag 2000a; 46: 14-35.

38. Sinclair RD, Ryan TJ. Types of chronic wounds: Indications for enzymatic debridement. In: Westerhof W, Vanscheidt W (eds.) Proteolytic Enzymes and Wound

Healing. New York, NY: Springer-Verlag, 1994: 7-20.

39. National Pressure Ulcer Advisory Panel (NPUAP) announces a change in terminology from pressure ulcer to pressure injury and updates the stages of pressure

injury. 13April2016. https://www.npuap.org/national-pressure-ulcer-advisory-panel-npuap-announces-a-change-in-terminology-from-pressure-ulcer-to-pressure-

injury-and-updates-the-stages-of-pressure-injury/ Accessed 01OCt2016.

40. Nemeth AJ, Eaglstein WH. Wound dressings and local treatment. In: Westerhof W (ed). Leg Ulcers: Diagnosis and Treatment. Amsterdam: Elsevier Science

Publishers, 1993: 325-33.

41. Ngan V. Leg ulcers. DermNet NZ. http://dermnetnz.org/site-age-specific/leg-ulcers.html. Updated February 25, 2012. Accessed August 8, 2012.

42. Pollack SV. The wound healing process. Clin Dermatol 1984; 2: 8-16.

http://www.mayoclinic.com/health/diabetic-neuropathy/DS01045

http://www.vascular.co.nz/chronic_venous_insufficiency

https://www.npuap.org/national-pressure-ulcer-advisory-panel-npuap-announces-a-change-in-terminology-from-pressure-ulcer-to-pressure-injury-and-updates-the-stages-of-pressure-injury/

http://dermnetnz.org/site-age-specific/leg-ulcers.html

References

43. Takahashi P. Chronic Ischemic, Venous and Neuropathic Ulcers in Long-Term Care. Annals of Long-Term Care. http://www.annalsoflongtermcare.com/article/5980.

Published September 5, 2008. Accessed September 26, 2016.

44. Tortora GJ and Grabowski SR. (1993) Principles of Anatomy and Physiology. Harper Collins College Publishers.

45. Webb LX. New techniques in wound management: Vacuum-assisted wound closure. J Am Acad Orthop Surg 2002; 10(5):303-11.

46. Rice et al. J MedEcon 2014;17(5): 347-356

47. Rice et al. Diabetes Care 2014;(3)651-658

48. Russo et al. Healthcare Cost and Utilization Project(HCUP) Statistical Briefs [Internet]

http://www.annalsoflongtermcare.com/article/5980

wound care in the post acute, rehabilitative setting care in the post acute, rehabilitative setting...

Documents