Types of Wounds

In This Chapter

The Different Types of Wounds . . . . . . . . . . . . . . . . . . 99

Acute Versus Chronic Wounds. . . . . . . . . . . . . . . . . . . 99

Pressure Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

Lower Extremity Wounds. . . . . . . . . . . . . . . . . . . . . . 101

Lymphedema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

Suspected Deep Tissue Injury . . . . . . . . . . . . . . . . . . 108

Kennedy Terminal Ulcers . . . . . . . . . . . . . . . . . . . . . . 110

Surgical Site Incision . . . . . . . . . . . . . . . . . . . . . . . . . 112

Skin Tears . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

Chapter 5

THE DIFFERENT

TYPES OF WOUNDS

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Chapter 5 � The Different Types of Wounds

The Different Types of Wounds

In the past, standard practice did not differentiate between thevarious types of wounds and consider how multiple factorsmight affect wound healing. In fact, we frequently spent moretime worrying about the “hole” in the patient (the wound)than assessing the “whole” patient. Current research, however,illustrates how important it is to carefully assess the woundand identify the correct treatment so we do not cause furtherharm; in other words, to work smart from the beginning.

A wound will most likely require different treatments as itprogresses. As the drainage slows, for example, the dressingchoice will no longer be one that absorbs exudate, butpossibly one that donates or retains moisture.

When assessing the wound and the patient, the best stepto make first is determining the etiology of the wound.Recognizing factors that affect the patient’s ability to healcan mean the difference between a slow-healing woundand a completely closed wound.

Acute Versus Chronic Wounds

Acute wounds heal uneventfully and within an expectedtime frame. However, complications can develop quicklyin some instances such as surgical incisions, gunshotwounds or abrasions and must be acted upon promptly.

Chronic wounds do not heal in the standard time frame andmay linger for weeks, months or even years. There are rela-tively few real complications, other than slow healing. Somechronic wounds are venous leg ulcers, arterial leg ulcers andneuropathic or diabetic ulcers and those caused by mechanicalinjury such as pressure ulcers. Usually, chronic wounds occurin an individual with an underlying pathology that preventsnormal wound healing.

Pressure Ulcers

Pressure ulcers, also known as pressure wounds,bedsores, or decubiti are described as a localized areaof tissue necrosis (death) that results from the compression

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Any patient thatspends a gooddeal of timesitting in a chair,wheelchair, orlying in bed is atrisk for developingpressure ulcers.

Worthremembering ...

The Wound Care Handbook

of soft tissue between a bony area and a surface. Bloodsupply to the tissue is decreased, which leads to vascularcompromise, tissue anoxia (lack of oxygen), and eventuallycell death that presents as a wound.

Two forces that lead to skin breakdown are friction andshear. Friction injuries occur when the skin moves across acoarse surface. Most of these injuries can be avoided by usingappropriate techniques when moving patients. Voluntary andinvoluntary movement by the patient can also lead to frictioninjuries, especially to elbows and heels. Shear injury occurswhen the skin remains stationary and the underlying tissueshifts. The shift reduces the blood supply to the skin that soonresults in ischemia and tissue damage. Most shear injuries canbe eliminated by proper turning and positioning.

According to the Centers for Medicare & Medicaid Services(CMS) guidelines, “A resident at risk can develop a pressureulcer within two to six hours of the onset of pressure.”Watch for a change in the temperature, feel or look of skin.Pay attention to areas that appear different from surroundingtissue. On darkly pigmented skin, damaged areas might lookdarker or lighter, and could be red, blue or purple in color.Look for redness that is “non-blanchable.” Healthy red areasturn white when pressed and released, while damaged areasare non-blanchable and remain red. Gently feel for changesin skin temperature and be suspicious of areas that feelspongy or harder than surrounding tissue. Check patientsfrom head to toe, paying special attention to bony promi-nences like the back of the head, ears, shoulder blades,coccyx, elbows and heels.

Patients must be well nourished if pressure ulcer preventionis a goal. Assist patients who are unable to feed themselvesand encourage or assist other patients to eat and drink. Keeppatients moving. Turn and reposition them at least everytwo hours and encourage them to make slight adjustmentsoften. For individuals who cannot move by themselves,schedule position changes and use pillows for support, ifneeded. Avoid shear and friction by using the appropriatebed linen. Do not use a blue underpad, or “chux,” to movepatients. If the patient can use their upper body to help withmovement, use a trapeze and keep their knees bent to preventsliding. Also use a skin lubricant, liquid skin barrier or powder.Ensure proper elevation by maintaining the head of the bed

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Patients with justone risk factor candevelop pressureulcers; therefore,every time youchange, dress,bathe, transfer, orturn a patient,check the skin.

TIPS!


at no more than a 30-degree angle. Keep heels elevated byplacing pillows under the legs and to prevent knees and heelsfrom rubbing together.

Lower Extremity Wounds

Lower extremity wounds are generally divided into venousulcers, arterial ulcers and neuropathic/diabetic wounds.Before treatment of any lower extremity wound begins,circulation must be assessed.

• Is there sufficient blood perfusion to close the wound?• Measure the ankle-brachial index (ABI) and check

the pedal pulses, color, temperature, location,muscle wasting and the patient’s lower extremityhair-growth pattern.

• Determine if the patient has diabetes and, if so,check the blood sugars and A1C levels.

• Is there any swelling that is affected by elevation?• Are there other skin changes such as staining in

the lower part of the leg or microvaricosities?• Is there a previous history of deep venous thrombosis

(DVT) or ulcers?• Is there pain? If so, have the patient describe the pain.

Answering these questions helps determine if this wound isa neuropathic/diabetic foot ulcer, a venous stasis problemrequiring some form of compression, or an arterial ulcer thatmay need to be referred to a surgeon for evaluation.

Arterial Leg UlcersArterial ulcers are also called ischemic ulcers. They arethe result of tissue ischemia due to arterial insufficiency.These ulcers account for 5 percent to 20 percent of all legulcers, and they occur at the distal (remote) end of thearterial system. They are often seen on the tips of the toes.When arterial blood flow is interrupted by an obstructionor narrowing of an artery, it causes arterial insufficiency,which can lead to arterial ulcers. Another cause of occlusionis artherosclerosis. Arterial perfusion of the lower extremityshould be assessed with Doppler ABI, flow studies or colorscans before aggressive treatment is initiated.

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Definition

Location

WoundMargin

Wound Bed

Wound Size

Exudate

Edema

Limb Staining

Ankle-BrachialIndex (ABI)

Pedal Pulses

Pain

Best Practice

Arterial

Wounds caused by ischemia,which is related to the pres-ence of arterial occlusivedisease.

The distal aspect of arterialcirculation can be anywhereon the leg, including the toesand feet.

“Punched out,” well-definedborders

Pale wound bed, little or nogranulation, necrotic tissue iscommon

Can be small, but often in-creases due to lack of arterialperfusion

Minimal to no exudate

If present, localized

Usually not present

< 0.8< 0.5 (indicates inability

to heal)

Usually reduced or absent

Occurs at rest, at night, orwhen the extremity is elevated

• If perfusion is not adequate,consider vascular consult

• If perfusion is adequate,follow protocol based onwound assessment andcharacteristics

• If dry and stable, leaveeschar intact

Neuropathic/Diabetic

Neuropathy is often associatedwith diabetes. Wounds result fromdamage to the autonomic, sensoryor motor nerves and have an arte-rial perfusion deficit.

Can be anywhere on the lowerextremity, usually located on thefoot.

Similar to arterial wounds, usuallywith a calloused edge

Similar to arterial wounds, usuallywith a calloused edge

Often small

Similar to arterial wounds



Not reliable, sometimes falselyevaluated due to calcification

Not reliable

Due to neuropathy, the painmay be absent or severe

Maintain optimal moisture• Control diabetes, if appropriate• Repetitive removal of callous• Bioburden control and

prevention of systemic infection• Remove pressure with

appropriate off-loading shoe orother appliance

The DifferentTypes of Wounds

Definition

Location

WoundMargin

Wound Bed

Wound Size

Exudate

Edema

Limb Staining

Ankle-BrachialIndex (ABI)

Pedal Pulses

Pain

Best Practice

Pressure

Damage to the skin orunderlying structures as aresult of tissue compressionand inadequate perfusion.

Usually over a bonyprominence.

Usually circular

Can have viable or necrotictissue

Can be very large orvery small

Can vary from noneto heavy

Can be localized, usually notseen

Usually not present

N/A

N/A

Usually present, but oftenundertreated

• Remove necrotic tissue• Maintain optimal moisture• Protect periwound skin• Control bioburden• Remove pressure

Venous

Failure of the venous valvefunction to return blood from thelower extremities to the heart.This causes venous congestionand leads to venous hypertension.

Located in the gaiter area (ankle tomid calf), it is often medial malle-olus and may be circumferential.

Irregular shaped

Usually shallow, can haveviable or necrotic tissue

Usually large

Can vary from none to heavy togeneralized weeping

Generalized edema to lowerextremity

Usually seen

> 0.8

Usually normal orundetectable due to edema.

Often occurs in a dependentposition along with edema.

• Compression• Remove necrotic tissue• Maintain optimal moisture• Protect periwound skin• Control bioburden• Ensure lower extremity

moisturization


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The DifferentTypes of Wounds


Venous Leg UlcersAny ulcer caused by stagnation of blood due to venouscongestion or venous hypertension is known as a venousleg ulcer. Venous ulcers require both an optimal moistwound healing environment and edema-control measures,typically with compression. The limb must have sufficientarterial flow and be free from acute cellulitis or uncontrolledcongestive heart failure. Therefore, determining perfusion isa key factor prior to applying any compression. Applyingcompression inappropriately can cause significantnegative outcomes.

A venous leg ulcer is usually located mid-calf to the heel,is medial or lateral, and can be circumferential. It is poorlydefined and often has jagged edges. The wound bed has ruddyred granulation tissue that is usually superficial and includesthe presence of yellow fibrin. The drainage is moderate toheavy, and edema is usually generalized to the lower extremity.The pulse may be difficult to assess secondary to the edema.The wound may be moderately painful, which will oftenimprove with a decrease in edema. Venous ulcers can occurin patients with superficial or perforator vein disease inaddition to patients with deep vein disease. These woundsare most common in older adults; however, they accountfor 70 to 90 percent of all leg ulcers.

Neuropathic/DiabeticNeuropathy is a nerve disorder that results in lost or impairedfunction in the tissues of the affected nerve fibers. It is oftenassociated with diabetes. Neuropathic/diabetic wounds resultfrom damage to the autonomic, sensory or motor nerves andhave an arterial perfusion deficit. They can be anywhere onthe lower extremity, usually located on the foot, and are calleddiabetic foot ulcers.

Lymphedema

Lymphedema is one of the most under-diagnosed andunder-treated conditions affecting wound healing. Thereis no known cure, but like many chronic diseases, it can bemanaged successfully by patients if they are knowledgeableof the disease and its treatment. It is estimated that up to 250million patients worldwide currently suffer with lymphedema.

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Lymphedema is oneof the most under-diagnosed andunder-treatedconditions affectingwound healing.

DID YOU KNOW


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The functioning lymphatic system is comprised of lymphaticvessels filled with lymphatic fluid, lymph nodes and organs.Think of the lymphatics as the “back up” system to removefluid from the interstitial tissue when the venous system isoverwhelmed. The lymphatic vessels closely mirror thevascular system. Its structure is similar to the venoussystem, consisting of one-way intraluminal valves toprevent reflux of lymph fluid.

The Progression of Lymphedema

� Serum proteins and and water leak into the interstitial space.� The lymphatic vessels absorb the excess fluid, now called

lymphatic fluid.� The lymphatic fluid re-enters the blood stream through the

lymph system, the spleen, and the vena cava.� Nearby sketetal muscles contract, placing external pressure

on the lymph channels, which propels the lymph forward.

Lymphatic dysfunction occurs from primary or secondarycauses. Primary lymphedema is caused by a structuralcongenital abnormality present at birth. While manypatients show clinical signs of lymphedema when theyare young, some cases do not appear until middle age.Secondary lymphedema has a readily identifiable sourcefrom structural damage to the lymphatic system. Thiscan occur from radiation, surgery, node dissection,obesity and burns.

Much like venous insufficiency, when there is structuraldamage to the lymph channels, valvular incompetenceensues. Subsequent fibrosis of the lymphatic vessel walloccurs and lymph channels become clogged with protein,thus blocking flow of fluid. This leads to lymph flow intothe dermal plexus, causing edema and marked inflammationdue to macrophage infiltration. Clinical evidence oflymphedema is categorized in four stages.


Stages of Lymphedema• Stage 0: This stage is subclinical. Impaired lymph

flow exists without clinical signs.• Stage I: Soft edema that usually resolves on its own.

The patient often reports that their legs are “puffy”after being upright for several hours, but the symptomdisappears when they lie down.

• Stage II: Pitting, brawny edema. The skin tissue isfirm and no longer soft, but not yet fibrotic.

• Stage III: Skin texture changes and displays “peau d’orange.” This type of skin has the look and texture ofan orange peel with prominent, indented pores. Theepidermis forms thick scaly areas with cracks or depositsthat may eventually develop a fibrotic warty-like tissue.Cracks and deep creases harbor bacteria and predisposethe patient to infection.

Patients in lymphedema Stage II and III often have repeatedepisodes of cellulitis, as the lymph system is unable to clearbacteria from the interstitium to the lymph nodes andspleen for their destruction. Often, the clinical hallmark ofundiagnosed lymphedema is numerous bouts of infectionor non-healing wounds in the affected area. Interstitialfluid accumulation impairs wound healing by pressing onthe vascular system, cutting off the delivery of oxygenationand nutrients. Local ischemia and resulting cellular wasteproducts cannot be removed. Should the area developweepy drainage, known as lymphorrhea, the proteins becomeirritating to the epidermis and subsequently contribute toa secondary infection. Other sequela associated with lym-phedema includes complex regional pain syndrome, decreasedsensation, limited range of motion and deconditioning.

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Stage III Lymphedema


Diagnosis is made on clinical examination. A thorough historyshould be taken because heart failure, DVT and other causesof edema should be considered in the differential diagnosis.Many patients with lower extremity lymphedema haveconcomitant venous hypertension with resultant venousinsufficiency. Malignancy associated with quick onset orrapidly progressive lymphedema should always be suspectedwith unilateral lymphedema.

A physical exam focuses on palpation of the soft tissueinvolved. Comparison to unaffected contralateral or adjacentareas is important. Hard fibrotic tissue is described as lipoder-matasclerosis for documentation purposes. Skin color, temper-ature, and the presence of weepy exudate with or withoutwounds are essential to assess, document and treat.

Treatment is focused on reducing protein accumulationand attempting to restore the flow of lymph through thelymphatic channels. As in many chronic diseases, treatmentis ongoing and requires active participation by the patient forself-management. It consists of two phases.

• Phase one involves manual lymph drainage (MLD) andshort-stretch compression bandaging until maximalfluid reduction has been achieved. MLD is a skinstretching/massage action to direct lymph flow in acertain direction to bypass any sclerotic or obstructedlymph channels. A thorough understanding of lymphchannels is necessary to perform this procedure. A certi-fied MLD therapist is essential to achieving these goals.This process usually takes three to eight weeks. Duringthis time, the patient is taught skin hygiene to reduceinfection and exercises to facilitate lymph drainage.

• Phase two of the treatment is often referred to as themaintenance stage. During this time, compressiongarments are used instead of short-stretch bandages tomaintain the limb or body part girth achieved throughMLD and bandaging. Skin and nail hygiene, exerciseand the importance of weight control are emphasized.Skin should be moisturized daily with a non-irritatingemollient after bathing.

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Even though research is not conclusive, some patientshave benefited from pneumatic intermittent compres-sion pumps.

Suspected Deep Tissue Injury

What is deep tissue injury and where does it come from? Isit a “purple pressure ulcer”? Is it a pressure ulcer at all sincethe skin is intact?

In an attempt to formally define this phenomenon, in 2007the National Pressure Ulcer Advisory Panel (NPUAP) proposedthe following definition:

“Purple or maroon localized area of discolored intactskin or blood-filled blister due to damage of underlyingsoft tissue from pressure and/or shear. The area may bepreceded by tissue that is painful, firm, mushy, boggy,warmer or cooler as compared to adjacent tissue.”

The wounds appear ischemic, and deterioration occurs in themetabolically active muscle bed. Ischemia may be due to directpressure or shearing injury to nutrient vessels. While thesedeep-tissue injuries clearly involve occlusion or infarction ofthe nutrient-rich arterial supply, the pathogenetic mechanismsof deep-tissue injury remain elusive. There is no discernablemass of blood, yet a DTI is described as, and often feels like, ahematoma. The role of shearing forces that stretch, kink, ortear the perforating blood vessels from underlying muscle orfascia has not been systematically studied, but shearing forcesshould be avoided. Direct pressure that occludes nutrientvessels could also be pathogenic.

How much time and how much pressure did it take tocompromise the deeper tissues? Remember, a small amountof pressure over a long period of time can do as much damageas a large amount of pressure over a short period of time.Cells need oxygen and nutrients in order to divide andmigrate. Without both components cell death and necrosisoccur. Also, friction, shear and increased torque on deepertissues and vessels increase the likelihood of deep tissueinjury and pressure ulcer formation.

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A small amountof pressure over along period of timecan do as muchdamage as a largeamount of pressureover a short periodof time.

Worthremembering ...


Deep tissue injury occurs either in the muscle bed orsubcutaneous fat. The damage is not quickly evidentbecause it presents itself slowly as the tissue deterioratesfrom the inside out, taking on the appearance of a bruisedor discolored area prior to surface skin opening (see theDTI diagram). The skin is usually intact at the time of initialassessment and is sometimes incorrectly described as a StageI pressure ulcer. However, its rapid deterioration to a full-thick-ness injury is unlike a true Stage I pressure ulcer, which is a re-solvable lesion. Areas of superficial blistering or broken blistersappear within 24 hours, similar to those seen with fractures orischemic flaps. The surface tissue may be hard (indurated), orsoft and mushy to the touch. It may be either warm or cold tothe touch depending on how much circulatory compromisehas taken place. The tissues evolve into full-thickness ulcersdespite the best of care.

Differential Diagnosis of Deep Tissue Injury

Bruise: To injure the underlying soft tissue or boneof part of the body without breaking the skin. Abruise usually heals in about two weeks undernormal conditions. History of trauma is common.

Calciphylaxis: An adaptive response following inducedsystemic hypersensitivity to a calcifying factor such asvitamin D and an agent such as a metallic salt, usuallyresulting in localized inflammation and calcification oftissues. Lesions may have a violet hue and be excruciat-ingly tender and extremely firm. Lesions are mostcommonly seen on the lower extremities, not bonyprominences. The incidence of these lesions is very low

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in the general patient population, but often seen inthose with end-stage renal disease.

Fournier gangrene: An intensely painful streptococcusinfection that affects the perineum. It may presentinitially as cellulitis.

Hematoma: A deep-seated purple nodule from clottedblood that is usually associated with trauma.

Perirectal abscess: This injury commonly presents as adull, aching or throbbing pain in the perianal area.The pain worsens when sitting and immediately beforedefecation. The pain abates after defecation. A tenderfluctuant mass may be felt at the anal edge. Theseabscesses can open to reveal large cavities that can beconfused with deep pressure ulcers.

We have to touch our patients as we assess them. If we arenot diligent in our assessment we can miss the early stages ofdeep tissue injury. Education is a key factor for all healthcareproviders. It will enable you to conduct thorough skin assess-ments and understand how to use precise terms to describethe deep tissue injury.

Kennedy Terminal Ulcers

The Kennedy Terminal Ulcer has a sudden onset andusually appears about two weeks before death. It is superficialbut progresses quickly in size and depth. It is generally pear-shaped; located at the base of the spine; and can be red, yellowand black. The borders of the ulcer are usually irregular. It isnot a cause of a patient's death, but it can appear as the dyingprocess begins. Residents on tube feedings or intravenoustherapy can develop the ulcers four to six weeks before death.It may be related to an overall breakdown in tissue due toa decline in circulation; pressure, or other causes yet tobe determined.

Treatment for Kennedy Terminal Ulcers is the same as for otherpressure ulcers based on clinical research. The use of dressings,adjunctive treatment modalities, support surfaces and otheroffloading devices are determined after a comprehensive

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assessment has been completed. Debridement will also bedetermined based on clinical assessment results.

The exact cause of Kennedy Terminal Ulcers is unknown, butthe skin is an organ and, as with other organ systems, organfailure is a possibility. One theory is that as people approachdeath, the internal organs may begin to slow down and gointo what is known as multi-organ failure. No particular set ofsymptoms may be identified except that the skin over bonyprominences starts to show the effects of pressure in a veryshort period of time. Turning a patient every two hours isstandard; however, now it may cause superficial tissue damage.If a Kennedy Terminal Ulcer surfaces, it may be time to addressend-of-life issues. Educate the patient as well as family mem-bers about a living will, power of attorney and organizing thepatient’s personal affairs. Ensure that the patient’s wishes andneeds are clearly known.

Kennedy Terminal Ulcers tend to be more prominent in thegeriatric population and are frequently seen in hospice pa-tients. Following are examples of Kennedy Terminal Ulcers.

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Kennedy Terminal Ulcer: Note variation in presentation.Photos courtesy of Karen Lou Kennedy-Evans


Surgical Site Incision

When a surgical incision results in a full-thickness openingthrough the skin, there are a few options for closure. In aclean, surgically-created wound the edges are typicallybrought together and sutured, stapled or secured in somemanner. The term for this process is primary intention.As a result, periwound redness is a standard element of thehealing process. As the redness fades, the wound will continueto heal at maximum strength for up to 18 months.

When a surgical wound is grossly contaminated and thepossibility of infection is great; or if the defect is too large,the wound is left to close through secondary intention. Inthis situation the wound edges are left open, and the woundheals as any other chronic wound. The wound will fill withgranulation and epithelialization, proceed through thematuration phase, and heal from the “bottom up.”

Another option is to surgically close the wound. This optionis used when there is an initial suspicion of infection, but after24 to 28 hours there is no evidence of an actual infection. Thisis referred to as tertiary closure or delayed primary closure.

Surgical wounds that open or dehisce (split) can be theresult of infection or various immunocompromised statesof the host, such as diabetes or malnutrition. When a surgicalwound dehisces or is non-healing, the patient must be assessedand stabilized if necessary. Often a systemic antibiotic orantimicrobial is ordered, and then the wound is treated.Following the principles of wound healing, you will needto address the optimal moist environment. Managingdraining wounds with absorptive dressing or a closed suctionsystem may be necessary. If the wound has stopped draining,a dressing that donates moisture and maintains the moistwound bed is necessary.

Assess the depth of the wound and evaluate it for fistulaformation. A fistula is an abnormal passage between twoareas, such as the small bowel and the skin, called anenterocutaneous fistula.

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The incidence ofskin tears is directlyrelated to a lack ofinternal hydrationand topicalmoisturization.

DID YOU KNOW


Ideally, the tissue in the wound bed is clean and granulating.However, in a chronic wound or dehisced surgical incision,there may be necrotic tissue, slough and eschar, which areknown to harbor bacteria and delay wound healing. Debride-ment may be necessary and should be achieved by the mosteffective and efficient method for the patient. In many casesthis is often achieved surgically.

A topical antimicrobial may also be necessary to treat anoverload of bacteria. Many products that contain silverare able to address this bioburden.

Skin Tears

A skin tear is a wound that results from either a separationof the epidermis and dermis, or both the epidermis anddermis from the underlying structures. There are differentdegrees of skin involvement and damage. Causes include butare not limited to trauma caused by bumping into equipmentand furniture, or transfer injuries that occur while getting inand out of motor vehicles and hitting the car door. Othertraumas include skin stripping from tape or device removaland lacerations from falls or foreign objects. Handling ofpatients with fragile skin may also result in tearing of theskin if a twisting motion is used on the forearm instead ofemploying a grab and release method. The most frequentinjuries occur on the upper extremities, with the legs andfeet reported as the next highest. Over half of the skintears reported have undetermined causes. Patients that aredependent upon caregivers for their activities of daily living(ADLs) are most at risk as they are “handled” the most often.The incidence of skin tears is directly related to a lack ofinternal hydration and topical moisturization. Topicalmoisturization using pH balanced cleansers and moisturizersare essential to maintaining skin health. Encourage fluidsunless the patient is on a fluid restriction. Patients thatare on steroid therapy may be at greater risk for impairedskin integrity and skin tears.

When assessing a skin tear, identify the causative factor.Does the patient have dry skin, requiring better moisturizationinternally and externally? What soaps, lotions and creamsare being used, and what is the pH of these products? Is the

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patient on medications that affect the integrity of the skin?Do the patient and caregivers need instructions about how toprotect the patient’s delicate skin and not cause further traumato the area? If these issues are addressed while the skin tear isbeing treated, further skin damage is less likely to occur.

Payne-Martin Classification System for Skin Tears

The Payne-Martin Classification for Skin Tears further definesand describes wounds that tend to occur more frequently inolder adults.

Risk factors include age, hydration status, medications,nutrition, immobility, increased caregiver handling injuries,edema and ecchymosis. Immature skin of infants and elderlyskin are at risk for tearing because of the fragility of thedermal-epidermal junction.

In 1990 Regina Payne and Marie-Lynn Martin developed aclassification tool for skin tears that groups characteristicsand degrees of damage exhibited by these injuries intothree categories.

� Category I: A skin tear without tissue loss.• Characteristics are based on whether the damage is

a linear tear or a skin-flap type tear. Both tears canbe fully approximated.

� Category II: A skin tear with partial tissue loss.• Tears will have a partial-thickness epidermal tissue

loss. The tears are further classified as scant versusmoderate to large tissue loss.

� Category III: A skin tear with complete tissue loss,• where the epidermal flap is absent.

These are wounds with complete tissue loss.

The tool should be used to quantify data, discover anddecrease causes of injury and plan treatment protocols.

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References:

Ankrom M, Bennett R, Sprigle S, et al. Pressure-related deep tissue injury underintact skin and the current pressure ulcer staging systems. Advances in Skin andWound Care. 2005:18.

Baranoski S, Ayello EA. Wound Care Essentials Practice Principles. Lippincott,Williams &Wilkins. 2003:4-57.

Black J. Deep tissue injury. Wounds: A compendium of clinical research andpractice. 2003;15(11):380.

Centers for Medicare & Medicaid Services. CMS manual system page. Avail-able at: http://www.cms.hhs.gov. Accessed January 23, 2007.

Creager MA, Libby P, eds. Peripheral arterial diseases. Braunwald's HeartDisease. 7th ed. Philadelphia, Pa: Elsevier Saunders; 2004:1437-1461.

Daniel RK, Kerrigan CL, ed. Principles and physiology of skin flap surgery.Plastic Surgery. Philadelphia, Pa: WB Saunders; 1990:275-328.

emedicine.com. Available at:http://www.emedicine.com/med/topic2722.htm. Accessed November 21, 2006.

Ford D. Pressure ulcer named after byron nurse who discovered it.People Northwest, Fort Wayne News Sentinal. October 8, 1992.

Giordano CP, Scott D, Koval KJ, et al. Fracture blister formation: a laboratorystudy. Journal of Trauma. 1995;38(6):907-9.

Groth KE. Clinical observations and experimental studies on the origin ofdecubiti. Acta Clin Scand. 1942;87(Suppl 76):S1-S209.

Husain T. An experimental study of some pressure effects on tissues, withreference to the bedsore problem. Journal of Pathology and Bacteria.1953:66,347-358.

Kennedy KL. Gaymar Pictorial Guide to Pressure Ulcer Assessment.Gaymar Industries, Inc.; 1997.

Kennedy KL. Strategies for the extended care professional; ask Mabel:What is a kennedy terminal ulcer? ECPN. 2002;81(3):36-38.

Kennedy KL. The prevalence of pressure ulcers in an intermediate care facility.Decubitus. 1989;2(2):44-45.

Kozier B, Erb G, Olivieri. Fundamentals of Nursing. 4th ed. Addison–Wesley;1991.

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lymphnet.org. Available at: http://www.lymphnet.org.Accessed November 21, 2006.

MacDonald JM. Wound healing and lymphedema: a new look at an old problem.Ostomy-Wound Management. 2001;47(4):52-57.

Mayer M, eds. Wound, Ostomy, Continence Nursing Secrets. Philadelphia, Pa:Hanley and Belfus, Inc.; 2003.

McCann S, Gruen G. Fracture blisters: a review of the literature. OrthopaedicNursing. 1997;16(2):17-22.

National Pressure Ulcer Advisory Panel. Deep Tissue Injury Task Force.Reston, Va. 2002.

Paget J. Clinical lecture on bed-sores. Student Journal and Hospital Gazette.1873:144-146.

Parks DS, Granger DN. Ischemia-reperfusion injury: a radical view. Hepatology.1988;8(3):680-682.

Payne RL, Martin ML. The epidemiology and management of skin tears in olderadults. Ostomy Wound Management. 1990;26:26-37.

Payne RL, Martin ML. Defining and classifying skin tears: need for a commonlanguage. Ostomy Wound Management. 1993;39(5):16-20,22-4,26.

Russell, L. Pressure ulcer classification: defining early skin damage.British Journal of Nursing. 2002;11(16): 33-41.

Shea JD. Pressure sores: classification and management. Clinical Orthopedics.1875:89-100,112.

Willms-Kretschmer K, Majno G. Ischemia of the skin. American Journal ofPathology. 1969;54(5):327-341.

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Documents

Types of Wounds