ulkus dekubitus med scape1

8/11/2019 Ulkus Dekubitus Med Scape1

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Diagnosis

1aboratory studies that may be helpful include the follo ing!

• 0omplete blood count (0&0) ith differential• Erythrocyte sedimentation rate (E-2)• Albumin and prealbumin• Transferrin• -erum protein

3hen indicated by the specific clinical situation, the follo ing should be obtained!

• Urinalysis and culture in the presence of urinary incontinence• -tool e#amination for fecal 3&0s and Clostridium difficile to#in hen pseudomembranous colitis

may be the cause of fecal incontinence• &lood cultures if bacteremia or sepsis is suggested

Additional studies that may be considered include the follo ing!

• Plain radiography• &one scan•

'agnetic resonance imaging• Tissue or bone biopsy-ee 3or up for more detail.

Management

4eneral principles of ound assessment and treatment are as follo s!• 3ound care may be broadly divided into nonoperative and operative methods• +or stage and pressure ulcers, ound care is usually conservative (ie, nonoperative)• +or stage and / lesions, surgical intervention (eg, flap reconstruction) may be re5uired,

though some of these lesions must be treated conservatively because of coe#isting medical problems 678

• Appro#imately 9:; <:; of pressure ulcers are superficial and heal by second intention-uccessful medical management of pressure ulcers relies on the follo ing ey principles!

• 2eduction of pressure• Ade5uate d=bridement of necrotic and devitali$ed tissue• 0ontrol of infection• 'eticulous ound care

f surgical reconstruction of a pressure ulcer is indicated, medical status must be optimi$ed beforereconstruction is attempted. 4eneral measures for optimi$ing medical status include the follo ing!

• 0ontrol of spasticity• Nutritional support as appropriate• 0essation of smo ing• Ade5uate pain control•

'aintenance of ade5uate blood volume• 0orrection of anemia• 'aintenance of the cleanliness of the ound and surrounding intact s in• 'anagement of urinary or fecal incontinence as appropriate• 'anagement of bacterial contamination or infection

Additional nonsurgical treatment measures include the follo ing!

• Pressure reduction 2epositioning and use of support surfaces• 3ound management %=bridement, cleansing agents, dressings, and antimicrobials

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• Ne er approaches still being studied 4ro th factors (eg, becaplermin), negative pressureound therapy, and electrotherapy

-urgical interventions that may be arranted include the follo ing!

• -urgical d=bridement• %iversion of the urinary or fecal stream•

2elease of fle#ion contractures• 3ound closure• Amputation

"ptions available for surgical management of pressure ulcers are as follo s!

• %irect closure (rarely usable for pressure ulcers being considered for surgical treatment)• - in grafts• - in flaps• 'yocutaneous (musculocutaneous) flaps• +ree flaps

The choice of reconstruction approach depends on the location of the pressure ulcer (eg, ischial, sacral,or trochanteric).

Prevention, if achievable, is optimal. Prevention of pressure ulcers has > main components!• dentification of patients at ris• nterventions designed to reduce the ris

-ee Treatmen t and 'edication for more detail.

Image Library

3ith gluteal thigh flap, superiorly based flap is elevated, ith inferior gluteal arterylocated bet een greater trochanter and ischial tuberosity as its a#is.

&ac groundThe terms decubitus ulcer (from 1atin decumbere, ?to lie do n@), pressure sore, and pressure ulcer oftenare used interchangeably in the medical community. o ever, as the name suggests, decubitus ulceroccurs at sites overlying bony structures that are prominent hen a person is recumbent. ence, it is notan accurate term for ulcers occurring in other positions, such as prolonged sitting (eg, ischial tuberosityulcer). &ecause the common denominator of all such ulcerations is pressure, pressure ulcer is the bestterm to use.

The National Pressure Ulcer Advisory Panel (NPUAP) is an independent nonprofit organi$ation formed in7<B9 and dedicated to the prevention, management, treatment, and research of pressure ulcers. TheNPUAP defines a pressure ulcer as an area of unrelieved pressure over a defined area, usually over abony prominence, resulting in ischemia, cell death, and tissue necrosis. 6>8

Pressure is e#erted on the s in, soft tissue, muscle, and bone by the eight of an individual against asurface beneath. These pressures often e#ceed capillary filling pressure (CD> mm g). n patients ithnormal sensitivity, mobility, and mental faculty, pressure ulcers do not occur. +eedbac , conscious and

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unconscious, from the areas of compression leads them to change their body position, and thesechanges shift the pressure before any irreversible tissue damage develops. (-ee Pathophysiology andEtiology.)

Those ho cannot avoid long term uninterrupted pressure over bony prominences (eg, persons ho areelderly, have neurologic impairment, or are undergoing acute hospitali$ation 6D8) are at increased ris forpressure ulcers. They cannot protect themselves from the pressure unless they consciously changeposition or are helped to do so. Even a highly conscientious patient ith an e#tensive support group andunlimited financial resources may develop ulceration resulting from a brief lapse in avoidance of the illeffects of pressure. 6 , F8

Addressing the overall management of pressure ulcers is no a prominent national healthcare issue.%espite current interest and advances in medicine, surgery, nursing care, and self care education,pressure ulcers remain a ma or cause of morbidity and mortality, and patients ith pressure ulcers areimportant users of medical resources. 6>, G, 9, B, <, 7:, 77, 7>8

'any factors are involved in the management of pressure ulcers. Nursing plays a pivotal role in thischallenging and comple# process, using a multifaceted approach that includes s in care, pressure relief,and nutritional support. Prevention is the ey to managing pressure ulcers, and it begins ith a completemedical and nursing history, a ris assessment, and s in e#amination hen the patient is admitted. 69, B,

7D8

(-ee Treatment.)+actors that sub ect the tissue at ris to potential s in brea do n should receive particular attention.Patients should be ept clean and dry and should be repositioned fre5uently. +or patients at ris ,ade5uate pressure relief must be provided, along ith ade5uate nutritional support.

+or patients ho develop pressure ulcers, these preventive measures must be used in con unction iththe techni5ues of general ound care. Nonoperative ound care may involve simple topical therapy, asfor pressure ulcers ith unbro en s in or superficial lesions ith nondraining, noninfected granulationtissue. +or draining necrotic or infected lesions, treatment also may include absorption agents, calciumalginate dressings, ound coverings, debridement, and antimicrobial therapy.

"ther therapeutic modalities, such as hirlpool, physical therapy, and specialty beds, may also be addedto the treatment regimen.

2esearch in the area of pressure ulcersHspecifically, in the characteri$ation, prevention, and treatment of these lesionsHis important for preventing secondary complications in persons ith disabilities. As thestandards of acute, posttraumatic, and rehabilitation care improve, the population of persons ith lifelongfunctional impairments continues to gro . 0onse5uently, the prevention of secondary complications hasbecome an increasingly prominent concern.

To date, clinical studies of pressure ulcers have been difficult to assess because they have often been5ualitatively based on random observation and uncontrolled studies. To arrive at more reliableconclusions, more fundamental approaches to these ulcers must be considered. Iuestions that might beas ed include the follo ing!

• 3hat are the basic histologic, pathologic, and biochemical mar ers in an evolving pressure ulcerJ• s it ethical to ta e a biopsy specimen of a human pressure ulcer for purposes of researchJ• 3hat are the multiple variables in the formation of pressure ulcers in the human environmentJ

A monograph prepared by the 2esearch 0ommittee of the NPUAP suggested the follo ing researchpriorities ith respect to pressure ulcers 6>8!

• "utcome focused research• ntervention and product efficacy studies• &asic research related to staging of ulcers• 2efinement of ris assessment methods• 2is based, multi interventional trials



Additional issues re5uiring investigation included cost issues, ethical decision ma ing, guidelinedissemination, public policy, and national outcome evaluations. 'ethodologic issues, such as researchdesign, study population, and control group use, also ere considered to arrant further investigation.

AnatomyPressure ulcers are typically described in terms of location and depth of involvement. The hip and buttoc

regions account for up to 9:; of all pressure ulcers, ith ischial tuberosity, trochanteric, and sacrallocations being most common. 67 8 The lo er e#tremities account for an additional 7F >F; of all pressureulcers, ith malleolar, heel, patellar, and pretibial locations being most common (see the images belo ).

Pressure ulcers of lateral aspect of right foot . eel pressure ulcer.The remaining small percentage of pressure ulcers may occur in any location that e#periences longperiods of uninterrupted pressure. 67 8 The nose, chin, forehead, occiput, chest, bac , and elbo are amongthe more common of the infre5uent sites for pressure ulceration. No surface of the body can beconsidered immune to the effects of pressure.

Pressure ulcers can involve different levels of tissue. 'uscle has been proved to be most susceptible topressure. o ever, %aniel and +aibisoff found that muscle rarely as interposed bet een bone and s inin normal eight bearing positions in cadaver and clinical dissections. 67F8

Pathophysiologyn 7B9D, -ir Kames Paget described the production of pressure ulcers remar ably ell, and his descriptionis still 5uite accurate today .67G8'any factors contribute to the development of pressure ulcers, but pressureleading to ischemia and necrosis is the final common path ay.

n this vie , pressure ulcers result from constant pressure sufficient to impair local blood flo to softtissue for an e#tended period. This e#ternal pressure must be greater than the arterial capillary pressure(D> mm g) to impair inflo and greater than the venous capillary closing pressure (B 7> mm g) toimpede the return of flo for an e#tended time.

Tissues are capable ithstanding enormous pressures for brief periods, but prolonged e#posure topressures ust slightly above capillary filling pressure initiates a do n ard spiral to ard tissue necrosisand ulceration .679, 7B8The inciting event is compression of the tissues against an e#ternal ob ect such as amattress, heelchair pad, bed rail, or other surface.

1indan et al documented ranges of pressure applied to various anatomic points in certain positions. 67<8Thepoints of highest pressure ith the patient supine included the sacrum, heel, and occiput ( : G: mm g).3ith the patient prone, the chest and nees absorbed the highest pressure (F: mm g). 3hen the patientis sitting, the ischial tuberosities ere under the most pressure (7:: mm g). "bviously, these pressuresare greater than the end capillary pressure, hich is hy these are the areas here pressure ulcers aremost common.

-hear forces and friction aggravate the effects of pressure and are important components of themechanism of in ury (see the image belo ). 6>:8 'aceration may occur in a patient ho has incontinence,predisposing the s in to in ury. Pressure, shear forces, and friction cause microcirculatory occlusion andconse5uent ischemia, hich leads to inflammation and tissue ano#ia. Tissue ano#ia leads to cell death,necrosis, and ulceration.

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Advanced sacral pressure ulcer sho s effects of pressure, shearing, and moisture."f the various tissues at ris for death due to pressure, muscle tissue is damaged first, before s in andsubcutaneous tissue, probably because of its increased need for o#ygen and higher metabolicre5uirements. 6>7, >>8 rreversible changes may occur during as little as > hours of uninterrupted pressure.- in can ithstand ischemia from direct pressure for up to 7> hours. &y the time ulceration is presentthrough the s in level, significant damage of underlying muscle may already have occurred, ma ing theoverall shape of the ulcer an inverted cone.

2eperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing anulcer to enlarge or become more chronicHas, for e#ample, hen a paraplegic or 5uadriplegic patient isturned from one side to the other in an attempt to combat prolonged pressure on a given side. The e#act

mechanism of ischemia reperfusion in ury is yet to be fully understood. 0ontinued production ofinflammatory mediators and reactive o#ygen species during ischemia reperfusion may contribute to thechronicity of pressure ulcers.

Etiologympaired mobility is probably the most common reason hy patients are e#posed to the prolongeduninterrupted pressure that causes pressure ulcers. This situation may be present in patients ho areneurologically impaired, heavily sedated or anestheti$ed, restrained, demented, or recovering from atraumatic in ury. These patients cannot alter their position far enough or often enough to relieve thepressure. Prolonged immobility may lead to muscle and soft tissue atrophy, decreasing the bul overhich bony prominences are supported.

0ontractures and spasticity often contribute to ulcer formation by repeatedly e#posing tissues to trauma

through fle#ion of a oint. 0ontractures rigidly hold a oint in fle#ion, hereas spasticity sub ects tissues torepeated friction and shear forces. - in brea do n and pressure ulcers may fre5uently be found underand bet een toes and on the palm of the hand.

nability to perceive pain, hether from neurologic impairment or from medication, contributes to pressureulceration by removing one of the most important stimuli for repositioning and pressure relief. 0onversely,pain from surgical incisions, fracture sites, or other sources may ma e the patient un illing or unable tochange position.

The 5uality of the s in also influences hether pressure leads to ulceration. Paralysis, insensibility, andaging lead to atrophy of the s in ith thinning of this protective barrier. A decrease in epidermal turnover,a flattening of the dermal epidermal unction, and a loss of vascularity occur ith advanced age.

n addition, the s in becomes more susceptible to minor traumatic forces, such as the friction and shear

forces typically e#erted during the moving of a patient. Trauma that causes de epitheliali$ation or s intears removes the barrier to bacterial contamination and leads to transdermal ater loss, creatingmaceration and causing the s in to adhere to clothing and bedding.

ncontinence or the presence of a fistula contributes to ulceration in several ays. These conditions causethe s in to be continually moist, thus leading to maceration. n addition, fre5uent soiling has the effect ofregularly introducing bacteria into an open ound.

&acterial contamination, though not truly an etiologic factor, must be considered in the treatment ofpressure ulcers, in that it can delay or prevent ound healing. These ulcers are arm, moist reservoirs for




bacterial overgro th, here antibiotic resistance may develop. A pressure ulcer may progress from simplecontamination (as in any open ound) to gross infection (indicating bacterial tissue invasion). This maylead to uncommon but life threatening complications (eg, bacteremia, sepsis, myonecrosis, gangrene, ornecroti$ing fasciitis).

'alnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute totissue vulnerability to trauma as ell as cause delayed ound healing. Poor nutritional status certainlycontributes to the chronicity often seen in these lesions and inhibits the ability of the immune system toprevent infections. Anemia indicates poor o#ygen carrying capacity of the blood. /ascular disease andhypovolemia also may impair blood flo to the region of ulceration.

n patients ith normal sensitivity, mobility, and mental faculty, pressure ulcers are unli ely. 0onscious orunconscious feedbac from the areas of compression leads them to change position, thereby shifting thepressure from one area to another long before any irreversible ischemic damage occurs. n individualsho cannot avoid long periods of uninterrupted pressure, the ris of necrosis and ulceration is increased.These individuals cannot protect themselves from the pressure unless they consciously change positionor are helped to do so.

EpidemiologyUnited States statistics

Pressure ulcers are common among patients hospitali$ed in acute and chronic care facilities. t has beenestimated that about 7 million pressure ulcers occur in the United -tatesL ho ever, definitive informationon the epidemiology and natural history of this condition is still limited. Unfortunately, studies to date havebeen encumbered by methodologic issues and variability in describing the lesions. 6>, >D8

2eported incidences of pressure ulcer in hospitali$ed patients range from >.9; to ><;, and reportedprevalences in hospitali$ed patients range from D.F; to G<;. 6> , >F, >G, >9, >B8 Patients in critical care units havean increased ris of pressure ulcers, as evidenced by a DD; incidence and a 7; prevalence. 6><, D:8

The fifth National Pressure Ulcer Prevalence -urvey, conducted in 7<<< among patients in acute carehospitals, sho ed an overall prevalence of 7 .B;, ith 9.7; of ulcers having occurred during thathospital visit. 6D78"f the various hospital settings, intensive care units ( 0Us) had the highest prevalence, at>7.F;. The largest single age group of patients ith pressure ulcers consisted of patients aged 97 B:years (><;).

Elderly patients admitted to acute care hospitals for nonelective orthopedic procedures are at evengreater ris for pressure ulcer than other hospitali$ed patients are, ith a GG; incidence. 6D>, DD8n a study ofGFB patients aged GF years or older ho under ent surgery for hip fracture , &aumgarten et al found thatDG.7; developed an ac5uired pressure ulcer ithin D> days after hospital admission. 6D 8

n nursing homes, the prevalence of pressure ulcers is >.G > ;. 6>D, DF8L the incidence is >F; in residentsadmitted from an acute care hospital. 6DF8Patients ith pree#isting pressure ulcers sho a >G; incidence of additional pressure ulcer formation over a G month period. The incidence in chronic care hospitals isreported to be 7:.B;, 6DG8hereas DD; of those admitted to a chronic care hospital have pressure ulcers.6D981ong term follo up demonstrates that most ulcers heal ithin 7 year. 6>D, DB8

Among patients ith neurologic impairments, pressure ulcers occur ith an incidence of 9 B; annually,6D<8ith a lifetime ris estimated to be >F BF; .6 :8 'oreover, pressure ulcers are listed as the direct cause ofdeath in 9 B; of all individuals ith paraplegiaL these individuals also have the highest recurrence rate(B:;) .6 78 n persons ith spinal cord in ury (-0 ) and associated comorbidity, the incidence of pressureulcer is in the range of >F GG;. 6 >, D, , F8

A study of the prevalence of pressure ulcers in community residents ith -0 demonstrated that thoseith higher level -0 lesions carry a greater ris of developing pressure ulcers than those ith lo er levellesions do. 6 >8"f 7:: patients ith pressure ulcers, DD had ulcers that ere classified as stage > or greater.&lac patients had more severe ulcers than other racial groups did.








-ome authors speculate that detecting erythema can be more difficult ith s in that has dar erpigmentation. 6 G8&ecause prolonged nonblanching erythema is typically an early arning sign of pressureulcer ris and development, difficulty in detecting erythema can result in failure to recogni$e grade pressure ulcers.

International statistics

n a study from 4ermany that revie ed the prevalence of pressure ulcer in more than 7B,::: patientsresiding in long term care facilities, the prevalence as found to have decreased from 7>.F; in >::> toF; in >::B. 6 98 This decrease is thought to be due to more effective management strategies and betterprevention.

Age-related demographics

The prevalence of pressure ulcer appears to have a bimodal age distribution. A small pea occurs duringthe third decade of life, reflecting ulceration in those ith traumatic neurologic in ury. mmobility and lacof sensation ma e these patients susceptible to developing pressure ulcers. Treatment of these lesions inthis patient population represents a financial challenge, ith one hospital reporting an average cost ofM9B,::: for each admission of a patient ith a pressure ulcer.

As patients move from the age category of : FB years to the age category of 9F years or older, a larger

increase in the incidence of pressure ulcers occurs.6 B8

T o thirds of pressure ulcers occur in patients olderthan 9: years. 6DG8 As elderly individuals become the fastest gro ing segment of the population, ith anestimated 7.F million people living in e#tended care facilities, the problem of pressure ulcers ill have aneven more profound influence on the American economy. 6 <8

Sex-related demographics

'ost younger individuals suffering from pressure ulceration are males. The higher incidence in malesreflects the greater number of men suffering traumatic -0 s. n the older population, most patients ithpressure ulcers are omen, as a conse5uence of their survival advantage over men.

Race-related demographics

A study by o ard and Taylor found the incidence of pressure ulceration in nursing home residents in thesoutheastern United -tates to be higher in blac patients than in hite ones. 6F:8The authors e#amined datafrom 77D,BG< nursing home residents, none of hom had pressure ulcers at nursing home admission.They determined that .9; of blac residents developed postadmission ulcerations, compared ith D. ;of hite residents.

n addition, the racial differences in pressure ulcer incidence displayed a se# predilection based on patientcharacteristics. 6F:8The variation in incidence bet een blac and hite males as noted in residents hoere dependent in mobility, hereas the difference in incidence bet een blac and hite females asnoted in residents ho ere bedfast and living in nursing homes ith fe er than >:: beds.

PrognosisPressure ulcers are listed as the direct cause of death in 9 B; of all patients ith paraplegia. 6F7, D<8 As manyas one third of hospitali$ed patients ith pressure ulcers die during their hospitali$ation. 'ore than half ofthose ho develop a pressure ulcer in the hospital ill die ithin the ne#t 7> months. As a rule, thesepatients die of their primary disease process rather than of pressure ulceration, but the pressure ulcermay be a contributing factor in some instances.

Each year, appro#imately G:,::: people die of complications of pressure ulcers. 6F>8 ndividuals ithpressure ulcers have a .F times greater ris of death than persons ith the same ris factors but ithoutpressure ulcers. 6G8 A secondary complication, ound related bacteremia, can increase the ris of mortalityto FF;. 6F>, FD, F , FF8



The most common causes of fatality for patients ith chronic pressure ulcers are renalfailure and amyloidosis . n general, mortality is higher for patients ho develop a ne pressure ulcer andin hom the ulcer fails to heal.

nfection is the most common ma or complication of pressure ulcers. The offending pathologic organismscan be either anaerobic or aerobic. Aerobic pathogens commonly are present in all pressure ulcers,6FG8hereas anaerobes tend to be present more often in larger ounds (GF; in grade and above). 6F98

The organisms most commonly isolated from pressure ulcers are as follo s!

• Proteus mirabilis• 4roup % streptococci• Escherichia coli • Staphylococcus• Pseudomonas• Corynebacterium

Patients ith bacteremia are more li ely to have Bacteroides species in their pressure ulcers. 6F98Theseounds need not be cultured routinely unless systemic signs of infection are present (eg, malodorousdrainage, leu ocytosis, fever, hypotension, increased heart rate, changes in mental status).

0linical alertness is vital because the signs commonly associated ith impeding or fulminating infectionare fre5uently absent in elderly or immunocompromised patients. n geriatric patients ith pressureulcers, bacteremia is reported to occur at a rate of D.F per 7:,::: hospital discharges. 6G8

n vie of the high mortality in this population (nearly F:;), 6F 8it is important that antibiotic treatment ofound infection or secondary bacteremia provide the appropriate spectrum of coverage specific to theoffending organisms. &ecause indiscriminate use of antibiotics leads to resistant organisms and becausethe specific drugs of choice and antimicrobial agents change rapidly, management of these comple#problems may be facilitated by consulting an infectious disease specialist.

-epsis also can occur secondary to osteomyelitis, hich has been reported to occur in >G; of nonhealingulcers .6G8 A prospective study demonstrated that osteomyelitis as associated ith nonhealing grade /pressure ulcers in BG; of the study population. 6FB, F<8This study utili$ed D phase technetium methyldiphosphate radionuclide flo to detect early osteomyelitis.

/arious tests can be used to diagnose osteomyelitis in patients ith pressure ulcers. Plain radiographshave a sensitivity of 9B; and a specificity of F:;, but radiographic findings often are not present in theearly stages of infection. &one scans are more sensitive, but their specificity is lo (F:;). &one biopsyhas the highest specificity (<G;) and sensitivity (9D;). 6FB, F<8

A combination of diagnostic tests (eg, hite blood cell 63&08 count, erythrocyte sedimentation rate 6E-28,and plain radiography) provides a sensitivity of B<; and a specificity of BB;. f all D test results arepositive, the positive predictive value of this combination is G<;. f all D test results are negative, thenegative predictive value is <G; .6FB, F<8

"steomyelitis should be considered henever an ulcer does not heal, especially if the ulcer is over abony prominence. 0linicians also should rule out other conditions associated ith nonhealing ulcers, suchas heterotopic calcification or ossification. 'ost findings indicate that antibiotic treatment for osteomyelitisshould last G B ee s. -urgery is needed for some cases of chronic osteomyelitis. 6 D8

-ystemic amyloidosis can result from chronic suppurative pressure ulcers. Additional complications ofpressure ulcers include spreading cellulitis, a sinus tract abscess, septic arthritis, s5uamous cellcarcinoma in the ulcer, a periurethral fistula, and heterotopic ossification. &ecause some of the secondarycomplications of pressure ulcers can preclude ound healing, they should be aggressively prevented andtreated. 6G:80omplications may include infection, pain, depression, and even death.











Patient EducationPatients and their support system must reali$e that it is their responsibility to avoid recurrent and neulceration and that this is a lifelong process. 6G78Education on the proper avoidance of pressure shouldbegin in the hospital and continue into the home.

+or patient education resources, see the - in, air, and Nails 0enter and %iabetes 0enter , as ell

as 3ound 0are and %iabetic +oot 0are .

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ulkus dekubitus med scape1

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