Pressure Sore Fix

7/30/2019 Pressure Sore Fix

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Berlian Indri Hapsari

Ayun Puji Lestari

Hendy Buana Vijaya

Coni Senopadang

Pembimbing : dr. Sulandri Gusasi, Sp.

BP


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.

Overview

Pressure sores/pressure ulcer soft-tissue injuries resulting from unrelievedpressure over a bony prominence

decubitus ulcer/bedsore (supine position)

In general, approximately 9% of allhospitalized patients develop pressuresores.

Association with other medical problems,including cardiovascular disease (41%),acute neurologic disease (27%), andorthopedic injury (15%).


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Factors such as poor nutrition, incontinence with

persistent soilage and moisture, dementia,

paralysis, friction, and shear make healing lesslikely

treatment frequently requires input from

orthopedic surgery, internal medicine,

endocrinology, in-/outpatient nursing, mentalhealth care, and, most importantly, plastic surgery

OVerview


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.

Risk Factor

risk factors in acute care pressure soredevelopment Braden Scale for PredictingPressure Sore Risk.

National Pressure Ulcer Prevalence Survey(1994) age, impaired sensory perception,moisture, immobility, poor nutrition, andfriction/shear

In terms of pressure sore location, 96% occurbelow the level of the umbilicus

For the majority of patients, wounds develop ineither the supine or seated position


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BRADEN SCALE


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National Pressure Sore Advisory PanelConsensus Development Conference (1989)

Staging


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Stage I

Discolouration of the skin, warmth, oedema, induration or hardness.

Protecting and monitoring mattress

A film dressing/thin hydrocplloid reduced friction/shearing


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Stage II

partial-thickness skin loss involving the epidermis, dermis or both.

The ulcer is superficial and presents clinically as an abrasion or

blister debridement


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Stage III Stage III

full-thickness skin loss involving damage to or necrosis of

subcutaneous tissue

absorbent dressings


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Stage IV

extensive destruction, tissue necrosis or damage to muscle, bone

or supporting structures with or without full-thickness skin loss

If there is bone exposed, consider infection in the bone

(osteomyelitis)


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Stage IV


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accelerated by infection, inflammation, edema,and factors that are not yet understood.

Patophysiology

Compression

of softtissues

ischemia

(if notrelieved)

necrosis and

ulceration


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capillary blood pressure in a single capillaryranged from 12 mm Hg on the venous end to

32 mm Hg on the arterial end

If the external compressive force exceedscapillary bed pressure, capillary perfusion is

impaired and ischemia will ensue

pressure of 70 mm Hg applied over 2 hours

was sufficient to cause pathologic changes indogs

pressure of 500 mm Hg applied for 2 hours, or

pressure of 100 mm Hg for 10 hours, was

sufficient to cause muscle necrosis.

1. PRESSURE


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pressure and its effects as it relates tolocation, time, and intensity

In the supine position, the maximal recorded

pressures were 40 to 60 mm Hg near theheels, buttock, and sacrum.

In the sitting position, pressures were greatest

near the ischial tuberosities.

1. PRESSURE


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Inverse relationship between time

and pressure in the formation of

pressure sores.


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Distribution of

pressures in a

normal man.


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2. INFECTION

bacterial counts increase in compressed areas.

Robson and Krizekincisions created in areas of

applied pressure and inoculated with knownconcentrations of organisms allowed for a 100-foldgreater bacterial growth than in areas not subjectedto pressure.

The proposed mechanisms include impairedlymphatic function, ischemia, and impaired immunefunction.


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Inflammation

When tissue is injured, there is a demargination

and influx of cells responsible for inflammation.

For injuries to heal, a series of events unfolds,

including vasoconstriction/vasodilatation,

coagulation, influx of proinflammatory cells like

neutrophils and macrophages, and, finally, matrix

formation/maturation

In chronic wounds, there is a breakdown in this

sequence, leading to a nonhealing wound.

3. INFLAMMATION


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pressureincreases

plasmaextravasation

Edemaformation

denervationloss ofsympathetic tone of the

blood vessels, leading to

vasodilatation, creating

greater engorgement of thevessels, and greater edema

As interstitial plasma

concentrations rise, the

concentration of sebum onthe skin surface is diluted.

Sebum has been shown to

be important in the defense

against both streptococcal

and staphylococcal

4. edema


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This approach may

require input from

internal medicine,

endocrinology,

neurology, urology,nutrition, physical

and occupational

therapy, and

psychiatry, as well asa wound care nurse

specialist

PREOPERATIVE

CARE

nutritionalassessment and

maintenance

pressureand

spasmrelief

control ofboth systemic

and localinfection


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Normal healing potential exists as long as serum

albumin is maintained above 2.0 g/dL.

1.5 to 3.0 g/kg/d of protein to restore lost lean

body mass, and 25 to 35 cal/kg of nonprotein

calories should be delivered daily

vitamins A and C proper wound healing

zinc epithelialization and fibroblast proliferation calcium is a cofactor for many enzymatic

pathways

Ferrous iron and copper collagen metabolism

1. NUTRITION


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Pressure sores may or may not present with local

infection.

Surgical debridement either at the bedside or

operating room is carried out to remove nonviabletissue

identify the types of bacteria present, and determine

antibiotic sensitivities

topical antimicrobial agents like Dakin solution at0.025%, silver sulfadiazine, or mafenide acetate, if an

eschar exists

The most common organisms cultured from pressure

sores are common skin flora (Staphylococcus,

2. INFECTION


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Wound healing will not

occur in the presence ofischemia or infection

Mattress and wheelchair

padding systems havebeen designed to relievepressure

Bedridden patients longstanding denervation

tightening of both musclesand joint capsules and are

common in hip flexors, trochanteric, knee, andankle ulcers

relieving the contractures physical therapy/

tenotomies

3. Relief

pressure4. Contracture


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Spasticity (spinal cord injuries) pressure sores

The more proximal the lesion, the higher the

incidence of spasm: near 100% in the cervicalregion, 75% in the thoracic region, and 50% in

the thoracolumbar region.

reduce spasm Valium, baclofen, and dantrolene.

surgical intervention

5. Spasm

SURGICAL


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A dilute solution of

methylene blue and

hydrogen peroxidehelp define the cavity

and leave a visual guide

for excision

removal of the necrotictissue

Postoperatively, the

wound is packed and

dressings changed

every 6 to 8 hours.

Radical ostectomy

should be avoided so

as to avoid excessivebleeding, skeletal

instability, and

redistribution of

pressure points toadjacent areas

SURGICAL

TREATMENT

1. DEBRIDEMENT 2. OSTEOKTOMY


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Skin grafting has only a 30% success rate as

grafting tends to provide unstable coverage

Musculocutaneous flaps provide blood supply,

bulky padding, and are effective in treating

infected wounds

Fasciocutaneous flaps offer an adequate bloodsupply, durable coverage, and minimal potential

for a functional deformity, and they more closely

reconstruct the normal anatomic arrangement

over bony prominences

3. Pressure Sore Closure


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>> seated position

high recurrence rate, as they almost always

return to sitting postoperatively

Medially based thigh flap and the gluteus

maximus myocutaneous flap, accomplished with

either fasciocutaneous or musculocutaneous

flaps The biceps femoris, semimembranosus, and

semitendinosus musculocutaneous flaps

effective for ischial ulcers and they can be re-

advanced

A. Ischial Defects


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several disadvantages closure is always under

tension, the scar is directly over the maximal

pressure point, and hip flexion tends to cause

dehiscence.

The tensor fascia lata (TFL) distal aspect of

the TFL flap is usually too thin to offer adequate

padding, making the TFL flap, in general, not the

best choice.

For more complex, deeper, or larger wounds, a

combination of flaps may need to be employed.


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Flaps for closure of ischial wounds.


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>> supine position musculocutaneous or fasciocutaneous flaps

The gluteal flap can be based superiorly or

inferiorly, part or all of the muscle or both muscles

may be used, it can be constructed of muscle or

muscle and skin, and it may be rotated,

advanced, or turned over

B. Sacral Defects


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Flaps for closure of the sacrum


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>> lie in lateral position (hip flexion contractures) >> TFL flap

Sensation from the nerve roots of L1, L2, and L3

by the lateral femoral cutaneous nerve makes this

a potentially sensate flap in patients with spinal

cord injury below L3, representing more than 60%

of meningomyelocele patients

Rotation of the TFL flap results in a T-shapedjunction between the flap and the closed donor

site and this area is prone to dehiscence.

C. Trochanteric Defects


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Post Operative Care

Nutrition,medical,

rehabilitative care

control ofurine and

stool

Drainpositioned avoidpressure

Carefulnursing care


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Pressure Sore Fix

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