















                       PREVENTION AND MANAGEMENT
                           OF PRESSURE SORES

                      EDWARD J. MATHES, RPA-C

                          Hahnemann University
                      Physician Assistant Program
                         Philadelphia, PA 19102

                                  and

                          The Genesee Hospital
                         Department of Surgery
                          224 Alexander Street
                          Rochester, NY 14607





        Written Comments invited at The Genesee Hospital Address





                   Abbreviated Title:  pressure sores
















                                ABSTRACT

    Pressure sores are a vexing problem estimated to affect 3-25% of
all patients in acute and long-term care facilities.  Entrinsic factors
that favor pressure sore development include pressure,
shear, friction, and moisture.  There are multiple intrinsic
contributors.  Frevention is preferable to treatment.  Using available
tools, patients at-risk for developing pressure sores can be identified
and preventive measures instituted.  When prevention fails, treatment,
based on 5 therapeutic principles, will facilitate healing.


                              EPIDEMIOLOGY

     Pressure ulcers (sores) are an unfortunate problem that carry
significant morbidity and mortality. Three distinct groups of patients
are affected: spinal-cord injured, geriatric, and orthopedic [1,2,3].
The National Pressure Ulcer Advisory Panel, at their 1988 meeting,
reported an incidence of 3% - 14% among all patients in acute care
institutions [4,5], rising to 15% - 25% if long-term care patients are
included [6].  Additionally, all patients who have or develop pressure
sores are hospitalized an average of five times longer, experience a
five-fold increase in mortality, and cost an average of $35,000.00
more, per patient, when compared to the general patient populations
[5,6,7,8].


                                ETIOLOGY

     There are 4 primary extrinsic factors associated with pressure
sore development:  pressure, shear, fricion, and moisture.

1).  Pressure: Most pressure sores occur in those areas where soft
tissue is compressed between bony prominences and a firm surface (focal
pressure).  80% occur on the lower body; the sacral-coccygeal area, the
greater trochanters, ischial tuberosities, malleoli, and heels being
most commonly affected [8].  Other sites include the elbows, occiput,
scapulae and spinus processes.
  External, focal pressure that exceeds capillary filling
pressure (32 mmHg) for as little as two hours can cause ischemic
change# [9,10].  As pressure is increased, ischemia occurrs over a
progressively shorter time [11]. Additionally, deeper tissues appear to
be more suceptible than skin to ischemia [12,13].

2).  Shear occurs when adjacent tissue surfaces (skin & fascia) slide,
creating a relative displacement of tissues, causing acute angulation
and stretch of blood vessels and lymphatics, resulting in decreased
perfusion, ischemia, and dermal undermining [14,15].

3).  Friction occurs when two surfaces are moved across one another.
Friction disrupts the protective outer layers of the skin, interfering
with the fibrinolytic activity of the dermis, making the skin more
suseptible to pressure necrosis [15].

4).  Moisture due to fecal and urinary incontinence causes tissue
maceration, accelerates skin breakdown, and increases the friction co-
efficient.
     There are a variety of intrinsic factors that contribute to
pressure sore formation.  Neurologic diseases that cause sensory
deficits rob the patient of the ability to sense the pain associated
with local tissue ischemia.  Immobility due to over-sedation,
contractures, fractures, spinal cord injury, and other causes interfere
with the patient's ability to change positions when pressure tolerances
are exceeded [16,17]. The loss of protective fat padding over bony
prominences occurs with weight loss.  Large and small vessel vascular
disease interferes with tissue perfusion.  skin changes associated with
age (inelasticity, transparency, etc), hypoalbuminemia, and
malnutrition have also been implicated [5,18,19,20].


                               PREVENTION

     Because of the financial, physical, and emotional morbidity
associated with pressure sores, prevention is preferable to treatment.
A simple program, stressing the total elimination of risk factors, is
usually the best.
     Nursing experts have developed many tools to help identify
patients at risk for pressure sore formation [21,22]. Most use a
scoring system that assigns a numeric value to selected risk factors.
Higher scores usually indicate greater risk.


                          PREVENTIVE MEASURES

     Once identified as `at-risk', prevention of skin breakdown is of
prime importance.  Underlying disease should be treated and/or
controlled, patients' skin should be inspected at regular intervals,
preferably daily, nutritional status assessed, and malnutrition
treated.
     Pressure Relief is effected by interposing soft material between
the, mattress and bony prominences frequent turning [23].  The goal is
to reduce pressure on the usual pressure ulcer sites below capillary
filling pressure (32mmHg).
     There are many mattress overlays and total bed systems available.
All have their advantages, disadvantages, and levels of effectiveness
[24]. A complete discussion is beyond the scope of this paper.
However, a brief description of a few types is presented.
     Convoluted Foam or eggcrate mattress overlays are relatively
inexpensive, easy to use, and may improve patient comfort.  Their
efficacy at preventing pressure ulcers is questionable as most do not
reduce focal pressure significantly.
     Air matresses come in many shapes and forms, including static
yair, alternating air-pressure, and low-air-loss systems.  Static air
mattresses are comparable to foam overlays.  Alternating pressure air
mattresses consist of a pump and multiple, interconnected cells that
alternately inflate and deflate to relieve pressure.  Low-air-loss beds
(Mediscus(R) & others) consist of multiple, individual, layered air
cells.  Pressure in each individual cell can be varied according to the
needs of the patient.
     Air Fluidized Beds (Clinitron(R) & others) consist of silicone
microspheres encased in an air and liquid permeable cover.  Warm air is
circulated in the cover, allowing the patient to "float" on a fluid-
like surface with less than l0mmHg pressure exerted [25].
     Your selection of an appropriate system should be based on it's
ability to protect patients at different levels of risk.  Foam
(eggcrate) overlays may be adequate for "low risk" patients, the air-
fluidized bed reserved for those at higher risk [26].

     FRlCTION is prevented by using lotion as a skin lubricant, lifting
(not dragging) the patient across the bed, and ensuring bedcloths are
wrinkle free.

     SHEAR is prevented by keeping the head of the bed lower than 30
degrees.

     IMMOBILE patients should be turned every two hours to relieve
pressure.  The 30 degree right and left lateral oblique positions will
relieve pressure on all bony prominences [23]. If the patient's
condition permits, range of motion exercises and ambulationshould be
incorporated into the prevention regimen.

     lNCONTlNENCE is a major source of moisture and bacterial
contamination.  Urinary incontinence can be contained with external
collection devices.  lndwelling bladder catheters work well, but serve
as a portal for bacterial entry.
     Bowel incontinence is more difficult to control.  External fecal
collection devices are available and, reportedly, easy to use.  Rectal
tubes, if improperly used, run the risk of anal stenosis, fistula
formation, or colonic perforation.  Adult diapers have the disadvantage
of keeping waste in contact with skin and can act as a barrier to
evaporation of excess moisture if not change frequently.


                               TREATMENT

     When Prevention fails, an aggressive approach to therapy is
warranted.
     ln 1988, the National Pressure Sore Advisory Panel adopted Shea's
pressure sore classification system (Figure 1-4) [4,27].
Treatment is guided by the five therapeutic principles outlined in
Table 1 [28,29].
     Improving the patient's general condition includes all the
measures discussed under `Prevention'.  Elimination of all risk factors
is essential.
     A complete nutritional assessment is advised. An adequate
number of calories must be provided, either enterally or with venous
hyperalimentation.  Several vitamins and minerals are important for
wound healin#. Vitamin A is essential for epithelial maturation and
collagen formations [30]. Vitamin C is needed for collaen synthesis,
maintenance of connective tissue, and leukocyte function [31].  Folic
acid is neyessary for protein synthesis and it enhances cell division
[32].  Zinc is essential for protein synthesis and tissue repair# [33].
All may be administered as oral supplements.
     Some caution in the use of vitamin and mineral supplements is
advised.  Serum zinc levels should be determined prior to starting
supplements because excess zinc can interfere with wound healing.
Additionally, zinc and folic acid bind to the same protein and must be
given 12 hours apart. Doses are: Zinc sulfate, 220mg PO daily; Folic
acid, lmg PO daily.
     Vitamin A is of special concern.  It has been shown to counter the
anti-inflammatory effects of steroids and stimulate wound healing.
Toxicity can occur with doses in excess of 25,000 IU per day for
several months [34,35,38].  I generally limit Vitamin A use to those
patients who are steroid dependant and/or malnurished.  Vitamin A dose
is 25,000 IU, p0 daily for 3-4 weeks.

     Relief of pressure is an absolute!  All measures discussed under
`PREVENTION' are applicable.  By their nature, Grade I
and many small Grade II pressure sores will heal with relief of
pressure alone.

     lN NO lNSTANCE should the patient lie directly on an existing
pressure sore.  If the patient cannot be turned frequently, or has
large sacral, bilateral ischial, or trochanteric ulcers, the use of a
low-air-loss or air fluidized bed should be considered.

     The goal of local disinfection is to lower the bacterial count of
the ulcer bed to less than 100,000 organisms/gram ulcer tissue.
Bacterial counts higher than this will delay healing by interfering
with wound granulation [15,28,29].
     The ideal disinfecting solution should not cause pain, change the
character of the ulcer (e.g.:iodine staining), injure healthy tissue,
or interfere with granulation tissue growth [29,36].
     Most of the topical disinfectants in use today are toxic to
fibroblasts and granulation tissue [37]. Their use in the wound is not
recommended.  However, all are appropriate for skin cleansing up to the
margin of the wound.  Wound disinfection is accomplished by frequent
irrigation, preferably under pressure (I use a waterpick), with sterile
normal saline, and a combination ofsharp and enzymatic debridement.
     Because bacterial infection is usually limited to the ulcer
itself, cultures and antibiotics are rarely indicated.
     Debridement is performed to remove necrotic tissue and eschar from
the ulcer bed.  Both impeed healing and create an environment for
bacterial proliferation.  The recommended approach is dailysharp
debridement until all necrotic tissue is removed [15,29].  If daily
sharp debridement cannot be done, proteolytic enzymes
(desoxyribonuclease, fibrinolysin, or collagenase) may be used.
     #equent dressing changes are also necessary. Gauze pads, moistened
with sterile normal saline and wrung-out, are applied to the wound two
or three times per day and allowed to dry. When the dressing is
changed, necrotic tissue and debris that has adhered to the auze are
removed with the dressing. This is an effective method of debridement,
but can be painful.  Unfortunately, it also removes healthy granulation
tissue with the debris.  Once the wound is clean, this method should be
discontinued.
     Other techniques of debridement include irrigation under pressure
and whirlpool baths.  Both work well but share the disadvanta#es of the
wet-to-dry dressing technique.
     Bedside debridement of large Grade 1II and IV ulcers may be
ineffective.  In these cases, surgical debridement under anesthesia may
be necessary.
     A favorable environment for granulation tissue formation exists
only if the ulcer is clean, moist, free of necrotic debris, with a
bacterial count less than 100,000 organisms/gram tissue [38,39,40].
Hydrophilic, occlusive, gas permeable dressings are recommended for
Grade II and small Grade III pressure sores.  Larger Grades III and IV
ulcers are kept moist by packing the wound with normal saline or
lactated ringer's moistened gauze that is kept moist between dressing
changes [29].

     Large Grade III and IV ulcers may require surgical repair with
skin grafts or myocutaneous flaps to replace skin and soft tissue
losses.  Additionally, modification of the bony prominence underlying
the ulcer may be necessary [41].
     This author's method of pressure sore treatment, based on the
available literature and personal experience, is also summarized in
Table 1.


                             COMPLICATIONS

     With few exceptions, routine wound cultures and systemic
antibiotics are not indicated in the treatment of the uncomplicated
pressure sore.  However, transient bacteremia can occur during
debridement sessions and dressing changes.  In the immunosupressed
patient, patients with a history of rheumatic heart disease, or in the
presence of orthopedic, cardiac or vascular prosthesis, prophylactic
antibiotics should be considered.
     Most pressure sores are polymicrobial, consisting of common gram
positive cocci and gram negative rods.  Without evidence of other
sources of infection, the appearance of fever, chills, and leukocytosis
indicates spread of infection beyond the pressure sore.
     Cellulitis is an inflammation of the subcutaneous tissue around
the pressure sore.  lt is characterized by swelling, redness, heat, and
pain extending away from the wound margins.  A moderate to high fever
and leukocytosis is usually present.  There can be accompaning
lymphangitis [42,43].
     Septicemia occurs when bacteria and their toxins are seeded
directly into the bloodstream from an infected pressure sore.
Septicemia is characterized by moderate to high fever, shaking chills.
and an elevated white blood cell count.  There may be a relative
bandemia on periPheral blood smear.  Septicemia is most frequently
associated with multiple pressure sores.  Mortality in this group of
patients approaches 50% [44,45].
     If cellulitis or septicemia are suspected, wound and blood
cultures for aerobes and anaerobes should be obtained.  Broad spectrum
antibiotics that cover common gram positive and negative pathogens
should be started. Antibiotic coverage can be tailored to the specific
pathogen(s) once culture results are available.
     Additional treatment for cellulitis includes elevation if an
extremity is involved, hot packs, and wound debridement.  Failure to
see improvement after 24 hours of appropriate treatment suggests the
presence of an abscess or a resistant organism.  An abscess requires
prompt surgical drainage [43]. The suspicion of a resistant organism
requires reconsideration of antibiotic coverage.
     In cases of septicemia, prompt recognition and treatment is
necessary to prevent frank sepsis.  Other supportive measures
(hemodynamic monitoring, blood pressure support, etc) may also be
necessary. If, on inspection, the pressure sores appear clean, other
sources of sepsis should be considered.
     Finally, because pressure ulcers occur in close proximity to bone,
osteomyelitis must be considered when a pressure sore penetrates to or
through periosteum, or if the ulcer fails to heal despite appropriate
therapy. The diagnosis is often difficult to make, requiring a high
index of suspicion [46].

      A number of studies looked at various radiologic aids to
diagnosing osteomelitis [47,48].  They concluded that a normal Tc99m
scan effectively ruled out osteomyelitis.  However, an abnormal scan
indicated the need for further testing (i.e.; needle bone biopsy) to
confirm the presence of osteomyelitis.  Plain radiographs proved useful
only in pinpointing the best location for biopsy.


                             OTHER THERAPY

     As our understanding of wound healing is increasing.  A variety of
new, and not so new, technologies is being applied to pressure sore
treatment with promising results.
     Transcutaneous measurement of skin oxygen tension allows the
direct measurement of the effects of pressure on skin perfusion[23].
Using the CO2 laser, the pressure sore can be excised, the ulcer bed
sterilized, and the wound closed primarily with little risk of
infection [49].
     Research on the use of platelet derived epidermal growth factors,
applied directly to the pressure sore or impregnated into dressings,
has been shown to speed epithelialization [50].
     Transcutaneous electrical stimulation of chronic pressure ulcers
has also been shown to stimulate healing [51,52].


                               CONCLUSION

     Pressure sores are an unfortunate problem that carries significant
financial, emotional, and physical morbidity.  Using existing
knowledge, tools, and techniques, "at-risk" patients can be identified
and preventive measures taken.  An organized approach consistin# of a
comprehensive, yet simple, prevention program is recommended.
     Treatment of existing pressure sores can be time consuming and
exasperating for patients, their families, and health care providers.
By following the 5 therapeutic principles outlined here.  improvement
and/or healing of these wounds will be facilitated.  Larger wounds
necessitate the early involvement of a general or plastic surgeon with
an interest in pressure sore management.
























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    FIGURE 1
    Grade I:  Localized area of heat, induration, and erythema with an
    irregular, ill defined border, usually over a bony prominence.
    Epidermis is usually intact, but there may be a shallow ulcer
    present [27].


   FlGURE 2
   Grade II:  All characteristics of Grade 1 but with an ulcer that
   extends through epidermis down to but not into subcutaneous tissue.
   May be tender to touch is sensation is intact [27].


   FlGURE 3
   Grade III:  Is a full-thickness wound extending to, but not through,
   fascia.  Dermal undermining is present for varying distances from
   the wound edge.  The sore is usually infected, foul smelling, with
   a necrotic base.  An eschar may be present [27].


   FIGURE 4
   Grade IV:  Has all the characteristics of Grade 3 but penetrates
   through fascia.  Muscle or bone may be visible in the ulcer base.
   Dermal undermining is usually extensive {27}.












 
                                TABLE 1
               APPROACHES TO TREATMENT OF PRESSURE SORES

Principle   Grade  1                    2                3        4


Pressure    Foam or static air    Alternating air      Low air loss or
 Relief      mattress overlay      pressure mattress    air-fluidized bed
                                                        system
            Turn q2h into 30 degree right and left lateral oblique

Shear       Head of bed flat/< 30 degrees

Dis-        none                                       Clean to wound
 Infection                                             edges using 0.001%
                                                       Providine-iodine
                                                       solution

Debridement none                                       Daily sharp removal
                                                        of eschar,necrotic
                                                        tissue, debris.

                                                       Colagenase used

                                                       Whirlpool qd-qod

                                                       Normal saline wet-
                                                        to-dry dressing
                                                        changes q8h until
                                                        wound clean

Promote                           Hydrocolloid         Ringer's solution
 Granulation                       occlusive            wet dressing:keep
                                   dressing             moist

                                                       General/Plastic
                                                        Surgery consult
                                                        for definative
                                                        repair