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INTRODUCTION

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DEFINITION OF TERMS

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EPIDEMIOLOGY

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ANATOMY/PHYSIOLOGY/KINESIOLOGY

ETIOLOGY
Causes Possible causes of pressure ulcers include:

immobility and decreased level of activity

friction causing damage to the epidermal and upper dermal skin layers
constant moisture on the skin causing tissue maceration
impaired hygiene status, such as with fecal incontinence, leading to skin breakdown
malnutrition (associated with pressure ulcer development)
medical conditions such as diabetes and orthopedic injuries (predispose to pressure
ulcer development)
psychological factors, such as depression and chronic emotional stresses (may
have a role in pressure ulcer development).
(Handbook Of Pathophysiology By Okdokey)

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PATHOPHYSIOLOGY/MECHANISM OF INJURY/PATHOLOGY
Pathophysiology
A pressure ulcer is caused by an injury to the skin and its underlying tissues. The pressure
exerted on the area causes ischemia and hypoxemia to the affected tissues because of
decreased blood flow to the site. As the capillaries collapse, thrombosis occurs, which
subsequently leads to tissue edema and progression to tissue necrosis. Ischemia also adds
to an accumulation of waste products at the site, which in turn leads to the production of
toxins. The toxins further break down the tissue and eventually lead to the death of the
cells.
(Handbook Of Pathophysiology By Okdokey)

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CLINICAL SIGNS & SYMPTOMS/PHYSICAL DISABILITIES/IMPAIRMENTS

Signs and symptoms
Signs and symptoms of pressure ulcers may include:

blanching erythema, varying from pink to bright red depending on the patient's skin
color; in dark-skinned people, purple discoloration or a darkening of normal skin
color (first clinical sign); when the examiner presses a finger on the reddened area,
the pressed on area whitens and color returns within 1 to 3 seconds if capillary
refill is good
pain at the site and surrounding area
localized edema due to the inflammatory response
increased body temperature due to initial inflammatory response (in more severe
cases, cool skin due to more severe damage or necrosis)
nonblanching erythema (more severe cases) ranging from dark red to purple or
cyanotic; indicates deeper dermal involvement
blisters, crusts, or scaling as the skin deteriorates and the ulcer progresses
usually dusky-red appearance, doesn't bleed easily, warm to the touch, and
possibly mottled (deep ulcer originating at the bony prominence below the skin
surface).
(Handbook Of Pathophysiology By Okdokey)

Complications
Possible complications of pressure ulcers include:

progression of the pressure ulcer to a more severe state (greatest risk)

secondary infections such as sepsis
loss of limb from bone involvement.
(Handbook Of Pathophysiology By Okdokey)

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DIAGNOSTIC TOOLS/TEST

DIFFERENTIAL DIAGNOSIS
Moisture-associated
dermatitis
Venous ulcers

Arterial ulcers

Diabetic neuropathy

Pyoderma
gangrenosum

Osteomyelitis

Pyoderma
gangrenosum

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Erythematous, macerated skin in an area that is

exposed to chronic moisture
Commonly occur on lower legs near ankles;
frequently accompanied by skin staining.
May be painful.
May be associated with lipodermatosclerosis, in
which the lower part of the leg is hardened
Found on feet, heels, or toes. Surrounding skin
often white and shiny.
Typically most painful in bed; pain sometimes
relieved by having the legs dependent.
Ulcers often have a pale base and a punchedout appearance.
Neuropathic diabetic ulcers are caused by
pressure resulting often from ill-fitting shoes or
failure to reposition limb due to impaired
perception of pain. Ulcers commonly occur on
the toes, the heels, or other parts of the foot
Most often affects people in their 40s or 50s.
In approximately 50% of patients, it is
associated with other conditions, including
inflammatory bowel disease.
Characteristically, the edge of an ulcer is purple
and undermined (tunnelled) as it enlarges.
Ulcers are painful and most commonly occur on
the legs.
Unlike pressure ulcers, pyoderma gangrenosum
ulcers start as a small discrete area and enlarge
rapidly
Typical symptoms are bone pain, tenderness,
and swelling. May be a previous history of
osteomyelitis, recent surgery, or penetrating
injury. If bone is exposed in a suspected
pressure ulcer, osteomyelitis should be excluded
Chronic ulcerative cutaneous disease of unknown
etiology. It is most often associated with systemic
disease, particularly the inflammatory bowel diseases
Crohns and ulcerative colitis where the occurrence
rate is approximately 50%. In addition, in about 30% of
cases, ulcerations can occur after injury or at sites of
trauma (pathergy). The lesions begin as an
inflammatory deep-seated painful pustule or nodule
which then enlarges and rapidly evolves into an ulcer.
These painful boggy ulcers have characteristically

Ecthyma gangrenosum

Warfarin necrosis

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undermined sharply marginated blue or violaceous

borders. The ulcers have perforations that drain pus
(sterile) and often show purulent hemorrhage at the
base. Often, smaller blue to violaceous satellite lesions
can appear in close proximity to the ulcer border, and
then coalesce to fuse with the central ulcer. The ulcers
heal with characteristic atrophic thin scars and
recurrences are not uncommon. The diagnosis of PG
remains one of exclusion as no histologic or serologic
features are present. Ulcers should be cultured (results
should be sterile) and treatment aimed at the
underlying disease. Consultation with a
gastroenterologist is advised. Systemic methods of
treatment include glucocorticoids,
immunosuppresants, immune globulins,
immunomodulators, and biologics. Management of
ulcers includes meticulous wound care, dressing
changes, and topical corticosteroids.
is an uncommon bacterial infection most often
secondary to the gram-negative organism
Pseudomonas aeruginosa. Although healthy patients
may occasionally develop EG, most patients are
chronically, critically or terminally ill, or
immunocompromised. Pseudomonal sepsis is typically
present. Lesions begin as pustules or vesicles
surrounded by thin pink to violaceous halos. (Culture of
the pustules at this stage will be positive for P.
aeruginosa.) The lesions soon become hemorrhagic
and rupture into round ulcers which quickly become
necrotic and remain surrounded by a narrow area of
erythema. Treatment with selective intravenous
antipseudomonal medications (combination
aminoglycosides, antipseudomonal penicillins, and/or
fluoroquinolones) should be prompt followed by
surgical debridement of ulcers if there is no response
to antimicrobial therapy.
This condition of tissue death is a rare but severe
complication of oral anticoagulation treatment.
Typically, warfarin necrosis occurs between the 3rd and
10th day of therapy with warfarin derivatives and is
often associated with larger loading doses at the
beginning of treatment (Schleicher & Fricker, 1980).
The patient, who is typically an obese menopausal
female, usually first complains of pain or diffuse
redness in the affected area. This may be accompanied
by parasthesias or a pressure sensation in the involved

area. Subcutaneous edema ensues, resulting in a peau

dorange appearance. The area then demonstrates
petechiae followed by purpura and often hemorrhagic
bullae. Eventually, left untreated, full-thickness skin
necrosis and eschar formation occur. Pain usually
progresses as the evolution of the lesion progresses.
Common areas of involvement are thighs, breasts,
abdomen, and buttocks, where underlying
subcutaneous fat is more abundant. The exact etiology
of this condition is not known, but current theories
include acquired or congenital coagulopathies (protein
C , protein S, factor VII deficiencies, inadequate
antithrombin III), a hypersensitivity reaction, or a direct
toxic effect

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MANAGEMENTS

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PHARMACOLOGICAL MANAGEMENT

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MEDICAL AND SURGICAL MANAGEMENT

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PHYSICAL THERAPY MANAGEMENT

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REFFERENCES