Showing posts with label BURN SURGERY. Show all posts
Showing posts with label BURN SURGERY. Show all posts
Wednesday, January 22, 2014
TREATMENT OF PRESSURE ULCERS
Pressure ulcers result from prolonged compression of soft tissues
overlying bony prominences ( Figure 21-9 ). However,
whether excessive pressure is suffi cient to create an ulcer
depends on the intensity and duration of the pressure as well
as on tissue tolerance. Factors that contribute to pressure
ulcer development are immobility, sensory and motor defi -
cits, reduced circulation, anemia, edema, infection, moisture,
shearing force, friction, and nutritional debilitation ( Cuzzell
and Workman, 2010 ). The most common sites of pressure
ulcers are the sacrum, the ischium, the trochanter, the malleolus,
and the heel; these are called decubitus ulcers. These ulcers
are different from chronic ulcers such as vascular, diabetic, and
neurogenic ulcers. Surgical interventions for pressure ulcers are usually based on ulcer staging (also referred to as grading ).
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In stage I the ulcer involves the epidermis and has soft tissue
swelling that is irregular and ill-defi ned; heat and erythema
at the ulcer site are characteristic. A stage II ulcer involves
the epidermis and dermis but not the subcutaneous fat. Stage
III ulcers show full-thickness skin loss with injury to underlying
tissue layers and may contain necrotic material. Thorough
excisional debridement is performed, and IV antibiotic
therapy is instituted. Although debrided stage III ulcers often
heal on their own, surgical excision and closure may be done
to prevent a lengthy spontaneous closure, which may result
in a weak, unstable scar with resultant recurrence. Stage IV
ulcers are the deepest, requiring more radical excisional
debridement. Adequate soft tissue cover may be obtained by
either split-thickness or full-thickness skin grafting or tissue
fl aps
overlying bony prominences ( Figure 21-9 ). However,
whether excessive pressure is suffi cient to create an ulcer
depends on the intensity and duration of the pressure as well
as on tissue tolerance. Factors that contribute to pressure
ulcer development are immobility, sensory and motor defi -
cits, reduced circulation, anemia, edema, infection, moisture,
shearing force, friction, and nutritional debilitation ( Cuzzell
and Workman, 2010 ). The most common sites of pressure
ulcers are the sacrum, the ischium, the trochanter, the malleolus,
and the heel; these are called decubitus ulcers. These ulcers
are different from chronic ulcers such as vascular, diabetic, and
neurogenic ulcers. Surgical interventions for pressure ulcers are usually based on ulcer staging (also referred to as grading ).
In stage I the ulcer involves the epidermis and has soft tissue
swelling that is irregular and ill-defi ned; heat and erythema
at the ulcer site are characteristic. A stage II ulcer involves
the epidermis and dermis but not the subcutaneous fat. Stage
III ulcers show full-thickness skin loss with injury to underlying
tissue layers and may contain necrotic material. Thorough
excisional debridement is performed, and IV antibiotic
therapy is instituted. Although debrided stage III ulcers often
heal on their own, surgical excision and closure may be done
to prevent a lengthy spontaneous closure, which may result
in a weak, unstable scar with resultant recurrence. Stage IV
ulcers are the deepest, requiring more radical excisional
debridement. Adequate soft tissue cover may be obtained by
either split-thickness or full-thickness skin grafting or tissue
fl aps
BURN SURGERY
A majority of burns result from exposure to high temperatures,
which injures the skin. Flame, scalding, or direct contact with
a hot object may cause thermal skin injury. Similar destruction
of skin can result from contact with chemicals such as acid or
alkali or contact with an electrical current. The latter, however,
often involves extensive destruction of the underlying tissue
and physiologic systems in addition to the skin. A 2007 fact
sheet on burn statistics includes the following information:
approximately 500,000 burn injuries receive medical treatment
yearly; 40,000 patients are hospitalized in the United States for
burn injuries, with 25,000 of those admitted to the 125 hospitals
with specialized burn centers (American Burn Association
[ABA], 2007).
Intact skin provides protection against the environment for
all underlying tissues and organs. It aids in heat regulation,
prevents water loss, and is the major barrier against bacterial
invasion. The tissue injury resulting from a burn disrupts this
normal protective function, resulting in local and systemic
effects ( Box 21-2 ). Burn patients are therefore some of the most
acutely ill patients brought to the OR. The greater the degree
of injury to the skin, expressed in percentage of total body surface
area (BSA) and depth of burn, the more severe the injury.
One method of measuring BSA in adults is by use of the rule of
nines
Partial-thickness (fi rst- and second-degree) burns heal by
regeneration of skin from dermal elements that remain intact.
First-degree burns involve the epidermis, which appears pink
or red; sunburn is usually a fi rst-degree burn. Second-degree
burns, also called partial-thickness burns, involve the epidermis
and some of the dermis. Full-thickness (third-degree)
burns ( Figure 21-8 ) involve the epidermis, the entire dermis,
and the subcutaneous tissues; they require skin grafting to
heal because no dermal elements remain intact. Both partialand
full-thickness burns may require debridement of necrotic
tissue (eschar) before healing can occur by skin regeneration
or grafting. An allograft may be used to cover the burned
area during the initial healing process. However, the allograft
must be carefully tested for immunodefi ciency diseases. A
xenograft (e.g., pig skin) may also be used for covering the
burned area.
which injures the skin. Flame, scalding, or direct contact with
a hot object may cause thermal skin injury. Similar destruction
of skin can result from contact with chemicals such as acid or
alkali or contact with an electrical current. The latter, however,
often involves extensive destruction of the underlying tissue
and physiologic systems in addition to the skin. A 2007 fact
sheet on burn statistics includes the following information:
approximately 500,000 burn injuries receive medical treatment
yearly; 40,000 patients are hospitalized in the United States for
burn injuries, with 25,000 of those admitted to the 125 hospitals
with specialized burn centers (American Burn Association
[ABA], 2007).
Intact skin provides protection against the environment for
all underlying tissues and organs. It aids in heat regulation,
prevents water loss, and is the major barrier against bacterial
invasion. The tissue injury resulting from a burn disrupts this
normal protective function, resulting in local and systemic
effects ( Box 21-2 ). Burn patients are therefore some of the most
acutely ill patients brought to the OR. The greater the degree
of injury to the skin, expressed in percentage of total body surface
area (BSA) and depth of burn, the more severe the injury.
One method of measuring BSA in adults is by use of the rule of
nines
regeneration of skin from dermal elements that remain intact.
First-degree burns involve the epidermis, which appears pink
or red; sunburn is usually a fi rst-degree burn. Second-degree
burns, also called partial-thickness burns, involve the epidermis
and some of the dermis. Full-thickness (third-degree)
burns ( Figure 21-8 ) involve the epidermis, the entire dermis,
and the subcutaneous tissues; they require skin grafting to
heal because no dermal elements remain intact. Both partialand
full-thickness burns may require debridement of necrotic
tissue (eschar) before healing can occur by skin regeneration
or grafting. An allograft may be used to cover the burned
area during the initial healing process. However, the allograft
must be carefully tested for immunodefi ciency diseases. A
xenograft (e.g., pig skin) may also be used for covering the
burned area.
