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    Pathophysiology of Pressure Ulcer

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    1. Pressure ulcers develop due to prolonged pressure on skin from lying or sitting in one position, which reduces blood flow and leads to tissue death if not relieved. 2. Factors that increase risk include sensory deficits, impaired mobility, malnutrition, moisture, shear forces, and friction on the skin. 3. Pressure ulcers are staged from I to IV based on depth of tissue damage, from non-blanchable redness to full thickness tissue loss exposing bone or muscle.

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    Pathophysiology of Pressure Ulcer

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    249 views1 page
    1. Pressure ulcers develop due to prolonged pressure on skin from lying or sitting in one position, which reduces blood flow and leads to tissue death if not relieved. 2. Factors that increase risk include sensory deficits, impaired mobility, malnutrition, moisture, shear forces, and friction on the skin. 3. Pressure ulcers are staged from I to IV based on depth of tissue damage, from non-blanchable redness to full thickness tissue loss exposing bone or muscle.

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    PATHOPHYSIOLOGY OF PRESSURE ULCER

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    1. Pressure ulcers develop due to prolonged pressure on skin from lying or sitting in one position, which reduces blood flow and leads to tissue death if not relieved. 2. Factors that increase risk include sensory deficits, impaired mobility, malnutrition, moisture, shear forces, and friction on the skin. 3. Pressure ulcers are staged from I to IV based on depth of tissue damage, from non-blanchable redness to full thickness tissue loss exposing bone or muscle.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    249 views1 page

    Pathophysiology of Pressure Ulcer

    Uploaded by

    STORAGE FILE
    1. Pressure ulcers develop due to prolonged pressure on skin from lying or sitting in one position, which reduces blood flow and leads to tissue death if not relieved. 2. Factors that increase risk include sensory deficits, impaired mobility, malnutrition, moisture, shear forces, and friction on the skin. 3. Pressure ulcers are staged from I to IV based on depth of tissue damage, from non-blanchable redness to full thickness tissue loss exposing bone or muscle.

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    PATHOPHYSIOLOGY OF PRESSURE ULCER

    Contributing Factors:
    Predisposing Factors:
    1. Chronic Medical Condition -
    1. Sensory Deficit
    Stroke, Diabetes, and
    2. Impaired Physical Mobility
    cardiovascular diseases.
    3. Altered level of
    2. Advanced Age (79 years old)
    Consciousness
    3. Excessive Body Heat
    4. Malnutrition

    Bed ridden or on Involuntary muscle Inability to move Bowel/Bladder Decrease in


    wheelchair. movement, passive well, aging skin incontinence, movement (Post
    repositioning of the (loss of elasticity and diaphoresis, CVA, coma, post-
    subcutaneous fat) surgery, etc.)
    torso wound drainage

    External Physical Moisture Limited Mobility


    Pressure Shear Forces Friction (Skin Maceration)

    Unrelieved Pressure
    greater than the
    LEGENDS: capillary pressure
    Pathophysiology
    Mechanism
    Sign/Symptoms/Lab
    findings Occlusion and tearing
    Complications of blood vessels

    Reduce tissue perfusion

    Ischemic Necrosis

    Pear-or butterfly- Kennedy


    PRESSURE ULCER shaped sacral Terminal Ulcer
    ulcer (Often precedes
    death)

    STAGE I STAGE II STAGE III STAGE IV Depth Unknown


    (non-blanchable (Partial thickness skin (Full-thickness skin loss; (Full-thickness (Eschar covers wound bed
    erythema of intact skin; loss) damage to subcutaneous tissue tissue loss) and obscure depth)
    heralds impending ulcer) but not underlying fascia)

    Bone, tendon, or Must remove eschar


    May be warmer, Erosion, serum-filed Exposed subcutaneous muscle exposed. to determine stage
    painful, edematous, blister, or shallow fat, may have slough, Slough or eschar is
    indurated, or ulcer with red-pink undermining, or present with
    discolored compared wound bed. tunnelling undermining or Bacterial invasion
    to surrounding tissue
    tunnelling
    via contiguous
    spread
    Elevated WBC,
    Fever, Dysuria, and
    High Bacterial Count,
    Abdominal Pain SEPSIS
    difficulty in urination Osteomyelitis

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