Wound Documentation, The Whole Picture

January 2, 2009 — Matthew Livingston R.N. C.W.S.

DOCUMENTATION

Document a full patient history including:

Initiating event and the duration of the wound

Previous treatments and their outcomes

Diabetes control and prior complications

Medical conditions that may interfere with wound healing

Medications that may interfere with wound healing

Underlying pathophysiology   

Psycho-social barriers to wound healing

Severity of pain

 

Other Important Wound Documentation

Routine skin assessment and care

Moisture management

Nutritional status

Change in clinical status or wound healing progress

Education and follow up with the patient, family, and caregivers

Discuss family adherence to plan of care

Repositioning and turning schedules

Pressure-reducing support surfaces (both bed and chair)

Document referral to specialist and/or programs including:

                Nutritional management

                Diabetes management

                Smoking cessation

                Vascular surgeon

                Interventional Radiologist

                Allergist

                Infectious Disease

 

 

 

 

 

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Wound Charting Tips

December 30, 2008 — Matthew Livingston R.N. C.W.S.

WOUND CHARTING SUGGESTIONS:

A. What is the underlying etiology contributing to the wound site?

Neuropathic, diabetic, end-stage renal disease, spinal cord injury, paraplegic, ischemic/pressure injury, dyspnea.

B. Where is the wound located anatomically?

Pressure points include: occiput (back of head), scapula, spine, elbow, sacrococcygeal, trocanter, ischial tuberosities, malleolus (ankle), heel.

Friction sites may include gluteal folds, under the abdominal pannus, any skin fold, under breasts, axilla, groin, buttocks (espcially if using briefs), heels.

Document in relation to head, feet, front, or back. Commonly used terms include: proximal/distal; superior/inferior; medial/lateral; anterior/posterior; dorsal/plantar.

C. What do the wound bed and wound edges look like?

Clean, raised, rolled, curled, smooth flat, irregular, clearly defined, epibole.

D. What size and shape is the wound?

Round, oval, semi-circular, T-shaped, rectangular, punched-out. Depth may be full thickness, partial thickness, unable to be assessed.

E. What kind of drainage is present, amount, color, and odor?

Serous, sanguinous, serosanguinous, purulent, tan, opaque, clear, cloudy. Odor may be foul or sweet, “yeasty”

F. What is the condition of the surrounding skin?

Smooth, glossy, moist, blistery, weepy, “woody”, intact, healthy, erythermatous, ecchymotic, macerated, dry callus, hyperpigmentation.

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Wagner Classification of Diabetic Foot Ulcers

December 5, 2008 — Matthew Livingston R.N. C.W.S.

WAGNER CLASSIFICATION OF DIABETIC FOOT ULCERS

 

Grade 0: No ulcer in a high risk foot.

Grade 1: Superficial ulcer involving the full skin thickness but not underlying tissues.

Grade 2: Deep ulcer, penetrating down to ligaments and muscle, but no bone involvement or abscess formation.

Grade 3: Deep ulcer with cellulitis or abscess formation, often with osteomyelitis.

Grade 4: Localized gangrene.

Grade 5: Extensive gangrene involving the whole foot.

 

Wagner, F., Levin, M., & O’Neal, L., 1983. Supplement: algorithms of foot care. In The Diabetic Foot. 3 rd ed. St. Louis, MO, CV. Mosby, 1983, p. 291–

302

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Stage One Pressure Ulcer Interventions

November 30, 2008 — Matthew Livingston R.N. C.W.S.

Stage I:Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.

Further description: The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk) (FROM THE NPUAP – 2007)

Intervention for Stage 1 pressure ulcers

Position patient off affected reddened area

Initiate turning schedule

Consider turning every two hours (3o degree turns off bone)

If the head of the bed has to be greater than 30 degrees turn every one hour

Keep skin clean, dry and supple.

Place protective barrier cream or hydrocolloid over the ulcer

Suspend heels or place in boots that will suspend the heels

Initiate a Dietary Consult (Nutrition assessment)

Remove the cause or the source of the ulcer including:

Divert urine moisture with catheterization

Divert liquid stool with Flexi-Seal Fecal Management System (ConvaTec)

Perform risk assessment and then place the patient on the appropriate pressure distribution mattress

Teach and document patient and family how to and the importance of shifting weight

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Wound Healing Phases

November 23, 2008 — Matthew Livingston R.N. C.W.S.

PHASES OF WOUND HEALING

Inflammatory phase (Start of injury up to 4 days)

Hemostasis

Vasoconstriction occurs soon after the tissue is damaged as injured vessels release serotonin, histamine, prostaglandins, and blood. Platelet aggregation and thromboplastin form a clot as fibrin binds the edges of the wound together and provides temporary wound closure.

Inflammation (1 to 4 days)

Lymphocytes trigger the inflammatory response, which increases capillary permeability (this causes wound edges to swell). Bacteria and other cellular debris (dead cells) are consumed by white blood cells. This reduces the formed clot. Macrophages mediate by releasing growth factors which increase the level of fibroblasts.

Proliferative phase (2-3 days to 30 days)

Fibroblasts lay the building blocks of the new extracellular matrix for collagen fibers and granulation tissue. Granulation tissue forms and that tissue fills in the open space of the wound. Angiogenesis, with capillary formation, connects blood flow into the newly developing granulating tissue. The wound begins to contract and epithelialization moves across and covers the surface of the wound.

Remodeling phase ( 3 weeks to 2 years)

Completion of contraction occurs as collagen fibers shorten and crosslink reducing the size of the scar, but increasing . This increases the tensile strength of the scar which will return to be approximately 80% as strong as the original tissue.

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