i bc27f85be50b71b1 (145 page)

BURNS AND WOUNDS

469

Table 7-11. Clinical Indicators of Vascular Insufficiency Wounds

and Diabctic Ulcers

Wound Etiology

Clinical Indicators

Arterial insuffi·

Intermirtent claudication

ciency

Extreme pain, decreased with rest and increased with

clevmion

Decreased or absent pedal pulses

Decreased temperaturc of the distal limb

Distinct, well-defined wound edges

Deep wound bed

Cyanosis

Venous

Localized limb pain, decreased with elevation and

Insufficiency

increased with srandmg

Pam with deep pressure or palpation

Pedal pulses present

Increased temperature around the wound

Indistinct, Irregular edges

Edema Mound the wound

Shallow wound bed

Suhsranrial drainage

Diabetic ulcer

Painless ulcer; however, general lower-limb pain is

present

Absent pedal pulses

Decreased temperature in the distal limb

Deep wound bed frequently located at pressure points

(e.g., metatarsal heads)

Shin}- skill on dlsral limb

Sources: D.lt.1

from JM �1cC:ulloch. r\'alu:lrion of P:lticnrs with Opcn Wounds. In LC

Kloth. KH M111er (cds), Wound Ilc:lhnlt: Alternatives in Management. Ph1ladelphia: FA

Da\·is, 1995; RG Sihbald. An approach to leg and foot ulcers: a bnef overv1ew. Ostomy

Wound MJnage 1998;44:29; RG �Ibbald. Venou!t leg ulcers. Osromy Wound Manage

1998;44:53; P Lamg. DI;Ibcrif.: foot ukcrs. AmJ Surg 1994;167(IA):31; and ML Levin,

LW O'Ncill, JII Bowker (cd�). Thc D1abetlc Foot (5th cd). St. loUIS: Mosby, 1993.

superficial veins in the subcutaneous tissue and [he overlying skin,

which causes widening of the capillary pores.J4.JS Clinically, this

would result In the first sign of venous disease, which is the presence

of a dilated long saphenous vein on the medial aspect of the calf. This

dIlation allows the escape of large macromolecules, including fibrinogen, into the interstitial space. This results in the development of edema toward the end of the day because of the pooling of fluid in the

470

AClITE CARE HANDBOOK FOR PHYSICAL TIIE.RAI'ISTS

dermis. In long-standing venous disease, fibrin accumulates in the dermis, creating a fibrin cuff that presents as hard, non pitting edema, and the surface skin is rigid and fixed. The theory states that this

fibrin cuff forms a mechanical barrier to the transfer of oxygen and

other nutrients, which progressively leads to cellular dysfunction, cell

death and skin ulceration.H."

Another hypothesis is called the white blood cell-trappil1g hypothesis. This theory states that transient elevations in venous pressures decrease capillary blood flow, resulting in trapping of white blood cells

at the capillary level, which in turn plugs capillary loops, resulting in

areas of localized ischemia." These white blood cells may also become

activated at this level, causing the release of various proteolytic

enzymes, superoxide free radicals, and chemotactic substances, which