Ulcers

Question 1

Types of Ulcers

Answer 1

Pressure
Venous
Arterial
Neurotrophic 
      Diabetic
Special Cases:
      Pyoderma gangrenosum
      Cancer

Question 2

Pressure Ulcer Staging

Answer 2

Stage I: non-blanchable erythema.
Stage II: like an unroofed blister, dermis exposed.
Stage III: exposed subdermal tissues, note undermined edges.
Stage IV: exposed tendon or bone.
Unstageable: any wound with unobservable base due to eschar, exudate, etc.
Suspected deep tissue injury: a newer idea, that I think best applies to Stage I lesions.

Question 3

Wound Healing steps

Answer 3

Wound healing process involves three overlapping processes:

1. Inflammation
2. Epitheilialization
3. Remodeling

Question 4

inflammation

Answer 4

The tissue injury causing the wound disrupts blood vessels, causing extravasation of blood components. A blood clot forms, providing a matrix for cell migration. Various chemotactic factors recruit and activate inflammatory cells. Infiltrating neutrophils and macrophages (activated monocytes) clean up foreign particles and bacteria. The monocytes also secrete growth factors which start the growth of new tissue and attract fibroblasts.

Note that by day 3 the primary process is inflammatory, but the re-epithelialization has already begun.

This is classic description of surgical wound healing. There is not much research on the healing of pressure sores.

Question 5

Epitheilialization

Answer 5

The formation of a richly vascular fibroblast stroma called granulation tissue provides a supportive base for the advancing epithelial tissue. Most of our wound treatments are predicated on providing an environment conducive to fibroblasts and the formation of granulation tissue. Unlike surgical wounds, pressure ulcers involve a large gap between the edges and no fibrin clot. This makes wound dressings more important and results in a much slower healing process.

Question 6

Remodeling

Answer 6

The remodeling phase consists of scar formation and contraction. Collagen secreted by fibroblasts is the primary ingredient. Pressure sores have more scar and less reepithelialization than surgical wounds.

In the case of pressure sores, wound care products replace the clot matrix and the time frame for healing is weeks to months rather than days.

Question 7

Pressure Ulcer Treatment

Answer 7

Managing tissue loads
Managing bacterial colonization/infection
Nutritional support
Local wound care
Operative repair

“Why did this happen?”

Question 8

First thing to do in treating ulcers

Answer 8

A good assessment of the wound (staging, description of exudate, necrosis, granulation, signs of infection, etc.) and a thorough appraisal of why the wound occurred in the first place should precede local treatment.

Examples of underlying causes for development of pressure sore:

occult fracture (hip, vertebral)
stroke
metabolic problem: hyponatremia, hyperosmolar, uremia
medications: sedative, anticholinergic, steroid

Question 9

Bacterial colonization/infection

Answer 9

All wounds are colonized, surface cultures are worthless.
Cleansing and debridement are key.
Two week trial of topical antibiotic?
Osteomyelitis: ESR, WBC, x-ray (69% sensitivity if all 3 abnl). MRI?

Sepsis, cellulitis, osteomyelitis require systemic antibiotics, often inpatient.

Surface cultures often yield exotic organisms which exist as surface colonizers on the wound, and do not need treatment. There is some evidence that reducing the total bacterial count with a limited course of topical antibiotic may aid healing.

If there is evidence of active infection, such as advancing erythema and fever, systemic antibiotics are needed rather than topical.

Question 10

Nutritional (catabolic) Support

Answer 10

Protein is key: 1.0-1.5 g/kg/day
Catabolic state

Healing requires extra calories: 30-35 kcal/kg/day

Tube feeding not helpful

Mineral (zinc) & vitamin (C) supplements not helpful

Question 11

Local Ulcer Care

Answer 11

The first step in local treatment of a pressure ulcer involves removal of dead tissue and excess exudate, which inhibit epithelialization. Note that the inflammatory phase of healing is able to handle small amounts of dead tissue and exudate through enzymatic and phagocytotic processes which are together referred to as autolysis.

Some of the traditional cleansing solutions, such as sodium hypochlorite, povidone-iodine (Betadine), peroxide, etc. have been shown to be cytotoxic to fibroblasts and should therefore be avoided.

Debridement & cleansing may be performed as one process if no eschar.

There are a multitude (5000+) of wound dressing products available. It is best to become familiar with one or two products in each category and use them consistently.

Question 12

Local care for stage 1 ulcer

Answer 12

Debridement: none

Cleansing: nondrying soap and water

Dressing: None or protective film

Central issues:
Pressure relief
Why did this happen?

Question 13

Local Care for Stage 2 Ulcer

Answer 13

Debridement: none.

Cleansing: Saline.

Dressing: Polyurethane film, hydrocolloid wafer.

Central issues:
provide moist wound bed
keep surrounding skin dry

Question 14

Local Care for Stage 3 Ulcer

Answer 14

Debridement: if eschar or slough present
autolytic, wet-to-dry, enzymatic, sharp

Cleansing: saline
Dressing: hydrocolloid, alginate, hydrogel
may need packing or foam if deep/undermined

Central issues:
debride necrotic tissue
protect granulation tissue

Question 15

Local Care for Stage 4 Ulcer

Answer 15

The same as stage 3.

Visible bone/tendon, even if superficially infected, does not mean it won’t heal.

Odor can be a problem
metronidazole gel
activated charcoal

Central issue: patience, pain control
End of life issues?

Question 16

Factors for Venous Ulcers

Answer 16

Overload
CHF, obesity

Obstruction
Clot, tumor

Pump malfunction
Neuro dz, injury
Inactivity

Question 17

Treatment of Venous Ulcers

Answer 17

Same cleansing and debridement principles as pressure ulcers.

Control of edema is essential.
Restore venous return by way of external compression (30-40 mm Hg @ ankle)
“TED” socks provide ~ 18 mm Hg pressure.
Unna boot
Compression hose
Compression pumps

Question 18

Arterial Ulcers

Answer 18

Circumscribed, “punched-out” ulcers, often multiple.
Occur in areas least well perfused: lateral malleolus, tibial, feet/toes.
Shiny, hairless skin.
Absent pulses.
Claudication.

Question 19

Venous leg ulcers

Answer 19

Medial malleolus is typical

Stasis dermatitis, hyperpigmentation

Chronic edema, will not diurese
Tender to palpate

Varicose veins?

Question 20

Ankle-Brachial Index (ABI)

Answer 20

The simplest measurement of flow into the leg is the quotient of the systolic BP at the ankle divided by the pressure at the brachial artery in the arm: “ankle-brachial index”, or ABI.

An ABI of less than 0.8 causes claudication with exercise, while an ABI below 0.4 causes pain without exercise. Arterial ulcers can occur with ABI’s of 0.8 and below.

The ABI predicts more than the risk of skin breakdown and claudication. Arteriosclerosis is usually a diffuse disease and people with stenoses in their leg arteries are at high risk for similar disease in the coronary and cerebral arteries. They often succumb to myocardial infarctions or strokes rather than complications of leg ischemia.

Question 21

Buerger’s Disease

Answer 21

Buerger’s disease represents an unusual sensitivity to the vasoactive effects of nicotine. These people have impaired endothelium-dependent relaxation in the peripheral vasculature, both arteries and veins. The disease progresses to amputation in 43% of those who continue smoking. Of those who quit smoking, only 6% require amputation.

The distinguishing factors between Buerger’s disease and atherosclerotic arterial ulcers are the presence of:

1. Both venous and arterial involvement in Buerger’s
2. More diffuse involvment of both upper and lower extremeties in Buerger’s.

Question 22

Allen Test

Answer 22

Occlude radial and ulnar arteries after making a fist to empty blood from the hand.
Open hand and release pressure over the ulnar artery.
Hand should refill with blood via ulnar artery, evidenced by return of pink color.

Positive = persistent pallor.

This tests for patency of the ulnar artery. A positive Allen test in a smoker with a leg ulcer would be strongly suggestive of Buerger’s disease, as you have documented arterial occlusive disease in both upper and lower extremities.

Question 23

Treatment of Arterial Ulcers

Answer 23

Same cleansing, debridement and dressing principles as pressure ulcers.

External compression is detrimental.
Smoking cessation.
Revascularization.
Skin graft.
Amputation.

Arterial ulcers require the same local care as pressure and venous ulcers to promote the growth of fibroblasts, resulting in granulation tissue. Unlike venous ulcers, external compression may worsen an ischemic ulcer by reducing arterial inflow. Management of risk factors for arterial disease, such as cigarette cessation, is essential. Revascularizatioin, either surgical or percutaneous angioplasty, is often helpful..

Skin grafting is sometimes helpful, but limited by the need for good perfusion to nourish the graft and ensure its survival. Amputation is an all-too-frequent sequela.

Question 24

Neurotrophic Ulcers

Answer 24

Plantar aspect of foot or toes is typical.

Prominent callus formation.

Caused by peripheral neuropathy, usually diabetic.

These lesions result from unrecognized, repetitive trauma due to a lack of sensation in the involved extremity. Diabetics have the added risk of arterial ischemia. The damage may not be limited to the skin, as the underlying bone and joint structure of the foot may also be destroyed (panels d & e).

Question 25

The Charcot Foot

Answer 25

The Charcot foot results from the collapse of the ankle and foot structure due to neuropathy. The foot assumes a “rocker bottom” appearance and there is usually deformity at the ankle as well. Ulcers often appear over the lateral plantar mid-foot and osteomyelitis is a frequent complication

Question 26

Treatment of Neurotrophic Ulcers

Answer 26

The same cleansing, debridement and dressing principles as pressure ulcers.
Protection: footwear, total contact cast?
Recombinant platelet-derived growth factor (becaplermin)?

Good diabetic management.
Beware of arterial insufficiency.
Beware of infection (osteomyelitis).

Question 27

Less Common Ulcers

Answer 27

Skin Cancer
Basal Cell Carcinoma
Squamous Cell Carcinoma

Pyoderma Gangrenosum

There are a host of less common conditions that result in ulcerating skin lesions. The usual hints that you are dealing with something unusual are:

1. It is in an unusual location and looks atypical. Be especially suspicious of lesions with a nodular component or swelling of regional lymph nodes.
2. It does not appear to heal (or progressively enlarges) despite good treatment.

Diagnosis of these lesions usually requires a biopsy for confirmation.

Question 28

Basal Cell Carcinoma

Answer 28

Most common skin cancer.
“Heaped up” or rolled edges.
Usually sun-exposed surfaces.
Does not metastasize

Question 29

Squamous Cell Skin Cancer

Answer 29

May occur as a complication of previously benign ulcer.

May metastasize, check regional lymph nodes.

If in doubt, biopsy.

Question 30

Pyoderma Gangrenosum

Answer 30

Margins are serpiginous and elevated.
Edges have blue or purple hue.
Pustule or blister precedes.
Assoc’d with inflammatory bowel, RA, leukemia.

Pyoderma gangrenosum usually occurs in association with an underlying inflammatory disease, such as Crohn’s or ulcerative colitis. It can also be seen with rheumatoid arthritis or leukemia.

It often starts with a pustular-appearing lesion. It grows rapidly and often has copious exudate with surrounding erythema, causing confusion with a bacterial infectious process. The blue or purplish discoloration around the periphery and the “scalloped” appearance of the edges can be clues.

Treatment is usually related to the underlying disease, often involving corticosteroids.