‘It Really Hurts When I Walk!’ Arterial Disease – Differential Diagnosis And Treatment

By Worley, Cynthia A

“In this age, which believes that there is a short cut to everything, the greatest lesson to be learned is that the most difficult way is, in the long run, the easiest.” – Henry Miller

I work in a large academic/teaching institution. As a nurse seeing patients all over the hospital, I don’t have a “slow gear.” My students frequently have trouble keeping up with me on our rounds and more than once I’ve found myself apparently “talking” to no one because my student has stopped several yards behind me in an attempt to halt a possible respiratory arrest. I recently began a fitness walking program. Unfortunately, my pace when fitness walking is sometimes so fast that my toes begin to cramp (got to get that heart rate up, right?). This is not from too much muscle activity, but from a lack of adequate “rebound” blood return. Not only do my toes become numb, the pain associated with my sometimes too-rapid walk is unlike anything I’ve previously experienced. Intense, gnawing, cramping pain that forces me to slow down. Patient’s with arterial disease use these terms to describe their pain.

When blood supply to tissue is compromised, the tissue is damaged. When blood supply to tissue is lost, the tissue dies. Arterial ulcers occur as a result of tissue ischemia. They are generally refractory to healing unless perfusion is improved. The key to diagnosis of lower-extremity arterial disease is the history obtained from the patient and appropriate interventions on the part of the wound care specialist.

Differential Diagnosis

The health care provider should assess the patient with possible arterial disease for the risk factors associated with the problem. Tobacco use, diabetes, hypertension, sedentary lifestyle, obesity, family history, hypercholesterolemia, cardiovascular disease, and elevated homocysteine levels all contribute to the picture of possible ischemic disease. However, pain is the most common presenting and diagnostic symptom. Location, characteristics, and exacerbating and relieving factors are all important to the differential diagnosis (rest pain indicates advanced disease). The ulcer history is also important; onset, precipitating factors, past and present management, and progress or regression in healing are all important bits of information that will help you put together a clinical picture of the patient’s problem (Young, 1983).

Arterial ulcers can be misdiagnosed as neuropathic ulcers. The greatest differentiating factors are pain and sensation. Patients with a neuropathic ulcer will not feel pain and/or sensation in the ulcer area (see Table 1).

Diagnostic Evaluation

The simplest, noninvasive method of confirmation for arterial disease is an ankle-brachial pressure index (ABI). This diagnostic procedure was discussed previously in “Wound Assessment and Evaluation” (Worley, 2007). In patients with diabetes or renal failure, the ABI is not the most diagnostic of tools because of the possibility of vessel calcification. Calcified vessels will not compress and the ABI values will be false because the blood pressure will be overestimated. In this case, a toe-brachial pressure index may be useful. Other noninvasive measurements of arterial perfusion include TCPO2 measurements and duplex ultrasound. Angiography is used to pinpoint, qualify, and quantify arterial blood flow and is used prior to surgical intervention.

Management of the Patient with Arterial Ulcers

As with any extremity ulceration, the first priority in management is to address the underlying etiology of the condition. Since the problem is a lack of tissue perfusion, it stands to reason that an adequate level of perfusion must be restored so that the ulcer may heal. There are several methods used to restore tissue perfusion in the ischemic patient.

Surgical options include bypass grafts, angioplasty and, unfortunately, amputation. The type of surgery is indicated by the patient’s current level of perfusion (ABI), previous response to nonsurgical interventions if any (drugs), severity of claudication, and presence of rest pain, infection, or gangrene (Fry, Marek, & Langfield, 1998). Bypass grafts utilize the patient’s saphenous vein or an upper-extremity vein if the saphenous is damaged. A synthetic graft is used in this case. The success rate is improved when the saphenous vein is used over a synthetic graft. Angioplasty is less invasive and is best when the occlusion is less than 10 cm in length. Balloon angioplasty, percutaneous placement of stents, and laser angioplasty (less common) are performed through an intra- arterial catheter and are done at the time of the arteri-ogram. These procedures cannot be used in all patients and generally have less long-term success than the more invasive bypass procedures. Amputation is reserved for irreversible ischemia (gangrene) and invasive infection (Biggs & Sykes, 2004; Fry et al., 1998; Holloway, 2001).

Pharmacologic options include the use of drugs which will prevent clotting, dilate vessels, decrease serum lipid levels or reduce concentration of fibrinogen. Low-dose aspirin does not affect arterial disease but other anti-platelet drugs such as dipyridamole (Persantine(TM)), cilostazol (Pletal(TM)) and clopidrogel (Plavix(TM)) have demonstrated effectiveness by antagonizing the specific receptors that activate platelets. Cilostazol has the added benefit of providing vasodilation and is currently the most commonly recommended drug for symptomatic arterial disease. Systemic vasodilators are usually not recommended in the treatment of arterial disease because the increased blood flow may be diverted away from the ischemic area. Hemorrheologics reduce concentrations of fibrinogen, a component in the viscosity of blood, and reduce rigidity of red blood cells thus allowing them to pass more readily through narrow vessels. Pentoxifylline (Trental(TM)) is the drug currently approved by the FDA for treatment of arterial disease but demonstrates only minimal to moderate clinical benefits. The gastrointestinal side effects produced require patients to take the drug with meals and should be given for no more than 8 to 12 weeks, at which point the patient should be re-evaluated for evidence of improvement of condition. Antilipemics are used to treat systemic atherosclerosis and have demonstrated an ability to slow disease progression and reduce severity of claudication. They include simvastatin (Zocor(TM)), chol-estyramine (Questran(TM)), and colestipol-niacin (Colestid(TM)) (Biggs & Sykes, 2004; Holloway, 2001).

Lifestyle changes must by implemented by the patient to modify correctable risk factors, improve tissue perfusion, and protect the compromised limb. Inform the patient of the benefits of therapeutic walking (30 minutes/3 times per week), encourage smoking cessation interventions, promote good skin care, and institute measures to minimize mechanical, chemical, and thermal trauma to the limb. Implementing limb-preservation strategies such as these will assist the patient in maintaining adequate tissue perfusion and promote wound healing (Biggs & Sykes, 2004; Holloway, 2001).

Topical treatment for the patient with an arterial ulcer is centered on the management of dry, non-infected necrotic wounds, and identification and management of infection. Dry intact tissue, in this instance, is a barrier against bacterial invasion and should be allowed to remain dry. Addition of moisture-retentive dressings will encourage autolytic debridement and will ultimately lead to bacterial invasion in a poorly perfused area. As this goes against everything we known about wound healing, I’ll explain why. It is thought that a closed wound on a poorly perfused area acts as a natural covering, preventing bacterial invasion likely to result in infection. Maintenance and careful monitoring of a closed wound in a poorly perfused area is the current standard of care recommended by wound care professionals. Prompt identification and aggressive treatment of infection is critical in managing a patient with a dry arterial ulceration. Even when infected, this patient will not manifest a normal inflammatory response nor display normal signs of infection. If the patient develops an infection, immediate actions should be taken to revascularize the ischemic area and provide appropriate topical wound care including debridement and appropriate dressing materials as well as systemic antibiotic coverage (Biggs & Sykes, 2004; Holloway, 2001).

Putting it Together

We’ve been discussing lower-extremity ulcers in this column for quite a while now. Students will frequently have difficulty differentiating between the different types of clinical conditions resulting in lower-extremity ulcers, namely venous, arterial, and neuropathic. Table 2 summarizes ulcer characteristics and common treatment.

References

Biggs, K., & Sykes, M. (2004). Arterial insufficiency ulcers; Principles of management. In P.J. Sheffield, C.E. Fife, & A.P.S. Smith (Eds.), Wound care practice. Flagstaff, AZ: Best Publishing Company.

Fry, D., Marek, J., & Langfield, M. (1998). Infection in the ischemic lower extremity. Surgery Clinics of North America, 78(3), 465.

Holloway, G. (2001). Arterial ulcers: Assessment, classification and management. In Krasner et al., (Eds.), Chronic wound care: A clinical source book for healthcare professionals (3rd ed.). Wayne, PA: HMP Publications.

Worley, C.A. (2007). ‘It hurts so much, I can’t walk!’ Arterial ulcers – etiology and assessment. Dermatology Nursing, 19(2), 175- 176, 181. Young, J.R. (1983). Differential diagnosis of leg ulcers. Cardiovascular Clinics, 13(2), 171-193.

Cynthia A.Worley, BSN, RN, COCN, CWCN, is a Board Certified Wound, Ostomy, and Continence Nurse, University of Texas, M.D. Anderson Cancer Center, Houston, TX; and a Dermatology Nursing Editorial Board Member.

Copyright Anthony J. Jannetti, Inc. Jun 2007

(c) 2007 Dermatology Nursing. Provided by ProQuest Information and Learning. All rights Reserved.