Be sure you’re familiar with these valuable resources for you and your patients.
Colorectal cancer resources
Fight Colorectal Cancer has a comprehensive resource library for patients, including:
a link to “My Colon Cancer Coach,” which provides a personalized report to help guide patients in making treatment decisions
archives of webinars (past topics include healthy changes that may reduce recurrence, highlights from a GI cancer symposium, and making sense of acronyms)
a link to the National Comprehensive Cancer Network guidelines for patients
videos on colon cancer signs and symptoms, peripheral neuropathy, and a patient answer line
a family history worksheet
a newly diagnosed information card and a screening information card that can be downloaded
Pressure-ulcer prevention and management guidelines recommend support-surface therapy to help prevent and treat pressure ulcers. Support surfaces include pads, mattresses, and cushions that redistribute pressure. Full cushions and cushion pads are considered therapeutic support surfaces if used to redistribute a patient’s pressure in a chair or wheelchair.
The National Pressure Ulcer Advisory Panel (NPUAP) defines support surfaces as “specialized devices for pressure redistribution designed for the management of tissue loads, microclimate, and/or other therapeutic functions.” These surfaces address the mechanical forces associated with skin and tissue injury, such as pressure, shear, friction, and excess moisture and heat. (See Clearing up the confusion.)
Incidence density best measure of pressure-ulcer prevention program According to the National Pressure Ulcer Advisory Panel (NPUAP), incidence density is the best quality measure of pressure-ulcer prevention programs. Pressure-ulcer incidence density is calculated by dividing the number of inpatients who develop a new pressure ulcer by 1,000 patient days. Using the larger denominator of patient days allows fair comparisons between institutions…
This issue’s resources include patient tools and new guidelines. Improving patient safety Research suggests that adverse events affect patients with limited English proficiency (LEP) more frequently, are commonly caused by communication problems, and are more likely to result in serious harm compared to adverse events affecting English-speaking patients. Your hospital can take steps to reduce risks of adverse events for…
By Debra Rose Wilson, PhD, MSN, RN, IBCLC, AHN-BC, and Dana Marie Dillard, MS, HSMI Like many clinicians, you may experience stress frequently, both on and off the job. Chronic stress can alter your equilibrium (homeostasis), activating physiologic reactive pathways that cause your body to shift its priorities. Physiologic effects of stress may include: slowed digestion delay in reproductive and…
By Pamela Anderson, MS, RN, APN-BC, CCRN, and Terri Townsend, MA, RN, CCRN-CMC, CVRN-BC Jan Smith, age 59, is admitted to the coronary intensive care unit with an acute inferior myocardial infarction (MI). Recently diagnosed with hypertension and hyperlipidemia, she smokes a pack and a half of cigarettes daily. She reports she has always been healthy and can’t believe she…
By: Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS Years ago, when I first started out in the wound care specialty, the only way to learn about new products and what was going on in the field was to “go to conference” (wound care conference). All year long, planning and excitement continued to build for our big trip. Not going…
By Cheryl Ericson, MS, RN, CCDS, CDIP Providers are often surprised at how pages upon pages of documentation in a patient’s health record can result in few reportable diagnosis and/or procedure codes, which often fail to capture the complexity of the patient’s condition. However, providers need to be aware of the implications of coding. As healthcare data become increasingly digital…
By Catherine R. Ratliff, PhD, APRN-BC, CWOCN, CFCN It’s estimated that about 70% of the 1 million ostomates in the United States and Canada will experience or have experienced stomal or peristomal complications. Peristomal complications are more common, although stomal complications (for example, retraction, stenosis, and mucocutaneous separation) can often contribute to peristomal problems by making it difficult to obtain…
By Nancy Morgan, RN, BSN, MBA, WOC, WCC, DWC, OMS Each issue, Apple Bites brings you a tool you can apply in your daily practice. The crusting procedure produces a dry surface and absorbs moisture from broken skin through an artificial scab that’s created by using skin barrier powder (stoma powder) and liquid polymer skin barrier. The crusting procedure is…
By Rosalyn S. Jordan, BSN, RN, MSc, CWOCN, WCC, and Sandra Phipps, BSN, RN, MBA, WCC Pressure-ulcer prevention and management guidelines recommend support-surface therapy to help prevent and treat pressure ulcers. Support surfaces include pads, mattresses, and cushions that redistribute pressure. Full cushions and cushion pads are considered therapeutic support surfaces if used to redistribute a patient’s pressure in a…
By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN Prevention of pressure ulcers and skin breakdown begins with a comprehensive risk assessment. Most providers use a skin risk assessment tool, such as the Braden or Norton scale. While these tools have been validated to predict pressure ulcer development, their use alone isn’t considered a comprehensive assessment, and frequently the individual risk…
Providers are often surprised at how pages upon pages of documentation in a patient’s health record can result in few reportable diagnosis and/or procedure codes, which often fail to capture the complexity of the patient’s condition. However, providers need to be aware of the implications of coding. As healthcare data become increasingly digital through initiatives such as meaningful use, coded data not only impact reimbursement but also are increasingly used to represent the quality of care provided. Here’s a closer look at how documentation and coding work in the context of wound care. (more…)
Incidence density best measure of pressure-ulcer prevention program
According to the National Pressure Ulcer Advisory Panel (NPUAP), incidence density is the best quality measure of pressure-ulcer prevention programs. Pressure-ulcer incidence density is calculated by dividing the number of inpatients who develop a new pressure ulcer by 1,000 patient days. Using the larger denominator of patient days allows fair comparisons between institutions of all sizes. (more…)
Margery Smith, age 82, arrives at your wound clinic for treatment of a shallow, painful ulcer on the lateral aspect of her right lower leg. On examination, you notice weeping and redness of both lower legs, 3+ pitting edema, several blisters, and considerable denudement of the periwound skin. She is wearing tennis shoes and her feet have relatively little edema, but her ankles are bulging over the edges of her shoes; both socks are wet. Stemmer’s sign is negative. The wound on the right leg is draining copious amounts of clear fluid; it’s dressed with an alginate, which is secured with conforming roll gauze. No signs or symptoms of infection are present.(more…)
Hospital pressure-ulcer comparison data not accurate
Performance scores for rates of hospital-acquired pressure ulcers might not be appropriate for comparing hospitals, according to a study in the Annals of Internal Medicine.
Here are some resources of value to your practice.
National Guideline Clearinghouse
The National Guideline Clearinghouse, supported by the Agency for Healthcare Research and Quality, summarizes many guidelines of interest to wound care, ostomy, and lymphedema clinicians. Here are some examples:
The ability to understand or “read” lower-extremity redness in your patient is essential to determining its cause and providing effective treatment. Redness can occur in multiple conditions—hemosiderin staining, lipodermatosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent rubor. This article provides clues to help you differentiate these conditions and identify the specific cause of your patient’s lower-extremity redness. (more…)
To begin appropriate treatment for chronic venous insufficiency (CVI), clinicians must be able to make the correct diagnosis. Part 1 (published in the March-April edition) described CVI and its presentation. This article provides details of the CVI diagnosis (including the differential diagnosis from other diseases), disease classification to help assess the extent of CVI, diagnostic studies used to diagnose CVI, and various treatment options to “rescue” the patient from CVI. (more…)
One of the worst fears of a wound care clinician is inadvertently compressing a leg with critical limb ischemia—a condition marked by barely enough blood flow to sustain tissue life. Compression (as well as infection or injury) could lead to necrosis, the need for amputation, or even death. The gold standard of practice is to obtain an ankle-brachial index (ABI) before applying compression. However, recent research and expert opinion indicate an elevated or normal ABI is deceptive in patients with advanced diabetes. What’s worse, in the diabetic foot, skin may die from chronic capillary ischemia even when total blood perfusion is normal. For information on how to perform an ABI and interpret results, click on this link. (more…)
Chronic venous insufficiency (CVI) is the most common cause of lower extremity wounds. The venous tree is defective, incapable of moving all the blood from the lower extremity back to the heart. This causes pooling of blood and intravascular fluid at the lowest gravitational point of the body—the ankle.
This article has two parts. Part 1 enhances your understanding of the disease and its clinical presentation. Part 2, which will appear in a later issue, explores the differential diagnosis of similar common diseases, the role that coexisting peripheral artery disease (PAD) may play, disease classification of venous insufficiency, and a general approach to therapy.
The most common form of lower extremity vascular disease, CVI affects 6 to 7 million people in the United States. Incidence increases with age and other risk factors. One study of 600 patients with CVI ulcers revealed that 50% had these ulcers for 7 to 9 months, 8% to 34% had them for more than 5 years, and 75% had recurrent ulcers.
Thrombotic complications of CVI include thrombophlebitis, which may range from superficial to extensive. If the thrombophlebitis extends up toward the common femoral vein leaving the leg, proximal ligation may be needed to prevent clot extension or embolization.
Understanding normal anatomy and physiology
Lower extremity veins flow horizontally from the superficial veins to the perforating veins and then into the deep veins. Normally, overall venous blood flows vertically against gravity from the foot and ankle upward toward the inferior vena cava (IVC). This antigravity flow toward the IVC results from muscular contraction around nonobstructed veins and one-way valves that close as blood passes them. These valves prevent abnormal backward blood flow toward the foot and ankle region.
The lower extremities have four types of veins. Superficial veins are located within the subcutaneous tissue between the dermis and muscular fascia. Examples are the greater and lesser (smaller) saphenous veins. Perforating veins connect the superficial veins to the deep veins of the leg. The deep veins are located below the muscular fascia. The communicating veins connect veins within the same system.
The greater saphenous vein is on the leg’s medial (inner) side. It originates from the dorsal veins on top of the foot and eventually drains into the common femoral vein in the groin region. By way of perforating veins, the greater saphenous vein drains into the deep venous system of both the calf and thigh.
The lesser saphenous vein is situated on the lateral (outer) side of the leg and originates from the lateral foot veins. As it ascends, it drains into the deep system at the popliteal vein behind the knee. Communicating veins connect the greater saphenous vein medially and the lesser saphenous vein laterally.
Intramuscular veins are the deep veins within the muscle itself, while the intermuscular veins are located between the muscle groups. The intermuscular veins are more important than other veins in development of chronic venous disease. Below the knee, the intermuscular veins are paired and take on the name of the artery they accompany—for example, paired anterior tibial, paired posterior tibial, and paired peroneal veins. Eventually, these veins form the popliteal vein behind the knee, which ultimately drains into the femoral vein of the groin.
As the common femoral vein travels below the inguinal ligament of the groin, it’s called the external iliac vein. Eventually, it becomes the common iliac vein, which drains directly into the IVC.
Pathophysiology
Abnormally elevated venous pressure stems from the leg’s inability to adequately drain blood from the leg toward the heart. Blood drainage from the leg requires the muscular pumping action of the leg onto the veins, which pump blood from the leg toward the heart as well as from the superficial veins toward the deep veins. Functioning one-way valves within the veins close when blood passes them, preventing blood from flowing backward toward the ankle. This process resembles what happens when you climb a ladder with intact rungs: As you step up from one rung to the next, you’re able to ascend.
CVI and the “broken rung” analogy
If the one-way valves are damaged or incompetent, the “broken rung” situation occurs. Think how hard it would be to climb a ladder with broken rungs: You might be able to ascend the ladder, but probably you would fall downward off the ladder due to the defective, broken rungs.
Normally, one-way valves ensure that blood flows from the lower leg toward the IVC and that the superficial venous system flows toward the deep venous system. The venous system must be patent (open) so blood flowing from the leg can flow upward toward the IVC. Blockage of a vein may result from an acute thrombosis (clot) in the superficial or deep systems. With time, blood may be rerouted around an obstructed vein. If the acute thrombosis involves one or more of the one-way valves, as the obstructing thrombosis opens up within the vein’s lumen, permanent valvular damage may occur, leading to post-thrombotic syndrome—a form of CVI.
CVI may result from an abnormality of any or all of the processes needed to drain blood from the leg—poor pumping action of the leg muscles, damage to the one-way valves, and blockage in the venous system. CVI commonly causes venous hypertension due to reversal of blood flow in the leg. Such abnormal flow may cause one or more of the following local effects:
leg swelling
tissue anoxia, inflammation, or necrosis
subcutaneous fibrosis
Compromised flow of venous blood or lymphatic fluid from the extremity.
“Water balloon” analogy
The effect of elevated venous pressure or hypertension is worst at the lowest gravitational point (around the ankle). Pooling of blood and intravascular fluid around the ankle causes a “water balloon” effect. A balloon inflated with water has a thin, easily traumatized wall. When it bursts, a large volume of fluid drains out. Due to its thicker wall, a collapsed balloon that contains less fluid is more difficult to break than one distended with water.
In a leg with CVI, subcutaneous fluid that builds up requires a weaker force to break the skin and ulcerate than does a nondistended leg with less fluid. This principle is the basis for compression therapy in treating and preventing CVI ulcers.
Effects of elevated venous pressure or hypertension
Increased pressure in the venous system causes:
abnormally high pressure in the superficial veins—60 to 90 mm Hg, compared to the normal pressure of 20 to 30 mm Hg
dilation and distortion of leg veins, because blood refluxes abnormally away from the heart and toward the lower leg and may move from the deep venous system into the superficial veins.
Abnormal vein swelling from elevated pressure in itself may impair an already abnormally functioning one-way valve. For instance, the valve may become more displaced due to the increase in intraluminal fluid, which may in turn worsen hypertension and cause an increase in leg swelling. Increased pressure from swollen veins also may dilate the capillary beds that drain into the veins; this may cause leakage of fluid and red blood cells from capillaries into the interstitial space, exacerbating leg swelling. Also, increased venous pressure may cause fibrinogen to leak from the intravascular plasma into the interstitial space. This leakage may create a fibrin cuff around the capillary bed, which may decrease the amount of oxygen entering the epidermis, increase tissue hypoxia, trigger leukocyte activation, increase capillary permeability, and cause local inflammation. These changes may lead to ulceration, lipodermatosclerosis, or both.
Visible changes may include dilated superficial veins, hemosiderin staining due to blood leakage from the venous tree, atrophie blanche, and lipodermatosclerosis. (See CVI glossary by clicking the PDF icon above.) Both atrophie blanche and lipodermatosclerosis result from local tissue scarring secondary to an inflammatory reaction of the leg distended with fluid.
Lipodermatosclerosis refers to scarring of subcutaneous tissue in severe venous insufficiency. Induration is associated with inflammation, which can cause the skin to bind to the subcutaneous tissue, causing narrowing of leg circumference. Lymphatic flow from the leg also may become compromised and inhibited in severe venous hypertension, causing additional leg swelling.
Patient history
In a patient with known or suspected CVI, a thorough history may lead to a working diagnosis. Be sure to ask the patient these questions:
Do you have pain?
Is your pain worse toward the end of the day?
Is the pain relieved with leg elevation at night?
Is it relieved with leg elevation during the day?
Do you have leg pain that awakens you at night?
How would you describe the pain?
Does the skin on your leg feel tight or irritated?
Have you noticed visible changes of your leg?
Do you have a leg ulcer?
Also determine if the patient has comorbidities that may exacerbate CVI, including PAD, renal failure, venous thrombosis, lymphedema, diabetes mellitus, heart failure, or malnutrition. (See CVI risk factors by clicking the PDF icon above .)
Common CVI symptoms
Approximately 20% of CVI patients have symptoms of the disease without physical findings. These symptoms may include:
tired, “heavy” legs that feel worse toward the end of the day
discomfort that worsens on standing
legs that feel best in the morning after sleeping or after the legs have been
elevated during the day.
Although patients may report leg discomfort, the history indicates that it doesn’t awaken them at night. Be aware that discomfort from CVI differs from that caused by PAD. With PAD, patients may report pain on exercise (claudication), pain with elevation (nocturnal pain), or constant pain (resting pain).
Signs of CVI (with or without ulcers) include:
leg swelling (seen in 25% to 75% of patients)
skin changes (such as hemosiderin staining or dermatitis)
telangiectasia, reticular veins, or both; while these are the most common signs, they represent an overall less severe finding
varicose veins with or without bleeding, occurring in one-third of patients with CVI.
Venous ulcers
Venous ulcers are the most common type of lower extremity ulcer. They’re commonly found on the medial aspect of the lower extremity, from the ankle to the more proximal calf area. Usually, they arise along the course of the greater saphenous vein, but also may be lateral and may occur at multiple locations. They aren’t found above the knee or on the forefoot. Venous ulcers are shallower than arterial ulcers and have considerable exudate consistent with drainage from a ruptured water balloon. They may extend completely around the leg.
CVI: From a heavy sensation to visible changes
In patients with CVI, blood flows within a lower extremity in an abnormal, reverse direction, causing build-up of blood and intravascular fluid around the ankle. Initially, this may cause only a sensation of heavy legs toward the end of the day, with no visible changes. Eventually, it may lead to venous ulcers or other visible changes. This abnormal blood flow results from dysfunction of the normal mechanisms that drain blood from the leg against gravity into the IVC.
Sardina D. Skin and Wound Management Course; Seminar Workbook. Wound Care Education Institute; 2011:92-112.
Donald A. Wollheim is a practicing wound care physician in southeastern Wisconsin. He also is an instructor for Wound Care Education Institute and Madison College. He serves on the Editorial Board for Wound Care Advisor.
Each month, Apple Bites brings you a tool you can apply in your daily practice.
Description
According to the American Diabetes Association, all patients with diabetes should be screened for loss of protective sensation in their feet (peripheral neuropathy) when they are diagnosed and at least annually thereafter, using simple clinical tests such as the Semmes-Weinstein monofilament exam.
The Semmes-Weinstein 5.07 monofilament nylon wire exerts 10 g of force when bowed into a C shape against the skin for 1 second. Patients who can’t reliably detect application of the 5.07, 10-g monofilament to designated sites on the plantar surface of their feet are considered to have lost protective sensation. (more…)
