Chronic venous insufficiency with lower extremity disease: Part 1

By Donald A. Wollheim, MD, WCC, DWC, FAPWCA

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.

Selected references

Alguire PC, Mathes BM. Clinical evaluation of lower extremity chronic venous disease. UpToDate. Last updated April 18, 2012. http://www.uptodate.com/contents/clinical-evaluation-of-lower-extremity-chronic-venous-disease?source=search_result&
search=Clinical+evaluation+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150
.  Accessed March 3, 2013.

Alguire PC, Mathes BM. Diagnostic evaluation of chronic venous insufficiency. UpToDate. Last updated May 7, 2012. www.uptodate.com/contents/diagnostic-evaluation-of-chronic-venous-insufficiency?source=search_result&search=Diagnostic+evaluation
+of+chronic+venous+insufficiency&selectedTitle=1%7E127
. Accessed March 3, 2013.

Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. UpToDate. Last updated April 12, 2012. www.uptodate.com/contents/pathophysiology-of-chronic-venous-disease?source=search_result&search=Pathophysiology+of+chronic+venous+disease
&selectedTitle=1%7E127
. Accessed March 3, 2013.

Alguire PC, Scovell S. Overview and management of lower extremity chronic venous disease. UpToDate. Last updated June 27, 2012. www.uptodate.com/contents/overview-and-management-of-lower-extremity-chronic-venous-disease?source=search_
result&search=Overview+and+management+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150
. Accessed March 3, 2013.

Moneta G. Classification of lower extremity chronic venous disorders. UpToDate. Last updated October 22, 2011. www.uptodate.com/contents/classification-of-lower-extremity-chronic-venous-disorders. Accessed March 3, 2013.

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.

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The “latest and greatest” vs. the basics

Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

If you’re keeping up on wound care, you know a lot of new things are coming to market with enough decent science behind them to make them reasonable options to consider in your practice. And as true-blooded Americans and citizens of the post-industrialized world, we want what’s newest, fastest, and best in class in everything. It’s just our nature.

But does it truly serve us to be eager to try new therapies even when the current treatment plan is successful? Perhaps. We know we must never close our eyes to new developments in our field that can lead to better outcomes. Knowing when and what to change can lead to better outcomes for the patient, the wound, and our collective pocketbook.

I’ve long maintained we can achieve excellent-quality wound care if we just stick to the basics the vast majority of the time. Why? Systemic, psychosocial, and local factors all affect wound healing—not just the dressing or cream. Our job is to provide the optimum environment possible for wound healing. That requires us to look at and support the whole body toward optimum health, not solely the wound.

The basics begin with identifying the cause of the wound and implementing interventions to reduce, control, or eliminate the cause. Next, we strive to manage local and psychosocial factors by choosing topical products that will maintain moisture balance, keep the wound warm, and protect it. If the wound doesn’t show progress toward healing within 2 weeks (or as expected, given the patient’s overall condition and ability to heal), we need to reevaluate the plan and begin making changes.

The best rule is to make one change at a time. That makes it much easier to determine what’s working and what isn’t. Once all the basics are in place and required changes have been made, if healing is still stalled or nonexistent, consider trying the available new products and specialty products.

Never close your clinical mind to advances in the field. To do that would be a disservice to your patients. But you should change the treatment plan only when a change is needed—not just for the sake of changing it.

Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
Editor-in-Chief
Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois

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Clinical Notes

Diabetes ‘ABC’ goals improve, but work remains

The number of people with diabetes who are meeting the ABC goals—hemoglobin A1C, blood pressure, and LDL cholesterol—has risen significantly in recent years, according to a study published by Diabetes Care. Patients meeting all three goals rose from about 2% in 1988 to about 19% in 2010.

Gains were made in each of the ABC goals, based on 2007 to 2010 data: 53% of patients met A1C goals, compared to 43% in 1988 to 1994 data; 51% met blood pressure goals, compared to 33%; and 56% met LDL goals, compared to 10%.

Younger people were less likely to meet A1C and cholesterol goals. Compared with non-
Hispanic whites, Mexican Americans were less likely to meet A1C and LDL goals and non-Hispanic blacks were less likely to meet blood pressure and LDL goals.

The prevalence of meeting A1C, blood pressure, and LDL goals among people with diabetes, 1988–2010” also found that statin use significantly increased from about 4% in 1988 to 1994 to about 51% in 2007 to 2010.

The researchers analyzed data from the National Health and Nutrition Examination Surveys from 1988–1994, 1999–2002, 2003–2006, and 2007–2010. Nearly 5,000 people age 20 or older participated.

Although progress had been made, the researchers conclude, “Despite significant improvement during the past decade, achieving the ABC goals remains suboptimal among adults with diabetes, particularly in some minority groups.”

Daily bathing with chlorhexidine-impregnated washcloths reduces infection risk

A study in The New England Journal of Medicine reports that daily bathing with chlorhexidine-impregnated washcloths reduces the risk of becoming infected with multidrug-resistant organisms and subsequent development of hospital-acquired bloodstream infections in intensive care unit patients.

Effect of daily chlorhexidine bathing on hospital-acquired infection” included 7,727 patients in nine intensive care and bone marrow units in six hospitals. The units were randomly assigned to bathe patients with either no-rinse 2% chlorhexidine-impregnated washcloths or nonantimicrobial washcloths for 6 months; then, the units switched to the opposite product for 6 months.

The rate of infection with multidrug-resistant organisms was 23% lower in the chlorhexidine group and the rate of hospital-acquired bloodstream infection was 28% lower in the chlorhexidine group.

Patients tend not to wear custom-made footwear for preventing diabetic foot ulcers

Adherence to wearing prescription custom-made footwear was low among patients with diabetes, neuropathy, and a recently healed plantar foot ulcer, according to a study in Diabetes Care. The low adherence was particularly notable at home, where patients did the most walking.

Adherence to wearing prescription custom-made footwear in patients with diabetes at high risk for plantar foot ulceration” studied 107 patients by using a shoe-worn, temperature-based monitor. The researchers also measured daily step count by using an
ankle-worn activity monitor.

Factors associated with higher adherence included lower body mass index, more severe foot deformity, and more appealing footwear.

Tedizolid works as well as linezolid in patients with acute bacterial skin infections

A JAMA study says that a 200-mg once-daily dose of oral tedizolid phosphate over 6 days was as effective as 600 mg of oral linezolid every 12 hours for 10 days in patients with acute bacterial skin and skin-structure infections, including cellulitis or erysipelas, major cutaneous abscesses, and wound infections.

Tedizolid phosphate vs linezolid for treatment of acute bacterial skin and skin structure infections: The ESTABLISH-1 Randomized Trial” reports a Phase 3, randomized, double-blind study conducted in 81 study centers with data analyzed from 667 adults.

A shorter course of tedizolid may be a “reasonable alternative” to linezolid for treating acute bacterial skin and skin-structure infections, the study concludes.

Water-based exercise improves ROM in patients with long-term arm lymphedema

A study of breast cancer survivors (median 10 years after surgery) with lymphedema found that a water-based exercise program improved shoulder range of motion (ROM).

Of the 29 eligible patients, 25 completed the study “Water-based exercise for patients with chronic arm lymphedema: A randomized controlled pilot trial,” published in the American Journal of Physical Medicine & Rehabilitation.

The program consisted of at least twice-weekly water-based exercise for 8 weeks. At first, participants were supervised, but later they exercised independently. Although lymphedema status didn’t change, those who performed water-based exercise had an increase in ROM, showing improvement years after surgery.

Dehydrated amniotic membrane allograft possible option for treating chronic wounds

A dehydrated amniotic membrane allograft (EpiFix) was used to treat four patients whose wounds hadn’t closed after conservative and advanced measures and who had been referred for plastic procedures. A variety of wounds healed (located on the elbow, knee, hand, and ankle) after one to three applications of the amniotic material, which patients tolerated well. The wounds remained closed several months later.

The authors of “Use of dehydrated human amniotic membrane allografts to promote healing in patients with refractory non healing wounds” recommend further investigation.

Mortality not linked to hospital readmissions in some patients

A study in JAMA reports that readmission rates aren’t linked to mortality rates in patients with an acute myocardial infarction or pneumonia and were only “weakly associated” for patients with heart failure.
Relationship between hospital readmission and mortality rates for patients hospitalized with acute myocardial infarction, heart failure, or pneumonia” studied Medicare beneficiaries. The study is likely to fuel ongoing discussions as to the value of using readmission and mortality rates as factors for reimbursement.

Study casts doubt on MLD’s role in breast cancer–related lymphedema

A meta-analysis published in the World Journal of Surgical Oncology found the “current evidence” from randomized clinical trials “does not support” the use of manual lymphatic drainage (MLD) in preventing or treating lymphedema in patients with breast cancer.

However, the authors of “Effects of manual lymphatic drainage on breast cancer–related lymphedema: a systematic review and meta-analysis of randomized controlled trials” note that the overall methodology of the studies was poor.

The authors analyzed 10 randomized clinical trials with 566 patients.

CDC issues additional prevention steps for carbapenem-resistant Enterobacteriaceae

On Feb. 14, the Centers for Disease Control and Prevention (CDC) issued additional prevention steps for carbapenem-resistant Enterobacteriaceae (CRE). Increased reports of CRE prompted the action: Of the 37 unusual forms of CRE reported in the U.S., the last 15 have been reported since July 2012.

Facilities should follow the CDC guidance for preventing the spread of CRE in healthcare settings. The CDC also now recommends the following:

• When a CRE is identified in a patient with a history of an overnight stay in a healthcare facility (within the last 6 months) outside the U.S., send the isolate to a reference laboratory for confirmatory susceptibility testing and test to determine the carbapenem resistance mechanism.
• For patients admitted to healthcare facilities in the U.S. after recently being hospitalized (within the last 6 months) in countries outside the U.S., consider performing rectal screening cultures to detect CRE colonization, and place patients on contact precautions while awaiting the results.

Examples of Enterobacteriaceae include Klebsiella species and Escherichia coli. CRE are Enterobacteriaceae with high levels of resistance to antibiotics, including carbapenems. CRE infections most commonly occur among patients who are receiving antibiotics and significant medical treatment for other conditions.

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Debridement options: BEAMS made easy

By Cindy Broadus, RN, BSHA, LNHA, CHCRM, CLNC, CLNI, WCC, DWC, OMS

At one time or another, all wound care professionals encounter a chronic wound, defined as a wound that fails to heal in an orderly and timely manner. Globally, about 67 million people (1% to 5% of the world’s population) suffer chronic wounds. In the United States, chronic wounds affect 6.5 million people and cost more than $25 billion annually to treat. (more…)

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Positive Stemmer’s sign yields a definitive lymphedema diagnosis in 10 seconds or less

By Robyn Bjork, MPT, CWS, WCC, CLT-LANA

In a busy wound clinic, quick and accurate differential diagnosis of edema is essential to appropriate treatment or referral for comprehensive care. According to a 2010 article in American Family Physician, 80% of lower extremity ulcers result from chronic venous insufficiency (CVI). In 2007, the German Bonn Vein Study found 100% of participants with active venous ulcers also had a positive Stemmer’s sign, indicating lymphedema. (more…)

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Clinical Notes

Guidelines for managing prosthetic joint infections released

The Infectious Diseases Society of America has released guidelines for diagnosing and managing prosthetic joint infections.
Diagnosis and management of prosthetic joint infection: Clinical practice guidelines by the Infectious Diseases Society of America,” published in Clinical Infectious Diseases, notes that of the 1 million people each year who have their hips or knees replaced, as many as 20,000 will get an infection in the new joint.
The guidelines describe the best methods for diagnosing these infections, which are not easy to identify. Specifically, infection should be suspected in a patient who has any of the following: persistent wound drainage in the skin over the joint replacement, sudden onset of a painful prosthesis, or ongoing pain after the prosthesis has been implanted, especially if there had been no pain for several years or if there is a history of prior wound healing problems or infections.
Guidelines for treating infections are included and note that 4 to 6 weeks of I.V. or highly bioavailable oral antibiotic therapy is almost always necessary to treat prosthetic joint infections.

A decade of TIME

The TIME acronym (tissue, infection/inflammation, moisture balance, and edge of wound) was first developed more than 10 years ago to provide a framework for a structured approach to wound bed preparation and a basis for optimizing the management of open chronic wounds healing by secondary intention. To mark the event, the International Wound Journal has published “Extending the TIME concept: What have we learned in the past 10 years?”
The review points out four key developments:
• recognition of the importance of biofilms (and the need for a simple diagnostic)
• use of negative-pressure wound therapy
• evolution of topical antiseptic therapy as dressings and for wound lavage (notably, silver and polyhexamethylene biguanide)
• expanded insight into the role of molecular biological processes in chronic wounds (with emerging diagnostics).
The authors conclude, “The TIME principle remains relevant 10 years on, with continuing important developments that incorporate new evidence for wound care.”

Bed alarms fail to reduce patient falls

A study in Annals of Internal Medicine found that the use of bed alarms had no statistical or clinical effect on falls in an urban community hospital.
The 18-month trial included 16 nursing units and 27,672 inpatients. There was no difference in fall rates per 1,000 patient-days, the number of patients who fell, or the number of patients physically restrained on units using bed alarms, compared with control units.
Authors of “Effects of an intervention to increase bed alarm use to prevent falls in hospitalized patients: A cluster randomized trial” speculate the lack of response may be related to “alarm fatigue.”

Drug for HIV might help in Staph infections

A study in Nature reports that the drug maraviroc, used to treat HIV, might be useful for treating Staphylococcus aureus infections.
CCR5 is a receptor for Staphylococcus aureus leukotoxin ED” found that the CCR5 receptor, which dots the surface of immune T cells, macrophages, and dendritic cells, is critical to the ability of certain strains of Staph to specifically target and kill cells with CCR5, which orchestrate an immune response against the bacteria. One of the toxins the bacterium releases, called LukED, latches on to CCR5 and subsequently punches holes through the membrane of immune cells, causing them to rapidly die.
When researchers treated cells with CCR5 with maraviroc and exposed the cells to the Staph toxin, they found maraviroc blocked toxic effects.

Dog able to sniff out C. difficile

A 2-year-old beagle trained to identify the smell of Clostridium difficile was 100% successful in identifying the bacteria in stool samples, and correctly identified 25 of 30 cases of patients with C. difficile, according to a study in BMJ.
Using a dog’s superior olfactory sensitivity to identify Clostridium difficile in stools and patients: Proof of principle study” discusses how the dog was trained to detect C. difficile and concludes that although more research is needed, dogs have the potential for screening for C. difficile infection.

After-hours access to providers reduces ED use

Patients who have access to their primary healthcare providers after hours use emergency departments (EDs) less frequently, according to a study in Health Affairs.
After-hours access to primary care practices linked with lower emergency department use and less unmet medical need” found that 30.4% of patients with after-hours access to their primary care providers reported ED use, compared with 37.7% of those without this access. In addition, those with after-hours access had lower rates of unmet needs (6.1% compared to 12.7%).
The findings come from the 2010 Health Tracking Household Survey of the Center for Studying Health System Change. The total sample included 9,577 respondents.

Neuropathic pain in patients with DPN might contribute to risk of falling

The presence of neuropathic pain in patients with diabetic peripheral neuropathy (DPN) contributes to gait variability, which could in turn contribute to the risk of falling, according to “Increased gait variability in diabetes mellitus patients with neuropathic pain.”
The study, published in the Journal of Diabetes and Its Complications, compared patients with at least moderate neuropathic pain with those who had no pain. Researchers used a portable device to measure gait parameters, such as step length and step velocity.

Amputation rates decrease significantly in patients with PAD

Temporal trends and geographic variation of lower-extremity amputation in patients with peripheral artery disease (PAD): Results from U.S. Medicare 2000–2008” found that amputation rates have decreased significantly, but that significant patient and geographic variations remain.
The study, published in the Journal of the American College of Cardiology, found that among 2,730,742 older patients with identified PAD, the overall rate of lower extremity amputation decreased from 7,258 per 100,000 patients to 5,790 per 100,000. Predictors of lower-extremity amputation included male sex, black race, diabetes mellitus, and renal disease.

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Hyperbaric oxygen therapy for treatment of diabetic foot ulcers

By Carrie Carls, BSN, RN, CWOCN, CHRN; Michael Molyneaux, MD; and William Ryan, CHT

Every year, 1.9% of patients with diabetes develop foot ulcers. Of those, 15% to 20% undergo an amputation within 5 years of ulcer onset. During their lifetimes, an estimated 25% of diabetic patients develop a foot ulcer. This article discusses use of hyperbaric oxygen therapy (HBOT) in treating diabetic foot ulcers, presenting several case studies.
HBOT involves intermittent administration of 100% oxygen inhaled at a pressure greater than sea level. It may be given in a:
• multi-place chamber (used to treat multiple patients at the same time), compressed to depth by air as the patient breathes 100% oxygen through a face mask or hood (more…)

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Feel more relaxed with restorative yoga

By Lisa Marie Bernardo, PhD, MPH, RN, HFI, RYT

Do you experience chronic stress? Is your body stiff and inflexible? Does your mind seem dull and sluggish, your spirit exhausted?
Restorative yoga may help “open” your joints, ease your mind, and revive your spirit. It’s based on the concept that we’re overstimulated and don’t get enough rest. Constant stimulation activates the sympathetic nervous system, overtaxing the fight-or-flight response. The body responds by increasing cortisol and glucose production, which (along with additional unhealthy responses) raises the risk of metabolic syndrome.
Restorative yoga promotes active relaxation, helping to halt the overstimulation cycle. It promotes balance by alternately stimulating and relaxing the body, which is supported in yoga poses with such props as blankets, pillows, yoga mat, and eye covers. Research suggests restorative yoga may ease hot flashes in postmenopausal women and may promote a calm, positive mood in women with ovarian or breast cancer.

Five facets of restorative yoga

Restorative yoga takes a five-faceted approach to relieve the effects of stress. Over time, you’re likely to notice a new awareness of and appreciation for your body, mind, and spirit.
Simply put, networking is an information exchange, a forum for communicating your needs or agenda and, in return, listening and responding to others’ needs or agendas. Good networking requires emotional reciprocity, which means caring about the needs and agendas of the people you network with. Caring about others’ needs is what nurses do, so networking really shouldn’t be that difficult for a nurse.
1. Using props, restorative yoga supports the body in yoga poses, helping muscles and joints release tension and achieve muscular balance.
2. The restorative poses move the spine in all directions—flexion, extension, rotation, and lateral flexion. This enhances spinal flex­-ibility, lubricates vertebrae, and strengthens the deep muscles that stabilize the spine.
3. Inverted poses, in which the feet and legs are elevated, counter the effects of gravity and promote lymph and fluid drainage to the heart.
4. The poses compress and release internal organs, cleansing them while aiding removal of cellular waste and renewing oxygen and nutrients.
5. Finally, the poses balance the body’s male (prana) and female (apana) energies.

Learning the poses

To learn the poses, consider taking a restorative yoga class. (See Finding an instructor.) Beforehand, make sure to tell the instructor about any special health concerns you have, so the instructor can modify the poses for you. Expect to bring your own blankets, pillows, eye covers, and yoga mat. The class will last from 60 to 90 minutes.
Restorative yoga typically doesn’t involve active (hatha) yoga poses, although it may include stretching poses to warm muscles and joints before the restorative poses begin. The instructor will help you use your props to make the poses right for you, and will direct you into a pose using them. Expect to stay in the pose for 5 to 10 minutes. The instructor will guide you by helping you focus on your breath and turn your attention inward. If your mind wanders and your body stays active, accept this reaction and don’t judge yourself. Over time, you’ll learn to use your breath to release tension and to focus and calm your mind.
After you hold the pose for the required duration, the instructor will help you into the next one. Generally, the class is near-silent, with minimal talking; the lights are low and music may play.
W­hen the class ends, you may feel more relaxed and in touch with yourself. If you feel restless and jittery instead, accept your reaction. Don’t judge yourself. Try again. Give yourself the opportunity to experience something different.
Restorative yoga is just one method to renew and reconnect with your inner being. Only you can know if it’s right for you. n

Selected references
Cohen B, Kanaya A, Macer J, Shen H, Chang A, Grady D. Feasibility and acceptability of restorative yoga for treatment of hot flushes: a pilot trial. Maturitas. 2007;56(2):198-204.
Danhauer SC, Tooze JA, Farmer DF, Campbell CR, McQuellon RP, Barrett R, Miller BE. Restorative yoga for women with ovarian or breast cancer: findings from a pilot study. J Soc Integr Oncol. 2008;6(2):47-58.

Lisa Marie Bernardo is the managing member of The PIlates Centre, LLC, in Hampton Township, Pennsylvania, and adjunct faculty at Carlow University School of Nursing in Pittsburgh, Pennsylvania.

To find a certified yoga instructor in your area, check the Yoga Alliance website at www.yogaalliance.com.  Restorative Yoga Teachers (www.restorativeyogateachers.com) focuses exclusively on restorative yoga. This site is operated by Judith Hansen Lasater, PhD, the leader in restorative yoga practice.

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Clinical Notes

NPUAP releases new position statement on exposed cartilage as Stage IV ulcer

The National Pressure Ulcer Advisory Panel (NPUAP) has released a new position statement, “Pressure ulcers with exposed cartilage are Stage IV pressure ulcers,” which states that pressure ulcers with exposed cartilage should be classified as Stage IV.
NPUAP notes that although the presence of “visible or palpable cartilage at the base of a pressure ulcer” wasn’t included in Stage IV terminology, cartilage “serves the same anatomical function as bone,” so it fits into the current Stage IV definition, “Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often including undermining and tunneling.”

Medicare expenditures for diabetic foot care varies significantly by region

Medicare spending on patients with diabetes who have foot ulcers and lower extremity amputations varies significantly by region, according to a study in Journal of Diabetes and Its Complications, but more spending doesn’t significantly reduce 1-year mortality.
Geographic variation in Medicare spending and mortality for diabetic patients with foot ulcers and amputations” examined data from 682,887 patients with foot ulcers and 151,752 patients with lower extremity amputations.
Macrovascular complications in patients with foot ulcers were associated with higher spending, and these complications in patients with amputations were more common in regions with higher mortality rates.
Rates of hospital admission were associated with higher spending and increased mortality rates for patients with foot ulcers and amputations.
“Geographic variation in Medicare spending and mortality rates for diabetic patients with foot ulcers and amputations is associated with regional differences in the utilization of inpatient services and the prevalence of macrovascular complications,” the study concludes.

Patients who develop pressure ulcers in hospital more likely to die

Medicare patients who develop pressure ulcers in the hospital are more likely to die during the hospital stay, have longer lengths of stay, and to be readmitted within 30 days after discharge, according to a study of 51,842 patients in the Journal of the American Geriatrics Society.
Hospital-acquired pressure ulcers: results from the National Medicare Patient Safety Monitoring System Study” found that 4.5% of patients developed at least one new pressure ulcer during their hospitalization. Length of stay averaged 4.8 days for patients who didn’t develop a pressure ulcer, compared to 11.2 days for those with a new pressure ulcer.

Patients with diabetic foot ulcers may have higher risk of death

Patients with diabetes who have foot ulcers have a higher risk of cardiovascular disease and mortality, according to a meta-analysis in Diabetologia.
The association of ulceration of the foot with cardiovascular and all-cause mortality in patients with diabetes: a meta-analysis” notes that the more frequent occurrence of cardiovascular disease only partly explains the increased mortality rate. Other explanations may include the more advanced stage of diabetes associated with those who had foot ulcers.
A Drugs.com article about the study reported that “analysis of data from more than 17,000 diabetes patients in eight studies found that the more than 3,000 patients with a history of foot ulcers had an extra 58 deaths per 1,000 people each year than those without foot ulcers.”
The study authors emphasize the importance of screening patients with diabetes for foot ulcers so intervention can begin early, as well as lowering cardiovascular risk factors.
Access patient information on foot care from the American Diabetes Association.

Nurse’s innovation for ostomy patients could improve quality of life

An oncology nurse in Australia has developed StomaLife, an alternative to ostomy bags.
StomaLife is a ceramic appliance that eliminates the need for an ostomy bag. According to the StomaLife website, the appliance uses a magnetic implant technology that provides a “pushing force” from within the body outward in order to keep the site intact, while a second part is placed on the stoma site. A cotton gauze pad is used between the skin and the appliance to keep the site separated and to provide air circulation to the surrounding skin.
“The benefits of StomaLife to ostomy patients are continence all day, reduced skin irritation and infection, odour and sound control, leak prevention, waste material flow control and on-demand gas release,” says Saied Sabeti.
StomaLife still needs to be tested and is not yet being produced.

View: StomaLife video

New laser-activated bio-adhesive polymer aims to replace sutures

The Journal of Visualized Experiments, a peer-reviewed video journal, has published “A chitosan based, laser activated thin film surgical adhesive, ‘SurgiLux’: preparation and demonstration.”
SurgiLux is a laser-activated, bio-adhesive polymer that is chitosan-based. Chitosan is a polymer derived from chitin, which is found in fungal cell walls or in exoskeletons of crustaceans and insects. This molecular component allows SurgiLux to form low-energy bonds between the polymer and the desired tissue when it absorbs light.
The technology may be able to replace traditional sutures in the clinical setting. SurgiLux polymer can achieve a uniform seal when activated by a laser and has antimicrobial properties, which help prevent a wound from becoming infected. It also maintains a barrier between the tissue and its surroundings.
SurgiLux has been tested both in vitro and in vivo on a variety of tissues, including nerve, intestine, dura mater, and cornea.

Palliative care raises patient satisfaction and reduces costs

Kaiser Permanente’s home-based palliative care program increased patient satisfaction and decreased emergency department visits, inpatient admissions, and costs, according to an innovation profile in the Agency for Healthcare Research and Quality’s Innovations Exchange.
In-home palliative care allows more patients to die at home, leading to higher satisfaction and lower acute care utilization and costs” notes that the program uses an interdisciplinary team of providers to manage symptoms and pain, provide emotional and spiritual support, and educate patients and family members on an ongoing basis about changes in the patient’s condition.
Other components of the program include a 24-hour nurse call center, biweekly team meetings, and bereavement services to the family after the patient dies.

More research needed to determine efficacy of maggot debridement therapy

The efficacy of maggot debridement therapy (MDT)—a review of comparative clinical trials” concludes that “poor quality of the data used for evaluating the efficacy of MDT highlights the need for more and better designed investigations.”
The authors of the article in International Wound Journal reviewed three randomized clinical trials and five nonrandomized clinical trials evaluating the efficacy of sterile Lucilia sericata applied on ulcers.
The studies found that MDT was “significantly more effective than hydrogel or a mixture of conventional therapy modalities, including hydrocolloid, hydrogel and saline moistened gauze,” but the designs of the study were “suboptimal.”

Use tool to select correct antimicrobial dressing

Ensuring that the correct antimicrobial dressing is selected,” in Wounds International, emphasizes that dressing selection should be based on assessment of the microbial burden in the wound, the wound type, and the location and condition of the wound.
The article includes a checklist that may be helpful for deciding on the level of bacterial burden in a wound. The checklist is used to determine four levels of risk—colonized: at risk; localized infection; spreading infection; and systemic infection. Each level has a corresponding definition.
A table of antimicrobial dressings reviews the antimicrobial agent and dressing form, and the article ends with a case study.

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Lymphedema 101 – Part 2: Treatment

By Steve Norton, CDT, CLT-LANA

Editor’s note: Part 1 of this series, published in the September-October issue, discussed lymphedema pathology and diagnosis. This article, Part 2, covers treatment.

Traditional treatment approaches

Traditionally, lymphedema treatment has been approached without a clear understanding of the underlying structure and function of lymphatic tissues. Ineffective traditional treatments include elevation, elastic garments, pneumatic pumps, surgery, diuretics, and benzopyrones (such as warfarin). Because many traditional treatments are still overused and some may be appropriate for limited use, it’s important for clinicians to understand these approaches.

Elevation

As a sole therapy for lymphedema, elevation of the affected part provides only short-lived results. Ever-increasing macromolecular wastes retain water against the effects of gravity. Increased interstitial colloid osmotic pressure must be addressed by interventions targeted at improving lymphatic function—not just a position change. Otherwise, lymphedema will progress. Furthermore, elevation alone is impractical, promotes deconditioning, and alters lifestyle for prolonged periods.

Elastic garments

Elastic garments prove inadequate because they attempt to treat lymphedema with compression alone. Medically correct garments are engineered with thoughtful attention to high-quality textiles and offer gradient support, which promotes proximal flow. However, without precise tissue stimulation leading to improved lymphangioactivity (lymph-vessel pulsation), macromolecular wastes can’t be removed.
Interstitial pressure increases caused by compression garments impede further fluid accumulation. When these garments are removed, the spontaneous girth increase causes an imprecise fit, and the garment rapidly leads to a countertherapeutic effect. Furthermore, compression garments don’t combat the osmotic forces generated by ever-increasing interstitial wastes. Except in patients diagnosed with stage 0 or stage 1 lymphedema, disease progression involving metaplasia ensues. Although elastic compression garments are a cornerstone of long-term management, they shouldn’t be used as a stand-alone treatment.

Pneumatic compression pump

Formerly, the pneumatic compression pump (PCP) was considered the standard of care for lymphedema. However, when inflated, the pump doesn’t increase the frequency of lymph-vessel contraction or enhance lymph capillary absorption. What’s more, accelerated fibrosis development and rapid tissue refilling occur when a PCP is removed. Also, PCP use disregards the ipsilateral territory of the excised regional nodes, effectively dumping fluid from the leg into the trunk. A PCP is appropriate only when nothing else is available, as it may worsen the patient’s condition.

Surgery

Surgical approaches to treating lymphedema involve either excisional (debulking) or microsurgical techniques. The most extensive surgical technique, the radical Charles procedure, completely debulks all involved tissue down to the muscle fascia. Split-thickness grafts are then harvested from excised skin and donor sites, and applied to the fascia to achieve so-called limb reduction.
Most debulking procedures have been applied to lower-extremity lymphedema and offer poor cosmetic results. Less radical surgeries favor long incisions, preserving the skin but excising subcutaneous edematous portions to reduce girth. Although less cosmetically alarming, these procedures effectively amputate the subcutaneous space where lymph vessels reside. Other surgical approaches are beyond the scope of this article.
Generally, surgery isn’t a good approach for any patient, as it’s linked to significant morbidity, such as skin necrosis, infection, and sensory changes. In the future, less invasive procedures may be available that yield significant improvement without these adverse effects.

Diuretics

Although diuretics are prescribed appropriately to address water-rich edemas of venous origin, they disregard the fact that lymphedema is a protein-rich edema. Long-term, high-dose diuretic therapy leads to treatment-resistant limbs, similar to those that have received intensive pneumatic compression.

Benzopyrones

Benzopyrones such as warfarin decrease swelling by combating protein accumulation in fluid. Such drugs have undergone clinical trials abroad. Their mechanism is to promote macrophage migration into interstitial fluid, as well as subsequent proteolysis. Due to significant risk of liver damage or failure, benzopyrones haven’t been approved for treating lymphedema.

Complete decongestive therapy: The current treatment approach

Currently, the gold standard for lymphedema treatment is complete decongestive therapy (CDT). Michael Foeldi and Etelka Foeldi, who originated this method, discovered a unique symbiotic relationship among five distinct modalities that addresses the challenges of lymphedema treatment. In 1989, CDT was brought to the United States by Robert Lerner and has become the mainstay of lymphedema treatment here.
CDT is a two-phase approach involving an intensive clinical effort followed by a semi-intensive home-care program geared toward autonomous management, stabilization, and continual improvement. It involves manual lymph drainage (MLD), compression bandaging, exercise, skin and nail hygiene, and self-care education. (See Phases of complete decongestive therapy by clicking the PDF icon above.)

Manual lymph drainage

A type of soft-tissue mobilization, MLD provides skin traction, stimulating superficial lymph vessels and nodes. Lymph capillaries contain large inter-endothelial inlets called swinging tips, akin to overlapping shingles. Each overlapping cell is tethered to the interstitial matrix by anchoring filaments, so that fluid increases cause immediate distention and lymph inflow. Manual skin traction using MLD promotes greater lymph fluid uptake by stretching these filamentous structures, opening the swinging tips.
MLD also provides extrinsic stimulation of the lymphangion (the segment of a lymph vessel between a distal and proximal valve), drawing fluid into the system at the capillary level and promoting flow at the vessel level toward regional lymph nodes. Usually, these segments contract and relax in a rhythmic fashion six times per minute. MLD triples this output to 18 or 20 times per minute, greatly enhancing systemic transport.
MLD requires intensive daily treatment sessions to strengthen collateral flow as a pathway to circumventing surgical or developmental lymphatic disruption. Treatment strategies further recruit more deeply situated lymphatics such as the thoracic duct, as well as lumbar trunks that empty at the juncture of the internal jugular and subclavian veins to improve global uptake. MLD thus stimulates deeper vessel angioactivity to help drain the superficial vessels that drain toward them.

Compression bandaging

Compression bandaging provides tissue support after MLD to prevent reflux, slow new fluid formation, and mechanically soften fibrotic areas. Bandaging techniques provide a high working pressure to harness the muscle and joint pumps as a propellant for lymph while resisting retrograde flow created by gravity and centrifugal forces during movement. Pure cotton materials coupled with specialized padding create a soft, castlike environment, which confines swollen tissues without constriction. By relying on high working pressure and low resting pressures to decrease limb swelling, this strategy achieves greater control over intensity (level of compression/pressure exerted), with little to no soft-tissue injury or discomfort.
The patient wears this bulky inelastic complex after each MLD treatment until the next day’s session to ensure limb-volume reduction in a stable, linear fashion. Once a plateau is reached, tissue stabilization and self-care education are the goals of additional sessions.

Exercise

Exercise always must be done with adequate support to counteract fluid formation. During the intensive CDT phase, limbs are bandaged to provide complete around-the-clock containment. Gentle exercises encourage blood flow into the muscle; during muscle contraction, this creates a favorable internal pressure that effectively squeezes the subcutaneous space between the bandage wall and muscle. Because every bandage strives to provide a gradient of support, fluid tends to drain proximally to the bandage—in most cases, to the trunk.

Skin and nail hygiene

Without intact, well-hydrated skin, cellulitic infections occur in many lymphedema patients whose immune response has been diminished by regional lymphadenectomy or inherited deficiencies. To prevent infection caused by avoidable external events, patients receive clear guidelines to reinforce appropriate behavior. As most cellulitis results from resident skin pathogens (streptococci and staphylococci), maintaining a low skin pH helps control colonization. Ways to avoid recurrent infections include maintaining an acid mantle on the skin using low-pH-formulated lotions and avoiding injury from daily tasks that may scratch, puncture, burn, or abrade the skin. Patients should receive lists of self-care precautions at the time of treatment.

Self-care education

Because lymphedema is a chronic condition, patients must receive self-care education for daily management to avoid lymphedema destabilization, which can lead to tissue saturation and subsequent skin changes. Therapists must provide patients with appropriate self-care tools and knowledge to maintain adequate treatment results. Teaching topics include how to apply and remove compression garments and bandages and how to exercise safely, preserve skin integrity, monitor for infection, and respond appropriately to infection and significant changes in limb mobility.

An underrecognized and mistreated problem

Lymphedema remains an underrecognized and mistreated condition, even though CDT yields safe, reliable results. Early detection, accurate staging, proper diagnosis, and appropriate treatment can slow the inevitable progression of lymphedema. Wound care specialists should adapt wound therapy to address not just the wound but the edematous environment responsible for delayed wound resolution.

Selected references
Al-Niaimi F, Cox N. Cellulitis and lymphedema: a vicious cycle. J Lymphoedema. 2009;4:38-42.

Browse N, Burnand KG, Mortimer PS. Diseases of the Lymphatics. London: Hodder Arnold; 2003.

Casley-Smith JR, Casley-Smith JR. Modern Treatment for Lymphoedema. 5th ed. The Lymphoedema Association of Australia; 1997.

Cooper R, White R. Cutaneous infections in lymphoedema. J Lymphoedema. 2009:4:44-8.

Foeldi M. Foeldi’s Textbook of Lymphology: For Physicians and Lymphedema Therapists. 3rd ed. St. Louis, MO: Mosby; 2012.

International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Consensus Document of the International Society of Lymphology. Lymphology. 2009 Jun;42(2):51-60.

Leduc A, Bastin R, Bourgeois P. Lymphatic reabsorption of proteins and pressotherapies. Progress in Lymphology XI. 1988:591-2.

National Lymphedema Network Medical Advisory Committee. Position Statement: Lymphedema Risk Reduction Practices. Revised May 2012. http://www.lymphnet.org/pdfDocs/nlnriskreduction.pdf. Accessed September 5, 2012.

Pappas CJ, O’Donnell TF Jr. Long-term results of compression treatment for lymphedema. J Vasc Surg. 1992 Oct;16(4):555-62.

Whittlinger H. Textbook of Dr. Vodder’s Manual Lymphatic Drainage. Vol 1. 7th ed. New York, NY: Thieme; 2003.

Steve Norton is cofounder of Lymphedema & Wound Care Education and executive director of the Norton School of Lymphatic Therapy in Matawan, New Jersey.

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MRSA: What wound care professionals need to know

By Joseph G. Garner, MD, FIDSA, FSHEA

Staphylococcus aureus is one of the most feared human pathogens, causing a wide range of infections. Most wound care professionals can expect to frequently encounter patients with S. aureus infections. Soft-tissue infections caused by S. aureus include impetigo, cellulitis, and cutaneous abscesses, as well as such life-threatening processes as necrotizing fasciitis and pyomyositis (a hematogenous intramuscular abscess). Serious non-soft-tissue infections include septic arthritis, osteomyelitis, pneumonia, endocarditis, and sepsis.

Why is S. aureus such a nasty bug?

S. aureus produces various cellular and extracellular factors involved in the pathogenesis of infection. S. aureus protein A, an important surface protein, helps the organism resist phagocytosis. Also, S. aureus produces several cytotoxins and enzymes that contribute to infection spread and severity. In addition, some strains produce toxins (including toxic shock syndrome toxin-1) that function as superantigens—molecules that nonspecifically trigger release of large amounts of cytokines, leading to a sepsislike condition. Taken together, such factors combine to make S. aureus a dangerous pathogen.

MRSA emergence

When penicillin was introduced in the 1940s, virtually all S. aureus isolates were sensitive to that drug. But soon thereafter, S. aureus strains that produced a β-lactamase enzyme capable of inactivating penicillin became widespread. During the 1950s, outbreaks of penicillin-resistant S. aureus occurred in many U.S. hospitals. Introduction of penicillinase-resistant antibiotics, such as methicillin and oxacillin, temporarily restored the ability to treat all strains of this pathogen using penicillin antibiotics. The first strain of methicillin-resistant S. aureus (MRSA) was described in 1961 shortly after introduction of penicillinase-resistant antibiotics.
The mechanism of methicillin resistance involves a mutation in one of the bacterial cell-wall proteins to which penicillins must bind to kill the bacterium. This mutation renders the organism resistant to all penicillins and penems and almost all cephalosporins.
MRSA incidence has increased steadily to the point where it currently constitutes up to 60% of S. aureus isolates in many U.S. hospitals. These organisms commonly carry genetic material that makes them resistant to various non-β lactam antibiotics as well, leading some to suggest that the term MRSA should stand for multiply resistant S. aureus.
S. aureus has continued to mutate in the face of persistent antibiotic pressure. Vancomycin-intermediate S. aureus (VISA) was described in 1997; vancomycin-resistant S. aureus (VRSA), in 2003. Fortunately, these two strains remain rare and haven’t become established pathogens. (See Strains of antibiotic-resistant S. aureus by clicking the PDF icon above.)

Healthcare- versus community-acquired MRSA

Although MRSA initially arose and spread within healthcare settings (chiefly acute-care hospitals), a community-based variant was described in 1998. Called community-
acquired MRSA (CA-MRSA), this variant differs from healthcare-associated MRSA (HCA-MRSA) in more ways than the acquisition site. CA-MRSA occurs predominately in otherwise healthy children and young adults.
It most commonly presents as recurrent cutaneous abscesses, although life-threatening infections (such as necrotizing fasciitis and pneumonia) also have occurred. The pro­pensity to cause cutaneous abscesses isn’t fully understood but may relate partly to production of the Panton-Valentine toxin by many CA-MRSA isolates.
In contrast, HCA-MRSA afflicts mainly older patients, particularly those with chronic illnesses, including chronic wounds. It typically causes wound infections, urinary tract infections, pneumonia, and bacteremia.
Besides these epidemiologic and clinical differences, many CA-MRSA isolates derive from a single clone, known as clone USA 300, whereas HCA-MRSA is composed of multiple non-USA 300 clones. Finally, many CA-MRSA isolates are sensitive to non-β
lactam antibiotics, whereas most HCA-MRSA isolates resist multiple antibiotics. More recently, the distinction between CA-MRSA and HCA-MRSA has been blurred as evidence emerges that CA-MRSA now is being transmitted in healthcare settings as well as in the community.

S. aureus carrier state

Staphylococci are frequent colonizers of humans. Common colonization sites include the skin, anterior nares, axillae, and inguinal regions. Individuals can be colonized continuously or transiently, with nasal carriage rates varying from 20% to 40%. Most S. aureus infections result from the strain carried by the infected patient.
Three patterns of S. aureus carriage exist in humans:
• 20% of individuals are continuously colonized.
• 30% of individuals are intermittently colonized.
• 50% of individuals are never colonized.

The highest carriage rates occur in patients receiving frequent injections (such as insulin-dependent diabetics, hemodialysis patients, and I.V. drug users) and those with chronic skin conditions (for instance, psoriasis or eczema). In the general population, MRSA carriage rates have increased to 1% or 2%, with clinical consequences hinging on the colonizing strain (CA-MRSA versus HCA-MRSA) and host characteristics. The most consistent carriage site is the anterior nares, but many other sites may carry this pathogen, including the axillae, inguinal regions, and perirectal area.

MRSA treatment

Therapy for MRSA infection depends on the infection location and antibiotic sensitivity of the infecting strain.
Cutaneous abscesses are treated by incision and drainage; antibiotics play a secondary role to adequate drainage.
• Therapy for necrotizing fasciitis caused by MRSA involves aggressive debridement with removal of all necrotic tissue, plus adequate antibiotic therapy. Typically, patients require serial debridement followed by subsequent careful wound care, often with eventual skin grafting.
Pyomyositis  treatment entails drainage of the muscle abscess (which sometimes can be done with percutaneous tube placement instead of open drain­age), plus appropriate antibiotic therapy.

Vancomycin has been the mainstay of I.V. therapy for MRSA for decades, but some clinicians are concerned that its effectiveness may be declining due to slowly increasing minimum inhibitory concentrations (the minimum concentration of an
antibiotic needed to inhibit pathogen growth). Other parenteral options have emerged in the last few years. (See I.V. drugs used to treat MRSA by clicking the PDF icon above.) Several oral antibiotics also are available for MRSA treatment. (See Oral agents used to treat MRSA by clicking the PDF icon above.)
Knowing the antibiotic sensitivity pattern of the infecting MRSA strain is crucial to ensuring that the patient receives an appropriate antibiotic. Treatment duration for soft-
tissue infections usually ranges from 7 to 14 days, but bacteremia and bone or joint infections call for more prolonged therapy.

Efforts to eradicate MRSA carriage

Because the carrier state increases the risk of subsequent S. aureus infection, efforts have been made to eradicate carriage. Unfortunately, this has proven to be difficult. A commonly used regimen involves 5 days of twice-daily mupirocin nasal ointment with either chlorhexidine gluconate showers or immersion up to the neck in a dilute bleach solution. However, success in eliminating carriage is limited, although the bleach bath seems to improve eradication rates better than other modalities.

Controlling MRSA in hospitals

How best to control MRSA spread within hospitals is controversial. Some experts advocate an aggressive, “search and destroy” approach involving screening all patients for nasal carriage on admission and initiating contact precautions with subsequent decolonization efforts. Others focus on improving the overall level of hand hygiene and other general infection-control measures, arguing that nasal screening misses at least 20% of MRSA-colonized patients and thus gives an unwarranted sense of security.
Many hospitals use a mixed approach, screening patients suspected to be at high risk for MRSA carriage (such as those admitted from extended-care facilities or to the intensive care unit), while simultaneously trying to improve hand hygiene and general infection-control measures. Recent data suggest MRSA colonization and infection rates have stopped increasing and are beginning to decline.
MRSA is one of the most problematic pathogens encountered on a regular basis, and among the most dangerous pathogens we face. While some MRSA infections are relatively mild, many are serious or life-threatening. Severe soft-tissue infections, such as necrotizing fasciitis and pyomyositis, require surgical debridement or drainage, appropriate antibiotic therapy, and assistance from a wound-care professional to achieve optimal outcomes. n

Selected references
Calfee DP. The epidemiology, treatment and prevention of transmission of methicillin-resistant Staphylococcus aureus. J Infus Nurs. 2011 Nov-Dec;34(6):359-64.

DeLeo FR, Otto M, Kreiswirth BN, Chambers HF. Community-associated meticillin-resistant Staphylococcus aureus. Lancet. 2010 May 1;375(9725): 1557-68.

Dryden MS. Complicated skin and soft tissue infection. J Antimicrob Chemother. 2010 Nov;65 Suppl 3:iii35-44.

Ippolito G, Leone S, Lauria FN, et al. Methicillin-resistant Staphylococcus aureus: the superbug. Int J Infect Dis. 2010 Oct;14 Suppl 4:S7-11.

Landrum ML, Neumann C, Cook C, et al. Epidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, 2005-2010. JAMA. July 4;308:50-9.

Lee AS, Huttner B, Harbarth S. Control of methicillin-resistant Staphylococcus aureus. Infect Dis Clin North Am. 2011 Mar;25(1):155-79.

Moellering RC Jr. MRSA: the first half century. J Antimicrob Chemother. 2012 Jan;67(1):4-11.

Otter JA, French GL. Community-associated meticillin-resistant Staphylococcus aureus strains as a cause of healthcare-associated infection. J Hosp Infect. 2011 Nov:79(3):189-93.

Rivera AM, Boucher HW. Current concepts in antimicrobial therapy against select gram-positive organisms: methicillin-resistant Staphylococcus aureus, penicillin-resistant pneumococci, and vancomycin-resistant enterococci. Mayo Clin Proc. 2011 Dec;86(12):1230-43.

Simor AE. Staphylococcal decolonization: an effective strategy for prevention of infection? Lancet Infect Dis. 2011 Dec;11(12):952-62.

Joseph G. Garner is director of the infectious disease division and hospital epidemiologist at the Hospital of Central Connecticut and a professor of medicine at the University of Connecticut.

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