Unfortunately, most clinicians can’t avoid having to work with difficult people. However we can learn how to be more effective in these situations, keeping in mind that learning to work with difficult people is both an art and a science.
How difficult people differ from the rest of us
We can all be difficult at times, but some people are difficult more often. They demonstrate such behaviors as arguing a point over and over, choosing their own self-interest over what’s best for the team, talking rather than listening, and showing disrespect. These behaviors can become habits. In most cases, difficult people have received feedback about their behavior at some time, but they haven’t made a consistent change. (See Is she a bully or a difficult person? by clicking the PDf icon above) (more…)
Achieving excellent wound care outcomes can be challenging, given the growing number of high-risk patients admitted to healthcare facilities today. Many of these patients have comorbidities, such as obesity, diabetes, renal disease, smoking, chronic obstructive pulmonary disease, and poor nutritional status. These conditions reduce wound-healing ability. (more…)
By Janice M. Beitz, PhD, RN, CS, CNOR, CWOCN, CRNP
Quality patient education is essential for comprehensive health care and will become reimbursable under healthcare reform in 2014. However, it’s difficult to provide effective education when time for patient interactions is limited. You can enhance your instruction time—and make your teaching more memorable—by using the techniques of analogy and metaphor. (more…)
As wound care professionals, we’ve all experienced a time when we felt that our patient didn’t have the appropriate wound treatment orders. However, the physician, nurse practitioner, or other prescriber wouldn’t follow your recommendation. This situation is not only frustrating but can delay the healing process. This article explores why a prescriber might not follow your recommendation and offers solutions. It focuses on physicians, because I’ve had the most experience with them. (more…)
Each month, Apple Bites brings you a tool you can apply in your daily practice.
Description
Xerosis, an abnormal dryness of the skin, is one of the most common skin conditions among patients with type 2 diabetes. While assessing for predictors of foot lesions in patients with diabetes, the authors of one study found that 82.1% of these patients had skin with dryness, cracks, or fissures. An unpublished survey of 105 consecutive patients with diabetes revealed that 75% had clinical manifestations of dry skin. (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…)
The elevator door opens and you step in to find yourself face to face with the important person you’ve wanted to meet to discuss your promising idea. It’s the chance you wouldn’t want to miss. But that chance lasts only as long as the elevator ride. You have less than a minute to make an impression. Do you have an elevator speech ready?
What’s an elevator speech?
An elevator speech is any short speech that sells an idea, promotes a business, or markets an individual. It’s a short summary, or pitch, that quickly describes the value of a service, product, or organization. The term is a metaphor for unexpected access to someone to whom you’d like to sell an idea or proposal. It derives from the early days of the Internet boom when web development companies needed venture capital. Firms were swamped with applications for funding, and in many cases, the companies that won the cash were those whose reps had a simple pitch and could explain a business proposal in an elevator in the time it took to ride to their floor.
A great elevator speech describes and sells an idea in less than a minute. Of course, it’s not restricted to elevators. It comes in handy any time and anywhere you need to give a concise presentation to capture someone’s interest so you can move to the next step—a follow-up call, a referral, a meeting, or a partnership.
Why clinicians need an elevator speech
You need to be able to describe what you do, what you’re interested in doing, and how you can be a resource to someone. The ability to sum up a unique aspect of your service or expertise in a way that excites others is a fundamental skill. Doing this in a brief, persuasive manner is an asset for any professional. A good elevator speech should grab one’s attention in a few words and make that person want to know more about you. Here are examples where a good elevator speech would be helpful:
• Thomas goes to a recruitment fair hoping to get an interview at a certain hospital.
• Mary is finishing her master of science degree and is interested in a position in a new wound care clinic.
• Caroline has written a book on grant writing and would like to present her ideas at a conference.
• Brian is interested in research and would like to join the research team.
• Mindy is trying to expand her wound consultation business.
You can use an elevator speech when you want to grab someone’s attention at a meeting, convention, or other social situation. In such situations, people typically ask, “What do you do?” A well-planned elevator speech can make the listener’s ears perk up and want to know more.
How to prepare an elevator speech
Before you can write an elevator speech, you need to know yourself, what you can offer, what problems you can solve, and what benefits you can bring to the prospective contact. For example, you may be an expert in professional communication and know strategies you can teach other staff to promote a better workplace environment.
You also need to know your audience. Will you direct your pitch to an administrator, a unit manager, or staff? You’re more likely to succeed if your elevator speech is targeted to a specific audience and you adjust it to that audience. Try to prepare different pitches for different audiences; a generic pitch is almost certain to fail. (See Key elements of a good elevator speech by clicking the PDF icon above.)
In today’s busy world, clinicians must be able to communicate in a succinct, persuasive manner. Your elevator speech is your introduction to others. It has to be good. Keep practicing it and perfecting it so you can speak with poise and polish. The more often you give it, the better it will become. It’s a great way to put your best foot forward when you have only a small window of opportunity to make a good impression.
Sjodin T. Small Message, Big Impact: The Elevator Speech Effect. New York, NY: Portfolio; 2012. Sprung S, Giang V. 6 keys to delivering a powerful elevator pitch. Business Insider Web site. www .businessinsider.com/terri-sjodin-how-to-deliver- an-elevator-speech-2012-10. October 26, 2012. Accessed October 26, 2012.
Kathleen D. Pagana is a keynote speaker and professor emeritus at Lycoming College in Williamsport, Pennsylvania. She is the author of The Nurse’s Communication Advantage and The Nurse’s Etiquette Advantage. She is also the coauthor of Mosby’s Diagnostic and Laboratory Test Reference, 11th ed. To contact her, visit www.KathleenPagana.com.
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.
January is traditionally the time of year when everyone starts the New Year fresh with resolutions for change—better organization, healthy living, new beginnings. This year, I want to challenge you to include your patients in your resolution planning. Work with each patient and come up with ideas to help improve their quality of life by, for instance, healing a wound, wearing a splint, keeping blood glucose levels within normal range, elevating the feet.
For resolutions to be effective, a “buy in” must exist. Most people don’t like
being told what they must do and would rather hear what they can do. So be sure to include your patients in the planning process. Ask them their opinion. Ask “What could I do differently to help you with this?” Determine if their treatments could be interfering with their lifestyle. Set mutually compatible goals. Most of all, help promote patients’ search for their own solutions.
To make an informed choice of can do instead of must do, patients must have a clear understanding of the facts, implications, and consequences. The Institute of Medicine defines health literacy as the degree to which individuals have the capacity to understand, obtain, and process basic health information needed to make appropriate health decisions. It’s easy to assume our patients know all the facts, especially if they have had the wound, ostomy, or diagnosis for many years. However, according to the 2003 National Assessment of Adult Literacy, almost 45% of the U.S. population (about 93 million Americans) have, at best, only basic health literacy skills.
To improve their health literacy, review your patients’ understanding of their situation and ask them to describe their diagnosis and treatment plan in their own words. If they can’t describe these correctly, reteach the information. Consider the possibility that you might have to use a new educational approach or method.
A new year and a new start, with a shared understanding of problems and potential solutions between the patient and wound care team can get you started on the pathway to success. To quote Zig Ziglar, “A goal properly set is halfway reached.”
Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS
Editor-in-Chief Wound Care Advisor
Cofounder, Wound Care Education Institute
Plainfield, Illinois
Complex wound failures are costly and time-consuming. They increase length of stay and contribute to morbidity and mortality in surgical patients. Negative-pressure wound therapy (NPWT)—a common adjunct to wound-care therapy—is used to accelerate wound healing in all fields of surgery. Using a vacuum device and wound-packing material, it applies subatmospheric pressure to complex wounds.
But NPWT alone doesn’t ensure adequate wound healing. Many physiologic factors—including infection, excessive moisture, nutrition, and medications—influence wound-healing success. Failure to account for these factors or improper application of NPWT can limit patient outcomes and cause debilitating complications.
For clinicians, applying and establishing an airtight seal on a complex wound is among the most dreaded, time-consuming, and challenging NPWT-related tasks. Simply applying NPWT material under layers of transparent drape may delay wound healing or exacerbate the wound. This article provides tips on safe application of NPWT to enhance the outcomes of patients with complex wounds.
Consider wound location
Wounds on the body’s anterior surfaces are less susceptible to the forces of pressure, friction, and shear than those on posterior and lateral surfaces. Posterior and lateral wounds commonly require posterior offloading or repositioning the patient in bed to reduce or eliminate direct pressure. This can be done with judicious and frequent patient turning using a specialty bed or support surface.
Bridge a posterior or lateral wound to an anterior surface by placing the drainage collection tubing to a nonpressure-bearing surface away from the wound. Bridging keeps the tubing from exerting pressure on intact skin and decreases the risk of a pressure ulcer. To create the bridge, cut foam into a single spiral of 0.5 to 1 cm, or if using gauze, fold gauze into 8 single layers.
Place the spiraled foam or gauze layers onto the drape, ensure the bridge is wider than the collection tubing disc, and secure it with an additional drape. Next, apply the NPWT collection tubing on the end of the bridge away from the wound. A wide bridge under the collection tubing disc will minimize the potential for periwound breakdown when negative pressure is initiated. You may modify this spiraling technique by varying the width of the foam to fill undermining and wounds of irregular configuration and depth.
Protect the periwound
An intact periwound may break down from exposure to moisture, injury from repetitive removal of a transparent drape, or NPWT material coming in contact with skin. Skin protection is critical in preventing additional breakdown stemming from contact with potentially damaging material.
Transparent drapes are designed to permit transmission of moisture vapor and oxygen. Avoid using multiple layers of transparent drapes to secure dressings over intact skin, as this can decrease the transmission of moisture vapor and oxygen, which in turn may increase the risk of fungal infection, maceration, and loss of an intact seal.
Periwound maceration also may indicate increased wound exudate, requiring an increase in negative pressure. Conversely, an ecchymotic periwound may indicate excessively high negative pressures. If either occurs, assess the need to adjust negative pressure and intervene accordingly. Reassess NPWT effectiveness with subsequent dressing changes.
Apply a protective liquid skin barrier to the periwound and adjacent healthy tissue to help protect the skin surface from body fluids. The skin barrier also helps prevent stripping of fragile skin by minimizing shear forces from repetitive or forceful removal of transparent drapes. Excessive moisture can be absorbed by using a light dusting of ostomy powder sealed with a skin barrier. A “window pane” of transparent drape or hydrocolloid dressing around the wound also can protect surface tissue from contactwith NPWT material and prevent maceration.
Avoid creating rolled wound edges
In the best-case scenario, epithelial tissue at the wound edge is attached to the wound bed and migrates across healthy granulation tissue, causing the wound to contract and finally close. With deep wound environments that lack moisture or healthy granulation tissue, the wound edges may roll downward and epibole may develop. Epibole is premature closure of the wound edges, which prevents epithelialization and wound closure when it comes in contact with a deeper wound bed. (See Picturing epibole by clicking the PDF icon above.)
Materials used in NPWT are primarily air-filled. Applying negative pressure causes air removal, leading to wound contraction by pulling on the wound edges—an action called macrostrain. Without sufficient NPWT material in the wound, macrostrain can cause the wound to contract downward and the wound edges to roll.
Ensure that enough NPWT material has been applied into the wound to enhance wound-edge approximation and avoid creating a potential defect as the wound heals. Before NPWT begins, material should be raised 1 to 2 cm above the intact skin. Additional material may be needed with subsequent changes if the NPWT material compresses below the periwound. The amount of NPWT material needed to remain above the periwound once NPWT starts varies with the amount of material compressed and the wound depth.
Reduce the infection risk
To some degree, all wounds are contaminated. Usually, the body’s immunologic response is able to clear bacterial organisms and wound healing isn’t delayed. But a patient who has an infection of a complex wound needs additional support.
Systemic antibiotics alone aren’t enough because they’re selective for specific organisms and don’t reach therapeutic levels in the wound bed. In contrast, topical antimicrobial adjuncts, such as controlled-release ionic silver, provide broad-spectrum antimicrobial coverage against fungi, viruses, yeasts, and gram-negative and gram-positive bacteria, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci.
Consider using controlled-release ionic silver for a wound known to be infected or at risk for infection due to its location or potential urine or fecal contamination. To be bactericidal, ionic silver must be in concentrations of at least 20 parts per million; also, it must be kept moist and must come in direct contact with infected wound bed. At lower concentrations, organisms may develop resistance. Ionic silver has no known resistance or contraindications. Dressings using it come in several forms, including a hydrogel sheet, perforated sheet, cavity version, and semiliquid hydrogel. Be sure the form you choose doesn’t occlude the NPWT material and compromise therapy. (See NPWT for a patient with necrotizing fasciitis by clicking the PDF icon above.)
One of the most daunting aspects of NPWT is obtaining and maintaining a good seal—in other words, avoiding the dreaded leak. Preventive skin measures may contribute to a poor seal; skin-care products containing glycerin, surfactant, or dimethicone may prevent adequate adhesion of NPWT drapes. Body oil, sweat, and hair may need to be minimized or removed.
To avoid leaks, don’t overlook the obvious—loose connections, a loose drainage collection canister, exposed NPWT material, and skinfolds extending beyond the transparent drape. Tincture of benzoin (with or without a thin hydrocolloid dressing) increases tackiness to enhance the adhesive property of a transparent drape on the diaphoretic patient and on hard-to-drape areas, such as the perineum. But be sure to use tincture of benzoin with discretion, as it may remove fragile periwound tissue when the dressing is removed.
Ostomy paste products can serve as effective filler. These pliable products can be spread into position to obtain a secure seal under the transparent drape in hard-to-seal areas, such as the perineum. Pastes remain flexible and can be removed without residue. Temporarily increasing NPWT pressure to a higher setting may help locate a subtle leak or provide enough negative pressure to self-seal the leak. Once the leak resolves, remember to return the pressure to the ordered setting.
Knowledge optimizes healing
It’s important to be aware of potential complications of NPWT (See Take care with NPWT by clicking on the PDF icon above). However, when applied correctly, NPWT is an effective option for managing complex wounds. Recognizing and managing potential complications at the wound site, ensuring periwound protection, minimizing epibole formation, and preventing wound infection can result in a better-prepared wound bed and promote optimal healing.
Selected references
Baranoski S, Ayello EA. (2012). Wound Care Essentials: Practice Principles. 3rd ed. Springhouse, PA; Lippincott Williams & Wilkins.
Bovill E, Banwell PE, Teot L, et al. Topical negative pressure wound therapy: a review of its role and guidelines for its use in the management of acute wounds. Int Wound J. 2008;5:511-529.
Sussman C, Bates-Jensen B. Wound Care: A Collaborative Practice Manual for Health Professionals. 4th ed. Baltimore, MD; Lippincott Williams & Wilkins; 2011.
Ronald Rock is an Adult Health Clinical Nurse Specialist in the Digestive Disease Institute at the Cleveland Clinic in Cleveland, Ohio.
By combining bioactive peptides, researchers have successfully stimulated wound healing in an in vitro and in vivo study. The studies, published in PLoS ONE, show that the combination of two peptides stimulates growth of blood vessels and promotes tissue re-growth of tissue. Further research into these peptides could potentially lead to new therapies for chronic and acute wounds.
The researchers evaluated a newly-created peptide, UN3, in pre-clinical models with the goal of simulating impaired wound healing as in patients suffering from peripheral vascular diseases or uncontrolled diabetes. They discovered that the peptide increased the development of blood vessel walls by 50%, with an 250% increase in blood vessel growth, and a 300% increase in cell migration in response to the injury. (more…)
Hansen’s disease, also called leprosy, is treatable today – and that’s partly thanks to a curious tree and the work of a pioneering young scientist in the 1920s. Centuries prior to her discovery, sufferers had no remedy for leprosy’s debilitating symptoms or its social stigma.
This young scientist, Alice Ball, laid fundamental groundwork for the first effective leprosy treatment globally. But her legacy still prompts conversations about the marginalization of women and people of color in science today.
Alice Augusta Ball, born in Seattle, Washington, in 1892, became the first woman and first African American to earn a master’s degree in science from the College of Hawaii in 1915, after completing her studies in pharmaceutical chemistry the year prior.
After she finished her master’s degree, the college hired her as a research chemist and instructor, and she became the first African American with that title in the chemistry department.
Doctors now understand that leprosy, also called Hansen’s disease, is minimally contagious. But in 1865, the fear and stigma associated with leprosy led authorities in Hawaii to implement a mandatory segregation policy, which ultimately isolated those with the disease on a remote peninsula on the island of Molokai. In 1910, over 600 leprosy sufferers were living in Molokai.
Doctors had attempted to use nearly every remedy imaginable to treat leprosy, even experimenting with dangerous substances such as arsenicand strychnine. But the lone consistently effective treatment was chaulmoogra oil.
Chaulmoogra oil is derived from the seeds of the chaulmoogra tree. Health practitioners in India and Burma had been using this oil for centuries as a treatment for various skin diseases. But there were limitations with the treatment, and it had only marginal effects on leprosy.
The oil is very thick and sticky, which makes it hard to rub into the skin. The drug is also notoriously bitter, and patients who ingested it would often start vomiting. Some physicians experimented with injections of the oil, but this produced painful pustules.
Dr. Isabel Kerr, a European missionary, administering to a patient a chaulmoogra oil treatment in 1915, prior to the invention of the Ball Method. George McGlashan Kerr, CC BY
The Ball Method
If researchers could harness chaulmoogra’s curative potential without the nasty side effects, the tree’s seeds could revolutionize leprosy treatment. So, Hollmann turned to Ball. In a 1922 article, Hollmann documents how the 23-year-old Ball discovered how to chemically adapt chaulmoogra into an injection that had none of the side effects.
The Ball Method, as Hollmann called her discovery, transformed chaulmoogra oil into the most effective treatment for leprosy until the introduction of sulfones in the late 1940s.
In 1920, the Ball Method successfully treated 78 patients in Honolulu. A year later, it treated 94 more, with the Public Health Service noting that the morale of all the patients drastically improved. For the first time, there was hope for a cure.
Ball’s death meant she didn’t have the opportunity to publish her research. Arthur Dean, chair of the College of Hawaii’s chemistry department, took over the project.
Dean mass-produced the treatment and published a series of articles on chaulmoogra oil. He renamed Ball’s method the “Dean Method,” and he never credited Ball for her work.
Ball’s other colleagues did attempt to protect Ball’s legacy. A 1920 article in the Journal of the American Medical Association praises the Ball Method, while Hollmann clearly credits Ball in his own 1922 article.
Ball is described at length in a 1922 article in volume 15, issue 5, of Current History, an academic publication on international affairs. That feature is excerpted in a June 1941 issue of Carter G. Woodson’s “Negro History Bulletin,” referring to Ball’s achievement and untimely death.
Joseph Dutton, a well-regarded religious volunteer at the leprosy settlements on Molokai, further referenced Ball’s work in a 1932 memoir broadly published for a popular audience.
Historians such as Paul Wermager later prompted a modern reckoning with Ball’s poor treatment by Dean and others, ensuring that Ball received proper credit for her work. Following Wermager’s and others’ work, the University of Hawaii honored Ball in 2000 with a bronze plaque, affixed to the last remaining chaulmoogra tree on campus.
In 2019, the London School of Hygiene and Tropical Medicine added Ball’s name to the outside of its building. Ball’s story was even featured in a 2020 short film, “The Ball Method.”
The Ball Method represents both a scientific achievement and a history of marginalization. A young woman of color pioneered a medical treatment for a highly stigmatizing disease that disproportionately affected an already disenfranchised Indigenous population.
In 2022, then-Gov. David Ige declared Feb. 28 Alice Augusta Ball Day in Hawaii. It was only fitting that the ceremony took place on the Mānoa campus in the shade of the chaulmoogra tree.
