Families, mothers, employers, and medical practices all interact in one way or another with a medical billing specialist. When medical billing is required, a qualified medical billing specialist can help you process your claim quickly and thoroughly. Medical billing specialists work in many different areas. A variety of tasks require a medical billing specialist to be familiar with medical transcription, medical codes, and electronic medical records (EMR).

This article not only explains the types of information a medical billing specialist should be familiar with but also the types of information that families, mothers, employers, and medical practices should be familiar with.

Medical Transcription

Medical transcription is the method of transferring medical information, such as diagnosis or interviews, from an audio format to a paper format or an electronic format. SOAP notes are recorded with a transcription machine before it is transferred to an electronic format. It becomes part of an electronic medical record or EMR.

A medical transcription job is often sent to a medical transcription company or processed with a medical transcription program. Medical transcription articles provide more information on the process of medical transcription as well as electronic medical records.

Medical Codes

Qualified medical billing specialists are also familiar with various medical codes, governing record-keeping, billing, and certification. CPT codes, HIPAA certification, ICD.9 codes, HCFA 1500 formats, etc. are just some of the important standards by which a qualified medical billing specialist performs his or her work. Other diagnosis codes and claim processing codes also play a continual role in medical billing, and a medical billing specialist should be aware of how they function.

Electronic Medical Records

An EMR, or electronic medical record, is a convenient way to process medical records in today’s business world. Databases are full of EMRs comprised of SOAP notes, billing information, medical history, and other relevant information. Electronic medical records must be carefully managed, backed up, and stored. They must also be kept secure.

Medical Practice Software

Medical practice software has helped to simplify the medical billing process, allowing a streamlined database of EMRs along with access to medical codes. Medical practices are beginning to adopt this type of software in order to cut their IT costs and set up fees and adopt a month by month cost on a secured system. Information may then be accessed from any computer or PDA by authorized individuals. Medical billing specialists are trained in software programs such as these.

Heart and organs failure is characterized by an inability of the myocardium to deliver sufficient oxygenated blood to meet the needs of tissues during exercise or at rest. Because diagnostic criteria for this clinical syndrome remain ill defined, the actual prevalence is difficult to determine. Heart failure is estimated to affect 2 to 4.5 million persons in the United States. (1-3) The condition is more common in men than in women, and its prevalence increases with age (1.1 percent in persons 25 to 54 years of age, 3.7 percent in persons 55 to 64 years, and 4.5 percent in persons 65 to 74 years). (3) Heart failure is becoming increasingly common as the U.S. population ages and survival rates after acute myocardial infarction increase.

The annual direct medical cost of caring for patients with heart failure is estimated to exceed $10 billion. (4) Furthermore, heart failure is a progressive condition: once symptoms appear, subsequent morbidity and mortality are high. In patients with heart failure identified by careful screening, five-year survival rates are only 59 percent in men and 45 percent in women. (5)

This article focuses on the diagnosis of heart failure from an evidence-based perspective. A clinical review (6) published in this issue examines the treatment of heart failure and the prognosis for affected patients.

Pathophysiology of Heart Failure
Normal myocardial function requires sufficient nutrient-rich, toxin-free blood at rest and during exercise; sequential depolarization of the myocardium; normal myocardial contractility during systole and relaxation during diastole; normal intracardiac volume before contraction (preload); and limited resistance to the flow of blood out of the heart (afterload). The capacity of the heart to adapt to short-term changes in preload or afterload is remarkable, but sudden or sustained changes in preload (e.g., acute mitral regurgitation, excessive intravenous hydration), afterload (e.g., aortic stenosis, severe uncontrolled hypertension), or demand (e.g., increased demand because of severe anemia or hyperthyroidism) may lead to progressive failure of myocardial function. Asymptomatic dysfunction progresses steadily to overt heart failure.

Coronary artery disease accounts for nearly 70 percent of all cases of heart failure. (7) Less frequent causes include diabetes mellitus and valvular heart disease (Table 1). Heart failure also can be multifactorial. For example, the disease can result from acute myocardial infarction (loss of myocardial contractility) with papillary muscle dysfunction (increased preload) and acute pulmonary edema (hypoxemia).

Heart failure may be classified into six types based on the role of diastolic or systolic dysfunction (Table 2). Diastolic dysfunction is heart failure caused by compromised myocardial relaxation in the presence of normal myocardial contractility and ejection fraction. It is associated most commonly with coronary artery disease, hypertension, aging, and infiltrative cardiomyopathy. Systolic dysfunction is caused by impaired myocardial contractility and low ejection fraction. It is associated most often with coronary artery disease (especially myocardial infarction), idiopathic dilated cardiomyopa-thy, hypertension, and valvular disease.

The five types of heart failure resulting from systolic dysfunction include high output heart failure, low cardiac output syndrome, right heart failure, left heart failure, and biventricular failure. High output heart failure occurs when the demand for blood exceeds the capacity of an otherwise normal heart to meet the demand. This type of heart failure may occur in patients with severe anemia, arteriovenous malformations with shunting of blood, or hyperthyroidism. Patients with low cardiac output syndrome have fatigue and loss of lean muscle mass as their most prominent symptoms, but they also may have dyspnea, impaired renal function, or altered mental status. Right heart failure is characterized by peripheral edema, whereas left heart failure is characterized by pulmonary congestion. Both systemic and pulmonary congestion are present in patients with biventricular heart failure.

Although the symptoms, causes, prevalence, and epidemiology of the six different types of heart failure are somewhat different, there is substantial overlap, and types may coexist. Therefore, this review presents an approach to diagnosis that is appropriate regardless of the type or cause of heart failure.

Overview of Diagnosis

The spectrum of patients who may be suspected of having heart failure ranges from those who are asymptomatic but at high risk for heart failure (i.e., patients who abuse alcohol or have coronary artery disease, hypertension, diabetes mellitus, exposure to cardiotoxic drugs, or familial history of cardiomyopathy) to those with florid signs and symptoms of heart failure.

Guidelines from the American College of Cardiology and the American Heart Association (8) identify four stages in the progression of heart failure. Patients in stage A have no structural abnormalities but are at high risk for heart failure. In stage B, patients are asymptomatic but have structural heart disease. Patients in stage C have structural abnormalities and past or present heart failure. In stage D, patients have end-stage heart failure and require mechanical circulatory support, infusion of inotropic agents, cardiac transplantation, or hospice care.

The diagnosis of vulvodynia is made after taking a careful history, ruling out infectious or dermatologic abnormalities, and eliciting pain in response to light pressure on the labia, introitus, or hymenal remnants. Several treatment options have been used, although the evidence for many of these treatments is incomplete. Treatments include oral medications that decrease nerve hypersensitivity (e.g., tricyclic antidepressants, selective serotonin reuptake inhibitors, anticonvulsants), pelvic floor biofeedback, cognitive behavioral therapy, local treatments, and (rarely) surgery. Most women experience substantial improvement when one or more treatments are used.

Vulvodynia is characterized by chronic discomfort in the vulvar region; the discomfort may range from mild to severe and debilitating. The diagnosis depends on a consistent history, lack of a documented infectious or dermatologic cause, and in most women, tenderness when gentle pressure is applied by a cotton swab to the vulva, introitus, or hymenal areas. The pain usually is present during and after intercourse, and other factors may exacerbate the pain (e.g., bicycle riding, tampon insertion, prolonged sitting, wearing tight clothes) (Table 1). (1) In some women the pain is spontaneous.

Although vulvodynia was described in 1889 as “excessive sensitivity” of the vulva, (2) it rarely was referred to in the medical literature until the 1980s. Recognition of this disorder and its effects on the lives of women worldwide led to the adoption of the term “vulvodynia” by the International Society for the Study of Vulvovaginal Diseases (ISSVD) in 1983. At the time, it was defined as “chronic vulvar discomfort that is characterized by the complaint of burning, stinging, irritation, or rawness” in the absence of skin disease or infection. (3) The ISSVD recently revised the definition to include two subgroups: localized and generalized vulvar dysesthesia. (4) Each of these subgroups is further categorized as provoked, spontaneous, or mixed. It is unclear whether these groups are separate disorders or different presentations of the same disorder. (1) The term “vulvar vestibulitis” is no longer used because inflammation is not a prominent component of the disorder; it is now referred to as localized vulvar dysesthesia (or vestibulodynia). (4)

Prevalence

Three studies (5-7) that systematically addressed prevalence in different settings found vulvar pain to be much more common than previously thought, with rates of 15 percent in one gynecologist’s practice, (5) 1.7 percent in an Internet survey, (6) and 8.6 percent in a population-based study of symptomatic women in the Boston area. (7) These findings would extrapolate to more than 2.4 million women in the United States and approximately 15 affected women in a family practice of 2,000 patients.

Characteristics of Women with Vulvodynia

Women presenting with vulvodynia typically are white; are in stable, long-term relationships; have had the pain for several years; and have been examined several times by multiple physicians before receiving the diagnosis. (6-9) The age range is broad, from children (rarely) to women 80 years and older, (6) but most women with this disorder are between 20 and 50 years of age.

Vulvodynia is not associated with sexually transmitted diseases (STDs) or STD risk factors, (8,10) but affected women often have been treated repeatedly for candidal vulvovaginitis. (8,10,11) In the past, it was theorized that the pain of vulvodynia was due to psychological issues. (12,13) However, recent data indicate that women with vulvodynia are psychologically comparable to women without the disorder (14-16) and are no more likely to have been abused. (8,14,17) Marital satisfaction levels also are similar. (14)

Although women with vulvodynia report that the quality and quantity of their sexual activity has decreased since the onset of symptoms, more than one half have had intercourse and have had an orgasm in the previous month. (18) These women were just as likely as women without pain to participate in other sexual activities (e.g., masturbation, receiving oral sex). (18)

Pathophysiology

Although research is ongoing, little is known about the causes of vulvodynia. Affected women are more likely to have altered contractile characteristics of the pelvic floor musculature (19); biofeedback therapy designed to address these alterations often results in improved muscle function and decreased vulvar pain. (20,21) Although women with vulvodynia were known to be sensitive to touch in the vestibular region, it has only recently become clear that women with vulvodynia also have increased sensitivity at peripheral sites, such as the upper arm or leg. (22,23) Whether these muscular changes and increased systemic sensitivity are primary or secondary to the pain disorder is unknown.

Several studies have identified minor immunologic changes in women with vulvodynia, such as altered levels of interleukin-1 and tumor necrosis factor-a in vestibular tissue (24); increased production of interleukin-1[beta] and decreased production of interleukin-1 receptor antagonist by lymphocytes following stimulation (25); decreased production of interferon-a26; and changes in the gene associated with interleukin-1 receptor antagonist. (27,28) These changes could result in a decreased ability to downregulate the inflammatory response, which in turn may be associated with neuropathic changes.

No matter if you are in an executive or a management role at an academic center or a private practice hospital, as a physician leader you want your medical staff to not only understand the principles and theories of the quality and safety movements, but also to put them into practice.

Though there may not yet be a burning national safety platform, for the best organizations the train has truly left the station. For leaders of health care organizations, it is not a question of if, but how to facilitate improvement in patient safety among medical staff. Changing people’s behavior is difficult and education alone is not enough.
In 1999, Children’s Hospitals and Clinics of Minnesota began a journey to improve patient safety. Our CEO at the time, Brock Nelson, had an epiphany that year that changed our organization and how we operate.

Nelson had been advised by our attorney not to disclose to a family that our pathologists made an error in a diagnosis. Nelson went against the advice and further decided that Children’s would always disclose the full truth. In addition, Children’s hired a world expert in patient safety–Julie Morath–as our chief operating officer. With these two key events, Children’s of Minnesota had begun the effort to change our culture.

We then developed a specific agenda that included readiness, accountability, infrastructure changes, empowerment of all employees and staff, high reliability training, and new safety technology.

Children’s medical staff not only concurred with the agenda but also took leadership roles in its development, through the vice president of medical affairs, the elected chief of staff, the chiefs of divisions, and by adding a new position, medical director of patient safety.

Over the past seven years, we have continually updated and revised our patient safety agenda to expand and enhance its effectiveness.

One recent enhancement is a relatively unusual commitment made by our medical staff: All members who are appointed (and at reappointment) will continue to have to meet traditional conditions such as maintaining their licenses, getting continuing medical education credits, showing competencies in their fields, and being good citizens.

In addition, each member must also pass a test that demonstrates understanding of safety and quality principles. At appointment, staff is now given a package of critical communication components to absorb, followed by a test of 10 questions. The medical leadership of Children’s of Minnesota took this step in order to raise the bar on safety. Medical staff members will not be appointed or reappointed without passing this test.

How we did it

In 2004, as Children’s vice president of medical affairs and chief medical officer, I recommended to the professional executive committee that we commit to an expectation of patient safety knowledge before allowing appointment to our medical staff.

The recommendation further stated that upon staff members’ application for reappointment every two years, Children’s would offer updated information and knowledge about patient safety, and members must renew their commitment by taking a test again.

The recommendation was supported by the leadership of the professional staff, including the chief of staff, division chiefs, community physicians and Children’s boards of directors.

With the guidance of our director of patient safety, Children’s created a package of critical communications that focused on nine areas of patient safety:

1. Stop the line policies

2. Chain of command

3. SBAR communications

4. “Do not use” abbreviations

5. Verbal order read backs

6. Rapid response teams

7. Medical accident reporting

8. Universal protocol

9. Disclosures

These recommendations were instituted in 2006. The new process began with all of Children’s employed physicians, followed by all of the private-practice (community) physicians and advance practice nurses who apply for appointment on a two-year cycle.

[ILLUSTRATION OMITTED]

The requirement can be fulfilled electronically or on paper. We have also created a CD-ROM with the information available for individuals to review the necessary communication skills.

Here’s a look at the test:

Children’s Professional Staff Patient Safety Training Questionnaire

Please circle the correct choice.

1. If someone invokes the “Stop-the-Line” rule:

A. All participants will immediately stop and respond to the request by re-assessing the patient’s safety.

B. Assistance by any means most expedient shall be sought.

C. Emergency interventions may be initiated without prior express physician order.

D. They are acting in a manner sanctioned and supported by Children’s professional staff.

E. All of the above.

2. The chain of command policy is a Children’s policy that describes how an employee or professional staff member is expected to escalate an issue of concern depending upon the patient’s acuity.

A. True

B. False

3. The obligation to provide disclosure does not require that harm has occurred.

Peripheral vascular disease is a manifestation of systemic atherosclerosis that leads to significant narrowing of arteries distal to the arch of the aorta. The most common symptom of peripheral vascular disease is intermittent claudication. At other times, peripheral vascular disease leads to acute or critical limb ischemia. Intermittent claudication manifests as pain in the muscles of the legs with exercise; it is experienced by 2 percent of persons older than 65 years. Physical findings include abnormal pedal pulses, femoral artery bruit, delayed venous filling time, cool skin, and abnormal skin color. Most patients present with subtle findings and lack classic symptoms, which makes the diagnosis difficult. The standard office-based test to determine the presence of peripheral vascular disease is calculation of the ankle-brachial index. Magnetic resonance arteriography, duplex scanning, and hemodynamic localization are noninvasive methods for lesion localization and may be helpful when symptoms or findings do not correlate with the ankle-brachial index. Contrast arteriography is used for definitive localization before intervention. Treatment is divided into lifestyle, medical, and surgical therapies. Lifestyle therapies focus on exercise, smoking cessation, and dietary modification. Medical therapy is directed at reducing platelet aggregation. In addition, patients with contributing disorders such as hypertension, diabetes, and hyperlipidemia need to have these conditions managed as aggressively as possible. Surgical therapies include stents, arterectomies, angioplasty, and bypass surgery.

Peripheral vascular disease (PVD) is the presence of systemic atherosclerosis in arteries distal to the arch of the aorta. As a result of the atherosclerotic process, patients with PVD develop narrowing of these arteries. The most common symptom of PVD is intermittentclaudication, which manifests as pain in the muscles of the legs with exercise and is experienced by 2 percent of persons older than 65 years. (1) In one study of outpatients in the United States, PVD was present in 29 percent of patients. (2) This study included patients older than 70 and patients 50 to 69 years of age with a history of cigarette smoking or diabetes mellitus. The greatest modifiable risk factor for the development and progression of PVD is cigarette smoking. Cigarette smoking increases the odds for PVD by 1.4 for every 10 cigarettes smoked per day. (3)

Screening and Primary Prevention

To date, no studies have attempted to document reductions in morbidity and mortality that result from screening for PVD in primary care. The U.S. Preventive Services Task Force has recommended against routine screening for peripheral arterial disease. (4)

Primary prevention of PVD consists of encouraging smoking cessation. Smoking cessation also is recommended for the prevention of coronary artery disease, chronic obstructive pulmonary disease, stroke, and lung cancer.

Diagnosis

The differential diagnosis of PVD includes musculoskeletal and neurologic causes. The most common entity that mimics PVD is spinal stenosis. Spinal stenosis can cause compression of the cauda equina, which results in pain that radiates down both legs. The pain occurs with walking (i.e., pseudoclaudication) or prolonged standing and does not subside rapidly with rest. Additional conditions to consider are acute embolism, deep or superficial venous thrombosis, restless legs syndrome, systemic vasculitides, nocturnal leg cramps, muscle or tendon strains, peripheral neuropathy, and arthritides (Table 1). (5)

Patients with PVD have a history of claudication, which manifests as cramp-like muscle pain occurring with exercise and subsiding rapidly with rest. In addition, later in the course of the disease, patients may present with night pain, nonhealing ulcers, and skin color changes. However, PVD is asymptomatic in almost 90 percent of patients. (2) The Edinburgh Claudication Questionnaire has been shown to be 91 percent specific and 99 percent sensitive for diagnosing intermittent claudication in symptomatic patients. (6) It is composed of a series of six questions and a pain diagram that are self-administered by the patient (Table 2). (6)

Classic risk factors for PVD are smoking, diabetes mellitus, hypertension, and hyperlipidemia. Recent trials have added chronic renal insufficiency, (7) elevated C-reactive protein levels, (8) and hyperhomocysteinemia (9) to the list of risk factors. In one series from the Netherlands, the likelihood of a patient having PVD (as defined by an anklebrachial index [ABI] of less than 0.9) was increased by being male (odds ratio [OR] 1.6); being older than 60 years (OR 4.1); having hypercholesterolemia (OR 1.9); having a history of ischemic heart disease (OR 3.5), cerebrovascular disease (OR 3.6), diabetes mellitus (OR 2.5), or intermittent claudication (OR 5.6); or smoking (OR 1.6). (9)

Physical examination findings in patients with PVD vary. They may include absent or diminished pulses, abnormal skin color, poor hair growth, and cool skin. The most reliable physical findings are diminished or absent pedal pulses, presence of femoral artery bruit, abnormal skin color, and cool skin (Table 3 (10)), but their absence does not preclude PVD.

Evidence summary

Electrocardiograms have been a mainstay in the evaluation for MI for many years. A systematic review of the workup of acute chest pain found that the ECG was the most useful bedside test for MI. (1) In this review, ST segment elevation and Q waves were found to be equally reliable predictors of MI (positive likelihood ratio [LR+] = 22). A normal ECG was also found to be the most important bedside finding for ruling out the diagnosis of MI (LR- = 0.2).
New ST segment elevation is the most important ECG feature in increasing the probability of diagnosing an MI, with LRs ranging from 5.7 to 53.9. (2) Another systematic review revealed similar findings where ST segment elevation (most commonly defined as at least 1 mm in 2 or more contiguous limb leads or at least 2 mm in 2 contiguous precordial leads) had a LR+ = 13.1 (95% confidence interval [CI], 8.28-20.6). (3) This review also found that a “completely normal” ECG is reasonably useful in ruling out MI with a LR- = 0.14 (95% CI, 0.11-0.20). (3)

In 2001, a working group of the National Heart Attack Alert Program (NHAAP) performed a systematic review to define the accuracy of “out of hospital” ECG in the diagnosis of acute cardiac ischemia (ACI) and MI. Based on the 8 studies for which data were available, the random effects pooled sensitivity for acute MI was 68% (95% CI, 59%-76%), the specificity was 97% (95% CI, 89%-92%), and the diagnostic odds ratio (DOR) was 104 (95% CI, 48-224). (4) (The DOR is the change in post-test odds from a negative test to a positive test. It is used as a summary measure in meta-analyses of diagnostic studies. A DOR of 1 represents a useless test, with higher values representing more useful tests.)

From tasting urine to microscopy to molecular testing, the sophistication of diagnostic techniques has come a long way and continues to develop at breakneck speed. The history of the laboratory is the story of medicine’s evolution from empirical to experimental techniques and proves that the clinical lab is the true source of medical authority. Part I in a 2-part series.

Three distinct periods in the history of medicine are associated with three different places and therefore different methods of determining diagnosis: From the middle ages to the 18th century, bedside medicine was prevalent; then between 1794 and 1848 came hospital medicine; and from that time forward, laboratory medicine has served as medicine’s lodestar. The laboratory’s contribution to modern medicine has only recently been recognized by historians as something more than the addition of another resource to medical science and is now being appreciated as the seat of medicine, where clinicians account for what they observe in their patients.

The first medical diagnoses made by humans were based on what ancient physicians could observe with their eyes and ears, which sometimes also included the examination of human specimens. The ancient Greeks attributed all disease to disorders of bodily fluids called humors, and during the late medieval period, doctors routinely performed uroscopy. Later, the microscope revealed not only the cellular structure of human tissue, but also the organisms that cause disease. More sophisticated diagnostic tools and techniques - such as the thermometer for measuring temperature and the stethoscope for measuring heart rate - were not in widespread use until the end of the 19th century. The clinical laboratory would not become a standard fixture of medicine until the beginning of the 20th century. This 2-part article reviews the history and development of diagnostic methods from ancient to modern times as well as the evolution of the clinical laboratory from the late 19th century to the present. Ancient diagnostic methods

In ancient Egypt and Mesopotamia, the earliest physicians made diagnoses and recommended treatments based primarily on observation of clinical symptoms. Palpation and auscultation were also used. Physicians were able to describe dysfunctions of the digestive tract, heart and circulation, the liver and spleen, and menstrual disturbances; unfortunately, this empiric medicine was reserved for royalty and the wealthy.

Other less-than-scientific methods of diagnosis used in treating the middle and lower classes included divination through ritual sacrifice to predict the outcome of illness. Usually a sheep would be killed before the statue of a god. Its liver was examined for malformations or peculiarities; the shape of the lobes and the orientation of the common duct were then used to predict the fate of the patient.

Ancient physicians also began the practice of examining patient specimens. The oldest known test on body fluids was done on urine in ancient times (before 400 BC). Urine was poured on the ground and observed to see whether it attracted insects. If it did, patients were diagnosed with boils.

The ancient Greeks also saw the value in examining body fluids to predict disease. At around 300 BC, Hippocrates promoted the use of the mind and senses as diagnostic tools, a principle that played a large part in his reputation as the “Father of Medicine.” The central Hippocratic doctrine of humoral pathology attributed all disease to disorders of fluids of the body. To obtain a clear picture of disease, Hippocrates advocated a diagnostic protocol that included tasting the patient’s urine, listening to the lungs, and observing skin color and other outward appearances. Beyond that, the physician was to “understand the patient as an individual.” Hippocrates related the appearance of bubbles on the surface of urine specimens to kidney disease and chronic illness. He also related certain urine sediments and blood and pus in urine to disease. The first description of hematuria, or the presence of blood in urine, by Rufus of Ephesus surfaced at around AD 50 and was attributed to the failure of kidneys to function properly in filtering the blood.

Later (c. AD 180), Galen (AD 131-201), who is recognized as the founder of experimental physiology, created a system of pathology that combined Hippocrates’ humoral theories with the Pythagorean theory, which held that the four elements (earth, air, fire, and water), corresponded to various combinations of the physiologic qualifies of dry, cold, hot, and moist. These combinations of physiologic characteristics corresponded roughly to the four humors of the human body: hot + moist = blood; hot + dry = yellow bile; cold + moist = phlegm; and cold + dry = black bile. Galen was known for explaining everything in light of his theory and for having an explanation for everything. He also described diabetes as “diarrhea of urine” and noted the normal relationship between fluid intake and urine volume. His unwavering belief in his own infallibility appealed to complacency and reverence for authority. That dogmatism essentially brought innovation and discovery in European medicine to a standstill for nearly 14 centuries. Anything relating to anatomy, physiology, and disease was simply referred back to Galen as the final authority from whom there could be no appeal.

Clinical introduction to medical acupuncture.
Aung, Steven K. H. and William P. D. Chen.

Thieme Medical Publishers

2007

324 pages

$99.95

Hardcover

RM184

This textbook introduces medical practitioners, students, and residents to the theoretical principles and fundamental techniques of medical acupuncture. Aung (dentistry, U. of Alberta) and Chen (ophthalmology, U. of California, Los Angeles) begin with an overview of Traditional Chinese Medicine (TCM), followed by a description of the channels and acupuncture points. Subsequent sections cover treatment techniques; diagnosis and differentiation of syndromes; and microsystems. Some of the specific applications addressed include treatments for osteoarthritis, menopause, and hypertension.

Typically considered a disease of affluent and rotund middle-aged men such as King Henry VIII, gout causes sudden, severe attacks of pain, redness, warmth, and swelling in some joints. It usually affects one joint at a time often starting in the big toe. This painful arthritic condition affects approximately 2.1 million Americans. It can occur at any age, but it often strikes men between the ages of 40 and 50, according to statistics from the Arthritis Foundation in Atlanta.

Gout occurs when there is a build-up of too much uric acid in the body, which forms crystals that deposit in joints and cause inflammation. Uric acid normally forms when the body breaks down waste products called purines.

Despite an understanding of its cause and the availability of treatments for both prevention and flares, until now there has been little consensus about how to diagnose and treat this painful, common condition. But the European League Against Rheumatism (EULAR) Gout Task Force now issued a two-part set of recommendations on gout diagnosis and treatment.

DIAGNOSIS: GOUT

When making a diagnosis of gout, taking a medical history alone is not sufficient. Doctors must demonstrate the presence of monosodium urate (MSU) crystals in the synovial fluid in the joints or a deposit of urates in the skin and tissue around a joint, the guidelines state.

Although x-rays can help doctors include gout in a differential diagnosis and may show typical features in chronic gout, they are not useful in confirming the diagnosis of early or acute gout, the guidelines state. Doctors should also look at risk factors for gout and associated conditions, including obesity and high blood sugar. High cholesterol and high blood pressure also should be assessed.

NSAIDS, COLCHICINE FIRST LINE TREATMENT

Gout attacks can occur after drinking too much alcohol, eating too much of certain foods, surgery, sudden, severe illness, crash diets and joint injury. Education on weight loss, diet and reduced alcohol (especially beer) are important parts of a gout treatment plan, the new guidelines state.

First-line treatments for flares should be either oral colchicine and/or nonsteroidal anti-inflammatory agents. These agents can help relieve the acute pain and inflammation of gout attacks. The panel concluded that acute attacks also can be effectively treated by removing fluids from within the inflamed joint or with an injection of a long-acting steroid.

NORMALIZE URIC ACID

At first, gout episodes are usually few and far between, but if the disease is not controlled by medication, episodes may occur more frequently and last longer.

When it comes to preventing gout attacks, drugs designed to normalize uric acid levels are key. If your body produces too much uric acid, your doctor may prescribe a drug called allopurinol to slow the rate of uric acid production. The goal should be to maintain levels of serum uric acid level below 360 [micro]mol /L. Because rapid reductions in serum uric acid levels can trigger flares, the guidelines suggest that colchicine and/or an NSAID be given as prophylaxis against acute attacks during the first months of urate-lowering therapy.

The guidelines recommend long-term allopurinol as an appropriate urate-lowering therapy and advise starting at a low dose (100 mg/day) and escalating by 100 mg every two to four weeks. Theses doses must be adjusted for people with kidney impairment. Alternatives do exist for people who can’t tolerate allpurinol.

DOCTOR’S PERSPECTIVE

FIRST-EVER SET OF GUIDELINES FOR GOUT TREATMENT

MICHAEL A. BECKER, MD, Professor of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL

“This is the first time that there is a coherent set of recommendations for the diagnosis and treatment of gout. I don’t agree with all of them, but they are not unreasonable and, in the aggregate, are useful in setting a target for lowering urate levels, stressing special caution when faced with impaired kidney function, and indicating a need for colchicines (or NSAID) for prophylaxis when initiating urate-lowering. In terms of treatment, the guideline authors suggest that a low-dose colchicine regimen may be sufficient to reverse inflammation in gout flares in a safer way than higher doses. Even though the quoted unit dose of 0.5 mg is not commonly available in the U.S., validation of this type of approach would be important. Still, the guidelines do provide some basis for telling physicians what they should be doing. Overall, there has been a deficit in the management of patients with gout in terms of making a sound diagnosis and treatment, and the guidelines are probably useful in providing the outline to do that. Patients may need to alert their doctors to the existence of these guidelines.”

Ristrom v. Twin Cities Area Asbestos Workers Local 34 Joint Apprenticeship Committee, 8th Cir., No. 03-1609, June 4, 2004.

An apprenticeship program was not guilty of disability discrimination against a participant who was diagnosed with attention deficit disorder (ADD) because the individual failed to establish that the impairment substantially limited his ability to learn, held the 8th U.S. Circuit Court of Appeals.

The Americans with Disabilities Act (ADA) requires individuals seeking the act’s protection to show their impairments substantially limited them compared to the average individual.

In 1995, Clayton Ristrom entered the Twin Cities Area Asbestos Workers Apprenticeship Program, operated by the Joint Apprenticeship Committee (JAC). The program offers participants an opportunity to perform on-the-job and classroom training to earn union journeyman status–and therefore higher wages.

Ristrom completed two years of the four-year program without problems and advanced to the program’s third year in the fall of 1997. At that time, he began experiencing difficulty with class work; he failed to improve despite assistance and tutoring provided by the JAC. During this period, Ristrom confided to his tutor that he had ADD and was suffering from depression.

The JAC determined that Ristrom should repeat the program’s third year. Ristrom continued to have problems and underwent a neurological examination in November 1998. The exam indicated some depression and anxiety, but did not yield a clear ADD diagnosis and did not show that Ristrom’s ability to learn was substantially impaired compared to the average person.

Ristrom did not immediately provide the results of his examination to the JAC, but began the second semester of the third-year program in January 1999. After he missed five of the first six classes, Ristrom was informed that if he did not complete his third-year classroom training, he would be dismissed. When Ristrom continued to miss classes, his participation in the program was cancelled.

Just prior to his termination from the program, Ristrom received a “preliminary diagnosis” of ADD and depression, which was provided to the JAC.

Ristrom sued the JAC, alleging disability discrimination and retaliation in violation of the ADA. The lower court granted summary judgment to the JAC, concluding that Ristrom failed to show he had an ADA-qualifying disability.

The 8th Circuit upheld the decision, finding that Ristrom had failed to offer evidence–medical or otherwise–proving his ADD or depression substantially limited his ability to learn to a considerable or large degree, compared to the average person.

Ristrom also failed to prove the JAC knew of his disability. As a result, the JAC could not be liable for violating the ADA.

RELATED ARTICLE: Professional Pointer

In a concurring opinion, one 8th Circuit judge found that regardless of whether Ristrom had an ADA-qualifying disability, his repeated unexcused absences from the program and apprenticeship jobs, in addition to his failing grades, created a legitimate nondiscriminatory reason for his termination from the program. Although not the basis for the 8th Circuit majority’s decision, that alternative rationale once again illustrates the importance of consistent application of policies and full and objective documentation.