I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.

At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.

In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.

I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.

Send your comments to ccjm@ccf.org. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.

I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.

At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.

In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.

I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.

Send your comments to ccjm@ccf.org. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.

I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.

At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.

In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.

I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.

Send your comments to ccjm@ccf.org. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.

A 68-year-old white woman with irritable bowel syndrome has had worsening symptoms of right-sided abdominal pain, excessive bloating, and loose stools. Her bowel movements have increased from one a day to two or three a day. She has not noted any mucus or blood in the stool. She cannot identify any alleviating or aggravating factors, and the pain is not related to eating.

She consumes a normal diet, including meat and dairy. Over-the-counter antidiarrheal medications do not relieve the symptoms. She has had no fevers, chills, or night sweats, and she has not lost weight over the past year.

Her medical history includes breast cancer (in remission), alcohol abuse (in remission), and hypothyroidism, osteoporosis, and supraventricular tachycardia, all controlled with treatment as noted below. She has never undergone abdominal surgery.

A general review of systems is normal. Her current medications include oxybutynin (available as Ditropan, others), calcium polycarbophil (FiberCon, others), risedronate (Actonel), levothyroxine (Synthroid, others), simethicone (Maalox Anti-Gas, others), atenolol (Tenormin), trazodone (Desyrel), a calcium supplement, and aspirin. She began taking duloxetine (Cymbalta) 18 months ago, and the dose was increased from 60 mg to 90 mg 1 week before this visit.

She has never smoked, and she has abstained from alcohol for 10 years. She has no family history of colon cancer, celiac disease, or inflammatory bowel disease. She has not traveled outside the country in the past several years, and she notes no change in her source of drinking water.

On physical examination, she does not appear to be in acute distress. Her pulse is 64 and her blood pressure is 112/78 mm Hg. The cardiopulmonary examination is normal. Her abdomen is soft, symmetrical, nondistended, and nontender. Bowel sounds are normal. No abdominal masses, palpable organomegaly, or abdominal bruits are noted.

Results of basic laboratory tests, including thyroid-stimulating hormone (TSH), complete blood count, blood chemistries, renal function, and liver function, are normal. Colonoscopy shows normal mucosa as far as the cecum.

DIFFERENTIAL DIAGNOSIS

1. In addition to irritable bowel syndrome, which of these can explain her symptoms?

• Ulcerative colitis
• Celiac disease
• Microscopic colitis
• Hyperthyroidism
• Lactase deficiency

Ulcerative colitis typically presents with blood and mucus in the stool and gross abnormalities on colonoscopy, none of which is present in this patient.

Hyperthyroidism can be ruled out by the normal TSH level.

Lactase deficiency or lactose intolerance is unlikely because it is present in only 15% of people of northern European descent (compared with 80% of blacks and Hispanics and up to 100% of Native Americans and Asians).¹ Furthermore, her pain is apparently not related to consuming dairy products.

The hydrogen breath test can aid in the diagnosis of lactase deficiency. This test relies on the breakdown of malabsorbed lactose by colonic flora. This is the most widely used test for this deficiency, but its high false-negative rate of 25% means that a negative result does not exclude the diagnosis and should not be relied on in working up a patient with chronic diarrhea.² Simply noting whether symptoms develop after ingesting 50 g of lactose is clinically useful when lactase deficiency is suspected.

Based on the information so far, it is reasonable in this patient to evaluate for celiac disease and for microscopic colitis.

Celiac disease, also called gluten-sensitive enteropathy, has a varied presentation that includes nonspecific symptoms such as those in this patient. Classically, it causes diarrhea, but patients may present with a single nutrient deficiency and no diarrhea.

This patient lacks the elevated alkaline phosphatase or evidence of vitamin deficiencies characteristic of malabsorption in celiac disease (ie, vitamins A, B₁₂, D, K, and folate)³. She also lacks evidence of malnutrition, such as iron deficiency anemia, weight loss, or low serum albumin. Finally, she does not have the dermatitis herpetiformis rash to suggest autoimmune gluten-sensitive enteropathy, nor does she have evidence of follicular hyperplasia or petechiae due to vitamin malabsorption.³

Because no single serologic test is ideal for diagnosing gluten-sensitive enteropathy, several tests are typically used: immunoglobulin A (IgA) antigliadin antibody, IgG antigliadin antibody, IgA antitransglutaminase antibody, and IgA antiendomysial antibody. IgA antitransglutaminase antibody is 92% to 98% sensitive and 91% to 100% specific for celiac disease. IgG antigliadin antibody is 92% to 97% sensitive and 99% specific. The positive predictive value of the IgA and IgG antigliadin antibody tests is less than 2% in the general population, whereas the positive predictive value for antiendomysial antibody and antitransglutaminase antibody are 15.7% and 21.8%, respectively.⁴ A positive serologic test for antiendomysial antibody is nearly 100% specific.

Our patient’s entire celiac antibody panel is negative, and thus celiac disease is unlikely.

In our patient, colonic biopsy reveals a mildly expanded lamina propria, intraepithelial lymphocytes, and a patchy but prominent thickening of the subepithelial collagen table. This set of features is consistent with collagenous colitis, a variant of microscopic colitis. Histologic signs on biopsy specimens are fairly specific for the disease.⁵

Chronic, intermittent, secretory diarrhea without bleeding is the hallmark of microscopic colitis. Associated symptoms may include abdominal pain, weight loss, and fatigue. If biopsies are not taken at the time of the initial evaluation, and the colonic pathology is overlooked, patients with collagenous colitis may be diagnosed with irritable bowel syndrome with diarrhea.⁶ The sedimentation rate is often elevated, and the antinuclear antibody test can be positive.⁷ Steatorrhea or protein-losing enteropathy can occur, and fecal leukocytes are present in more than 50% of patients.⁸

This patient fits well the demographics of the typical collagenous colitis patient: ie, a middle-aged woman in her 6th decade in otherwise good general health. The female-to-male ratio is 15:1 overall, although the relative frequency of collagenous colitis in women is greater than that of lymphocytic colitis.⁹ In a population-based study, the incidence of collagenous colitis was 5.1 per 100,000 per year, with a prevalence of 36 per 100,000; the incidence of lymphocytic colitis was 9.8 per 100,000 per year, with a prevalence of 64 per 100,000.¹⁰

Symptoms are typically vague and range from an annoyance to more than 20 non-bloody stools per day. The course of the disease also varies. Case series have reported a spontaneous remission rate of 15% to 20%,¹¹ though flare-ups are common. Microscopic colitis is largely a benign disease. It does not increase a person’s risk of colon cancer.

CAUSES OF COLLAGENOUS COLITIS

2. What causes of collagenous colitis have been identified?

• Alcohol abuse
• Previous gastrointestinal surgery
• Drug-induced injury to colon

Neither alcohol use nor previous gastrointestinal surgery has been associated with the development of collagenous colitis.

Collagenous colitis has, however, been linked to several causes. Abnormal collagen metabolism has been demonstrated in patients as a result of increased expression of procollagen I and metalloproteinase inhibitor TIMP-1.¹² Bacterial toxins and a bile-acid malabsorption defect in the terminal ileum and subsequent exposure of the colon to high concentrations of bile acids have also been linked to the development of collagenous colitis.

Many drugs have been linked to the development of collagenous colitis. Damage to the large intestine related to the use of non-steroidal anti-inflammatory drugs has been attributed to the blockage of prostaglandin synthesis.¹³ Simvastatin (Zocor), lansoprazole (Prilosec), and ticlopidine (Ticlid) have been linked to collagenous colitis; ticlopidine, flutamide (Eulexin), gold salts, lansoprazole, and sertraline (Zoloft) have been linked to the development of lymphocytic colitis.¹⁴ In one small series, patients developed colitis after switching from omeprazole (Prevacid) to lansoprazole. All patients had their symptoms and biopsy findings resolve within 1 week of stopping the drug.¹⁵

WHICH DRUG IS BEST?

3. Which drug is best for microscopic colitis, based on the current evidence?

• Bismuth (eg, Kaopectate, Pepto-Bismol)
• Sulfasalazine (Sulfazine)
• Budesonide (Entocort)
• Prednisolone

Studies have evaluated bismuth subsalicylate, Boswellia serrata extract, probiotics, prednisolone, budesonide, and other drugs for treating collagenous colitis.¹⁶

Bismuth trials have been small. In an open-label study of bismuth,¹⁷ symptoms improved in 11 of 12 patients.

Prednisolone recipients had a trend towards clinical response with treatment vs placebo, but it was not statistically significant, and there was incomplete remission of disease.¹⁸

Boswellia serrataextract¹⁹ and probiotics²⁰ showed no clinical improvement.

Cholestyramine has been shown to be helpful when used in conjunction with an anti-inflammatory agent,²¹ and it may be helpful when used alone.

Aminosalicylate compounds have not been tested in prospective randomized trials, even though they are the cornerstone of treatment for ulcerative colitis. Retrospective trials have been equivocal.²²

Budesonide currently has the best evidence of efficacy in collagenous colitis,^23,24 and some evidence suggests it is also effective for other variants of microscopic colitis.

A total of 94 patients were enrolled in three placebo-controlled trials of budesonide at 9 mg daily or on a tapering schedule for 6 to 8 weeks. The pooled odds ratio for clinical response to treatment with budesonide was 12.32 (95% confidence interval 5.53–27.46), with a number needed to treat of 1.58. Significant histologic improvement with treatment was noted in all three trials.²³

Quality of life has also been studied in patients with microscopic colitis who take budesonide. Symptoms, emotional functioning, and physical functioning are improved. Budesonide also improved stool consistency and significantly reduced the mean stool frequency compared with placebo.²⁴

Compared with cortisol, budesonide has a 200 times greater affinity for the glucocorticoid receptor, and a 1,000 times greater topical anti-inflammatory potency. It is also well absorbed in the gastrointestinal tract but is substantially modified into very weak metabolites as a result of first-pass metabolism in the liver.²⁵ This localized effect further supports the use of budesonide in patients with any form of microscopic colitis.

Although studies have shown budesonide to be effective, not every patient with a histologic diagnosis of microscopic colitis needs it. It is reasonable to try antidiarrheal agents, bismuth, or both as a first step because they are inexpensive and have few side effects. If budesonide is used, it should be given for 6 to 8 weeks, then stopped, and the patient should then be monitored for symptom recurrence. If a flare does occur, budesonide can be restarted and continued as maintenance therapy.

KEY CONSIDERATIONS

Microscopic colitis is diagnosed histologically, while irritable bowel syndrome is a clinical diagnosis. In population-based cohorts of histologically confirmed microscopic colitis, 50% to 70% met symptom-based Rome criteria for the diagnosis of irritable bowel syndrome. The clinical symptom-based criteria for irritable bowel syndrome are not specific enough to rule out the diagnosis of microscopic colitis. Therefore, patients with suspected diarrhea-predominant irritable bowel syndrome should undergo colonoscopy with biopsy to investigate microscopic colitis if symptoms are not well controlled by antidiarrheal therapy.²⁶ The patient’s management may be very different depending on whether colonoscopy is done.

Management of microscopic colitis should include stopping any drugs associated with it. Simple antidiarrheal agents should be tried first to manage symptoms. If symptoms persist, patients can be treated with budesonide (Entocort EC) 9 mg by mouth daily for 8 weeks to induce remission, or 6 mg by mouth daily for 3 months as maintenance therapy.

OUR PATIENT’S COURSE

Our patient’s medication list includes duloxetine, a serotonin-norepinephrine reuptake inhibitor related to drugs that have been associated with the development of microscopic colitis. We tapered the duloxetine, and her symptoms improved by 50%. Her symptoms were eventually controlled after an 8-week course of oral budesonide 9 mg and ongoing intermittent use of loperamide (Imodium).

A 68-year-old white woman with irritable bowel syndrome has had worsening symptoms of right-sided abdominal pain, excessive bloating, and loose stools. Her bowel movements have increased from one a day to two or three a day. She has not noted any mucus or blood in the stool. She cannot identify any alleviating or aggravating factors, and the pain is not related to eating.

She consumes a normal diet, including meat and dairy. Over-the-counter antidiarrheal medications do not relieve the symptoms. She has had no fevers, chills, or night sweats, and she has not lost weight over the past year.

Her medical history includes breast cancer (in remission), alcohol abuse (in remission), and hypothyroidism, osteoporosis, and supraventricular tachycardia, all controlled with treatment as noted below. She has never undergone abdominal surgery.

A general review of systems is normal. Her current medications include oxybutynin (available as Ditropan, others), calcium polycarbophil (FiberCon, others), risedronate (Actonel), levothyroxine (Synthroid, others), simethicone (Maalox Anti-Gas, others), atenolol (Tenormin), trazodone (Desyrel), a calcium supplement, and aspirin. She began taking duloxetine (Cymbalta) 18 months ago, and the dose was increased from 60 mg to 90 mg 1 week before this visit.

She has never smoked, and she has abstained from alcohol for 10 years. She has no family history of colon cancer, celiac disease, or inflammatory bowel disease. She has not traveled outside the country in the past several years, and she notes no change in her source of drinking water.

On physical examination, she does not appear to be in acute distress. Her pulse is 64 and her blood pressure is 112/78 mm Hg. The cardiopulmonary examination is normal. Her abdomen is soft, symmetrical, nondistended, and nontender. Bowel sounds are normal. No abdominal masses, palpable organomegaly, or abdominal bruits are noted.

Results of basic laboratory tests, including thyroid-stimulating hormone (TSH), complete blood count, blood chemistries, renal function, and liver function, are normal. Colonoscopy shows normal mucosa as far as the cecum.

DIFFERENTIAL DIAGNOSIS

1. In addition to irritable bowel syndrome, which of these can explain her symptoms?

• Ulcerative colitis
• Celiac disease
• Microscopic colitis
• Hyperthyroidism
• Lactase deficiency

Ulcerative colitis typically presents with blood and mucus in the stool and gross abnormalities on colonoscopy, none of which is present in this patient.

Hyperthyroidism can be ruled out by the normal TSH level.

Lactase deficiency or lactose intolerance is unlikely because it is present in only 15% of people of northern European descent (compared with 80% of blacks and Hispanics and up to 100% of Native Americans and Asians).¹ Furthermore, her pain is apparently not related to consuming dairy products.

The hydrogen breath test can aid in the diagnosis of lactase deficiency. This test relies on the breakdown of malabsorbed lactose by colonic flora. This is the most widely used test for this deficiency, but its high false-negative rate of 25% means that a negative result does not exclude the diagnosis and should not be relied on in working up a patient with chronic diarrhea.² Simply noting whether symptoms develop after ingesting 50 g of lactose is clinically useful when lactase deficiency is suspected.

Based on the information so far, it is reasonable in this patient to evaluate for celiac disease and for microscopic colitis.

Celiac disease, also called gluten-sensitive enteropathy, has a varied presentation that includes nonspecific symptoms such as those in this patient. Classically, it causes diarrhea, but patients may present with a single nutrient deficiency and no diarrhea.

This patient lacks the elevated alkaline phosphatase or evidence of vitamin deficiencies characteristic of malabsorption in celiac disease (ie, vitamins A, B₁₂, D, K, and folate)³. She also lacks evidence of malnutrition, such as iron deficiency anemia, weight loss, or low serum albumin. Finally, she does not have the dermatitis herpetiformis rash to suggest autoimmune gluten-sensitive enteropathy, nor does she have evidence of follicular hyperplasia or petechiae due to vitamin malabsorption.³

Because no single serologic test is ideal for diagnosing gluten-sensitive enteropathy, several tests are typically used: immunoglobulin A (IgA) antigliadin antibody, IgG antigliadin antibody, IgA antitransglutaminase antibody, and IgA antiendomysial antibody. IgA antitransglutaminase antibody is 92% to 98% sensitive and 91% to 100% specific for celiac disease. IgG antigliadin antibody is 92% to 97% sensitive and 99% specific. The positive predictive value of the IgA and IgG antigliadin antibody tests is less than 2% in the general population, whereas the positive predictive value for antiendomysial antibody and antitransglutaminase antibody are 15.7% and 21.8%, respectively.⁴ A positive serologic test for antiendomysial antibody is nearly 100% specific.

Our patient’s entire celiac antibody panel is negative, and thus celiac disease is unlikely.

In our patient, colonic biopsy reveals a mildly expanded lamina propria, intraepithelial lymphocytes, and a patchy but prominent thickening of the subepithelial collagen table. This set of features is consistent with collagenous colitis, a variant of microscopic colitis. Histologic signs on biopsy specimens are fairly specific for the disease.⁵

Chronic, intermittent, secretory diarrhea without bleeding is the hallmark of microscopic colitis. Associated symptoms may include abdominal pain, weight loss, and fatigue. If biopsies are not taken at the time of the initial evaluation, and the colonic pathology is overlooked, patients with collagenous colitis may be diagnosed with irritable bowel syndrome with diarrhea.⁶ The sedimentation rate is often elevated, and the antinuclear antibody test can be positive.⁷ Steatorrhea or protein-losing enteropathy can occur, and fecal leukocytes are present in more than 50% of patients.⁸

This patient fits well the demographics of the typical collagenous colitis patient: ie, a middle-aged woman in her 6th decade in otherwise good general health. The female-to-male ratio is 15:1 overall, although the relative frequency of collagenous colitis in women is greater than that of lymphocytic colitis.⁹ In a population-based study, the incidence of collagenous colitis was 5.1 per 100,000 per year, with a prevalence of 36 per 100,000; the incidence of lymphocytic colitis was 9.8 per 100,000 per year, with a prevalence of 64 per 100,000.¹⁰

Symptoms are typically vague and range from an annoyance to more than 20 non-bloody stools per day. The course of the disease also varies. Case series have reported a spontaneous remission rate of 15% to 20%,¹¹ though flare-ups are common. Microscopic colitis is largely a benign disease. It does not increase a person’s risk of colon cancer.

CAUSES OF COLLAGENOUS COLITIS

2. What causes of collagenous colitis have been identified?

• Alcohol abuse
• Previous gastrointestinal surgery
• Drug-induced injury to colon

Neither alcohol use nor previous gastrointestinal surgery has been associated with the development of collagenous colitis.

Collagenous colitis has, however, been linked to several causes. Abnormal collagen metabolism has been demonstrated in patients as a result of increased expression of procollagen I and metalloproteinase inhibitor TIMP-1.¹² Bacterial toxins and a bile-acid malabsorption defect in the terminal ileum and subsequent exposure of the colon to high concentrations of bile acids have also been linked to the development of collagenous colitis.

Many drugs have been linked to the development of collagenous colitis. Damage to the large intestine related to the use of non-steroidal anti-inflammatory drugs has been attributed to the blockage of prostaglandin synthesis.¹³ Simvastatin (Zocor), lansoprazole (Prilosec), and ticlopidine (Ticlid) have been linked to collagenous colitis; ticlopidine, flutamide (Eulexin), gold salts, lansoprazole, and sertraline (Zoloft) have been linked to the development of lymphocytic colitis.¹⁴ In one small series, patients developed colitis after switching from omeprazole (Prevacid) to lansoprazole. All patients had their symptoms and biopsy findings resolve within 1 week of stopping the drug.¹⁵

WHICH DRUG IS BEST?

3. Which drug is best for microscopic colitis, based on the current evidence?

• Bismuth (eg, Kaopectate, Pepto-Bismol)
• Sulfasalazine (Sulfazine)
• Budesonide (Entocort)
• Prednisolone

Studies have evaluated bismuth subsalicylate, Boswellia serrata extract, probiotics, prednisolone, budesonide, and other drugs for treating collagenous colitis.¹⁶

Bismuth trials have been small. In an open-label study of bismuth,¹⁷ symptoms improved in 11 of 12 patients.

Prednisolone recipients had a trend towards clinical response with treatment vs placebo, but it was not statistically significant, and there was incomplete remission of disease.¹⁸

Boswellia serrataextract¹⁹ and probiotics²⁰ showed no clinical improvement.

Cholestyramine has been shown to be helpful when used in conjunction with an anti-inflammatory agent,²¹ and it may be helpful when used alone.

Aminosalicylate compounds have not been tested in prospective randomized trials, even though they are the cornerstone of treatment for ulcerative colitis. Retrospective trials have been equivocal.²²

Budesonide currently has the best evidence of efficacy in collagenous colitis,^23,24 and some evidence suggests it is also effective for other variants of microscopic colitis.

A total of 94 patients were enrolled in three placebo-controlled trials of budesonide at 9 mg daily or on a tapering schedule for 6 to 8 weeks. The pooled odds ratio for clinical response to treatment with budesonide was 12.32 (95% confidence interval 5.53–27.46), with a number needed to treat of 1.58. Significant histologic improvement with treatment was noted in all three trials.²³

Quality of life has also been studied in patients with microscopic colitis who take budesonide. Symptoms, emotional functioning, and physical functioning are improved. Budesonide also improved stool consistency and significantly reduced the mean stool frequency compared with placebo.²⁴

Compared with cortisol, budesonide has a 200 times greater affinity for the glucocorticoid receptor, and a 1,000 times greater topical anti-inflammatory potency. It is also well absorbed in the gastrointestinal tract but is substantially modified into very weak metabolites as a result of first-pass metabolism in the liver.²⁵ This localized effect further supports the use of budesonide in patients with any form of microscopic colitis.

Although studies have shown budesonide to be effective, not every patient with a histologic diagnosis of microscopic colitis needs it. It is reasonable to try antidiarrheal agents, bismuth, or both as a first step because they are inexpensive and have few side effects. If budesonide is used, it should be given for 6 to 8 weeks, then stopped, and the patient should then be monitored for symptom recurrence. If a flare does occur, budesonide can be restarted and continued as maintenance therapy.

KEY CONSIDERATIONS

Microscopic colitis is diagnosed histologically, while irritable bowel syndrome is a clinical diagnosis. In population-based cohorts of histologically confirmed microscopic colitis, 50% to 70% met symptom-based Rome criteria for the diagnosis of irritable bowel syndrome. The clinical symptom-based criteria for irritable bowel syndrome are not specific enough to rule out the diagnosis of microscopic colitis. Therefore, patients with suspected diarrhea-predominant irritable bowel syndrome should undergo colonoscopy with biopsy to investigate microscopic colitis if symptoms are not well controlled by antidiarrheal therapy.²⁶ The patient’s management may be very different depending on whether colonoscopy is done.

Management of microscopic colitis should include stopping any drugs associated with it. Simple antidiarrheal agents should be tried first to manage symptoms. If symptoms persist, patients can be treated with budesonide (Entocort EC) 9 mg by mouth daily for 8 weeks to induce remission, or 6 mg by mouth daily for 3 months as maintenance therapy.

OUR PATIENT’S COURSE

Our patient’s medication list includes duloxetine, a serotonin-norepinephrine reuptake inhibitor related to drugs that have been associated with the development of microscopic colitis. We tapered the duloxetine, and her symptoms improved by 50%. Her symptoms were eventually controlled after an 8-week course of oral budesonide 9 mg and ongoing intermittent use of loperamide (Imodium).

A 68-year-old white woman with irritable bowel syndrome has had worsening symptoms of right-sided abdominal pain, excessive bloating, and loose stools. Her bowel movements have increased from one a day to two or three a day. She has not noted any mucus or blood in the stool. She cannot identify any alleviating or aggravating factors, and the pain is not related to eating.

She consumes a normal diet, including meat and dairy. Over-the-counter antidiarrheal medications do not relieve the symptoms. She has had no fevers, chills, or night sweats, and she has not lost weight over the past year.

Her medical history includes breast cancer (in remission), alcohol abuse (in remission), and hypothyroidism, osteoporosis, and supraventricular tachycardia, all controlled with treatment as noted below. She has never undergone abdominal surgery.

A general review of systems is normal. Her current medications include oxybutynin (available as Ditropan, others), calcium polycarbophil (FiberCon, others), risedronate (Actonel), levothyroxine (Synthroid, others), simethicone (Maalox Anti-Gas, others), atenolol (Tenormin), trazodone (Desyrel), a calcium supplement, and aspirin. She began taking duloxetine (Cymbalta) 18 months ago, and the dose was increased from 60 mg to 90 mg 1 week before this visit.

She has never smoked, and she has abstained from alcohol for 10 years. She has no family history of colon cancer, celiac disease, or inflammatory bowel disease. She has not traveled outside the country in the past several years, and she notes no change in her source of drinking water.

On physical examination, she does not appear to be in acute distress. Her pulse is 64 and her blood pressure is 112/78 mm Hg. The cardiopulmonary examination is normal. Her abdomen is soft, symmetrical, nondistended, and nontender. Bowel sounds are normal. No abdominal masses, palpable organomegaly, or abdominal bruits are noted.

Results of basic laboratory tests, including thyroid-stimulating hormone (TSH), complete blood count, blood chemistries, renal function, and liver function, are normal. Colonoscopy shows normal mucosa as far as the cecum.

DIFFERENTIAL DIAGNOSIS

1. In addition to irritable bowel syndrome, which of these can explain her symptoms?

• Ulcerative colitis
• Celiac disease
• Microscopic colitis
• Hyperthyroidism
• Lactase deficiency

Ulcerative colitis typically presents with blood and mucus in the stool and gross abnormalities on colonoscopy, none of which is present in this patient.

Hyperthyroidism can be ruled out by the normal TSH level.

Lactase deficiency or lactose intolerance is unlikely because it is present in only 15% of people of northern European descent (compared with 80% of blacks and Hispanics and up to 100% of Native Americans and Asians).¹ Furthermore, her pain is apparently not related to consuming dairy products.

The hydrogen breath test can aid in the diagnosis of lactase deficiency. This test relies on the breakdown of malabsorbed lactose by colonic flora. This is the most widely used test for this deficiency, but its high false-negative rate of 25% means that a negative result does not exclude the diagnosis and should not be relied on in working up a patient with chronic diarrhea.² Simply noting whether symptoms develop after ingesting 50 g of lactose is clinically useful when lactase deficiency is suspected.

Based on the information so far, it is reasonable in this patient to evaluate for celiac disease and for microscopic colitis.

Celiac disease, also called gluten-sensitive enteropathy, has a varied presentation that includes nonspecific symptoms such as those in this patient. Classically, it causes diarrhea, but patients may present with a single nutrient deficiency and no diarrhea.

This patient lacks the elevated alkaline phosphatase or evidence of vitamin deficiencies characteristic of malabsorption in celiac disease (ie, vitamins A, B₁₂, D, K, and folate)³. She also lacks evidence of malnutrition, such as iron deficiency anemia, weight loss, or low serum albumin. Finally, she does not have the dermatitis herpetiformis rash to suggest autoimmune gluten-sensitive enteropathy, nor does she have evidence of follicular hyperplasia or petechiae due to vitamin malabsorption.³

Because no single serologic test is ideal for diagnosing gluten-sensitive enteropathy, several tests are typically used: immunoglobulin A (IgA) antigliadin antibody, IgG antigliadin antibody, IgA antitransglutaminase antibody, and IgA antiendomysial antibody. IgA antitransglutaminase antibody is 92% to 98% sensitive and 91% to 100% specific for celiac disease. IgG antigliadin antibody is 92% to 97% sensitive and 99% specific. The positive predictive value of the IgA and IgG antigliadin antibody tests is less than 2% in the general population, whereas the positive predictive value for antiendomysial antibody and antitransglutaminase antibody are 15.7% and 21.8%, respectively.⁴ A positive serologic test for antiendomysial antibody is nearly 100% specific.

Our patient’s entire celiac antibody panel is negative, and thus celiac disease is unlikely.

In our patient, colonic biopsy reveals a mildly expanded lamina propria, intraepithelial lymphocytes, and a patchy but prominent thickening of the subepithelial collagen table. This set of features is consistent with collagenous colitis, a variant of microscopic colitis. Histologic signs on biopsy specimens are fairly specific for the disease.⁵

Chronic, intermittent, secretory diarrhea without bleeding is the hallmark of microscopic colitis. Associated symptoms may include abdominal pain, weight loss, and fatigue. If biopsies are not taken at the time of the initial evaluation, and the colonic pathology is overlooked, patients with collagenous colitis may be diagnosed with irritable bowel syndrome with diarrhea.⁶ The sedimentation rate is often elevated, and the antinuclear antibody test can be positive.⁷ Steatorrhea or protein-losing enteropathy can occur, and fecal leukocytes are present in more than 50% of patients.⁸

This patient fits well the demographics of the typical collagenous colitis patient: ie, a middle-aged woman in her 6th decade in otherwise good general health. The female-to-male ratio is 15:1 overall, although the relative frequency of collagenous colitis in women is greater than that of lymphocytic colitis.⁹ In a population-based study, the incidence of collagenous colitis was 5.1 per 100,000 per year, with a prevalence of 36 per 100,000; the incidence of lymphocytic colitis was 9.8 per 100,000 per year, with a prevalence of 64 per 100,000.¹⁰

Symptoms are typically vague and range from an annoyance to more than 20 non-bloody stools per day. The course of the disease also varies. Case series have reported a spontaneous remission rate of 15% to 20%,¹¹ though flare-ups are common. Microscopic colitis is largely a benign disease. It does not increase a person’s risk of colon cancer.

CAUSES OF COLLAGENOUS COLITIS

2. What causes of collagenous colitis have been identified?

• Alcohol abuse
• Previous gastrointestinal surgery
• Drug-induced injury to colon

Neither alcohol use nor previous gastrointestinal surgery has been associated with the development of collagenous colitis.

Collagenous colitis has, however, been linked to several causes. Abnormal collagen metabolism has been demonstrated in patients as a result of increased expression of procollagen I and metalloproteinase inhibitor TIMP-1.¹² Bacterial toxins and a bile-acid malabsorption defect in the terminal ileum and subsequent exposure of the colon to high concentrations of bile acids have also been linked to the development of collagenous colitis.

Many drugs have been linked to the development of collagenous colitis. Damage to the large intestine related to the use of non-steroidal anti-inflammatory drugs has been attributed to the blockage of prostaglandin synthesis.¹³ Simvastatin (Zocor), lansoprazole (Prilosec), and ticlopidine (Ticlid) have been linked to collagenous colitis; ticlopidine, flutamide (Eulexin), gold salts, lansoprazole, and sertraline (Zoloft) have been linked to the development of lymphocytic colitis.¹⁴ In one small series, patients developed colitis after switching from omeprazole (Prevacid) to lansoprazole. All patients had their symptoms and biopsy findings resolve within 1 week of stopping the drug.¹⁵

WHICH DRUG IS BEST?

3. Which drug is best for microscopic colitis, based on the current evidence?

• Bismuth (eg, Kaopectate, Pepto-Bismol)
• Sulfasalazine (Sulfazine)
• Budesonide (Entocort)
• Prednisolone

Studies have evaluated bismuth subsalicylate, Boswellia serrata extract, probiotics, prednisolone, budesonide, and other drugs for treating collagenous colitis.¹⁶

Bismuth trials have been small. In an open-label study of bismuth,¹⁷ symptoms improved in 11 of 12 patients.

Prednisolone recipients had a trend towards clinical response with treatment vs placebo, but it was not statistically significant, and there was incomplete remission of disease.¹⁸

Boswellia serrataextract¹⁹ and probiotics²⁰ showed no clinical improvement.

Cholestyramine has been shown to be helpful when used in conjunction with an anti-inflammatory agent,²¹ and it may be helpful when used alone.

Aminosalicylate compounds have not been tested in prospective randomized trials, even though they are the cornerstone of treatment for ulcerative colitis. Retrospective trials have been equivocal.²²

Budesonide currently has the best evidence of efficacy in collagenous colitis,^23,24 and some evidence suggests it is also effective for other variants of microscopic colitis.

A total of 94 patients were enrolled in three placebo-controlled trials of budesonide at 9 mg daily or on a tapering schedule for 6 to 8 weeks. The pooled odds ratio for clinical response to treatment with budesonide was 12.32 (95% confidence interval 5.53–27.46), with a number needed to treat of 1.58. Significant histologic improvement with treatment was noted in all three trials.²³

Quality of life has also been studied in patients with microscopic colitis who take budesonide. Symptoms, emotional functioning, and physical functioning are improved. Budesonide also improved stool consistency and significantly reduced the mean stool frequency compared with placebo.²⁴

Compared with cortisol, budesonide has a 200 times greater affinity for the glucocorticoid receptor, and a 1,000 times greater topical anti-inflammatory potency. It is also well absorbed in the gastrointestinal tract but is substantially modified into very weak metabolites as a result of first-pass metabolism in the liver.²⁵ This localized effect further supports the use of budesonide in patients with any form of microscopic colitis.

Although studies have shown budesonide to be effective, not every patient with a histologic diagnosis of microscopic colitis needs it. It is reasonable to try antidiarrheal agents, bismuth, or both as a first step because they are inexpensive and have few side effects. If budesonide is used, it should be given for 6 to 8 weeks, then stopped, and the patient should then be monitored for symptom recurrence. If a flare does occur, budesonide can be restarted and continued as maintenance therapy.

KEY CONSIDERATIONS

Microscopic colitis is diagnosed histologically, while irritable bowel syndrome is a clinical diagnosis. In population-based cohorts of histologically confirmed microscopic colitis, 50% to 70% met symptom-based Rome criteria for the diagnosis of irritable bowel syndrome. The clinical symptom-based criteria for irritable bowel syndrome are not specific enough to rule out the diagnosis of microscopic colitis. Therefore, patients with suspected diarrhea-predominant irritable bowel syndrome should undergo colonoscopy with biopsy to investigate microscopic colitis if symptoms are not well controlled by antidiarrheal therapy.²⁶ The patient’s management may be very different depending on whether colonoscopy is done.

Management of microscopic colitis should include stopping any drugs associated with it. Simple antidiarrheal agents should be tried first to manage symptoms. If symptoms persist, patients can be treated with budesonide (Entocort EC) 9 mg by mouth daily for 8 weeks to induce remission, or 6 mg by mouth daily for 3 months as maintenance therapy.

OUR PATIENT’S COURSE

Our patient’s medication list includes duloxetine, a serotonin-norepinephrine reuptake inhibitor related to drugs that have been associated with the development of microscopic colitis. We tapered the duloxetine, and her symptoms improved by 50%. Her symptoms were eventually controlled after an 8-week course of oral budesonide 9 mg and ongoing intermittent use of loperamide (Imodium).

Editor’s note: We are interested in your thoughts on this article. See the Editor-in-Chief’s comments.

I use to be a hospital guy. I was only a few days into my third-year medicine clerkship in medical school nearly three decades ago when I fell in love with the hospital and knew I was going to be an internist. The hospital wasn’t called a medical center back then. It was a fascinating and magical place, where internists were fired in the furnace of rounds, night call, and morning report. I loved the association with the great case, the flush of excitement that accompanied the difficult diagnosis, the hard-earned annual promotion through the hierarchy of trainees seeking the rarefied air of the attending physicians. We bonded as fellow house officers more tightly than with friends outside the hospital. We prowled the wards, intensive care units, emergency room, and laboratories and never slept. The hospital was the most exclusive of clubs, and our training granted us lifelong membership.

A humming beehive of academic activity, the hospital was also a web of powerful social relationships. Everybody knew everybody, from the hospital CEO to the night security officer. The nurses called you by your first name and worked with you for weeks at a time, fostering mutual respect and sometimes even affection. In those days, nurses actually nursed their patients, spoon-feeding them broth with their medications, washing them in bed and bathroom, holding their hands and heads. Patients came to the hospital to be diagnosed and treated until they recovered from whatever illness had felled them. They stayed long enough so that you knew them and their families as well as you knew your own.

I have been a general internist and clinician-educator for 23 years, working in two university hospitals and one community hospital. That’s more than seven generations of house staff with whom I’ve toiled and learned. Somewhere along the way, I became increasingly aware that teaching clinical medicine to students, interns, and residents was getting harder and harder. The patients were sicker and stayed only 3.2 days in the hospital. What we were teaching wasn’t how to diagnose and treat diseases, but how to manage only their most serious complications—the respiratory distress from pneumonia, the ketosis of uncontrolled diabetes, the septic shock from infections. The wards became intensive care units, and the critical care units the province of “intensivists” who were more adept than we were at taming all the machinery and technology. We struggled to keep up with the unending deluge of arcane demands from the accreditation organizations watchdogging our teaching efforts. We pretended that we somehow distinguished teaching rounds from working rounds, and documented the silliness in computer files. Medical education slowly slipped from being a calling to folks like me, finally succumbing to bureaucratic lunacy. The pace of teaching and caring for acutely ill patients became intolerable. Rounds went from the bedside to the classroom to the cell phone. The house staff were getting cheated out of the whole point of residency—the miracle of turning medical students into attending physicians in a little over a thousand days.

Worse, though, was the ebbing of the lifeblood of the hospital. Now the medical center, riddled with “centers of excellence” instead of departments, answered only to administrators who cared nothing about medical education, except for the Medicare dollars they would lose if they cut the training programs. They spent enormous amounts of money marketing the centers of excellence, and they cut everything else to manipulate the bottom line.

The biggest casualty, of course, was the nursing staff. Underpaid, depleted of leadership and morale, they simply disappeared. They were replaced by agency nurses who worked their shifts and didn’t know the doctors or the patients. The complex bedside care of increasingly sick, old, and vulnerable patients was delegated to people with high school equivalency degrees. Nurses now cared for their patients by managing their own support staff, and spent much of their time entering useless information in the computer. The doctor-nurse collaboration I grew up with as a trainee and young attending didn’t exist any-more, and patients suffered as a result.

In 2000, the Institute of Medicine informed the public and the medical community that being a patient in an American hospital was dangerous.1 We were told that at least 44,000 and perhaps as many as 98,000 patients die annually in US hospitals as the result of preventable medical mishaps, more deaths than are attributable yearly to motor vehicle accidents, breast cancer, or AIDS.1 Although there has been an emerging body of literature pertaining to this epidemic, not much has changed, at least not in my hospital. We remain absurdly complacent about rising iatrogenic infection rates, knowing all too well that we are allowing immunocompromised patients to die unnecessarily in our intensive care units. There are alcohol-based hand-washing gels everywhere, but no police or policy with teeth in it to enforce handwashing. We lurch toward physician computer order entry, clinging to the false belief that software programs will prevent adverse drug reactions and delivery of the wrong dangerous drug to the wrong patient. We understaff our pharmacies so that they can’t get the medications to the patients on time or alert us to our own prescribing errors. We burn out our nurses despite years of loyal service. And worst of all, we capitulate to the for-profit insurance industry that informs us they won’t pay for day 4 of Mr. Jones’ hospitalization because he has failed to meet some arbitrary criteria in their manual.

I stepped down as chairman of my department 3 years ago because I couldn’t stand it any longer. I couldn’t stand the management retreats in which we obsessed about “customer service” while the waiting time in the emergency department ballooned to 12 hours because there were “no beds.” There were plenty of beds, but no nurses to staff them. I was marginalized when I protested the budget cycles bleeding out support of medical education in favor of the annual purchase of new scanners and surgical gizmos. I couldn’t get anybody fired up about patient safety.

Retreating to the privacy of clinical medicine, I realized the other day that my real job is not to diagnose, treat, and teach about diseases anymore. My real job is to do everything in my power to keep my patients out of the medical center. I walk the halls now and don’t recognize the institution I grew up in and came to love. Everywhere I look, I see not magic and promise, but dirt and danger.

I’m not a hospital guy anymore.

Editor’s note: We are interested in your thoughts on this article. See the Editor-in-Chief’s comments.

I use to be a hospital guy. I was only a few days into my third-year medicine clerkship in medical school nearly three decades ago when I fell in love with the hospital and knew I was going to be an internist. The hospital wasn’t called a medical center back then. It was a fascinating and magical place, where internists were fired in the furnace of rounds, night call, and morning report. I loved the association with the great case, the flush of excitement that accompanied the difficult diagnosis, the hard-earned annual promotion through the hierarchy of trainees seeking the rarefied air of the attending physicians. We bonded as fellow house officers more tightly than with friends outside the hospital. We prowled the wards, intensive care units, emergency room, and laboratories and never slept. The hospital was the most exclusive of clubs, and our training granted us lifelong membership.

A humming beehive of academic activity, the hospital was also a web of powerful social relationships. Everybody knew everybody, from the hospital CEO to the night security officer. The nurses called you by your first name and worked with you for weeks at a time, fostering mutual respect and sometimes even affection. In those days, nurses actually nursed their patients, spoon-feeding them broth with their medications, washing them in bed and bathroom, holding their hands and heads. Patients came to the hospital to be diagnosed and treated until they recovered from whatever illness had felled them. They stayed long enough so that you knew them and their families as well as you knew your own.

I have been a general internist and clinician-educator for 23 years, working in two university hospitals and one community hospital. That’s more than seven generations of house staff with whom I’ve toiled and learned. Somewhere along the way, I became increasingly aware that teaching clinical medicine to students, interns, and residents was getting harder and harder. The patients were sicker and stayed only 3.2 days in the hospital. What we were teaching wasn’t how to diagnose and treat diseases, but how to manage only their most serious complications—the respiratory distress from pneumonia, the ketosis of uncontrolled diabetes, the septic shock from infections. The wards became intensive care units, and the critical care units the province of “intensivists” who were more adept than we were at taming all the machinery and technology. We struggled to keep up with the unending deluge of arcane demands from the accreditation organizations watchdogging our teaching efforts. We pretended that we somehow distinguished teaching rounds from working rounds, and documented the silliness in computer files. Medical education slowly slipped from being a calling to folks like me, finally succumbing to bureaucratic lunacy. The pace of teaching and caring for acutely ill patients became intolerable. Rounds went from the bedside to the classroom to the cell phone. The house staff were getting cheated out of the whole point of residency—the miracle of turning medical students into attending physicians in a little over a thousand days.

Worse, though, was the ebbing of the lifeblood of the hospital. Now the medical center, riddled with “centers of excellence” instead of departments, answered only to administrators who cared nothing about medical education, except for the Medicare dollars they would lose if they cut the training programs. They spent enormous amounts of money marketing the centers of excellence, and they cut everything else to manipulate the bottom line.

The biggest casualty, of course, was the nursing staff. Underpaid, depleted of leadership and morale, they simply disappeared. They were replaced by agency nurses who worked their shifts and didn’t know the doctors or the patients. The complex bedside care of increasingly sick, old, and vulnerable patients was delegated to people with high school equivalency degrees. Nurses now cared for their patients by managing their own support staff, and spent much of their time entering useless information in the computer. The doctor-nurse collaboration I grew up with as a trainee and young attending didn’t exist any-more, and patients suffered as a result.

In 2000, the Institute of Medicine informed the public and the medical community that being a patient in an American hospital was dangerous.1 We were told that at least 44,000 and perhaps as many as 98,000 patients die annually in US hospitals as the result of preventable medical mishaps, more deaths than are attributable yearly to motor vehicle accidents, breast cancer, or AIDS.1 Although there has been an emerging body of literature pertaining to this epidemic, not much has changed, at least not in my hospital. We remain absurdly complacent about rising iatrogenic infection rates, knowing all too well that we are allowing immunocompromised patients to die unnecessarily in our intensive care units. There are alcohol-based hand-washing gels everywhere, but no police or policy with teeth in it to enforce handwashing. We lurch toward physician computer order entry, clinging to the false belief that software programs will prevent adverse drug reactions and delivery of the wrong dangerous drug to the wrong patient. We understaff our pharmacies so that they can’t get the medications to the patients on time or alert us to our own prescribing errors. We burn out our nurses despite years of loyal service. And worst of all, we capitulate to the for-profit insurance industry that informs us they won’t pay for day 4 of Mr. Jones’ hospitalization because he has failed to meet some arbitrary criteria in their manual.

I stepped down as chairman of my department 3 years ago because I couldn’t stand it any longer. I couldn’t stand the management retreats in which we obsessed about “customer service” while the waiting time in the emergency department ballooned to 12 hours because there were “no beds.” There were plenty of beds, but no nurses to staff them. I was marginalized when I protested the budget cycles bleeding out support of medical education in favor of the annual purchase of new scanners and surgical gizmos. I couldn’t get anybody fired up about patient safety.

Retreating to the privacy of clinical medicine, I realized the other day that my real job is not to diagnose, treat, and teach about diseases anymore. My real job is to do everything in my power to keep my patients out of the medical center. I walk the halls now and don’t recognize the institution I grew up in and came to love. Everywhere I look, I see not magic and promise, but dirt and danger.

I’m not a hospital guy anymore.

Editor’s note: We are interested in your thoughts on this article. See the Editor-in-Chief’s comments.

I use to be a hospital guy. I was only a few days into my third-year medicine clerkship in medical school nearly three decades ago when I fell in love with the hospital and knew I was going to be an internist. The hospital wasn’t called a medical center back then. It was a fascinating and magical place, where internists were fired in the furnace of rounds, night call, and morning report. I loved the association with the great case, the flush of excitement that accompanied the difficult diagnosis, the hard-earned annual promotion through the hierarchy of trainees seeking the rarefied air of the attending physicians. We bonded as fellow house officers more tightly than with friends outside the hospital. We prowled the wards, intensive care units, emergency room, and laboratories and never slept. The hospital was the most exclusive of clubs, and our training granted us lifelong membership.

A humming beehive of academic activity, the hospital was also a web of powerful social relationships. Everybody knew everybody, from the hospital CEO to the night security officer. The nurses called you by your first name and worked with you for weeks at a time, fostering mutual respect and sometimes even affection. In those days, nurses actually nursed their patients, spoon-feeding them broth with their medications, washing them in bed and bathroom, holding their hands and heads. Patients came to the hospital to be diagnosed and treated until they recovered from whatever illness had felled them. They stayed long enough so that you knew them and their families as well as you knew your own.

I have been a general internist and clinician-educator for 23 years, working in two university hospitals and one community hospital. That’s more than seven generations of house staff with whom I’ve toiled and learned. Somewhere along the way, I became increasingly aware that teaching clinical medicine to students, interns, and residents was getting harder and harder. The patients were sicker and stayed only 3.2 days in the hospital. What we were teaching wasn’t how to diagnose and treat diseases, but how to manage only their most serious complications—the respiratory distress from pneumonia, the ketosis of uncontrolled diabetes, the septic shock from infections. The wards became intensive care units, and the critical care units the province of “intensivists” who were more adept than we were at taming all the machinery and technology. We struggled to keep up with the unending deluge of arcane demands from the accreditation organizations watchdogging our teaching efforts. We pretended that we somehow distinguished teaching rounds from working rounds, and documented the silliness in computer files. Medical education slowly slipped from being a calling to folks like me, finally succumbing to bureaucratic lunacy. The pace of teaching and caring for acutely ill patients became intolerable. Rounds went from the bedside to the classroom to the cell phone. The house staff were getting cheated out of the whole point of residency—the miracle of turning medical students into attending physicians in a little over a thousand days.

Worse, though, was the ebbing of the lifeblood of the hospital. Now the medical center, riddled with “centers of excellence” instead of departments, answered only to administrators who cared nothing about medical education, except for the Medicare dollars they would lose if they cut the training programs. They spent enormous amounts of money marketing the centers of excellence, and they cut everything else to manipulate the bottom line.

The biggest casualty, of course, was the nursing staff. Underpaid, depleted of leadership and morale, they simply disappeared. They were replaced by agency nurses who worked their shifts and didn’t know the doctors or the patients. The complex bedside care of increasingly sick, old, and vulnerable patients was delegated to people with high school equivalency degrees. Nurses now cared for their patients by managing their own support staff, and spent much of their time entering useless information in the computer. The doctor-nurse collaboration I grew up with as a trainee and young attending didn’t exist any-more, and patients suffered as a result.

In 2000, the Institute of Medicine informed the public and the medical community that being a patient in an American hospital was dangerous.1 We were told that at least 44,000 and perhaps as many as 98,000 patients die annually in US hospitals as the result of preventable medical mishaps, more deaths than are attributable yearly to motor vehicle accidents, breast cancer, or AIDS.1 Although there has been an emerging body of literature pertaining to this epidemic, not much has changed, at least not in my hospital. We remain absurdly complacent about rising iatrogenic infection rates, knowing all too well that we are allowing immunocompromised patients to die unnecessarily in our intensive care units. There are alcohol-based hand-washing gels everywhere, but no police or policy with teeth in it to enforce handwashing. We lurch toward physician computer order entry, clinging to the false belief that software programs will prevent adverse drug reactions and delivery of the wrong dangerous drug to the wrong patient. We understaff our pharmacies so that they can’t get the medications to the patients on time or alert us to our own prescribing errors. We burn out our nurses despite years of loyal service. And worst of all, we capitulate to the for-profit insurance industry that informs us they won’t pay for day 4 of Mr. Jones’ hospitalization because he has failed to meet some arbitrary criteria in their manual.

I stepped down as chairman of my department 3 years ago because I couldn’t stand it any longer. I couldn’t stand the management retreats in which we obsessed about “customer service” while the waiting time in the emergency department ballooned to 12 hours because there were “no beds.” There were plenty of beds, but no nurses to staff them. I was marginalized when I protested the budget cycles bleeding out support of medical education in favor of the annual purchase of new scanners and surgical gizmos. I couldn’t get anybody fired up about patient safety.

Retreating to the privacy of clinical medicine, I realized the other day that my real job is not to diagnose, treat, and teach about diseases anymore. My real job is to do everything in my power to keep my patients out of the medical center. I walk the halls now and don’t recognize the institution I grew up in and came to love. Everywhere I look, I see not magic and promise, but dirt and danger.

I’m not a hospital guy anymore.

Seemingly diverse autism mutations may share the same underlying mechanism, according to Eric M. Morrow, MD, PhD, Instructor in Psychiatry at Harvard Medical School in Boston, and colleagues.
“The regulation of expression of some autism candidate genes by neuronal membrane depolarization suggests the appealing hypothesis that neural activity–dependent regulation of synapse development may be a mechanism common to several autism mutations,” stated Dr. Morrow and colleagues in the July 11 Science. “Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.”
The researchers studied 88 large families—in which both parents shared recent ancestors—to find inherited causes of autism spectrum disorders. The families, who came from Jordan, Saudi Arabia, Kuwait, Oman, Pakistan, Qatar, Turkey, and the United Arab Emirates, were selected to emphasize the role of inherited genetic mutations.
The investigators gathered data with use of homozygosity mapping and compared the DNA of family members with and without autism to identify recessive mutations. Most individuals exhibited different genetic causes with little overlap between families, but a few exceptions were observed.
“Although the large size of linked loci precluded systemic gene sequencing in most cases, we were surprised to see that several consanguineous pedigrees showed large, rare, inherited homozygous deletions within linked regions, some of which are very likely causative mutations,” Dr. Morrow and colleagues said. Specifically, such deletions linked to autism were found in five families, or 6.4% of the study sample. Family members with one remaining functional copy of their genome segments did not have autism, while those with both copies missing did have autism.
The investigators found six gene disruptions that contributed to autism spectrum disorders. The largest of these gene disruptions involved genes essential for learning in the brain, as they are regulated either directly or indirectly by neuronal activity triggered by experience. Not all the genes were deleted—the remaining genes were simply turned off, leaving room for therapies to possibly turn these genes back on.
“Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity,” the investigators stated. “In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation.... The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development.”
The researchers’ findings also pointed to potential genetic similarities, such as inherited recessive causes, between autism and other neurologic disorders. Among families in the present study who had one member with autism, there was a relatively equivalent male/female ratio compared with other families with autism, indicating that parents who shared a common recent ancestor was a determining factor. In families with more than one member with autism, the male/female ratio was even more balanced.
“The accumulating number of distinct, individually rare genetic causes in autism suggests that the genetic architecture of autism resembles that of mental retardation and epilepsy, with many syndromes, each individually rare, as well as other cases potentially reflecting complex interactions between inherited changes,” Dr. Morrow and colleagues elaborated. “The relatively reduced male/female ratio of affected children and the reduced rate of linked de novo copy number variants in the consanguineous sample [of the present study] ... both suggest that consanguineous pedigrees with autism are enriched for autosomal recessive causes similar to other congenital neurological disorders in consanguineous populations.”
The research team stated that although their findings support recent studies that suggest autism is highly heterogeneous genetically, homozygosity mapping appears to be an effective way to find underlying shared mechanisms. Understanding these genetic underpinnings could eventually help direct various therapies for the different clinical manifestations of autism.
“Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism,” the researchers concluded. In addition, their “data implicating noncoding elements in patients with shared ancestry, as well as the heterozygous nonsense changes in patients without shared ancestry, suggest that loss of proper regulation of gene dosage may be an important genetic mechanism in autism.”

Seemingly diverse autism mutations may share the same underlying mechanism, according to Eric M. Morrow, MD, PhD, Instructor in Psychiatry at Harvard Medical School in Boston, and colleagues.
“The regulation of expression of some autism candidate genes by neuronal membrane depolarization suggests the appealing hypothesis that neural activity–dependent regulation of synapse development may be a mechanism common to several autism mutations,” stated Dr. Morrow and colleagues in the July 11 Science. “Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.”
The researchers studied 88 large families—in which both parents shared recent ancestors—to find inherited causes of autism spectrum disorders. The families, who came from Jordan, Saudi Arabia, Kuwait, Oman, Pakistan, Qatar, Turkey, and the United Arab Emirates, were selected to emphasize the role of inherited genetic mutations.
The investigators gathered data with use of homozygosity mapping and compared the DNA of family members with and without autism to identify recessive mutations. Most individuals exhibited different genetic causes with little overlap between families, but a few exceptions were observed.
“Although the large size of linked loci precluded systemic gene sequencing in most cases, we were surprised to see that several consanguineous pedigrees showed large, rare, inherited homozygous deletions within linked regions, some of which are very likely causative mutations,” Dr. Morrow and colleagues said. Specifically, such deletions linked to autism were found in five families, or 6.4% of the study sample. Family members with one remaining functional copy of their genome segments did not have autism, while those with both copies missing did have autism.
The investigators found six gene disruptions that contributed to autism spectrum disorders. The largest of these gene disruptions involved genes essential for learning in the brain, as they are regulated either directly or indirectly by neuronal activity triggered by experience. Not all the genes were deleted—the remaining genes were simply turned off, leaving room for therapies to possibly turn these genes back on.
“Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity,” the investigators stated. “In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation.... The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development.”
The researchers’ findings also pointed to potential genetic similarities, such as inherited recessive causes, between autism and other neurologic disorders. Among families in the present study who had one member with autism, there was a relatively equivalent male/female ratio compared with other families with autism, indicating that parents who shared a common recent ancestor was a determining factor. In families with more than one member with autism, the male/female ratio was even more balanced.
“The accumulating number of distinct, individually rare genetic causes in autism suggests that the genetic architecture of autism resembles that of mental retardation and epilepsy, with many syndromes, each individually rare, as well as other cases potentially reflecting complex interactions between inherited changes,” Dr. Morrow and colleagues elaborated. “The relatively reduced male/female ratio of affected children and the reduced rate of linked de novo copy number variants in the consanguineous sample [of the present study] ... both suggest that consanguineous pedigrees with autism are enriched for autosomal recessive causes similar to other congenital neurological disorders in consanguineous populations.”
The research team stated that although their findings support recent studies that suggest autism is highly heterogeneous genetically, homozygosity mapping appears to be an effective way to find underlying shared mechanisms. Understanding these genetic underpinnings could eventually help direct various therapies for the different clinical manifestations of autism.
“Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism,” the researchers concluded. In addition, their “data implicating noncoding elements in patients with shared ancestry, as well as the heterozygous nonsense changes in patients without shared ancestry, suggest that loss of proper regulation of gene dosage may be an important genetic mechanism in autism.”

Seemingly diverse autism mutations may share the same underlying mechanism, according to Eric M. Morrow, MD, PhD, Instructor in Psychiatry at Harvard Medical School in Boston, and colleagues.
“The regulation of expression of some autism candidate genes by neuronal membrane depolarization suggests the appealing hypothesis that neural activity–dependent regulation of synapse development may be a mechanism common to several autism mutations,” stated Dr. Morrow and colleagues in the July 11 Science. “Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.”
The researchers studied 88 large families—in which both parents shared recent ancestors—to find inherited causes of autism spectrum disorders. The families, who came from Jordan, Saudi Arabia, Kuwait, Oman, Pakistan, Qatar, Turkey, and the United Arab Emirates, were selected to emphasize the role of inherited genetic mutations.
The investigators gathered data with use of homozygosity mapping and compared the DNA of family members with and without autism to identify recessive mutations. Most individuals exhibited different genetic causes with little overlap between families, but a few exceptions were observed.
“Although the large size of linked loci precluded systemic gene sequencing in most cases, we were surprised to see that several consanguineous pedigrees showed large, rare, inherited homozygous deletions within linked regions, some of which are very likely causative mutations,” Dr. Morrow and colleagues said. Specifically, such deletions linked to autism were found in five families, or 6.4% of the study sample. Family members with one remaining functional copy of their genome segments did not have autism, while those with both copies missing did have autism.
The investigators found six gene disruptions that contributed to autism spectrum disorders. The largest of these gene disruptions involved genes essential for learning in the brain, as they are regulated either directly or indirectly by neuronal activity triggered by experience. Not all the genes were deleted—the remaining genes were simply turned off, leaving room for therapies to possibly turn these genes back on.
“Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity,” the investigators stated. “In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation.... The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development.”
The researchers’ findings also pointed to potential genetic similarities, such as inherited recessive causes, between autism and other neurologic disorders. Among families in the present study who had one member with autism, there was a relatively equivalent male/female ratio compared with other families with autism, indicating that parents who shared a common recent ancestor was a determining factor. In families with more than one member with autism, the male/female ratio was even more balanced.
“The accumulating number of distinct, individually rare genetic causes in autism suggests that the genetic architecture of autism resembles that of mental retardation and epilepsy, with many syndromes, each individually rare, as well as other cases potentially reflecting complex interactions between inherited changes,” Dr. Morrow and colleagues elaborated. “The relatively reduced male/female ratio of affected children and the reduced rate of linked de novo copy number variants in the consanguineous sample [of the present study] ... both suggest that consanguineous pedigrees with autism are enriched for autosomal recessive causes similar to other congenital neurological disorders in consanguineous populations.”
The research team stated that although their findings support recent studies that suggest autism is highly heterogeneous genetically, homozygosity mapping appears to be an effective way to find underlying shared mechanisms. Understanding these genetic underpinnings could eventually help direct various therapies for the different clinical manifestations of autism.
“Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism,” the researchers concluded. In addition, their “data implicating noncoding elements in patients with shared ancestry, as well as the heterozygous nonsense changes in patients without shared ancestry, suggest that loss of proper regulation of gene dosage may be an important genetic mechanism in autism.”

FAILED HOME BIRTH, NOW IN THE ED

You are at the hospital, caring for your patients in labor, when a 32-year-old G3P2 with two prior cesarean section deliveries is brought to the emergency department in labor after a failed home birth.

“Will you assume care for this woman?” the nursing administrator asks you. Quickly! What would you do?

29%  Assume her care and recommend cesarean section

46%  Assume her care and recommend cesarean section—plus, later, report the responsible midwife to the department of public health and her credentialing organization

18%  Agree to assume her care as long as the hospital’s attorney and risk management team indemnify you

FAILED HOME BIRTH, NOW IN THE ED

You are at the hospital, caring for your patients in labor, when a 32-year-old G3P2 with two prior cesarean section deliveries is brought to the emergency department in labor after a failed home birth.

“Will you assume care for this woman?” the nursing administrator asks you. Quickly! What would you do?

29%  Assume her care and recommend cesarean section

46%  Assume her care and recommend cesarean section—plus, later, report the responsible midwife to the department of public health and her credentialing organization

18%  Agree to assume her care as long as the hospital’s attorney and risk management team indemnify you

FAILED HOME BIRTH, NOW IN THE ED

You are at the hospital, caring for your patients in labor, when a 32-year-old G3P2 with two prior cesarean section deliveries is brought to the emergency department in labor after a failed home birth.

“Will you assume care for this woman?” the nursing administrator asks you. Quickly! What would you do?

29%  Assume her care and recommend cesarean section

46%  Assume her care and recommend cesarean section—plus, later, report the responsible midwife to the department of public health and her credentialing organization

18%  Agree to assume her care as long as the hospital’s attorney and risk management team indemnify you

The author reports no financial relationships relevant to this article.

OBs get codes for unremarkable sonograms ordered on the basis of suspicion. For gyn practice, options expand for abnormal Pap smear results. Here are the details.

Revisions and additions to the International Classification of Diseases, Clinical Modification (ICD-9-CM) for 2009, which take effect on October 1, 2008, bring especially good news to obstetricians who are testing for “conditions not found,” evaluating or treating twin-to-twin transfusion syndrome, dealing with the aftermath of maternal surgery, and providing the correct diagnostic code match for screening tests.

Gyn practitioners, don’t feel slighted: Many new codes take effect on that October day, covering abnormal Pap smear results, prophylactic drug treatment, breast conditions, and taking a patient’s personal history.

Remember: 1) October 1 is the key date here—when all the new and revised codes described in this article (and others not reviewed here) are added to the national code set, and 2) as in past years, there will be no grace period!

New and revised OB codes

FOR “CONDITIONS NOT FOUND”

How many times have you ordered a sonogram for a suspected problem with a pregnancy, only to have the scan reveal that all is normal? You then had to use either 1) a screening code for the condition or 2) an unspecified code because you could not assign a code that gave a condition to the patient that she did not have.

With addition of a new category of codes (V89), this obstetrical problem will be solved.

V89.01  Suspected problem with amniotic cavity and membrane not found

V89.02  Suspected placenta not found

V89.03  Suspected fetal anomaly not found

V89.04  Suspected problem with fetal growth not found

V89.05  Suspected cervical shortening not found

V89.09  Other suspected maternal and fetal condition not found

CERVICAL SHORTENING

Women undergo cervical shortening normally as their body prepares for labor, of course, but, on occasion, cervical shortening can indicate impending premature birth. Until now, you might have reflected this condition with 654.5x (Cervical incompetence complicating pregnancy), 654.6x (Other congenital or acquired abnormality of cervix), or 644.1x (Other threatened labor). Starting October 1, however, you’ll have a more precise code available to report this condition: 649.7x (Cervical shortening).

HIGH-RISK PREGNANCY

The V23 category of codes, which represent supervision of high-risk pregnancy, becomes more specific with two additions: V23.85 (Pregnancy resulting from assisted reproductive technology) and V23.86 (Pregnancy with history of in utero procedure during previous pregnancy).

ANTENATAL SCREENING

How to select the right code to report a screening test has been less than clear. Were you performing it to screen for malformation of a fetus? Some other reason? Three new antenatal codes and revision of an existing code (V28.3) clarify the distinction.

V28.3  Encounter for routine screening for malformation using ultrasonics

V28.81  Encounter for fetal anatomic survey

V28.82  Encounter for screening for risk of preterm labor

V28.89  Other specified antenatal screening

ICD-9-CM now directs that the latter code, V28.89, be reported for screening as part of chorionic villus sampling, nuchal translucency testing, genomic screening, and proteomic screening.

COMPLICATIONS OF PREGNANCY AND IN UTERO PROCEDURES

At last, you have a specific code for fetal conjoined twins (678.1x) and one for such fetal hematologic conditions as fetal anemia, thrombocytopenia, and twin-to-twin transfusion syndrome (678.0x).

In addition, complications from an in utero procedure will have two new codes: 679.0x (Maternal complications from in utero procedure) and 679.1x (Fetal complications from in utero procedure).

Gynecologic code changes and additions

ABNORMAL RESULTS OF A PAP SMEAR

You already know to look at the 795 series for ICD-9 codes to support various abnormal Pap smear results; after October 1, you’ll have a lot of new options.

Key developments:

• The risk of dysplasia and carcinoma is the same for the anus as it is for the cervix, so physicians can take anal cytologic smears.
  
• The cervix and the anus both have transformation zones where mucosa turns from squamous to columnar, so parallel codes have been created for anal smears.
  

The new codes are listed below.

CERVIX

795.07  Satisfactory cervical smear but lacking transformation zone

VAGINA AND VULVA

795.10  Abnormal Papanicolaou smear of vagina

795.11  Papanicolaou smear of vagina with atypical squamous cells of undetermined significance (ASC-US)

795.12  Papanicolaou smear of vagina with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

795.13  Papanicolaou smear of vagina with low grade squamous intraepithelial lesion (LGSIL)

795.14  Papanicolaou smear of vagina with high grade squamous intraepithelial lesion (HGSIL)

795.15  Vaginal high risk papillomavirus (HPV) DNA test positive

795.16  Papanicolaou smear of vagina with cytologic evidence of malignancy

795.18  Unsatisfactory cytology smear

795.19  Other abnormal smear of vagina and vaginal HPV

ANUS

796.70  Abnormal glandular Papanicolaou smear of anus

796.71  Papanicolaou smear of anus with atypical squamous cells of undetermined significance (ASC-US)

796.72  Papanicolaou smear of anus with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

796.73  Papanicolaou smear of anus with low grade squamous intraepithelial lesion (LGSIL)

796.74  Papanicolaou smear of anus with high grade squamous intraepithelial lesion (HGSIL)

796.75  Anal high risk human papillomavirus (HPV) DNA test positive

796.76  Papanicolaou smear of anus with cytologic evidence of malignancy

796.77  Satisfactory anal smear but lacking transformation zone

796.78  Unsatisfactory anal cytology smear

796.79  Other abnormal Papanicolaou smear of anus and anal HPV

There is also a new code, 569.44 (Dysplasia of anus), to report anal dysplasia. In the past, this condition was reported using 569.49 (Other specified disorders of rectum and anus).

ACQUIRED ABSENCE CODES

Until now, only V45.77 (Acquired absence of genital organs) could be used to report this patient status. As of October 1, you’ll have to be more specific about what is absent, using any of the following three new codes. You might find these codes helpful in supporting the performance of screening Pap smears:

V88.01  Acquired absence of both cervix and uterus

V88.02  Acquired absence of uterus with remaining cervical stump

V88.03  Acquired absence of cervix with remaining uterus

These new codes can be reported in conjunction with V67.01 (Follow-up vaginal Pap smear) and V76.47 (Special screening for malignant neoplasm of vagina).

URINARY PROBLEMS

Use these three new codes to report various presentations of hematuria:

599.70  Hematuria, unspecified

599.71  Gross hematuria

599.72  Microscopic hematuria

Note: The old code for hematuria (599.7) did not require a fifth digit; after October 1, using that old code will trigger a denial of your claim.

In addition, you have two new codes with which to report urinary symptoms:

788.91  Functional urinary incontinence

788.99  Other symptoms involving urinary symptoms

VULVODYNIA AND VULVAR VESTIBULITIS

A single code (625.8) has been available to describe vulvodynia, and it was grouped into a general category that covered symptoms. This condition has been given three new codes.

625.70  Vulvodynia, unspecified

625.71  Vulvar vestibulitis

625.79  Other vulvodynia

BREAST DISORDERS

New codes for breast conditions are about to take effect. These include ptosis (611.81), hypoplasia (611.82), and other disorders of the breast, such as capsular contracture of a breast implant (611.89).

For surgeons who handle follow-up after breast surgery, two new codes describe problems with the reconstructed breast: 612.0 (Deformity of reconstructed breast) and 612.1 (Disproportion of reconstructed breast).

WOUND DISRUPTION

Under current ICD-9-CM guidelines, you must specify “external wound” or “internal wound” to code correctly for dehiscence. On October 1, you have the option to report an unspecified code, 998.30 (Disruption of wound, unspecified) if the record does not specify the type of wound.

PROPHYLACTIC USE OF AGENTS AFFECTING ESTROGEN RECEPTORS AND ESTROGEN LEVELS

ICD-9-CM created a V code to capture data on the many women who receive tamoxifen and raloxifene after treatment of breast cancer. This code has been expanded to include V codes for different classes of drugs used for this type of therapy:

V07.51  Prophylactic use of selective estrogen receptor modulators (SERMs)

V07.52  Prophylactic use of aromatase inhibitors

V07.59  Prophylactic use of agents affecting estrogen receptors and estrogen levels

From a guideline perspective, you can use the cancer code with one of these codes throughout the course of treatment, including during routine chemotherapy and radiation therapy. Long-term use of a drug that falls under the V07.5x category doesn’t require continued use of the cancer code, however.

You can provide additional information on your patient by reporting her estrogen receptor-positive status (V86.0), personal or family history of breast cancer (V10.3/V16.3), genetic susceptibility to cancer (V84.01–V84.09), and postmenopausal status (V49.81).

TAKING A PERSONAL HISTORY

This year, 11 codes make their debut to allow you to report a patient’s personal history. Use them for encounters in which the personal history has a direct impact on the patient’s complaints or status.

V13.51  Personal history of pathologic fracture

V13.52  Personal history of stress fracture

V13.59  Personal history of other musculoskeletal disorders

V15.51  Personal history of traumatic fracture

V15.59  Personal history of other injury

V15.21  Personal history of undergoing in utero procedure during pregnancy

V15.22  Personal history of undergoing in utero procedure while a fetus

V15.29  Personal history of surgery to other organs

V87.41  Personal history of antineoplastic chemotherapy

V87.42  Personal history of monoclonal drug therapy

V87.49  Personal history of other drug therapy

The author reports no financial relationships relevant to this article.

OBs get codes for unremarkable sonograms ordered on the basis of suspicion. For gyn practice, options expand for abnormal Pap smear results. Here are the details.

Revisions and additions to the International Classification of Diseases, Clinical Modification (ICD-9-CM) for 2009, which take effect on October 1, 2008, bring especially good news to obstetricians who are testing for “conditions not found,” evaluating or treating twin-to-twin transfusion syndrome, dealing with the aftermath of maternal surgery, and providing the correct diagnostic code match for screening tests.

Gyn practitioners, don’t feel slighted: Many new codes take effect on that October day, covering abnormal Pap smear results, prophylactic drug treatment, breast conditions, and taking a patient’s personal history.

Remember: 1) October 1 is the key date here—when all the new and revised codes described in this article (and others not reviewed here) are added to the national code set, and 2) as in past years, there will be no grace period!

New and revised OB codes

FOR “CONDITIONS NOT FOUND”

How many times have you ordered a sonogram for a suspected problem with a pregnancy, only to have the scan reveal that all is normal? You then had to use either 1) a screening code for the condition or 2) an unspecified code because you could not assign a code that gave a condition to the patient that she did not have.

With addition of a new category of codes (V89), this obstetrical problem will be solved.

V89.01  Suspected problem with amniotic cavity and membrane not found

V89.02  Suspected placenta not found

V89.03  Suspected fetal anomaly not found

V89.04  Suspected problem with fetal growth not found

V89.05  Suspected cervical shortening not found

V89.09  Other suspected maternal and fetal condition not found

CERVICAL SHORTENING

Women undergo cervical shortening normally as their body prepares for labor, of course, but, on occasion, cervical shortening can indicate impending premature birth. Until now, you might have reflected this condition with 654.5x (Cervical incompetence complicating pregnancy), 654.6x (Other congenital or acquired abnormality of cervix), or 644.1x (Other threatened labor). Starting October 1, however, you’ll have a more precise code available to report this condition: 649.7x (Cervical shortening).

HIGH-RISK PREGNANCY

The V23 category of codes, which represent supervision of high-risk pregnancy, becomes more specific with two additions: V23.85 (Pregnancy resulting from assisted reproductive technology) and V23.86 (Pregnancy with history of in utero procedure during previous pregnancy).

ANTENATAL SCREENING

How to select the right code to report a screening test has been less than clear. Were you performing it to screen for malformation of a fetus? Some other reason? Three new antenatal codes and revision of an existing code (V28.3) clarify the distinction.

V28.3  Encounter for routine screening for malformation using ultrasonics

V28.81  Encounter for fetal anatomic survey

V28.82  Encounter for screening for risk of preterm labor

V28.89  Other specified antenatal screening

ICD-9-CM now directs that the latter code, V28.89, be reported for screening as part of chorionic villus sampling, nuchal translucency testing, genomic screening, and proteomic screening.

COMPLICATIONS OF PREGNANCY AND IN UTERO PROCEDURES

At last, you have a specific code for fetal conjoined twins (678.1x) and one for such fetal hematologic conditions as fetal anemia, thrombocytopenia, and twin-to-twin transfusion syndrome (678.0x).

In addition, complications from an in utero procedure will have two new codes: 679.0x (Maternal complications from in utero procedure) and 679.1x (Fetal complications from in utero procedure).

Gynecologic code changes and additions

ABNORMAL RESULTS OF A PAP SMEAR

You already know to look at the 795 series for ICD-9 codes to support various abnormal Pap smear results; after October 1, you’ll have a lot of new options.

Key developments:

• The risk of dysplasia and carcinoma is the same for the anus as it is for the cervix, so physicians can take anal cytologic smears.
  
• The cervix and the anus both have transformation zones where mucosa turns from squamous to columnar, so parallel codes have been created for anal smears.
  

The new codes are listed below.

CERVIX

795.07  Satisfactory cervical smear but lacking transformation zone

VAGINA AND VULVA

795.10  Abnormal Papanicolaou smear of vagina

795.11  Papanicolaou smear of vagina with atypical squamous cells of undetermined significance (ASC-US)

795.12  Papanicolaou smear of vagina with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

795.13  Papanicolaou smear of vagina with low grade squamous intraepithelial lesion (LGSIL)

795.14  Papanicolaou smear of vagina with high grade squamous intraepithelial lesion (HGSIL)

795.15  Vaginal high risk papillomavirus (HPV) DNA test positive

795.16  Papanicolaou smear of vagina with cytologic evidence of malignancy

795.18  Unsatisfactory cytology smear

795.19  Other abnormal smear of vagina and vaginal HPV

ANUS

796.70  Abnormal glandular Papanicolaou smear of anus

796.71  Papanicolaou smear of anus with atypical squamous cells of undetermined significance (ASC-US)

796.72  Papanicolaou smear of anus with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

796.73  Papanicolaou smear of anus with low grade squamous intraepithelial lesion (LGSIL)

796.74  Papanicolaou smear of anus with high grade squamous intraepithelial lesion (HGSIL)

796.75  Anal high risk human papillomavirus (HPV) DNA test positive

796.76  Papanicolaou smear of anus with cytologic evidence of malignancy

796.77  Satisfactory anal smear but lacking transformation zone

796.78  Unsatisfactory anal cytology smear

796.79  Other abnormal Papanicolaou smear of anus and anal HPV

There is also a new code, 569.44 (Dysplasia of anus), to report anal dysplasia. In the past, this condition was reported using 569.49 (Other specified disorders of rectum and anus).

ACQUIRED ABSENCE CODES

Until now, only V45.77 (Acquired absence of genital organs) could be used to report this patient status. As of October 1, you’ll have to be more specific about what is absent, using any of the following three new codes. You might find these codes helpful in supporting the performance of screening Pap smears:

V88.01  Acquired absence of both cervix and uterus

V88.02  Acquired absence of uterus with remaining cervical stump

V88.03  Acquired absence of cervix with remaining uterus

These new codes can be reported in conjunction with V67.01 (Follow-up vaginal Pap smear) and V76.47 (Special screening for malignant neoplasm of vagina).

URINARY PROBLEMS

Use these three new codes to report various presentations of hematuria:

599.70  Hematuria, unspecified

599.71  Gross hematuria

599.72  Microscopic hematuria

Note: The old code for hematuria (599.7) did not require a fifth digit; after October 1, using that old code will trigger a denial of your claim.

In addition, you have two new codes with which to report urinary symptoms:

788.91  Functional urinary incontinence

788.99  Other symptoms involving urinary symptoms

VULVODYNIA AND VULVAR VESTIBULITIS

A single code (625.8) has been available to describe vulvodynia, and it was grouped into a general category that covered symptoms. This condition has been given three new codes.

625.70  Vulvodynia, unspecified

625.71  Vulvar vestibulitis

625.79  Other vulvodynia

BREAST DISORDERS

New codes for breast conditions are about to take effect. These include ptosis (611.81), hypoplasia (611.82), and other disorders of the breast, such as capsular contracture of a breast implant (611.89).

For surgeons who handle follow-up after breast surgery, two new codes describe problems with the reconstructed breast: 612.0 (Deformity of reconstructed breast) and 612.1 (Disproportion of reconstructed breast).

WOUND DISRUPTION

Under current ICD-9-CM guidelines, you must specify “external wound” or “internal wound” to code correctly for dehiscence. On October 1, you have the option to report an unspecified code, 998.30 (Disruption of wound, unspecified) if the record does not specify the type of wound.

PROPHYLACTIC USE OF AGENTS AFFECTING ESTROGEN RECEPTORS AND ESTROGEN LEVELS

ICD-9-CM created a V code to capture data on the many women who receive tamoxifen and raloxifene after treatment of breast cancer. This code has been expanded to include V codes for different classes of drugs used for this type of therapy:

V07.51  Prophylactic use of selective estrogen receptor modulators (SERMs)

V07.52  Prophylactic use of aromatase inhibitors

V07.59  Prophylactic use of agents affecting estrogen receptors and estrogen levels

From a guideline perspective, you can use the cancer code with one of these codes throughout the course of treatment, including during routine chemotherapy and radiation therapy. Long-term use of a drug that falls under the V07.5x category doesn’t require continued use of the cancer code, however.

You can provide additional information on your patient by reporting her estrogen receptor-positive status (V86.0), personal or family history of breast cancer (V10.3/V16.3), genetic susceptibility to cancer (V84.01–V84.09), and postmenopausal status (V49.81).

TAKING A PERSONAL HISTORY

This year, 11 codes make their debut to allow you to report a patient’s personal history. Use them for encounters in which the personal history has a direct impact on the patient’s complaints or status.

V13.51  Personal history of pathologic fracture

V13.52  Personal history of stress fracture

V13.59  Personal history of other musculoskeletal disorders

V15.51  Personal history of traumatic fracture

V15.59  Personal history of other injury

V15.21  Personal history of undergoing in utero procedure during pregnancy

V15.22  Personal history of undergoing in utero procedure while a fetus

V15.29  Personal history of surgery to other organs

V87.41  Personal history of antineoplastic chemotherapy

V87.42  Personal history of monoclonal drug therapy

V87.49  Personal history of other drug therapy

The author reports no financial relationships relevant to this article.

OBs get codes for unremarkable sonograms ordered on the basis of suspicion. For gyn practice, options expand for abnormal Pap smear results. Here are the details.

Revisions and additions to the International Classification of Diseases, Clinical Modification (ICD-9-CM) for 2009, which take effect on October 1, 2008, bring especially good news to obstetricians who are testing for “conditions not found,” evaluating or treating twin-to-twin transfusion syndrome, dealing with the aftermath of maternal surgery, and providing the correct diagnostic code match for screening tests.

Gyn practitioners, don’t feel slighted: Many new codes take effect on that October day, covering abnormal Pap smear results, prophylactic drug treatment, breast conditions, and taking a patient’s personal history.

Remember: 1) October 1 is the key date here—when all the new and revised codes described in this article (and others not reviewed here) are added to the national code set, and 2) as in past years, there will be no grace period!

New and revised OB codes

FOR “CONDITIONS NOT FOUND”

How many times have you ordered a sonogram for a suspected problem with a pregnancy, only to have the scan reveal that all is normal? You then had to use either 1) a screening code for the condition or 2) an unspecified code because you could not assign a code that gave a condition to the patient that she did not have.

With addition of a new category of codes (V89), this obstetrical problem will be solved.

V89.01  Suspected problem with amniotic cavity and membrane not found

V89.02  Suspected placenta not found

V89.03  Suspected fetal anomaly not found

V89.04  Suspected problem with fetal growth not found

V89.05  Suspected cervical shortening not found

V89.09  Other suspected maternal and fetal condition not found

CERVICAL SHORTENING

Women undergo cervical shortening normally as their body prepares for labor, of course, but, on occasion, cervical shortening can indicate impending premature birth. Until now, you might have reflected this condition with 654.5x (Cervical incompetence complicating pregnancy), 654.6x (Other congenital or acquired abnormality of cervix), or 644.1x (Other threatened labor). Starting October 1, however, you’ll have a more precise code available to report this condition: 649.7x (Cervical shortening).

HIGH-RISK PREGNANCY

The V23 category of codes, which represent supervision of high-risk pregnancy, becomes more specific with two additions: V23.85 (Pregnancy resulting from assisted reproductive technology) and V23.86 (Pregnancy with history of in utero procedure during previous pregnancy).

ANTENATAL SCREENING

How to select the right code to report a screening test has been less than clear. Were you performing it to screen for malformation of a fetus? Some other reason? Three new antenatal codes and revision of an existing code (V28.3) clarify the distinction.

V28.3  Encounter for routine screening for malformation using ultrasonics

V28.81  Encounter for fetal anatomic survey

V28.82  Encounter for screening for risk of preterm labor

V28.89  Other specified antenatal screening

ICD-9-CM now directs that the latter code, V28.89, be reported for screening as part of chorionic villus sampling, nuchal translucency testing, genomic screening, and proteomic screening.

COMPLICATIONS OF PREGNANCY AND IN UTERO PROCEDURES

At last, you have a specific code for fetal conjoined twins (678.1x) and one for such fetal hematologic conditions as fetal anemia, thrombocytopenia, and twin-to-twin transfusion syndrome (678.0x).

In addition, complications from an in utero procedure will have two new codes: 679.0x (Maternal complications from in utero procedure) and 679.1x (Fetal complications from in utero procedure).

Gynecologic code changes and additions

ABNORMAL RESULTS OF A PAP SMEAR

You already know to look at the 795 series for ICD-9 codes to support various abnormal Pap smear results; after October 1, you’ll have a lot of new options.

Key developments:

• The risk of dysplasia and carcinoma is the same for the anus as it is for the cervix, so physicians can take anal cytologic smears.
  
• The cervix and the anus both have transformation zones where mucosa turns from squamous to columnar, so parallel codes have been created for anal smears.
  

The new codes are listed below.

CERVIX

795.07  Satisfactory cervical smear but lacking transformation zone

VAGINA AND VULVA

795.10  Abnormal Papanicolaou smear of vagina

795.11  Papanicolaou smear of vagina with atypical squamous cells of undetermined significance (ASC-US)

795.12  Papanicolaou smear of vagina with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

795.13  Papanicolaou smear of vagina with low grade squamous intraepithelial lesion (LGSIL)

795.14  Papanicolaou smear of vagina with high grade squamous intraepithelial lesion (HGSIL)

795.15  Vaginal high risk papillomavirus (HPV) DNA test positive

795.16  Papanicolaou smear of vagina with cytologic evidence of malignancy

795.18  Unsatisfactory cytology smear

795.19  Other abnormal smear of vagina and vaginal HPV

ANUS

796.70  Abnormal glandular Papanicolaou smear of anus

796.71  Papanicolaou smear of anus with atypical squamous cells of undetermined significance (ASC-US)

796.72  Papanicolaou smear of anus with atypical squamous cells cannot exclude high grade squamous intraepithelial lesion (ASC-H)

796.73  Papanicolaou smear of anus with low grade squamous intraepithelial lesion (LGSIL)

796.74  Papanicolaou smear of anus with high grade squamous intraepithelial lesion (HGSIL)

796.75  Anal high risk human papillomavirus (HPV) DNA test positive

796.76  Papanicolaou smear of anus with cytologic evidence of malignancy

796.77  Satisfactory anal smear but lacking transformation zone

796.78  Unsatisfactory anal cytology smear

796.79  Other abnormal Papanicolaou smear of anus and anal HPV

There is also a new code, 569.44 (Dysplasia of anus), to report anal dysplasia. In the past, this condition was reported using 569.49 (Other specified disorders of rectum and anus).

ACQUIRED ABSENCE CODES

Until now, only V45.77 (Acquired absence of genital organs) could be used to report this patient status. As of October 1, you’ll have to be more specific about what is absent, using any of the following three new codes. You might find these codes helpful in supporting the performance of screening Pap smears:

V88.01  Acquired absence of both cervix and uterus

V88.02  Acquired absence of uterus with remaining cervical stump

V88.03  Acquired absence of cervix with remaining uterus

These new codes can be reported in conjunction with V67.01 (Follow-up vaginal Pap smear) and V76.47 (Special screening for malignant neoplasm of vagina).

URINARY PROBLEMS

Use these three new codes to report various presentations of hematuria:

599.70  Hematuria, unspecified

599.71  Gross hematuria

599.72  Microscopic hematuria

Note: The old code for hematuria (599.7) did not require a fifth digit; after October 1, using that old code will trigger a denial of your claim.

In addition, you have two new codes with which to report urinary symptoms:

788.91  Functional urinary incontinence

788.99  Other symptoms involving urinary symptoms

VULVODYNIA AND VULVAR VESTIBULITIS

A single code (625.8) has been available to describe vulvodynia, and it was grouped into a general category that covered symptoms. This condition has been given three new codes.

625.70  Vulvodynia, unspecified

625.71  Vulvar vestibulitis

625.79  Other vulvodynia

BREAST DISORDERS

New codes for breast conditions are about to take effect. These include ptosis (611.81), hypoplasia (611.82), and other disorders of the breast, such as capsular contracture of a breast implant (611.89).

For surgeons who handle follow-up after breast surgery, two new codes describe problems with the reconstructed breast: 612.0 (Deformity of reconstructed breast) and 612.1 (Disproportion of reconstructed breast).

WOUND DISRUPTION

Under current ICD-9-CM guidelines, you must specify “external wound” or “internal wound” to code correctly for dehiscence. On October 1, you have the option to report an unspecified code, 998.30 (Disruption of wound, unspecified) if the record does not specify the type of wound.

PROPHYLACTIC USE OF AGENTS AFFECTING ESTROGEN RECEPTORS AND ESTROGEN LEVELS

ICD-9-CM created a V code to capture data on the many women who receive tamoxifen and raloxifene after treatment of breast cancer. This code has been expanded to include V codes for different classes of drugs used for this type of therapy:

V07.51  Prophylactic use of selective estrogen receptor modulators (SERMs)

V07.52  Prophylactic use of aromatase inhibitors

V07.59  Prophylactic use of agents affecting estrogen receptors and estrogen levels

From a guideline perspective, you can use the cancer code with one of these codes throughout the course of treatment, including during routine chemotherapy and radiation therapy. Long-term use of a drug that falls under the V07.5x category doesn’t require continued use of the cancer code, however.

You can provide additional information on your patient by reporting her estrogen receptor-positive status (V86.0), personal or family history of breast cancer (V10.3/V16.3), genetic susceptibility to cancer (V84.01–V84.09), and postmenopausal status (V49.81).

TAKING A PERSONAL HISTORY

This year, 11 codes make their debut to allow you to report a patient’s personal history. Use them for encounters in which the personal history has a direct impact on the patient’s complaints or status.

V13.51  Personal history of pathologic fracture

V13.52  Personal history of stress fracture

V13.59  Personal history of other musculoskeletal disorders

V15.51  Personal history of traumatic fracture

V15.59  Personal history of other injury

V15.21  Personal history of undergoing in utero procedure during pregnancy

V15.22  Personal history of undergoing in utero procedure while a fetus

V15.29  Personal history of surgery to other organs

V87.41  Personal history of antineoplastic chemotherapy

V87.42  Personal history of monoclonal drug therapy

V87.49  Personal history of other drug therapy

ILLUSTRATIVE CASE

A 48-year-old man comes to your office for a routine physical. He has a 30 pack-year smoking history. When you talk to him about smoking cessation, he tells you he’s tried to stop more than once, but he can’t seem to stay motivated. You find no evidence of chronic lung disease and do not perform spirometry screening. (The US Preventive Services Task Force does not recommend spirometry for asymptomatic patients.) But could spirometry have therapeutic value in this case?

Smoking is the leading modifiable risk factor for mortality in the United States,² and smoking cessation is the most effective intervention. Nortriptyline, bupropion, nicotine replacement agents, and varenicline are effective pharmacological treatments.³ Adding counseling to medication significantly improves quit rates (estimated odds ratio [OR]=1.4; 95% confidence interval [CI], 1.2-1.6).³ Nonetheless, physicians’ efforts to help patients stop smoking frequently fail.

But another option has caught—and held—the attention of researchers.

The promise of biomarkers

It has long been suspected that presenting smokers with evidence of tobacco’s harmful effect on their bodies—biomarkers—might encourage them to stop. Biomarkers that have been tested in randomized controlled trials (RCTs) include spirometry, exhaled carbon monoxide measurement, ultrasonography of carotid and femoral arteries, and genetic susceptibility to lung cancer, as well as combinations of these markers. But the results of most biomarker studies have been disappointing. A 2005 Cochrane Database review found insufficient evidence of the effectiveness of these markers in boosting quit rates.⁴

Lung age, a biomarker that’s easily understood

Lung age, a clever presentation of spirometry results, had not been tested in an RCT prior to the study we summarize below. Defined in 1985, lung age refers to the average age of a nonsmoker with a forced expiratory volume at 1 second (FEV₁) equal to that of the person being tested ( FIGURE 1 ). The primary purpose was to make spirometry results easier for patients to understand, but researchers also envisioned it as a way to demonstrate the premature lung damage suffered as a consequence of smoking.⁵

FIGURE 1
Translating FEV₁ into lung age¹

STUDY SUMMARY: Graphic display more effective than FEV₁ results

This study was a well-done, multicenter RCT evaluating the effect on tobacco quit rates of informing adult smokers of their lung age.¹ Smokers ages 35 and older from 5 general practices in England were invited to participate. The authors excluded patients using oxygen and those with a history of tuberculosis, lung cancer, asbestosis, bronchiectasis, silicosis, or pneumonectomy. The study included 561 participants with an average of 33 pack-years of smoking, who underwent spirometry before being divided into an intervention or a control group. The researchers used standardized instruments to confirm the baseline comparability of the 2 groups.

Subjects in both groups were given information about local smoking cessation clinics and strongly encouraged to quit. All were told that their lung function would be retested in 12 months.

The controls received letters with their spirometry results presented as FEV₁. In contrast, participants in the intervention group received the results in the form of a computer-generated graphic display of lung age ( FIGURE 2 ), which was further explained by a health care worker. They also received a letter within 1 month containing the same data. Participants were evaluated for smoking cessation at 12 months, and those who reported quitting received confirmatory carbon monoxide breath testing and salivary cotinine testing. Eleven percent of the subjects were lost to follow-up.

FIGURE 2
Lung age helps spirometry pack a bigger punch

Quit rates higher when patients know lung age

At 1 year, verified quit rates were 13.6% in the intervention group and 6.4% in the control group (a difference of 7.2%, 95% CI, 2.2%-12.1%; P=.005). This means that for every 14 smokers who are told their lung age and shown a graphic display of this biomarker, 1 additional smoker will quit after 1 year.

Contrary to what might be expected, the investigators found that quitting did not depend on the degree of lung damage. Patients with both normal and abnormal lung age quit smoking at similar rates.

WHAT’S NEW: Lung age resonates more than spirometry alone

This is the first RCT demonstrating that informing smokers of their lung age can help them quit, and the first well-designed study to demonstrate improved cessation rates using a physiological biomarker. The research also suggests that successful quitting may have less to do with spirometry results—the level of severity of lung damage it shows—than with the way the results are presented. Giving patients information about their lung function in an easily understandable format, the authors observe, appears to result in higher quit rates.

CAVEATS: Young smokers weren’t studied

The study did not test to see if this intervention would work in younger adults, as only those 35 years of age and older were enrolled. This is a single study, and it is possible that the findings cannot be generalized to other groups or are due to unmeasured confounding factors. However, the intervention is unlikely to cause any significant harm, so we see no risks associated with it other than the cost of spirometry.

CHALLENGES TO IMPLEMENTATION: Time and expense of spirometry

We suspect the biggest challenges to implementing this recommendation in clinical practice are the expense of obtaining a spirometer ( TABLE ), staff training for those practices without one, and the time needed for the intervention. The average time to perform spirometry on study participants was 30 minutes; a health care worker spent, on average, another 15 minutes reviewing results with each member of the intervention group.

Another challenge: Not all spirometers calculate lung age or can create a graphic similar to FIGURE 2 . However, any FEV₁ measurement, whether it is generated by formal pulmonary function testing or by an inexpensive hand-held meter, can easily be converted to lung age using the formula shown in FIGURE 1 . If desired, the same elements—the patient’s age, height, and gender as well as FEV₁—could also be used to create a computer-generated graphic display.

TABLE
Spirometry: equipment costs

This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.

PURL METHODOLOGY
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 48-year-old man comes to your office for a routine physical. He has a 30 pack-year smoking history. When you talk to him about smoking cessation, he tells you he’s tried to stop more than once, but he can’t seem to stay motivated. You find no evidence of chronic lung disease and do not perform spirometry screening. (The US Preventive Services Task Force does not recommend spirometry for asymptomatic patients.) But could spirometry have therapeutic value in this case?

Smoking is the leading modifiable risk factor for mortality in the United States,² and smoking cessation is the most effective intervention. Nortriptyline, bupropion, nicotine replacement agents, and varenicline are effective pharmacological treatments.³ Adding counseling to medication significantly improves quit rates (estimated odds ratio [OR]=1.4; 95% confidence interval [CI], 1.2-1.6).³ Nonetheless, physicians’ efforts to help patients stop smoking frequently fail.

But another option has caught—and held—the attention of researchers.

The promise of biomarkers

It has long been suspected that presenting smokers with evidence of tobacco’s harmful effect on their bodies—biomarkers—might encourage them to stop. Biomarkers that have been tested in randomized controlled trials (RCTs) include spirometry, exhaled carbon monoxide measurement, ultrasonography of carotid and femoral arteries, and genetic susceptibility to lung cancer, as well as combinations of these markers. But the results of most biomarker studies have been disappointing. A 2005 Cochrane Database review found insufficient evidence of the effectiveness of these markers in boosting quit rates.⁴

Lung age, a biomarker that’s easily understood

Lung age, a clever presentation of spirometry results, had not been tested in an RCT prior to the study we summarize below. Defined in 1985, lung age refers to the average age of a nonsmoker with a forced expiratory volume at 1 second (FEV₁) equal to that of the person being tested ( FIGURE 1 ). The primary purpose was to make spirometry results easier for patients to understand, but researchers also envisioned it as a way to demonstrate the premature lung damage suffered as a consequence of smoking.⁵

FIGURE 1
Translating FEV₁ into lung age¹

STUDY SUMMARY: Graphic display more effective than FEV₁ results

This study was a well-done, multicenter RCT evaluating the effect on tobacco quit rates of informing adult smokers of their lung age.¹ Smokers ages 35 and older from 5 general practices in England were invited to participate. The authors excluded patients using oxygen and those with a history of tuberculosis, lung cancer, asbestosis, bronchiectasis, silicosis, or pneumonectomy. The study included 561 participants with an average of 33 pack-years of smoking, who underwent spirometry before being divided into an intervention or a control group. The researchers used standardized instruments to confirm the baseline comparability of the 2 groups.

Subjects in both groups were given information about local smoking cessation clinics and strongly encouraged to quit. All were told that their lung function would be retested in 12 months.

The controls received letters with their spirometry results presented as FEV₁. In contrast, participants in the intervention group received the results in the form of a computer-generated graphic display of lung age ( FIGURE 2 ), which was further explained by a health care worker. They also received a letter within 1 month containing the same data. Participants were evaluated for smoking cessation at 12 months, and those who reported quitting received confirmatory carbon monoxide breath testing and salivary cotinine testing. Eleven percent of the subjects were lost to follow-up.

FIGURE 2
Lung age helps spirometry pack a bigger punch

Quit rates higher when patients know lung age

At 1 year, verified quit rates were 13.6% in the intervention group and 6.4% in the control group (a difference of 7.2%, 95% CI, 2.2%-12.1%; P=.005). This means that for every 14 smokers who are told their lung age and shown a graphic display of this biomarker, 1 additional smoker will quit after 1 year.

Contrary to what might be expected, the investigators found that quitting did not depend on the degree of lung damage. Patients with both normal and abnormal lung age quit smoking at similar rates.

WHAT’S NEW: Lung age resonates more than spirometry alone

This is the first RCT demonstrating that informing smokers of their lung age can help them quit, and the first well-designed study to demonstrate improved cessation rates using a physiological biomarker. The research also suggests that successful quitting may have less to do with spirometry results—the level of severity of lung damage it shows—than with the way the results are presented. Giving patients information about their lung function in an easily understandable format, the authors observe, appears to result in higher quit rates.

CAVEATS: Young smokers weren’t studied

The study did not test to see if this intervention would work in younger adults, as only those 35 years of age and older were enrolled. This is a single study, and it is possible that the findings cannot be generalized to other groups or are due to unmeasured confounding factors. However, the intervention is unlikely to cause any significant harm, so we see no risks associated with it other than the cost of spirometry.

CHALLENGES TO IMPLEMENTATION: Time and expense of spirometry

We suspect the biggest challenges to implementing this recommendation in clinical practice are the expense of obtaining a spirometer ( TABLE ), staff training for those practices without one, and the time needed for the intervention. The average time to perform spirometry on study participants was 30 minutes; a health care worker spent, on average, another 15 minutes reviewing results with each member of the intervention group.

Another challenge: Not all spirometers calculate lung age or can create a graphic similar to FIGURE 2 . However, any FEV₁ measurement, whether it is generated by formal pulmonary function testing or by an inexpensive hand-held meter, can easily be converted to lung age using the formula shown in FIGURE 1 . If desired, the same elements—the patient’s age, height, and gender as well as FEV₁—could also be used to create a computer-generated graphic display.

TABLE
Spirometry: equipment costs

This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.

PURL METHODOLOGY
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 48-year-old man comes to your office for a routine physical. He has a 30 pack-year smoking history. When you talk to him about smoking cessation, he tells you he’s tried to stop more than once, but he can’t seem to stay motivated. You find no evidence of chronic lung disease and do not perform spirometry screening. (The US Preventive Services Task Force does not recommend spirometry for asymptomatic patients.) But could spirometry have therapeutic value in this case?

Smoking is the leading modifiable risk factor for mortality in the United States,² and smoking cessation is the most effective intervention. Nortriptyline, bupropion, nicotine replacement agents, and varenicline are effective pharmacological treatments.³ Adding counseling to medication significantly improves quit rates (estimated odds ratio [OR]=1.4; 95% confidence interval [CI], 1.2-1.6).³ Nonetheless, physicians’ efforts to help patients stop smoking frequently fail.

But another option has caught—and held—the attention of researchers.

The promise of biomarkers

It has long been suspected that presenting smokers with evidence of tobacco’s harmful effect on their bodies—biomarkers—might encourage them to stop. Biomarkers that have been tested in randomized controlled trials (RCTs) include spirometry, exhaled carbon monoxide measurement, ultrasonography of carotid and femoral arteries, and genetic susceptibility to lung cancer, as well as combinations of these markers. But the results of most biomarker studies have been disappointing. A 2005 Cochrane Database review found insufficient evidence of the effectiveness of these markers in boosting quit rates.⁴

Lung age, a biomarker that’s easily understood

Lung age, a clever presentation of spirometry results, had not been tested in an RCT prior to the study we summarize below. Defined in 1985, lung age refers to the average age of a nonsmoker with a forced expiratory volume at 1 second (FEV₁) equal to that of the person being tested ( FIGURE 1 ). The primary purpose was to make spirometry results easier for patients to understand, but researchers also envisioned it as a way to demonstrate the premature lung damage suffered as a consequence of smoking.⁵

FIGURE 1
Translating FEV₁ into lung age¹

STUDY SUMMARY: Graphic display more effective than FEV₁ results

This study was a well-done, multicenter RCT evaluating the effect on tobacco quit rates of informing adult smokers of their lung age.¹ Smokers ages 35 and older from 5 general practices in England were invited to participate. The authors excluded patients using oxygen and those with a history of tuberculosis, lung cancer, asbestosis, bronchiectasis, silicosis, or pneumonectomy. The study included 561 participants with an average of 33 pack-years of smoking, who underwent spirometry before being divided into an intervention or a control group. The researchers used standardized instruments to confirm the baseline comparability of the 2 groups.

Subjects in both groups were given information about local smoking cessation clinics and strongly encouraged to quit. All were told that their lung function would be retested in 12 months.

The controls received letters with their spirometry results presented as FEV₁. In contrast, participants in the intervention group received the results in the form of a computer-generated graphic display of lung age ( FIGURE 2 ), which was further explained by a health care worker. They also received a letter within 1 month containing the same data. Participants were evaluated for smoking cessation at 12 months, and those who reported quitting received confirmatory carbon monoxide breath testing and salivary cotinine testing. Eleven percent of the subjects were lost to follow-up.

FIGURE 2
Lung age helps spirometry pack a bigger punch

Quit rates higher when patients know lung age

At 1 year, verified quit rates were 13.6% in the intervention group and 6.4% in the control group (a difference of 7.2%, 95% CI, 2.2%-12.1%; P=.005). This means that for every 14 smokers who are told their lung age and shown a graphic display of this biomarker, 1 additional smoker will quit after 1 year.

Contrary to what might be expected, the investigators found that quitting did not depend on the degree of lung damage. Patients with both normal and abnormal lung age quit smoking at similar rates.

WHAT’S NEW: Lung age resonates more than spirometry alone

This is the first RCT demonstrating that informing smokers of their lung age can help them quit, and the first well-designed study to demonstrate improved cessation rates using a physiological biomarker. The research also suggests that successful quitting may have less to do with spirometry results—the level of severity of lung damage it shows—than with the way the results are presented. Giving patients information about their lung function in an easily understandable format, the authors observe, appears to result in higher quit rates.

CAVEATS: Young smokers weren’t studied

The study did not test to see if this intervention would work in younger adults, as only those 35 years of age and older were enrolled. This is a single study, and it is possible that the findings cannot be generalized to other groups or are due to unmeasured confounding factors. However, the intervention is unlikely to cause any significant harm, so we see no risks associated with it other than the cost of spirometry.

CHALLENGES TO IMPLEMENTATION: Time and expense of spirometry

We suspect the biggest challenges to implementing this recommendation in clinical practice are the expense of obtaining a spirometer ( TABLE ), staff training for those practices without one, and the time needed for the intervention. The average time to perform spirometry on study participants was 30 minutes; a health care worker spent, on average, another 15 minutes reviewing results with each member of the intervention group.

Another challenge: Not all spirometers calculate lung age or can create a graphic similar to FIGURE 2 . However, any FEV₁ measurement, whether it is generated by formal pulmonary function testing or by an inexpensive hand-held meter, can easily be converted to lung age using the formula shown in FIGURE 1 . If desired, the same elements—the patient’s age, height, and gender as well as FEV₁—could also be used to create a computer-generated graphic display.

TABLE
Spirometry: equipment costs

This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.

PURL METHODOLOGY
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

JJ, a 4-year-old boy, was taken to an urgent care clinic 3 times last winter for “recurrent bronchitis” and given a 7-day course of prednisone and antibiotics at each visit. His mother reports that “his colds always seem to go to his chest” and his skin is always dry. She was given a nebulizer and albuterol for use when JJ begins wheezing, which often happens when he has a cold, plays vigorously, or visits a friend who has cats.

JJ is one of approximately 6.7 million children—and 22.9 million US residents—who have asthma.¹ To help guide the care of patients like JJ, the National Heart, Lung, and Blood Institute (NHLBI) and National Asthma Education and Prevention Program (NAEPP) released the third expert panel report (EPR-3) in 2007. Available at http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm, the EPR-3 provides the most comprehensive evidence-based guidance for the diagnosis and management of asthma to date.²

The guidelines were an invaluable resource for JJ’s family physician, who referred to them to categorize the severity of JJ’s asthma as “mild persistent.” In initiating treatment, JJ’s physician relied on specific recommendations for children 0 to 4 years of age to prescribe low-dose inhaled corticosteroids (ICS). Without the new guidelines, which underscore the safety of controller medication for young children, JJ’s physician would likely have been reluctant to place a 4-year-old on ICS.

This review highlights the EPR-3’s key recommendations to encourage widespread implementation by family physicians.

The EPR-3: What’s changed

The 2007 guidelines:
Recommend assessing asthma severity before starting treatment and assessing asthma control to guide adjustments in treatment.
Address both severity and control in terms of impairment and risk.
Feature 3 age breakdowns (0-4 years, 5-11 years, and ≥12 years) and a 6-step approach to asthma management.
Make it easier to individualize and adjust treatment.

What’s changed?

There’s a new paradigm

The 2007 update to guidelines released in 1997 and 2002 reflects a paradigm shift in the overall approach to asthma management. The change in focus addresses the highly variable nature of asthma² and the recognition that asthma severity and asthma control are distinct concepts serving different functions in clinical practice.

Severity and control in 2 domains. Asthma severity—a measure of the intrinsic intensity of the disease process—is ideally assessed before initiating treatment. In contrast, asthma control is monitored over time to guide adjustments to therapy. The guidelines call for assessing severity and control within the domains of:

• impairment, based on asthma symptoms (identified by patient or caregiver recall of the past 2-4 weeks), quality of life, and functional limitations; and
• risk, of asthma exacerbations, progressive decline in pulmonary function (or reduced lung growth in children), or adverse events. Predictors of increased risk for exacerbations or death include persistent and/or severe airflow obstruction; at least 2 visits to the emergency department or hospitalizations for asthma within the past year; and a history of intubation or admission to intensive care, especially within the past 5 years.

The specific criteria for determining asthma severity and assessing asthma control are detailed in FIGURES 1 AND 2, respectively. Because treatment affects impairment and risk differently, this dual assessment helps ensure that therapeutic interventions minimize all manifestations of asthma as much as possible.

More steps and age-specific interventions. The EPR-3’s stepwise approach to asthma therapy has gone from 4 steps to 6, and the recommended treatments, as well as the levels of severity and criteria for assessing control that guide them, are now divided into 3 age groups: 0 to 4 years, 5 to 11 years, and ≥12 years (FIGURE 3). The previous guidelines, issued in 2002, divided treatment recommendations into 2 age groups: ≤5 years and >5 years. The EPR-3’s expansion makes it easier for physicians to initiate, individualize, and adjust treatment.

FIGURE 1
Classifying asthma severity and initiating therapy in children, adolescents, and adults

FIGURE 2
Assessing asthma control and adjusting therapy

FIGURE 3
Stepwise approach for managing asthma

Putting guidelines into practice begins with the history

A detailed medical history and a physical examination focusing on the upper respiratory tract, chest, and skin are needed to arrive at an asthma diagnosis. JJ’s physician asked his mother to describe recent symptoms and inquired about comorbid conditions that can aggravate asthma. He also identified viral respiratory infections, environmental causes, and activity as precipitating factors.

In considering an asthma diagnosis, try to determine the presence of episodic symptoms of airflow obstruction or bronchial hyperresponsiveness, as well as airflow obstruction that is at least partly reversible (an increase in forced expiratory volume in 1 second [FEV₁] of >200 mL and ≥12% from baseline or an increase of ≥10% of predicted FEV₁), and to exclude alternative diagnoses.

EPR-3 emphasizes spirometry

Recognizing that patients’ perception of airflow obstruction is highly variable and that pulmonary function measures do not always correlate directly with symptoms,^3,4 the EPR-3 recommends spirometry for patients ≥5 years of age, both before and after bronchodilation. In addition to helping to confirm an asthma diagnosis, spirometry is the preferred measure of pulmonary function in classifying severity, because peak expiratory flow (PEF) testing has not proven reliable.^5,6

Objective measurement of pulmonary function is difficult to obtain in children <5 years of age. If diagnosis remains uncertain for patients in this age group, a therapeutic trial of medication is recommended. In JJ’s case, however, 3 courses of oral corticosteroids (OCS) in less than 6 months were indicative of persistent asthma.

Spirometry is often underutilized. For patients ≥5 years of age, spirometry is a vital tool, but often underutilized in family practice. A recent study by Yawn and colleagues found that family physicians made changes in the management of approximately half of the asthma patients who underwent spirometry.⁷ (Information about spirometry training is available through the National Institute for Occupational Safety and Health at http://www.cdc.gov/niosh.) Referral to a specialist is recommended if the physician has difficulty making a differential diagnosis or is unable to perform spirometry on a patient who presents with atypical signs and symptoms of asthma.

What is the patient’s level of severity?

In patients who are not yet receiving long-term controller therapy, severity level is based on an assessment of impairment and risk (FIGURE 1). For patients who are already receiving treatment, severity is determined by the minimum pharmacologic therapy needed to maintain asthma control.

The severity classification—intermittent asthma or persistent asthma that is mild, moderate, or severe—is determined by the most severe category in which any feature occurs. (In children, FEV₁/FVC [forced vital capacity] ratio has been shown to be a more sensitive determinant of severity than FEV₁,⁴ which may be more useful in predicting exacerbations.⁸)

Asthma management: Preferred and alternative Tx

The recommended stepwise interventions include both preferred therapies (evidence-based) and alternative treatments (listed alphabetically in FIGURE 3 because there is insufficient evidence to rank them). The additional steps and age categories support the goal of using the least possible medication needed to maintain good control and minimize the potential for adverse events.

In initiating treatment, select the step that corresponds to the level of severity in the bottom row of FIGURE 1; to adjust medications, determine the patient’s level of asthma control and follow the corresponding guidance in the bottom row of FIGURE 2.

Inhaled corticosteroids remain the bedrock of therapy

ICS, the most potent and consistently effective long-term controller therapy, remain the foundation of therapy for patients of all ages who have persistent asthma. (Evidence: A).

Several of the age-based recommendations follow, with a focus on preferred treatments:

Children 0 to 4 years of age

• The guidelines recommend low-dose ICS at Step 2 (Evidence: A) and medium-dose ICS at Step 3 (Evidence: D), as inhaled corticosteroids have been shown to reduce impairment and risk in this age group.^9-16 The potential risk is generally limited to a small reduction in growth velocity during the first year of treatment, and offset by the benefits of therapy.^15,16
• Add a long-acting β₂-adrenergic agonist (LABA) or montelukast to medium-dose ICS therapy at Step 4 rather than increasing the ICS dose (Evidence: D) to avoid the risk of side effects associated with high-dose ICS. Montelukast has demonstrated efficacy in children 2 to 5 years of age with persistent asthma.¹⁷
• Recommendations for preferred therapy at Steps 5 (high-dose ICS + LABA or montelukast) and 6 (Step 5 therapy + OCS) are based on expert panel judgment (Evidence: D). When severe persistent asthma warrants Step 6 therapy, start with a 2-week course of the lowest possible dose of OCS to confirm reversibility.
• In this age group, a therapeutic trial with close monitoring is recommended for patients whose asthma is not well controlled. If there is no response in 4 to 6 weeks, consider alternative therapies or diagnoses (Evidence: D).

Children 5 to 11 years of age

• For Step 3 therapy, the guidelines recommend either low-dose ICS plus a LABA, leukotriene receptor antagonist (LTRA), or theophylline; or medium-dose ICS (Evidence: B). Treatment decisions at Step 3 depend on whether impairment or risk is the chief concern, as well as on safety considerations.
• For Steps 4 and 5, ICS (medium dose for Step 5 and high dose for Step 6) plus a LABA is preferred, based on studies of patients ≥12 years of age (Evidence: B). Step 6 builds on Step 5, adding an OCS to the LABA/ICS combination (Evidence: D).
• If theophylline is prescribed—a viable option if cost and adherence to inhaled medications are key concerns—serum levels must be closely monitored because of the risk of toxicity.
• Closely monitor and be prepared to identify and respond to anaphylaxis in a child at Step 2, 3, or 4 who is receiving allergen immunotherapy.

Adolescents ≥12 years of age and adults

• There are 2 preferred Step 3 treatments: Low-dose ICS plus a LABA, or medium-dose ICS. The combination therapy has shown greater improvement in impairment^24,25 and risk^24-26 compared with the higher dose of ICS.
• Preferred treatments at Steps 4, 5, and 6 are the same as those for children ages 5 to 11 years, with one exception: Subcutaneous anti-IgE therapy (omalizumab) may be added to the regimen at Steps 5 and 6 for adolescents and adults with severe persistent allergic asthma to reduce the risk of exacerbations.²⁷

Weigh the benefits and risks of therapy

Safety is a key consideration for all asthma patients. Carefully weigh the benefits and risks of therapy, including the rare but potential risk of life-threatening or fatal exacerbations with daily LABA therapy²⁸ and systemic effects with higher doses of ICS.²³ Patients who begin receiving oral corticosteroids require close monitoring, regardless of age.

Regular reassessment and monitoring are critical

Schedule visits at 2- to 6-week intervals for those who are starting therapy or require a step up to achieve or regain asthma control. After control is achieved, reassess at least every 1 to 6 months. Measures of asthma control are the same as those used to assess severity, with the addition of validated multidimensional questionnaires (eg, Asthma Control Test [ACT])²⁹ to gauge impairment.

JJ’s physician scheduled a follow-up visit in 4 weeks, at which time he did a reassessment based on a physical exam and symptom recall. Finding JJ’s asthma to be well controlled, the physician asked the boy’s mother to bring him back to the office in 2 months, or earlier if symptoms recurred.

TABLE W1
Asthma education resources

Does your patient require a step down or step up?

A step down is recommended for patients whose asthma is well controlled for 3 months or more. Reduce the dose of ICS gradually, about 25% to 50% every 3 months, because deterioration in asthma control is highly variable. Review adherence and medication administration technique with patients whose asthma is not well controlled, and consider a step up in treatment. If an alternative treatment is used but does not result in an adequate response, it should be discontinued and the preferred treatment used before stepping up. Refer patients to an asthma specialist if their asthma does not respond to these adjustments.

Partner with patients for optimal care

The EPR-3 recommends the integration of patient education into all aspects of asthma care. To forge an active partnership, identify and address concerns about the condition and its treatment and involve the patient and family in developing treatment goals and making treatment decisions. If the patient is old enough, encourage self-monitoring and management.

The EPR-3 recommends that physicians give every patient a written asthma action plan that addresses individual symptoms and/or PEF measurements and includes instructions for self-management. Daily PEF monitoring can be useful in identifying early changes in the disease state and evaluating response to changes in therapy. It is ideal for those who have moderate to severe persistent asthma, difficulty recognizing signs of exacerbations, or a history of severe exacerbations.

Correspondence
Stuart W. Stoloff, MD, Clinical Professor, Department of Family and Community Medicine, University of Nevada–Reno, 1200 Mountain Street, Suite 220, Carson City, NV 89703; drstoloff@sbcglobal.net.

JJ, a 4-year-old boy, was taken to an urgent care clinic 3 times last winter for “recurrent bronchitis” and given a 7-day course of prednisone and antibiotics at each visit. His mother reports that “his colds always seem to go to his chest” and his skin is always dry. She was given a nebulizer and albuterol for use when JJ begins wheezing, which often happens when he has a cold, plays vigorously, or visits a friend who has cats.

JJ is one of approximately 6.7 million children—and 22.9 million US residents—who have asthma.¹ To help guide the care of patients like JJ, the National Heart, Lung, and Blood Institute (NHLBI) and National Asthma Education and Prevention Program (NAEPP) released the third expert panel report (EPR-3) in 2007. Available at http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm, the EPR-3 provides the most comprehensive evidence-based guidance for the diagnosis and management of asthma to date.²

The guidelines were an invaluable resource for JJ’s family physician, who referred to them to categorize the severity of JJ’s asthma as “mild persistent.” In initiating treatment, JJ’s physician relied on specific recommendations for children 0 to 4 years of age to prescribe low-dose inhaled corticosteroids (ICS). Without the new guidelines, which underscore the safety of controller medication for young children, JJ’s physician would likely have been reluctant to place a 4-year-old on ICS.

This review highlights the EPR-3’s key recommendations to encourage widespread implementation by family physicians.

The EPR-3: What’s changed

The 2007 guidelines:
Recommend assessing asthma severity before starting treatment and assessing asthma control to guide adjustments in treatment.
Address both severity and control in terms of impairment and risk.
Feature 3 age breakdowns (0-4 years, 5-11 years, and ≥12 years) and a 6-step approach to asthma management.
Make it easier to individualize and adjust treatment.

What’s changed?

There’s a new paradigm

The 2007 update to guidelines released in 1997 and 2002 reflects a paradigm shift in the overall approach to asthma management. The change in focus addresses the highly variable nature of asthma² and the recognition that asthma severity and asthma control are distinct concepts serving different functions in clinical practice.

Severity and control in 2 domains. Asthma severity—a measure of the intrinsic intensity of the disease process—is ideally assessed before initiating treatment. In contrast, asthma control is monitored over time to guide adjustments to therapy. The guidelines call for assessing severity and control within the domains of:

• impairment, based on asthma symptoms (identified by patient or caregiver recall of the past 2-4 weeks), quality of life, and functional limitations; and
• risk, of asthma exacerbations, progressive decline in pulmonary function (or reduced lung growth in children), or adverse events. Predictors of increased risk for exacerbations or death include persistent and/or severe airflow obstruction; at least 2 visits to the emergency department or hospitalizations for asthma within the past year; and a history of intubation or admission to intensive care, especially within the past 5 years.

The specific criteria for determining asthma severity and assessing asthma control are detailed in FIGURES 1 AND 2, respectively. Because treatment affects impairment and risk differently, this dual assessment helps ensure that therapeutic interventions minimize all manifestations of asthma as much as possible.

More steps and age-specific interventions. The EPR-3’s stepwise approach to asthma therapy has gone from 4 steps to 6, and the recommended treatments, as well as the levels of severity and criteria for assessing control that guide them, are now divided into 3 age groups: 0 to 4 years, 5 to 11 years, and ≥12 years (FIGURE 3). The previous guidelines, issued in 2002, divided treatment recommendations into 2 age groups: ≤5 years and >5 years. The EPR-3’s expansion makes it easier for physicians to initiate, individualize, and adjust treatment.

FIGURE 1
Classifying asthma severity and initiating therapy in children, adolescents, and adults

FIGURE 2
Assessing asthma control and adjusting therapy

FIGURE 3
Stepwise approach for managing asthma

Putting guidelines into practice begins with the history

A detailed medical history and a physical examination focusing on the upper respiratory tract, chest, and skin are needed to arrive at an asthma diagnosis. JJ’s physician asked his mother to describe recent symptoms and inquired about comorbid conditions that can aggravate asthma. He also identified viral respiratory infections, environmental causes, and activity as precipitating factors.

In considering an asthma diagnosis, try to determine the presence of episodic symptoms of airflow obstruction or bronchial hyperresponsiveness, as well as airflow obstruction that is at least partly reversible (an increase in forced expiratory volume in 1 second [FEV₁] of >200 mL and ≥12% from baseline or an increase of ≥10% of predicted FEV₁), and to exclude alternative diagnoses.

EPR-3 emphasizes spirometry

Recognizing that patients’ perception of airflow obstruction is highly variable and that pulmonary function measures do not always correlate directly with symptoms,^3,4 the EPR-3 recommends spirometry for patients ≥5 years of age, both before and after bronchodilation. In addition to helping to confirm an asthma diagnosis, spirometry is the preferred measure of pulmonary function in classifying severity, because peak expiratory flow (PEF) testing has not proven reliable.^5,6

Objective measurement of pulmonary function is difficult to obtain in children <5 years of age. If diagnosis remains uncertain for patients in this age group, a therapeutic trial of medication is recommended. In JJ’s case, however, 3 courses of oral corticosteroids (OCS) in less than 6 months were indicative of persistent asthma.

Spirometry is often underutilized. For patients ≥5 years of age, spirometry is a vital tool, but often underutilized in family practice. A recent study by Yawn and colleagues found that family physicians made changes in the management of approximately half of the asthma patients who underwent spirometry.⁷ (Information about spirometry training is available through the National Institute for Occupational Safety and Health at http://www.cdc.gov/niosh.) Referral to a specialist is recommended if the physician has difficulty making a differential diagnosis or is unable to perform spirometry on a patient who presents with atypical signs and symptoms of asthma.

What is the patient’s level of severity?

In patients who are not yet receiving long-term controller therapy, severity level is based on an assessment of impairment and risk (FIGURE 1). For patients who are already receiving treatment, severity is determined by the minimum pharmacologic therapy needed to maintain asthma control.

The severity classification—intermittent asthma or persistent asthma that is mild, moderate, or severe—is determined by the most severe category in which any feature occurs. (In children, FEV₁/FVC [forced vital capacity] ratio has been shown to be a more sensitive determinant of severity than FEV₁,⁴ which may be more useful in predicting exacerbations.⁸)

Asthma management: Preferred and alternative Tx

The recommended stepwise interventions include both preferred therapies (evidence-based) and alternative treatments (listed alphabetically in FIGURE 3 because there is insufficient evidence to rank them). The additional steps and age categories support the goal of using the least possible medication needed to maintain good control and minimize the potential for adverse events.

In initiating treatment, select the step that corresponds to the level of severity in the bottom row of FIGURE 1; to adjust medications, determine the patient’s level of asthma control and follow the corresponding guidance in the bottom row of FIGURE 2.

Inhaled corticosteroids remain the bedrock of therapy

ICS, the most potent and consistently effective long-term controller therapy, remain the foundation of therapy for patients of all ages who have persistent asthma. (Evidence: A).

Several of the age-based recommendations follow, with a focus on preferred treatments:

Children 0 to 4 years of age

• The guidelines recommend low-dose ICS at Step 2 (Evidence: A) and medium-dose ICS at Step 3 (Evidence: D), as inhaled corticosteroids have been shown to reduce impairment and risk in this age group.^9-16 The potential risk is generally limited to a small reduction in growth velocity during the first year of treatment, and offset by the benefits of therapy.^15,16
• Add a long-acting β₂-adrenergic agonist (LABA) or montelukast to medium-dose ICS therapy at Step 4 rather than increasing the ICS dose (Evidence: D) to avoid the risk of side effects associated with high-dose ICS. Montelukast has demonstrated efficacy in children 2 to 5 years of age with persistent asthma.¹⁷
• Recommendations for preferred therapy at Steps 5 (high-dose ICS + LABA or montelukast) and 6 (Step 5 therapy + OCS) are based on expert panel judgment (Evidence: D). When severe persistent asthma warrants Step 6 therapy, start with a 2-week course of the lowest possible dose of OCS to confirm reversibility.
• In this age group, a therapeutic trial with close monitoring is recommended for patients whose asthma is not well controlled. If there is no response in 4 to 6 weeks, consider alternative therapies or diagnoses (Evidence: D).

Children 5 to 11 years of age

• For Step 3 therapy, the guidelines recommend either low-dose ICS plus a LABA, leukotriene receptor antagonist (LTRA), or theophylline; or medium-dose ICS (Evidence: B). Treatment decisions at Step 3 depend on whether impairment or risk is the chief concern, as well as on safety considerations.
• For Steps 4 and 5, ICS (medium dose for Step 5 and high dose for Step 6) plus a LABA is preferred, based on studies of patients ≥12 years of age (Evidence: B). Step 6 builds on Step 5, adding an OCS to the LABA/ICS combination (Evidence: D).
• If theophylline is prescribed—a viable option if cost and adherence to inhaled medications are key concerns—serum levels must be closely monitored because of the risk of toxicity.
• Closely monitor and be prepared to identify and respond to anaphylaxis in a child at Step 2, 3, or 4 who is receiving allergen immunotherapy.

Adolescents ≥12 years of age and adults

• There are 2 preferred Step 3 treatments: Low-dose ICS plus a LABA, or medium-dose ICS. The combination therapy has shown greater improvement in impairment^24,25 and risk^24-26 compared with the higher dose of ICS.
• Preferred treatments at Steps 4, 5, and 6 are the same as those for children ages 5 to 11 years, with one exception: Subcutaneous anti-IgE therapy (omalizumab) may be added to the regimen at Steps 5 and 6 for adolescents and adults with severe persistent allergic asthma to reduce the risk of exacerbations.²⁷

Weigh the benefits and risks of therapy

Safety is a key consideration for all asthma patients. Carefully weigh the benefits and risks of therapy, including the rare but potential risk of life-threatening or fatal exacerbations with daily LABA therapy²⁸ and systemic effects with higher doses of ICS.²³ Patients who begin receiving oral corticosteroids require close monitoring, regardless of age.

Regular reassessment and monitoring are critical

Schedule visits at 2- to 6-week intervals for those who are starting therapy or require a step up to achieve or regain asthma control. After control is achieved, reassess at least every 1 to 6 months. Measures of asthma control are the same as those used to assess severity, with the addition of validated multidimensional questionnaires (eg, Asthma Control Test [ACT])²⁹ to gauge impairment.

JJ’s physician scheduled a follow-up visit in 4 weeks, at which time he did a reassessment based on a physical exam and symptom recall. Finding JJ’s asthma to be well controlled, the physician asked the boy’s mother to bring him back to the office in 2 months, or earlier if symptoms recurred.

TABLE W1
Asthma education resources

Does your patient require a step down or step up?

A step down is recommended for patients whose asthma is well controlled for 3 months or more. Reduce the dose of ICS gradually, about 25% to 50% every 3 months, because deterioration in asthma control is highly variable. Review adherence and medication administration technique with patients whose asthma is not well controlled, and consider a step up in treatment. If an alternative treatment is used but does not result in an adequate response, it should be discontinued and the preferred treatment used before stepping up. Refer patients to an asthma specialist if their asthma does not respond to these adjustments.

Partner with patients for optimal care

The EPR-3 recommends the integration of patient education into all aspects of asthma care. To forge an active partnership, identify and address concerns about the condition and its treatment and involve the patient and family in developing treatment goals and making treatment decisions. If the patient is old enough, encourage self-monitoring and management.

The EPR-3 recommends that physicians give every patient a written asthma action plan that addresses individual symptoms and/or PEF measurements and includes instructions for self-management. Daily PEF monitoring can be useful in identifying early changes in the disease state and evaluating response to changes in therapy. It is ideal for those who have moderate to severe persistent asthma, difficulty recognizing signs of exacerbations, or a history of severe exacerbations.

Correspondence
Stuart W. Stoloff, MD, Clinical Professor, Department of Family and Community Medicine, University of Nevada–Reno, 1200 Mountain Street, Suite 220, Carson City, NV 89703; drstoloff@sbcglobal.net.

JJ, a 4-year-old boy, was taken to an urgent care clinic 3 times last winter for “recurrent bronchitis” and given a 7-day course of prednisone and antibiotics at each visit. His mother reports that “his colds always seem to go to his chest” and his skin is always dry. She was given a nebulizer and albuterol for use when JJ begins wheezing, which often happens when he has a cold, plays vigorously, or visits a friend who has cats.

JJ is one of approximately 6.7 million children—and 22.9 million US residents—who have asthma.¹ To help guide the care of patients like JJ, the National Heart, Lung, and Blood Institute (NHLBI) and National Asthma Education and Prevention Program (NAEPP) released the third expert panel report (EPR-3) in 2007. Available at http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm, the EPR-3 provides the most comprehensive evidence-based guidance for the diagnosis and management of asthma to date.²

The guidelines were an invaluable resource for JJ’s family physician, who referred to them to categorize the severity of JJ’s asthma as “mild persistent.” In initiating treatment, JJ’s physician relied on specific recommendations for children 0 to 4 years of age to prescribe low-dose inhaled corticosteroids (ICS). Without the new guidelines, which underscore the safety of controller medication for young children, JJ’s physician would likely have been reluctant to place a 4-year-old on ICS.

This review highlights the EPR-3’s key recommendations to encourage widespread implementation by family physicians.

The EPR-3: What’s changed

The 2007 guidelines:
Recommend assessing asthma severity before starting treatment and assessing asthma control to guide adjustments in treatment.
Address both severity and control in terms of impairment and risk.
Feature 3 age breakdowns (0-4 years, 5-11 years, and ≥12 years) and a 6-step approach to asthma management.
Make it easier to individualize and adjust treatment.

What’s changed?

There’s a new paradigm

The 2007 update to guidelines released in 1997 and 2002 reflects a paradigm shift in the overall approach to asthma management. The change in focus addresses the highly variable nature of asthma² and the recognition that asthma severity and asthma control are distinct concepts serving different functions in clinical practice.

Severity and control in 2 domains. Asthma severity—a measure of the intrinsic intensity of the disease process—is ideally assessed before initiating treatment. In contrast, asthma control is monitored over time to guide adjustments to therapy. The guidelines call for assessing severity and control within the domains of:

• impairment, based on asthma symptoms (identified by patient or caregiver recall of the past 2-4 weeks), quality of life, and functional limitations; and
• risk, of asthma exacerbations, progressive decline in pulmonary function (or reduced lung growth in children), or adverse events. Predictors of increased risk for exacerbations or death include persistent and/or severe airflow obstruction; at least 2 visits to the emergency department or hospitalizations for asthma within the past year; and a history of intubation or admission to intensive care, especially within the past 5 years.

The specific criteria for determining asthma severity and assessing asthma control are detailed in FIGURES 1 AND 2, respectively. Because treatment affects impairment and risk differently, this dual assessment helps ensure that therapeutic interventions minimize all manifestations of asthma as much as possible.

More steps and age-specific interventions. The EPR-3’s stepwise approach to asthma therapy has gone from 4 steps to 6, and the recommended treatments, as well as the levels of severity and criteria for assessing control that guide them, are now divided into 3 age groups: 0 to 4 years, 5 to 11 years, and ≥12 years (FIGURE 3). The previous guidelines, issued in 2002, divided treatment recommendations into 2 age groups: ≤5 years and >5 years. The EPR-3’s expansion makes it easier for physicians to initiate, individualize, and adjust treatment.

FIGURE 1
Classifying asthma severity and initiating therapy in children, adolescents, and adults

FIGURE 2
Assessing asthma control and adjusting therapy

FIGURE 3
Stepwise approach for managing asthma

Putting guidelines into practice begins with the history

A detailed medical history and a physical examination focusing on the upper respiratory tract, chest, and skin are needed to arrive at an asthma diagnosis. JJ’s physician asked his mother to describe recent symptoms and inquired about comorbid conditions that can aggravate asthma. He also identified viral respiratory infections, environmental causes, and activity as precipitating factors.

In considering an asthma diagnosis, try to determine the presence of episodic symptoms of airflow obstruction or bronchial hyperresponsiveness, as well as airflow obstruction that is at least partly reversible (an increase in forced expiratory volume in 1 second [FEV₁] of >200 mL and ≥12% from baseline or an increase of ≥10% of predicted FEV₁), and to exclude alternative diagnoses.

EPR-3 emphasizes spirometry

Recognizing that patients’ perception of airflow obstruction is highly variable and that pulmonary function measures do not always correlate directly with symptoms,^3,4 the EPR-3 recommends spirometry for patients ≥5 years of age, both before and after bronchodilation. In addition to helping to confirm an asthma diagnosis, spirometry is the preferred measure of pulmonary function in classifying severity, because peak expiratory flow (PEF) testing has not proven reliable.^5,6

Objective measurement of pulmonary function is difficult to obtain in children <5 years of age. If diagnosis remains uncertain for patients in this age group, a therapeutic trial of medication is recommended. In JJ’s case, however, 3 courses of oral corticosteroids (OCS) in less than 6 months were indicative of persistent asthma.

Spirometry is often underutilized. For patients ≥5 years of age, spirometry is a vital tool, but often underutilized in family practice. A recent study by Yawn and colleagues found that family physicians made changes in the management of approximately half of the asthma patients who underwent spirometry.⁷ (Information about spirometry training is available through the National Institute for Occupational Safety and Health at http://www.cdc.gov/niosh.) Referral to a specialist is recommended if the physician has difficulty making a differential diagnosis or is unable to perform spirometry on a patient who presents with atypical signs and symptoms of asthma.

What is the patient’s level of severity?

In patients who are not yet receiving long-term controller therapy, severity level is based on an assessment of impairment and risk (FIGURE 1). For patients who are already receiving treatment, severity is determined by the minimum pharmacologic therapy needed to maintain asthma control.

The severity classification—intermittent asthma or persistent asthma that is mild, moderate, or severe—is determined by the most severe category in which any feature occurs. (In children, FEV₁/FVC [forced vital capacity] ratio has been shown to be a more sensitive determinant of severity than FEV₁,⁴ which may be more useful in predicting exacerbations.⁸)

Asthma management: Preferred and alternative Tx

The recommended stepwise interventions include both preferred therapies (evidence-based) and alternative treatments (listed alphabetically in FIGURE 3 because there is insufficient evidence to rank them). The additional steps and age categories support the goal of using the least possible medication needed to maintain good control and minimize the potential for adverse events.

In initiating treatment, select the step that corresponds to the level of severity in the bottom row of FIGURE 1; to adjust medications, determine the patient’s level of asthma control and follow the corresponding guidance in the bottom row of FIGURE 2.

Inhaled corticosteroids remain the bedrock of therapy

ICS, the most potent and consistently effective long-term controller therapy, remain the foundation of therapy for patients of all ages who have persistent asthma. (Evidence: A).

Several of the age-based recommendations follow, with a focus on preferred treatments:

Children 0 to 4 years of age

• The guidelines recommend low-dose ICS at Step 2 (Evidence: A) and medium-dose ICS at Step 3 (Evidence: D), as inhaled corticosteroids have been shown to reduce impairment and risk in this age group.^9-16 The potential risk is generally limited to a small reduction in growth velocity during the first year of treatment, and offset by the benefits of therapy.^15,16
• Add a long-acting β₂-adrenergic agonist (LABA) or montelukast to medium-dose ICS therapy at Step 4 rather than increasing the ICS dose (Evidence: D) to avoid the risk of side effects associated with high-dose ICS. Montelukast has demonstrated efficacy in children 2 to 5 years of age with persistent asthma.¹⁷
• Recommendations for preferred therapy at Steps 5 (high-dose ICS + LABA or montelukast) and 6 (Step 5 therapy + OCS) are based on expert panel judgment (Evidence: D). When severe persistent asthma warrants Step 6 therapy, start with a 2-week course of the lowest possible dose of OCS to confirm reversibility.
• In this age group, a therapeutic trial with close monitoring is recommended for patients whose asthma is not well controlled. If there is no response in 4 to 6 weeks, consider alternative therapies or diagnoses (Evidence: D).

Children 5 to 11 years of age

• For Step 3 therapy, the guidelines recommend either low-dose ICS plus a LABA, leukotriene receptor antagonist (LTRA), or theophylline; or medium-dose ICS (Evidence: B). Treatment decisions at Step 3 depend on whether impairment or risk is the chief concern, as well as on safety considerations.
• For Steps 4 and 5, ICS (medium dose for Step 5 and high dose for Step 6) plus a LABA is preferred, based on studies of patients ≥12 years of age (Evidence: B). Step 6 builds on Step 5, adding an OCS to the LABA/ICS combination (Evidence: D).
• If theophylline is prescribed—a viable option if cost and adherence to inhaled medications are key concerns—serum levels must be closely monitored because of the risk of toxicity.
• Closely monitor and be prepared to identify and respond to anaphylaxis in a child at Step 2, 3, or 4 who is receiving allergen immunotherapy.

Adolescents ≥12 years of age and adults

• There are 2 preferred Step 3 treatments: Low-dose ICS plus a LABA, or medium-dose ICS. The combination therapy has shown greater improvement in impairment^24,25 and risk^24-26 compared with the higher dose of ICS.
• Preferred treatments at Steps 4, 5, and 6 are the same as those for children ages 5 to 11 years, with one exception: Subcutaneous anti-IgE therapy (omalizumab) may be added to the regimen at Steps 5 and 6 for adolescents and adults with severe persistent allergic asthma to reduce the risk of exacerbations.²⁷

Weigh the benefits and risks of therapy

Safety is a key consideration for all asthma patients. Carefully weigh the benefits and risks of therapy, including the rare but potential risk of life-threatening or fatal exacerbations with daily LABA therapy²⁸ and systemic effects with higher doses of ICS.²³ Patients who begin receiving oral corticosteroids require close monitoring, regardless of age.

Regular reassessment and monitoring are critical

Schedule visits at 2- to 6-week intervals for those who are starting therapy or require a step up to achieve or regain asthma control. After control is achieved, reassess at least every 1 to 6 months. Measures of asthma control are the same as those used to assess severity, with the addition of validated multidimensional questionnaires (eg, Asthma Control Test [ACT])²⁹ to gauge impairment.

JJ’s physician scheduled a follow-up visit in 4 weeks, at which time he did a reassessment based on a physical exam and symptom recall. Finding JJ’s asthma to be well controlled, the physician asked the boy’s mother to bring him back to the office in 2 months, or earlier if symptoms recurred.

TABLE W1
Asthma education resources

Does your patient require a step down or step up?

A step down is recommended for patients whose asthma is well controlled for 3 months or more. Reduce the dose of ICS gradually, about 25% to 50% every 3 months, because deterioration in asthma control is highly variable. Review adherence and medication administration technique with patients whose asthma is not well controlled, and consider a step up in treatment. If an alternative treatment is used but does not result in an adequate response, it should be discontinued and the preferred treatment used before stepping up. Refer patients to an asthma specialist if their asthma does not respond to these adjustments.

Partner with patients for optimal care

The EPR-3 recommends the integration of patient education into all aspects of asthma care. To forge an active partnership, identify and address concerns about the condition and its treatment and involve the patient and family in developing treatment goals and making treatment decisions. If the patient is old enough, encourage self-monitoring and management.

The EPR-3 recommends that physicians give every patient a written asthma action plan that addresses individual symptoms and/or PEF measurements and includes instructions for self-management. Daily PEF monitoring can be useful in identifying early changes in the disease state and evaluating response to changes in therapy. It is ideal for those who have moderate to severe persistent asthma, difficulty recognizing signs of exacerbations, or a history of severe exacerbations.

Correspondence
Stuart W. Stoloff, MD, Clinical Professor, Department of Family and Community Medicine, University of Nevada–Reno, 1200 Mountain Street, Suite 220, Carson City, NV 89703; drstoloff@sbcglobal.net.

The viability of primary care in the United States is in question, attributable in large part to declining provider payments in the face of rising medical school debt and fee-for-service pressures to increase patient volume.^1-3 Congress—which has authority over Medicare and its price-setting function for provider reimbursement overall—is seemingly unaware of the problems facing primary care, including barriers to payment reform. The future of our specialty may hinge on our ability to persuade Congress that these problems are dire. A growing body of evidence supports the essential and integrative function primary care plays in health systems, and its positive impact on quality of care and costs.^4-6

The confused order of things now

Advantages of primary care are proven. Regions with higher ratios of primary care physicians relative to specialists have lower rates of hospitalizations, lower Medicare costs, and higher quality of care.^7,8 People with a primary care physician are more satisfied with their care and more likely to receive preventive services and better chronic disease management.^9-11 Most countries that have built their health care systems on a strong foundation of primary care demonstrate better health outcomes, fewer health care disparities, and lower costs.^4,6 Thus the waning of primary care presents risks to both personal and population health.

Still, society undervalues primary care. Despite evidence of the benefits just cited, the income disparity between primary care physicians and specialists continues to grow, discouraging medical students from entering primary care careers.¹² The Medical Group Management Association shows that between 2000 and 2004, the median income for a family physician increased 7.5% to $156,000; for invasive cardiologists, 16.9% to $428,000; and for diagnostic radiologists, 36.2% to $407,000. Adjusted for inflation, primary care income fell 10% from 1995 to 2004.¹³

No wonder students shy away from primary care. Though there is little public sympathy for the financial woes of primary care doctors, lower incomes are contributing to a drying of the primary care pipeline.^14,15 The number of US medical school graduates choosing family medicine residencies dropped by 50% between 1997 and 2005.¹⁶ From 1998 to 2004, the number of internal medicine residents choosing careers in primary care plummeted from 54% to 25%.^17,18 This waning interest in primary care coincides, unfortunately, with the aging of the US baby boomers and an increasing prevalence of chronic disease.

How Congress could help fix the disparity

Medicare reimbursement has 2 components that Congress could amend to narrow the payment gap and help open the primary care pipeline: the Sustainable Growth Rate (SGR) and the Resource-Based Relative Value Scale (RBRVS) process.

The SGR formula sets a target for Medicare physician expenditures each year. Recently, physician expenditure growth has exceeded the target and, by law, the difference is subtracted from the fees paid to all physicians. According to the Medicare Payment Advisory Commission (MedPAC), much of the excess spending has come from rapidly increasing volumes of procedures used by specialists.¹⁹ The SGR system therefore disproportionately penalizes primary care physicians because payments to all physicians are cut regardless of which specialties are responsible for excess spending.

RBRVS is the system of relative values applied to every procedure and office visit. The Relative Value Units (RVUs) for each procedure or office visit are multiplied by a conversion factor determined by the SGR formula. RVUs are largely governed by the Relative Value Scale Update Committee (RUC), which advises the Centers for Medicare and Medicaid Services (CMS) on revisions to physician reimbursement.

The RUC reviews the relative value scale at least every 5 years. Though primary care physicians provide about half of Medicare physician visits, they represent just 15% of the RUC’s voting members.¹²

The committee’s reevaluation process tends to raise some RVUs without sufficiently deflating others.²⁰ The resulting overall inflation of fees forces CMS to reduce payments equally to all physicians, meaning primary care is again disproportionately penalized. Moreover, both Medicare and private insurance companies follow the RUC’s recommendations.

Influencing Congress: Where to begin? As Congress escalates its deliberations on Medicare physician spending, we investigated how key legislators perceive issues in primary care and physician payment.

Methods

To better understand perspectives of congressional committees with jurisdiction over health care spending, we conducted semistructured key informant interviews in March 2007 with 14 health staff aides to members of Congress who have jurisdiction over Medicare. Interviews were done face to face and lasted 30 to 60 minutes.

The congressional committees with jurisdiction over Medicare physician payment are Senate Finance, House Ways and Means, and House Energy and Commerce. Each committee has 1 majority and 1 minority staffer specializing in Medicare part B, which includes physician payment. Of these 6 specialized staffers, 5 agreed to participate in semistructured interviews. Other staffers were contacted by using a purposeful sampling technique known as “snowballing” or chain-referral, whereby participants with whom contact has been made refer the researcher to other potential interviewees. This process yielded another 9 interviewees to total 14.

The aides identified several other information sources, and we interviewed 1 staff member each from 3 of these sources: MedPAC, the Congressional Budget Office (CBO), and the Government Accountability Office (GAO).

Interviews covered several topics, including views on the state of primary care and physician payment (TABLE). Three researchers separately reviewed the interview notes to identify and compile themes.

TABLE
6 Questions we asked the congressional staffers

Results

Of the 14 congressional staffers, 8 were Republican and 6 were Democrat; 5 were committee staff and 9 were general staff. Committee representation was fairly even among staffers: Senate Finance (4), House Ways and Means (5), and House Energy and Commerce (5). Range of experience on Capitol Hill was 3 months to 9 years.

Some staffers are empathetic, others unaware. Most respondents expressed concern about the decreasing number of students entering primary care careers and the potential impact on patient access to care. One staffer acknowledged, “the way our reimbursement system works, primary care is not an option for students…reimbursement is so low…the number of primary care physicians is going down relative to other specialties.”

Another participant added that most staffers “recognize a role for primary care. It’s also tough because of how strong the specialty community is.” One staffer advised, “The Alliance of Specialty Medicine goes along with the AMA, trying to represent a coordinated front…I don’t see this much coordination around primary care.”

A few staffers did not understand the definition of primary care or did not know which physician groups represent primary care.

Legislation to improve US health care—and primary care. Participants varied in their input on this subject. One staffer stated that primary care is “important but rarely singled out…usually the goal is broader reform so [primary care] is still a goal, but unstated.”

Some committee staff described the need to incentivize greater use of primary care and increase coordination of care. A few proposed reevaluating RBRVS to help primary care, and they spontaneously raised the Medical Home concept as a way to encourage growth of primary care. The Medical Home involves pairing each Medicare beneficiary with a patient-centered practice that meets certain criteria including continuity with a personal physician, care coordination, quality assurance, increased access, and specific payment.²¹ A pilot project in North Carolina that incorporates the Medical Home is saving the state about $162 million annually.^22,23 One staffer championed primary care, but pointed out that a critical barrier preventing Congress from investing in it is the CBO, which is not convinced that primary care can save money over the long term.

The SGR dominates discussions on physician payment

All respondents had a functional understanding of the SGR and desired reform, but few understood how the SGR contributes to the payment gap. Many staffers would like to do away with the SGR, but CBO estimates show that this would be cost-prohibitive.²⁴

A few staffers believed that SGR reform may not happen until 2009, after the next president takes office. Some participants also predicted that SGR reform will not happen until more physicians refuse to see Medicare patients. To date, MedPAC has reported each year that there is no Medicare access crisis. Staffers from rural districts, however, affirmed that constituents are having difficulty finding primary care doctors who take Medicare.

Staffers uniformly agreed that nobody has the answer to fix the SGR. Several staffers commented on the complexity of the problem, pointing out that MedPAC’s March 2007 SGR report did not achieve a consensus on how to restructure the rate. Many participants were disappointed with the MedPAC report and want solutions to fix physician payment that are more directed and “convincing.”

Some expressed a need for “hands-on models and demonstration projects.” Although these staffers have heard of models that would split the SGR by specialty or geography, they remain skeptical about such proposals without evidence of efficacy. Staffers were also wary of splitting the SGR by specialty, believing it would cause infighting among physicians.

Staffers know far less about RBRVS than they do about the SGR. One staffer admitted, “I won’t pay attention until something is at a crisis point or we have a hearing or a vote.” A few staffers asserted that there should be a more rigorous RUC review to examine what services are over- and undervalued.

Government agencies are not asked to address primary care. At the time of interview (March 2007), staff from MedPAC, GAO, and CBO said that Congress had not asked them to study issues in primary care. One CBO analyst asserted that “nobody’s been able to demonstrate significant changes in volume or outcome [as a result of investing in primary care]…we need empirical data.” The analyst also mentioned CMS demonstration projects as a way to gather data. According to a Capitol Hill veteran, the CBO believes that even if primary care extends a person’s life, this may not necessarily save money.

Discussion

Although most of the interviewed congressional staffers recognize the payment gap and understand that the number of physicians entering primary care is decreasing, Congress has not taken action to address these issues. Several factors explain this.

SGR is the 800-pound gorilla. When discussing physician payment, congressional staffers appear far more concerned with reforming the SGR than addressing problems in primary care. This perception is supported by the fact that Congress has asked MedPAC and CBO to investigate the SGR, but has not asked them to examine issues in primary care. For Congress, the dilemma is to hold down physician spending while keeping physicians in the Medicare market. Staffers are dissatisfied with SGR reform proposals from MedPAC and are eager to learn about new possible solutions.

No one perceives a crisis in access to Medicare providers. According to annual MedPAC reports, the number of primary care doctors accepting Medicare patients is sufficient. Staff for members of Congress from rural areas, however, contend that some constituents cannot find a primary care provider who accepts Medicare.

Congress is not convinced that primary care saves money. Although some staffers believe that primary care can reduce costs, the CBO argues that this is not necessarily true. It is indeed difficult to prove cost savings from investing in preventive services because there is greater upfront cost, and extending people’s lives could incur higher future costs. Research, however, shows that primary care-oriented systems reduce preventable hospitalizations, which decreases costs.^4,5,7,8 It seems that either the existing evidence is insufficient to convince the CBO or the evidence has not been communicated effectively.

Strategic leverage moving forward

The time is ripe for SGR reform because most staffers conveyed a desire for solutions. Because the SGR appears to take priority over primary care issues, it must be dealt with first. It is possible, however, for policy makers to address the SGR and RBRVS reforms while simultaneously investing in primary care. The SGR and RBRVS reforms could hold specialties accountable for their own volume growth and protect specialties with minimal volume growth.

The Medical Home is a concept gaining recognition among congressional staff and could involve restructured physician payment. In its Tax Relief and Health Care Act of 2006, Congress mandated a 3-year Medical Home demonstration to be conducted across multiple demographic communities in up to 8 states. The concept encompasses “large or small medical practices where a physician provides comprehensive and coordinated patient centered medical care and acts as the ‘personal physician’ to the patient.”²⁵ (The Medical Home is also a focus of The Patient-Centered Primary Care Collaborative [http://www.pcpcc.net/], a coalition of medical societies, employers, insurers, consumer groups, and others that is exploring the concept as a way to contain health care costs and also achieve fair remuneration for physicians.)

The demonstration must be carefully crafted to test the concept fairly. Even before the demonstration begins, Congress could ask the CBO and GAO to investigate existing evidence of primary care’s cost-effectiveness. Support from the CBO is essential for Congress to invest in primary care.

Other experiments are underway. As of this publication, several major insurers are beginning regional experiments in raising fees for primary care visits in an effort to avoid greater costs down the road.²³

Access issue needs further study. Our interviews revealed that while MedPAC asserts there is no primary care access issue, staffers from rural districts disagree. In fact, had Congress not over-ridden President Bush’s recent veto of a Medicare bill to increase physicians’ fees, doctors in urban areas would also have stopped accepting new Medicare patients.²⁶ Additional physician workforce studies are necessary to fully understand the current primary care physician supply. Also useful would be studies by Medicaid and Medicare that investigate thresholds at which physicians stop seeing patients with low-paying coverage.

Advocacy is needed, too. Congressional staffers appear to understand some of the difficulties in primary care, but give priority to broader SGR reform. Further research and advocacy on the value of primary care and payment reform solutions will be necessary to establish primary care as a means to cost-effective, high-quality care in the United States.

Acknowledgment

Part of the content in this article was presented as a poster at the North American Primary Care Research Group Conference in Vancouver, British Columbia, October 2007.

Correspondence
Brian Yoshio Laing, MD, San Francisco General Hospital, 995 Potrero Avenue, Building 80, Ward 83, San Francisco, CA 94110; yoshi.laing@ucsf.edu.

The viability of primary care in the United States is in question, attributable in large part to declining provider payments in the face of rising medical school debt and fee-for-service pressures to increase patient volume.^1-3 Congress—which has authority over Medicare and its price-setting function for provider reimbursement overall—is seemingly unaware of the problems facing primary care, including barriers to payment reform. The future of our specialty may hinge on our ability to persuade Congress that these problems are dire. A growing body of evidence supports the essential and integrative function primary care plays in health systems, and its positive impact on quality of care and costs.^4-6

The confused order of things now

Advantages of primary care are proven. Regions with higher ratios of primary care physicians relative to specialists have lower rates of hospitalizations, lower Medicare costs, and higher quality of care.^7,8 People with a primary care physician are more satisfied with their care and more likely to receive preventive services and better chronic disease management.^9-11 Most countries that have built their health care systems on a strong foundation of primary care demonstrate better health outcomes, fewer health care disparities, and lower costs.^4,6 Thus the waning of primary care presents risks to both personal and population health.

Still, society undervalues primary care. Despite evidence of the benefits just cited, the income disparity between primary care physicians and specialists continues to grow, discouraging medical students from entering primary care careers.¹² The Medical Group Management Association shows that between 2000 and 2004, the median income for a family physician increased 7.5% to $156,000; for invasive cardiologists, 16.9% to $428,000; and for diagnostic radiologists, 36.2% to $407,000. Adjusted for inflation, primary care income fell 10% from 1995 to 2004.¹³

No wonder students shy away from primary care. Though there is little public sympathy for the financial woes of primary care doctors, lower incomes are contributing to a drying of the primary care pipeline.^14,15 The number of US medical school graduates choosing family medicine residencies dropped by 50% between 1997 and 2005.¹⁶ From 1998 to 2004, the number of internal medicine residents choosing careers in primary care plummeted from 54% to 25%.^17,18 This waning interest in primary care coincides, unfortunately, with the aging of the US baby boomers and an increasing prevalence of chronic disease.

How Congress could help fix the disparity

Medicare reimbursement has 2 components that Congress could amend to narrow the payment gap and help open the primary care pipeline: the Sustainable Growth Rate (SGR) and the Resource-Based Relative Value Scale (RBRVS) process.

The SGR formula sets a target for Medicare physician expenditures each year. Recently, physician expenditure growth has exceeded the target and, by law, the difference is subtracted from the fees paid to all physicians. According to the Medicare Payment Advisory Commission (MedPAC), much of the excess spending has come from rapidly increasing volumes of procedures used by specialists.¹⁹ The SGR system therefore disproportionately penalizes primary care physicians because payments to all physicians are cut regardless of which specialties are responsible for excess spending.

RBRVS is the system of relative values applied to every procedure and office visit. The Relative Value Units (RVUs) for each procedure or office visit are multiplied by a conversion factor determined by the SGR formula. RVUs are largely governed by the Relative Value Scale Update Committee (RUC), which advises the Centers for Medicare and Medicaid Services (CMS) on revisions to physician reimbursement.

The RUC reviews the relative value scale at least every 5 years. Though primary care physicians provide about half of Medicare physician visits, they represent just 15% of the RUC’s voting members.¹²

The committee’s reevaluation process tends to raise some RVUs without sufficiently deflating others.²⁰ The resulting overall inflation of fees forces CMS to reduce payments equally to all physicians, meaning primary care is again disproportionately penalized. Moreover, both Medicare and private insurance companies follow the RUC’s recommendations.

Influencing Congress: Where to begin? As Congress escalates its deliberations on Medicare physician spending, we investigated how key legislators perceive issues in primary care and physician payment.

Methods

To better understand perspectives of congressional committees with jurisdiction over health care spending, we conducted semistructured key informant interviews in March 2007 with 14 health staff aides to members of Congress who have jurisdiction over Medicare. Interviews were done face to face and lasted 30 to 60 minutes.

The congressional committees with jurisdiction over Medicare physician payment are Senate Finance, House Ways and Means, and House Energy and Commerce. Each committee has 1 majority and 1 minority staffer specializing in Medicare part B, which includes physician payment. Of these 6 specialized staffers, 5 agreed to participate in semistructured interviews. Other staffers were contacted by using a purposeful sampling technique known as “snowballing” or chain-referral, whereby participants with whom contact has been made refer the researcher to other potential interviewees. This process yielded another 9 interviewees to total 14.

The aides identified several other information sources, and we interviewed 1 staff member each from 3 of these sources: MedPAC, the Congressional Budget Office (CBO), and the Government Accountability Office (GAO).

Interviews covered several topics, including views on the state of primary care and physician payment (TABLE). Three researchers separately reviewed the interview notes to identify and compile themes.

TABLE
6 Questions we asked the congressional staffers

Results

Of the 14 congressional staffers, 8 were Republican and 6 were Democrat; 5 were committee staff and 9 were general staff. Committee representation was fairly even among staffers: Senate Finance (4), House Ways and Means (5), and House Energy and Commerce (5). Range of experience on Capitol Hill was 3 months to 9 years.

Some staffers are empathetic, others unaware. Most respondents expressed concern about the decreasing number of students entering primary care careers and the potential impact on patient access to care. One staffer acknowledged, “the way our reimbursement system works, primary care is not an option for students…reimbursement is so low…the number of primary care physicians is going down relative to other specialties.”

Another participant added that most staffers “recognize a role for primary care. It’s also tough because of how strong the specialty community is.” One staffer advised, “The Alliance of Specialty Medicine goes along with the AMA, trying to represent a coordinated front…I don’t see this much coordination around primary care.”

A few staffers did not understand the definition of primary care or did not know which physician groups represent primary care.

Legislation to improve US health care—and primary care. Participants varied in their input on this subject. One staffer stated that primary care is “important but rarely singled out…usually the goal is broader reform so [primary care] is still a goal, but unstated.”

Some committee staff described the need to incentivize greater use of primary care and increase coordination of care. A few proposed reevaluating RBRVS to help primary care, and they spontaneously raised the Medical Home concept as a way to encourage growth of primary care. The Medical Home involves pairing each Medicare beneficiary with a patient-centered practice that meets certain criteria including continuity with a personal physician, care coordination, quality assurance, increased access, and specific payment.²¹ A pilot project in North Carolina that incorporates the Medical Home is saving the state about $162 million annually.^22,23 One staffer championed primary care, but pointed out that a critical barrier preventing Congress from investing in it is the CBO, which is not convinced that primary care can save money over the long term.

The SGR dominates discussions on physician payment

All respondents had a functional understanding of the SGR and desired reform, but few understood how the SGR contributes to the payment gap. Many staffers would like to do away with the SGR, but CBO estimates show that this would be cost-prohibitive.²⁴

A few staffers believed that SGR reform may not happen until 2009, after the next president takes office. Some participants also predicted that SGR reform will not happen until more physicians refuse to see Medicare patients. To date, MedPAC has reported each year that there is no Medicare access crisis. Staffers from rural districts, however, affirmed that constituents are having difficulty finding primary care doctors who take Medicare.

Staffers uniformly agreed that nobody has the answer to fix the SGR. Several staffers commented on the complexity of the problem, pointing out that MedPAC’s March 2007 SGR report did not achieve a consensus on how to restructure the rate. Many participants were disappointed with the MedPAC report and want solutions to fix physician payment that are more directed and “convincing.”

Some expressed a need for “hands-on models and demonstration projects.” Although these staffers have heard of models that would split the SGR by specialty or geography, they remain skeptical about such proposals without evidence of efficacy. Staffers were also wary of splitting the SGR by specialty, believing it would cause infighting among physicians.

Staffers know far less about RBRVS than they do about the SGR. One staffer admitted, “I won’t pay attention until something is at a crisis point or we have a hearing or a vote.” A few staffers asserted that there should be a more rigorous RUC review to examine what services are over- and undervalued.

Government agencies are not asked to address primary care. At the time of interview (March 2007), staff from MedPAC, GAO, and CBO said that Congress had not asked them to study issues in primary care. One CBO analyst asserted that “nobody’s been able to demonstrate significant changes in volume or outcome [as a result of investing in primary care]…we need empirical data.” The analyst also mentioned CMS demonstration projects as a way to gather data. According to a Capitol Hill veteran, the CBO believes that even if primary care extends a person’s life, this may not necessarily save money.

Discussion

Although most of the interviewed congressional staffers recognize the payment gap and understand that the number of physicians entering primary care is decreasing, Congress has not taken action to address these issues. Several factors explain this.

SGR is the 800-pound gorilla. When discussing physician payment, congressional staffers appear far more concerned with reforming the SGR than addressing problems in primary care. This perception is supported by the fact that Congress has asked MedPAC and CBO to investigate the SGR, but has not asked them to examine issues in primary care. For Congress, the dilemma is to hold down physician spending while keeping physicians in the Medicare market. Staffers are dissatisfied with SGR reform proposals from MedPAC and are eager to learn about new possible solutions.

No one perceives a crisis in access to Medicare providers. According to annual MedPAC reports, the number of primary care doctors accepting Medicare patients is sufficient. Staff for members of Congress from rural areas, however, contend that some constituents cannot find a primary care provider who accepts Medicare.

Congress is not convinced that primary care saves money. Although some staffers believe that primary care can reduce costs, the CBO argues that this is not necessarily true. It is indeed difficult to prove cost savings from investing in preventive services because there is greater upfront cost, and extending people’s lives could incur higher future costs. Research, however, shows that primary care-oriented systems reduce preventable hospitalizations, which decreases costs.^4,5,7,8 It seems that either the existing evidence is insufficient to convince the CBO or the evidence has not been communicated effectively.

Strategic leverage moving forward

The time is ripe for SGR reform because most staffers conveyed a desire for solutions. Because the SGR appears to take priority over primary care issues, it must be dealt with first. It is possible, however, for policy makers to address the SGR and RBRVS reforms while simultaneously investing in primary care. The SGR and RBRVS reforms could hold specialties accountable for their own volume growth and protect specialties with minimal volume growth.

The Medical Home is a concept gaining recognition among congressional staff and could involve restructured physician payment. In its Tax Relief and Health Care Act of 2006, Congress mandated a 3-year Medical Home demonstration to be conducted across multiple demographic communities in up to 8 states. The concept encompasses “large or small medical practices where a physician provides comprehensive and coordinated patient centered medical care and acts as the ‘personal physician’ to the patient.”²⁵ (The Medical Home is also a focus of The Patient-Centered Primary Care Collaborative [http://www.pcpcc.net/], a coalition of medical societies, employers, insurers, consumer groups, and others that is exploring the concept as a way to contain health care costs and also achieve fair remuneration for physicians.)

The demonstration must be carefully crafted to test the concept fairly. Even before the demonstration begins, Congress could ask the CBO and GAO to investigate existing evidence of primary care’s cost-effectiveness. Support from the CBO is essential for Congress to invest in primary care.

Other experiments are underway. As of this publication, several major insurers are beginning regional experiments in raising fees for primary care visits in an effort to avoid greater costs down the road.²³

Access issue needs further study. Our interviews revealed that while MedPAC asserts there is no primary care access issue, staffers from rural districts disagree. In fact, had Congress not over-ridden President Bush’s recent veto of a Medicare bill to increase physicians’ fees, doctors in urban areas would also have stopped accepting new Medicare patients.²⁶ Additional physician workforce studies are necessary to fully understand the current primary care physician supply. Also useful would be studies by Medicaid and Medicare that investigate thresholds at which physicians stop seeing patients with low-paying coverage.

Advocacy is needed, too. Congressional staffers appear to understand some of the difficulties in primary care, but give priority to broader SGR reform. Further research and advocacy on the value of primary care and payment reform solutions will be necessary to establish primary care as a means to cost-effective, high-quality care in the United States.

Acknowledgment

Part of the content in this article was presented as a poster at the North American Primary Care Research Group Conference in Vancouver, British Columbia, October 2007.

Correspondence
Brian Yoshio Laing, MD, San Francisco General Hospital, 995 Potrero Avenue, Building 80, Ward 83, San Francisco, CA 94110; yoshi.laing@ucsf.edu.

The viability of primary care in the United States is in question, attributable in large part to declining provider payments in the face of rising medical school debt and fee-for-service pressures to increase patient volume.^1-3 Congress—which has authority over Medicare and its price-setting function for provider reimbursement overall—is seemingly unaware of the problems facing primary care, including barriers to payment reform. The future of our specialty may hinge on our ability to persuade Congress that these problems are dire. A growing body of evidence supports the essential and integrative function primary care plays in health systems, and its positive impact on quality of care and costs.^4-6

The confused order of things now

Advantages of primary care are proven. Regions with higher ratios of primary care physicians relative to specialists have lower rates of hospitalizations, lower Medicare costs, and higher quality of care.^7,8 People with a primary care physician are more satisfied with their care and more likely to receive preventive services and better chronic disease management.^9-11 Most countries that have built their health care systems on a strong foundation of primary care demonstrate better health outcomes, fewer health care disparities, and lower costs.^4,6 Thus the waning of primary care presents risks to both personal and population health.

Still, society undervalues primary care. Despite evidence of the benefits just cited, the income disparity between primary care physicians and specialists continues to grow, discouraging medical students from entering primary care careers.¹² The Medical Group Management Association shows that between 2000 and 2004, the median income for a family physician increased 7.5% to $156,000; for invasive cardiologists, 16.9% to $428,000; and for diagnostic radiologists, 36.2% to $407,000. Adjusted for inflation, primary care income fell 10% from 1995 to 2004.¹³

No wonder students shy away from primary care. Though there is little public sympathy for the financial woes of primary care doctors, lower incomes are contributing to a drying of the primary care pipeline.^14,15 The number of US medical school graduates choosing family medicine residencies dropped by 50% between 1997 and 2005.¹⁶ From 1998 to 2004, the number of internal medicine residents choosing careers in primary care plummeted from 54% to 25%.^17,18 This waning interest in primary care coincides, unfortunately, with the aging of the US baby boomers and an increasing prevalence of chronic disease.

How Congress could help fix the disparity

Medicare reimbursement has 2 components that Congress could amend to narrow the payment gap and help open the primary care pipeline: the Sustainable Growth Rate (SGR) and the Resource-Based Relative Value Scale (RBRVS) process.

The SGR formula sets a target for Medicare physician expenditures each year. Recently, physician expenditure growth has exceeded the target and, by law, the difference is subtracted from the fees paid to all physicians. According to the Medicare Payment Advisory Commission (MedPAC), much of the excess spending has come from rapidly increasing volumes of procedures used by specialists.¹⁹ The SGR system therefore disproportionately penalizes primary care physicians because payments to all physicians are cut regardless of which specialties are responsible for excess spending.

RBRVS is the system of relative values applied to every procedure and office visit. The Relative Value Units (RVUs) for each procedure or office visit are multiplied by a conversion factor determined by the SGR formula. RVUs are largely governed by the Relative Value Scale Update Committee (RUC), which advises the Centers for Medicare and Medicaid Services (CMS) on revisions to physician reimbursement.

The RUC reviews the relative value scale at least every 5 years. Though primary care physicians provide about half of Medicare physician visits, they represent just 15% of the RUC’s voting members.¹²

The committee’s reevaluation process tends to raise some RVUs without sufficiently deflating others.²⁰ The resulting overall inflation of fees forces CMS to reduce payments equally to all physicians, meaning primary care is again disproportionately penalized. Moreover, both Medicare and private insurance companies follow the RUC’s recommendations.

Influencing Congress: Where to begin? As Congress escalates its deliberations on Medicare physician spending, we investigated how key legislators perceive issues in primary care and physician payment.

Methods

To better understand perspectives of congressional committees with jurisdiction over health care spending, we conducted semistructured key informant interviews in March 2007 with 14 health staff aides to members of Congress who have jurisdiction over Medicare. Interviews were done face to face and lasted 30 to 60 minutes.

The congressional committees with jurisdiction over Medicare physician payment are Senate Finance, House Ways and Means, and House Energy and Commerce. Each committee has 1 majority and 1 minority staffer specializing in Medicare part B, which includes physician payment. Of these 6 specialized staffers, 5 agreed to participate in semistructured interviews. Other staffers were contacted by using a purposeful sampling technique known as “snowballing” or chain-referral, whereby participants with whom contact has been made refer the researcher to other potential interviewees. This process yielded another 9 interviewees to total 14.

The aides identified several other information sources, and we interviewed 1 staff member each from 3 of these sources: MedPAC, the Congressional Budget Office (CBO), and the Government Accountability Office (GAO).

Interviews covered several topics, including views on the state of primary care and physician payment (TABLE). Three researchers separately reviewed the interview notes to identify and compile themes.

TABLE
6 Questions we asked the congressional staffers

Results

Of the 14 congressional staffers, 8 were Republican and 6 were Democrat; 5 were committee staff and 9 were general staff. Committee representation was fairly even among staffers: Senate Finance (4), House Ways and Means (5), and House Energy and Commerce (5). Range of experience on Capitol Hill was 3 months to 9 years.

Some staffers are empathetic, others unaware. Most respondents expressed concern about the decreasing number of students entering primary care careers and the potential impact on patient access to care. One staffer acknowledged, “the way our reimbursement system works, primary care is not an option for students…reimbursement is so low…the number of primary care physicians is going down relative to other specialties.”

Another participant added that most staffers “recognize a role for primary care. It’s also tough because of how strong the specialty community is.” One staffer advised, “The Alliance of Specialty Medicine goes along with the AMA, trying to represent a coordinated front…I don’t see this much coordination around primary care.”

A few staffers did not understand the definition of primary care or did not know which physician groups represent primary care.

Legislation to improve US health care—and primary care. Participants varied in their input on this subject. One staffer stated that primary care is “important but rarely singled out…usually the goal is broader reform so [primary care] is still a goal, but unstated.”

Some committee staff described the need to incentivize greater use of primary care and increase coordination of care. A few proposed reevaluating RBRVS to help primary care, and they spontaneously raised the Medical Home concept as a way to encourage growth of primary care. The Medical Home involves pairing each Medicare beneficiary with a patient-centered practice that meets certain criteria including continuity with a personal physician, care coordination, quality assurance, increased access, and specific payment.²¹ A pilot project in North Carolina that incorporates the Medical Home is saving the state about $162 million annually.^22,23 One staffer championed primary care, but pointed out that a critical barrier preventing Congress from investing in it is the CBO, which is not convinced that primary care can save money over the long term.

The SGR dominates discussions on physician payment

All respondents had a functional understanding of the SGR and desired reform, but few understood how the SGR contributes to the payment gap. Many staffers would like to do away with the SGR, but CBO estimates show that this would be cost-prohibitive.²⁴

A few staffers believed that SGR reform may not happen until 2009, after the next president takes office. Some participants also predicted that SGR reform will not happen until more physicians refuse to see Medicare patients. To date, MedPAC has reported each year that there is no Medicare access crisis. Staffers from rural districts, however, affirmed that constituents are having difficulty finding primary care doctors who take Medicare.

Staffers uniformly agreed that nobody has the answer to fix the SGR. Several staffers commented on the complexity of the problem, pointing out that MedPAC’s March 2007 SGR report did not achieve a consensus on how to restructure the rate. Many participants were disappointed with the MedPAC report and want solutions to fix physician payment that are more directed and “convincing.”

Some expressed a need for “hands-on models and demonstration projects.” Although these staffers have heard of models that would split the SGR by specialty or geography, they remain skeptical about such proposals without evidence of efficacy. Staffers were also wary of splitting the SGR by specialty, believing it would cause infighting among physicians.

Staffers know far less about RBRVS than they do about the SGR. One staffer admitted, “I won’t pay attention until something is at a crisis point or we have a hearing or a vote.” A few staffers asserted that there should be a more rigorous RUC review to examine what services are over- and undervalued.

Government agencies are not asked to address primary care. At the time of interview (March 2007), staff from MedPAC, GAO, and CBO said that Congress had not asked them to study issues in primary care. One CBO analyst asserted that “nobody’s been able to demonstrate significant changes in volume or outcome [as a result of investing in primary care]…we need empirical data.” The analyst also mentioned CMS demonstration projects as a way to gather data. According to a Capitol Hill veteran, the CBO believes that even if primary care extends a person’s life, this may not necessarily save money.

Discussion

Although most of the interviewed congressional staffers recognize the payment gap and understand that the number of physicians entering primary care is decreasing, Congress has not taken action to address these issues. Several factors explain this.

SGR is the 800-pound gorilla. When discussing physician payment, congressional staffers appear far more concerned with reforming the SGR than addressing problems in primary care. This perception is supported by the fact that Congress has asked MedPAC and CBO to investigate the SGR, but has not asked them to examine issues in primary care. For Congress, the dilemma is to hold down physician spending while keeping physicians in the Medicare market. Staffers are dissatisfied with SGR reform proposals from MedPAC and are eager to learn about new possible solutions.

No one perceives a crisis in access to Medicare providers. According to annual MedPAC reports, the number of primary care doctors accepting Medicare patients is sufficient. Staff for members of Congress from rural areas, however, contend that some constituents cannot find a primary care provider who accepts Medicare.

Congress is not convinced that primary care saves money. Although some staffers believe that primary care can reduce costs, the CBO argues that this is not necessarily true. It is indeed difficult to prove cost savings from investing in preventive services because there is greater upfront cost, and extending people’s lives could incur higher future costs. Research, however, shows that primary care-oriented systems reduce preventable hospitalizations, which decreases costs.^4,5,7,8 It seems that either the existing evidence is insufficient to convince the CBO or the evidence has not been communicated effectively.

Strategic leverage moving forward

The time is ripe for SGR reform because most staffers conveyed a desire for solutions. Because the SGR appears to take priority over primary care issues, it must be dealt with first. It is possible, however, for policy makers to address the SGR and RBRVS reforms while simultaneously investing in primary care. The SGR and RBRVS reforms could hold specialties accountable for their own volume growth and protect specialties with minimal volume growth.

The Medical Home is a concept gaining recognition among congressional staff and could involve restructured physician payment. In its Tax Relief and Health Care Act of 2006, Congress mandated a 3-year Medical Home demonstration to be conducted across multiple demographic communities in up to 8 states. The concept encompasses “large or small medical practices where a physician provides comprehensive and coordinated patient centered medical care and acts as the ‘personal physician’ to the patient.”²⁵ (The Medical Home is also a focus of The Patient-Centered Primary Care Collaborative [http://www.pcpcc.net/], a coalition of medical societies, employers, insurers, consumer groups, and others that is exploring the concept as a way to contain health care costs and also achieve fair remuneration for physicians.)

The demonstration must be carefully crafted to test the concept fairly. Even before the demonstration begins, Congress could ask the CBO and GAO to investigate existing evidence of primary care’s cost-effectiveness. Support from the CBO is essential for Congress to invest in primary care.

Other experiments are underway. As of this publication, several major insurers are beginning regional experiments in raising fees for primary care visits in an effort to avoid greater costs down the road.²³

Access issue needs further study. Our interviews revealed that while MedPAC asserts there is no primary care access issue, staffers from rural districts disagree. In fact, had Congress not over-ridden President Bush’s recent veto of a Medicare bill to increase physicians’ fees, doctors in urban areas would also have stopped accepting new Medicare patients.²⁶ Additional physician workforce studies are necessary to fully understand the current primary care physician supply. Also useful would be studies by Medicaid and Medicare that investigate thresholds at which physicians stop seeing patients with low-paying coverage.

Advocacy is needed, too. Congressional staffers appear to understand some of the difficulties in primary care, but give priority to broader SGR reform. Further research and advocacy on the value of primary care and payment reform solutions will be necessary to establish primary care as a means to cost-effective, high-quality care in the United States.

Acknowledgment

Part of the content in this article was presented as a poster at the North American Primary Care Research Group Conference in Vancouver, British Columbia, October 2007.

Correspondence
Brian Yoshio Laing, MD, San Francisco General Hospital, 995 Potrero Avenue, Building 80, Ward 83, San Francisco, CA 94110; yoshi.laing@ucsf.edu.

Mr. Z, age 42, is referred by his primary care physician with symptoms suggesting attention-deficit/hyperactivity disorder (ADHD). Mr. Z has seen his physician sporadically for 10 years and acknowledges not following dietary and exercise advice. He has had intermittent “minor” depression, is overweight, and is a smoker with a family history of cardiovascular disease and diabetes.

A salesman, Mr. Z recently was promoted to an administrative position that substantially increased his paperwork. He is having difficulty performing his job because of longstanding forgetfulness and disorganization. He says he feels “like I’m in grade school again, lost in paperwork.” He also describes a recent educational assessment for his son, age 7, who may have ADHD. Similarities between Mr. Z’s and his son’s early childhood academic struggles are striking.

Like Mr. Z, adults with ADHD commonly seek treatment when increasing stressors and demands overwhelm their cognitive-attentional abilities. Some may be “healthy” men and women without psychiatric histories, whose disorganization, forgetfulness, or impulsivity contributes to functional impairment, including nonadherence with medical advice. For others, such as those with known psychiatric disorders, ADHD may be a hidden comorbidity contributing to seemingly refractory depression or anxiety disorder.

Despite growing evidence related to adult ADHD, individualizing and maintaining treatment over time can be challenging for clinicians and patients. Fortunately, new tools and multiple stimulant and nonstimulant medications can help you screen for, assess, and treat adult ADHD.

ADHD diagnosis

To diagnose ADHD in an adult patient, first establish that symptoms have existed from childhood to adulthood. One approach is to review DSM-IV-TR criteria for ADHD with your patient and ask him or her to reflect on childhood symptoms and dysfunction. Begin with orienting questions, such as “Do you remember your first grade teacher, your school, where you lived?” ADHD symptoms might have been present even if the patient maintained acceptable grades, particularly in elementary school, as dedicated parents or teachers might have contributed to early academic success.

Next, turn to diagnostic language that captures ADHD symptoms in adults. For example, the 18-item World Health Organization Adult ADHD Self-Report Scale (ASRS-v1.1) prompts individuals to self-report DSM-IV ADHD symptoms, and a 6-item subset (Table 1) is a highly specific screener (see Related Resources). The ASRS is most reliable in adults with limited psychiatric comorbidity.¹

Adults often describe fluctuations in symptom severity over time. Symptoms may have less impact with more physically demanding work—such as sales—and greater impact with organizationally demanding work—such as administration.

Base your summary ADHD diagnosis on DSM-IV-TR criteria, including:

• lifetime persistence of symptoms, beginning before age 7
• functional impairment in ≥2 life settings, such as work, school, or home
• lack of another medical or psychiatric condition sufficient to explain the symptoms.

Table 1

Adult Self-Report Scale-v1.1 WHO 6-question screening tool for ADHD*

CASE CONTINUED: ‘All the time, every day’

Mr. Z completes the ASRS self-report symptom checklist and brings his wife to the next appointment. He rated all 6 screening symptoms and most others as occurring “often” or “very often.” He describes functional impairments “essentially all the time, basically every day” at work, home, and socially. His wife confirms these symptoms and the frustrations and conflicts they have caused.

Mr. Z describes ADHD symptoms from early elementary school to college. He was held back in kindergarten for being “immature,” his academic performance was inconsistent, and he “just got by…by cramming” in high school and college. His school performance pattern does not suggest a learning disability; he did not need special help in 1 subject more than others, and under pressure he could achieve average grades.

Medical review excludes explanations other than ADHD for his inattention, restlessness, and impulsivity. You conclude that Mr. Z meets criteria for ADHD, combined subtype, and discuss medication treatment.

FDA-approved medications

Medication for ADHD is appropriate only if symptoms are impairing. Five effective and generally well-tolerated medications are FDA-approved for adults with ADHD (Table 2):

• extended-release mixed amphetamine (Adderall XR)
• extended-release OROS methylphenidate (Concerta)
• extended-release dexmethylphenidate (Focalin XR)
• atomoxetine (Strattera)
• lisdexamfetamine (Vyvanse).

Efficacy. A meta-analysis of 29 pediatric ADHD trials across 30 years demonstrated greater effect size for stimulant class medications (immediate- and long-acting), compared with nonstimulant medications (including bupropion, atomoxetine, and modafinil).² This finding is consistent with the American Academy of Child and Adolescent Psychiatry’s recommendation of stimulant medications as first-line agents for pediatric ADHD.³ A similar meta-analysis of 6 controlled studies of methylphenidate-class medications in adults found a large mean effect size (0.9), with greater effects associated with higher doses.⁴

Atomoxetine, a norepinephrine reuptake inhibitor, is the only nonstimulant medication FDA-approved for ADHD in adults. More than 6,000 children, adolescents, and adults have taken atomoxetine in clinical trials for ADHD (Lilly, prescribing information), with 4 years of open treatment data showing benefit being maintained over time.⁵

Tolerability. Although ADHD medications are generally well-tolerated by healthy adults, assess for a history of potential contraindications:

• unstable medical condition, hyperthyroidism, glaucoma
• treatment with a monoamine oxidase inhibitor or other pressor agents because of possible effects on blood pressure and heart rate
• use of cytochrome P450 2D6 inhibitors, which may increase atomoxetine steady-state plasma concentrations
• cardiovascular disease or family history of early cardiac disease (Box 1)^6,7
• history of or active substance use disorder, such as alcohol dependence, cocaine or heroin abuse
• history of psychosis, bipolar disorder, or an active clinically significant psychiatric comorbidity (major depression, agitated state, suicidality).

Clinically, some patients appear to tolerate 1 class of stimulant (such as methylphenidate or amphetamine) over another. Consider switching to an alternate stimulant if your patient has bothersome side effects—mild low appetite, insomnia, tension, or jitteriness—or has received limited or partial benefit during an initial stimulant trial.

Box 1

Extended-release formulations. Early adult studies demonstrated the efficacy of immediate-release stimulants, but adults with ADHD’s inherent deficits in organization and memory may have higher adherence rates and greater success with once-daily, extended-release formulations.^8-11 Unless your patient wants to begin with small, short-acting dosages (5 to 10 mg) or desires to target treatment to specific times of day (such as in the morning for administrative work only), many appreciate once-daily formulations. Extended-release formulations also may be the simplest stimulants with which to begin ADHD treatment.

Over time, patients may benefit from an immediate-release form:

• added for certain times of day—such as in late afternoon, when the morning extended-release dose has worn off (Box 2)^12,13
• to use as an alternative to extended-release formulations when more or less flexibly is desired, such as on weekends.

Table 2

Administering medications approved for adult ADHD

CASE CONTINUED: Feeling ‘calm, less frenetic’

During the next 6 months, you start Mr. Z on stimulant treatment at robust dosing consistent with his weight (90 kg). He complains that extended-duration methylphenidate (MPH)—titrated to 90 mg/d—doesn’t last into the late afternoon, and he feels mildly tense with a low appetite. Because of an apparent partial response and relatively mild adverse effects, you discontinue MPH and try an extended-duration amphetamine, titrated to 60 mg.

Mr. Z’s blood pressure and heart rate remain stable. He begins to exercise regularly and reduce his use of tobacco and caffeine drinks, as you recommend. He says he feels “calm, less frenetic.” He reports no tension on this medication and only mild reduced appetite. With a plan to continue taking the stimulant medication with regular monitoring, he then disappears from treatment.

Promoting adherence

Treatment nonadherence is an issue throughout medicine, and individuals with disorganization, forgetfulness, and impulsivity may be at higher-than-usual risk of not following through on medication regimens.

Box 2

In addition, restrictions on stimulant-class medications do not permit multiple-month prescribing (refills), as is allowed with non-scheduled medications such as atomoxetine. Discuss with patients how they will obtain stimulant medications on a regular, monthly or bimonthly basis. In our experience, the practical challenges of remaining in treatment at times may limit patients’ adherence to ADHD medications more than a lack of response or tolerability concerns.

Explain to patients early in treatment that they might need to try several different medications before settling on 1 that is optimally tolerated and efficacious. Because stimulants are generally quite effective for ADHD symptoms, set your goal to identify adverse effects and aim for a patient response of “this works well, and I don’t feel any different on it.”

CASE CONTINUED: Ready to try again

Three years later, Mr. Z returns and reports gradually discontinuing the stimulant because he “wanted to go it on my own.” He functioned relatively well at first, but errors and conflicts at his job led to his dismissal.

Since then, he has been unemployed. He is increasingly depressed and reports drinking and smoking “more heavily than in college.” He asks about resuming ADHD treatment.

Mr. Z does not meet DSM-IV-TR criteria for major depressive disorder or alcohol abuse/dependence. His depressed mood appears to be linked to his marked ADHD symptoms. Mr. Z agrees to a new treatment plan that includes starting atomoxetine at 25 mg to allow for flexible titration and psychotherapy to monitor his mood and achieve sobriety.

ADHD and substance abuse

Clinical judgment determines whether an adult with ADHD and a history of substance use disorders may safely benefit from treatment with a stimulant. The relationship between ADHD and substance use disorders is of clinical concern, but ADHD medications have not been shown to increase risk for later substance use disorders in children.¹⁴ Conversely, effective ADHD treatment appears to reduce later cigarette and substance use.¹⁵

Consider using a nonstimulant-class medication in adults with ADHD and active substance use disorders. In a 12-week, double-blind, controlled trial, atomoxetine improved ADHD symptoms significantly more than placebo in adults meeting DS-MIV-TR criteria for comorbid alcohol use disorders. After 4 to 30 days of alcohol abstinence, 72 patients were randomly assigned to atomoxetine, 25 to 100 mg/d (mean final dose 90 mg/d), and 75 patients to placebo. Although estimated times to initial relapse to heavy drinking did not differ:

• atomoxetine-treated subjects had 26% fewer cumulative heavy drinking days than placebo-treated subjects (P=0.023)
• the difference in cumulative heavy drinking days between the atomoxetine and placebo groups became statistically significant after 55 days of treatment.¹⁶

Related resources

• World Health Organization Adult Self-Report Scale (ASRS) 18-item instrument and 6-item screener. www.med.nyu.edu/psych/psychiatrist/adhd.html.
• Volkow ND, Swanson JM. Does childhood treatment of ADHD with stimulant medication affect substance abuse in adulthood? Am J Psychiatry 2008;165:553-5.
• Adler LA, Spencer TJ, Levine LR, et al. Functional outcomes in the treatment of adults with ADHD. J Atten Disord 2008; 11:720-7.

Drug brand names

• Atomoxetine • Strattera
• Bupropion • Wellbutrin
• Extended-release mixed amphetamine • Adderall XR
• Extended duration OROS methylphenidate • Concerta
• Extended-release dexmethylphenidate • Focalin XR
• Lisdexamfetamine • Vyvanse
• Modafinil • Provigil

Disclosure

Dr. Hammerness has received research support from and is on the speakers bureau for Shire Pharmaceuticals. He has received support for CME activities and talks from Shire Pharmaceuticals, Ortho-McNeil, and Abbott Laboratories.

Dr. Surman receives research support and/or is a speaker for Abbott Laboratories, Cephalon, Eli Lilly and Company, Janssen, Ortho-McNeil, Merck, New River Pharmaceuticals, Novartis, Pfizer Inc., Shire Pharmaceuticals, and Takeda Pharmaceutical Company.

Dr. Sassi reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgement

Clinical research assistant Katherine Miller, BA, contributed to the literature review for this article and assisted in preparing the manuscript.