Additions and revision to this year’s International Classification of Diseases, Clinical Modification (ICD-9-CM)—which go into effect on October 1—reflect tinkering with existing codes and expansion of others to boost granularity and clarity in your reporting of diagnostic work. To that add a number of new codes—including one that acknowledges the arrival of the H1N1 (swine flu) virus nationwide.

In obstetrics, there are now specific codes for different types of puerperal infection and a requirement for more diagnostic information when a patient has venous complications during pregnancy and intrapartum.

On the gynecology side, changes include the way you report a finding of endometrial intraepithelial neoplasia. New codes have been created to report:

• visits and procedures for fertility preservation
  
• inconclusive mammography
  
• preprocedural laboratory testing.
  

Remember: On October 1, 2009, the new and revised codes discussed here, plus others, will be added to the national ICD-9-CM code set. Be cautioned that, as in past years, there is no grace period!

Changes to obstetric codes

PUERPERAL INFECTIONS

Before October 1, 2009, all puerperal infections were lumped into one code: 670.0 (Major puerperal infection). This changes now: You’ll be required to document, more specifically, the type of infection that your patient has.

Continue to report code 670.0 for an unspecified puerperal infection; but, if you admit the patient to the hospital, using that unspecified code may lead to a first-submission denial of claim. A fifth digit is also required for the unspecified and new more specific codes: 0 (unspecified as to episode of care or not applicable), 2 (delivered with mention of postpartum complication), or 4 (postpartum condition or complication) (to be reported only once the patient is discharged after delivery).

670.1x [0,2,4]  Puerperal endometritis

670.2x [0,2,4]  Puerperal sepsis

670.3x [0,2,4]  Puerperal septic thrombophlebitis

670.8x [0,2,4]  Other major puerperal infection

VENOUS COMPLICATIONS IN PREGNANCY AND PUERPERIUM

Code category 671 (venous complications in pregnancy and the puerperium) retains its current codes, but ICD-9 has added notes to clarify that additional information is required.

For example: When a patient has deep-vein thrombosis, either antepartum (671.3x) or postpartum (671.4x), assign a secondary diagnosis from code category 453 (Other venous embolism and thrombosis). If, in addition, the patient has been taking an anticoagulant for a long time and is currently taking it, report code V56.81, as well, to indicate this.

Gyn code changes

HYPERPLASIA

Over time, codes for hyperplasia have evolved from a system that described mild, moderate, severe, or atypical, to one in which hyperplasia was subdivided by architectural complexity, such as simple versus complex and whether or not atypia were present. Even this terminology fails, however, to adequately identify patients’ risk of cancer to improve therapeutic triaging.

In more recent years, physicians and pathologists have begun to distinguish benign hormonal effects of unopposed estrogen, classified as benign hyperplasia, from pre-cancerous lesions classified as endometrial intraepithelial neoplasia (EIN). To capture this newer terminology, ICD-9 has added two new codes.

ICD-9 has elected to retain existing codes in this area of diagnosis and assessment because the old terminology is still used by many older practicing physicians. The hope, however, is that, over time, more accurate distinctions between the types of hyperplasia will replace the older distinctions.

A note in ICD-9 will instruct providers that older codes may not be reported if one of the newer codes is assigned.

An additional note that accompanies the EIN diagnosis indicates that, if a patient is given a diagnosis of malignant neoplasm of the endometrium with endometrial intraepithelial neoplasia, the code for the malignancy (182.0, Malignant neoplasm of body of uterus; corpus uteri, except isthmus) would be reported instead of the EIN code.

621.34  Benign endometrial hyperplasia

621.35  Endometrial intraepithelial neoplasia

INCONCLUSIVE MAMMOGRAM

Routine mammograms are, as you know, sometimes labeled “inconclusive” because of what are termed “dense breasts.” This finding isn’t considered to represent an abnormal condition, but it does require further testing to confirm that no malignant condition exists that cannot be seen on mammogram.

Because many payers cover a repeat mammogram only when an abnormal finding is reported, a new code has been needed—and has now been added—to explain the reason for a second mammogram.

Because of the added code, ICD-9 also decided to revise wording for the 793 code category (until now, it’s been Nonspecific abnormal findings on radiological and other examination of body structure) to a more general heading of Nonspecific findings, which covers inconclusive and abnormal findings.

793.82  Inconclusive mammogram

FERTILITY PRESERVATION PRIOR TO ANTINEOPLASTIC THERAPY

Two new codes have been added to this area of practice at the request of the American Society for Reproductive Medicine (ASRM) and ACOG. They allow you to report visits and procedures aimed at preserving fertility in women who must undergo chemotherapy, surgery, or radiation therapy that might otherwise leave them sterile.

The codes reflect that, before a patient is treated, you may discuss a range of options that can increase her chances of becoming pregnant, including:

• conception before cancer treatment
  
• banking of sperm, eggs, ovarian tissue, and embryos
  
• protecting the ovaries during radiation therapy
  
• modifying surgery to spare the uterus.
  

V26.42  Encounter for fertility preservation counseling

V26.82  Encounter for fertility preservation procedure

PREPROCEDURAL EVALUATIONS

Code category V72.6 has been expanded from four to five digits to better capture reasons for ordering or performing laboratory tests that are not specifically linked to a medical diagnosis.

For example: If you order routine tests as part of a routine, general medical or gyn annual examination, report code V72.62. For routine preoperative lab tests, report V72.63 instead.

ICD-9 has clarified that V72.61 can be reported for testing of immune status, and that current code V72.83 (Other specified pre-operative examination) is the one to report when an exam precedes chemotherapy.

Note: ICD-9 rules require that you list the preprocedural examination code as the primary diagnosis, followed by the code that represents the reason for the surgery or procedure.

V72.60  Laboratory examination, unspecified

V72.61  Antibody response examination

V72.62  Laboratory examination ordered as part of a routine general medical examination

V72.63  Preprocedural laboratory examination

V72.69  Other laboratory examination

PERSONAL HISTORY CODES

A history of drug therapy can affect the care that you are giving a patient now, and may require testing from time to time to assess the consequences of such therapy.

Two examples are long-term estrogen therapy, which may increase a woman’s risk of developing breast cancer, and inhaled steroids, which can decrease bone density. In the absence of a known problem with these (or other) therapies in a given patient, new history codes listed below may be useful in communicating with a payer about ongoing follow-up care or testing that you are providing.

V87.43  Personal history of estrogen therapy

V87.44  Personal history of inhaled steroid therapy

V87.45  Personal history of systemic steroid therapy

V87.46  Personal history of immunosuppressive therapy

Plus a number of miscellaneous additions and changes

Here are few more new codes that may better explain why you saw a patient, provided:

• the new code for swine flu is reported only for a confirmed case, per ICD-9 rules
  
• the new V codes are reported only if the personal history or family circumstance affected treatment at the time of the visit, or if the patient was receiving counseling concerning only those issues.
  

995.24  Failed moderate sedation during procedure

V10.90  Personal history of unspecified type of malignant neoplasm

V15.80  Personal history of failed moderate sedation

V61.07  Family disruption due to death of family member

V61.08  Family disruption due to other extended absence of a family member

V61.42  Substance abuse in family

Additions and revision to this year’s International Classification of Diseases, Clinical Modification (ICD-9-CM)—which go into effect on October 1—reflect tinkering with existing codes and expansion of others to boost granularity and clarity in your reporting of diagnostic work. To that add a number of new codes—including one that acknowledges the arrival of the H1N1 (swine flu) virus nationwide.

In obstetrics, there are now specific codes for different types of puerperal infection and a requirement for more diagnostic information when a patient has venous complications during pregnancy and intrapartum.

On the gynecology side, changes include the way you report a finding of endometrial intraepithelial neoplasia. New codes have been created to report:

• visits and procedures for fertility preservation
  
• inconclusive mammography
  
• preprocedural laboratory testing.
  

Remember: On October 1, 2009, the new and revised codes discussed here, plus others, will be added to the national ICD-9-CM code set. Be cautioned that, as in past years, there is no grace period!

Changes to obstetric codes

PUERPERAL INFECTIONS

Before October 1, 2009, all puerperal infections were lumped into one code: 670.0 (Major puerperal infection). This changes now: You’ll be required to document, more specifically, the type of infection that your patient has.

Continue to report code 670.0 for an unspecified puerperal infection; but, if you admit the patient to the hospital, using that unspecified code may lead to a first-submission denial of claim. A fifth digit is also required for the unspecified and new more specific codes: 0 (unspecified as to episode of care or not applicable), 2 (delivered with mention of postpartum complication), or 4 (postpartum condition or complication) (to be reported only once the patient is discharged after delivery).

670.1x [0,2,4]  Puerperal endometritis

670.2x [0,2,4]  Puerperal sepsis

670.3x [0,2,4]  Puerperal septic thrombophlebitis

670.8x [0,2,4]  Other major puerperal infection

VENOUS COMPLICATIONS IN PREGNANCY AND PUERPERIUM

Code category 671 (venous complications in pregnancy and the puerperium) retains its current codes, but ICD-9 has added notes to clarify that additional information is required.

For example: When a patient has deep-vein thrombosis, either antepartum (671.3x) or postpartum (671.4x), assign a secondary diagnosis from code category 453 (Other venous embolism and thrombosis). If, in addition, the patient has been taking an anticoagulant for a long time and is currently taking it, report code V56.81, as well, to indicate this.

Gyn code changes

HYPERPLASIA

Over time, codes for hyperplasia have evolved from a system that described mild, moderate, severe, or atypical, to one in which hyperplasia was subdivided by architectural complexity, such as simple versus complex and whether or not atypia were present. Even this terminology fails, however, to adequately identify patients’ risk of cancer to improve therapeutic triaging.

In more recent years, physicians and pathologists have begun to distinguish benign hormonal effects of unopposed estrogen, classified as benign hyperplasia, from pre-cancerous lesions classified as endometrial intraepithelial neoplasia (EIN). To capture this newer terminology, ICD-9 has added two new codes.

ICD-9 has elected to retain existing codes in this area of diagnosis and assessment because the old terminology is still used by many older practicing physicians. The hope, however, is that, over time, more accurate distinctions between the types of hyperplasia will replace the older distinctions.

A note in ICD-9 will instruct providers that older codes may not be reported if one of the newer codes is assigned.

An additional note that accompanies the EIN diagnosis indicates that, if a patient is given a diagnosis of malignant neoplasm of the endometrium with endometrial intraepithelial neoplasia, the code for the malignancy (182.0, Malignant neoplasm of body of uterus; corpus uteri, except isthmus) would be reported instead of the EIN code.

621.34  Benign endometrial hyperplasia

621.35  Endometrial intraepithelial neoplasia

INCONCLUSIVE MAMMOGRAM

Routine mammograms are, as you know, sometimes labeled “inconclusive” because of what are termed “dense breasts.” This finding isn’t considered to represent an abnormal condition, but it does require further testing to confirm that no malignant condition exists that cannot be seen on mammogram.

Because many payers cover a repeat mammogram only when an abnormal finding is reported, a new code has been needed—and has now been added—to explain the reason for a second mammogram.

Because of the added code, ICD-9 also decided to revise wording for the 793 code category (until now, it’s been Nonspecific abnormal findings on radiological and other examination of body structure) to a more general heading of Nonspecific findings, which covers inconclusive and abnormal findings.

793.82  Inconclusive mammogram

FERTILITY PRESERVATION PRIOR TO ANTINEOPLASTIC THERAPY

Two new codes have been added to this area of practice at the request of the American Society for Reproductive Medicine (ASRM) and ACOG. They allow you to report visits and procedures aimed at preserving fertility in women who must undergo chemotherapy, surgery, or radiation therapy that might otherwise leave them sterile.

The codes reflect that, before a patient is treated, you may discuss a range of options that can increase her chances of becoming pregnant, including:

• conception before cancer treatment
  
• banking of sperm, eggs, ovarian tissue, and embryos
  
• protecting the ovaries during radiation therapy
  
• modifying surgery to spare the uterus.
  

V26.42  Encounter for fertility preservation counseling

V26.82  Encounter for fertility preservation procedure

PREPROCEDURAL EVALUATIONS

Code category V72.6 has been expanded from four to five digits to better capture reasons for ordering or performing laboratory tests that are not specifically linked to a medical diagnosis.

For example: If you order routine tests as part of a routine, general medical or gyn annual examination, report code V72.62. For routine preoperative lab tests, report V72.63 instead.

ICD-9 has clarified that V72.61 can be reported for testing of immune status, and that current code V72.83 (Other specified pre-operative examination) is the one to report when an exam precedes chemotherapy.

Note: ICD-9 rules require that you list the preprocedural examination code as the primary diagnosis, followed by the code that represents the reason for the surgery or procedure.

V72.60  Laboratory examination, unspecified

V72.61  Antibody response examination

V72.62  Laboratory examination ordered as part of a routine general medical examination

V72.63  Preprocedural laboratory examination

V72.69  Other laboratory examination

PERSONAL HISTORY CODES

A history of drug therapy can affect the care that you are giving a patient now, and may require testing from time to time to assess the consequences of such therapy.

Two examples are long-term estrogen therapy, which may increase a woman’s risk of developing breast cancer, and inhaled steroids, which can decrease bone density. In the absence of a known problem with these (or other) therapies in a given patient, new history codes listed below may be useful in communicating with a payer about ongoing follow-up care or testing that you are providing.

V87.43  Personal history of estrogen therapy

V87.44  Personal history of inhaled steroid therapy

V87.45  Personal history of systemic steroid therapy

V87.46  Personal history of immunosuppressive therapy

Plus a number of miscellaneous additions and changes

Here are few more new codes that may better explain why you saw a patient, provided:

• the new code for swine flu is reported only for a confirmed case, per ICD-9 rules
  
• the new V codes are reported only if the personal history or family circumstance affected treatment at the time of the visit, or if the patient was receiving counseling concerning only those issues.
  

995.24  Failed moderate sedation during procedure

V10.90  Personal history of unspecified type of malignant neoplasm

V15.80  Personal history of failed moderate sedation

V61.07  Family disruption due to death of family member

V61.08  Family disruption due to other extended absence of a family member

V61.42  Substance abuse in family

Additions and revision to this year’s International Classification of Diseases, Clinical Modification (ICD-9-CM)—which go into effect on October 1—reflect tinkering with existing codes and expansion of others to boost granularity and clarity in your reporting of diagnostic work. To that add a number of new codes—including one that acknowledges the arrival of the H1N1 (swine flu) virus nationwide.

In obstetrics, there are now specific codes for different types of puerperal infection and a requirement for more diagnostic information when a patient has venous complications during pregnancy and intrapartum.

On the gynecology side, changes include the way you report a finding of endometrial intraepithelial neoplasia. New codes have been created to report:

• visits and procedures for fertility preservation
  
• inconclusive mammography
  
• preprocedural laboratory testing.
  

Remember: On October 1, 2009, the new and revised codes discussed here, plus others, will be added to the national ICD-9-CM code set. Be cautioned that, as in past years, there is no grace period!

Changes to obstetric codes

PUERPERAL INFECTIONS

Before October 1, 2009, all puerperal infections were lumped into one code: 670.0 (Major puerperal infection). This changes now: You’ll be required to document, more specifically, the type of infection that your patient has.

Continue to report code 670.0 for an unspecified puerperal infection; but, if you admit the patient to the hospital, using that unspecified code may lead to a first-submission denial of claim. A fifth digit is also required for the unspecified and new more specific codes: 0 (unspecified as to episode of care or not applicable), 2 (delivered with mention of postpartum complication), or 4 (postpartum condition or complication) (to be reported only once the patient is discharged after delivery).

670.1x [0,2,4]  Puerperal endometritis

670.2x [0,2,4]  Puerperal sepsis

670.3x [0,2,4]  Puerperal septic thrombophlebitis

670.8x [0,2,4]  Other major puerperal infection

VENOUS COMPLICATIONS IN PREGNANCY AND PUERPERIUM

Code category 671 (venous complications in pregnancy and the puerperium) retains its current codes, but ICD-9 has added notes to clarify that additional information is required.

For example: When a patient has deep-vein thrombosis, either antepartum (671.3x) or postpartum (671.4x), assign a secondary diagnosis from code category 453 (Other venous embolism and thrombosis). If, in addition, the patient has been taking an anticoagulant for a long time and is currently taking it, report code V56.81, as well, to indicate this.

Gyn code changes

HYPERPLASIA

Over time, codes for hyperplasia have evolved from a system that described mild, moderate, severe, or atypical, to one in which hyperplasia was subdivided by architectural complexity, such as simple versus complex and whether or not atypia were present. Even this terminology fails, however, to adequately identify patients’ risk of cancer to improve therapeutic triaging.

In more recent years, physicians and pathologists have begun to distinguish benign hormonal effects of unopposed estrogen, classified as benign hyperplasia, from pre-cancerous lesions classified as endometrial intraepithelial neoplasia (EIN). To capture this newer terminology, ICD-9 has added two new codes.

ICD-9 has elected to retain existing codes in this area of diagnosis and assessment because the old terminology is still used by many older practicing physicians. The hope, however, is that, over time, more accurate distinctions between the types of hyperplasia will replace the older distinctions.

A note in ICD-9 will instruct providers that older codes may not be reported if one of the newer codes is assigned.

An additional note that accompanies the EIN diagnosis indicates that, if a patient is given a diagnosis of malignant neoplasm of the endometrium with endometrial intraepithelial neoplasia, the code for the malignancy (182.0, Malignant neoplasm of body of uterus; corpus uteri, except isthmus) would be reported instead of the EIN code.

621.34  Benign endometrial hyperplasia

621.35  Endometrial intraepithelial neoplasia

INCONCLUSIVE MAMMOGRAM

Routine mammograms are, as you know, sometimes labeled “inconclusive” because of what are termed “dense breasts.” This finding isn’t considered to represent an abnormal condition, but it does require further testing to confirm that no malignant condition exists that cannot be seen on mammogram.

Because many payers cover a repeat mammogram only when an abnormal finding is reported, a new code has been needed—and has now been added—to explain the reason for a second mammogram.

Because of the added code, ICD-9 also decided to revise wording for the 793 code category (until now, it’s been Nonspecific abnormal findings on radiological and other examination of body structure) to a more general heading of Nonspecific findings, which covers inconclusive and abnormal findings.

793.82  Inconclusive mammogram

FERTILITY PRESERVATION PRIOR TO ANTINEOPLASTIC THERAPY

Two new codes have been added to this area of practice at the request of the American Society for Reproductive Medicine (ASRM) and ACOG. They allow you to report visits and procedures aimed at preserving fertility in women who must undergo chemotherapy, surgery, or radiation therapy that might otherwise leave them sterile.

The codes reflect that, before a patient is treated, you may discuss a range of options that can increase her chances of becoming pregnant, including:

• conception before cancer treatment
  
• banking of sperm, eggs, ovarian tissue, and embryos
  
• protecting the ovaries during radiation therapy
  
• modifying surgery to spare the uterus.
  

V26.42  Encounter for fertility preservation counseling

V26.82  Encounter for fertility preservation procedure

PREPROCEDURAL EVALUATIONS

Code category V72.6 has been expanded from four to five digits to better capture reasons for ordering or performing laboratory tests that are not specifically linked to a medical diagnosis.

For example: If you order routine tests as part of a routine, general medical or gyn annual examination, report code V72.62. For routine preoperative lab tests, report V72.63 instead.

ICD-9 has clarified that V72.61 can be reported for testing of immune status, and that current code V72.83 (Other specified pre-operative examination) is the one to report when an exam precedes chemotherapy.

Note: ICD-9 rules require that you list the preprocedural examination code as the primary diagnosis, followed by the code that represents the reason for the surgery or procedure.

V72.60  Laboratory examination, unspecified

V72.61  Antibody response examination

V72.62  Laboratory examination ordered as part of a routine general medical examination

V72.63  Preprocedural laboratory examination

V72.69  Other laboratory examination

PERSONAL HISTORY CODES

A history of drug therapy can affect the care that you are giving a patient now, and may require testing from time to time to assess the consequences of such therapy.

Two examples are long-term estrogen therapy, which may increase a woman’s risk of developing breast cancer, and inhaled steroids, which can decrease bone density. In the absence of a known problem with these (or other) therapies in a given patient, new history codes listed below may be useful in communicating with a payer about ongoing follow-up care or testing that you are providing.

V87.43  Personal history of estrogen therapy

V87.44  Personal history of inhaled steroid therapy

V87.45  Personal history of systemic steroid therapy

V87.46  Personal history of immunosuppressive therapy

Plus a number of miscellaneous additions and changes

Here are few more new codes that may better explain why you saw a patient, provided:

• the new code for swine flu is reported only for a confirmed case, per ICD-9 rules
  
• the new V codes are reported only if the personal history or family circumstance affected treatment at the time of the visit, or if the patient was receiving counseling concerning only those issues.
  

995.24  Failed moderate sedation during procedure

V10.90  Personal history of unspecified type of malignant neoplasm

V15.80  Personal history of failed moderate sedation

V61.07  Family disruption due to death of family member

V61.08  Family disruption due to other extended absence of a family member

V61.42  Substance abuse in family

This coming flu season will be interesting—and confusing. As of August 6, 2009, the Centers for Disease Control and Prevention (CDC) reported 6506 hospitalized cases and 436 deaths from the pandemic H1N1 flu virus since the first US cases were reported in April 2009.¹ (Reporting on individual confirmed and probable cases has been discontinued.) On July 31, the World Health Organization reported pandemic influenza in 168 countries, with 162,380 reported cases and 1154 deaths.² At the same time the pandemic was developing, the seasonal flu of 2009—a relatively mild year—was tapering off. The pandemic influenza has continued to cause widespread disease in the United States throughout the summer, a somewhat unusual pattern for influenza.

So far, pandemic H1N1 flu is relatively benign, treatable

The pandemic virus, though highly infectious, has had a low case fatality rate up to now. Deaths have occurred predominantly in those with underlying medical conditions that put them at high risk of infection. Attack rates for those older than age 65 have been lower than expected, indicating that this age group may have some immunity based on past infection. The pandemic virus so far has been sensitive to both oseltamivir (Tamiflu) and zanamivir (Relenza). The resistance patterns of the key viruses from last flu season showed that the H1N1 seasonal virus was resistant to oseltamivir but sensitive to zanamivir and the adamantanes (rimantadine and amantadine), while the H3N2 virus that circulated last year was sensitive to oseltamivir.³

Fall flu season: Be prepared

So, what can you expect this fall? With pandemic H1N1 still causing illness and strains of seasonal virus circulating elsewhere in the world, no one knows for sure. But it is very likely that we will experience much higher rates of pandemic influenza once schools reopen and children begin to congregate. It is also likely we will have pandemic influenza circulating along with seasonal influenza viruses this fall and into 2010.

Immunize for seasonal flu, now

The 2009-2010 seasonal influenza vaccine will contain antigens from 3 strains: a nonpandemic H1N1 influenza A strain, an H3N2 influenza A strain, and an influenza B strain.⁴ These 3 antigens will be in all seasonal influenza vaccine products, whether they are the trivalent influenza vaccine given by injection or the live attenuated influenza vaccine provided as a nasal spray. The CDC is recommending immunization against seasonal influenza as soon as the vaccine is available.

The groups for whom seasonal influenza vaccine is recommended have not changed from last year. The recommendations are summarized in the TABLE.

TABLE
Who should get seasonal flu vaccine, 2009-2010?

Pandemic flu vaccine will be available in the fall

The vaccine for pandemic H1N1 is being produced, and the Department of Health and Human Services is projecting it to be available starting in mid- to late October. The supply will be limited at first, with increasing quantities produced as time progresses. The intent is to produce 600 million doses, or 2 per US resident, since 2 doses will be required.

Who should get the vaccine for pandemic H1N1? At its meeting at the end of July, the Advisory Committee on Immunization Practices (ACIP) recommended that vaccination efforts focus on 5 key populations:

• pregnant women
• people who live with, or care for, children <6 months of age
• health care and emergency services personnel
• individuals between the ages of 6 months and 24 years
• individuals 25 to 64 years of age who are at higher risk for novel H1N1 because of chronic health disorders or compromised immune systems.

In the event of initial shortages of the vaccine, the first 3 groups listed above should be given priority, along with children 6 months through 4 years of age and children 5 through 18 years who have chronic medical conditions.⁵ In the event of a vaccine surplus (due to low demand and/or faster-than-expected supply), prioritization will not apply and the vaccine should be administered to anyone requesting it who does not have a contraindication.

It is not known how the pandemic influenza vaccine will be distributed and administered. The extent of involvement by physician offices and clinics is undetermined and may vary by locale. There may be extensive use of mass immunization clinics and school clinics to administer the vaccine quickly. Administration will be complicated by the need for 2 doses for protection and a perception by the public that the pandemic virus is not a major concern.

Medical practices may be administering 2 influenza vaccines with different dose requirements: a single dose for seasonal influenza vaccine (except for children <9 years who are being vaccinated for the first time; they get 2 doses), and 2 doses for pandemic vaccine.

Antivirals protect vulnerable patients

Antiviral medications can be used for chemoprophylaxis, both to prevent infection in patients with a high-risk medical condition who are not, or cannot be, vaccinated (chemoprevention), and for post-exposure prophylaxis (PEP) for those who are at risk for complications or want to avoid illness. PEP is time limited (5 days), while chemoprevention may be needed for the duration of potential exposure during an outbreak or epidemic.

PEP should be considered for residents in an assisted living facility during an influenza outbreak, and for individuals who are at higher risk for influenza-related complications and who have had recent household or other close contact with a person with laboratory-confirmed influenza. Chemoprevention is an option with limited applicability at this time. If the pandemic virus were to become more virulent, it might be considered for health care workers until they had received 2 doses of vaccine.

Follow recommendations for antiviral treatment

Because resistance patterns differ among flu viruses, the decision on which antiviral or combination of antivirals to use depends on the predominant viruses circulating in the community and on laboratory tests from the infected patient to determine the influenza type involved. Current recommendations for seasonal influenza can be found at http://www2a.cdc.gov/han/ArchiveSys/ViewMsgV.asp?AlertNum=00279, and recommendations for pandemic influenza are at http://www.cdc.gov/h1n1flu/recommendations.htm#table1. These recommendations may change as the season progresses and viral resistance patterns are determined.

Consider antiviral treatment for those at high risk for complications from the virus. These include anyone hospitalized for influenza, children <5 years of age (especially those <2 years), adults ≥65 years of age, and individuals with the following conditions:

• chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, hematologic (including sickle cell disease), neurologic, neuromuscular, or metabolic disorders (including diabetes mellitus)
• immunosuppression, including that caused by medications or by HIV
• pregnant women
• individuals <19 years of age who are receiving long-term aspirin therapy
• residents of nursing homes and other chronic-care facilities.

The evidence for antiviral effectiveness is strongest if it is given within the first 48 hours of symptom onset, although in hospitalized patients, there is some evidence of effectiveness if started after this time.

Be diligent about infection control

Physicians and other health care workers will need to practice good infection control this flu season. This has been the topic of a previous Practice Alert.⁶ All health care workers should be fully immunized against influenza—seasonal and pandemic. In addition, each clinical practice should plan on implementing policies to prevent the spread of infection within the clinic or office. Such policies might include scheduling patients with respiratory illnesses for later in the day, separating patients with respiratory illnesses from other patients, requiring patients to cover their nose and mouth when they cough or sneeze, and providing tissues and hand sanitizers for patients and staff.

Physicians and staff will need to take measures to protect themselves from infection by frequent hand washing, avoiding work when ill, and using personal protective equipment when there is potential exposure to respiratory droplets.⁷ It will also be important to teach families to follow infection control practices at home whenever a household member has an influenza-like illness. Recommendations for home care can be found at www.cdc.gov/h1n1flu/guidance_homecare.htm/?x_cid=ccu071309_HomeCareGuidance_e.

Stay on top of the situation

As this influenza season progresses, keeping current about influenza recommendations will be crucial. The 3 issues to say on top of are:

1. Who should receive the vaccine for pandemic influenza and where will it be administered?
2. What influenza viruses are circulating in the community?
3. What is happening to antiviral resistance patterns and how are changes in these patterns affecting recommendations for treatment and chemoprophylaxis?

Web sites that will keep you up to date

• The CDC influenza Web site: http://www.cdc.gov/flu
• Your local and state public health department Web sites
• The American Academy of Family Physicians (AAFP) Web site: http://www.aafp.org/online/en/home.html.

CORRESPONDENCE
Doug Campos-Outcalt, MD, MPA, 550 E. Van Buren, Phoenix, AZ 85004; dougco@u.arizona.edu

This coming flu season will be interesting—and confusing. As of August 6, 2009, the Centers for Disease Control and Prevention (CDC) reported 6506 hospitalized cases and 436 deaths from the pandemic H1N1 flu virus since the first US cases were reported in April 2009.¹ (Reporting on individual confirmed and probable cases has been discontinued.) On July 31, the World Health Organization reported pandemic influenza in 168 countries, with 162,380 reported cases and 1154 deaths.² At the same time the pandemic was developing, the seasonal flu of 2009—a relatively mild year—was tapering off. The pandemic influenza has continued to cause widespread disease in the United States throughout the summer, a somewhat unusual pattern for influenza.

So far, pandemic H1N1 flu is relatively benign, treatable

The pandemic virus, though highly infectious, has had a low case fatality rate up to now. Deaths have occurred predominantly in those with underlying medical conditions that put them at high risk of infection. Attack rates for those older than age 65 have been lower than expected, indicating that this age group may have some immunity based on past infection. The pandemic virus so far has been sensitive to both oseltamivir (Tamiflu) and zanamivir (Relenza). The resistance patterns of the key viruses from last flu season showed that the H1N1 seasonal virus was resistant to oseltamivir but sensitive to zanamivir and the adamantanes (rimantadine and amantadine), while the H3N2 virus that circulated last year was sensitive to oseltamivir.³

Fall flu season: Be prepared

So, what can you expect this fall? With pandemic H1N1 still causing illness and strains of seasonal virus circulating elsewhere in the world, no one knows for sure. But it is very likely that we will experience much higher rates of pandemic influenza once schools reopen and children begin to congregate. It is also likely we will have pandemic influenza circulating along with seasonal influenza viruses this fall and into 2010.

Immunize for seasonal flu, now

The 2009-2010 seasonal influenza vaccine will contain antigens from 3 strains: a nonpandemic H1N1 influenza A strain, an H3N2 influenza A strain, and an influenza B strain.⁴ These 3 antigens will be in all seasonal influenza vaccine products, whether they are the trivalent influenza vaccine given by injection or the live attenuated influenza vaccine provided as a nasal spray. The CDC is recommending immunization against seasonal influenza as soon as the vaccine is available.

The groups for whom seasonal influenza vaccine is recommended have not changed from last year. The recommendations are summarized in the TABLE.

TABLE
Who should get seasonal flu vaccine, 2009-2010?

Pandemic flu vaccine will be available in the fall

The vaccine for pandemic H1N1 is being produced, and the Department of Health and Human Services is projecting it to be available starting in mid- to late October. The supply will be limited at first, with increasing quantities produced as time progresses. The intent is to produce 600 million doses, or 2 per US resident, since 2 doses will be required.

Who should get the vaccine for pandemic H1N1? At its meeting at the end of July, the Advisory Committee on Immunization Practices (ACIP) recommended that vaccination efforts focus on 5 key populations:

• pregnant women
• people who live with, or care for, children <6 months of age
• health care and emergency services personnel
• individuals between the ages of 6 months and 24 years
• individuals 25 to 64 years of age who are at higher risk for novel H1N1 because of chronic health disorders or compromised immune systems.

In the event of initial shortages of the vaccine, the first 3 groups listed above should be given priority, along with children 6 months through 4 years of age and children 5 through 18 years who have chronic medical conditions.⁵ In the event of a vaccine surplus (due to low demand and/or faster-than-expected supply), prioritization will not apply and the vaccine should be administered to anyone requesting it who does not have a contraindication.

It is not known how the pandemic influenza vaccine will be distributed and administered. The extent of involvement by physician offices and clinics is undetermined and may vary by locale. There may be extensive use of mass immunization clinics and school clinics to administer the vaccine quickly. Administration will be complicated by the need for 2 doses for protection and a perception by the public that the pandemic virus is not a major concern.

Medical practices may be administering 2 influenza vaccines with different dose requirements: a single dose for seasonal influenza vaccine (except for children <9 years who are being vaccinated for the first time; they get 2 doses), and 2 doses for pandemic vaccine.

Antivirals protect vulnerable patients

Antiviral medications can be used for chemoprophylaxis, both to prevent infection in patients with a high-risk medical condition who are not, or cannot be, vaccinated (chemoprevention), and for post-exposure prophylaxis (PEP) for those who are at risk for complications or want to avoid illness. PEP is time limited (5 days), while chemoprevention may be needed for the duration of potential exposure during an outbreak or epidemic.

PEP should be considered for residents in an assisted living facility during an influenza outbreak, and for individuals who are at higher risk for influenza-related complications and who have had recent household or other close contact with a person with laboratory-confirmed influenza. Chemoprevention is an option with limited applicability at this time. If the pandemic virus were to become more virulent, it might be considered for health care workers until they had received 2 doses of vaccine.

Follow recommendations for antiviral treatment

Because resistance patterns differ among flu viruses, the decision on which antiviral or combination of antivirals to use depends on the predominant viruses circulating in the community and on laboratory tests from the infected patient to determine the influenza type involved. Current recommendations for seasonal influenza can be found at http://www2a.cdc.gov/han/ArchiveSys/ViewMsgV.asp?AlertNum=00279, and recommendations for pandemic influenza are at http://www.cdc.gov/h1n1flu/recommendations.htm#table1. These recommendations may change as the season progresses and viral resistance patterns are determined.

Consider antiviral treatment for those at high risk for complications from the virus. These include anyone hospitalized for influenza, children <5 years of age (especially those <2 years), adults ≥65 years of age, and individuals with the following conditions:

• chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, hematologic (including sickle cell disease), neurologic, neuromuscular, or metabolic disorders (including diabetes mellitus)
• immunosuppression, including that caused by medications or by HIV
• pregnant women
• individuals <19 years of age who are receiving long-term aspirin therapy
• residents of nursing homes and other chronic-care facilities.

The evidence for antiviral effectiveness is strongest if it is given within the first 48 hours of symptom onset, although in hospitalized patients, there is some evidence of effectiveness if started after this time.

Be diligent about infection control

Physicians and other health care workers will need to practice good infection control this flu season. This has been the topic of a previous Practice Alert.⁶ All health care workers should be fully immunized against influenza—seasonal and pandemic. In addition, each clinical practice should plan on implementing policies to prevent the spread of infection within the clinic or office. Such policies might include scheduling patients with respiratory illnesses for later in the day, separating patients with respiratory illnesses from other patients, requiring patients to cover their nose and mouth when they cough or sneeze, and providing tissues and hand sanitizers for patients and staff.

Physicians and staff will need to take measures to protect themselves from infection by frequent hand washing, avoiding work when ill, and using personal protective equipment when there is potential exposure to respiratory droplets.⁷ It will also be important to teach families to follow infection control practices at home whenever a household member has an influenza-like illness. Recommendations for home care can be found at www.cdc.gov/h1n1flu/guidance_homecare.htm/?x_cid=ccu071309_HomeCareGuidance_e.

Stay on top of the situation

As this influenza season progresses, keeping current about influenza recommendations will be crucial. The 3 issues to say on top of are:

1. Who should receive the vaccine for pandemic influenza and where will it be administered?
2. What influenza viruses are circulating in the community?
3. What is happening to antiviral resistance patterns and how are changes in these patterns affecting recommendations for treatment and chemoprophylaxis?

Web sites that will keep you up to date

• The CDC influenza Web site: http://www.cdc.gov/flu
• Your local and state public health department Web sites
• The American Academy of Family Physicians (AAFP) Web site: http://www.aafp.org/online/en/home.html.

CORRESPONDENCE
Doug Campos-Outcalt, MD, MPA, 550 E. Van Buren, Phoenix, AZ 85004; dougco@u.arizona.edu

This coming flu season will be interesting—and confusing. As of August 6, 2009, the Centers for Disease Control and Prevention (CDC) reported 6506 hospitalized cases and 436 deaths from the pandemic H1N1 flu virus since the first US cases were reported in April 2009.¹ (Reporting on individual confirmed and probable cases has been discontinued.) On July 31, the World Health Organization reported pandemic influenza in 168 countries, with 162,380 reported cases and 1154 deaths.² At the same time the pandemic was developing, the seasonal flu of 2009—a relatively mild year—was tapering off. The pandemic influenza has continued to cause widespread disease in the United States throughout the summer, a somewhat unusual pattern for influenza.

So far, pandemic H1N1 flu is relatively benign, treatable

The pandemic virus, though highly infectious, has had a low case fatality rate up to now. Deaths have occurred predominantly in those with underlying medical conditions that put them at high risk of infection. Attack rates for those older than age 65 have been lower than expected, indicating that this age group may have some immunity based on past infection. The pandemic virus so far has been sensitive to both oseltamivir (Tamiflu) and zanamivir (Relenza). The resistance patterns of the key viruses from last flu season showed that the H1N1 seasonal virus was resistant to oseltamivir but sensitive to zanamivir and the adamantanes (rimantadine and amantadine), while the H3N2 virus that circulated last year was sensitive to oseltamivir.³

Fall flu season: Be prepared

So, what can you expect this fall? With pandemic H1N1 still causing illness and strains of seasonal virus circulating elsewhere in the world, no one knows for sure. But it is very likely that we will experience much higher rates of pandemic influenza once schools reopen and children begin to congregate. It is also likely we will have pandemic influenza circulating along with seasonal influenza viruses this fall and into 2010.

Immunize for seasonal flu, now

The 2009-2010 seasonal influenza vaccine will contain antigens from 3 strains: a nonpandemic H1N1 influenza A strain, an H3N2 influenza A strain, and an influenza B strain.⁴ These 3 antigens will be in all seasonal influenza vaccine products, whether they are the trivalent influenza vaccine given by injection or the live attenuated influenza vaccine provided as a nasal spray. The CDC is recommending immunization against seasonal influenza as soon as the vaccine is available.

The groups for whom seasonal influenza vaccine is recommended have not changed from last year. The recommendations are summarized in the TABLE.

TABLE
Who should get seasonal flu vaccine, 2009-2010?

Pandemic flu vaccine will be available in the fall

The vaccine for pandemic H1N1 is being produced, and the Department of Health and Human Services is projecting it to be available starting in mid- to late October. The supply will be limited at first, with increasing quantities produced as time progresses. The intent is to produce 600 million doses, or 2 per US resident, since 2 doses will be required.

Who should get the vaccine for pandemic H1N1? At its meeting at the end of July, the Advisory Committee on Immunization Practices (ACIP) recommended that vaccination efforts focus on 5 key populations:

• pregnant women
• people who live with, or care for, children <6 months of age
• health care and emergency services personnel
• individuals between the ages of 6 months and 24 years
• individuals 25 to 64 years of age who are at higher risk for novel H1N1 because of chronic health disorders or compromised immune systems.

In the event of initial shortages of the vaccine, the first 3 groups listed above should be given priority, along with children 6 months through 4 years of age and children 5 through 18 years who have chronic medical conditions.⁵ In the event of a vaccine surplus (due to low demand and/or faster-than-expected supply), prioritization will not apply and the vaccine should be administered to anyone requesting it who does not have a contraindication.

It is not known how the pandemic influenza vaccine will be distributed and administered. The extent of involvement by physician offices and clinics is undetermined and may vary by locale. There may be extensive use of mass immunization clinics and school clinics to administer the vaccine quickly. Administration will be complicated by the need for 2 doses for protection and a perception by the public that the pandemic virus is not a major concern.

Medical practices may be administering 2 influenza vaccines with different dose requirements: a single dose for seasonal influenza vaccine (except for children <9 years who are being vaccinated for the first time; they get 2 doses), and 2 doses for pandemic vaccine.

Antivirals protect vulnerable patients

Antiviral medications can be used for chemoprophylaxis, both to prevent infection in patients with a high-risk medical condition who are not, or cannot be, vaccinated (chemoprevention), and for post-exposure prophylaxis (PEP) for those who are at risk for complications or want to avoid illness. PEP is time limited (5 days), while chemoprevention may be needed for the duration of potential exposure during an outbreak or epidemic.

PEP should be considered for residents in an assisted living facility during an influenza outbreak, and for individuals who are at higher risk for influenza-related complications and who have had recent household or other close contact with a person with laboratory-confirmed influenza. Chemoprevention is an option with limited applicability at this time. If the pandemic virus were to become more virulent, it might be considered for health care workers until they had received 2 doses of vaccine.

Follow recommendations for antiviral treatment

Because resistance patterns differ among flu viruses, the decision on which antiviral or combination of antivirals to use depends on the predominant viruses circulating in the community and on laboratory tests from the infected patient to determine the influenza type involved. Current recommendations for seasonal influenza can be found at http://www2a.cdc.gov/han/ArchiveSys/ViewMsgV.asp?AlertNum=00279, and recommendations for pandemic influenza are at http://www.cdc.gov/h1n1flu/recommendations.htm#table1. These recommendations may change as the season progresses and viral resistance patterns are determined.

Consider antiviral treatment for those at high risk for complications from the virus. These include anyone hospitalized for influenza, children <5 years of age (especially those <2 years), adults ≥65 years of age, and individuals with the following conditions:

• chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, hematologic (including sickle cell disease), neurologic, neuromuscular, or metabolic disorders (including diabetes mellitus)
• immunosuppression, including that caused by medications or by HIV
• pregnant women
• individuals <19 years of age who are receiving long-term aspirin therapy
• residents of nursing homes and other chronic-care facilities.

The evidence for antiviral effectiveness is strongest if it is given within the first 48 hours of symptom onset, although in hospitalized patients, there is some evidence of effectiveness if started after this time.

Be diligent about infection control

Physicians and other health care workers will need to practice good infection control this flu season. This has been the topic of a previous Practice Alert.⁶ All health care workers should be fully immunized against influenza—seasonal and pandemic. In addition, each clinical practice should plan on implementing policies to prevent the spread of infection within the clinic or office. Such policies might include scheduling patients with respiratory illnesses for later in the day, separating patients with respiratory illnesses from other patients, requiring patients to cover their nose and mouth when they cough or sneeze, and providing tissues and hand sanitizers for patients and staff.

Physicians and staff will need to take measures to protect themselves from infection by frequent hand washing, avoiding work when ill, and using personal protective equipment when there is potential exposure to respiratory droplets.⁷ It will also be important to teach families to follow infection control practices at home whenever a household member has an influenza-like illness. Recommendations for home care can be found at www.cdc.gov/h1n1flu/guidance_homecare.htm/?x_cid=ccu071309_HomeCareGuidance_e.

Stay on top of the situation

As this influenza season progresses, keeping current about influenza recommendations will be crucial. The 3 issues to say on top of are:

1. Who should receive the vaccine for pandemic influenza and where will it be administered?
2. What influenza viruses are circulating in the community?
3. What is happening to antiviral resistance patterns and how are changes in these patterns affecting recommendations for treatment and chemoprophylaxis?

Web sites that will keep you up to date

• The CDC influenza Web site: http://www.cdc.gov/flu
• Your local and state public health department Web sites
• The American Academy of Family Physicians (AAFP) Web site: http://www.aafp.org/online/en/home.html.

CORRESPONDENCE
Doug Campos-Outcalt, MD, MPA, 550 E. Van Buren, Phoenix, AZ 85004; dougco@u.arizona.edu

Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; krafczm@slhn.org

Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; krafczm@slhn.org

Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; krafczm@slhn.org

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

pdnews@elsevier.com

Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

pdnews@elsevier.com

Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

pdnews@elsevier.com

Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”