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Your guide to the new pneumococcal vaccine for children
A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.1 PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.1
Invasive pneumococcal disease in kids has diminished substantially
Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.3 This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.
However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.3 The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.3
Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.3 As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.3
Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.6 Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.
The dosing schedule is complicated
The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.
The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.
TABLE 1
PCV13: Routine vaccination schedule
Age at first dose | Primary series* | Booster dose† |
---|---|---|
2-6 months | 3 doses | 1 dose, 12-15 months |
7-11 months | 2 doses | 1 dose, 12-15 months |
12-23 months | 2 doses | None |
24-59 months, healthy children | 1 dose | None |
24-71 months for children with certain chronic diseases or immunocompromising conditions (see TABLE 3) | 2 doses | None |
*Minimum interval between doses is 8 weeks, except for children vaccinated at <12 months for whom the minimum interval is 4 weeks. Minimum age for first dose is 6 weeks. | ||
†Given at least 8 weeks after previous dose. | ||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
TABLE 2
In transition: From PCV7 to PCV13
Infant series | Booster dose | Supplemental PCV13 dose | ||
---|---|---|---|---|
2 months | 4 months | 6 months | ≥12 months* | 14-59 months† |
PCV7 | PCV13 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV7 | PCV13 |
*No additional PCV13 doses are indicated for children ages 12-23 months who have received 2 or 3 doses of PCV before age 12 months and at least 1 dose of PCV13 at ≥12 months. | ||||
†For children with underlying medical conditions (see TABLE 3), a single supplemental PCV13 dose is recommended through age 71 months. | ||||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.
If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.1)
Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.
Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).
Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.
Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.1
TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease
Risk group | Condition |
---|---|
Immunocompetent children | Chronic heart disease* |
Chronic lung disease† | |
Diabetes mellitus | |
Cerebrospinal fluid leaks | |
Cochlear implant | |
Children with functional or anatomic asplenia | Sickle cell disease and other hemoglobulinopathies |
Congenital or acquired asplenia or splenic dysfunction | |
Children with immunocompromising conditions | HIV infection |
Chronic renal failure and nephrotic syndrome | |
Diseases associated with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin’s disease; or solid organ transplantation | |
Congenital immunodeficiency‡ | |
*Particularly cyanotic congenital heart disease and cardiac failure. | |
†Including asthma if treated with prolonged high-dose oral corticosteroids. | |
‡Includes B- (humoral) or T-lymphocyte deficiency; complement deficiencies, particularly C1, C2, C3, and C4 deficiency; and phagocytic disorders (excluding chronic granulomatous disease). | |
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
Recommendations for children at higher risk
Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.
However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.9
The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.9 This, however, is an off-label recommendation.
The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.1
A useful vaccine, with its share of challenges
The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.
The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.10 Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.11
With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.
1. CDC. Licensure of a 13-valent pneumococcal conjugate vaccine (PCV13) and recommendations for use among children—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2010;59:258-261.
2. Hicks LA, Harrison LH, Flannery B, et al. Incidence of pneumococcal disease due to nonpneumococcal conjugate vaccine (PCV7) serotypes in the United States during the era of widespread PCV7 vaccination, 1998-2004. J Infect Dis. 2007;196:1346-1354.
3. Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis. 2010;201:32-41.
4. Whitney CG, Farley MM, Hadler J, et al. Decline in invasive pneumococcal disease after the introduction of protein-polysaccharide conjugate vaccine. N Engl J Med. 2003;348:1737-1746.
5. Direct and indirect effects of routine vaccination of children with 7-valent pneumococcal conjugate vaccine on incidence of invasive pneumococcal disease—United States, 1998-2003. MMWR Morb Mortal Wkly Rep. 2005;54:893-897.
6. CDC. Invasive pneumococcal disease in young children before licensure of 13-valent pneumococcal conjugate vaccine—United States, 2007. MMWR Morb Mortal Wkly Rep. 2010;59:253-257.
7. CDC. Preventing pneumococcal disease among infants and young children: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2000;49(RR-9):1-35.
8. CDC. Updated recommendation from the Advisory Committee on Immunization Practices (ACIP) for use of 7-valent pneumococcal conjugate vaccine (PCV7) in children aged 24-59 months who are not completely vaccinated. MMWR Morb Mortal Wkly Rep. 2008;57:343-344.
9. ACIP provisional recommendations for use of 13-valent pneumococcal conjugate vaccine (PCV13) among infants and children. March 3, 2010. Available at: www.cdc.gov/vaccines/recs/provisional/downloads/pcv13-mar-2010-508.pdf. Accessed May 24, 2010.
10. CDC vaccine price list. Available at: www.cdc.gov/vaccines/programs/vfc/cdc-vac-price-list.htm. Accessed May 22, 2010.
11. Vaccines for Children Program. FAQs from providers. Available at www.cdc.gov/vaccines/programs/vfc/providers/faq-hcp. htm. Accessed May 22, 2010.
A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.1 PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.1
Invasive pneumococcal disease in kids has diminished substantially
Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.3 This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.
However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.3 The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.3
Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.3 As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.3
Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.6 Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.
The dosing schedule is complicated
The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.
The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.
TABLE 1
PCV13: Routine vaccination schedule
Age at first dose | Primary series* | Booster dose† |
---|---|---|
2-6 months | 3 doses | 1 dose, 12-15 months |
7-11 months | 2 doses | 1 dose, 12-15 months |
12-23 months | 2 doses | None |
24-59 months, healthy children | 1 dose | None |
24-71 months for children with certain chronic diseases or immunocompromising conditions (see TABLE 3) | 2 doses | None |
*Minimum interval between doses is 8 weeks, except for children vaccinated at <12 months for whom the minimum interval is 4 weeks. Minimum age for first dose is 6 weeks. | ||
†Given at least 8 weeks after previous dose. | ||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
TABLE 2
In transition: From PCV7 to PCV13
Infant series | Booster dose | Supplemental PCV13 dose | ||
---|---|---|---|---|
2 months | 4 months | 6 months | ≥12 months* | 14-59 months† |
PCV7 | PCV13 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV7 | PCV13 |
*No additional PCV13 doses are indicated for children ages 12-23 months who have received 2 or 3 doses of PCV before age 12 months and at least 1 dose of PCV13 at ≥12 months. | ||||
†For children with underlying medical conditions (see TABLE 3), a single supplemental PCV13 dose is recommended through age 71 months. | ||||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.
If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.1)
Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.
Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).
Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.
Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.1
TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease
Risk group | Condition |
---|---|
Immunocompetent children | Chronic heart disease* |
Chronic lung disease† | |
Diabetes mellitus | |
Cerebrospinal fluid leaks | |
Cochlear implant | |
Children with functional or anatomic asplenia | Sickle cell disease and other hemoglobulinopathies |
Congenital or acquired asplenia or splenic dysfunction | |
Children with immunocompromising conditions | HIV infection |
Chronic renal failure and nephrotic syndrome | |
Diseases associated with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin’s disease; or solid organ transplantation | |
Congenital immunodeficiency‡ | |
*Particularly cyanotic congenital heart disease and cardiac failure. | |
†Including asthma if treated with prolonged high-dose oral corticosteroids. | |
‡Includes B- (humoral) or T-lymphocyte deficiency; complement deficiencies, particularly C1, C2, C3, and C4 deficiency; and phagocytic disorders (excluding chronic granulomatous disease). | |
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
Recommendations for children at higher risk
Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.
However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.9
The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.9 This, however, is an off-label recommendation.
The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.1
A useful vaccine, with its share of challenges
The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.
The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.10 Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.11
With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.
A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.1 PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.1
Invasive pneumococcal disease in kids has diminished substantially
Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.3 This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.
However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.3 The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.3
Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.3 As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.3
Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.6 Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.
The dosing schedule is complicated
The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.
The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.
TABLE 1
PCV13: Routine vaccination schedule
Age at first dose | Primary series* | Booster dose† |
---|---|---|
2-6 months | 3 doses | 1 dose, 12-15 months |
7-11 months | 2 doses | 1 dose, 12-15 months |
12-23 months | 2 doses | None |
24-59 months, healthy children | 1 dose | None |
24-71 months for children with certain chronic diseases or immunocompromising conditions (see TABLE 3) | 2 doses | None |
*Minimum interval between doses is 8 weeks, except for children vaccinated at <12 months for whom the minimum interval is 4 weeks. Minimum age for first dose is 6 weeks. | ||
†Given at least 8 weeks after previous dose. | ||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
TABLE 2
In transition: From PCV7 to PCV13
Infant series | Booster dose | Supplemental PCV13 dose | ||
---|---|---|---|---|
2 months | 4 months | 6 months | ≥12 months* | 14-59 months† |
PCV7 | PCV13 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV13 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV13 | None |
PCV7 | PCV7 | PCV7 | PCV7 | PCV13 |
*No additional PCV13 doses are indicated for children ages 12-23 months who have received 2 or 3 doses of PCV before age 12 months and at least 1 dose of PCV13 at ≥12 months. | ||||
†For children with underlying medical conditions (see TABLE 3), a single supplemental PCV13 dose is recommended through age 71 months. | ||||
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.
If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.1)
Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.
Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).
Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.
Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.1
TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease
Risk group | Condition |
---|---|
Immunocompetent children | Chronic heart disease* |
Chronic lung disease† | |
Diabetes mellitus | |
Cerebrospinal fluid leaks | |
Cochlear implant | |
Children with functional or anatomic asplenia | Sickle cell disease and other hemoglobulinopathies |
Congenital or acquired asplenia or splenic dysfunction | |
Children with immunocompromising conditions | HIV infection |
Chronic renal failure and nephrotic syndrome | |
Diseases associated with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin’s disease; or solid organ transplantation | |
Congenital immunodeficiency‡ | |
*Particularly cyanotic congenital heart disease and cardiac failure. | |
†Including asthma if treated with prolonged high-dose oral corticosteroids. | |
‡Includes B- (humoral) or T-lymphocyte deficiency; complement deficiencies, particularly C1, C2, C3, and C4 deficiency; and phagocytic disorders (excluding chronic granulomatous disease). | |
Source: CDC. MMWR Morb Mortal Wkly Rep. 2010.1 |
Recommendations for children at higher risk
Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.
However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.9
The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.9 This, however, is an off-label recommendation.
The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.1
A useful vaccine, with its share of challenges
The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.
The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.10 Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.11
With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.
1. CDC. Licensure of a 13-valent pneumococcal conjugate vaccine (PCV13) and recommendations for use among children—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2010;59:258-261.
2. Hicks LA, Harrison LH, Flannery B, et al. Incidence of pneumococcal disease due to nonpneumococcal conjugate vaccine (PCV7) serotypes in the United States during the era of widespread PCV7 vaccination, 1998-2004. J Infect Dis. 2007;196:1346-1354.
3. Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis. 2010;201:32-41.
4. Whitney CG, Farley MM, Hadler J, et al. Decline in invasive pneumococcal disease after the introduction of protein-polysaccharide conjugate vaccine. N Engl J Med. 2003;348:1737-1746.
5. Direct and indirect effects of routine vaccination of children with 7-valent pneumococcal conjugate vaccine on incidence of invasive pneumococcal disease—United States, 1998-2003. MMWR Morb Mortal Wkly Rep. 2005;54:893-897.
6. CDC. Invasive pneumococcal disease in young children before licensure of 13-valent pneumococcal conjugate vaccine—United States, 2007. MMWR Morb Mortal Wkly Rep. 2010;59:253-257.
7. CDC. Preventing pneumococcal disease among infants and young children: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2000;49(RR-9):1-35.
8. CDC. Updated recommendation from the Advisory Committee on Immunization Practices (ACIP) for use of 7-valent pneumococcal conjugate vaccine (PCV7) in children aged 24-59 months who are not completely vaccinated. MMWR Morb Mortal Wkly Rep. 2008;57:343-344.
9. ACIP provisional recommendations for use of 13-valent pneumococcal conjugate vaccine (PCV13) among infants and children. March 3, 2010. Available at: www.cdc.gov/vaccines/recs/provisional/downloads/pcv13-mar-2010-508.pdf. Accessed May 24, 2010.
10. CDC vaccine price list. Available at: www.cdc.gov/vaccines/programs/vfc/cdc-vac-price-list.htm. Accessed May 22, 2010.
11. Vaccines for Children Program. FAQs from providers. Available at www.cdc.gov/vaccines/programs/vfc/providers/faq-hcp. htm. Accessed May 22, 2010.
1. CDC. Licensure of a 13-valent pneumococcal conjugate vaccine (PCV13) and recommendations for use among children—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2010;59:258-261.
2. Hicks LA, Harrison LH, Flannery B, et al. Incidence of pneumococcal disease due to nonpneumococcal conjugate vaccine (PCV7) serotypes in the United States during the era of widespread PCV7 vaccination, 1998-2004. J Infect Dis. 2007;196:1346-1354.
3. Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis. 2010;201:32-41.
4. Whitney CG, Farley MM, Hadler J, et al. Decline in invasive pneumococcal disease after the introduction of protein-polysaccharide conjugate vaccine. N Engl J Med. 2003;348:1737-1746.
5. Direct and indirect effects of routine vaccination of children with 7-valent pneumococcal conjugate vaccine on incidence of invasive pneumococcal disease—United States, 1998-2003. MMWR Morb Mortal Wkly Rep. 2005;54:893-897.
6. CDC. Invasive pneumococcal disease in young children before licensure of 13-valent pneumococcal conjugate vaccine—United States, 2007. MMWR Morb Mortal Wkly Rep. 2010;59:253-257.
7. CDC. Preventing pneumococcal disease among infants and young children: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2000;49(RR-9):1-35.
8. CDC. Updated recommendation from the Advisory Committee on Immunization Practices (ACIP) for use of 7-valent pneumococcal conjugate vaccine (PCV7) in children aged 24-59 months who are not completely vaccinated. MMWR Morb Mortal Wkly Rep. 2008;57:343-344.
9. ACIP provisional recommendations for use of 13-valent pneumococcal conjugate vaccine (PCV13) among infants and children. March 3, 2010. Available at: www.cdc.gov/vaccines/recs/provisional/downloads/pcv13-mar-2010-508.pdf. Accessed May 24, 2010.
10. CDC vaccine price list. Available at: www.cdc.gov/vaccines/programs/vfc/cdc-vac-price-list.htm. Accessed May 22, 2010.
11. Vaccines for Children Program. FAQs from providers. Available at www.cdc.gov/vaccines/programs/vfc/providers/faq-hcp. htm. Accessed May 22, 2010.
Propranolol for anxiety
How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.
Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ
The authors respond
In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.1 Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.2,3 We found only 2 studies examining adjunctive use of propranolol.4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.
Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital
Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC
1. Granville-Grossman KL, Turner P. The effect of propranolol on anxiety. Lancet. 1966;1:788-790.
2. Hayes PE, Schulz SC. Beta-blockers in anxiety disorder. J Affect Disord. 1987;13:119-130.
3. Tyrer P. Anxiolytics not acting at the benzodiazepine receptor: beta blockers. Prog Neuropsychopharmacol Biol Psychiatry. 1992;16:17-26.
4. Shehi M, Patterson WM. Treatment of panic attacks with alprazolam and propranolol. Am J Psychiatry. 1984;141(7):900-901.
5. Mendels J, Chernoff RW, Blatt M. Alprazolam as an adjunct to propranolol in anxious outpatients with stable angina pectoris. J Clin Psychiatry. 1986;47(1):8-11.
How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.
Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ
The authors respond
In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.1 Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.2,3 We found only 2 studies examining adjunctive use of propranolol.4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.
Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital
Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC
How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.
Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ
The authors respond
In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.1 Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.2,3 We found only 2 studies examining adjunctive use of propranolol.4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.
Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital
Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC
1. Granville-Grossman KL, Turner P. The effect of propranolol on anxiety. Lancet. 1966;1:788-790.
2. Hayes PE, Schulz SC. Beta-blockers in anxiety disorder. J Affect Disord. 1987;13:119-130.
3. Tyrer P. Anxiolytics not acting at the benzodiazepine receptor: beta blockers. Prog Neuropsychopharmacol Biol Psychiatry. 1992;16:17-26.
4. Shehi M, Patterson WM. Treatment of panic attacks with alprazolam and propranolol. Am J Psychiatry. 1984;141(7):900-901.
5. Mendels J, Chernoff RW, Blatt M. Alprazolam as an adjunct to propranolol in anxious outpatients with stable angina pectoris. J Clin Psychiatry. 1986;47(1):8-11.
1. Granville-Grossman KL, Turner P. The effect of propranolol on anxiety. Lancet. 1966;1:788-790.
2. Hayes PE, Schulz SC. Beta-blockers in anxiety disorder. J Affect Disord. 1987;13:119-130.
3. Tyrer P. Anxiolytics not acting at the benzodiazepine receptor: beta blockers. Prog Neuropsychopharmacol Biol Psychiatry. 1992;16:17-26.
4. Shehi M, Patterson WM. Treatment of panic attacks with alprazolam and propranolol. Am J Psychiatry. 1984;141(7):900-901.
5. Mendels J, Chernoff RW, Blatt M. Alprazolam as an adjunct to propranolol in anxious outpatients with stable angina pectoris. J Clin Psychiatry. 1986;47(1):8-11.
The Child or Adolescent With Anxiety
Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?
Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?
Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.
Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.
When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.
For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).
It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.
Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues
When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.
Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?
Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”
Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).
Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.
Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?
Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?
Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.
Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.
When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.
For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).
It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.
Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues
When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.
Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?
Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”
Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).
Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.
Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?
Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?
Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.
Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.
When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.
For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).
It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.
Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues
When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.
Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?
Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”
Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).
Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.
Urge Parents to React Calmly to Sibling Rivalry
www.CHADIS.com[email protected]
From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.
Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.
Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.
But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).
Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.
So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.
The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.
Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.
In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.
Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.
The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?
Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).
Corporal punishment in the family makes rivalry worse as well.
Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.
When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.
I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.
Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.
Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.
Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.
When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.
Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.
A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).
Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.
Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.
If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”
If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”
Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.
Whatever the solution, it should be brief.
Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.
Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.
www.CHADIS.com[email protected]
From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.
Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.
Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.
But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).
Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.
So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.
The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.
Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.
In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.
Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.
The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?
Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).
Corporal punishment in the family makes rivalry worse as well.
Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.
When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.
I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.
Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.
Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.
Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.
When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.
Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.
A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).
Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.
Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.
If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”
If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”
Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.
Whatever the solution, it should be brief.
Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.
Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.
www.CHADIS.com[email protected]
From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.
Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.
Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.
But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).
Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.
So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.
The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.
Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.
In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.
Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.
The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?
Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).
Corporal punishment in the family makes rivalry worse as well.
Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.
When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.
I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.
Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.
Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.
Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.
When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.
Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.
A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).
Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.
Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.
If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”
If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”
Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.
Whatever the solution, it should be brief.
Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.
Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.
MGMA Releases Compensation and Productivity Data
New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.
“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”
The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.
The report also shows the median number of work RVUs at 4,107 per hospitalist per year.
SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.
The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.
Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”
New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.
“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”
The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.
The report also shows the median number of work RVUs at 4,107 per hospitalist per year.
SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.
The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.
Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”
New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.
“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”
The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.
The report also shows the median number of work RVUs at 4,107 per hospitalist per year.
SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.
The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.
Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”
Belt Tightening
Let the debate formally begin.
Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).
“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.
The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.
The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.
“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”
In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).
“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”
Let the debate formally begin.
Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).
“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.
The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.
The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.
“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”
In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).
“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”
Let the debate formally begin.
Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).
“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.
The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.
The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.
“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”
In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).
“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”
Save Time, Save Money
A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.
James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.
“It’s like translating 43 different languages to consolidate it and manage it,” he says.
His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.
Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.
“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”
A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.
James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.
“It’s like translating 43 different languages to consolidate it and manage it,” he says.
His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.
Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.
“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”
A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.
James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.
“It’s like translating 43 different languages to consolidate it and manage it,” he says.
His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.
Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.
“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”
In the Literature: Research You Need to Know
Clinical question: Does a resident’s ability to make decisions in the management of critically ill patients deteriorate with longer periods of wakefulness?
Background: Residents work long shifts, particularly in the ICU. Their cognitive performance on standardized tests and clinical performance in surgical simulators deteriorates with sleep deprivation. The effect of prolonged wakefulness on resident management of critically ill patients is not known.
Study design: Experimental within-subjects comparison.
Setting: Simulator at the Centre of Excellence for Surgical Education and Innovation, Vancouver General Hospital, Canada.
Synopsis: Twelve internal medicine residents at various levels of training from the University of British Columbia were studied. The residents provided simulated care for critically ill patients at four time points over 26 hours of wakefulness. At each time point, the residents first managed a cardiac dysrhythmia, then a complex patient scenario that would require ICU-level care. They were then scored for errors and given a global score by two of the investigators.
Resident errors in the management of dysrhythmias decreased at the first time point, and remained stable through the next two time points. The mean error rate for the complex patient scenarios increased from 0.92, with a steady rate of rise to 1.58 at the last session. The mean global score for the complex patient scenario showed a trend toward decline as well. Despite this being a small study with relatively subjective outcomes, the results are consistent with previous studies and raise concern for increasing the risk for error in the care of highly vulnerable critically ill patients by residents working long hours.
Bottom line: There is a progressive decrement in resident performance with increasing periods of wakefulness when delivering ICU-level patient-management decisions in a simulator environment.
Citation: Sharpe R, Koval V, Ronco JJ, et al. The impact of prolonged continuous wakefulness on resident clinical performance in the intensive care unit: A patient simulator study. Crit Care Med. 2010;38:766-770.
Reviewed for TH eWire by Dimitriy Levin, MD, Jeffrey Carter, MD, Erin Egan, MD, JD, Jonathan Pell, MD, Laura Rosenthal, MSN, ACNP, Nichole Zehnder, MD, Hospital Medicine Group, University of Colorado Denver
For more physician reviews of HM-related research, visit our website.
Clinical question: Does a resident’s ability to make decisions in the management of critically ill patients deteriorate with longer periods of wakefulness?
Background: Residents work long shifts, particularly in the ICU. Their cognitive performance on standardized tests and clinical performance in surgical simulators deteriorates with sleep deprivation. The effect of prolonged wakefulness on resident management of critically ill patients is not known.
Study design: Experimental within-subjects comparison.
Setting: Simulator at the Centre of Excellence for Surgical Education and Innovation, Vancouver General Hospital, Canada.
Synopsis: Twelve internal medicine residents at various levels of training from the University of British Columbia were studied. The residents provided simulated care for critically ill patients at four time points over 26 hours of wakefulness. At each time point, the residents first managed a cardiac dysrhythmia, then a complex patient scenario that would require ICU-level care. They were then scored for errors and given a global score by two of the investigators.
Resident errors in the management of dysrhythmias decreased at the first time point, and remained stable through the next two time points. The mean error rate for the complex patient scenarios increased from 0.92, with a steady rate of rise to 1.58 at the last session. The mean global score for the complex patient scenario showed a trend toward decline as well. Despite this being a small study with relatively subjective outcomes, the results are consistent with previous studies and raise concern for increasing the risk for error in the care of highly vulnerable critically ill patients by residents working long hours.
Bottom line: There is a progressive decrement in resident performance with increasing periods of wakefulness when delivering ICU-level patient-management decisions in a simulator environment.
Citation: Sharpe R, Koval V, Ronco JJ, et al. The impact of prolonged continuous wakefulness on resident clinical performance in the intensive care unit: A patient simulator study. Crit Care Med. 2010;38:766-770.
Reviewed for TH eWire by Dimitriy Levin, MD, Jeffrey Carter, MD, Erin Egan, MD, JD, Jonathan Pell, MD, Laura Rosenthal, MSN, ACNP, Nichole Zehnder, MD, Hospital Medicine Group, University of Colorado Denver
For more physician reviews of HM-related research, visit our website.
Clinical question: Does a resident’s ability to make decisions in the management of critically ill patients deteriorate with longer periods of wakefulness?
Background: Residents work long shifts, particularly in the ICU. Their cognitive performance on standardized tests and clinical performance in surgical simulators deteriorates with sleep deprivation. The effect of prolonged wakefulness on resident management of critically ill patients is not known.
Study design: Experimental within-subjects comparison.
Setting: Simulator at the Centre of Excellence for Surgical Education and Innovation, Vancouver General Hospital, Canada.
Synopsis: Twelve internal medicine residents at various levels of training from the University of British Columbia were studied. The residents provided simulated care for critically ill patients at four time points over 26 hours of wakefulness. At each time point, the residents first managed a cardiac dysrhythmia, then a complex patient scenario that would require ICU-level care. They were then scored for errors and given a global score by two of the investigators.
Resident errors in the management of dysrhythmias decreased at the first time point, and remained stable through the next two time points. The mean error rate for the complex patient scenarios increased from 0.92, with a steady rate of rise to 1.58 at the last session. The mean global score for the complex patient scenario showed a trend toward decline as well. Despite this being a small study with relatively subjective outcomes, the results are consistent with previous studies and raise concern for increasing the risk for error in the care of highly vulnerable critically ill patients by residents working long hours.
Bottom line: There is a progressive decrement in resident performance with increasing periods of wakefulness when delivering ICU-level patient-management decisions in a simulator environment.
Citation: Sharpe R, Koval V, Ronco JJ, et al. The impact of prolonged continuous wakefulness on resident clinical performance in the intensive care unit: A patient simulator study. Crit Care Med. 2010;38:766-770.
Reviewed for TH eWire by Dimitriy Levin, MD, Jeffrey Carter, MD, Erin Egan, MD, JD, Jonathan Pell, MD, Laura Rosenthal, MSN, ACNP, Nichole Zehnder, MD, Hospital Medicine Group, University of Colorado Denver
For more physician reviews of HM-related research, visit our website.
Short‐term Femoral Vein Catheterization
Central venous catheters (CVC) are routinely used to deliver medications and monitor intravascular pressures of critically ill patients. Experts and national regulatory bodies have questioned the safety of femoral vein catheterization (FVC), and currently recommend against venous access at this site whenever possible. 13 However, a large prospective nonrandomized study has suggested that rates of FVC infections are not higher than jugular or subclavian sites. 4 Some authors have suggested that increased risk of deep vein thrombosis (DVT) also relatively contraindicates the femoral site. 5 No study has prospectively examined rates of DVT in patients receiving FVC for short durations (<72 hours). In this brief report, we prospectively examined the rates of catheter‐related bloodstream infections (CRBI) and DVT in critically ill patients receiving CVC.
Methods
This prospective observational cohort study was conducted in the medical intensive care unit (MICU) of Bridgeport Hospital, a 350‐bed community teaching hospital. The hospital's Institutional Review Board approved the study and waived the informed consent requirement because it has been the practice for the past decade to favor use of the femoral site for initial resuscitations with very low complication rates. All patients admitted to the MICU between September 1, 2008 and March 31, 2009 were eligible. VC were defined as catheters placed in the jugular, subclavian or femoral veins or peripherally inserted and guided to a central intrathoracic vein (PICC). CVC refers to catheters placed directly into central veins. In early 2008, a hospital‐wide initiative was introduced to insert all CVC using the Pronovost check‐list. 1 VC sites were chosen at the discretion of caregivers in the emergency department and MICU. The policy of our intensive care units is to use only saline flushes of VCs.
Demographic data including age, gender, and body mass index, were collected on all patients. In addition the following parameters were monitored for the duration of ICU stay for the purpose of this study: (1) site and duration of installation of all intravascular catheters, (2) level of training of clinician inserting CVC, (3) catheter/blood culture results. For the purposes of this study, bilateral femoral Doppler compression ultrasound studies were expected to be performed by radiology house officers within 24 hours of removing and again 5 to 7 days following removal of FVC. Local VC complications, methods of thromboprophylaxis and risk factors for venous thromboembolism (VTE) were recorded. Patient outcomes and disposition destinations were also recorded.
CRBI were defined using the Centers for Disease Control definitions. 2 CRBI were identified by daily review of all positive blood cultures and review of patients' medical records. In addition, Infection Control Committee data were reviewed to corroborate contemporaneously determined CRBI during the study period and for 1 year prior to the study period. Patients with FVC were examined each day for signs or symptoms of thrombosis (tenderness along the vein, leg swelling, pitting edema or visible collateral superficial veins). Patients were followed up until death or hospital discharge for clinical signs, symptoms or diagnosis of thromboembolic disease.
Bedside Duplex ultrasounds of bilateral common femoral and superficial femoral veins were performed using graded compression and color Doppler techniques. The leg without FVC served as the control. Evaluations were conducted by senior radiology residents (>100 hours training) utilizing a high‐resolution (>7.5 MHz) linear array transducer. Frame capture images were digitally stored and subsequently reviewed by a Board‐certified radiologist, who was blinded to side of insertion and clinical outcomes, and rendered a final interpretation.
Values are listed as means standard deviations. Comparisons of group means were performed using nonpaired Student's t tests. A P value of <0.05 signified statistical significance.
Results
During the study period, 675 patients were admitted to the MICU. VCs were inserted in 238 (35% of) patients. During their MICU stay, 182 (77% of) patients had 1 VC, 48 (20%) had 2 VC, and 8 (3%) had 3 VC. On admission, 38 patients (6%) had preexisting VC (tunneled catheter 58%, PICC 32%, and dialysis catheters 10%). Additional VCs were placed in 10 of these patients (26%).
Of the 302 VC, 85 (28%) were PICCs and 217 were CVC (107, 49% FVC; 82, 38% internal jugular; 28, 13% subclavian). A total of 151 (28%) patients had radial arterial catheters placed around the time of admission. The types of CVC included triple lumen in 164 (75%), dialysis catheters in 29 (13%), single‐lumen large bore catheters in 17 (8%), and tunneled catheters in 4 patients (2%). The average duration (standard deviation [SD]) of CVC was 2.7 2.2 days for FVC, 5.7 9.6 days for internal jugular and 3.6 3.1 days for subclavian vein catheters.
During these seven months, including 1200 catheter‐days, only 1 CRBI was identified in a patient who only had a PICC, yielding an infection rate of 0.83 CRBI per 1000 catheter‐days. No femoral, subclavian or internal jugular catheter infections were detected. Hospital epidemiologic data confirmed this finding, and demonstrated only 1 other CRBI during 3721 line‐days, in the 7 months of this study and 12 months before, yielding an average of 0.40 CRBI/1000 catheter‐days.
Of 107 FVC, 101 were placed during initial resuscitations and 6 as second‐access sites, (2 for dialysis, 4 triple lumen catheters). Thromboprophylaxis was administered to 104 (97% of) patients with FVC. Thromboprophylaxis was pharmacological (heparins) in 63 (59% of) patients and mechanical (pneumatic compression) in 46 (43%). Five patients had both mechanical and pharmacological prophylaxis. Catheters were placed by a critical care or emergency department attending in 11%, critical care fellows in 11%, and residents in 78%. Ultrasound studies of the legs were performed in 57 patients; 56 had studies within 24 hours of removing FVC. Of these 56 patients, 53 studies were interpreted as negative and 3 were considered incomplete. The 3 initially incomplete studies were repeated, and found to be negative. Six patients were discharged from the hospital before the post‐FVC‐removal ultrasound could be performed. Of the 50 patients who had both ultrasounds (initial and follow up 57 days after removal of FVC), none had a DVT on the side of the catheter or in the control leg. Of the 50 patients with no ultrasound follow‐up, no patient developed clinically detected VTE; these patients had FVC for shorter duration (2.4 2.4 vs. 3.4 1.9 days for those with 2 Duplex; P = 0.02) and their ICU length of stay was shorter (3.8 4.6 vs. 6.6 5.6 days for those with 2 Duplex; P = 0.01).
Since no VTE or CRBI were detected further analyses regarding risks for these complications was not possible.
Discussion
Contrary to regulatory guidelines suggesting a poor safety profile, we found that short‐term FVC was associated with no episode of DVT or CRBI. While the incidence of complications is lower in more experienced operators, 6 most FVC in our hospital were placed by resident‐trainees (78%) with or without supervision from an attending physician. There were no immediate or subacute (ie, thrombosis, infection) major complications. There are a number of features that favor short‐term FVC for initial resuscitation of critically ill patients. Subclavian and intrajugular CVC require prolonged Trendelenburg position, which may not be well tolerated by some patients. FVC does not require Trendelenburg position. Major bleeding1.0% to 1.5% for all the CVCis minimized because direct compression of femoral vessels is possible. Compression of subclavian hemorrhage is impossible while compression of the jugular vessels is uncomfortable. Pneumothorax, while uncommon in the subclavian and intrajugular approaches, 7 has serious consequences for an unstable patient, whereas FVC obviates the risk. Some might argue that FVC cannot accurately reflect cardiovascular filling thereby defeating 1 of the important purposes of the catheter. While this is certainly true in patients with raised intraabdominal pressures, a small case series suggests that (longer‐than‐normal) FVC can accurately measure central filling pressures. 8 Another potential shortcoming of FVC is that if used only for short durations during initial resuscitationsas in this studysome patients will require a second CVC or PICC with incumbent risks.
Our study differs from previous studies that have shown infection rates ranging from 1.5/1000 to 20/1000 catheter‐days 4, 9, 10 and thrombosis rates of 6.6% to 25%. 5, 1013 Some previous studies have suggested higher rates of infection of FVC relative to internal jugular or subclavian sites (3.7/1000 vs. 20/1000 catheter‐days) 9 while others found similar infection or colonization rates between femoral and nonfemoral sites. 4, 10 Our 0.83 CRBSI per 1000 catheter‐day rate is similar to that of Pronovost et al. 1 who avoided FVC, whereas it was the preferred site (nearly half of all CVC) in our MICU. The incidence of VTE in critically ill patients ranges from 9% to 33 %, 14, 15 and CVC are a well recognized risk factor of VTE. 5 The reported incidence of DVT in patients with CVC varies widely from 3% to 10% in subclavian catheters 9 to 6.6% to 25% in FVC. 11, 12 We attribute the remarkable difference in our results to the fact that FVC was used for brief durations (mean 2.7 days, range 116 days) for the primary purpose of resuscitating critically ill patients. Also, techniques introduced by Pronovost et al. 1 to reduce CRBI had permeated our institutional practices by the time of this study; our results match his, of very low rates of CRBI when checklists are employed. In previous studies, FVC was used for extended durations similar to other CVC sites (ranging from 4 to 9.6 days). 5, 9, 12, 13, 16 Additionally, almost all of our patients received VTE prophylaxis whereas rates were variable in previous studies.
This study has several limitations. First, catheter insertion sites were not randomly assigned. This can introduce selection bias. For example, often femoral access is used in more unstable patients 4 who are less tolerant of Trendelenberg position whereas it is often avoided in obese patients. Another important limitation is that ultrasound studies were not performed in 47% of patients who had FVC. While these missed cases were not advertent (eg, CVC on weekends when no study personnel available), we cannot exclude the possibility of bias. However, no FVC patients who did not have ultrasounds developed clinically detected VTE. It is also possible that DVT could have appeared >5 to 7 days after our follow‐up ultrasound, though later development might favor spontaneous DVT unrelated to CVC. Finally, this was a relatively small study, but it appears that the rate of DVT from FVC, if placed for short durations and accompanied by thromboprophylaxis, is very low.
In conclusion, short‐term FVC was used safelywith no major complicationsin our MICU. Our data support that short‐term FVC (with thromboprophylaxis) has a reasonable safety profile for initial resuscitation of critically ill patients. Notwithstanding the limitations of our study, we suggest that it may be premature to abandon entirely 3, 17 the use of FVC for resuscitation of critically ill patients. We propose that our data suggest the need for a larger study to examine more definitively the safety profile of short‐term FVC.
- An intervention to decrease catheter related bloodstream infections in the ICU. N Engl J Med. 2006; 355: 2725– 2732. , , , et al.
- http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5110a1.htm. Accessed February 2010. , , , et al. Guidelines for the prevention of intravascular catheter‐related infection. MMWR Website. Available at:
- Joint Commission. National Accreditation: Hospital Patient Safety Goals. Available at: http://www.jointcommission.org/NR/rdonlyres/31666E86‐E7F4‐423E‐9BE8‐F05BD1CB0AA8/0/HAP_NPSG.pdf. Accessed February 2010.
- The incidence of infectious complications of central venous catheters at the subclavian, internal jugular and femoral sites in an intensive care unit population. Crit Care Med. 2005; 33: 13– 20. , , , et al.
- Femoral deep vein thrombosis associated with central venous catheterization: Results from a prospective, randomized trial. Crit Care Med. 1995; 23: 52– 59. , , , .
- Central vein catheterization. Failure and complicagtion rates by three percutaneous approaches. Arch Intern Med. 1986; 146: 259– 261. , , , , .
- Complications of central venous catheters: internal jugular versus subclavian access—a systematic review. Crit Care Med. 2002; 30: 454– 460. , , .
- Comparison of intrathoracic and intra‐abdominal measurements of central venous pressure. Lancet. 1996; 347: 1155– 1157. , , , , , .
- Complications of femoral and subclavian venous catheterization in critically ill patients. A randomized controlled trial. JAMA. 2001; 286: 700– 707. , , , et al.
- Femoral vs jugular venous catheterization and risk of nosocomial events in adults requiring acute renal replacement therapy. A randomized trial. JAMA. 2008; 299: 2413– 2422. , , , et al.
- A prospective evaluation of the use of femoral venous catheters in critically ill adults. Crit Care Med. 1997; 25: 1986– 1989. , , , , , .
- Lower extremity deep vein thrombosis: a prospective, randomized, controlled trial in comatose or sedated patients undergoing femoral vein catheterization. Crit Care Med. 1997; 25: 1982– 1985. , , , , .
- Deep venous thrombosis caused by femoral venous catheters in critically ill adult patients. Chest. 2000; 117: 178– 183. , , , , .
- The incidence of deep venous thrombosis in ICU patients. Chest. 1997; 111: 661– 664. , , .
- Deep venous thrombosis in medical‐surgical critically il patients: prevalence, incidence and risk factors. Crit Care Med. 2005; 33: 1565– 1571. , , , et al.
- Central vein catheter related thrombosis in intensive care patients: incidence, risk factors and relationship with catheter related sepsis. Chest. 1998; 114: 207– 213. , , , et al.
- Institute for Healthcare Improvement. Optimal catheter site selection, with avoidance of the femoral vein for central venous access in adults. Available at: http://www.ihi.org/IHI/Topics/CriticalCare/IntensiveCare/Changes/IndividualChanges/OptimalCatheterSiteSelectionwithAvoidanceofFemoralVeinforCentralVenousAccessinAdultPatients.htm. Accessed February 2010.
Central venous catheters (CVC) are routinely used to deliver medications and monitor intravascular pressures of critically ill patients. Experts and national regulatory bodies have questioned the safety of femoral vein catheterization (FVC), and currently recommend against venous access at this site whenever possible. 13 However, a large prospective nonrandomized study has suggested that rates of FVC infections are not higher than jugular or subclavian sites. 4 Some authors have suggested that increased risk of deep vein thrombosis (DVT) also relatively contraindicates the femoral site. 5 No study has prospectively examined rates of DVT in patients receiving FVC for short durations (<72 hours). In this brief report, we prospectively examined the rates of catheter‐related bloodstream infections (CRBI) and DVT in critically ill patients receiving CVC.
Methods
This prospective observational cohort study was conducted in the medical intensive care unit (MICU) of Bridgeport Hospital, a 350‐bed community teaching hospital. The hospital's Institutional Review Board approved the study and waived the informed consent requirement because it has been the practice for the past decade to favor use of the femoral site for initial resuscitations with very low complication rates. All patients admitted to the MICU between September 1, 2008 and March 31, 2009 were eligible. VC were defined as catheters placed in the jugular, subclavian or femoral veins or peripherally inserted and guided to a central intrathoracic vein (PICC). CVC refers to catheters placed directly into central veins. In early 2008, a hospital‐wide initiative was introduced to insert all CVC using the Pronovost check‐list. 1 VC sites were chosen at the discretion of caregivers in the emergency department and MICU. The policy of our intensive care units is to use only saline flushes of VCs.
Demographic data including age, gender, and body mass index, were collected on all patients. In addition the following parameters were monitored for the duration of ICU stay for the purpose of this study: (1) site and duration of installation of all intravascular catheters, (2) level of training of clinician inserting CVC, (3) catheter/blood culture results. For the purposes of this study, bilateral femoral Doppler compression ultrasound studies were expected to be performed by radiology house officers within 24 hours of removing and again 5 to 7 days following removal of FVC. Local VC complications, methods of thromboprophylaxis and risk factors for venous thromboembolism (VTE) were recorded. Patient outcomes and disposition destinations were also recorded.
CRBI were defined using the Centers for Disease Control definitions. 2 CRBI were identified by daily review of all positive blood cultures and review of patients' medical records. In addition, Infection Control Committee data were reviewed to corroborate contemporaneously determined CRBI during the study period and for 1 year prior to the study period. Patients with FVC were examined each day for signs or symptoms of thrombosis (tenderness along the vein, leg swelling, pitting edema or visible collateral superficial veins). Patients were followed up until death or hospital discharge for clinical signs, symptoms or diagnosis of thromboembolic disease.
Bedside Duplex ultrasounds of bilateral common femoral and superficial femoral veins were performed using graded compression and color Doppler techniques. The leg without FVC served as the control. Evaluations were conducted by senior radiology residents (>100 hours training) utilizing a high‐resolution (>7.5 MHz) linear array transducer. Frame capture images were digitally stored and subsequently reviewed by a Board‐certified radiologist, who was blinded to side of insertion and clinical outcomes, and rendered a final interpretation.
Values are listed as means standard deviations. Comparisons of group means were performed using nonpaired Student's t tests. A P value of <0.05 signified statistical significance.
Results
During the study period, 675 patients were admitted to the MICU. VCs were inserted in 238 (35% of) patients. During their MICU stay, 182 (77% of) patients had 1 VC, 48 (20%) had 2 VC, and 8 (3%) had 3 VC. On admission, 38 patients (6%) had preexisting VC (tunneled catheter 58%, PICC 32%, and dialysis catheters 10%). Additional VCs were placed in 10 of these patients (26%).
Of the 302 VC, 85 (28%) were PICCs and 217 were CVC (107, 49% FVC; 82, 38% internal jugular; 28, 13% subclavian). A total of 151 (28%) patients had radial arterial catheters placed around the time of admission. The types of CVC included triple lumen in 164 (75%), dialysis catheters in 29 (13%), single‐lumen large bore catheters in 17 (8%), and tunneled catheters in 4 patients (2%). The average duration (standard deviation [SD]) of CVC was 2.7 2.2 days for FVC, 5.7 9.6 days for internal jugular and 3.6 3.1 days for subclavian vein catheters.
During these seven months, including 1200 catheter‐days, only 1 CRBI was identified in a patient who only had a PICC, yielding an infection rate of 0.83 CRBI per 1000 catheter‐days. No femoral, subclavian or internal jugular catheter infections were detected. Hospital epidemiologic data confirmed this finding, and demonstrated only 1 other CRBI during 3721 line‐days, in the 7 months of this study and 12 months before, yielding an average of 0.40 CRBI/1000 catheter‐days.
Of 107 FVC, 101 were placed during initial resuscitations and 6 as second‐access sites, (2 for dialysis, 4 triple lumen catheters). Thromboprophylaxis was administered to 104 (97% of) patients with FVC. Thromboprophylaxis was pharmacological (heparins) in 63 (59% of) patients and mechanical (pneumatic compression) in 46 (43%). Five patients had both mechanical and pharmacological prophylaxis. Catheters were placed by a critical care or emergency department attending in 11%, critical care fellows in 11%, and residents in 78%. Ultrasound studies of the legs were performed in 57 patients; 56 had studies within 24 hours of removing FVC. Of these 56 patients, 53 studies were interpreted as negative and 3 were considered incomplete. The 3 initially incomplete studies were repeated, and found to be negative. Six patients were discharged from the hospital before the post‐FVC‐removal ultrasound could be performed. Of the 50 patients who had both ultrasounds (initial and follow up 57 days after removal of FVC), none had a DVT on the side of the catheter or in the control leg. Of the 50 patients with no ultrasound follow‐up, no patient developed clinically detected VTE; these patients had FVC for shorter duration (2.4 2.4 vs. 3.4 1.9 days for those with 2 Duplex; P = 0.02) and their ICU length of stay was shorter (3.8 4.6 vs. 6.6 5.6 days for those with 2 Duplex; P = 0.01).
Since no VTE or CRBI were detected further analyses regarding risks for these complications was not possible.
Discussion
Contrary to regulatory guidelines suggesting a poor safety profile, we found that short‐term FVC was associated with no episode of DVT or CRBI. While the incidence of complications is lower in more experienced operators, 6 most FVC in our hospital were placed by resident‐trainees (78%) with or without supervision from an attending physician. There were no immediate or subacute (ie, thrombosis, infection) major complications. There are a number of features that favor short‐term FVC for initial resuscitation of critically ill patients. Subclavian and intrajugular CVC require prolonged Trendelenburg position, which may not be well tolerated by some patients. FVC does not require Trendelenburg position. Major bleeding1.0% to 1.5% for all the CVCis minimized because direct compression of femoral vessels is possible. Compression of subclavian hemorrhage is impossible while compression of the jugular vessels is uncomfortable. Pneumothorax, while uncommon in the subclavian and intrajugular approaches, 7 has serious consequences for an unstable patient, whereas FVC obviates the risk. Some might argue that FVC cannot accurately reflect cardiovascular filling thereby defeating 1 of the important purposes of the catheter. While this is certainly true in patients with raised intraabdominal pressures, a small case series suggests that (longer‐than‐normal) FVC can accurately measure central filling pressures. 8 Another potential shortcoming of FVC is that if used only for short durations during initial resuscitationsas in this studysome patients will require a second CVC or PICC with incumbent risks.
Our study differs from previous studies that have shown infection rates ranging from 1.5/1000 to 20/1000 catheter‐days 4, 9, 10 and thrombosis rates of 6.6% to 25%. 5, 1013 Some previous studies have suggested higher rates of infection of FVC relative to internal jugular or subclavian sites (3.7/1000 vs. 20/1000 catheter‐days) 9 while others found similar infection or colonization rates between femoral and nonfemoral sites. 4, 10 Our 0.83 CRBSI per 1000 catheter‐day rate is similar to that of Pronovost et al. 1 who avoided FVC, whereas it was the preferred site (nearly half of all CVC) in our MICU. The incidence of VTE in critically ill patients ranges from 9% to 33 %, 14, 15 and CVC are a well recognized risk factor of VTE. 5 The reported incidence of DVT in patients with CVC varies widely from 3% to 10% in subclavian catheters 9 to 6.6% to 25% in FVC. 11, 12 We attribute the remarkable difference in our results to the fact that FVC was used for brief durations (mean 2.7 days, range 116 days) for the primary purpose of resuscitating critically ill patients. Also, techniques introduced by Pronovost et al. 1 to reduce CRBI had permeated our institutional practices by the time of this study; our results match his, of very low rates of CRBI when checklists are employed. In previous studies, FVC was used for extended durations similar to other CVC sites (ranging from 4 to 9.6 days). 5, 9, 12, 13, 16 Additionally, almost all of our patients received VTE prophylaxis whereas rates were variable in previous studies.
This study has several limitations. First, catheter insertion sites were not randomly assigned. This can introduce selection bias. For example, often femoral access is used in more unstable patients 4 who are less tolerant of Trendelenberg position whereas it is often avoided in obese patients. Another important limitation is that ultrasound studies were not performed in 47% of patients who had FVC. While these missed cases were not advertent (eg, CVC on weekends when no study personnel available), we cannot exclude the possibility of bias. However, no FVC patients who did not have ultrasounds developed clinically detected VTE. It is also possible that DVT could have appeared >5 to 7 days after our follow‐up ultrasound, though later development might favor spontaneous DVT unrelated to CVC. Finally, this was a relatively small study, but it appears that the rate of DVT from FVC, if placed for short durations and accompanied by thromboprophylaxis, is very low.
In conclusion, short‐term FVC was used safelywith no major complicationsin our MICU. Our data support that short‐term FVC (with thromboprophylaxis) has a reasonable safety profile for initial resuscitation of critically ill patients. Notwithstanding the limitations of our study, we suggest that it may be premature to abandon entirely 3, 17 the use of FVC for resuscitation of critically ill patients. We propose that our data suggest the need for a larger study to examine more definitively the safety profile of short‐term FVC.
Central venous catheters (CVC) are routinely used to deliver medications and monitor intravascular pressures of critically ill patients. Experts and national regulatory bodies have questioned the safety of femoral vein catheterization (FVC), and currently recommend against venous access at this site whenever possible. 13 However, a large prospective nonrandomized study has suggested that rates of FVC infections are not higher than jugular or subclavian sites. 4 Some authors have suggested that increased risk of deep vein thrombosis (DVT) also relatively contraindicates the femoral site. 5 No study has prospectively examined rates of DVT in patients receiving FVC for short durations (<72 hours). In this brief report, we prospectively examined the rates of catheter‐related bloodstream infections (CRBI) and DVT in critically ill patients receiving CVC.
Methods
This prospective observational cohort study was conducted in the medical intensive care unit (MICU) of Bridgeport Hospital, a 350‐bed community teaching hospital. The hospital's Institutional Review Board approved the study and waived the informed consent requirement because it has been the practice for the past decade to favor use of the femoral site for initial resuscitations with very low complication rates. All patients admitted to the MICU between September 1, 2008 and March 31, 2009 were eligible. VC were defined as catheters placed in the jugular, subclavian or femoral veins or peripherally inserted and guided to a central intrathoracic vein (PICC). CVC refers to catheters placed directly into central veins. In early 2008, a hospital‐wide initiative was introduced to insert all CVC using the Pronovost check‐list. 1 VC sites were chosen at the discretion of caregivers in the emergency department and MICU. The policy of our intensive care units is to use only saline flushes of VCs.
Demographic data including age, gender, and body mass index, were collected on all patients. In addition the following parameters were monitored for the duration of ICU stay for the purpose of this study: (1) site and duration of installation of all intravascular catheters, (2) level of training of clinician inserting CVC, (3) catheter/blood culture results. For the purposes of this study, bilateral femoral Doppler compression ultrasound studies were expected to be performed by radiology house officers within 24 hours of removing and again 5 to 7 days following removal of FVC. Local VC complications, methods of thromboprophylaxis and risk factors for venous thromboembolism (VTE) were recorded. Patient outcomes and disposition destinations were also recorded.
CRBI were defined using the Centers for Disease Control definitions. 2 CRBI were identified by daily review of all positive blood cultures and review of patients' medical records. In addition, Infection Control Committee data were reviewed to corroborate contemporaneously determined CRBI during the study period and for 1 year prior to the study period. Patients with FVC were examined each day for signs or symptoms of thrombosis (tenderness along the vein, leg swelling, pitting edema or visible collateral superficial veins). Patients were followed up until death or hospital discharge for clinical signs, symptoms or diagnosis of thromboembolic disease.
Bedside Duplex ultrasounds of bilateral common femoral and superficial femoral veins were performed using graded compression and color Doppler techniques. The leg without FVC served as the control. Evaluations were conducted by senior radiology residents (>100 hours training) utilizing a high‐resolution (>7.5 MHz) linear array transducer. Frame capture images were digitally stored and subsequently reviewed by a Board‐certified radiologist, who was blinded to side of insertion and clinical outcomes, and rendered a final interpretation.
Values are listed as means standard deviations. Comparisons of group means were performed using nonpaired Student's t tests. A P value of <0.05 signified statistical significance.
Results
During the study period, 675 patients were admitted to the MICU. VCs were inserted in 238 (35% of) patients. During their MICU stay, 182 (77% of) patients had 1 VC, 48 (20%) had 2 VC, and 8 (3%) had 3 VC. On admission, 38 patients (6%) had preexisting VC (tunneled catheter 58%, PICC 32%, and dialysis catheters 10%). Additional VCs were placed in 10 of these patients (26%).
Of the 302 VC, 85 (28%) were PICCs and 217 were CVC (107, 49% FVC; 82, 38% internal jugular; 28, 13% subclavian). A total of 151 (28%) patients had radial arterial catheters placed around the time of admission. The types of CVC included triple lumen in 164 (75%), dialysis catheters in 29 (13%), single‐lumen large bore catheters in 17 (8%), and tunneled catheters in 4 patients (2%). The average duration (standard deviation [SD]) of CVC was 2.7 2.2 days for FVC, 5.7 9.6 days for internal jugular and 3.6 3.1 days for subclavian vein catheters.
During these seven months, including 1200 catheter‐days, only 1 CRBI was identified in a patient who only had a PICC, yielding an infection rate of 0.83 CRBI per 1000 catheter‐days. No femoral, subclavian or internal jugular catheter infections were detected. Hospital epidemiologic data confirmed this finding, and demonstrated only 1 other CRBI during 3721 line‐days, in the 7 months of this study and 12 months before, yielding an average of 0.40 CRBI/1000 catheter‐days.
Of 107 FVC, 101 were placed during initial resuscitations and 6 as second‐access sites, (2 for dialysis, 4 triple lumen catheters). Thromboprophylaxis was administered to 104 (97% of) patients with FVC. Thromboprophylaxis was pharmacological (heparins) in 63 (59% of) patients and mechanical (pneumatic compression) in 46 (43%). Five patients had both mechanical and pharmacological prophylaxis. Catheters were placed by a critical care or emergency department attending in 11%, critical care fellows in 11%, and residents in 78%. Ultrasound studies of the legs were performed in 57 patients; 56 had studies within 24 hours of removing FVC. Of these 56 patients, 53 studies were interpreted as negative and 3 were considered incomplete. The 3 initially incomplete studies were repeated, and found to be negative. Six patients were discharged from the hospital before the post‐FVC‐removal ultrasound could be performed. Of the 50 patients who had both ultrasounds (initial and follow up 57 days after removal of FVC), none had a DVT on the side of the catheter or in the control leg. Of the 50 patients with no ultrasound follow‐up, no patient developed clinically detected VTE; these patients had FVC for shorter duration (2.4 2.4 vs. 3.4 1.9 days for those with 2 Duplex; P = 0.02) and their ICU length of stay was shorter (3.8 4.6 vs. 6.6 5.6 days for those with 2 Duplex; P = 0.01).
Since no VTE or CRBI were detected further analyses regarding risks for these complications was not possible.
Discussion
Contrary to regulatory guidelines suggesting a poor safety profile, we found that short‐term FVC was associated with no episode of DVT or CRBI. While the incidence of complications is lower in more experienced operators, 6 most FVC in our hospital were placed by resident‐trainees (78%) with or without supervision from an attending physician. There were no immediate or subacute (ie, thrombosis, infection) major complications. There are a number of features that favor short‐term FVC for initial resuscitation of critically ill patients. Subclavian and intrajugular CVC require prolonged Trendelenburg position, which may not be well tolerated by some patients. FVC does not require Trendelenburg position. Major bleeding1.0% to 1.5% for all the CVCis minimized because direct compression of femoral vessels is possible. Compression of subclavian hemorrhage is impossible while compression of the jugular vessels is uncomfortable. Pneumothorax, while uncommon in the subclavian and intrajugular approaches, 7 has serious consequences for an unstable patient, whereas FVC obviates the risk. Some might argue that FVC cannot accurately reflect cardiovascular filling thereby defeating 1 of the important purposes of the catheter. While this is certainly true in patients with raised intraabdominal pressures, a small case series suggests that (longer‐than‐normal) FVC can accurately measure central filling pressures. 8 Another potential shortcoming of FVC is that if used only for short durations during initial resuscitationsas in this studysome patients will require a second CVC or PICC with incumbent risks.
Our study differs from previous studies that have shown infection rates ranging from 1.5/1000 to 20/1000 catheter‐days 4, 9, 10 and thrombosis rates of 6.6% to 25%. 5, 1013 Some previous studies have suggested higher rates of infection of FVC relative to internal jugular or subclavian sites (3.7/1000 vs. 20/1000 catheter‐days) 9 while others found similar infection or colonization rates between femoral and nonfemoral sites. 4, 10 Our 0.83 CRBSI per 1000 catheter‐day rate is similar to that of Pronovost et al. 1 who avoided FVC, whereas it was the preferred site (nearly half of all CVC) in our MICU. The incidence of VTE in critically ill patients ranges from 9% to 33 %, 14, 15 and CVC are a well recognized risk factor of VTE. 5 The reported incidence of DVT in patients with CVC varies widely from 3% to 10% in subclavian catheters 9 to 6.6% to 25% in FVC. 11, 12 We attribute the remarkable difference in our results to the fact that FVC was used for brief durations (mean 2.7 days, range 116 days) for the primary purpose of resuscitating critically ill patients. Also, techniques introduced by Pronovost et al. 1 to reduce CRBI had permeated our institutional practices by the time of this study; our results match his, of very low rates of CRBI when checklists are employed. In previous studies, FVC was used for extended durations similar to other CVC sites (ranging from 4 to 9.6 days). 5, 9, 12, 13, 16 Additionally, almost all of our patients received VTE prophylaxis whereas rates were variable in previous studies.
This study has several limitations. First, catheter insertion sites were not randomly assigned. This can introduce selection bias. For example, often femoral access is used in more unstable patients 4 who are less tolerant of Trendelenberg position whereas it is often avoided in obese patients. Another important limitation is that ultrasound studies were not performed in 47% of patients who had FVC. While these missed cases were not advertent (eg, CVC on weekends when no study personnel available), we cannot exclude the possibility of bias. However, no FVC patients who did not have ultrasounds developed clinically detected VTE. It is also possible that DVT could have appeared >5 to 7 days after our follow‐up ultrasound, though later development might favor spontaneous DVT unrelated to CVC. Finally, this was a relatively small study, but it appears that the rate of DVT from FVC, if placed for short durations and accompanied by thromboprophylaxis, is very low.
In conclusion, short‐term FVC was used safelywith no major complicationsin our MICU. Our data support that short‐term FVC (with thromboprophylaxis) has a reasonable safety profile for initial resuscitation of critically ill patients. Notwithstanding the limitations of our study, we suggest that it may be premature to abandon entirely 3, 17 the use of FVC for resuscitation of critically ill patients. We propose that our data suggest the need for a larger study to examine more definitively the safety profile of short‐term FVC.
- An intervention to decrease catheter related bloodstream infections in the ICU. N Engl J Med. 2006; 355: 2725– 2732. , , , et al.
- http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5110a1.htm. Accessed February 2010. , , , et al. Guidelines for the prevention of intravascular catheter‐related infection. MMWR Website. Available at:
- Joint Commission. National Accreditation: Hospital Patient Safety Goals. Available at: http://www.jointcommission.org/NR/rdonlyres/31666E86‐E7F4‐423E‐9BE8‐F05BD1CB0AA8/0/HAP_NPSG.pdf. Accessed February 2010.
- The incidence of infectious complications of central venous catheters at the subclavian, internal jugular and femoral sites in an intensive care unit population. Crit Care Med. 2005; 33: 13– 20. , , , et al.
- Femoral deep vein thrombosis associated with central venous catheterization: Results from a prospective, randomized trial. Crit Care Med. 1995; 23: 52– 59. , , , .
- Central vein catheterization. Failure and complicagtion rates by three percutaneous approaches. Arch Intern Med. 1986; 146: 259– 261. , , , , .
- Complications of central venous catheters: internal jugular versus subclavian access—a systematic review. Crit Care Med. 2002; 30: 454– 460. , , .
- Comparison of intrathoracic and intra‐abdominal measurements of central venous pressure. Lancet. 1996; 347: 1155– 1157. , , , , , .
- Complications of femoral and subclavian venous catheterization in critically ill patients. A randomized controlled trial. JAMA. 2001; 286: 700– 707. , , , et al.
- Femoral vs jugular venous catheterization and risk of nosocomial events in adults requiring acute renal replacement therapy. A randomized trial. JAMA. 2008; 299: 2413– 2422. , , , et al.
- A prospective evaluation of the use of femoral venous catheters in critically ill adults. Crit Care Med. 1997; 25: 1986– 1989. , , , , , .
- Lower extremity deep vein thrombosis: a prospective, randomized, controlled trial in comatose or sedated patients undergoing femoral vein catheterization. Crit Care Med. 1997; 25: 1982– 1985. , , , , .
- Deep venous thrombosis caused by femoral venous catheters in critically ill adult patients. Chest. 2000; 117: 178– 183. , , , , .
- The incidence of deep venous thrombosis in ICU patients. Chest. 1997; 111: 661– 664. , , .
- Deep venous thrombosis in medical‐surgical critically il patients: prevalence, incidence and risk factors. Crit Care Med. 2005; 33: 1565– 1571. , , , et al.
- Central vein catheter related thrombosis in intensive care patients: incidence, risk factors and relationship with catheter related sepsis. Chest. 1998; 114: 207– 213. , , , et al.
- Institute for Healthcare Improvement. Optimal catheter site selection, with avoidance of the femoral vein for central venous access in adults. Available at: http://www.ihi.org/IHI/Topics/CriticalCare/IntensiveCare/Changes/IndividualChanges/OptimalCatheterSiteSelectionwithAvoidanceofFemoralVeinforCentralVenousAccessinAdultPatients.htm. Accessed February 2010.
- An intervention to decrease catheter related bloodstream infections in the ICU. N Engl J Med. 2006; 355: 2725– 2732. , , , et al.
- http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5110a1.htm. Accessed February 2010. , , , et al. Guidelines for the prevention of intravascular catheter‐related infection. MMWR Website. Available at:
- Joint Commission. National Accreditation: Hospital Patient Safety Goals. Available at: http://www.jointcommission.org/NR/rdonlyres/31666E86‐E7F4‐423E‐9BE8‐F05BD1CB0AA8/0/HAP_NPSG.pdf. Accessed February 2010.
- The incidence of infectious complications of central venous catheters at the subclavian, internal jugular and femoral sites in an intensive care unit population. Crit Care Med. 2005; 33: 13– 20. , , , et al.
- Femoral deep vein thrombosis associated with central venous catheterization: Results from a prospective, randomized trial. Crit Care Med. 1995; 23: 52– 59. , , , .
- Central vein catheterization. Failure and complicagtion rates by three percutaneous approaches. Arch Intern Med. 1986; 146: 259– 261. , , , , .
- Complications of central venous catheters: internal jugular versus subclavian access—a systematic review. Crit Care Med. 2002; 30: 454– 460. , , .
- Comparison of intrathoracic and intra‐abdominal measurements of central venous pressure. Lancet. 1996; 347: 1155– 1157. , , , , , .
- Complications of femoral and subclavian venous catheterization in critically ill patients. A randomized controlled trial. JAMA. 2001; 286: 700– 707. , , , et al.
- Femoral vs jugular venous catheterization and risk of nosocomial events in adults requiring acute renal replacement therapy. A randomized trial. JAMA. 2008; 299: 2413– 2422. , , , et al.
- A prospective evaluation of the use of femoral venous catheters in critically ill adults. Crit Care Med. 1997; 25: 1986– 1989. , , , , , .
- Lower extremity deep vein thrombosis: a prospective, randomized, controlled trial in comatose or sedated patients undergoing femoral vein catheterization. Crit Care Med. 1997; 25: 1982– 1985. , , , , .
- Deep venous thrombosis caused by femoral venous catheters in critically ill adult patients. Chest. 2000; 117: 178– 183. , , , , .
- The incidence of deep venous thrombosis in ICU patients. Chest. 1997; 111: 661– 664. , , .
- Deep venous thrombosis in medical‐surgical critically il patients: prevalence, incidence and risk factors. Crit Care Med. 2005; 33: 1565– 1571. , , , et al.
- Central vein catheter related thrombosis in intensive care patients: incidence, risk factors and relationship with catheter related sepsis. Chest. 1998; 114: 207– 213. , , , et al.
- Institute for Healthcare Improvement. Optimal catheter site selection, with avoidance of the femoral vein for central venous access in adults. Available at: http://www.ihi.org/IHI/Topics/CriticalCare/IntensiveCare/Changes/IndividualChanges/OptimalCatheterSiteSelectionwithAvoidanceofFemoralVeinforCentralVenousAccessinAdultPatients.htm. Accessed February 2010.
Trends in Thrombolytic Use for Stroke
Recombinant tissue plasminogen activator (tPA), approved for use in the United States for the treatment for acute ischemic stroke since 1996, improves overall outcomes from ischemic stroke when administered to selected patients.14 Several prominent guidelines, including the Brain Attack Coalition and the American Stroke Association, have recommended increasing the use of tPA for acute ischemic stroke.57 In addition, in 2003 the Joint Commission on Accreditation of Healthcare Organizations developed a disease‐specific certification program to designate certain institutions Primary Stroke Centers, with one of the performance measures being the availability of thrombolysis.8
Despite guidelines and regulatory agencies promoting the use of thrombolysis for ischemic stroke, previous studies have shown disappointingly low rates of use.912 The goals of this study were to assess whether national trends in the use of thrombolysis for acute ischemic stroke have increased in light of increased regulatory activity as well as to identify patient characteristics associated with thrombolytic administration.
Materials and Methods
Data for this study were obtained from the 2001 through 2006 National Hospital Discharge Survey (NHDS), a nationally representative sample of inpatient hospitalizations conducted annually by the National Center for Health Statistics.13 The NHDS collects data on approximately 300,000 patients from about 500 short‐stay nonfederal hospitals in the United States and uses a 3‐stage sampling strategy that allows for extrapolation to national level estimates. Response rates typically exceed 90% from participating hospitals. The survey collects demographic data, including age, sex, race, hospital geographic region, hospital bedsize and patient insurance status. In addition, up to 7 diagnostic and 4 procedural codes from the hospitalization are available, as is hospitalization length of stay and patient discharge disposition. No information on timing of symptoms, degree of neurologic compromise, or results of imaging tests were available in the NHDS.
We searched for all patients age 18 years or older with a primary diagnostic code of ischemic stroke using the International Classification of Diseases, 9th Edition, Clinical Modification (ICD‐9‐CM) codes 433, 434, 436, 437.0, and 437.1, excluding codes with a fifth digit of 0 (which indicated arterial occlusion without mention of cerebral infarction). We then searched for the presence of an ICD‐9‐CM procedure code for injection or infusion of thrombolytic agent (code 99.10). Specific comorbid conditions associated with ischemic stroke were identified by searching for specific ICD‐9‐CM codes, including for heart failure, coronary artery disease, hypertension, diabetes mellitus, and atrial fibrillation. To provide a general assessment of the severity of illness of the patients, we calculated an adapted Charlson comorbidity score for each patient using available secondary discharge diagnosis codes.14 We also searched for codes corresponding to intracranial hemorrhage, a complication associated with tPA administration.
Statistical Analysis
We defined thrombolytic utilization rates as the number of patients hospitalized with a primary diagnosis of ischemic stroke who had a procedure code for thrombolysis divided by the total number of patients hospitalized with ischemic stroke. To calculate nationally representative prevalence rates, we used the sample weights provided by the NHDS to account for the complex sampling design of the survey. Differences in thrombolytic administration rates by patient and hospital characteristics were tested using chi‐squared tests for categorical variables and t‐tests for continuous variables. Variables underwent a backwards selection process with a significance level of 0.05 to develop the final multivariable model of predictors of thrombolytic administration. Length of stay and hospital discharge status were not included in the variable selection process, as the focus was on predictors of initial administration of thrombolytics. All analyses were conducted using SAS Version 9.1 (SAS Institute Inc., Cary, NC).
Results
From years 2001 through 2006, we identified 22,842 patients with a primary diagnosis of ischemic stroke. Of these, 313 (1.37%, 95% confidence interval [CI], 1.22‐1.53%) had a procedure code for injection or infusion of thrombolysis. Using NHDS sample weights, these numbers corresponded to an estimated 2.55 million hospitalizations for ischemic stroke in the United States during the time period and to 35,082 patients receiving intravenous thrombolytics. Although the overall rate of thrombolysis administration was quite low overall, the administration rate increased over time, from 0.87% [95% CI, 0.61‐1.22%] of stroke patients in year 2001 to 2.40% [95% CI, 1.95‐2.93%] in year 2006 and with a particular increase especially noted after year 2003 (P <0.001 for trend, Figure 1).

On bivariate analysis, a lower proportion of African‐American patients received tPA compared to white patients (0.8% vs. 1.5%, P = 0.003), while a higher proportion of patients with atrial fibrillation received tPA (2.3% vs. 1.2%, P < 0.001). Older patients were less likely than younger patients to receive tPA (Table 1). The rate of intracranial hemorrhage was significantly higher in patients who received tPA (5.4% vs. 0.6%, P < 0.001) and the overall inpatient mortality in patients who received tPA was 9.0%. Mortality in patients receiving tPA continued to be higher than in patients who did not receive tPA even when patients with intracranial hemorrhage were excluded (8.1% vs. 5.3%, P < 0.001). Larger hospitals were more likely to administer tPA to patients with ischemic stroke, with a 1.79% administration rate in hospitals with 300 beds compared to 0.90% in hospitals with 100 to 199 beds and 0.52% in hospitals with 6 to 99 beds (P < 0.001).
Thrombolysis, n (%) | No Thrombolysis, n (%) | P Value | |
---|---|---|---|
| |||
Age | 0.001 | ||
<60 | 76 (24.3) | 4478 (19.9) | |
60‐69 | 73 (23.3) | 3942 (17.5) | |
70‐79 | 82 (26.2) | 6265 (27.8) | |
80+ | 82 (26.2) | 7844 (34.8) | |
Female | 155 (49.5) | 12625 (56.0) | 0.02 |
Race | 0.003 | ||
White | 173 (55.3) | 11542 (51.2) | |
African American | 29 (9.3) | 3774 (16.8) | |
Other | 16 (5.1) | 814 (3.6) | |
Not stated | 95 (30.4) | 6399 (28.4) | |
Region | 0.05 | ||
Northeast | 78 (24.9) | 4570 (20.3) | |
Midwest | 84 (26.8) | 6924 (30.7) | |
South | 104 (33.2) | 8284 (36.8) | |
West | 47 (15.0) | 2751 (12.2) | |
Type of admission | <0.001 | ||
Emergent | 247 (78.9) | 14233 (63.2) | |
Urgent | 33 (10.5) | 3703 (16.4) | |
Elective | 5 (1.6) | 1346 (6.0) | |
Unknown | 28 (9.0) | 3247 (14.4) | |
Length of stay, days [95% CI] | 7.2 [6.6‐7.8] | 6.0 [5.9‐6.1] | <0.001 |
Hospital bedsize | <0.001 | ||
6‐99 | 16 (5.1) | 3065 (13.6) | |
100‐199 | 48 (15.3) | 5289 (23.5) | |
200‐299 | 86 (27.5) | 5212 (23.1) | |
300+ | 163 (52.1) | 8963 (39.8) | |
Payment type | <0.001 | ||
Medicare | 176 (56.2) | 15197 (67.5) | |
Medicaid | 21 (6.7) | 1245 (5.5) | |
Private | 45 (14.4) | 2483 (11.0) | |
HMO/PPO | 39 (12.5) | 2224 (9.9) | |
Other/unknown | 32 (10.2) | 1380 (6.1) | |
Discharge status | <0.001 | ||
Home | 98 (31.3) | 9507 (42.2) | |
Short term care facility | 25 (8.0) | 1271 (5.6) | |
Long term care facility | 62 (19.8) | 5400 (24.0) | |
Alive, status unknown | 89 (28.4) | 4514 (20.0) | |
Death | 28 (9.0) | 1218 (5.4) | |
Unknown | 11 (3.5) | 619 (2.8) | |
Comorbid conditions | |||
Congestive heart failure | 48 (15.3) | 2769 (12.3) | 0.10 |
Coronary artery disease | 49 (15.7) | 4082 (18.1) | 0.26 |
Hypertension | 164 (52.4) | 12480 (55.4) | 0.29 |
Diabetes mellitus | 42 (13.4) | 4965 (22.0) | <0.001 |
Atrial fibrillation | 96 (30.7) | 4096 (18.2) | <0.001 |
Intracranial hemorrhage | 17 (5.4) | 139 (0.6) | <0.001 |
Charlson score14 (mean) | 2.48 [2.32‐2.64] | 2.38 [2.36‐2.40] | 0.23 |
After adjusting for patient and hospital characteristics, the absolute rate of thrombolysis administration increased by an average of 0.19% per year (95% CI, 0.12‐0.26%). Factors that were significantly associated with administration of thrombolytics included being hospitalized in a larger hospital, having a history of atrial fibrillation, and a higher Charlson comorbidity index (Table 2). Patients aged 80 years or older, African American patients, and those with diabetes mellitus were significantly less likely to receive thrombolysis.
Characteristic | Adjusted OR (95% CI) |
---|---|
| |
Year (per year, from 2001 to 2006) | 1.2 (1.1‐1.3) |
Age, years | |
<60 | Referent |
60‐69 | 1.0 (0.7‐1.4) |
70‐79 | 0.6 (0.5‐0.9) |
80+ | 0.4 (0.3‐0.6) |
Race | |
Not African American | Referent |
African‐American | 0.4 (0.3‐0.7) |
Unknown | 1.0 (0.8‐1.2) |
Hospital bedsize | |
6‐99 | Referent |
100‐199 | 1.7 (1.0‐3.1) |
200‐299 | 3.2 (1.8‐5.4) |
300+ | 3.3 (2.0‐5.6) |
Diabetes mellitus | 0.5 (0.3‐0.6) |
Atrial fibrillation | 2.2 (1.7‐2.9) |
Charlson comorbidity score14 (per point increase) | 1.1 (1.1‐1.2) |
Discussion
Despite strong recommendations from guidelines and regulatory agencies, national rates of intravenous thrombolysis for ischemic stroke continue to be quite low overall. However, tPA administration appears to have increased from previous years and particularly increased in years after the Joint Commission began to accredit institutions as Primary Stroke Centers.11 The oldest patients and African Americans were less likely to receive thrombolytics, while patients with atrial fibrillation were more likely to receive thrombolysis, potentially related to atrial fibrillation causing more severe strokes.15 A total of 5.4% of patients who received tPA were diagnosed with intracranial hemorrhage, and the inpatient mortality rate of patients with tPA was 9.0%.
The exact optimal rate of thrombolysis administration for the patients in our study is unknown, as the NHDS database lacked detailed information on factors that would preclude tPA administration such as late timing of presentation and mild stroke symptoms.3 Studies conducted in stroke registries and regional settings have found that only approximately 15% to 32% of patients presenting with ischemic stroke arrive within 3 hours of symptom onset, and of these, only about 40% to 50% are eligible for tPA clinically.9, 10, 1619 However, even among presumed eligible patients, tPA administration rates only range between 25% and 43%,17, 19, 20 and the ideal rate is likely to be higher than the very low rates we observed in our study. Newer evidence that extending the time window where tPA may be given safely may increase the number of eligible patients.21
Patients who received thrombolysis had higher mortality rates than patients who did not. Although we were unable to determine a causal association, prior observational studies of tPA administration for acute stroke have found that patients with more severe neurologic deficits were more likely to receive thrombolysis.17, 18 The 9.0% inpatient case‐fatality rate observed in our study compares favorably to the 13.4% mortality rate after tPA reported in a post‐approval meta‐analysis of safety outcomes22 and the rate of intracranial hemorrhage in our analysis was similar to those observed in other settings.9, 2225 We were unable to determine whether intracranial hemorrhages in our study were as a result of tPA administration or whether patients who received tPA were more likely to have intracranial hemorrhages detected, such as may be due to increased frequency of head imaging.
Larger hospitals were more likely to administer tPA. This may reflect regionalization of stroke care, particularly in those designated as stroke centers of excellence. As well, there is some evidence that there is a learning curve with thrombolysis administration, where guideline‐recommended practice and use of tPA increases with additional experience with the drug.9, 26 Promoting systems that allow for rapid triage and diagnosis of acute stroke should be encouraged and hospital leaders should develop strategies that allow for early recognition of potential tPA candidates.
There are several limitations to our analysis. The NHDS does not collect detailed data on clinical or presenting features of stroke, and so we lacked information on stroke severity and eligibility for administration of thrombolysis. Our study may have underestimated the overall rates of thrombolysis, as it was dependent on diagnostic codes. A previous study of 34 patients who received tPA found that although the 99.10 code was 100% specific, the code identified only 17 patients who actually received tPA (sensitivity of 50%).20 Another study comparing Medicare administrative claims data to actual pharmacy billing charges for tPA found that administrative data underestimated the rate of tPA administration by approximately 25% to 30%.12 If a diagnostic code sensitivity of 50% was assumed, rates of tPA administration in our study may have been as high as 4.8% (95% CI, 4.1‐5.5%) by year 2006.
Conclusion
In conclusion, the use of intravenous thrombolysis in patients admitted with acute ischemic stroke in the United States has risen over time, but overall use remains very low. Further efforts to improve appropriate administration rates should be encouraged, particularly as the acceptable time‐window for using tPA widens.
Acknowledgements
The authors thank Mr. Loren Yglecias for his assistance with manuscript text and references.
- The National Institute of Neurological Disorders and Stroke rt‐PA Stroke Study Group.Tissue plasminogen activator for acute ischemic stroke.N Engl J Med.1995;333:1581–1587.
- Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group.N Engl J Med.1999;340:1781–1787. , , , et al.
- Association of outcome with early stroke treatment: Pooled analysis of ATLANTIS, ECASS, and NINDS rT‐PA stroke trials.Lancet.2004;363:768–774. , , , et al.
- Thrombolysis with alteplase for acute ischaemic stroke in the safe implementation of thrombolysis in stroke‐monitoring study (SITS‐MOST): An observational study.Lancet.2007;369:275–282. , , , et al.
- Recommendations for the establishment of primary stroke centers.JAMA.2000;283:3102–3109. , , , et al.
- Management of acute ischaemic stroke: new guidelines from the American Stroke Association and European Stroke Initiative.Lancet Neurol.2003;2:698–701. , .
- Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.Circulation.2007;115:e478–534. , , , et al.
- The Joint Commission Primary Stroke Center Certification. Available at: http://www.jointcommission.org/CertificationPrograms/PrimaryStrokeCenters. Accessed February 2010.
- Use of tissue‐type plasminogen activator for acute ischemic stroke: The Cleveland area experience.JAMA.2000;283:1151–1158. , , , et al.
- California Acute Stroke Pilot Registry (CASPR) Investigators.Prioritizing interventions to improve rates of thrombolysis for ischemic stroke.Neurology.2005;64:654–659.
- Thrombolysis for ischemic stroke in the united states: Data from National Hospital Discharge Survey 1999–2001.Neurosurgery.2005;57:647–654; discussion647–654. , , , et al.
- National US estimates of recombinant tissue plasminogen activator use: ICD‐9 codes substantially underestimate.Stroke.2008;39:924–928. , , , , .
- US Department of Health and Human Services Public Health Service and National Center for Health Statistics.National Hospital Discharge Durvey 1991–2006. Multi‐year public‐use data file documentation.
- Adapting a clinical comorbidity index for use with ICD‐9‐CM administrative databases.J Clin Epidemiol.1992;45:613–619. , , .
- Stroke severity in atrial fibrillation. The Framingham study.Stroke.1996;27:1760–1764. , , , et al.
- Why are stroke patients excluded from tPA therapy? An analysis of patient eligibility.Neurology.2001;57:1739–1740. , , , , .
- Utilization of intravenous tissue plasminogen activator for acute ischemic stroke.Arch Neurol.2004;61:346–350. , , , , , .
- Eligibility for recombinant tissue plasminogen activator in acute ischemic stroke: a population‐based study.Stroke.2004;35:27–29. , , , et al.
- Tpa use for stroke in the registry of the Canadian stroke network.Can J Neurol Sci.2005;32:433–439. , , , et al.
- Utilization of intravenous tissue‐type plasminogen activator for ischemic stroke at academic medical centers: the influence of ethnicity.Stroke.2001;32:1061–1068. , , , et al.
- Number needed to treat to benefit and to harm for intravenous tissue plasminogen activator therapy in the 3‐ to 4.5‐hour window: Joint outcome table analysis of the ECASS 3 trial.Stroke.2009;40:2433–2437. , , , et al.
- Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta‐analysis of safety data.Stroke.2003;34:2847–2850. .
- Early intravenous thrombolysis for acute ischemic stroke in a community‐based approach.Stroke.1998;29:1544–1549. , , , et al.
- Factors associated with in‐hospital mortality after administration of thrombolysis in acute ischemic stroke patients: an analysis of the Nationwide Inpatient Sample 1999 to 2002.Stroke.2006;37:440–446. , , , et al.
- Intravenous t‐PA for acute ischemic stroke: therapeutic yield of a stroke code system.Neurology.1998;50:501–503. , , , et al.
- Intravenous tissue‐type plasminogen activator therapy for ischemic stroke: Houston experience 1996 to 2000.Arch Neurol.2001;58:2009–2013. , , , et al.
Recombinant tissue plasminogen activator (tPA), approved for use in the United States for the treatment for acute ischemic stroke since 1996, improves overall outcomes from ischemic stroke when administered to selected patients.14 Several prominent guidelines, including the Brain Attack Coalition and the American Stroke Association, have recommended increasing the use of tPA for acute ischemic stroke.57 In addition, in 2003 the Joint Commission on Accreditation of Healthcare Organizations developed a disease‐specific certification program to designate certain institutions Primary Stroke Centers, with one of the performance measures being the availability of thrombolysis.8
Despite guidelines and regulatory agencies promoting the use of thrombolysis for ischemic stroke, previous studies have shown disappointingly low rates of use.912 The goals of this study were to assess whether national trends in the use of thrombolysis for acute ischemic stroke have increased in light of increased regulatory activity as well as to identify patient characteristics associated with thrombolytic administration.
Materials and Methods
Data for this study were obtained from the 2001 through 2006 National Hospital Discharge Survey (NHDS), a nationally representative sample of inpatient hospitalizations conducted annually by the National Center for Health Statistics.13 The NHDS collects data on approximately 300,000 patients from about 500 short‐stay nonfederal hospitals in the United States and uses a 3‐stage sampling strategy that allows for extrapolation to national level estimates. Response rates typically exceed 90% from participating hospitals. The survey collects demographic data, including age, sex, race, hospital geographic region, hospital bedsize and patient insurance status. In addition, up to 7 diagnostic and 4 procedural codes from the hospitalization are available, as is hospitalization length of stay and patient discharge disposition. No information on timing of symptoms, degree of neurologic compromise, or results of imaging tests were available in the NHDS.
We searched for all patients age 18 years or older with a primary diagnostic code of ischemic stroke using the International Classification of Diseases, 9th Edition, Clinical Modification (ICD‐9‐CM) codes 433, 434, 436, 437.0, and 437.1, excluding codes with a fifth digit of 0 (which indicated arterial occlusion without mention of cerebral infarction). We then searched for the presence of an ICD‐9‐CM procedure code for injection or infusion of thrombolytic agent (code 99.10). Specific comorbid conditions associated with ischemic stroke were identified by searching for specific ICD‐9‐CM codes, including for heart failure, coronary artery disease, hypertension, diabetes mellitus, and atrial fibrillation. To provide a general assessment of the severity of illness of the patients, we calculated an adapted Charlson comorbidity score for each patient using available secondary discharge diagnosis codes.14 We also searched for codes corresponding to intracranial hemorrhage, a complication associated with tPA administration.
Statistical Analysis
We defined thrombolytic utilization rates as the number of patients hospitalized with a primary diagnosis of ischemic stroke who had a procedure code for thrombolysis divided by the total number of patients hospitalized with ischemic stroke. To calculate nationally representative prevalence rates, we used the sample weights provided by the NHDS to account for the complex sampling design of the survey. Differences in thrombolytic administration rates by patient and hospital characteristics were tested using chi‐squared tests for categorical variables and t‐tests for continuous variables. Variables underwent a backwards selection process with a significance level of 0.05 to develop the final multivariable model of predictors of thrombolytic administration. Length of stay and hospital discharge status were not included in the variable selection process, as the focus was on predictors of initial administration of thrombolytics. All analyses were conducted using SAS Version 9.1 (SAS Institute Inc., Cary, NC).
Results
From years 2001 through 2006, we identified 22,842 patients with a primary diagnosis of ischemic stroke. Of these, 313 (1.37%, 95% confidence interval [CI], 1.22‐1.53%) had a procedure code for injection or infusion of thrombolysis. Using NHDS sample weights, these numbers corresponded to an estimated 2.55 million hospitalizations for ischemic stroke in the United States during the time period and to 35,082 patients receiving intravenous thrombolytics. Although the overall rate of thrombolysis administration was quite low overall, the administration rate increased over time, from 0.87% [95% CI, 0.61‐1.22%] of stroke patients in year 2001 to 2.40% [95% CI, 1.95‐2.93%] in year 2006 and with a particular increase especially noted after year 2003 (P <0.001 for trend, Figure 1).

On bivariate analysis, a lower proportion of African‐American patients received tPA compared to white patients (0.8% vs. 1.5%, P = 0.003), while a higher proportion of patients with atrial fibrillation received tPA (2.3% vs. 1.2%, P < 0.001). Older patients were less likely than younger patients to receive tPA (Table 1). The rate of intracranial hemorrhage was significantly higher in patients who received tPA (5.4% vs. 0.6%, P < 0.001) and the overall inpatient mortality in patients who received tPA was 9.0%. Mortality in patients receiving tPA continued to be higher than in patients who did not receive tPA even when patients with intracranial hemorrhage were excluded (8.1% vs. 5.3%, P < 0.001). Larger hospitals were more likely to administer tPA to patients with ischemic stroke, with a 1.79% administration rate in hospitals with 300 beds compared to 0.90% in hospitals with 100 to 199 beds and 0.52% in hospitals with 6 to 99 beds (P < 0.001).
Thrombolysis, n (%) | No Thrombolysis, n (%) | P Value | |
---|---|---|---|
| |||
Age | 0.001 | ||
<60 | 76 (24.3) | 4478 (19.9) | |
60‐69 | 73 (23.3) | 3942 (17.5) | |
70‐79 | 82 (26.2) | 6265 (27.8) | |
80+ | 82 (26.2) | 7844 (34.8) | |
Female | 155 (49.5) | 12625 (56.0) | 0.02 |
Race | 0.003 | ||
White | 173 (55.3) | 11542 (51.2) | |
African American | 29 (9.3) | 3774 (16.8) | |
Other | 16 (5.1) | 814 (3.6) | |
Not stated | 95 (30.4) | 6399 (28.4) | |
Region | 0.05 | ||
Northeast | 78 (24.9) | 4570 (20.3) | |
Midwest | 84 (26.8) | 6924 (30.7) | |
South | 104 (33.2) | 8284 (36.8) | |
West | 47 (15.0) | 2751 (12.2) | |
Type of admission | <0.001 | ||
Emergent | 247 (78.9) | 14233 (63.2) | |
Urgent | 33 (10.5) | 3703 (16.4) | |
Elective | 5 (1.6) | 1346 (6.0) | |
Unknown | 28 (9.0) | 3247 (14.4) | |
Length of stay, days [95% CI] | 7.2 [6.6‐7.8] | 6.0 [5.9‐6.1] | <0.001 |
Hospital bedsize | <0.001 | ||
6‐99 | 16 (5.1) | 3065 (13.6) | |
100‐199 | 48 (15.3) | 5289 (23.5) | |
200‐299 | 86 (27.5) | 5212 (23.1) | |
300+ | 163 (52.1) | 8963 (39.8) | |
Payment type | <0.001 | ||
Medicare | 176 (56.2) | 15197 (67.5) | |
Medicaid | 21 (6.7) | 1245 (5.5) | |
Private | 45 (14.4) | 2483 (11.0) | |
HMO/PPO | 39 (12.5) | 2224 (9.9) | |
Other/unknown | 32 (10.2) | 1380 (6.1) | |
Discharge status | <0.001 | ||
Home | 98 (31.3) | 9507 (42.2) | |
Short term care facility | 25 (8.0) | 1271 (5.6) | |
Long term care facility | 62 (19.8) | 5400 (24.0) | |
Alive, status unknown | 89 (28.4) | 4514 (20.0) | |
Death | 28 (9.0) | 1218 (5.4) | |
Unknown | 11 (3.5) | 619 (2.8) | |
Comorbid conditions | |||
Congestive heart failure | 48 (15.3) | 2769 (12.3) | 0.10 |
Coronary artery disease | 49 (15.7) | 4082 (18.1) | 0.26 |
Hypertension | 164 (52.4) | 12480 (55.4) | 0.29 |
Diabetes mellitus | 42 (13.4) | 4965 (22.0) | <0.001 |
Atrial fibrillation | 96 (30.7) | 4096 (18.2) | <0.001 |
Intracranial hemorrhage | 17 (5.4) | 139 (0.6) | <0.001 |
Charlson score14 (mean) | 2.48 [2.32‐2.64] | 2.38 [2.36‐2.40] | 0.23 |
After adjusting for patient and hospital characteristics, the absolute rate of thrombolysis administration increased by an average of 0.19% per year (95% CI, 0.12‐0.26%). Factors that were significantly associated with administration of thrombolytics included being hospitalized in a larger hospital, having a history of atrial fibrillation, and a higher Charlson comorbidity index (Table 2). Patients aged 80 years or older, African American patients, and those with diabetes mellitus were significantly less likely to receive thrombolysis.
Characteristic | Adjusted OR (95% CI) |
---|---|
| |
Year (per year, from 2001 to 2006) | 1.2 (1.1‐1.3) |
Age, years | |
<60 | Referent |
60‐69 | 1.0 (0.7‐1.4) |
70‐79 | 0.6 (0.5‐0.9) |
80+ | 0.4 (0.3‐0.6) |
Race | |
Not African American | Referent |
African‐American | 0.4 (0.3‐0.7) |
Unknown | 1.0 (0.8‐1.2) |
Hospital bedsize | |
6‐99 | Referent |
100‐199 | 1.7 (1.0‐3.1) |
200‐299 | 3.2 (1.8‐5.4) |
300+ | 3.3 (2.0‐5.6) |
Diabetes mellitus | 0.5 (0.3‐0.6) |
Atrial fibrillation | 2.2 (1.7‐2.9) |
Charlson comorbidity score14 (per point increase) | 1.1 (1.1‐1.2) |
Discussion
Despite strong recommendations from guidelines and regulatory agencies, national rates of intravenous thrombolysis for ischemic stroke continue to be quite low overall. However, tPA administration appears to have increased from previous years and particularly increased in years after the Joint Commission began to accredit institutions as Primary Stroke Centers.11 The oldest patients and African Americans were less likely to receive thrombolytics, while patients with atrial fibrillation were more likely to receive thrombolysis, potentially related to atrial fibrillation causing more severe strokes.15 A total of 5.4% of patients who received tPA were diagnosed with intracranial hemorrhage, and the inpatient mortality rate of patients with tPA was 9.0%.
The exact optimal rate of thrombolysis administration for the patients in our study is unknown, as the NHDS database lacked detailed information on factors that would preclude tPA administration such as late timing of presentation and mild stroke symptoms.3 Studies conducted in stroke registries and regional settings have found that only approximately 15% to 32% of patients presenting with ischemic stroke arrive within 3 hours of symptom onset, and of these, only about 40% to 50% are eligible for tPA clinically.9, 10, 1619 However, even among presumed eligible patients, tPA administration rates only range between 25% and 43%,17, 19, 20 and the ideal rate is likely to be higher than the very low rates we observed in our study. Newer evidence that extending the time window where tPA may be given safely may increase the number of eligible patients.21
Patients who received thrombolysis had higher mortality rates than patients who did not. Although we were unable to determine a causal association, prior observational studies of tPA administration for acute stroke have found that patients with more severe neurologic deficits were more likely to receive thrombolysis.17, 18 The 9.0% inpatient case‐fatality rate observed in our study compares favorably to the 13.4% mortality rate after tPA reported in a post‐approval meta‐analysis of safety outcomes22 and the rate of intracranial hemorrhage in our analysis was similar to those observed in other settings.9, 2225 We were unable to determine whether intracranial hemorrhages in our study were as a result of tPA administration or whether patients who received tPA were more likely to have intracranial hemorrhages detected, such as may be due to increased frequency of head imaging.
Larger hospitals were more likely to administer tPA. This may reflect regionalization of stroke care, particularly in those designated as stroke centers of excellence. As well, there is some evidence that there is a learning curve with thrombolysis administration, where guideline‐recommended practice and use of tPA increases with additional experience with the drug.9, 26 Promoting systems that allow for rapid triage and diagnosis of acute stroke should be encouraged and hospital leaders should develop strategies that allow for early recognition of potential tPA candidates.
There are several limitations to our analysis. The NHDS does not collect detailed data on clinical or presenting features of stroke, and so we lacked information on stroke severity and eligibility for administration of thrombolysis. Our study may have underestimated the overall rates of thrombolysis, as it was dependent on diagnostic codes. A previous study of 34 patients who received tPA found that although the 99.10 code was 100% specific, the code identified only 17 patients who actually received tPA (sensitivity of 50%).20 Another study comparing Medicare administrative claims data to actual pharmacy billing charges for tPA found that administrative data underestimated the rate of tPA administration by approximately 25% to 30%.12 If a diagnostic code sensitivity of 50% was assumed, rates of tPA administration in our study may have been as high as 4.8% (95% CI, 4.1‐5.5%) by year 2006.
Conclusion
In conclusion, the use of intravenous thrombolysis in patients admitted with acute ischemic stroke in the United States has risen over time, but overall use remains very low. Further efforts to improve appropriate administration rates should be encouraged, particularly as the acceptable time‐window for using tPA widens.
Acknowledgements
The authors thank Mr. Loren Yglecias for his assistance with manuscript text and references.
Recombinant tissue plasminogen activator (tPA), approved for use in the United States for the treatment for acute ischemic stroke since 1996, improves overall outcomes from ischemic stroke when administered to selected patients.14 Several prominent guidelines, including the Brain Attack Coalition and the American Stroke Association, have recommended increasing the use of tPA for acute ischemic stroke.57 In addition, in 2003 the Joint Commission on Accreditation of Healthcare Organizations developed a disease‐specific certification program to designate certain institutions Primary Stroke Centers, with one of the performance measures being the availability of thrombolysis.8
Despite guidelines and regulatory agencies promoting the use of thrombolysis for ischemic stroke, previous studies have shown disappointingly low rates of use.912 The goals of this study were to assess whether national trends in the use of thrombolysis for acute ischemic stroke have increased in light of increased regulatory activity as well as to identify patient characteristics associated with thrombolytic administration.
Materials and Methods
Data for this study were obtained from the 2001 through 2006 National Hospital Discharge Survey (NHDS), a nationally representative sample of inpatient hospitalizations conducted annually by the National Center for Health Statistics.13 The NHDS collects data on approximately 300,000 patients from about 500 short‐stay nonfederal hospitals in the United States and uses a 3‐stage sampling strategy that allows for extrapolation to national level estimates. Response rates typically exceed 90% from participating hospitals. The survey collects demographic data, including age, sex, race, hospital geographic region, hospital bedsize and patient insurance status. In addition, up to 7 diagnostic and 4 procedural codes from the hospitalization are available, as is hospitalization length of stay and patient discharge disposition. No information on timing of symptoms, degree of neurologic compromise, or results of imaging tests were available in the NHDS.
We searched for all patients age 18 years or older with a primary diagnostic code of ischemic stroke using the International Classification of Diseases, 9th Edition, Clinical Modification (ICD‐9‐CM) codes 433, 434, 436, 437.0, and 437.1, excluding codes with a fifth digit of 0 (which indicated arterial occlusion without mention of cerebral infarction). We then searched for the presence of an ICD‐9‐CM procedure code for injection or infusion of thrombolytic agent (code 99.10). Specific comorbid conditions associated with ischemic stroke were identified by searching for specific ICD‐9‐CM codes, including for heart failure, coronary artery disease, hypertension, diabetes mellitus, and atrial fibrillation. To provide a general assessment of the severity of illness of the patients, we calculated an adapted Charlson comorbidity score for each patient using available secondary discharge diagnosis codes.14 We also searched for codes corresponding to intracranial hemorrhage, a complication associated with tPA administration.
Statistical Analysis
We defined thrombolytic utilization rates as the number of patients hospitalized with a primary diagnosis of ischemic stroke who had a procedure code for thrombolysis divided by the total number of patients hospitalized with ischemic stroke. To calculate nationally representative prevalence rates, we used the sample weights provided by the NHDS to account for the complex sampling design of the survey. Differences in thrombolytic administration rates by patient and hospital characteristics were tested using chi‐squared tests for categorical variables and t‐tests for continuous variables. Variables underwent a backwards selection process with a significance level of 0.05 to develop the final multivariable model of predictors of thrombolytic administration. Length of stay and hospital discharge status were not included in the variable selection process, as the focus was on predictors of initial administration of thrombolytics. All analyses were conducted using SAS Version 9.1 (SAS Institute Inc., Cary, NC).
Results
From years 2001 through 2006, we identified 22,842 patients with a primary diagnosis of ischemic stroke. Of these, 313 (1.37%, 95% confidence interval [CI], 1.22‐1.53%) had a procedure code for injection or infusion of thrombolysis. Using NHDS sample weights, these numbers corresponded to an estimated 2.55 million hospitalizations for ischemic stroke in the United States during the time period and to 35,082 patients receiving intravenous thrombolytics. Although the overall rate of thrombolysis administration was quite low overall, the administration rate increased over time, from 0.87% [95% CI, 0.61‐1.22%] of stroke patients in year 2001 to 2.40% [95% CI, 1.95‐2.93%] in year 2006 and with a particular increase especially noted after year 2003 (P <0.001 for trend, Figure 1).

On bivariate analysis, a lower proportion of African‐American patients received tPA compared to white patients (0.8% vs. 1.5%, P = 0.003), while a higher proportion of patients with atrial fibrillation received tPA (2.3% vs. 1.2%, P < 0.001). Older patients were less likely than younger patients to receive tPA (Table 1). The rate of intracranial hemorrhage was significantly higher in patients who received tPA (5.4% vs. 0.6%, P < 0.001) and the overall inpatient mortality in patients who received tPA was 9.0%. Mortality in patients receiving tPA continued to be higher than in patients who did not receive tPA even when patients with intracranial hemorrhage were excluded (8.1% vs. 5.3%, P < 0.001). Larger hospitals were more likely to administer tPA to patients with ischemic stroke, with a 1.79% administration rate in hospitals with 300 beds compared to 0.90% in hospitals with 100 to 199 beds and 0.52% in hospitals with 6 to 99 beds (P < 0.001).
Thrombolysis, n (%) | No Thrombolysis, n (%) | P Value | |
---|---|---|---|
| |||
Age | 0.001 | ||
<60 | 76 (24.3) | 4478 (19.9) | |
60‐69 | 73 (23.3) | 3942 (17.5) | |
70‐79 | 82 (26.2) | 6265 (27.8) | |
80+ | 82 (26.2) | 7844 (34.8) | |
Female | 155 (49.5) | 12625 (56.0) | 0.02 |
Race | 0.003 | ||
White | 173 (55.3) | 11542 (51.2) | |
African American | 29 (9.3) | 3774 (16.8) | |
Other | 16 (5.1) | 814 (3.6) | |
Not stated | 95 (30.4) | 6399 (28.4) | |
Region | 0.05 | ||
Northeast | 78 (24.9) | 4570 (20.3) | |
Midwest | 84 (26.8) | 6924 (30.7) | |
South | 104 (33.2) | 8284 (36.8) | |
West | 47 (15.0) | 2751 (12.2) | |
Type of admission | <0.001 | ||
Emergent | 247 (78.9) | 14233 (63.2) | |
Urgent | 33 (10.5) | 3703 (16.4) | |
Elective | 5 (1.6) | 1346 (6.0) | |
Unknown | 28 (9.0) | 3247 (14.4) | |
Length of stay, days [95% CI] | 7.2 [6.6‐7.8] | 6.0 [5.9‐6.1] | <0.001 |
Hospital bedsize | <0.001 | ||
6‐99 | 16 (5.1) | 3065 (13.6) | |
100‐199 | 48 (15.3) | 5289 (23.5) | |
200‐299 | 86 (27.5) | 5212 (23.1) | |
300+ | 163 (52.1) | 8963 (39.8) | |
Payment type | <0.001 | ||
Medicare | 176 (56.2) | 15197 (67.5) | |
Medicaid | 21 (6.7) | 1245 (5.5) | |
Private | 45 (14.4) | 2483 (11.0) | |
HMO/PPO | 39 (12.5) | 2224 (9.9) | |
Other/unknown | 32 (10.2) | 1380 (6.1) | |
Discharge status | <0.001 | ||
Home | 98 (31.3) | 9507 (42.2) | |
Short term care facility | 25 (8.0) | 1271 (5.6) | |
Long term care facility | 62 (19.8) | 5400 (24.0) | |
Alive, status unknown | 89 (28.4) | 4514 (20.0) | |
Death | 28 (9.0) | 1218 (5.4) | |
Unknown | 11 (3.5) | 619 (2.8) | |
Comorbid conditions | |||
Congestive heart failure | 48 (15.3) | 2769 (12.3) | 0.10 |
Coronary artery disease | 49 (15.7) | 4082 (18.1) | 0.26 |
Hypertension | 164 (52.4) | 12480 (55.4) | 0.29 |
Diabetes mellitus | 42 (13.4) | 4965 (22.0) | <0.001 |
Atrial fibrillation | 96 (30.7) | 4096 (18.2) | <0.001 |
Intracranial hemorrhage | 17 (5.4) | 139 (0.6) | <0.001 |
Charlson score14 (mean) | 2.48 [2.32‐2.64] | 2.38 [2.36‐2.40] | 0.23 |
After adjusting for patient and hospital characteristics, the absolute rate of thrombolysis administration increased by an average of 0.19% per year (95% CI, 0.12‐0.26%). Factors that were significantly associated with administration of thrombolytics included being hospitalized in a larger hospital, having a history of atrial fibrillation, and a higher Charlson comorbidity index (Table 2). Patients aged 80 years or older, African American patients, and those with diabetes mellitus were significantly less likely to receive thrombolysis.
Characteristic | Adjusted OR (95% CI) |
---|---|
| |
Year (per year, from 2001 to 2006) | 1.2 (1.1‐1.3) |
Age, years | |
<60 | Referent |
60‐69 | 1.0 (0.7‐1.4) |
70‐79 | 0.6 (0.5‐0.9) |
80+ | 0.4 (0.3‐0.6) |
Race | |
Not African American | Referent |
African‐American | 0.4 (0.3‐0.7) |
Unknown | 1.0 (0.8‐1.2) |
Hospital bedsize | |
6‐99 | Referent |
100‐199 | 1.7 (1.0‐3.1) |
200‐299 | 3.2 (1.8‐5.4) |
300+ | 3.3 (2.0‐5.6) |
Diabetes mellitus | 0.5 (0.3‐0.6) |
Atrial fibrillation | 2.2 (1.7‐2.9) |
Charlson comorbidity score14 (per point increase) | 1.1 (1.1‐1.2) |
Discussion
Despite strong recommendations from guidelines and regulatory agencies, national rates of intravenous thrombolysis for ischemic stroke continue to be quite low overall. However, tPA administration appears to have increased from previous years and particularly increased in years after the Joint Commission began to accredit institutions as Primary Stroke Centers.11 The oldest patients and African Americans were less likely to receive thrombolytics, while patients with atrial fibrillation were more likely to receive thrombolysis, potentially related to atrial fibrillation causing more severe strokes.15 A total of 5.4% of patients who received tPA were diagnosed with intracranial hemorrhage, and the inpatient mortality rate of patients with tPA was 9.0%.
The exact optimal rate of thrombolysis administration for the patients in our study is unknown, as the NHDS database lacked detailed information on factors that would preclude tPA administration such as late timing of presentation and mild stroke symptoms.3 Studies conducted in stroke registries and regional settings have found that only approximately 15% to 32% of patients presenting with ischemic stroke arrive within 3 hours of symptom onset, and of these, only about 40% to 50% are eligible for tPA clinically.9, 10, 1619 However, even among presumed eligible patients, tPA administration rates only range between 25% and 43%,17, 19, 20 and the ideal rate is likely to be higher than the very low rates we observed in our study. Newer evidence that extending the time window where tPA may be given safely may increase the number of eligible patients.21
Patients who received thrombolysis had higher mortality rates than patients who did not. Although we were unable to determine a causal association, prior observational studies of tPA administration for acute stroke have found that patients with more severe neurologic deficits were more likely to receive thrombolysis.17, 18 The 9.0% inpatient case‐fatality rate observed in our study compares favorably to the 13.4% mortality rate after tPA reported in a post‐approval meta‐analysis of safety outcomes22 and the rate of intracranial hemorrhage in our analysis was similar to those observed in other settings.9, 2225 We were unable to determine whether intracranial hemorrhages in our study were as a result of tPA administration or whether patients who received tPA were more likely to have intracranial hemorrhages detected, such as may be due to increased frequency of head imaging.
Larger hospitals were more likely to administer tPA. This may reflect regionalization of stroke care, particularly in those designated as stroke centers of excellence. As well, there is some evidence that there is a learning curve with thrombolysis administration, where guideline‐recommended practice and use of tPA increases with additional experience with the drug.9, 26 Promoting systems that allow for rapid triage and diagnosis of acute stroke should be encouraged and hospital leaders should develop strategies that allow for early recognition of potential tPA candidates.
There are several limitations to our analysis. The NHDS does not collect detailed data on clinical or presenting features of stroke, and so we lacked information on stroke severity and eligibility for administration of thrombolysis. Our study may have underestimated the overall rates of thrombolysis, as it was dependent on diagnostic codes. A previous study of 34 patients who received tPA found that although the 99.10 code was 100% specific, the code identified only 17 patients who actually received tPA (sensitivity of 50%).20 Another study comparing Medicare administrative claims data to actual pharmacy billing charges for tPA found that administrative data underestimated the rate of tPA administration by approximately 25% to 30%.12 If a diagnostic code sensitivity of 50% was assumed, rates of tPA administration in our study may have been as high as 4.8% (95% CI, 4.1‐5.5%) by year 2006.
Conclusion
In conclusion, the use of intravenous thrombolysis in patients admitted with acute ischemic stroke in the United States has risen over time, but overall use remains very low. Further efforts to improve appropriate administration rates should be encouraged, particularly as the acceptable time‐window for using tPA widens.
Acknowledgements
The authors thank Mr. Loren Yglecias for his assistance with manuscript text and references.
- The National Institute of Neurological Disorders and Stroke rt‐PA Stroke Study Group.Tissue plasminogen activator for acute ischemic stroke.N Engl J Med.1995;333:1581–1587.
- Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group.N Engl J Med.1999;340:1781–1787. , , , et al.
- Association of outcome with early stroke treatment: Pooled analysis of ATLANTIS, ECASS, and NINDS rT‐PA stroke trials.Lancet.2004;363:768–774. , , , et al.
- Thrombolysis with alteplase for acute ischaemic stroke in the safe implementation of thrombolysis in stroke‐monitoring study (SITS‐MOST): An observational study.Lancet.2007;369:275–282. , , , et al.
- Recommendations for the establishment of primary stroke centers.JAMA.2000;283:3102–3109. , , , et al.
- Management of acute ischaemic stroke: new guidelines from the American Stroke Association and European Stroke Initiative.Lancet Neurol.2003;2:698–701. , .
- Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.Circulation.2007;115:e478–534. , , , et al.
- The Joint Commission Primary Stroke Center Certification. Available at: http://www.jointcommission.org/CertificationPrograms/PrimaryStrokeCenters. Accessed February 2010.
- Use of tissue‐type plasminogen activator for acute ischemic stroke: The Cleveland area experience.JAMA.2000;283:1151–1158. , , , et al.
- California Acute Stroke Pilot Registry (CASPR) Investigators.Prioritizing interventions to improve rates of thrombolysis for ischemic stroke.Neurology.2005;64:654–659.
- Thrombolysis for ischemic stroke in the united states: Data from National Hospital Discharge Survey 1999–2001.Neurosurgery.2005;57:647–654; discussion647–654. , , , et al.
- National US estimates of recombinant tissue plasminogen activator use: ICD‐9 codes substantially underestimate.Stroke.2008;39:924–928. , , , , .
- US Department of Health and Human Services Public Health Service and National Center for Health Statistics.National Hospital Discharge Durvey 1991–2006. Multi‐year public‐use data file documentation.
- Adapting a clinical comorbidity index for use with ICD‐9‐CM administrative databases.J Clin Epidemiol.1992;45:613–619. , , .
- Stroke severity in atrial fibrillation. The Framingham study.Stroke.1996;27:1760–1764. , , , et al.
- Why are stroke patients excluded from tPA therapy? An analysis of patient eligibility.Neurology.2001;57:1739–1740. , , , , .
- Utilization of intravenous tissue plasminogen activator for acute ischemic stroke.Arch Neurol.2004;61:346–350. , , , , , .
- Eligibility for recombinant tissue plasminogen activator in acute ischemic stroke: a population‐based study.Stroke.2004;35:27–29. , , , et al.
- Tpa use for stroke in the registry of the Canadian stroke network.Can J Neurol Sci.2005;32:433–439. , , , et al.
- Utilization of intravenous tissue‐type plasminogen activator for ischemic stroke at academic medical centers: the influence of ethnicity.Stroke.2001;32:1061–1068. , , , et al.
- Number needed to treat to benefit and to harm for intravenous tissue plasminogen activator therapy in the 3‐ to 4.5‐hour window: Joint outcome table analysis of the ECASS 3 trial.Stroke.2009;40:2433–2437. , , , et al.
- Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta‐analysis of safety data.Stroke.2003;34:2847–2850. .
- Early intravenous thrombolysis for acute ischemic stroke in a community‐based approach.Stroke.1998;29:1544–1549. , , , et al.
- Factors associated with in‐hospital mortality after administration of thrombolysis in acute ischemic stroke patients: an analysis of the Nationwide Inpatient Sample 1999 to 2002.Stroke.2006;37:440–446. , , , et al.
- Intravenous t‐PA for acute ischemic stroke: therapeutic yield of a stroke code system.Neurology.1998;50:501–503. , , , et al.
- Intravenous tissue‐type plasminogen activator therapy for ischemic stroke: Houston experience 1996 to 2000.Arch Neurol.2001;58:2009–2013. , , , et al.
- The National Institute of Neurological Disorders and Stroke rt‐PA Stroke Study Group.Tissue plasminogen activator for acute ischemic stroke.N Engl J Med.1995;333:1581–1587.
- Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group.N Engl J Med.1999;340:1781–1787. , , , et al.
- Association of outcome with early stroke treatment: Pooled analysis of ATLANTIS, ECASS, and NINDS rT‐PA stroke trials.Lancet.2004;363:768–774. , , , et al.
- Thrombolysis with alteplase for acute ischaemic stroke in the safe implementation of thrombolysis in stroke‐monitoring study (SITS‐MOST): An observational study.Lancet.2007;369:275–282. , , , et al.
- Recommendations for the establishment of primary stroke centers.JAMA.2000;283:3102–3109. , , , et al.
- Management of acute ischaemic stroke: new guidelines from the American Stroke Association and European Stroke Initiative.Lancet Neurol.2003;2:698–701. , .
- Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.Circulation.2007;115:e478–534. , , , et al.
- The Joint Commission Primary Stroke Center Certification. Available at: http://www.jointcommission.org/CertificationPrograms/PrimaryStrokeCenters. Accessed February 2010.
- Use of tissue‐type plasminogen activator for acute ischemic stroke: The Cleveland area experience.JAMA.2000;283:1151–1158. , , , et al.
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