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Oxford: Oxford University Press. p. 17. ISBN 0-19-517022-9. - American Psychiatric Association (June 2000). Diagnostic and Statistical Manual of Mental Disorders-IV (Text Revision).
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Is maternal PTSD associated with greater exposure of very young children to violent media? Journal of Trauma and Stress. 22(6), 658-62. - Briere, John (1992). "Methodological Issues in the Study of Sexual Abuse Effects" (PDF).
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- Giannini, AJ (1997). Drugs of Abuse (2nd ed.). Los Angeles: Practice Management Information Corp. ISBN 1-57066-053-0. - International Society for the Study of Trauma and Dissociation - The official journal of the International Society for the Study of Dissociation (ISSD), published between 1988 and 1997
Coding for Whooping Cough For The Record Vol. 25 No. 12 P. 26 Pertussis, which is more commonly known as whooping cough, is a highly contagious bacterial infection of the respiratory system. Commonly caused by Bordetella pertussis, its trademark symptom is severe coughing spells followed by a high-pitched “whoop” sound during inhalation.
Coding for Whooping Cough For The Record Vol. 25 No. 12 P. 26 Pertussis, which is more commonly known as whooping cough, is a highly contagious bacterial infection of the respiratory system. Commonly caused by Bordetella pertussis, its trademark symptom is severe coughing spells followed by a high-pitched “whoop” sound during inhalation. A vaccination is available to prevent the disease and consists of a series of five injections at the following ages: 2 months, 4 months, 6 months, between 15 and 18 months, and between 4 and 6 years.
12 P. 26 Pertussis, which is more commonly known as whooping cough, is a highly contagious bacterial infection of the respiratory system. Commonly caused by Bordetella pertussis, its trademark symptom is severe coughing spells followed by a high-pitched “whoop” sound during inhalation. A vaccination is available to prevent the disease and consists of a series of five injections at the following ages: 2 months, 4 months, 6 months, between 15 and 18 months, and between 4 and 6 years. This vaccination is called DTaP and is given in combination with vaccinations for diphtheria and tetanus. Because the immunity from the vaccination can fade away, a booster shot called Tdap is given between the ages of 11 and 18 and then every 10 years thereafter.
A vaccination is available to prevent the disease and consists of a series of five injections at the following ages: 2 months, 4 months, 6 months, between 15 and 18 months, and between 4 and 6 years. This vaccination is called DTaP and is given in combination with vaccinations for diphtheria and tetanus. Because the immunity from the vaccination can fade away, a booster shot called Tdap is given between the ages of 11 and 18 and then every 10 years thereafter. The Tdap vaccine is similar to DTaP but with lower concentrations of diphtheria and pertussis. Despite the availability of a vaccination to prevent whooping cough, the number of confirmed cases each year in the United States is on the rise.
The Tdap vaccine is similar to DTaP but with lower concentrations of diphtheria and pertussis. Despite the availability of a vaccination to prevent whooping cough, the number of confirmed cases each year in the United States is on the rise. According to the Centers for Disease Control and Prevention, in 2012 there were more than 41,000 whooping cough cases in the United States, including 18 deaths. The condition typically affects children who are too young to have received at least the first three vaccinations. It also may affect teenagers and adults without enough immunity to fight the bacteria and who have not received the booster shot.
Common complications include an abdominal hernia, broken blood vessels affecting the skin or eyes, and fractured or bruised ribs. Infants with whooping cough may experience complications such as apnea, brain damage, dehydration, ear infections, pneumonia, and seizures. ICD-9-CM Code Classifications Whooping cough is classified to ICD-9-CM category 033. A fourth-digit subcategory is available to identify the organism involved, as follows: • 033.0, Bordetella pertussis; • 033.1, Bordetella parapertussis; and • 033.8, Whooping cough due to other specified organism, which also includes Bordetella bronchiseptica. If the organism is not specified, assign code 033.9.
Infants with whooping cough may experience complications such as apnea, brain damage, dehydration, ear infections, pneumonia, and seizures. ICD-9-CM Code Classifications Whooping cough is classified to ICD-9-CM category 033. A fourth-digit subcategory is available to identify the organism involved, as follows: • 033.0, Bordetella pertussis; • 033.1, Bordetella parapertussis; and • 033.8, Whooping cough due to other specified organism, which also includes Bordetella bronchiseptica. If the organism is not specified, assign code 033.9. Pneumonia associated with whooping cough is classified as code 484.3, Pneumonia in whooping cough, sequenced as the secondary diagnosis.
ICD-9-CM Code Classifications Whooping cough is classified to ICD-9-CM category 033. A fourth-digit subcategory is available to identify the organism involved, as follows: • 033.0, Bordetella pertussis; • 033.1, Bordetella parapertussis; and • 033.8, Whooping cough due to other specified organism, which also includes Bordetella bronchiseptica. If the organism is not specified, assign code 033.9. Pneumonia associated with whooping cough is classified as code 484.3, Pneumonia in whooping cough, sequenced as the secondary diagnosis. If the patient receives a vaccination against pertussis alone, assign code V03.6.
A fourth-digit subcategory is available to identify the organism involved, as follows: • 033.0, Bordetella pertussis; • 033.1, Bordetella parapertussis; and • 033.8, Whooping cough due to other specified organism, which also includes Bordetella bronchiseptica. If the organism is not specified, assign code 033.9. Pneumonia associated with whooping cough is classified as code 484.3, Pneumonia in whooping cough, sequenced as the secondary diagnosis. If the patient receives a vaccination against pertussis alone, assign code V03.6. If the vaccination is combined with DTaP, then assign code V06.1.
If the organism is not specified, assign code 033.9. Pneumonia associated with whooping cough is classified as code 484.3, Pneumonia in whooping cough, sequenced as the secondary diagnosis. If the patient receives a vaccination against pertussis alone, assign code V03.6. If the vaccination is combined with DTaP, then assign code V06.1. Other codes that are available for vaccinations given in combination include the following: • V06.2, DTaP with typhoid-paratyphoid; • V06.3, DTaP with poliomyelitis; and • V06.8, DTaP with hemophilus influence B. Whooping cough may be confirmed by a nose or throat culture to identify the organism.
Pneumonia associated with whooping cough is classified as code 484.3, Pneumonia in whooping cough, sequenced as the secondary diagnosis. If the patient receives a vaccination against pertussis alone, assign code V03.6. If the vaccination is combined with DTaP, then assign code V06.1. Other codes that are available for vaccinations given in combination include the following: • V06.2, DTaP with typhoid-paratyphoid; • V06.3, DTaP with poliomyelitis; and • V06.8, DTaP with hemophilus influence B. Whooping cough may be confirmed by a nose or throat culture to identify the organism. The physician also may order blood tests.
If the patient receives a vaccination against pertussis alone, assign code V03.6. If the vaccination is combined with DTaP, then assign code V06.1. Other codes that are available for vaccinations given in combination include the following: • V06.2, DTaP with typhoid-paratyphoid; • V06.3, DTaP with poliomyelitis; and • V06.8, DTaP with hemophilus influence B. Whooping cough may be confirmed by a nose or throat culture to identify the organism. The physician also may order blood tests. If the patient’s white blood cell count is elevated, it may indicate the patient is fighting an infection.
However, infants with whooping cough typically are hospitalized to treat the infection and any associated symptoms and complications. Coding and sequencing for whooping cough depend on the physician documentation in the medical record and application of the Official Coding Guidelines for inpatient care. Use specific AHA Coding Clinic for ICD-9-CM and American Medical Association CPT Assistant references to ensure complete and accurate coding. — This information was prepared by Audrey Howard, RHIA, senior consultant with 3M Consulting Services. 3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to more than 5,000 healthcare providers.
Use specific AHA Coding Clinic for ICD-9-CM and American Medical Association CPT Assistant references to ensure complete and accurate coding. — This information was prepared by Audrey Howard, RHIA, senior consultant with 3M Consulting Services. 3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to more than 5,000 healthcare providers. The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447.
3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to more than 5,000 healthcare providers. The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447. ICD-10-CM Coding for Whooping Cough The coding classification for whooping cough is similar in ICD-10-CM. The one major difference is that instead of assigning a separate code for any associated pneumonia as a secondary diagnosis, there now is a combination code for whooping cough and pneumonia.
The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447. ICD-10-CM Coding for Whooping Cough The coding classification for whooping cough is similar in ICD-10-CM. The one major difference is that instead of assigning a separate code for any associated pneumonia as a secondary diagnosis, there now is a combination code for whooping cough and pneumonia. Category A37 has codes available for whooping cough caused by Bordetella pertussis, Bordetella parapertussis, and other Bordetella species (including Bordetella bronchiseptica).
The one major difference is that instead of assigning a separate code for any associated pneumonia as a secondary diagnosis, there now is a combination code for whooping cough and pneumonia. Category A37 has codes available for whooping cough caused by Bordetella pertussis, Bordetella parapertussis, and other Bordetella species (including Bordetella bronchiseptica). The fifth character of 1 will identify that there is associated pneumonia.
1. (MeSH)A childhood disorder predominately affecting boys and similar to autism (AUTISTIC DISORDER). It is characterized by severe, sustained, clinically significant impairment of social interaction, and restricted repetitive and stereotyped patterns of behavior.
It differs from other autism spectrum disorders by its relative preservation of linguistic and cognitive development. Although not required for diagnosis, physical clumsiness and atypical use of language are frequently reported. The syndrome is named after the Austrian pediatrician Hans Asperger who, in 1944, studied and described children in his practice who lacked nonverbal communication skills, demonstrated limited empathy with their peers, and were physically clumsy. The modern conception of Asperger syndrome came into existence in 1981 and went through a period of popularization, becoming standardized as a diagnosis in the early 1990s. Many questions remain about aspects of the disorder.
Although not required for diagnosis, physical clumsiness and atypical use of language are frequently reported. The syndrome is named after the Austrian pediatrician Hans Asperger who, in 1944, studied and described children in his practice who lacked nonverbal communication skills, demonstrated limited empathy with their peers, and were physically clumsy. The modern conception of Asperger syndrome came into existence in 1981 and went through a period of popularization, becoming standardized as a diagnosis in the early 1990s. Many questions remain about aspects of the disorder. For example, there is doubt about whether it is distinct from high-functioning autism (HFA); partly because of this, its prevalence is not firmly established.
The extent of the overlap between AS and high-functioning autism (HFA—autism unaccompanied by mental retardation) is unclear. The current ASD classification is to some extent an artifact of how autism was discovered, and may not reflect the true nature of the spectrum; methodological problems have beset Asperger syndrome as a valid diagnosis from the outset. One of the proposed changes to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), to be published in May 2013, would eliminate Asperger syndrome as a separate diagnosis, and fold it under autistic disorder (autism spectrum disorder), which would be rated on a severity scale. Like the diagnosis of Asperger syndrome, the proposed change is controversial, and it has been argued that the syndrome's diagnostic criteria should be broadened. Asperger syndrome is also called Asperger's syndrome (AS), Asperger (or Asperger's) disorder (AD), or just Asperger's.
The hypothesis that individuals with AS are predisposed to violent or criminal behavior has been investigated but is not supported by data. More evidence suggests children with AS are victims rather than victimizers. A 2008 review found that an overwhelming number of reported violent criminals with AS had coexisting psychiatric disorders such as schizoaffective disorder. People with Asperger syndrome often display behavior, interests, and activities that are restricted and repetitive and are sometimes abnormally intense or focused. They may stick to inflexible routines, move in stereotyped and repetitive ways, or preoccupy themselves with parts of objects.
Individuals with AS may collect volumes of detailed information on a relatively narrow topic such as weather data or star names, without necessarily having a genuine understanding of the broader topic. For example, a child might memorize camera model numbers while caring little about photography. This behavior is usually apparent by grade school, typically age 5 or 6 in the United States. Although these special interests may change from time to time, they typically become more unusual and narrowly focused, and often dominate social interaction so much that the entire family may become immersed. Because narrow topics often capture the interest of children, this symptom may go unrecognized.
For example, one study found that activation is delayed in the core circuit for imitation in individuals with AS. This theory maps well to social cognition theories like the theory of mind, which hypothesizes that autistic behavior arises from impairments in ascribing mental states to oneself and others, or hyper-systemizing, which hypothesizes that autistic individuals can systematize internal operation to handle internal events but are less effective at empathizing by handling events generated by other agents. Parents of children with Asperger syndrome can typically trace differences in their children's development to as early as 30 months of age. Developmental screening during a routine check-up by a general practitioner or pediatrician may identify signs that warrant further investigation. The diagnosis of AS is complicated by the use of several different screening instruments, including the Asperger Syndrome Diagnostic Scale (ASDS), Autism Spectrum Screening Questionnaire (ASSQ), Childhood Asperger Syndrome Test (CAST), Gilliam Asperger's Disorder Scale (GADS), Krug Asperger's Disorder Index (KADI), and the Autism Spectrum Quotient (AQ; with versions for children, adolescents and adults).
The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine, and sertraline have been effective in treating restricted and repetitive interests and behaviors. Care must be taken with medications, as side effects may be more common and harder to evaluate in individuals with AS, and tests of drugs' effectiveness against comorbid conditions routinely exclude individuals from the autism spectrum. Abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications, along with serious long-term neurological side effects. SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression, and sleep disturbance. Weight gain and fatigue are commonly reported side effects of risperidone, which may also lead to increased risk for extrapyramidal symptoms such as restlessness and dystonia and increased serum prolactin levels.
Sedative side-effects in school-age children have ramifications for classroom learning. Individuals with AS may be unable to identify and communicate their internal moods and emotions or to tolerate side effects that for most people would not be problematic. There is some evidence that children with AS may see a lessening of symptoms; up to 20% of children may no longer meet the diagnostic criteria as adults, although social and communication difficulties may persist. As of 2006, no studies addressing the long-term outcome of individuals with Asperger syndrome are available and there are no systematic long-term follow-up studies of children with AS. Individuals with AS appear to have normal life expectancy, but have an increased prevalence of comorbid psychiatric conditions, such as major depressive disorder and anxiety disorder that may significantly affect prognosis.
There are legal implications for individuals with AS as they run the risk of exploitation by others and may be unable to comprehend the societal implications of their actions. Prevalence estimates vary enormously. A 2003 review of epidemiological studies of children found autism prevalence rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1; combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000. Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria.
A 2003 review of epidemiological studies of children found autism prevalence rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1; combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000. Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria. Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%.
Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria. Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%. Depression is common in adolescents and adults; children are likely to present with ADHD.
For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria. Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%. Depression is common in adolescents and adults; children are likely to present with ADHD. [unreliable medical source?]
[unreliable medical source?] Reports have associated AS with medical conditions such as aminoaciduria and ligamentous laxity, but these have been case reports or small studies and no factors have been associated with AS across studies. One study of males with AS found an increased rate of epilepsy and a high rate (51%) of nonverbal learning disorder. AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive-compulsive disorder and obsessive-compulsive personality disorder. However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common.
AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive-compulsive disorder and obsessive-compulsive personality disorder. However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common. Named after the Austrian pediatrician Hans Asperger (1906–1980), Asperger syndrome is a relatively new diagnosis in the field of autism. As a child, Asperger appears to have exhibited some features of the very condition named after him, such as remoteness and talent in language. In 1944, Asperger described four children in his practice who had difficulty in integrating themselves socially.
Named after the Austrian pediatrician Hans Asperger (1906–1980), Asperger syndrome is a relatively new diagnosis in the field of autism. As a child, Asperger appears to have exhibited some features of the very condition named after him, such as remoteness and talent in language. In 1944, Asperger described four children in his practice who had difficulty in integrating themselves socially. The children lacked nonverbal communication skills, failed to demonstrate empathy with their peers, and were physically clumsy. Asperger called the condition "autistic psychopathy" and described it as primarily marked by social isolation.
Asperger also called his young patients "little professors", and believed some would be capable of exceptional achievement and original thought later in life. His paper was published during wartime and in German, so it was not widely read elsewhere. Lorna Wing popularized the term Asperger syndrome in the English-speaking medical community in her 1981 publication of a series of case studies of children showing similar symptoms, and Uta Frith translated Asperger's paper to English in 1991. Sets of diagnostic criteria were outlined by Gillberg and Gillberg in 1989 and by Szatmari et al. in the same year.
Sets of diagnostic criteria were outlined by Gillberg and Gillberg in 1989 and by Szatmari et al. in the same year. AS became a standard diagnosis in 1992, when it was included in the tenth edition of the World Health Organization's diagnostic manual, International Classification of Diseases (ICD-10); in 1994, it was added to the fourth edition of the American Psychiatric Association's diagnostic reference, Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup. Whether it should be seen as distinct from high-functioning autism is a fundamental issue requiring further study, and there are questions about the empirical validation of the DSM-IV and ICD-10 criteria.
AS became a standard diagnosis in 1992, when it was included in the tenth edition of the World Health Organization's diagnostic manual, International Classification of Diseases (ICD-10); in 1994, it was added to the fourth edition of the American Psychiatric Association's diagnostic reference, Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup. Whether it should be seen as distinct from high-functioning autism is a fundamental issue requiring further study, and there are questions about the empirical validation of the DSM-IV and ICD-10 criteria. People identifying with Asperger syndrome may refer to themselves in casual conversation as aspies (a term first used in print by Liane Holliday Willey in 1999). The word neurotypical (abbreviated NT) describes a person whose neurological development and state are typical, and is often used to refer to non-autistic people.
Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup. Whether it should be seen as distinct from high-functioning autism is a fundamental issue requiring further study, and there are questions about the empirical validation of the DSM-IV and ICD-10 criteria. People identifying with Asperger syndrome may refer to themselves in casual conversation as aspies (a term first used in print by Liane Holliday Willey in 1999). The word neurotypical (abbreviated NT) describes a person whose neurological development and state are typical, and is often used to refer to non-autistic people. The Internet has allowed individuals with AS to communicate and celebrate diversity with each other in a way that was not previously possible because of their rarity and geographic dispersal.
There is a contrast between the attitude of adults with self-identified AS, who typically do not want to be cured and are proud of their identity, and parents of children with AS, who typically seek assistance and a cure for their children. Some researchers have argued that AS can be viewed as a different cognitive style, not a disorder or a disability, and that it should be removed from the standard Diagnostic and Statistical Manual, much as homosexuality was removed. In a 2002 paper, Simon Baron-Cohen wrote of those with AS, "In the social world, there is no great benefit to a precise eye for detail, but in the worlds of maths, computing, cataloguing, music, linguistics, engineering, and science, such an eye for detail can lead to success rather than failure." Baron-Cohen cited two reasons why it might still be useful to consider AS to be a disability: to ensure provision for legally required special support, and to recognize emotional difficulties from reduced empathy. It has been argued that the genes for Asperger's combination of abilities have operated throughout recent human evolution and have made remarkable contributions to human history.
EPA's Report on the Environment: External Review Draft Birth Defects Prevalence and Mortality Note to reviewers of this draft revised ROE: This indicator reflects data through 2010. EPA anticipates updating this indicator in 2014. Birth defects or congenital anomalies are structural or functional anomalies causing physical or mental disability, some of which can be fatal.
EPA's Report on the Environment: External Review Draft Birth Defects Prevalence and Mortality Note to reviewers of this draft revised ROE: This indicator reflects data through 2010. EPA anticipates updating this indicator in 2014. Birth defects or congenital anomalies are structural or functional anomalies causing physical or mental disability, some of which can be fatal. Although birth defects are the leading cause of infant mortality (deaths occurring to those under 1 year of age) in the U.S., the cause is unknown for approximately 70 percent of all cases (Infant Mortality indicator) (CDC, 2011).
EPA anticipates updating this indicator in 2014. Birth defects or congenital anomalies are structural or functional anomalies causing physical or mental disability, some of which can be fatal. Although birth defects are the leading cause of infant mortality (deaths occurring to those under 1 year of age) in the U.S., the cause is unknown for approximately 70 percent of all cases (Infant Mortality indicator) (CDC, 2011). Many different factors may be associated with the development of birth defects, such as genetic and/or chromosomal aberrations, in utero exposure to viruses or bacteria, uncontrolled maternal diabetes, maternal cigarette smoke, maternal use of drugs and alcohol during pregnancy, and prenatal exposure to chemicals. All of these factors may influence normal infant growth or development, resulting in different types of birth defects (NICHD, 2012).
Although birth defects are the leading cause of infant mortality (deaths occurring to those under 1 year of age) in the U.S., the cause is unknown for approximately 70 percent of all cases (Infant Mortality indicator) (CDC, 2011). Many different factors may be associated with the development of birth defects, such as genetic and/or chromosomal aberrations, in utero exposure to viruses or bacteria, uncontrolled maternal diabetes, maternal cigarette smoke, maternal use of drugs and alcohol during pregnancy, and prenatal exposure to chemicals. All of these factors may influence normal infant growth or development, resulting in different types of birth defects (NICHD, 2012). This indicator presents birth defects prevalence at birth for five specified congenital anomalies (anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele) that are consistently reported on both the 2003 (revised) and 1989 U.S. Standard Certificates of Live Birth and mortality rates among infants in the U.S. as recorded in the National Vital Statistics System (NVSS), which registers virtually all births and deaths nationwide. Birth defects data are currently collected on birth certificates and death certificates from all 50 states and the District of Columbia.
Many different factors may be associated with the development of birth defects, such as genetic and/or chromosomal aberrations, in utero exposure to viruses or bacteria, uncontrolled maternal diabetes, maternal cigarette smoke, maternal use of drugs and alcohol during pregnancy, and prenatal exposure to chemicals. All of these factors may influence normal infant growth or development, resulting in different types of birth defects (NICHD, 2012). This indicator presents birth defects prevalence at birth for five specified congenital anomalies (anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele) that are consistently reported on both the 2003 (revised) and 1989 U.S. Standard Certificates of Live Birth and mortality rates among infants in the U.S. as recorded in the National Vital Statistics System (NVSS), which registers virtually all births and deaths nationwide. Birth defects data are currently collected on birth certificates and death certificates from all 50 states and the District of Columbia. Reported race and ethnicity data are based on the race and ethnicity of the mother.
All of these factors may influence normal infant growth or development, resulting in different types of birth defects (NICHD, 2012). This indicator presents birth defects prevalence at birth for five specified congenital anomalies (anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele) that are consistently reported on both the 2003 (revised) and 1989 U.S. Standard Certificates of Live Birth and mortality rates among infants in the U.S. as recorded in the National Vital Statistics System (NVSS), which registers virtually all births and deaths nationwide. Birth defects data are currently collected on birth certificates and death certificates from all 50 states and the District of Columbia. Reported race and ethnicity data are based on the race and ethnicity of the mother. What the Data Show Exhibit 1 presents the prevalence of live births with identified specific congenital anomalies between 1999 and 2010.
Birth defects data are currently collected on birth certificates and death certificates from all 50 states and the District of Columbia. Reported race and ethnicity data are based on the race and ethnicity of the mother. What the Data Show Exhibit 1 presents the prevalence of live births with identified specific congenital anomalies between 1999 and 2010. While the rates of birth defects are rare and underreported, as stated in the Limitations, it is possible to make some general inferences based on the available data. For example, as Exhibit 1 shows, the rates for cleft lip or palate and spina bifida or meningomyelocele decreased slightly over the last decade.
What the Data Show Exhibit 1 presents the prevalence of live births with identified specific congenital anomalies between 1999 and 2010. While the rates of birth defects are rare and underreported, as stated in the Limitations, it is possible to make some general inferences based on the available data. For example, as Exhibit 1 shows, the rates for cleft lip or palate and spina bifida or meningomyelocele decreased slightly over the last decade. Rates for the other three fluctuated over time with a slight increase in rates since 1999. Rates for certain types of anomalies differ widely with maternal age.
While the rates of birth defects are rare and underreported, as stated in the Limitations, it is possible to make some general inferences based on the available data. For example, as Exhibit 1 shows, the rates for cleft lip or palate and spina bifida or meningomyelocele decreased slightly over the last decade. Rates for the other three fluctuated over time with a slight increase in rates since 1999. Rates for certain types of anomalies differ widely with maternal age. For example, in 2010 as in past years, infants of the youngest mothers (under 20 years of age) have the highest rates for omphalocele orgastroschisis, a defect or abnormality of the anterior abdominal wall (102.1 per 100,000 live births); infants of mothers age 40-54 years have the highest rates for Down syndrome (333.9 per 100,000 live births).
Rates for the other three fluctuated over time with a slight increase in rates since 1999. Rates for certain types of anomalies differ widely with maternal age. For example, in 2010 as in past years, infants of the youngest mothers (under 20 years of age) have the highest rates for omphalocele orgastroschisis, a defect or abnormality of the anterior abdominal wall (102.1 per 100,000 live births); infants of mothers age 40-54 years have the highest rates for Down syndrome (333.9 per 100,000 live births). Birth defects continue to be the leading cause of infant mortality, accounting for 5,319 (20.1 percent) of the 26,412 infant deaths in 2009 (Exhibit 2, Infant Mortality indicator). Between 1979 and 1998, a decline in the national birth defects mortality rate has been observed, ranging from 255.4 per 100,000 live births in 1979 to 157.6 per 100,000 live births in 1998.
Rates for certain types of anomalies differ widely with maternal age. For example, in 2010 as in past years, infants of the youngest mothers (under 20 years of age) have the highest rates for omphalocele orgastroschisis, a defect or abnormality of the anterior abdominal wall (102.1 per 100,000 live births); infants of mothers age 40-54 years have the highest rates for Down syndrome (333.9 per 100,000 live births). Birth defects continue to be the leading cause of infant mortality, accounting for 5,319 (20.1 percent) of the 26,412 infant deaths in 2009 (Exhibit 2, Infant Mortality indicator). Between 1979 and 1998, a decline in the national birth defects mortality rate has been observed, ranging from 255.4 per 100,000 live births in 1979 to 157.6 per 100,000 live births in 1998. From 1999 to 2009, the birth defects mortality rates ranged from a high of 150.9 in 2000 to a low of 124.8 per 100,000 live births in 2009.
For example, in 2010 as in past years, infants of the youngest mothers (under 20 years of age) have the highest rates for omphalocele orgastroschisis, a defect or abnormality of the anterior abdominal wall (102.1 per 100,000 live births); infants of mothers age 40-54 years have the highest rates for Down syndrome (333.9 per 100,000 live births). Birth defects continue to be the leading cause of infant mortality, accounting for 5,319 (20.1 percent) of the 26,412 infant deaths in 2009 (Exhibit 2, Infant Mortality indicator). Between 1979 and 1998, a decline in the national birth defects mortality rate has been observed, ranging from 255.4 per 100,000 live births in 1979 to 157.6 per 100,000 live births in 1998. From 1999 to 2009, the birth defects mortality rates ranged from a high of 150.9 in 2000 to a low of 124.8 per 100,000 live births in 2009. (Data not shown.)
Birth defects continue to be the leading cause of infant mortality, accounting for 5,319 (20.1 percent) of the 26,412 infant deaths in 2009 (Exhibit 2, Infant Mortality indicator). Between 1979 and 1998, a decline in the national birth defects mortality rate has been observed, ranging from 255.4 per 100,000 live births in 1979 to 157.6 per 100,000 live births in 1998. From 1999 to 2009, the birth defects mortality rates ranged from a high of 150.9 in 2000 to a low of 124.8 per 100,000 live births in 2009. (Data not shown.) Birth defect mortality rates differ by sex, race, and ethnicity.
(Data not shown.) Birth defect mortality rates differ by sex, race, and ethnicity. From 1999 to 2009, females had lower rates for each individual year than males, but the range in rates was similar between the two sexes. Specifically, birth defect mortality rates for females ranged from a high of 146.2 (2000) to a low of 122.6 (2009) per 100,000 live births compared to a high of 155.4 (2000) and a low of 127.0 (2009) per live births for males. Asian or Pacific Islanders consistently had the lowest rates of mortality from birth defects among the reported racial groups from 1999 to 2009.
Birth defect mortality rates differ by sex, race, and ethnicity. From 1999 to 2009, females had lower rates for each individual year than males, but the range in rates was similar between the two sexes. Specifically, birth defect mortality rates for females ranged from a high of 146.2 (2000) to a low of 122.6 (2009) per 100,000 live births compared to a high of 155.4 (2000) and a low of 127.0 (2009) per live births for males. Asian or Pacific Islanders consistently had the lowest rates of mortality from birth defects among the reported racial groups from 1999 to 2009. During the 11-year period from 1999-2009, Blacks or African Americans had the second highest birth defect mortality rates for seven years, while American Indians/Alaska Natives had the second highest rates for four years.
Specifically, birth defect mortality rates for females ranged from a high of 146.2 (2000) to a low of 122.6 (2009) per 100,000 live births compared to a high of 155.4 (2000) and a low of 127.0 (2009) per live births for males. Asian or Pacific Islanders consistently had the lowest rates of mortality from birth defects among the reported racial groups from 1999 to 2009. During the 11-year period from 1999-2009, Blacks or African Americans had the second highest birth defect mortality rates for seven years, while American Indians/Alaska Natives had the second highest rates for four years. Whites did not have the highest or lowest birth defects mortality rate for any of these years. For each year during 1999 to 2009, Hispanics or Latinos had higher birth defects mortality rates than non-Hispanics except for two years: 1999 and 2009.
During the 11-year period from 1999-2009, Blacks or African Americans had the second highest birth defect mortality rates for seven years, while American Indians/Alaska Natives had the second highest rates for four years. Whites did not have the highest or lowest birth defects mortality rate for any of these years. For each year during 1999 to 2009, Hispanics or Latinos had higher birth defects mortality rates than non-Hispanics except for two years: 1999 and 2009. (Data not shown.) - In order to enable comparisons over time, this indicator represents only a subset of possible birth defects.
(Data not shown.) - In order to enable comparisons over time, this indicator represents only a subset of possible birth defects. This is necessary because of changes made to the U.S. Standard Certificate of Live Birth in 2003. Consistent with NCHS reporting in its recent "Births: Final Data" publications, only the five congenital anomalies reported on both the 2003 and 1989 U.S. Standard Certificates of Live Birth are included (i.e., anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele). - Birth defects are often underreported on both birth and death certificates (Boulet et al., 2011; Friis and Sellers, 1999).
- In order to enable comparisons over time, this indicator represents only a subset of possible birth defects. This is necessary because of changes made to the U.S. Standard Certificate of Live Birth in 2003. Consistent with NCHS reporting in its recent "Births: Final Data" publications, only the five congenital anomalies reported on both the 2003 and 1989 U.S. Standard Certificates of Live Birth are included (i.e., anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele). - Birth defects are often underreported on both birth and death certificates (Boulet et al., 2011; Friis and Sellers, 1999). Many anomalies are hard to detect at birth, which limits early ascertainment and complete reporting.
This is necessary because of changes made to the U.S. Standard Certificate of Live Birth in 2003. Consistent with NCHS reporting in its recent "Births: Final Data" publications, only the five congenital anomalies reported on both the 2003 and 1989 U.S. Standard Certificates of Live Birth are included (i.e., anencephaly, cleft lip or palate, Down syndrome, omphalocele or gastroschisis, and spina bifida or meningomyelocele). - Birth defects are often underreported on both birth and death certificates (Boulet et al., 2011; Friis and Sellers, 1999). Many anomalies are hard to detect at birth, which limits early ascertainment and complete reporting. While the most serious and/or apparent anomalies are more likely to be identified and reported prior to hospital discharge, studies have reported low overall sensitivity (e.g., 23-28%) of selected birth defects reported on birth certificates (Boulet et al., 2011; Honein et al., 2001).
- Birth defects are often underreported on both birth and death certificates (Boulet et al., 2011; Friis and Sellers, 1999). Many anomalies are hard to detect at birth, which limits early ascertainment and complete reporting. While the most serious and/or apparent anomalies are more likely to be identified and reported prior to hospital discharge, studies have reported low overall sensitivity (e.g., 23-28%) of selected birth defects reported on birth certificates (Boulet et al., 2011; Honein et al., 2001). Research shows that the NVSS birth records can produce prevalence estimates that are 2 to 3 times lower than those based on ascertainment of congenital defects using records from active surveillance efforts (Parker et al., 2010). - The congenital anomalies reported on birth certificates are rare events.
Many anomalies are hard to detect at birth, which limits early ascertainment and complete reporting. While the most serious and/or apparent anomalies are more likely to be identified and reported prior to hospital discharge, studies have reported low overall sensitivity (e.g., 23-28%) of selected birth defects reported on birth certificates (Boulet et al., 2011; Honein et al., 2001). Research shows that the NVSS birth records can produce prevalence estimates that are 2 to 3 times lower than those based on ascertainment of congenital defects using records from active surveillance efforts (Parker et al., 2010). - The congenital anomalies reported on birth certificates are rare events. Since a small change in the number of anomalies reported can result in a relatively large change in rates, caution should also be used in comparing yearly rates for a specific anomaly.
Incorrect coding and low rates of autopsies that confirm the cause of death may occur. Additionally, some individuals may have had competing causes of death. When more than one cause or condition is entered by the physician, the underlying cause is determined by the sequence of conditions on the certificate, provisions of the ICD [International Classification of Diseases], and associated selection rules and modifications. Consequently, some misclassification of reported mortality might occur in individuals with competing causes of death, as well as underreporting of some birth defects as the cause of death. - The International Classification of Diseases 9th Revision (ICD-9) codes were used to specify underlying cause of death for years 1979-1998.
When more than one cause or condition is entered by the physician, the underlying cause is determined by the sequence of conditions on the certificate, provisions of the ICD [International Classification of Diseases], and associated selection rules and modifications. Consequently, some misclassification of reported mortality might occur in individuals with competing causes of death, as well as underreporting of some birth defects as the cause of death. - The International Classification of Diseases 9th Revision (ICD-9) codes were used to specify underlying cause of death for years 1979-1998. Beginning in 1999, cause of death is specified with the International Classification of Diseases 10th Revision (ICD-10) codes. The two revisions differ substantially, and to prevent confusion about the significance of any specific disease code, data queries are separate.
Consequently, some misclassification of reported mortality might occur in individuals with competing causes of death, as well as underreporting of some birth defects as the cause of death. - The International Classification of Diseases 9th Revision (ICD-9) codes were used to specify underlying cause of death for years 1979-1998. Beginning in 1999, cause of death is specified with the International Classification of Diseases 10th Revision (ICD-10) codes. The two revisions differ substantially, and to prevent confusion about the significance of any specific disease code, data queries are separate. The relatively large difference between birth defects mortality rates reported from 1979 through 1998 and those reported beginning in 1999 may be due to some changes in the criteria used to report birth defects mortality during the switch from ICD-9 to ICD-10.
Beginning in 1999, cause of death is specified with the International Classification of Diseases 10th Revision (ICD-10) codes. The two revisions differ substantially, and to prevent confusion about the significance of any specific disease code, data queries are separate. The relatively large difference between birth defects mortality rates reported from 1979 through 1998 and those reported beginning in 1999 may be due to some changes in the criteria used to report birth defects mortality during the switch from ICD-9 to ICD-10. The birth defects rate data used for this indicator are from National Vital Statistics Reports published by the Centers for Disease Control and Prevention's National Center for Health Statistics (NCHS, 2001, 2002a,b, 2003, 2005, 2006, 2007, 2009, 2010a,b, 2012a,b). The birth defects mortality data were obtained from CDC's compressed mortality files (underlying cause of death), accessed via CDC WONDER (CDC, 2012), at http://wonder.cdc.gov.