Fetal alcohol spectrum disturbance ( FASD ) is a group of conditions that can occur in someone whose mother drinks alcohol during pregnancy. Problems may include abnormal appearance, short height, low weight, small head size, poor coordination, low intelligence, behavior problems, and hearing or vision problems. Those affected are more likely to have problems at school, legal issues, participate in high-risk behaviors, and have problems with alcohol or other drugs. The most severe form of this condition is known as fetal alcohol syndrome ( FAS ). Other types include partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorders (ARND) and alcohol-related birth defects (ARBD). Some simply accept FAS as a diagnosis, seeing evidence as inconclusive with respect to other types.
Fetal alcohol spectrum disorders are caused by drinking alcohol during pregnancy. Surveys from the United States have found about 10% of pregnant women drink alcohol in the past month, and 20% to 30% drink at some point during pregnancy. About 4.7% of pregnant North American women are alcoholics. The risk of the problem depends on the amount consumed and the frequency of consumption as well as when during pregnancy the alcohol is consumed. Other risk factors include older mothers, smoking, and poor diet. There is no known safe amount or safe time to take during pregnancy. When drinking small amounts of alcohol does not cause abnormalities in the face, it can cause behavior problems. Alcohol crosses the blood barrier of the brain and either directly or indirectly affects the developing baby. Diagnosis is based on signs and symptoms on the person.
Fetal alcohol spectrum disorders can be prevented by avoiding alcohol. For this reason, medical authorities advise no alcohol during pregnancy or when trying to get pregnant. Although the condition is permanent, treatment can improve results. Interventions may include parent-child interaction therapy, attempts to modify child behavior, and possibly drugs.
FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. FAS is believed to occur between 0.2 and 9 per 1,000 live births in the United States. In South Africa, some populations have rates as high as 9%. The negative effects of alcohol during pregnancy have been described since ancient times. The cost of a child's lifetime with FAS is $ 2,000,000 in 2002 in the US. The term fetal alcohol syndrome was first used in 1973.
Video Fetal alcohol spectrum disorder
Type
FASDs cover a wide range of physical and neurodevelopmental problems that can result from exposure to prenatal alcohol. The most severe condition is called fetal alcohol syndrome (FAS), which refers to individuals with birth defects and neurodevelopmental disorders characteristic of diagnosis.
Some simply accept FAS as a diagnosis, seeing evidence as inconclusive with respect to other types. Partial fetal alcohol syndrome (pFAS) refers to individuals with a history of known or highly suspected prenatal alcohol exposure that have physical deficits and neurological development associated with alcohol that do not meet the complete criteria for FAS. The pFAS subtype is an alcohol-related neurodevelopmental disorder (ARND) and an alcohol-related birth defect (ARBD). In addition to FAS, pFAS, ARND, and ARBD, any other conditions believed to be associated with prenatal alcohol exposure, such as spontaneous abortion and sudden infant death syndrome (SIDS), are also considered to be on the spectrum of related disorders. It is unclear by 2017 if identifying the FASD-related conditions benefits the individual.
Maps Fetal alcohol spectrum disorder
Signs and symptoms
The FASD lock may vary between individuals exposed to alcohol during pregnancy. While consensus exists for the definition and diagnosis of FAS, small variations between systems lead to different definitions and diagnostic cut-off criteria for other diagnoses across the FASD sequence. Criteria of damage to the central nervous system are especially lacking a clear consensus. Knowledge that works on key features is helpful in understanding the diagnosis and condition of the FASD, and each is looked at with attention to similarities and differences across the four diagnostic systems. More than 400 problems, however, can occur with FASD.
Growth
In the case of FASD, growth deficiency is defined significantly below the mean height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifetime. Measurement of growth should be adjusted for parental height, gestational age (for premature infants), and other postnatal contempt (eg, malnutrition), although height and birth weight are the preferred measure. Disadvantages are documented when height or weight drops at or below the 10th percentile of a standard growth chart corresponding to the population.
The criteria for FASD are at least specific in the IOM diagnostic system ("low birth weight..., weight loss is not due to nutrition..., [or] low weight disproportionate to high" p.4 of the executive summary), while The Canadian CDC and guidelines use the 10th percentile as a cut-off to determine growth deficiencies. The "4-Digit Diagnostic Code" allows for mid-range gradation in growth deficiencies (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile. Growth deficiencies (at the level of severe, moderate, or mild) contribute to the diagnosis of FAS and pFAS, but not ARND or static encephalopathy.
The growth deficiency is ranked as follows by "4-Digit Diagnostic Code":
- Severe: Height and weight at or below the 3rd percentile.
- Medium: Either height or weight in or below the 3rd percentile, but not both.
- Lightweight: Either height or weight or both between the 3rd and 10th percentiles.
- Nothing: Height and weight are both above the 10th percentile.
In a preliminary study that found FAS, growth deficiency was a requirement to be included in the study; thus, all indigenous people with FAS have growth deficiencies as sampling characteristic artifacts used to establish criteria for the syndrome. That is, growth deficiency is a key feature of FASD because growth deficiency is a criterion for inclusion in studies that define FAS. This suggests that growth deficiency may be less important for understanding FASD defects than neurobehavioral sequelae of brain damage.
Facial features
Some abnormalities of craniofacial characteristics are often seen in individuals with FAS. The presence of facial features of FAS shows brain damage, although brain damage may also exist when they are absent. FAS facial features (and most others seen, but not diagnostic, defective) are believed to be caused primarily during the 10 and 20th gestational weeks.
Refinements in diagnostic criteria since 1975 have resulted in three distinct and distinctive facial features known to be due to pranatal alcohol exposure and distinguishing FAS from other interference with partial overlap characteristics. Three facial features of FAS are:
- Fine liquids: Divot or groove between the nose and the upper lip flat with an increased prenatal alcohol display.
- Thin vermilion: Lips over dilated with increased pranatal alcohol exposure.
- Small palpebraic fissure: The widening of the eye decreases with an increase in prenatal alcohol exposure.
FAS face features measurements using criteria developed by the University of Washington. Lips and philtrum were measured by a trained doctor with Lip-Philtrum Guide, a five-point Likert Scale with representative photographs of lips and philtrum ranging from normal (rank 1) to weight (rank 5). The length of the palpebra fissure (PFL) is measured in millimeters with clear calipers or ruler and then compared with the PFL growth chart, also developed by the University of Washington.
The feature ranking of the FAS face is complicated because three separate facial features can be affected independently by prenatal alcohol. Summary of the following criteria:
- Severe: The three facial features have severe independent rankings (4 or 5 lip ratings, philtrum in rank 4 or 5, and PFL of two or more standard deviations below average).
- Medium: Two facial features are rated as weight and one feature rank as moderate (lips or 3rd rank, or PFL between one and two below standard deviations ).
- Lightweight: FAS's lightweight feature set includes a variety of facial features:
- Two facial features were ranked severe and one ranked within normal limits,
- One face feature has a weight rating and two moderate ratings, or
- One feature of a severe rank face, one moderate rank and one rank within normal limits.
- None: All three face features rank within normal limits.
Central nervous system
Central nervous system damage (CNS) is a key feature of FASD diagnosis. Prenatal alcohol exposure, classified as teratogens, can damage the brain throughout the continuum of severe to fine disorders, depending on the amount, timing, and frequency of exposure and fetal and maternal genetic predisposition. While functional abnormalities are the behavioral and cognitive expressions of FASD defects, CNS damage can be assessed in three areas: structural, neurological, and functional disorders.
The four diagnostic systems allow assessment of CNS damage in this area, but the criteria vary. The IOM system requires structural or neurological disorders for FAS diagnosis, but also allows "complex patterns" of functional anomalies to diagnose PFAS and ARND. The "4-Digit Diagnostic Code" and CDC guidelines allow for positive CNS findings in one of three areas for FASD diagnosis, but functional anomalies should measure on two standard deviations or worse in three or more functional domains for FAS diagnosis. , PFAS, and ARND. The "4-Digit Diagnostic Code" also allows for the diagnosis of FASD when only two functional domains are measured on two standard deviations or worse. The "4-Digit Diagnostic Code" further outlines the extent of CNS damage by four ratings:
- Definitely: Structural damage or neurological disorders for FAS or static encephalopathy.
- Possible: Significant dysfunction of two standard deviations or worse in three or more functional domains.
- Possible: Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by the clinical evaluation team's assessment that CNS damage can not be dismissed.
- Not possible: There is no evidence of CNS damage.
Structure
Brain structure abnormalities can be observed, physical damage to the brain or brain structures caused by exposure to prenatal alcohol. Structural damage may include microcephaly (small head size) of two or more below average standard deviations, or other abnormalities in the brain structure (eg, agenesis of the corpus callosum, cerebellar hypoplasia).
Microcephaly is determined by comparing the head circumference (often called occipitofrontal circumference, or OFC) for appropriate OFC growth charts. Other structural damage should be observed through medical imaging techniques by trained physicians. Because imaging procedures are expensive and relatively inaccessible to most people, the diagnosis of FAS is not often done through structural disorders, except for microcephaly.
The evidence of CNS structural damage due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional disorders are highly likely.
During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural defects or deficits in the brain. During the third trimester, damage can occur to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create nervous and functional impairment as well.
In 2002, there were 25 autopsy reports in infants known to have FAS. The first was in 1973, in infants who died soon after birth. This examination reveals extensive brain damage, including microcephaly, anomalous migration, callosal dysgenesis, and large neuroglial, leptomeningeal heterotopia that covers the left hemisphere.
In 1977, Dr. Clarren described the second baby whose mother was a party drinker. The baby died ten days after birth. Autopsies show severe hydrocephalus, abnormal neuronal migration, and small corpus callosum (which connect the two brain hemispheres) and the cerebellum. FAS has also been associated with brain stem and cerebellar changes, corpus callosum agenesis and anterior commissures, neuronal migration errors, no olfactory balls, meningomyelocele, and porencephaly.
Neurological
When structural disorders can not be observed or absent, neurologic disorders are assessed. In the context of FASD, neurological disorders are caused by exposure to prenatal alcohol which causes general neurological damage to the central nervous system (CNS), peripheral nervous system, or autonomic nervous system. The determination of neurological problems should be done by a trained doctor, and should not be caused by postnatal insults, such as high fever, concussion, traumatic brain injury, etc.
The four diagnostic systems demonstrate a virtual agreement on their criteria for CNS damage at the neurological level, and evidence of CNS neurological disorders caused by prenatal alcohol exposure will result in a FAS or pFAS diagnosis, and functional impairment is highly likely.
Neurologic problems are expressed as harsh signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or mild signs. Wider gentle markings, nonspecific neurological disorders, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, awkwardness, poor eye-hand coordination. Many soft signs have criteria referenced by the norm, while others are determined by clinical judgment. "Clinical assessment" is only as good as doctors, and soft signs should be assessed by a pediatric neurologist, a child neuropsychologist, or both.
Functional
When structural or neurological disorders are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairment. Functional disorders are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (not the cause of heredity or postpartum insults) in the observable and measurable domains associated with daily functioning, often referred to as developmental defects. There is no consensus on the specific pattern of functional impairment due to prenatal alcohol exposure and only delaying the development of such CDC label labels, so the criteria (and FASD diagnosis) are somewhat different across the diagnostic system.
Four diagnostic systems listing various CNS domains that can qualify for functional disorders that can determine the diagnosis of FASD:
- Evidence of complex behavior patterns or cognitive abnormalities inconsistent with levels of development within the following CNS domains - Sufficient for diagnosis of pFAS or ARND using IOM guidelines
- Learning difficulties, academic achievement, impulse control, perception social, communication, abstraction, math skills, memory, attention, judgment
- Performance on two or more standard deviations on standardized testing in three or more of the following CNS domains - Sufficient for FAS, pFAS or static encephalopathy diagnosis using 4-Digit Diagnostic Code
- Executive functions, memory, cognition, social/adaptive skills, academic achievement, language, motor skills, attention, activity level
- Common cognitive deficits (eg, IQ) at or below the 3rd percentile on standard testing - Sufficient for FAS diagnosis using CDC guidelines
- Performance at or below the 16th percentile on standardized testing in three or more of the following CNS domains - Sufficient for diagnosis of FAS using CDC guidelines
- Cognition, executive function, motor function, attention and hyperactivity issues, social skills, sensory processing impairments, social communication, memory, difficulty responding to general parenting practices
- Performance on two or more standard deviations on standardized testing in three or more of the following CNS domains - Sufficient for FAS diagnosis using Canadian guidelines
- Cognition, communication, academic achievement, memory, executive function, adaptive behavior, motor skills, social skills, social communication
Related signs
Other conditions may occur simultaneously with FAS, which results from exposure to prenatal alcohol. However, this condition is considered an alcohol-related birth defect and not a diagnostic criterion for FAS.
- Heart: A whisper of the heart that often disappears at the age of one year. The ventricular septal defect is most commonly seen, followed by an atrial septal defect.
- Bone: The joint anomaly includes abnormal position and function, altering palmar fold pattern, small distal phalanx, and fifth finger node.
- Kidney: Horseshoe, aplastic, dysplastic, or hipoplastic kidney.
- Eyes: Strabismus, optic nerve hypoplasia (which can cause light sensitivity, decreased visual acuity, or unconscious eye movements).
- Occasionally problems: eyelid ptosis, microophthalmia, cleft lip with or without cleft palate, webbed neck, short neck, tetralogy Fallot, coarctation of aorta, spina bifida, and hydrocephalus.
Cause
Fetal alcohol syndrome usually occurs when a pregnant woman has more than four standard drinks per day. Lighter symptoms have been found with two drinks per day during the early part of pregnancy. Among those who are alcoholic about one-third of children have FAS.
The evidence of harm from less than two drinks per day or 10 drinks per week is unclear. Although small amounts of alcohol do not cause abnormal appearance, this can lead to behavioral problems. There is conflicting evidence as to whether drinking by the father before conception can lead to FAS.
Mechanism
Despite intensive research efforts, it has not been possible to identify a clear mechanism for the development of FAS or FASD. In contrast, clinical and animal studies have identified a broad spectrum of pathways in which maternal alcohol can have a negative impact on pregnancy outcomes. Clear conclusions with universal validity are difficult to draw, since different ethnic groups exhibit considerable genetic polymorphisms for liver enzymes responsible for the detoxification of ethanol.
Genetic testing has demonstrated a long-term continuum of molecular effects that are not only time-specific but also dose-specific; even with moderate amounts capable of causing change.
A human fetus appears to be at risk three times the consumption of maternal alcohol:
- Placenta allows the entry of free ethanol and toxic metabolites such as acetaldehyde into the fetal compartment. Placental barrier is called no barrier with respect to ethanol.
- The developing fetal nervous system appears highly sensitive to ethanol toxicity. The latter negatively affects proliferation, differentiation, neuronal migration, axonic growth, integration and synaptic tissue adjustment. In short, all the major processes in the developing central nervous system appear to be disrupted.
- The fetal network is very different from the adult network in function and purpose. For example, the main detoxifying organ in adults is the liver, whereas the fetal liver is unable to detoxify ethanol, since ADH and ALDH enzymes have not been expressed at this early stage. Until long term, fetal tissue does not have significant capacity to detoxify ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for a much longer period of time than ethanol decay in the mother's circulation. Generally, fetal tissue has much less antioxidant protection than adult tissue, as they do not show significant amounts of ADH and ALDH, and much fewer amounts of antioxidant enzymes, such as SOD, glutathione transferases, and glutathione peroxidases.
Diagnosis
Because the inclusion of alcohol use during pregnancy can stigmatize mothers who give birth, many are reluctant to admit drinking or provide accurate reports of the quantity they drink. This complicates the diagnosis and treatment of the syndrome. Consequently, the diagnosis of FASD severity depends on the protocol of physiological observation and child behavior rather than self-reporting. Currently, four FASD diagnostic systems that diagnose FAS and other FASD conditions have been developed in North America:
- The Institute of Medicine Guidelines for FAS, the first system to standardize the diagnosis of individuals with prenatal alcohol exposure;
- The University of Washington "The 4-Digit Diagnostic Code," which composes four main features of FASD on a Likert scale of one to four and produces 256 descriptive codes that can be categorized into 22 different clinical categories, ranging from FAS to no findings ;
- Control Center for Fetal Alcohol Syndrome: Guidelines for Reference and Diagnosis, "which establishes a consensus on FAS diagnosis in the US, but suspends other FASD conditions, and
- The Canadian Guidelines for FASD diagnosis, which sets the criteria for diagnosing FASD in Canada and aligning most of the differences between the IOM system and the University of Washington.
Each diagnostic system requires that a complete FASD evaluation includes an assessment of the four key features of the FASD, described below. Positive findings on all four features are necessary for FAS diagnosis. However, prenatal alcohol exposure and central nervous system damage are important elements of the FASD spectrum, and positive findings in these two features are sufficient for a FASD diagnosis that is not "full-blown FAS".
While four diagnostic systems basically agree on the criteria for fetal alcohol syndrome (FAS), there are still differences when the complete criteria for FAS are not met. This has resulted in a different nomenclature and evolved for other conditions across the FASD spectrum, which can account for a variety of terminologies. Most individuals with deficits resulting from prenatal alcohol exposure do not express all features of FAS and fall into other FASD conditions. Canadian Guidelines recommend a descriptive assessment and "4-Digit Diagnostic Code" for each of the major FASD features and IOM terminology in the diagnostic category, excluding ARBD.
Thus, other FASD conditions are partial FAS expression. However, other FASD conditions may create defects similar to FAS if the key area of ​​central nervous system damage shows clinical deficits in two or more than ten domains of brain function. Basically, although FAS facial growth and/or facial deficiencies may be mild or absent under other FASD conditions, clinically significant brain damage from the central nervous system is present. Under other FASD conditions, an individual may have a greater risk for adverse outcomes because brain damage is present without poor visual growth-related cues or "FAS face" which can usually lead to FASD evaluation. Such individuals may be misdiagnosed with a primary mental health disorder such as ADHD or an oppositional disagreement disorder without appreciation that brain damage is the underlying cause of this disorder, which requires a different treatment paradigm of a typical mental health disorder. While other FASD conditions may not have been included as a diagnosis of ICD or DSM-IV-TR, they still cause significant disruption in functional behavior due to underlying brain damage.
Fetal alcohol syndrome
The following criteria must be fully met for FAS diagnosis:
- Growth deficiency: The height or weight of prenatal or postnatal (or both) at or below the 10th percentile
- FAS facial features: The three features of FAS face display
- Central nervous system damage: Clinically significant neurological structural, or functional impairment
- Prenatal alcohol exposure: Confirmed or unknown prenatal alcohol exposure
Fetal alcohol syndrome (FAS) is the first diagnosed FASD diagnosis. FAS is the only FASD expression that has garnered consensus among experts to be the official diagnosis of ICD-9 and ICD-10. To make this diagnosis or determine the FASD condition, a multi-disciplinary evaluation is required to assess each of the four key features for assessment. Generally, trained doctors will determine the growth deficiency and facial features of FAS. While qualified physicians may also assess structural abnormalities of the central nervous system and/or neurological problems, usually central nervous system damage is determined through psychological assessment, speech, and occupational therapy to ensure clinically significant disorders in three or more of the Ten Domain Brains. The risk of prenatal alcohol exposure may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. These professionals work together as a team to assess and interpret data from each major feature for assessment and develop an integrative, multidisciplinary report to diagnose FAS (or other FASD conditions) within an individual.
Partial FAS
Partial FAS (pFAS), formerly known as atypical FAS in the 1997 edition of "4-Digit Diagnostic Code". People with pFAS have a history of confirmation of prenatal alcohol exposure, but may lack a complete growth deficiency or facial stigmata. Central nervous system damage is present at the same level as FAS. These people have the same functional disability but "look" less like FAS.
The following criteria must be fully met for the diagnosis of Partial FAS:
- Growth deficiency: Growth or height can range from normal to deficient
- FAS facial features: Two or three FAS facial features present
- Significant central nervous system damage: Clinical, neurological, or clinically significant dysfunction in three or more of the Top Ten Brain Domains
- Prenatal alcohol exposure: Confirmed prenatal alcohol exposure
Fetal alcohol effect
The fetal alcohol effect (FAE) is an earlier term for alcohol-related neurodevelopmental disorders and alcohol-related birth defects. It was originally used in research to describe humans and animals in which the teratogenic effects were seen after prenatal alcoholic exposure was confirmed (or exposure not known to humans), but without clear physical anomalies. Smith (1981) described the FAE as "a very important concept" to highlight the effects of debilitating brain damage, regardless of growth or facial features. This term is disliked by doctors because it is often regarded by the public as a less severe handicap than FAS, when in fact its effects can be just as detrimental.
Alcohol-related developmental disorders (ARND) were initially suggested by the Institute of Medicine to replace the FAE term and focus on central nervous system damage, rather than growth deficiency or facial features of FAS. The Canadian Guide also uses this diagnosis and the same criteria. While the "4-Digit Diagnostic Code" includes these criteria for its three diagnostic categories, it refers to this condition as static encephalopathy. The effects of ARND behavior are not always unique to alcohol, so the use of the term should be within the context of prenatal alcohol exposure confirmed. ARND may gain acceptance of the terms FAE and ARBD to describe FASD conditions with central nervous system abnormalities or behavioral or cognitive abnormalities or both due to prenatal alcohol exposure regardless of growth deficiency or FAS facial features.
The following criteria must be fully met for the diagnosis of ARND or static encephalopathy:
- Growth deficiency: Growth or height can range from the normal to the most imperfect
- FAS facial features: Minimum or no FAS facial features are present
- Significant central nervous system damage: Clinical, neurological, or clinically significant dysfunction in three or more of the Top Ten Brain Domains
- Prenatal alcohol exposure: Confirmed prenatal alcohol exposure; 0
Alcohol-related birth defects (ARBD), formerly known as the fetal alcohol effect (PFAE), is a proposed term as an alternative to FAE and PFAE IOM presents ARBD as a list of congenital anomalies associated with maternal alcohol use but has no major FASD features. PFAE and ARBD are not preferred because these anomalies are not necessarily specific for maternal alcohol consumption and not the criteria for FASD diagnosis. The Canadian Guidelines recommend that ARBD should not be used as an umbrella term or diagnostic category for FASD.
Exposure
Prenatal alcohol exposure is determined by interviewing biological mothers or other family members who know the use of maternal alcohol during pregnancy (where available), prenatal health records (where available), and review of available birth records, court records (if any), chemical dependence treatment records (if any), or other reliable sources.
Exposure levels are rated as confirmed exposure , unknown exposure , and confirming the absence of exposure by IOM, CDC and Canadian diagnostic systems. The "4-Digit Diagnostic Code" further distinguishes the confirmed exposure as High Risk and Some Risk :
- High Risk: Alcohol use confirmed during pregnancy is known to be at high blood alcohol levels (100 mg/dL or greater) given at least weekly in early pregnancy.
- Some Risks: Alcohol use confirmed during pregnancy using less of the High Risk or unknown pattern of use.
- Unknown Risk: Unknown alcohol use during pregnancy.
- No Risk: No confirmed prenatal alcohol exposure.
Confirmed exposure
The amount, frequency, and timing of prenatal alcohol use can dramatically affect the three other major FASD features. Although consensus states that alcohol is teratogenic, there is no clear consensus about what levels of exposure are toxic. The CDC guides are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, recognizing the importance of significant alcohol exposure from regular or severe episodic alcohol intake in determining, but not offering a standard for diagnosis. The Canadian Guidelines address this vagueness and familially indicate that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode at five days or more over a 30 day period.
The "4-Digit Diagnostic Code" rating system distinguishes between prenatal alcohol exposure levels as high risk and some risks. It operates a high risk exposure as blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least every week in early pregnancy. This BAC level is usually achieved by a 55 kg woman drinking six to eight beers in one sitting.
Unknown view
For many adopted or adults and children in care, records or other reliable sources may not be available for review. Reporting on the use of alcohol during pregnancy may also stigmatize mothers who give birth, especially if alcohol use is ongoing. In this case, all diagnostic systems use an unknown prenatal appointment of alcoholic exposure. The FAS diagnosis is still possible with unknown levels of exposure if other key features of the FASD are present at the clinical level.
Missing exposure confirmed
The absence of confirmed exposure will apply to planned pregnancy where no alcohol is used or pregnancy women who do not use alcohol or report it is pointless during pregnancy. This appointment is relatively rare, as most people who do FASD evaluations are at least suspected have had prenatal alcohol exposure due to other key features of the FASD.
Ten brain domains
Recent attempts to standardize the functional CNS damage assessment have been suggested by an experienced FASD diagnostic team in Minnesota. The proposed framework tries to align the IOM, 4-Digit Diagnostic Code, CDC, and Canadian guidelines to measure CNS damage vis-Ã -vis evaluation and FASD diagnosis. The standard approach is called the Ten Brain Domains and includes aspects of all four diagnostic system recommendations for assessing CNS damage due to prenatal alcohol exposure. This framework provides a clear definition of brain dysfunction, determines the empirical data required for accurate diagnosis, and defines consideration of interventions that address the complex nature of FASD with a view to avoiding common secondary defects.
Ten proposed Brain Domains include:
- Achievement, adaptive behavior, attention, cognition, executive function, language, memory, motor skills, multisensor integration or gentle neurological issues, social communication
The Fetal Alcohol Diagnostic Program (FADP) uses the unpublished Minnesota performance criteria at 1.5 or more standard deviations on standardized testing in three or more of the Ten Brain Domains to determine CNS damage. However, the Ten Brain Domains are easily incorporated into any of the four criteria of CNS diagnostic system damage, since the framework only proposes domains, rather than the cut-off criteria for FASD.
Differential diagnosis
CDC reviews nine syndromes that feature overlap with FAS; However, none of these syndromes encompasses all three facial features of FAS, and none is the result of prenatal alcohol exposure:
- Aarskog Syndrome
- Williams Syndrome
- Noonan Syndrome
- Dubowitz syndrome
- Brachman-DeLange syndrome
- Toluene syndrome
- fetal hidantoin syndrome
- Fetal valproat syndrome
- Maternal PKU fetal effects
Prevention
The only particular way to prevent FAS is to avoid drinking alcohol during pregnancy. In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use during pregnancy or when planning a pregnancy, the last to avoid damage even at an early stage (even weeks) of pregnancy, such as the woman may not be aware that she has been pregnant. In the United States, federal law requires that warning labels be placed on all alcoholic beverages since 1988 under the Alcoholic Beverage Labeling Act.
There is some controversy surrounding the "zero tolerance" approach taken by many countries when it comes to alcohol consumption during pregnancy. The statement that moderate drinking causes FAS is said to be lacking strong evidence and, in fact, the practice of equalizing responsible levels of drinking with potential harm to the fetus may have negative social, legal, and health impacts. In addition, special attention should be taken when considering statistics on this disease, since prevalence and causes are often associated with FASD, which is more common and causes less harm, compared to FAS.
Treatment
There is no cure for FASD, but treatment is possible. Because CNS damage, symptoms, secondary defects, and needs vary individually, no one type of treatment works for everyone.
Medication
Psychoactive drugs are often tried on those with FASD because many of the symptoms of FASD are erroneous or overlap with other disorders, especially ADHD.
Behavioral intervention
Behavioral interventions are based on learning theory, which is the basis for many strategies and nurturing and professional interventions. Along with the usual parenting style, such strategies are often used by default to treat them with FAS, such as the diagnosis of oppositional opposition disorder (ODD), behavioral disorders, reactive attachment disorder (RAD) often overlap with FAS (along with ADHD), and this is sometimes considered to be beneficial from behavioral interventions. Often, a poor academic achievement of a person produces specialized educational services, which also use principles of learning theory, behavior modification, and results-based education.
Developmental template
Many books and flyers in the FAS recommend a developmental approach, based on developmental psychology, although most do not set it and provide a little theoretical background. Optimal human development generally occurs at identifiable stages (eg, Jean Piaget's cognitive developmental theory, Erikson's stage of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development, which can lead to delayed, skipped, or immature phases. Over time, an unaffected child can negotiate the rising demands of life by progressing through normal developmental stages, but not so for a child with FAS.
By knowing what stages of development and tasks that children follow, care and interventions for the FAS can be tailored to help one fulfill development tasks and demands succeed. If a person is delayed in the adaptive behavior domain, for example, interventions will be recommended to target certain delays through additional education and training (for example, instructions practiced on shoelaces), provide reminders, or make accommodation (for example, using slip- on shoes) to support the desired level of functionality. This approach is an improvement over behavioral intervention, as it takes the context of person's development into account when developing interventions.
Advocacy model
The advocacy model takes the point of view that one is required to actively mediate between the environment and the person with the FAS. Advocacy activities are conducted by an advocate (eg, a family member, friend, or case manager) and fall into three basic categories. An advocate for the FAS: (1) interpret the FAS and the defects that arise from it and explain it to the environment in which the person operates; (2) incur change or accommodation on behalf of that person; and (3) assist the person in developing and achieving the target achieved.
Advocacy models are often recommended, for example, when developing Individual Education Program (IEP) for the progress of people at school.
Understanding the development framework is likely to inform and improve the advocacy model, but advocacy also implies interventions at the system level as well, such as educating schools, social workers, and so on best practices for FAS. However, some organizations devoted to the FAS also use advocacy models at the community practice level as well.
Health and public policy
Treating FAS at public health and public policy levels encourages the prevention and diversion of public resources to assist those with FAS. This is related to the advocacy model but promoted at the system level (not with individuals or families), such as developing education and community support, state or provincial prevention efforts (eg, screening for maternal alcohol use during OB/GYN or prenatal health care visits ), or a national awareness program. Several US organizations and agencies are dedicated to this type of intervention.
The US Centers for Disease Control estimates that 3 million women in the United States are at risk of having babies with FASD, and recommend that women of childbearing age should be in birth control or not drinking alcohol as the safest way to avoid this.
Prognosis
Main flaw
FAS primary defects are functional difficulties in which a child is born as a result of CNS damage due to prenatal alcohol exposure. Often, primary defects are mistaken as behavioral problems, but the underlying damage to CNS is a source derived from functional difficulties, rather than mental health conditions, which are considered secondary defects.
The exact mechanisms for functional problems of primary defects are not always fully understood, but animal studies have begun to explain some of the correlations between functional problems and brain structures impaired by prenatal alcohol exposure. Representative examples include:
- Learning attenuation is associated with dendritic disorders of the hippocampus
- Impaired motor development and function associated with reduced small brain size
- Hyperactivity is associated with a decrease in the size of the corpus callosum
Functional difficulties can result from CNS damage in more than one domain, but general functional difficulties by the domain include: Note that this is not a complete list of difficulties.
- Achievements: Learning difficulties
- Adaptive behavior: Poor impulse control, poor personal constraints, poor anger management, stubbornness, disruptive behavior, too friendly with strangers, poor daily living skills, developmental delays
- Caution: Attention-Deficit/Hyperactivity Disorder (ADHD), poor attention or concentration, may be disrupted
- Cognition: intellectual disability, confusion under stress, poor abstract ability, difficulty distinguishing between fantasy and reality, slower cognitive processing
- Executive function: Poor judgment, impaired information processing, poor understanding of patterns, causes and reasons of poor effects, inconsistent in correlating words with actions, poor generalization skills
- Language: Expressive or receptive language disorder, grasp part but not whole concept, lack understanding of metaphors, idioms, or sarcasm
- Memory: Poor short-term memory, inconsistent memory, and knowledge base
- Motor skills: Poor handwriting, poor fine motor skills, poor rough motor skills, delayed motor skills development (eg, riding a bike at the right age)
- Sensory processing and soft neurological problems: sensory processing impairment, sensory defensive, insensitivity to stimulation
- Social communication: Encouraging conversation, inability to read nonverbal or social cues, "fussy" but without substance
Secondary flaw
Secondary FAS defects are those that appear later in the aftermath of CNS damage. This disability often arises over time due to incompatibility between primary defects and environmental expectations; secondary disability can be corrected with early intervention and appropriate support services.
Six primary secondary disabilities were identified in a University of Washington research study of 473 subjects diagnosed with FAS, PFAS (partial fetal alcohol syndrome), and ARND (alcohol-related neurodevelopmental disorder):
- Mental health problems: Diagnosed with ADHD, Clinical Depression, or other mental illness, experienced by more than 90% of subjects
- Disturbed school experience: Suspended or excluded from school or dropping out, experienced by 60% of subjects (age 12 and over)
- Difficulties with the law: Charged or punished with crime, experienced by 60% of subjects (age 12 and over)
- Confinement: For inpatient psychiatric care, chemical dependency treatment in hospitalization, or jail for crime, experienced about 50% of subjects (age 12 and older)
- Inappropriate sexual behavior: Sexual progression, sexual touch, or promiscuity, experienced by approximately 50% of subjects (age 12 and over)
- Alcohol and drug problems: Harassment or dependence, experienced by 35% of subjects (age 12 and over)
Two additional secondary defects exist for adults: Dependent life: Home group, living with family or friends, or some sort of living assisted, is experienced by 80% of the subject (ages 21 and older)
Protective factors and strengths
Eight factors were identified in the same study as a universal protective factor that reduced the rate of occurrence of secondary defects:
- Stay in a stable home and care for more than 73% of life
- Diagnosed with FAS before the age of six
- Never experience violence
- Remains in any life situation for at least 2.8 years
- Experience "quality homes" (meet 10 or more specified qualities) from ages 8 to 12
- Was found eligible for disabled development service (DD)
- Have basic needs for at least 13% of life
- Have a FAS diagnosis (rather than other FASD conditions)
Malbin (2002) has identified the following areas of interest and talent as a force that often stands out for those who have FASD and should be utilized, like any power, in care planning:
- Music, playing instruments, composing, singing, art, spelling, reading, computer, mechanics, carpentry, skilled calls (welding, electricians, etc.), writing, poetry
- Participation in non-impact sports or physical fitness activities Epidemiology
- Smoking and pregnancy
- Fetal alcohol spectrum disorders in Curlie (based on DMOZ)
- Center for Disease Control page on Fetal Alcohol Spectrum Disorders (FASDs)
FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. FAS is believed to occur between 0.2 and 9 per 1,000 live births in the United States. The cost of an individual's lifetime with FAS is estimated at two million USD in 2002.
Australia
FASD among Australian youth is more common among indigenous Australians. The only countries that have recorded birth defects in Australian youth are Western Australia, New South Wales, Victoria and South Australia. In Australia, only 12% of Australian health experts are aware of FASD diagnostics and symptoms. In Western Australia, the birth rate that generates FASD is 0.02 per 1000 births for non-Indigenous Australians, but among native births, this figure is 2.76 per 1000 births. In Victoria, no FASD-related births were registered for indigenous Australians, but the rate for the general population in Victoria was 0.01-0.03 per 1000 births. There are no special FASD clinics in Western Australia, but there are also no nationally supported diagnostic criteria anywhere in Australia. Passive surveillance is a prevention technique used in Australia to help monitor and define the defects that are detected during pregnancy and childhood.
History
From the 1960s to the 1980s, alcohol was generally used as tocolytic, a method of stopping premature labor. This method is from Dr. Fritz Fuchs, head of the department of obstetrics and gynecology at Cornell University Medical College. Doctors recommend a small amount of alcohol to calm the uterus during contractions early in pregnancy or Braxton Hicks contractions. In the late stages of pregnancy, alcohol is given intravenously and often in large quantities. "Women experience the same effects as those on oral ingestion, including poisoning, nausea and vomiting, and potential alcohol poisoning, followed by hangovers when alcohol is stopped." Vomiting puts the mother at high risk for aspiration and "brutal procedures for all involved." Because alcohol is given intravenously, doctors can continue to provide care to the mother long after she passes out, so she becomes more drunk than she should be. Such severe poisoning is likely to contribute to FASD.
Historical reference
Anecdotal notes about the prohibition of maternal alcohol use from ancient Bible, ancient Greek and Roman sources imply a historical awareness of the relationship between maternal alcohol use and negative child outcomes. For example, in the Bible, Judges 13: 4 (addressed to a woman who will have a baby) read: "Therefore be careful not to drink wine or liquor, and eat unclean ones" (ESV). In 1725 British physicians petitioned the House of Commons about the effects of liquor when consumed by pregnant women who said that drinking like that was "... too often the cause of weak, weak, and depressed children, which should, not profits and strength, cost to their country. "There are many other historical references. In Gaelic Scotland, mothers and nurses are not allowed to consume ale during pregnancy and breast-feeding (Martin Martin). The claim that alcohol consumption caused ignorance was part of Teetotalism's message in the nineteenth century, but the claim, despite some attempts to offer evidence, was ignored because no mechanism could be proposed.
The earliest recorded observation of the possible link between maternal alcohol use and fetal damage was done in 1899. William Sullivan, a Liverpool prison doctor who recorded a higher birthrate for 120 female alcohol inmates than their drunken relatives; he suggests a causal agent to use alcohol. This is contrary to the dominating beliefs at the time that heredity causes intellectual disability, poverty, and criminal behavior, which contemporary studies on the subject are usually inferred. A case study by Henry H. Goddard of the Kallikak family - popular in the early 1900s - represented this early perspective, although researchers later suggested that Kallikaks almost certainly had FAS. General studies and discussions about alcoholism throughout the mid-1900s are usually based on hereditary arguments.
Before fetal alcohol syndrome was specifically identified and named in 1973, only a few studies noted differences between children of mothers who used alcohol during pregnancy or breast-feeding and those who did not, and identified the use of alcohol as a factor that might contribute to offspring.
Recognition as syndrome
Fetal Alcohol Syndrome was named in 1973 by two dysmorphologists, Drs. Kenneth Lyons Jones and David Weyhe Smith from the University of Washington Medical School in Seattle, USA. They identified patterns of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficits and developmental delays" in eight unrelated children from three ethnic groups, all born to mothers who were alcoholics. The pattern of malformations indicates that the damage is prenatal. The news of the discovery surprised some, while others were skeptical of the find.
Dr. Paul Lemoine from Nantes, France has published a study in the French medical journal in 1968 about children with a characteristic whose mother is an alcoholic, and in the US, Christy Ulleland and colleagues at the University of Washington Medical School have conducted 18 studies months in 1968-1969 documented the risk of maternal alcohol consumption among the offspring of 11 mothers of alcohol. The findings of Washington and Nantes were confirmed by a research group in Gothenburg, Sweden in 1979. Researchers in France, Sweden, and the United States were struck by how similar these children are, even if they are unrelated, and how they behave in a similarly unfocused and Hyperactive.
In nine years of Washington's discovery, research on animals, including non-human monkey studies conducted at the University of Washington Primate Center by Dr. Sterling Clarren, has asserted that alcohol is a teratogen. In 1978, 245 cases of FAS have been reported by medical researchers, and the syndrome began to be described as the most common cause of intellectual disability.
While many syndromes are eponymous, it is named after the first physician to report symptom associations, Dr. Smith was named FAS after the causative agent of symptoms. He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption causes syndrome, then abstinence during pregnancy would follow from patient education and public awareness. At that time, no one was aware of the various possible birth defects of the FAS or its prevalence rate. Over time, as subsequent research and clinical experience suggested that various effects (including physical, behavioral, and cognitive) may arise from prenatal alcohol exposure, the term Fetal Alcohol Spectrum Disorder (FASD) was developed to include FAS as well as other conditions. resulting from exposure to prenatal alcohol. Currently, FAS is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Health Problems Associated and assigned ICD-9 and diagnosis.
See also
References
External links
Source of the article : Wikipedia
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