Medical-Legal Neurologic

Aspects of Problems

Gerald S. Golden, M.D.

Introduction Medical-legal issues have intruded into medical practice in a number of ways. The most obvious is that of the “malpractice crisis” that is never far from the thoughts of every physician. The ramifications of this concern are manifold, ranging from subtle or obvious changes in the nature of the physicianpatient relationship to modifications of practice itself. The practice of defensive medicine is a reality that cannot be escaped. An increasing number of physicians also find themselves involved in a second medical-legal area, that of being asked to testify as a witness in a lawsuit. This may require being an unwilling participant as a plaintiff or a neutral actor as a fact witness. The court appearance may also represent the physician’s willingness to serve as an expert witness. A necessary part of any medical-legal action is an injury to the patient. If this injury is permanent and impairs the person’s function in a significant fashion, the plaintiff’s ability to win a large settlement is enhanced. Injuries to the nervous system share these two important characteristics, making neurologic problems a frequent and important part of many medical liability suits. It is this portion of the broad spectrum of medical-legal problems that is the subject of this review.

Gerald S. Golden, M.D., is Director, Boling Center for Developmental Disabilities, and Shainberg Professor of Pediatrics and Professor of Neurology, The University of Tennessee, Memphis, College of Medicine, Memphis.

Medical-Legal Issues and the Pediatrician Pediatricians are not immune from medical liability suits. A survey of pediatricians in 1990 showed that 29% reported having had claims filed against them, and the average pediatrician has been sued 1.6 times.l There was an out-of-court settlement in 31.2% of the cases, the claim was dropped by the plaintiff in 29.8% of the cases, and the pediatrician won in court in 9.8% of the suits. The remainder were still in progress. No case in the recent survey period was lost in court, but this probably reflects the relative frequency of out-of-court settlements. The settlement was less than $115,000 in 71% of the cases that were settled, and was above $950,000 in 3.5% of them. Common Causes of Claims The legal basis behind many medical-legal claims is the failure of the practitioner to meet the standard of care. This is a legal concept which implies that there is a well-recognized and widely accepted standard that must be met in all situations involving medical diagnosis and treatment. Although this was originally a standard applied on a local or regional basis, the rapid dissemination of medical information has made a more general standard applicable to most situations . The concept of standard of care, as used in the courts, is a troublesome one for the physician. This test does not allow for differences in clinical judgment and experience, and is obviously much more easily applied in retrospect. Events and decisions always are more obvious the next day. Ultimately, the

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decision as to whether or not there was a breach in the standard of care is decided by a jury after weighing the opinions of expert witnesses who usually have diametricany opposing views. Determination that the standard of care was not met is not sufficient, however, for the plaintiff to prevail. It must be shown also that the medical negligence was causally related to the injury in question Both components are required for a judgment in favor of the plaintiff. Diagnostic errors are one of the most common specific claims made in medical-legal actions. Delay in the diagnosis of meningitis and meningococcal infections is the single most common cause of a malpractice suit in pediatric practice.’ It is obvious that delays in diagnosis, or an incorrect diagnosis, can be the first step in a cascade of errors. Pitfalls in treatment are many. Delay in the initiation of correct treatment, or institution of inappropriate treatment, can severely compromise the outcome of the condition. Closely related is the failure to recognize adverse effects of treatment, take remedial action, and substitute an alternative therapy. Another area often incorporated into lawsuits is failure of informed consent. This can be avoided most easily by complete discussion with the family of the working diagnosis and the level of certainty of this diagnosis, treatment options, the reasons for recommending a particular treatment, potential side effects and adverse reactions to treatment, and expectations for outcome. A good result should never be promised. An attempt should be made to be certain that the family understands the issues and options, and this should be noted in the medical record. The pediatrician, unless acting as an expert witness, is not usually involved in issues of product liablity. These claims are made against the manufacturers of vaccines, other biologic products, and drugs. There are, however, two issues concerning drugs and related products that are of importance to the physician. The first is the status of the package insert, either supplied with the drug or published in the Physician’s Desk Reference. Although this document can be introduced into court, its validity is not absolute and an expert witness can disagree with any portion of the recommendations if support for this disagreement can be demonstrated. The second issue of special concern to pediatricians is the statement in the package insert that the drug has not been approved for use in children younger than a certain age. The usual meaning of this statement is that studies to obtain approval in the specific age group in question have not been carried out. These statements do not represent an absolute prohibition

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to the use of the drug, as long as reasons for its use can be supported.3 Issues Specific to Pediatrics The legal status of children raises several issues that complicate their treatment and the consequences of errors in treatment and diagnosis or adverse outcomes for any reason. The most obvious is that surrogates, usually the parents, must make decisions for the child and give consent for treatment. The family’s opinions may appear inappropriate or illadvised to the physician, and not in the best interests of the child. Although competent adults generally have the legal right to make medical decisions adverse to their well-being, the courts may have to intervene if the health and welfare of children are at risk. This can put the physician and the family in an adversarial position, increasing the risk of legal action if there is a poor outcome. A second problem unique to the practice of pediatrics is that in most states the statute of limitations does not begin to run until children reach a specific age, usually their legal majority. The physician’s liability continues for a prolonged period after the acts in question, and it may be difficult to marshal1 a strong defense if records are no longer available, witnesses cannot be found, and time has dulled or distorted the memories of all involved. In addition, the child may institute a suit on his or her own behalf after achieving legal majority. Finally, the assumption is generally made that children will have a long life span following many injuries, even those that are quite severe. Life span is a significant factor in determining the size of an award if the plaintiff should prevail.

General Medical-Legal Aspects of Neurologic Problems Medical-legal claims involving children are based most commonly on an adverse neurologic outcome; the two most common specific issues relate to the diagnosis and treatment of meningitis and claims of injury suffered in the perinatal period. Large settlements are sought in these cases for a number of interrelated reasons. First, as noted, is the assumption that most children will have a long life span and the special needs will continue for many years. Evidence that this assumption is not correct has been obtained recently. A follow-up study of children with cerebral palsy demonstrated that those who also had severe or profound mental retardation had a survival rate of 68% at age 5 years and 54% at 10 years.4 The most significant factors that predict life span are the severity of the deficit in cognitive function, limitation of

mobility, incontinence, and inability to eat without assistance.5 In the group of patients with severe or profound mental retardation who were immobile, incontinent, and required feeding by a tube, only 58.6% were alive at the age of 1 year; 21% at 5 years; 7.2% at 10 years; and 2.5% at 15 years old. Of the individuals with mental retardation who were immobile and incontinent but could be fed by others, 17% were alive at 15 years. In the group of patients who were incontinent but ambulatory and could be fed by others, 56.7% survived until the age of 15 years. Analyzing the data from another perspective showed that in the group requiring feeding by a tube, additional average life expectancy was 4 to 5 years while individuals who could be fed by others had an average additional life expectancy of 8 years. Patients who were mobile but not ambulatory had a life expectancy of approximately 23 additional years. Life expectancy data raise an additional issue related to the site at which services are provided to the individual with a severe handicap. The claim is made frequently that there is excess mortality in institutional settings, and that the individual’s life would be prolonged with skilled nursing and attendant care at home or in a community-based facility. It is clear that institutional mortality rates are higher among residents of state facilities admitted in 1980 than those admitted in 1970.6 This appears to be related to the trend toward admission of individuals with physical disabilities and who require special care, as less severely handicapped individuals have been moved into community placement. The institutions now have an increasing percentage of patients with the type and severity of handicaps that would be associated with a high mortality rate in any setting. A second factor related to the size of the claim for damages is that the needs of a child with significant neurologic damage are numerous, specialized, and expensive. In addition to medical expenses, the patient may never achieve full independent function and will have a lifelong requirement for personal assistance with self-care. It may be necessary to provide supervised living arrangements and adaptive equipment (e.g., motorized wheelchairs, augmentative communications equipment). These expenses, when projected over a period of 40 or 50 years and indexed for inflation, can grow to astronomic levels. A contentious issue relates to the need for special education. The plaintiff often presents the claim that educational needs can only be met in a private school or private residential facility. In fact, Public Law 94-142, the Education for All Handicapped Children Act (EHA), mandates that every child of school age is entitled to an appropriate, free, public

education in the least restrictive environment.7 This special education is defined in the regulations written for the implementation of the EHA as “specially designed instruction, at no cost to the parent, to meet the unique needs of a handicapped child”. The school must evaluate the child’s needs and develop an Individual Educational Plan (IEP) which is acceptable to the parents. The IEP also must provide for educationally relevant related services including early identification and assessment of disabilities, medical services for diagnostic or evaluation purposes, physical and occupational therapy services, speech pathology and audiology, psychological services, counseling services, recreation, school health services, school social services, and parent counseling and training. ’ If there is disagreement between the family and the school on the adequacy of services, an appeal process is available. If the conflict still cannot be resolved, the parents can obtain legal counsel and take the matter to court. Guidance and legal assistance are generally available through the state protection and advocacy agency. If the child’s demonstrated needs cannot be met by the school, the school system becomes responsible for purchasing the required services at no cost to the family. For these reasons, it should be unnecessary to include the cost of the educational and related services in a judgment. A recent ruling by the Office of Special Education and Rehabilitative Services of the U.S. Department of Education has clarified the right of the family to obtain assistive technology under Part B of the EHA.9 Assistive technology devices are those that enhance the child’s learning, mobility, communication, and/or interaction with nondisabled peers, and include such things as motorized wheelchairs, computer-based communication devices, and mechanical ventilators. The right of the child to obtain these, without cost to the family, derives from the interpretation of the regulations written for the implementation of the EHA that the list of related services “is not exhaustive and may include other developmental, corrective, or other supported services . . . if they are required to assist a handicapped child to benefit from special education.“9 The mechanism by which the child becomes eligible is the same as for other services provided through the EHA; that is, the need for the devices must be determined as part of the development of the IEP. Public Law 99-457, the Early Childhood Education Act, is now in its implementation phase in the individual states. lo Within a few years all children with neurologic handicaps, from birth through the age of 21 or 22 years, will be eligible to obtain educational and related services within their local school

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system or in agencies under contract to the school systems. There will be no need for the family to obtain the funds to purchase services for the child on their own. Another major factor leading to large awards if a child suffers serious neurologic impairment is loss of earnings. An attempt is made to predict the type of work that the child, if neurologically normal, might have been able to engage in, and to extrapolate what this lost income would be. Additional amounts are often claimed for subjective factors such as pain and suffering, loss of enjoyment of life, and loss of companionship. Some states are examining the issue of tort reform and other legislative modifications related to medical 1iablity.i’ There is also movement toward limitation of the total amount awarded for claims of pain and suffering and loss of companionship, which may be important but are difficult to quantify.

Background

Issues

Static Brain Dysfunction Although the nervous system is complex and is capable of a wide range of activities and responses, the general types of dysfunction secondary to developmental abnormalities or damage early in life can be categorized into a relative few major types. Those most frequently encountered are motor disabilities, cognitive and behavioral abnormalities, impairment of special senses, and seizure disorders. These divisions are somewhat arbitrary, as any patient may have one or more disabilities; this is more common than a single one occurring in isolation. It is also important to realize that the specific abnormality, or pattern of abnormalities, rarely correlates with a single etiologic factor. Some statistical associations can be made, such as that of spastic diplegia most frequently resulting from periventricular leukomalacia in children of low birth weight, but diagnostic constellations of symptoms are a rarity. As these diagnoses are the most frequent ones referred to in claims of medical negligence, it is important that they be defined and some of the diagnostic pitfalls outlined. Cerebral palsy refers to a condition in which there is a motor disability due to a static abnormality of the brain, first becoming manifest early in life. The incidence of this condition in the general population is l.O/l,OOO live births of infants weighing 2,500 g or more; the rate increases with decreasing birth weights. r2 It is now clear that most cases of cerebral palsy are probably due to intrauterine abnormalities, either developmental or acquired.i3 The

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concept that cerebral palsy is usually the outcome of adverse perinatal events can no longer be supported. The perinatal factors that demonstrate the strongest statistical relationship with cerebral palsy are low birth weight and short gestation period.14 This is discussed in more detail in the section on perinatal asphyxia. An important clinical characteristic of cerebral palsy that often plays a role in attempts to implicate a postnatal event as an etiologic factor is that the diagnosis is virtually impossible to make at birth.15 This difficulty also is a factor in claims of diagnostic delay. Children who are severely involved with spastic or atonic quadriplegia show a severe motor delay in early infancy, but it is usually several months before the clinical characteristics of the motor disability become clear. Spastic hemiplegia is rarely diagnosed until the age of 4 to 6 months when premature hand preference becomes evident; if the leg is predominantly involved, diagnosis may easily be delayed until the child is approximately 1 year old. Spastic diplegia may be suspected if the child demonstrates abnormalities in sitting and crawling, but may not become obvious until the child begins to stand and attempts to walk independently. Children with athetosis have generally delayed motor development, but the adventitious movements rarely start until the second year of life. It is difficult to classify the child whose motor abnormalities are limited to fine motor skills; the majority of these children also have learning disabilities. An additional confounding issue related to the diagnosis of cerebral palsy is the disappearance of motor symptoms in many of the patients, especially those with less severe involvement. Longitudinal assessment of 115 high-risk infants showed that one half of infants thought to be “neurologically suspicious” at 12 months were normal at the age of 24 months.r6 Those considered to be either normal or abnormal at 12 months tended to remain in the same category at 24 months. A follow-up study of 229 children diagnosed as having cerebral palsy at 1 year demonstrated that only 48% still carried this diagnosis at the age of 7 years.17 Resolution of the motor disability was most likely in those children with mild symptoms, monoparesis, ataxia, dyskinesia, or diplegia. The group of children who “outgrew” cerebral palsy do, however, have an increased incidence of mental retardation, epilepsy, speech articulation problems, oculomotor abnormalities, and behavior problems compared with the control population. An additional study, based on long-term follow-up of a defined population, showed a resolution rate of 86% for mild cerebral palsy.4 Abnormalities of cognitive function can be global

(mental retardation) or more specific (learning and language disabilities). Mental retardation is best defined by using the criteria of the American Association on Mental Deficiency.” The condition is present if there is significantly subaverage intellectual functioning associated with impairment in adaptive behavior and manifested in the developmental period. The important feature of this definition is that deficits in adaptive function, the person’s ability to carry out the activities expected of other individuals of the same age, must be present as well as an intelligence quotient (IQ) 2 or more standard deviations below the mean. As adaptive demands vary with age, the prevalence of mental retardation also changes with age. Prevalence reaches a peak of 3% in the lo- to lPyear-old group and is closer to 1% in individuals who are younger than 5 years and older than 21 years. The diagnosis of mental retardation, like that of cerebral palsy, is rarely made in early infancy. This has implications for attempts to implicate postnatal events as being causative and in claims of delayed diagnosis. If the level of mental retardation is severe or profound, it will be apparent within the first year of life. Moderate mental retardation is often suspected first in the second year of life when language development is noted to be significantly delayed. Mild mental retardation is most frequently discovered when testing is performed to determine why a child is not learning adequately in a preschool program or in school. Specific cognitive deficits also cannot be diagnosed until after the age at which the abilities would be expected to be found in a normal child. For this reason, language disorders are usually first diagnosed when the child is approximately 3 years old. Learning disabilities can be defined in a number of ways. Many states have educational regulations which require that if learning in at least one academic area, as measured by standardized tests, is 1 or more standard deviations below the level expected based on the overall IQ, a child is labeled as learning disabled. This discrepancy criterion is easily applied, but would label approximately 15% of the population as having a learning disability. Neuropsychological testing for specific cognitive abnormalities is a potentially more useful approach, but is not available in most school districts. An important point, however, regardless of the defining criteria, is that the diagnosis of a learning disability should not be made until it has been demonstrated that the child fails at attempts at learning in school. An older concept of learning disabilities was to view them as part of the syndrome of minimal brain dysfunction with the implication that they were part

of the “spectrum of reproductive casualty.” Attempts to correlate learning disabilities with adverse perinatal events have not been successful, however. There is a growing body of evidence that developmental malformations of the brain, or damage sustained early in intrauterine life, are causative in many cases. Problems with behavior, especially attention deficit-hyperactivity disorder (ADHD), were also said to be part of the complex of minimal brain dysfunction. As in the case of learning disabilities, it is difficult to support this concept. Reasons include the difficulty in differentiating ADHD from behavioral problems such as conduct disorder, accumulating evidence that there may be a biochemical basis for ADHD, and the suspicion that the disorder may have a genetic component. Acute Encephalopathies The term encephalopathy refers to any disease of the brain. It has little value without further elaboration in a specific case, as can be seen by its use in conditions as different as the metabolic encephalopathy of hepatic failure and anoxic encephalopathy following near-drowning. It is important to understand that illnesses characterized by severe, acute neurologic abnormalities are not rare in childhood. The child may recover completely, or be left with a permanent deficit. The background rate of these disorders mandates caution before raising the possibility of a causative relationship between the neurologic illness and other events such as an illness, accident, or immunization. The British National Childhood Encephalopathy Study (NCES), a case-control study, attempted to determine if there was a relationship between immunizations and acute encephalopathies in childhood. One striking finding was that 96.5% of cases of encephalopathy occurred 1 week or longer after immunization and could not have been associated with the vaccine.i’ A recent study from India demonstrated that it was impossible to define a cause in 50% of encephalopathies in 740 children aged 6 months to 12 years. ” Although the total population base was not specified in this article, and so no incidence data can be developed, the study does confirm that encephalopathies are seen in childhood, and that the cause can often not be determined by the studies available. Age-Related Disorders Many neurologic disorders of childhood are timelimited in their appearance or have characteristic ages of onset. An example is infantile spasms, which have an onset restricted to the first year of life and a

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peak age of onset of 5 to 6 months. A more common condition with a predictable age of occurrence is febrile seizures; these are unusual before the age of 6 months or after 5 years. The importance of recognizing the typical age of occurrence of these and other conditions is to allow understanding of the hazards of drawing causal relationships with events that are linked in time fortuitously. The peak onset of infantile spasms is clearly during the months in which diphtheria-tetanus-pertussis (DTP) immunizations are administered. A temporal association between the immunization and the onset of the seizure disorder would clearly be expected, although studies have not supported a causal relationship. The Role of Newer Diagnostic Techniques Concepts of causal relationships change as new and more sensitive diagnostic techniques become available. It has become possible to demonstrate the existence of congenital malformations of the brain in many patients in whom no cause for a neurologic disability could be found. An important association that is becoming more evident since magnetic resonance imaging (MRI) scans have become easily available is that between various types of neuronal migration defects, mental retardation, and seizures, especially infantile spasms.‘l MRI scanning, chromosomal analysis, and studies directed toward defining metabolic disorders should be considered strongly when evaluating a patient in whom a causal link between a neurologic disability and an external factor has been postulated. Specific Disorders An attempt is now made to examine those neurological disorders in which there is a significant possibility of an outcome which includes damage to, or abnormalities of, the function of the nervous system. It is these conditions, and factors related to their diagnosis and treatment, that are associated with a high risk of a claim of medical negligence. Potential causal relationships between the condition and antecedent factors, especially those factors that are often considered in legal claims, are also evaluated, and pitfalls for the pediatrician examined. The analysis and opinions that follow are those of the author, and are meant in no way to represent an authoritative guide to the standard of care of these conditions.

Perinatal Asphyxia The perinatal period carries the greatest risk for claims of medical negligence. Information obtained

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from the State Volunteer Mutual Insurance Company of Tennessee reveals that there were approximately 66 claims made of neurologic damage to a child in the period 1977 to 1988. Forty-nine of these claims alleged errors in management during labor and delivery, while an additional 14 claims involved events in the immediate neonatal period. In attempting to evaluate the relationship between perinatal events and adverse neurologic outcomes, four questions must be asked: Was there evidence of significant perinatal asphyxia? Did the infant show a characteristic clinical picture in the neonatal period? Was the outcome consistent with hypoxic-ischemic encephalopathy? Have other conditions been ruled out?” From the medical-legal perspective, it also must be determined whether the perinatal asphyxia was preventable or the result of negligence. The most common clinical tool in the diagnosis of perinatal asphyxia is the Apgar score, although it is inappropriate to use this score as the sole criterion for asphyxia. The Apgar score can be low in the normal premature infant, in any infant after the administration of maternal sedation or analgesia, and in children with preexisting neurologic abnormalities or diseases of the cardiorespiratory system.23 There is generally agreement that in a full-term infant a score of 0 to 3 is significantly depressed, but there is less certainty about the significance of a score of 4 to 7, especially the l-minute score. The second is the finding that it may be necessary to continue measuring the Apgar score for as long as 20 minutes following the birth of the infant in order to obtain significant information. The routine in most institutions, however, is to measure it only at 1 and 5 minutes. The usefulness of the Apgar score alone as a predictor of cerebral palsy is limited. The largest body of information comes from the National Collaborative Perinatal Project (NCPP), in which 54,000 singleton pregnancies were studied and the great majority of the children followed to the age of 7 years. Almost three-fourths of the children who had cerebral palsy at age 7 years had Apgar scores of 7 to 10 at 5 minutes.24 In the group of infants who had Apgar scores of 0 to 3 at 10, 15, or 20 minutes and survived, only 12% had cerebral palsy; the majority of the children with cerebral palsy were multiply handicapped and also had severe mental retardation. Eight percent of the children with persistently low Apgar scores did not have cerebral palsy but had other neurologic disabilities. It should be noted that 80% of the children who had Apgar scores of 0 to 3 at 10, 15, and 20 minutes did not have major handicaps at the time of school entrance. Other evidence of perinatal asphyxia can be ob-

tained from measurement of the physiologic effects of the insult. A severe metabolic acidosis would be expected to be present if the child were compromised significantly.25 The most important diagnostic tool, however, is the clinical status of the child. Significant asphyxia should be associated with a clinical syndrome consistent with hypoxic-ischemic encephalopathy.26 In the first 12 hours of life, the child would typically be stuporous or comatose and hypotonic. Seizures, which can present diagnostic difficulties in neonates, are almost always present and manifested by eye movements, mouth movements, swimming movements of the limbs, or apneic spells. During the second 12 hours the child may appear more alert but is jittery. More seizures and apneic spells occur, and weakness is found on examination. The second and third postpartum days are characterized by a return of stupor or coma, signs of brain stem dysfunction, and respiratory arrest. Improvement will then occur, but abnormalities of tone, strength, and feeding ability remain. There is often evidence of compromise of other organ systems, particularly the heart and the kidneys. The importance of clinical signs in the neonatal period has been further confirmed by analysis of data from the NCPP. A significant increase in the risk of cerebral palsy was present when there was diminished activity or a diminished cry for more than 1 day, thermal instability, the need for gavage feeding, abnormalities of muscle tone, or apneic spells.27 Another powerful predictor was the global impression by the attending physician that brain dysfunction was present. If complications in late pregnancy or the perinatal period were present, but the child was asymptomatic in the newborn nursery, the rate of cerebal palsy at the age of 7 years was identical to that in the control group of infants who had no birth complications.” As in the previous analysis, the risk of cerebral palsy increased if transient neonatal abnormalities were present, and was highest if the neurologic signs were persistent. The issue of the prevention of perinatal asphyxia relates primarily to the use of fetal heart rate monitoring during labor and measurement of cord pH values at the time of delivery. There is a poor correlation of cord pH alone with perinatal asphyxia.‘” Continuous electronic fetal monitoring during highrisk pregnancies has been compared with routine auscultation of the fetal heart rate in two large studies .30, 31 Neither study showed a better outcome for the group that had been monitored. It appears that the standard of care applied in the management of many pregnancies may have little support from the published literature. The relationship between perinatal asphyxia, as

defined by any of the criteria outlined, and neurologic abnormalities remains the fundamental question. Further detailed analyses of the data obtained in the NCPP have been directed toward clarifying these relationships. Univariate analysis was carried out initially, and demonstrated significant correlations between a number of factors and cerebral palsy.32 Maternal factors included mental retardation, seizure disorders, hyperthyroidism, and the administration of thyroid hormone or estrogen during pregnancy. Other risk factors were significant predictors of cerebral palsy only because of their association with low birth weight or a low Apgar score. Factors that were not related to cerebral palsy included the use of anesthetic agents or oxytocic drugs and the duration of labor. Multivariate analysis of the data from the NCPP has also been performed. 33 The most significant predictive factors for cerebral palsy were maternal mental retardation, fetal malformations, and a birth weight lower than 2,001 g. Twenty-one percent of the children with cerebral palsy had clinical evidence of perinatal asphyxia. Forty-three percent of these children had major congenital malformations, however, suggesting a cause of the cerebral palsy antedating the birth process. The role of preexisting congenital malformations can be seen in the analysis of breech delivery. Breech presentation was a risk factor, while breech delivery was not; it was found that one third of the children with cerebral palsy who had a breech presentation had major extracerebral congenital anomalies. It can be estimated that of the children followed as part of the NCPP, only between 3% and 13% of cases of cerebral palsy appeared to be due to perinatal injury.34 A more recent analysis of 43,437 full-term children studied in the NCPP confirmed the findings of the earlier analyses and provided additional data.35 A presumptive cause was determined in 71% of the children with quadriplegia. Fifty-three percent of the children in this group had congenital disorders while in only 14% could the cerebral palsy be attributed to perinatal asphyxia. In the nonquadriplegic group, 35% had congenital disorders and in 2.5% of the cases perinatal asphyxia was the most likely cause. Clinical signs such as meconium staining of the amniotic fluid, low lo-minute Apgar scores, neonatal apneic spells, seizures, persistent neurologic abnormalities, and slow head growth after birth were more commonly found in children without asphyxia as a cause of cerebral palsy than in those with perinatal asphyxia. Perinatal factors that were not associated with an increased risk of cerebral palsy included the use of oxytocic drugs, gas anesthesia, and fetal or neonatal hypoglycemia.

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Data from the Western Australia Cerebral Palsy Register, covering all children with cerebral palsy born between 1975 and 1980 and compared to a matched control group, indicated that there was an association between clinically observed perinatal signs of birth asphyxia and spastic cerebral palsy.36 The overall estimate from this study was that intrapartum asphyxia possibly played a role in only 8.2% of cases of spastic cerebral palsy. In fact, in only 4.9% of cases was asphyxia considered very likely using rigorous criteria; it was considered possible in another 3.3% of cases of cerebral palsy. Prenatal and perinatal risk factors were investigated in the California Child Health and Development Studies. A total of 19,044 children born to mothers who had their pregnancy monitored were followed for at least 5 years.37 A diagnosis of cerebral palsy was made in 0.2% of this group, and these children were compared to the entire group without cerebral palsy. The factors that were significant indicators of cerebral palsy included the presence of congenital anomalies, low birth weight, low placental weight, abnormal fetal position, and premature separation of the placenta. Abnormal delivery and delayed crying associated with perinatal asphyxia were significant perinatal factors. Unusually long or short intervals between pregnancies and excessively long menstrual periods in the mother also were predictors of cerebral palsy. The overall analysis demonstrated that 78% of children with cerebral palsy did not have birth asphyxia; 22% had evidence of birth asphyxia but also had other prenatal risk factors that may have compromised the final outcome. The data available no longer support a causative role of perinatal events in the genesis of most cases of cerebral palsy. Before implicating obstetric factors, it is most important to define fetal compromise during labor, determine that the clinical findings in the neonatal period are consistent with hypoxia, and rigorously rule out underlying problems such as congenital malformations of the brain and extracerebra1 malformations. In those cases where significant asphyxia does play a causative role in the etiology of the cerebral palsy, the child will almost certainly also have mental retardation and an increased risk for a seizure disorder.

Perinatal Trauma Claims of neurologic damage due to perinatal trauma often arise when a child demonstrates developmental abnormalities and the history indicates that the labor was prolonged, the delivery difficult, or bruising or forceps marks were present on the child’s head at the time of birth. Caput succeda-

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neum and subgaleal hemorrhage are findings that are present commonly in the perinatal period and do not, as isolated findings, indicate that intracranial injury has taken place. Cephalohematomas are found in 1% to 3% of live births, and are associated with an underlying skull fracture in 10% to 25% of cases.38 The fracture itself is of no significance, although investigation for intracranial injury is appropriate if clinical signs suggesting injury are present. Computed tomography (CT) scan is appropriate if a depressed fracture is present. Traumatic intracranial hemorrhage is most common in full-term infants.39 The most common symptoms are seizures and respiratory abnormalities including grunting respirations and apneic spells. Abnormalities of muscle tone, poor feeding, an abnormal cry, lethargy, and hypothermia are present in varying numbers of these patients. The bleeding is usually present in several different regions, with tentorial and supratentorial subdural hemorrhage being the most common. Outcome in the survivors is as dependent on the severity of any associated perinatal asphyxia as it is on the traumatic lesion itself.

Seizure Disorders

and Antiepileptic

Drugs

Etiology of Seizures Seizures, including those associated with fever, occur in as many as 4% of all children. Epilepsy, defined as recurrent seizures without a definable precipitating cause for each episode, has an average annual incidence of approximately 80/100,000 population and a lifetime prevalence of approximately drugs (AEDs) lO/l,OOO population. 4o Antiepileptic can provide full control in 65% of patients; a significant reduction of seizures can be obtained in an additional 20% of patients, but the remaining 15% have intractable seizures. If complete control of the seizures can be maintained for several years, AED treatment can be discontinued and only between 11% and 33% of patients without other neurologic abnormalities will have a recurrence of their disorder. 41, 42 The exact recurrence risk varies with the type of seizure and is higher in children with other evidence of neurologic dysfunction. The critical medical-legal consideration is whether epilepsy is caused, in a given case, by a preventable brain injury, especially a perinatal injury. A case-control study of generalized tonic-clonic seizures found that risk factors that were significantly associated with seizures included convulsions in the mother, febrile seizures, and head trauma.43 A large number of prenatal and perinatal risk factors

were examined, and no correlations were found with the later onset of generalized tonic-clonic seizures. These included advanced maternal age, previous miscarriages, toxemia or eclampsia, bleeding during pregnancy, low birth weight, asphyxia, and postmaturity. The relationship of nonfebrile seizures and possible etiologic factors was also studied in the cohort of children in the NCPP.44 The incidence of seizures was 0.8%. When the entire group of children with seizures was examined, the important predictors were neonatal seizures, a number of types of neurologic conditions in the family, and congenital anomalies. The familial conditions associated with epilepsy in the index case included a previous sibling with cerebral palsy, maternal seizures, and maternal mental retardation. Congenital anomalies were those involving the brain as well as extracranial malformations such as vertebral and genital abnormalities. Although fetal bradycardia with a heart rate below 60 beats/min and evidence of uterine dysfunction were associated with an increased risk for seizures, these factors did not strongly affect the outcome. In children with epilepsy who had neither cerebral palsy nor minor motor seizures, maternal seizures and neonatal seizures remained the strongest predictive factors. There was only a weak association with prenatal and perinatal factors in this group of patients. Minor motor seizures are often associated with mental retardation and cerebral palsy and are difficult to treat. Although univariate analysis showed correlations with a number of perinatal factors, simultaneous examination of all factors showed the strongest predictors to be fetal malformation, maternal mental retardation, and primiparity. There was also some predictive value to meconium staining of the amniotic fluid and the use of oxytocin during a prolonged first stage of labor. Predictors of neonatal seizures were also examined. Initial analysis showed some significant correlations with a number of prenatal and perinatal factors. Following sequential analysis, however, the major predictors were fetal brain malformations, abnormal cry in the delivery room, and a low Apgar score. The difficulty in applying statistical correlations to individual patients can be seen by examination of the overall NCPP series. Although the 5% of children who had the strongest risk factors made up 21% of the population of patients with seizures, 79% of all seizure disorders were found in patients who were not in this high-risk group. There was a higher level of predictability in the group of patients with minor motor seizures. The 5% of children at highest

risk accounted for 44% of the minor motor seizures; the highest 1% of children accounted for 26% of the cases. Predictive ability was also reasonably strong for neonatal seizures. Forty-seven percent of neonatal seizures occurred in the 5% of children at highest risk. One additional important factor was the strong predictive value of congenital malformations. Brain malformations were present in 13% of the children with minor motor seizures, compared to 0.5% in the population without seizures. In addition, more than one fourth of patients with neonatal seizures and one third of those with minor motor seizures had major extracerebral malformations. Minor congenital anomalies, unassociated with major malformations, were present in 11% of all children with seizures; this factor was a predictor of seizures on the univariate, but not the multivariate, analysis. Status epilepticus is a medical emergency that calls for the prompt initiation of treatment. Older studies reported a mortality rate as high as 11% in children. 45 More recent ana 1ys es indicated mortality rates of 3.6% to 6.0% within a period of days to weeks following the seizure.46Z 47 Although new neurologic abnormalities may be found following an episode of status epilepticus, both injury and death appear to be a result of the underlying acute or progressive neurologic disorder. It is rare to see either death or deterioration of the neurologic status in a patient who has idiopathic epilepsy or a static underlying condition. Febrile status epilepticus, even prolonged over 2 hours, does not appear to be associated with death or the development of new neurologic deficits. 48 The child with neurologic abnormalities is at increased risk for subsequent febrile and afebrile seizures, while the previously normal child is not. There are a number of significant risks in the use of AEDs, the most important being serious idiosyncratic reactions, dose-related toxicity, and teratogenie effects. The patient and family should be made aware of these risks before treatment begins, and they should be given explicit instructions to call if any untoward effects occur or are suspected. Children with epilepsy are also at increased risk of drowning as compared to the general population.49 The child and family should be advised against unsupervised swimming, as should all children and adults, and warned about the increased risk. Antiepileptic Drugs Idiosyncratic side effects vary with the specific AED, and these are discussed in detail in the package inserts and most standard texts. The side effects of

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several drugs are potentially life-threatening and worth noting; the family should be given specific warning about the possibility of these reactions. Phenytoin has been associated with a hypersensitivity reaction manifested by a combination of symptoms that can include rash, fever, lymphadenopathy, eosinophilia, abnormal liver function, blood dyscrasia, serum sickness, renal failure, and polymyositis. 5o These reactions usually occur within 2 months of starting therapy. Hepatic necrosis51 and Stevens-Johnson syndrome5’ have also been reported with the use of phenytoin. The most serious side effect of valproic acid is fatal hepatotoxicity. The highest risk (l/500) was found in children younger than 2 years who were being treated with valproic acid and one or more additional AEDs and who had preexisting neurologic abnormalities.53 The risk rapidly declined with age, and was greatly reduced by the use of valproic acid as monotherapy. There were no reports of fatal liver disease in patients older than 10 years who took valproic acid as the only drug. The overall estimated risk of a hepatic fatality with valproic acid monotherapy was l/37,000. Although carbamazepine had been considered to be a drug with a high risk of serious hepatic and bone marrow toxicity, it now appears that the hazards of this drug are relatively low. It has been estimated that approximately 6 patients/l million population/year are at risk for agranulocytosis and 2 patients/l million population/year are at risk for aplastic anemia.54 Transient or persistent leukopenia and thrombocytopenia are common, and the manufacturer recommends that patients with these disorders be monitored closely. A baseline hematologic evaluation should be obtained before therapy is started, and the patient’s hematologic status should be monitored regularly. Dose-related side effects also vary with the AED being used, but most of these pharmacologic agents can interfere with cognition, behavior, and coordination when toxic blood levels are present. These reactions can have adverse effects on school performance and motor incoordination, and can increase the risk of accidental injury. There is little or no consistency in the data concerning adverse effects on cognition and behavior when the blood level of an AED is within the therapeutic range. Although most of the commonly used drugs do not produce clinically significant problems, there has been some concern raised about the longterm use of phenobarbital in the treatment of febrile seizures.” IQ scores were measured in a group of children with febrile seizures who were randomly assigned to receive either phenobarbital or placebo.

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After 2 years, the mean IQ of the group of patients taking phenobarbital was 8.4 points lower than that of the placebo group. Six months later, after the medication had been discontinued, the IQ was again measured and was 5.2 points lower. Parents of the children treated with phenobarbital also reported more behavioral abnormalities early in the study, but this effect disappeared. It was also found that the proportion of children remaining seizure-free following cessation of treatment did not differ between the two groups. Phenobarbital use may also be associated with the development of a major depressive disorder in children with epilepsy, and patients should be monitored for this problem.56 The issue of teratogenicity of AEDs is a complex one. Several studies have suggested that there is an increase in serious malformations, particularly cleft lip and palate,57 and minor and major malformations as well as failure to thrive and Gesell development quotients less than 90 in children exposed to anticonvulsants in utero.58 It then became apparent, however, that the presence of a seizure disorder, with or without treatment with AEDs, places the pregnancy and the fetus at risk.59 Adverse outcomes were found in 20% of pregnancies of women with epilepsy and consisted of stillbirth, microcephaly, mental retardation, and nonfebrile seizure disorders. There was not an increased risk for spontaneous abortion, low birth weight, or neonatal seizures. The study was unable to demonstrate an increased risk when the woman was taking AEDs. The data on potential AED teratogenicity must, therefore, be viewed against this high background rate of fetal malformation in children born to epileptic women. The fetal hydantoin syndrome, most commonly ascribed to exposure to phenytoin, consists of a number of minor malformations, the most consistent of which is nail hypoplasia. The children have some resemblance to those affected by the fetal alcohol syndrome. In families with one child with the syndrome, there is an increased risk for subsequent children; if the index case is unaffected, the risk is lower.60 It has been suggested that the teratogenicity is the result of failure to excrete an abnormal metabolite of the drug because of low levels of epoxide hydrolase activity. Measurement of this enzyme in the fetus has been successful in predicting which fetuses will be affected, and may prove to be useful in genetic counseling, although this is not yet an established technique.” It has been suggested that carbamazepine therapy during pregnancy may be associated with fetal malformations similar to those found in the fetal hydantoin syndrome. 62 There was an increased incidence of craniofacial defects, fingernail hypoplasia,

and developmental delays in children who were exposed prenatally to carbamazepine alone. It was hypothesized that this drug, like phenytoin, is metabolized through an epoxide intermediate, and that the metabolic product may be teratogenic. Trimethadione is not commonly used at this time, but is a valuable adjunct in the treatment of some patients with intractable epilepsy. A fetal tridistinct from the fetal hymethadione syndrome, dantoin syndrome, has been reported.63 This syndrome, or fetal loss, may occur in as many as 87% of pregnancies in which there is prenatal exposure to this drug. 64 There are also case reports of primidone embryopathy, the affected infants having a broad range of malformations.65, 66 An increase in both major and minor malformations, which may be dose-related, has been reported with the use of valproic acid during pregnancy.67 The possibility of pregnancy is a real concern when any adolescent girl including those being treated with an AED. Initial and ongoing reproductive counseling is of great importance and, if the girl is sexually active, appropriate contraceptive advice should be provided. One problem that arises in the choice of a contraceptive method is that AEDs have numerous interactions with other pharmacologic agents. 68 A risk of contracep tive failure has been suggested with the use of both phenobarbital and phenytoin. 69, 7o It is important to make a firm clinical judgment that the use of an AED is required and, if seizures have been under control for several years, to consider discontinuing the medication. An attempt should be made to use the AED with the least potential for teratogenicity, and to provide counseling concerning the risk of fetal malformation to the young woman and her family. Seizures and Accidents One issue that will eventually face children with epilepsy is their ability to drive as adolescents and adults. The laws vary from state to state. In some cases there is a specified seizure-free interval and the patient must be under a physician’s care. In other jurisdictions, the patient can obtain a driver’s license if the physician is willing to state that the individual should be allowed to drive. There are several states in which the physician must report the names of patients with epilepsy or recurrent lapses of consciousness to the motor vehicle department. The question of the physician’s liability if the adolescent with epilepsy is involved in a motor vehicle accident is unsettled. 71 The physician is well advised to discuss the patient’s responsibility for notifying the motor vehicle department about his or her sei-

zures, and recording notes on the conversation in the patient’s chart. A population-based study has explored the level of risk for automobile accidents in patients with epilepsy. 72 There was a slightly increased risk of accidents causing injury with a standardized mishap ratio of 1.63 (95% confidence limits, 0.95 to 2.60). There was also an increased frequency of speeding violations and violations involving drugs and alcohol. The increased risk of accidents was highest in those patients younger than 25 years. The authors expressed the opinion that the increased risk was small, and was not great enough to warrant further restrictions on driving.

Irreversible Coma and the Termination of Treatment Brain Death Problems related to the termination of treatment of patients with brain death or in a chronic vegetative state are complex because of the intersection of medical, ethical, and legal issues. The complexity of these areas of decision making has been further increased by the growing need for organs for transplantation. The courts have also become deeply involved and have taken on the task of trying to balance the rights of the infant, the interest of the state in the preservation of life, and the rights and responsibilities of the parents as surrogate decision makers for the child. There has also been enormous political pressure brought to bear on the courts and legislative bodies from activists espousing personal choice or a viewpoint which is against any action that will shorten life. The issues facing the pediatrician are the diagnosis of brain death in a child, the diagnosis and management of the child in a chronic vegetative state, the intensity of treatment offered to a child with a severe handicap, and the use of the anencephalic infant as an organ donor. The allowable courses of action in these areas change almost daily on the basis of court decisions, many of which are contradictory, and so this review is restricted to selected material in the medical literature. The definition of brain death, or irreversible coma, was first formalized in 1968 by an Ad Hoc Committee of the Harvard Medical Schoo1.73 The basic concepts were that a number of clinical criteria could be used to determine that the patient would never emerge from the comatose state and that irreversible coma was an alternative definition of death. When brain death was present, the patient was, in fact, dead and artificial support of cardiorespiratory

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function could be discontinued. The clinical criteria were unreceptivity and unresponsivity, no movements or breathing, no reflexes, and a flat recording on an electroencephalogram (EEG). The basic concepts of the Harvard criteria were accepted and elaborated by the President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research.74 Complicating factors that required caution in making the diagnosis of brain death were drug and metabolic intoxication, hypothermia, and shock. The medical consultants to the commission also considered the diagnosis of brain death in children to be a complicating condition. They stated that because the brains of infants and young children may have increased resistance to damage and may recover substantial function after longer periods of unresponsiveness, compared with adults, physicians should be cautious in applying the usual criteria to children younger than 5 years. A Task Force for the Determination of Brain Death in Children, made up of representatives of the American Bar Association and the major pediatric and neurologic societies in this country, published their report in 1987.75 The criteria established were that coma and apnea must coexist, absence of brain stem function must be documented, the patient must not be hypothermic or hypotensive, flaccid tone and absence of spontaneous or induced movements must be demonstrated, and findings consistent with brain death must be maintained throughout the observation and testing period. The recommended period of observation varied with the patient’s age. Children between 7 days and 2 months old required two examinations and two EEGs 48 hours apart. If the patient was between 2 months and 1 year old, the examinations and EEGs could be separated by 24 hours. For older patients, it was recommended that observation be continued for at least 12 hours. A caveat was given concerning hypoxic-ischemic encephalopathy, and the period of observation of these patients, especially if seen shortly after the acute event, was at least 24 hours. This time period could be shortened if the EEG confirmed electrocortical silence or cerebral radionuclide angiography demonstrated no flow through the cerebral arteries. Clinical studies have supported the validity of the task force’s criteria for children older than 2 months. 76 It has been demonstrated that there is no difference in the time needed to confirm the diagnosis in children 2 months to 1 year old, those older than 1 year, and those older than 5 years. The usefulness of the EEG in supporting the diagnosis of brain death has been confirmed for children older than 3 months.77

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The issue of diagnostic criteria for brain death in infants younger than 1 month is beginning to be clarified.78 Standard clinical criteria of coma, apnea, and absent brain stem reflexes were used. Term infants who maintained clinical features of brain death for 2 days and preterm infants who maintained these clinical features for 3 days did not recover, even if there was evidence of electrocortical activity or intracranial blood flow demonstrated on radionuelide angiography. The neurodiagnostic studies did not confirm the diagnosis of brain death in one half to two thirds of patients, although the prognosis was set by the clinical criteria. Absence of radionuelide uptake in the presence of electrocortical silence confirmed the diagnosis. A confounding factor was a phenobarbital level greater than 25 .pg/mL, which could suppress electrocortical activity. Chronic Vegetative State The chronic vegetative state can be defined as a condition of permanent unconsciousness in which the person’s eyes are open and there are wake-sleep cycles.79 There is, however, no evidence that the patient is aware of the environment or that there is any self-awareness. This state, in pediatric practice, most commonly occurs following severe, closed head injury or hypoxic-ischemic encephalopathy such as occurs with near-drowning. Patients in a chronic vegetative state can survive for many years if they are given adequate nutrition and meticulous medical care. This has led to requests on the part of families and guardians of these patients to discontinue the provision of food and water and to allow the patient to die. Court decisions have been somewhat contradictory, but have generally allowed discontinuation of treatment if it was clear that the patient had expressed the wish, at a time when they were legally competent, not to be subjected to artificial means of life support. A position statement from the American Academy of Neurology is worth noting, although it contains little specific guidance for the management of children in the chronic vegetative state.791 So This statement defines the chronic vegetative state and provides the basis for the argument that these patients do not have the capacity to experience pain or suffering. This conclusion is based on clinical observations, the results of postmortem examinations, and the study of the metabolic rate of glucose utilization of the cerebral cortex. The position then taken is that the artificial means of providing nutrition and hydration are forms of medical treatment and may be discontinued following the guidelines for the withholding or discontinuation of any medical treatment. The statement also notes that diagnostic cer-

tainty of the chronic vegetative state cannot be achieved, until the patient has been observed for at least 1 to 3 months, and that it is good medical practice to provide nutrition and hydration during that time period. Finally, the ethical issues and central role of the family in the decision-making process are discussed. Until more data are available in children, it would seem appropriate to apply the principles and guidelines that have been developed by the American Academy of Neurology. There is still some uncertainty concerning the status of the infant and very young child, as there was until recently concerning the issue of brain death. More clinical studies are needed before firm conclusions can be drawn for the youngest patients. Severely Handicapped Infants and Children The issue of withholding or withdrawing treatment from severely handicapped infants and children shares the legal and ethical issues raised by the patient in irreversible coma or the chronic vegetative state. These include the role of surrogate decision makers, the state’s interest in the preservation of life as expressed by the courts, and the underlying ethical issues concerning life and death. An additional level of complexity arises because the group of patients under consideration do have the ability to experience pain and suffering and have levels of cognitive function ranging from normal to severely impaired. The fundamental issue becomes one of quality of life, not one based on the presence or absence of higher cortical function. The legal issues related to the care of the severely handicapped infant became formalized by the “Baby Doe” rules issued by the Department of Health and Human Services.‘i The rule making took the approach that any action taken solely because of an infant’s handicap, and which would have an adverse outcome for the infant, denied the child’s civil rights and was prohibited. The promulgation of these rules caused a great deal of controversy in the medical community. The claim was made that this represented governmental interference in clinical decision making and inserted the government in the physician-patient relationship. There was also great consternation about the establishment of the toll-free Handicapped Infant Hotline, which allowed any individual who believed that an infant’s rights were being violated to call, lodge a complaint, and initiate an investigation. Responses in the literature suggested mechanisms for developing policies and procedures for situations in which life-saving care would be withheld. The establishment of infant bioethical committees

was also discussed. s2, 83 Although the literature reflected a good deal of discussion about the conceptual bases behind these committees, there have been few reports of their utility in the clinical setting. The reports that have been published have expressed satisfaction with this mechanism.84, 85 A number of issues remain unclear, and the degrees of freedom in making clinical decisions are often limited by court decisions; these court decisions, however, are usually very narrowly drawn and may be contradictory from jurisdiction to jurisdiction. The decision to withhold or discontinue treatment is usually limited to life-saving or life-sustaining procedures that have been sometimes termed “heroic.” The definition of what is heroic may be subjective and has never been clearly defined. A reasonable suggestion is to provide all patients with nutrition, hydration, and remedies to ensure freedom from pain. Most clinicians would consider the use of antibiotics to treat infections to be routine care. Procedures such as transfusion of blood components would have to be viewed in the specific clinical context, while hemodialysis, ventilatory assistance, and cardiopulmonary resuscitation would seem to be beyond routine care. In the absence of specific legal guidelines, each hospital should have clearly defined policies and procedures, these policies and procedures should be followed, and the child’s family must be continuously involved in the decision-making process. It is also important to understand that no course of action is irrevocable, and that a decision entailing a specific course of action can be modified as the clinical situation and the family’s perception of the child’s needs change. Caution would also dictate consultation with the hospital’s legal staff so that the impact of the most recent court decisions can be understood. Anencephalic Infants as Organ Donors There is a great need for organs for transplantation, especially for young children. Donors are usually individuals with devastating brain injuries who are otherwise normal. The necessity of protecting the rights of patients who are being considered as organ donors has driven the development of specific guidelines for brain death. Anencephalic infants have intact brain stem function and, although they have no functioning cortical tissue and almost never survive beyond the first week of life, do not fulfill the accepted criteria of brain death. Because of the lack of all but the most primitive neurologic functions and the certain outcome, the suggestion has been made that these infants should serve as organ donors. This issue has been reviewed in detail by a

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task force consisting of members of a number of professional societies with interest and expertise in the related problems.s6 No specific guidance for the clinician was offered, but possible modes of action were outlined. This area, like all other areas related to the termination of life, is currently in flux.

Adverse Rections to Immunizations The number of lawsuits related to claims of adverse reactions to immunizations can be represented by an epidemic growth curve, especially those suits related to pertussis vaccine. One lawsuit was filed against vaccine manufacturers in 1978 and one in 1979.87 There was then a gradual increase to 73 lawsuits in 1984 and an explosion to 219 claims filed in 1985 and 255 claims in 1986. There were 178 additional claims in 1987 and 114 in 1988. During the peak year of 1986, this amounted to one lawsuit for every 76,200 doses administered. The amount claimed per suit reached a peak of $46,000,000 in 1984 and averaged $21,410,000 over the period of time studied. It should also be noted that the cost per dose of vaccine purchased by public sector providers rose from $O.l5/dose prior to 1983 to $9.62/dose during the first 5 months of 1988. This represents a price increase of 6400%. The most common causes of claims made against pediatricians are the failure to provide informed consent, including a discussion of possible adverse reactions, and administering immunizations despite the presence of contraindications. A recent survey has shown that 88.4% of pediatricians who administer vaccines in a primary health care setting always verbally discuss the benefits and risks of DTP vaccine before the first administration and an additional 10.2% sometimes do.’ Written information is always distributed 73% of the time, and an additional 13.3% of respondents sometimes do. In the case of oral polio vaccine (OPV), 79.2% of pediatricians always discuss benefits and risks and 18.5% sometimes do; 65.4% always distribute written information, while 12.9% sometimes do. Documentation of the information given to the family is noted in the chart by the pediatricians surveyed always or sometimes 79.4% of the time for DTP and 73.4% of the time for OPV. A signature is obtained always from a family member 54.2% of the time for DTP and 51.7% of the time for OPV. The most common guides for contraindications are the manufacturer’s package insert and the “Red Book,” published by the American Academy of Pediatrics.88 This publication is the Report of the Committee on Infectious Diseases and represents a con-

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sensus developed by members of the committee in consultation with liaison representatives from other organizations and collaborators contacted by the committee. Attorneys often ask expert witnesses if the Red Book is authoritative. The answer to that question should be modified by reference to the introduction to the 1988 edition which states that I/ . . . the Committee attempts to provide guidelines and information that in conjunction with clinical judgment will facilitate well-reasoned decisions.“” General guidance in the area of immunization has also been provided by the Immunization Practices Advisory Committee (ACIP) of the Centers for Disease Controls’ Claims against pediatricians are accompanied often by claims against the manufacturer of the vaccine. The bases of the suits against the manufacturer are that the currently produced whole-cell pertussis vaccine is inherently toxic and dangerous, and that the manufacturers have delayed developing a less toxic acellular vaccine, modeled after the acellular vaccines that are in use or being studied in a number of countries. Although these vaccines have been in use for a number of years, it is still too early to provide a firm estimate of the rate of various serious adverse reactions. A great proportion of the literature concerning acellular vaccines is from Japan but in that country, the first dose of DTP is given at the age of 2 years. It does appear, however, that the incidence of troublesome but minor reactions, such as fever and swelling at the injection site, is lower.” These minor reactions, and behavioral reactions such as sleepiness and prolonged crying, do not indicate or predict neurologic damage and are seen in up to 36% of children receiving placebo injections.” Pertussis Vaccine The first case report suggesting that the administration of pertussis vaccine could be followed by the onset of serious neurologic injury was published in 1933.92 Additional case reports demonstrated a temporal relationship between vaccination and the onset of clinical events such as acute encephalopathy, seizures including infantile spasms, and sudden infant death syndrome (SIDS). A causal relationship became widely accepted as fact, despite the absence of a definable syndrome or syndromes, lack of a plausible mechanism, and the absence of a reproducible animal model for the condition.93 Postmortem studies of children dying of alleged pertussis vaccine-induced encephalopathy failed to demonstrate any specific neuropathologic findings.94 The first large epidemiologic study to investigate the relationship was the National Childhood En-

cephalopathy Study (NCES) in Great Britain. An attempt was made to ascertain all children with severe acute neurologic disorders who were admitted to hospitals over a 3-year period.95 Two matched control subjects were assigned to each case patient and the vaccination status of each child was determined. An initial analysis of the first 1,000 cases found that 3.5% of the children with neurologic illnesses had been immunized within the previous 7 days, while 1.7% of the control subjects had received the vaccine in the previous week. The authors calculated an attributable risk for the development of an acute neurologic reaction following immunization of 1: 110,000 injections (95% confidence limits, 1:360,000 to 1: 44,000), and a risk of permanent neurologic damage of 1:360,000 immunizations (95% confidence limits, 1: 5,310,OOO to 1: 54,000). The risk figures from this study are widely quoted, and appear in the package insert of some of the vaccine products. Two of the authors of the study subsequently provided commentary that should be noted, however.96 They pointed out that the analysis included all children, even if there was an alternative explanation for the findings. The relative risk, they noted, was small and was concentrated in the first 72 hours after immunization, and the majority of children recovered quickly and were apparently normal on follow-up at 1 year. They also pointed out that if cases with other etiologic causes were discounted, there were only four children with no other explanation for the illness and caution that the vaccine is given at the age when children are most likely to manifest serious neurologic disorders. The authors also stated that it is “clearly unwise to attribute a causal connection in individual cases.“96 A critique of the NCES occurred as part of a trial in Great Britain, Loveday z, Renton and the Wellcome Foundation.97, 98 Reanalysis of the primary data by Lord Justice Stuart-Smith indicated that no child who was previously normal sustained permanent neurologic damage. The conclusion reached was that despite the administration of more than 1 million doses of vaccine, the probability that pertussis vaccine could cause permanent brain damage could not be supported. Three additional epidemiologic studies were carried out in this country and Great Britain.‘“~~iol Although there was a cumulative total of over 500,000 doses of vaccine administered in these studies, there was no case in which the vaccine could be implicated with certainty in the onset of serious neurologic disease and no case of what has been described as pertussis vaccine-induced encephalopathy. Although convulsions and hypotonic-hyporesponsive

episodes were each present at a rate of 1: 1,750 injections in one series, none of these children had residua on follow-up.99 The evidence in the recent medical literature also does not support a causal relationship between DTP vaccine and epilepsy. 99, 1o1-1o3 Those seizures that occur with a temporal association following the immunization are most probably accidents of timing. Seizures associated with fever may follow DTP immunizations, but they have all the clinical and demographic characteristics of febrile seizures, and do not produce any permanent residua.lo2, lo4 Although a prolonged seizure associated with fever may occur, it appears that febrile status epilepticus can be expected to have a good outcome.48 Special attention has been given to the issue of infantile spasms since the first suggestion that there could be a causal relationship with DTP vaccine.lo5 Analysis of the data from the NCES showed no relationship in the 28 days following immunization.106 What appeared to be a clustering of new cases in the first 7 days following immunization was followed by fewer cases than expected in the next 3 weeks. This was interpreted as possibly meaning that the vaccine triggered the onset of infantile spasms in a child who was going to develop the condition under any circumstances. Previous studies from Japan and Denmark failed to demonstrate a causal relationship between the vaccine and infantile spasms.107, lo8 Japan has had a compensation system for alleged vaccine damage since 1970. As a result of the studies cited, damages are no longer awarded for cases of infantile spasms. lo9 An additional condition for which a relationship with DTP vaccine has been suggested is SIDS.ll’ A small study comparing children with SIDS with two age-matched control subjects demonstrated that the children with SIDS were less likely to have been vaccinated.“’ A similar finding came out of the analysis of the Cooperative Epidemiological Study of Sudden Infant Death Syndrome Risk Factors.“’ Epidemiologic studies in Tennessee and France also failed to document increased risk or a causal relationship.l13, “* A survey was recently conducted by the Child Neurology Society, in which the membership was asked to provide answers to a series of three questions concerning neurologic injury resulting from pertussis vaccine. The questions, and the percentage of respondents agreeing with each statement, were as followsn5: 1. Administration of pertussis vaccine is associated with a short-term increased risk of seizures, most

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of these being febrile seizure, and a complete recovery is expected. (96.9% agreement) 2. Case reports have raised the question as to whether there is an association between pertussis vaccine and progressive or chronic neurologic disorders, but controlled studies have failed to prove such an association. (94.6% agreement) 3. At the present time, there is no means by which a diagnosis of pertussis vaccine-induced encephalopathy can be established in an individual case. (90.4% agreement) Of the 357 respondents, 86.5% agreed with all three statements and only 1 individual disagreed with all of the statements. Despite the lack of support found in the literature for a causal relationship between pertussis vaccine and serious neurologic disorders, it is prudent in most cases to follow the guidelines in the Red Book and the manufacturer’s package insert. The currently recommended contraindications for further administration of pertussis vaccine are: encephalopathy occurring within 7 days, a convulsion with or without fever occurring within 3 days, persistent inconsolable screaming or crying for 3 or more hours, collapse or shocklike state occurring within 48 hours, temperature of 40.5” C within 48 hours, or an immediate severe or anaphylactic allergic reaction.88 A number of indications for deferral or omission of pertussis vaccine in children with underlying neurologic disorders are also delineated. These include progressive developmental delay or changing neurologic findings and neurologic conditions that predispose either to seizures or to neurologic deterioration. Note is taken of the fact that infants and children with a personal history of convulsions are at increased risk of having a convulsion following the administration of pertussis vaccine, and this is given as a reason for deferral or omission of the immunization. It is then stated, however, that there is no evidence that these seizures produce permanent brain damage or aggravate existing neurologic conditions, and that children with well-controlled seizures or those in whom a seizure is unlikely to recur may be vaccinated. The recommendations in the Red Book are clear in stating that a family history of seizure disorders, SIDS, or severe reactions following administration of pertussis vaccine are not contraindications to pertussis immunization. The ACIP guidelines also state that the following are not contraindications to immunization”: reaction to a previous dose of DTP that caused only soreness, redness, and swelling at the injection site or a temperature less than 40.5” C;

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a family history of convulsions; a family history SIDS; and a family history of adverse reactions.

of

Poliomyelitis Immunization There is a small risk of paralytic disease following the administration of OPV; this vaccine contains a live attenuated virus. Disease may occur in the individual who received the vaccine or in a contact, as live virus is excreted in the stool.ii’ A recent study in Washington found a rate of 6.4 cases/million live births in vaccine recipients and contacts.ii7 Two of the 10 cases were the infants who had been immunized, while the other cases occurred in adult contacts. Five of the contacts had never been immunized, while the others had received either inactivated polio vaccine (IPV) or an incomplete course of OPV. The Red Book gives an approximate risk for paralytic disease in immunologically normal vaccine recipients of 1 ease/7.8 million doses of vaccine; the estimate for household and community contacts is 1 ease/5.5 million doses.88 The risk of paralytic disease is increased in vaccine recipients who are immunocompromised. These infants should only receive IPV, and IPV should also be used for the immunization of family contacts of immunocompromised patients. Other indications for the use of IPV, rather than OPV, are patients with human immunodeficiency virus (HIV) infections, unimmunized adults who reside in households where children will be immunized with OPV or who are at risk for exposure to poliomyelitis, partially immunized adults who are at risk of exposure to poliomyelitis, and adults at risk of exposure to poliomyelitis who have had a primary series of IIJv.88 Other Vaccines The Red Book provides the most comprehensive guide to vaccine reactions.s8 Measles vaccine may cause fever and a transient rash. The reported incidence of encephalopathy is 1: 3 million doses, which is considerably lower than the background rate of encephalopathy, suggesting that the association is only temporal. It is such a rare occurrence that it would be impossible to define a causal relationship in an individual case. Although febrile seizures may follow immunization with measles vaccine, there is no evidence that this puts the child at increased risk for neurologic injury or the subsequent development of epilepsy. A personal or family history of seizures increases the risk of a seizure following immunization, but is not a contraindication for administration of the vaccine. The widespread use of measles vaccine has been

followed by a dramatic decrease in the incidence of subacute sclerosing panencephalitis (SSPE), a chronic progressive neurologic disease that is associated with infection by wild strain measles virus. The development of SSPE in vaccinated children probably represents prior exposure to the measles virus or incomplete vaccine efficacy. There is no evidence that the vaccine virus can cause SSPE.iis Mumps vaccine is associated rarely with a febrile seizure. Transient paresthesias and pain may follow rubella immunization. Vaccine Compensation Act The US Congress began serious study of the possibility of development of a vaccine injury compensation act in 1980 following the publication of a report by the Office of Technology Assessment.“’ The driving forces for the exploration of a vaccine injury compensation system included the plan by the Secretary of the US Department of Health, Education, and Welfare to initiate a national immunization initiative; the publicity surrounding the swine flu immunization program; and media attention in other countries concerning adverse reactions to immunizations. lzci Legislation was first introduced in 1983, but the act did not become law until December 1986. One year later, funding provisions were in place. In the period from 1983 to 1986 there were a number of crises affecting the availability of adequate supplies of DTP vaccine with manufacturers discontinuing production of the vaccine or limiting its sale. The price of the vaccine escalated rapidly. Vaccines specifically covered under the act are all pertussis-containing vaccines; measles, mumps, rubella, or any vaccine containing these; DT, Td, or tetanus toxoid; live polio vaccines and IPVs. The act states that children with claims of injury before October 1, 1988, are free to sue under the laws of their state of residence.i’i Those with claims involving immunization after that date must file a claim against the US Department of Health and Human Services. If compensation is accepted under the provisions of the act, no other legal action against the manufacturer of the vaccine remains open to the family. If compensation is not awarded, or if the family rejects the award, they are free to file suit but would obviously have a rather weak case. Compensation is awarded if the plaintiff is successful in showing that the injury suffered appears in the Vaccine Injury Table which is part of the act. The table lists the vaccines covered by the act, the nature of the reactions, an explanation of qualifications, aids to interpretation, and the time limits within which the reaction must have occurred. Al-

leged injuries other than those that occur in the table can be compensated, but the burden of proof is on the plaintiff. 12’ The funds for the payment of compensation were initially appropriated by Congress. Continued funding will be from an excise tax on vaccines. The legislation places a limit on the number of claims that can be compensated each year. Recovery of damages by the plaintiff is limited to the costs incurred for medical treatment and rehabilitation and which are not covered by third-party payers. There are also limits for payment for wrongful death and for pain and suffering. Attorneys’ fees can be awarded if the suit was reasonable, even if compensation is not awarded.“l The act does not, at this time, protect from liability the person who administered the vaccine. In addition, requirements for record keeping and the reporting of vaccine reactions have been made more rigorous. Medical records must note, for each administration of vaccine, the date of administration; the manufacturer and lot number of the vaccine; and the name, address, and title of the person administering the vaccine. i2’ A new reporting system, the Vaccine Adverse Event Reporting System (VAERS), became effective as of November 1, 1990.123 The reportable events are virtually identical to those listed in the Vaccine Injury Table but include, in addition, “events in vaccinees described in manufacturer’s package insert as contraindications to additional doses of vaccine.” A footnote to the table of reportable events further states that the health care provider must refer to the contraindication section of the manufacturer’s package insert for each vactine . It is important to differentiate the status of the scientific knowledge concerning the issue of vaccine injury to the central nervous system from the compensable injuries defined in the act. The legislation was developed to further a number of social and legal goals and to help ensure the continued production of vaccines and continuation of the vaccination initiative in this country. The distinction between science and public policy must remain clear.

Chloride-Deficient Formulas A group of infants with hypokalemic metabolic alkalosis, growth failure, and delayed development in infancy was reported in 1979.1z4 Further investigation showed that this syndrome was caused by two infant formulas that were deficient in chloride. As many as 20,000 infants may have used these formulas. The question of long-term neurologic dysfunc-

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tion in these children remains relevant because of the long statute of limitations in cases involving minors. A follow-up study of ten children, all of whom had severe hypochloremic metabolic alkalosis and growth failure as infants, showed normal growth and at least average intellectual ability at the ages of 4 to 5 years. lz5 Three of the children had behavioral problems, although none had evidence suggesting a learning disability. Another study that attempted to differentiate the effects of general malnutrition from the specific effects of the chloride deficiency in the genesis of the cognitive dysfunction appeared to demonstrate a role for the latter.iz6 Results of a questionnaire study suggested an increased incidence of learning disabilities but was difficult to interpret as there were no control subjects and the authors relied on reports in the literature to estimate the community incidence of school bias in and learning problems. lz7 An additional this study was a selected patient population that was obtained through a parent advocacy organization. The Centers for Disease Control has an ongoing follow-up study of children who had been exposed to chloride-deficient formulas as infants. Eighteen children were evaluated at 2 years and then again at the age of 4 years.lz8 Those children who received no nutritional supplementation demonstrated a negative dose-response effect when the duration of time on the formula was compared to the score on standardized cognitive testing. Clinical data, other than the number of weeks of exclusive use of the formula, were not analyzed and not correlated with the results. A second study investigated 42 children who had used the deficient formulas and 66 control children.lz9 The mean age of the children was 7.8 years. Initial analysis of the results obtained on the McCarthy Scales of Children’s Abilities showed a statistically significant decrease only in the quantitative score in the group fed the deficient formula. Reanalysis of adjusted difference between the subjects and the control children also showed a 4.86-point decrease in the general cognitive index, which was statistically significant. The clinical significance of this difference is not clear, however. Neither Centers for Disease Control study included in the analysis the metabolic status of the child while ingesting the formula. This may be the critical factor, as it now appears that in the absence of documented hypochloremic alkalosis there are no definable long-term adverse effects on cognitive development. i3’ The authors stated that follow-up of children who had documented metabolic impairment is in progress.

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Bacterial Meningitis Delayed diagnosis of bacterial meningitis is a common cause of malpractice claims.’ As in any suit involving an allegation of medical negligence, the plaintiff must demonstrate that the physician’s actions did not meet the appropriate standard of care and that the deviation was the cause of the injury to the child. The natural history of bacterial meningitis must be understood to permit evaluation of the role, if any, of the delay in diagnosis. Long-term follow-up of 185 infants and children who had bacterial meningitis demonstrated that 37% had neurologic abnormalities 1 month after the illness. i3i Many of the deficits resolved. On further follow-up, 10% had sensorineural hearing loss, 7% had afebrile seizures, and 4% had multiple neurologic abnormalities. Epilepsy was found most frequently in the children with abnormal findings on neurologic examinations. In another study, 97 school-age children who had Hemophilus influenzae meningitis were evaluated and compared to sibling controls.132 Acute neurologic complications occurred in 58% of the patients but on follow-up only 14% had abnormalities. Sensorineural hearing loss was present in 11%; 2 patients had a seizure disorder and 1 had hemiplegia and mental retardation. Low socioeconomic status and a low cerebrospinal fluid-blood ratio for glucose were associated with the presence of residua. Delayed clearance of bacteria from the cerebrospinal fluid increases the risk of an adverse outcome133 while the presence of subdural effusions does not.134 Academic achievement was assessed in a group of 23 children, aged 10 to 12 years, after treatment of H. infltrenzue meningitis. 135The children with meningitis were compared to control subjects, and scored in the average range on all measures of academic performance. Minor areas of weakness were found in some reading skills, but the children’s parents spent more time helping them and the children were able to perform satisfactorily in school. Because of the high incidence of sensorineural deafness following meningitis, the question of the risk of this disability related to the rapidity with which the diagnosis was made and treatment was instituted was examined. Information now available documents that hearing loss occurs early in the course of meningitis, is independent of the specific antibiotics used, and is not prevented by early treatment.136, 137 Improvement in the degree of hearing loss may also occur over a period of time.138 Because of the high risk of sensorineural hearing loss following meningitis, it is appropriate to obtain evaluation of the child’s hearing at the time of hospital discharge or soon after.

Minor Closed Head Trauma Penetrating head wounds and severe closed head injury followed by coma are major causes of neurologic disability in children and especially in adolescents.139, i4’ An important issue that arises in the medical-legal context is that of sequelae resulting from minor head trauma. A l-month follow-up of 321 children with minor head injury demonstrated few physical abnormalities; 6.9% of the children had headaches and only 1% or fewer had any other physical complaints. i41 There was an increased incidence of behavior problems, compared to the normal population, that was thought to have been the result of parental overreaction. A British study of 114 children showed that children with head injuries were identical to the normal population in all respects except for the teacher’s report of hyperactivity.i4’ After control for hyperactivity at age 5, the increase in hyperactivity was small, amounting to only 0.4 standard deviation. There is evidence that functional morbidity following minor head injuries is related to parental anxiety and can be lessened by focusing on the minor nature of the injury and the need for the children to return to their usual routine.143 Skull roentgenograms and CT scans of the brain have become almost routine for all children seen in emergency rooms with a history of head trauma. This is another example of the practice of defensive medicine. The finding of a skull fracture in a child who does not have any clinical evidence of intracranial injury is rare, and the presence of a fracture will not usually modify clinical decision making, treatment, or prognosis. 144 Although parietal skull fractures are associated frequently with intracranial complications, it is the patients who have clinical signs of neurologic dysfunction who have serious injuries and who have abnormalities on CT scans of the head.145 Clinical features in patients without skull fractures can also be used to predict, with a high rate of accuracy, those patients who will have abnormalities demonstrated on CT scans of the head.146 No patient with mild or moderate head trauma had an abnormality on the CT scan. Patients with abnormal clinical signs, however, had a high probability of having an abnormality demonstrated, even with a Glasgow coma score of 12 or greater.

Hydrocephalus The data from the State Volunteer Mutual Insurance Company in Tennessee indicate that there were several claims related to either failure of early diagnosis of hydrocephalus or delayed treatment of shunt malfunction. The infant with hydrocephalus, especially

early in the evolution of the problem, may have no clinical signs except for a head circumference that is growing at an accelerated rate and changing percentiles. The most accurate method of monitoring head growth is to record the occipital-frontal circumference at every visit and to plot the measurement on a standard head growth chart. If there is any suspicion that head growth is too rapid, ultrasonography is a rapid, noninvasive method of assessing ventricular size, and is useful in any child with an open fontanel. 147 Shunt malfunction may be acute, in which case it presents with headache, vomiting, and progressive obtundation. In some patients the rise in intracranial pressure may be more insidious; one diagnostic clue is a return to an accelerated rate of head growth. This is noted most easily by plotting the head circumference on a growth chart. One possible complication of shunt malfunction is permanent visual 10~s.~~~

Intracranial Neoplasms Delayed diagnosis of brain tumors in children is a problem, as one study documented that only 38% of primary brain tumors were diagnosed within 1 month of the onset of symptoms.‘49 The most common symptoms in children from birth to 5 years old were gait disturbances and ataxia while in the 6- to lo- and ll- to 20-year-old groups, headache, nausea, and vomiting were the chief complaints. The evaluation of headaches in children presents a dilemma to the physician. By the age of 7 years, 40% of children will have had complaints of headache.isO Three fourths of all children will have headaches by the time they are 15 years old, and 5.3% will have severe headaches that are probably migrainous. It is clearly inefficient and inappropriate to obtain a CT or MRI scan in every child with a headache. A number of clinical clues are useful and should raise the suspicion that a tumor might be present.151 These include the onset of a neurologic abnormality, including papilledema or loss of vision, vomiting in association with headaches, a change in the character of the headache, and headaches that awaken the child from sleep or are present in the morning. Suspicion of a tumor should also be raised when any child younger than 3 years or a child with neurofibromatosis or tuberous sclerosis has headaches. The symptoms associated with midline tumors are less well known to the pediatrician. These include visual loss, endocrine dysfunction, especially secondary growth failure, changes in appetite, and precocious puberty in males; personality change; and increased intracranial pressure without localiz-

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ing neurologic signs.r5* Diabetes insipidus may also become evident. Height, weight, and head circumference should continue to be monitored and plotted on standard charts throughout childhood. This may provide the first clue of a change in the child’s growth rate. Unfortunately, visual function is difficult to assess in young children, and there may be significant visual loss before it can be detected clinitally .

Risk Reduction The medical dictum that prevention is always better than treatment holds also for medical-legal issues. Prevention strategies begin with an understanding of the clinical issues involved in a specific case and the pitfalls that lie in the path of diagnosis and treatment. This article has attempted to outline information in the literature that may be useful in fostering this understanding. An error in diagnosis and treatment is a necessary ingredient of a successful medical-legal claim against the physician. Not all such misadventures trigger lawsuits, however, and there is good evidence that the relationship between the family and the physician, and the degree to which communications are timely, accurate, and honest are factors that impinge on the course of action taken by the family. Technical issues, such as complete and accurate record keeping, will not prevent a claim from being made, but will be of great importance in the development of an adequate defense. There are several guides which can help the physician develop personal and office practices that will reduce risk and be valuable in the defense of any claim made.153, 154

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Medical-legal aspects of neurologic problems.

Medical-Legal Neurologic Aspects of Problems Gerald S. Golden, M.D. Introduction Medical-legal issues have intruded into medical practice in a numb...
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