NEONATOLOGY: MANAGEMENT, PROCEDURES, ON-CALL PROBLEMS, DISEASES, AND DRUGS - part 8 ppsx

3. Consumption of high-dose folic acid must be under a physician's supervision because there is still little information regarding its long-term effects and symptoms of pernicious anemia may be obscured, with the potential to result in serious neurologic damage. 4. Because 4 mg of folic acid did not prevent all NTDs in the MRC study, patients should be cautioned that folic acid supplementation does not preclude the need for counseling or consideration of prenatal testing for NTDs. C. The American Academy of Pediatrics Committee on Genetics has endorsed the U.S. Department of Health and Human Services (1992) recommendation, as follows: 1. All women of childbearing age (15-44 years) in the United States who are capable of becoming pregnant should consume 0.4 mg of folic acid per day for the purpose of reducing their risk of having a pregnancy affected by spina bifida or other NTDs. This amount of folic acid is estimated to reduce the NTD risk by 50-70%. This amount (0.4 mg) is also the US Recommended Daily Allowance of folic acid. 2. An intake of >1 mg is not generally recommended. 3. Folic acid should ideally be taken at least 1 month before conception and at least through the first month of gestation. D. Sources of folic acid 1. Dietary. The average diet in the United States contains 0.2 mg of folate, which is less bioavailable than folic acid. Folate intake of 0.4 mg/day can be achieved through careful selection of folate-rich foods (spinach and other leafy green vegetables, dried beans, peas, liver, and citrus fruits). Some breakfast cereals are fortified with folic acid. Since January 1998, enriched foods (including flour, cornmeal, pasta, and rice) are fortified in folic acid by order of the US Food and Drug Administration. 2. Supplementation. Folic acid is available over the counter in dosages up to 0.8 mg. Folic acid is also available by prescription in 1-mg tablets. Prenatal vitamins contain 0.8 or 1 mg of folic acid. A survey by the March of Dimes revealed that only 27% of nonpregnant women 18-45 years of age took a vitamin preparation containing folic acid in 2001. Awareness of the U.S. Public Health Service recommendation regarding folic acid did more than double from 1995 to 2002 (from 15 to 32%) for the same group. Multiple sources are available to provide educational material to the public (March of Dimes: 1-888-MODIMES or http://www.marchofdimes.org, http://www.cdc.gov, http://www.aap. org, http://www.acog.org). E. Current epidemiologic and biochemical evidence suggests that NTDs are not primarily due to folate insufficiency but rather arise from changes in the metabolism of folate and possibly B 12 in predisposed women. The mechanisms may also involve homocysteine metabolism. Polymorphisms of methylene tetrahydrofolate reductase and other genes encoding proteins involved in folate metabolism may be associated with an increased frequency of NTDs. Of further interest is that the homocysteine-lowering effect of folic acid supplementation may also reduce the risk for cardiovascular disease. F. Intestinal hydrolysis of dietary folate is not impaired in mothers who have had infants with NTDs, although the response curve to a folate-enriched meal appears to differ significantly from that of mothers who have not had infants with NTDs. V. Prenatal detection of NTDs A. Prenatal screen using maternal serum AFP at 14-16 weeks' gestation. Elevated levels (>2.5 multiples of the mean, which are adjusted to gestational age) are indicative of open NTDs at a sensitivity of 90-100%, a specificity of 96%, and a negative predictive value of 99-100% but a low positive predictive value. B. Prenatal diagnosis. Documentation of an elevated maternal serum AFP is followed by: 1. Genetic counseling. The physician needs to make sure that the patient receives information regarding her risk for NTDs and other conditions with elevated AFP (gastroschisis or other conditions leading to fetal skin defects), to evaluate causes of possible false-positive results (imprecise dates or twin pregnancies), to learn about options regarding further evaluation (see later discussion), and to provide nondirective counseling regarding treatment options. 2. Detailed fetal ultrasonography with anomaly screening. In skilled hands, a detailed ultrasonogram can be extremely sensitive and specific for detection of NTDs. Sonographic determination of the level of the lesion has been shown to be useful in predicting the ambulatory potential of fetuses with NTDs. Ultrasonography is also done to rule out other major congenital defects. 3. Measurement of the amniotic fluid AFP and acetylcholinesterase. Amniocentesis is usually done between 16 and 18 weeks' gestation, although it can technically be done as early as 14 weeks' gestation. If indicated, karyotype can also be obtained. The detection rate for anencephaly and open spina bifida is 100% when results of amniotic fluid acetylcholinesterase and AFP are combined, with a false-positive rate of only 0.04%. VI. Management: anencephaly A. Approximately 75% are stillborn, and most live-born infants with anencephaly die within the first 2 weeks of birth. B. Considering the 100% lethality of anencephaly, usually only supportive care is given: warmth, comfort, and enteral nutrition. Support services for the family, including social work and genetic and general counseling, are essential. There are some ethically controversial issues regarding the extent of care and other issues (eg, organ donation), and it may be advisable to involve other support systems (eg, ethics committees, support groups, or religious guidance [if desired by the family]). VII. Management: encephalocele A. Physical examination and initial management. In addition to the general principles of neonatal resuscitation, an especially careful physical examination is indicated. Look for associated malformations. As mentioned in Neural Tube Defects, section III,C, some genetic publications list up to 50 syndromes associated with NTDs. We recommend that the child be given nothing by mouth until the consultations by subspecialties such as neurosurgery and, if indicated, genetic tests are done and the need for immediate treatment (perhaps surgery) is assessed. Imaging studies (ultrasonography, CT, and MRI) should be arranged. B. Neurosurgical intervention may be indicated to prevent ulceration and infection, except in those cases with massive lesions and marked microcephaly. The encephalocele and its contents are often excised because the brain tissue within is frequently infarcted and distorted. Surgery may be deferred, depending on the size, skin coverage, and location. Ventriculoperitoneal shunt (VP) placement may be required because as many as 50% of cases have secondary hydrocephalus. C. Counseling and long-term outcome. A multidisciplinary approach is necessary to counsel the family regarding recurrence risk, long-term outcome, and follow-up. The family should be informed about the availability of support groups (March of Dimes and others; March of Dimes Birth Defect Foundation can be reached at 1-888-MODIMES). The degree of developmental deficits is determined mainly by the extent of herniation and location; cerebral hemispheres from both sides or one side, the cerebellum, and even the brainstem can be involved. Visual deficits are common with occipital encephaloceles. Motor and intellectual deficits are found in ~50% of patients. VIII. Management: myelomeningocele. Although fetal surgery for NTDs remains controversial, many maternal-fetal specialists believe that this option should be mentioned to parents. After birth, a multidisciplinary team approach, including the primary care physician, geneticist, genetic counselor, neonatologist, urologist, neurosurgeon, orthopedic surgeon, and social worker, is necessary. A. Physical examination should include careful evaluation for other malformations (see section VII,A). In addition, special efforts should be made to correlate motor, sensory, and sphincter function and reflexes to the functional level of lesion (Table 72-2). 1. Extent of neurologic dysfunction correlates with the level of the spinal cord lesion. 2. Paraplegia below the level of the defect. 3. The presence of the anal wink and anal sphincter tone suggests functioning sacral spinal segments and is prognostically important. In one study, 90% of patients with a positive anocutaneous reflex were determined to be "dry" on a regimen of intermittent catheterization as opposed to 50% of those with a negative reflex. B. Initial management. In addition to following the general principles of neonatal resuscitation and newborn care, appropriate management of the spinal lesion is essential. 1. There are institutional differences in the specifics of how to cover the lesion, and provision of a sterile cover can be achieved by several means. Some surgeons do prefer to have only a sterile plastic material or wrap applied to the lesion and ask to avoid contact with gauze or other material that could adhere to the tissue and result in mechanical damage when removed. It is advisable to try to keep the defective area moist while avoiding bacterial contamination. If tolerated, the patient should be positioned on the side. TABLE 72-1. CAUSES OF NEONATAL SEIZURES Perinatal asphyxia Intracranial hemorrhage Subarachnoid hemorrhage Periventricular or intraventricular hemorrhage Subdural hemorrhage Metabolic abnormalities Hypoglycemia Hypocalcemia Electrolyte disturbances: hypo- and hypernatremia Amino acid disorders Congenital malformations Infections Meningitis Encephalitis Syphilis, cytomegalovirus infections, toxoplasmosis Cerebral abscess Drug withdrawal Toxin exposure (particular local anesthetics) Inherited seizure disorders Benign familial epilepsy Tuberous sclerosis Zellweger syndrome Pyridoxine dependency TABLE 72-2. CORRELATION AMONG LEVEL OF MYELOMENINGOCELE, LEVEL OF CUTANEOUS SENSATION, SPHINCTER FUNCTION, REFLEXES, AND POTENTIAL FOR AMBULATION Level of lesion Innervation Cutaneous sensation (pinprick) Sphincter function Reflexes Ambulation potential Thoracolumbar T12-L2 Groin (L1) Anterior upper thigh (L2)     Full braces Wheelchair bound Lumbar L3-L4 Anterior lower thigh and knee (L3) Medial leg (L4)  Knee jerk May ambulate with braces and crutches Lumbosacral L5-S1 Lateral leg and medial foot (L5) Sole of foot (S1)  Ankle jerk May ambulate with or without short leg braces Sacral S2-S4 Posterior leg and thigh (S2) Middle of buttock (S3) Medial buttock (S4) Bladder and rectal function Anal wink May ambulate without braces Voluntary muscle movements are difficult to elicit in newborns with myelomeningocele and are, therefore, not helpful during initial evaluation. Furthermore, motor examination may be distorted initially by reversible spinal cord dysfunction above the level of the actual defect induced by exposure of the open cord. 2. Be aware that a high rate of latex allergies has been reported in patients with NTDs. In some centers, all patients with myelodysplasia are, therefore, considered at risk for anaphylaxis and other allergic complications, and latex avoidance is practiced as a preventive protocol. One study showed that after 6 years of a latex-free environment the prevalence of latex sensitization fell from 26.7% to 4.5% of children with spina bifida. 3. In most centers, patients are started on antibiotics (ampicillin and gentamicin) and are given nothing by mouth. 4. Arrange for imaging studies to evaluate for hydrocephalus or other malformations detected or suspected on physical examination. C. Surgical management. Usually, closure of the back lesion is done within 24 or 48 h to prevent infection and further loss of function. D. Hydrocephalus is common and often noncommunicative secondary to Arnold-Chiari malformation of the foramen magnum and upper cervical canal (usually type II), with resultant downward displacement of the medulla, pons, and cerebellum and obstruction of CSF flow. 1. The risk of hydrocephalus is 95% for infants with thoracolumbar, lumbar, and lumbosacral lesions and 63% for those with occipital, cervical, thoracic, or sacral lesions. 2. In most cases, hydrocephalus is not evident until after closure of the myelomeningocele, and placement of a VP shunt may be required at a later date. 3. Aggressive treatment with early VP shunt placement may improve cognitive function. 4. Serial ultrasound scans are necessary to monitor progression of hydrocephalus because ventricular dilation may occur without rapid head growth or signs of increased ICP. The hydrocephalus usually becomes clinically overt 2-3 weeks after birth. 5. Despite treatment of the myelomeningocele and hydrocephalus, ~50% of these infants may still succumb to death from aspiration, laryngeal stridor, and apnea attributable to the hindbrain anomaly. E. Urinary tract dysfunction is one of the major causes of morbidity and mortality after the first year of life. 1. More than 85% of myelomeningoceles located above S2 are associated with neurogenic bladder dysfunction, with urinary incontinence and ureteral reflux. Poor bladder emptying immediately after NTD closure may be temporary ("spinal shock"), and improvement of bladder function may be observed up to 6 weeks after repair. 2. Without proper management, hydronephrosis develops with progressive scarring and destruction of the kidneys. Many of these infants succumb to urosepsis. 3. Renal ultrasonography and a voiding cystourethrogram may identify patients who could benefit from anticholinergic medication, clean and intermittent catheterization, prophylactic antibiotics, or early surgical intervention of the urinary tract. 4. Other associated renal anomalies include renal agenesis, horseshoe kidney, and ureteral duplications. F. Orthopedic complications 1. The lower extremities lack innervation and become atrophied. 2. Deformities of the foot, knee, hip, and spine are common as a result of muscle imbalance, abnormal in utero positioning, or teratologic factors. 3. Hip dislocation or subluxation is usually evident within the first year of life, especially in patients with midlumbar myelomeningocele. 4. Treatment of orthopedic abnormalities be instituted as soon as there is sufficient healing of the back wound. 5. Physical therapists assist with proper positioning of the extremities to minimize contractures and to maximize function. G. Outcome of aggressive therapy 1. The overall mortality rate is now <15% by 3-7 years of age. One study revealed a survival rate of infants with spina bifida of 87.2% for the first year. In multivariable analysis, factors associated with increased mortality were low birth weight and high lesions. 2. Infants with sacral lesions have essentially no mortality. 3. The outcome in regard to the highest potential for ambulation depends largely on the level of the original lesion (see Table 72-2) and is modified by the orthopedic treatment and complications (see section VIII,F). 4. The majority of children with lumbar myelomeningocele score within the normal range on intelligence and achievement tests, with the greatest and possibly progressive deficits on performance IQ, arithmetic achievement, and visuomotor integration, while keeping pace on reading and spelling. 5. An IQ >80 is found in essentially all patients with lesions below S1. 6. Approximately 50% of survivors with thoracolumbar lesions have IQ >80. 7. Cognitive function is improved in the presence of favorable socioeconomic and environmental factors. IX. Management: spina bifida occulta A. Neonatal features. The presence of spina bifida occulta is suggested by overlying abnormal collections of hair, hemangioma, pigmented macule, aplasia cutis congenita, skin tag, subcutaneous mass, cutaneous dimples, or tracts. B. If undetected in the neonatal period, clinical presentation later in infancy includes the following: 1. Delay in development of sphincter control. 2. Delay in walking. 3. Development of a foot deformity. 4. Recurrent meningitis. 5. A sudden deterioration may represent vascular insufficiency produced by tension on a tethered cord, angulation of the cord around fibrous or related structures, or cord compression from a tumor or cyst. C. Diagnosis 1. Ultrasonography is useful for screening. 2. MRI provides superior anatomic details. The advantages of MRI are that contrast is not needed and the infants are not exposed to radiation. D. Surgical correction may be necessary in the newborn period to avoid the onset of symptoms. Surgical release of a tethered cord or decompression of the spinal cord within 48 h of sudden deterioration may completely or partially reverse recently acquired deficits. REFERENCES Agarwal SK et al: Outcome analysis of vesicoureteral reflux in children with myelodysplasia. J Urol 1997;157:980. Anderson GD et al: The effect of cesarean section on intraventricular hemorrhage in the preterm infant. Am J Obstet Gynecol 1992;166:1091. Aziz K et al: Province-based study of neurologic disability of children weighing 500 through 1249 grams at birth in relation to neonatal cerebral ultrasound findings. Pediatrics 1995;95:837. Batton DG et al: Current gestational age-related incidence of major intraventricular hemorrhage. J Pediatr 1994;125:623. Bender J: Parental occupation and neural tube defect-affected pregnancies among Mexican Americans. J Occup Environ Med 2002;44:650. Bernes SM, Kaplan AM: Evolution of neonatal seizures. Pediatr Clin North Am 1994;41:1069. Biggio et al: Can prenatal ultrasound findings predict the ambulatory status in fetuses with open spina bifida? Am J Obstet Gynecol 2001;185:1016. Birmingham PK et al: Do latex precautions in children with myelodysplasia reduce intraoperative allergic reactions? J Pediatr Orthop 1996;16:799. Bluml S et al: Differentiation between cortical atrophy and hydrocephalus using 1 H MRS. Magn Reson Med 1997;37:395. Bower C et al: Absorption of pteroylpolyglutamates in mothers of infants with neural tube defects. Br J Nutr 1993a;69:827. Bower C et al: Maternal folate status and the risk for neural tube defects. The role of dietary folate. Ann NY Acad Sci 1993b;678:146. Brock DJH et al: Prenatal diagnosis of neural tube defects with monoclonal antibody specific for acetylcholinesterase. Lancet 1985;21:5. Centers for Disease Control and Prevention: Economic costs of birth defects and cerebral palsyUnited States, 1992. MMWR Morb Mortal Wkly Rep 1995;44:694. Centers for Disease Control and Prevention: Knowledge and use of folic acid by women of childbearing ageUnited States, 1997. MMWR Morb Mortal Wkly Rep 1997;46:721. Clark RH et al: Intraventricular hemorrhage and high-frequency ventilation: a meta-analysis of prospective clinical trials. Pediatrics 1996;98:1058. Committee on Genetics: Folic acid for the prevention of neural tube defects. Pediatrics 1993; 92:493. Dansky LV et al: Mechanisms of teratogenesis: folic acid and antiepileptic therapy. Neurology 1992;42(suppl 5):32. Dimmick JE, Kalousek DK: Developmental Pathology of the Embryo & Fetus. Lippincott, 1992. Donn SM et al: Prevention of intraventricular hemorrhage with phenobarbital therapy: Now what? Pediatrics 1986;77:779. Dykes FD et al: Intraventricular hemorrhage: a prospective evaluation of etiopathogenesis. Pediatrics 1980;66:42. Dykes FD et al: Posthemorrhagic hydrocephalus in high-risk preterm infants: natural history, management and long-term outcome. J Pediatr 1989;114:611. Fohr IP et al: 5,10-Methylentetrahydrofolate reductase genotype determines the plasma homocysteine lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr 2002;75:275. Fraser RK et al: The unstable hip and mid-lumbar myelomeningocele. J Bone Joint Surg 1992; 74:143. Garland JS et al: Effect of maternal glucocorticoid exposure on risk of severe intraventricular hemorrhage in surfactant-treated preterm infants. J Pediatr 1995;126:272. Gilman JT et al: Rapid sequential phenobarbital treatment of neonatal seizures. Pediatrics 1989; 83:674. Glick PL et al: Management of ventriculomegaly in the fetus. J Pediatr 1984;105:97. Goh D, Minns RA: Intracranial pressure and cerebral arterial flow velocity indices in childhood hydrocephalus: current review. Child Nerv Syst 1995;11:392. Green DW et al: Nucleated erythrocytes and intraventricular hemorrhage in preterm neonates. Pediatrics 1995;96:475. Greitz D et al: A new view on the CSF-circulation with the potential for pharmacological treatment of childhood hydrocephalus. Acta Paediatr 1997;86:125. Hanlo PW et al: Relationship between anterior fontanelle pressure measurements and clinical signs in infantile hydrocephalus. Child Nerv Syst 1996;12:200. Horbar JD: Prevention of periventricular-intraventricular hemorrhage. In Sinclair J, Bracken MB (eds): Effective Care of the Newborn Infant. Oxford University Press, 1992. Hudgins RJ et al: Natural history of fetal ventriculomegaly. Pediatrics 1988;82:692. Hudgins RJ et al: Treatment of intraventricular hemorrhage in the premature infant with urokinase. Pediatr Neurosurg 1994;20:190. Kaempf JW et al: Antenatal phenobarbital for the prevention of periventricular and intraventricular hemorrhage: a double-blind, randomized, placebo-controlled, multihospital trial. J Pediatr 1990;117:933. Laurence KM et al: Double blind randomized controlled trial of folate treatment before conception to prevent recurrence of neural tube defects. BMJ 1981;282:1509. Lazzara A et al: Clinical predictability of intraventricular hemorrhage in preterm infants. Pediatrics 1980;65:30. Lemire RJ: Neural tube defects: clinical correlations. Clin Neurosurg 1983;30:165. Lemire RJ et al: Neural tube defects. JAMA 1988;259:558. Leviton A, Gilles F: Ventriculomegaly, delayed myelination, white matter hypoplasia, and "periventricular" leukomalacia: how are they related? Pediatr Neurol 1996;15:127. Leviton A et al: Antenatal corticosteroids appear to reduce the risk of postnatal germinal matrix hemorrhage in intubated low birth weight newborns. Pediatrics 1993;91:1083. Lott JW et al: Umbilical artery catheter blood sampling alters cerebral blood flow velocity in preterm infants. J Perinatol 1996;15:341. Main DM, Mennuti MT: Neural tube defects: issues in prenatal diagnosis and counseling. Obstet Gynecol 1986;67:1. March of Dimes and the Gallop Organization: Folic Acid and the Prevention of Birth Defects. A National Survey of Pre-pregnancy Awareness and Behavior Among Women of Childbearing Age 1995-2001. March of Dimes, 2001. Massager N et al: Anterior fontanelle pressure monitoring for the evaluation of asymptomatic infants with increased head growth rate. Child Nerv Syst 1996;12:38. McCullough DC, Balzer-Martin LA: Current prognosis in overt neonatal hydrocephalus. J Neurosurg 1982;57:378. Medical Research Council Vitamin Study Research Group: Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 1991;338:131. Meeropol E et al: Allergic reaction to rubber in patients with myelodysplasia. N Engl J Med 1990;323:1072. Ment LR et al: Antenatal steroids, delivery mode, and intraventricular hemorrhage in preterm infants. Am J Obstet Gynecol 1995;172:795. Ment LR et al: Low-dose indomethacin and prevention of intraventricular hemorrhage: a multicenter randomized trial. Pediatrics 1994a;93:543. Ment LR et al: Low-dose indomethacin therapy and extension of intraventricular hemorrhage: a multicenter randomized trial. J Pediatr 1994b;124:951. Ment LR et al: Neurodevelopmental outcome at 36 months' corrected age of preterm infants in the multicenter indomethacin intraventricular hemorrhage prevention trial. Pediatrics 1996; 98:714. Michejda M et al: Present status of intrauterine treatment of hydrocephalus and its future. Am J Obstet Gynecol 1986;155:873. Mills JL, Raymond E: Effects of recent research on recommendations for periconceptional folate supplement use. Ann NY Acad Sci 1993;678:137. Morrow JD, Wachs TD: Infants with myelomeningocele: visual recognition memory and [...]... Pediatrics 19 98; 102 :88 5 Hall RT et al: High-dose phenobarbital therapy in term newborn infants with severe perinatal asphyxia: a randomized prospective study with three-year follow-up J Pediatr 19 98; 132:345 Harbord MG, Weston PF: Somatosensory evoked potentials predict neurologic outcome in full-term neonates with asphyxia J Paediatr Child Health 1995;31:1 48 Hull J, Dodd KL: Falling incidence of hypoxic-ischemic... cases of spina bifida and other neural tube defects MMWR Morb Mortal Wkly Rep 1992;41(RR-14):1 Resch B et al: Neurodevelopmental outcome of hydrocephalus following intra-/periventricular hemorrhage in preterm infants: short- and long-term results Child Nerv Syst 1996;12:27 Robbin M et al: Elevated levels of amniotic fluid α-fetoprotein: sonographic evaluation Radiology 1993; 188 :165 Rodgers WB et al:... Intraventricular hemorrhage in preterm infants: declining incidence in the 1 980 s Pediatrics 1 989 ;84 :797 Poland RL: Vitamin E for prevention of perinatal intracranial hemorrhage Pediatrics 1990 ;85 : 86 5 Rasmussen AG et al: A comparison of amniotic fluid alpha-fetoprotein and acetylcholinesterase in the prenatal diagnosis of open neural tube defects and anterior abdominal wall defects Prenat Diagn 1993;13:93 Recommendations... patterns that vary with PCA: at 2 6-3 2 weeks, the lateral thalami are primarily affected; at 3 4-3 6 weeks, the lentiform nucleus and hippocampus and the perirolandic cortex are affected; and by 40 weeks, the corticospinal tracts from the internal capsule to the perirolandic cortex are affected More severe or prolonged events result in injury to the optic radiations 8 MRI demonstrates the structural sequelae... excitation of the N-methyl-D- aspartate type of glutamate receptors and competitively blocks Ca2+ entry through voltage-dependent Ca2+ channels during hypoxia Apnea may occur, and higher doses carry a significant risk of hypotension Use of magnesium sulfate (MgSO4) remains controversial 2 Prevention of free radical formation a Xanthine oxidase inhibitor In a pilot study (Van Bel et al, 19 98) , allopurinol... acuity scores and smaller visual fields B Nondisabled survivors of moderate HIE have delayed skills in reading, spelling, or arithmetic and have more difficulties with attention and short-term recall than survivors of mild HIE and normal individuals X Ethics Decision making is often difficult, but it is easier if the medical team and families communicate openly and clearly (See also Chapters 15 and 32.)... a partnership between parents and the physician and potentially reduces conflicts Discussing best- and worst-case outcomes may help to define the range of potential outcome XI Medicolegal issues A Fetal monitoring In the presence of a reactive FHR pattern and normal fetal movement, the key is to monitor the baseline rate (Phelan & Kim, 2000) A rise or fall in FHR baseline should alert the labor and. .. Pediatr 19 98; 132:619 Clancy RR et al: Hypoxic-ischemic spinal cord injury following perinatal asphyxia Ann Neurol 1 989 ;25: 185 Cordes I et al: Early prediction of the development of microcephaly after hypoxic-ischemic encephalopathy in the full-term newborn Pediatrics 1994;93:703 Eken P et al: Predictive value of early neuroimaging, pulsed Doppler and neurophysiology in full term infants with hypoxic-ischaemic... caused by hypoxia resulting in neurologic injury or by inappropriate intrapartum management II Incidence of asphyxia and its relationship to CP The incidence of HIE is 2-9 in 1000 live term births The incidence of CP has not fallen despite improved obstetric and neonatal interventions and remains at 1-2 in 1000 live term births Only 8- 1 7% of CP in term infants is associated with adverse perinatal events... phenotypically distinct neural tube defects among 0.7 million California births, 1 98 3-1 987 Teratology 1994;49:143 Shaw GM et al: Maternal periconceptional vitamin use, genetic variation of infant reduced folate carrier (A80G), and risk of spina bifida Am J Med Genet 2002;1 08: 1 Shaw GM et al: Risk of neural tube defect-affected pregnancies among obese women JAMA 1996;275:1093 Smithells RW et al: Further . of Dimes and others; March of Dimes Birth Defect Foundation can be reached at 1 -8 8 8- MODIMES). The degree of developmental deficits is determined mainly by the extent of herniation and location;. public (March of Dimes: 1 -8 8 8- MODIMES or http://www.marchofdimes.org, http://www.cdc.gov, http://www.aap. org, http://www.acog.org). E. Current epidemiologic and biochemical evidence suggests. diagnosis and counseling. Obstet Gynecol 1 986 ;67:1. March of Dimes and the Gallop Organization: Folic Acid and the Prevention of Birth Defects. A National Survey of Pre-pregnancy Awareness and