the infant of drug dependent mother ma. teresa c. ambat, md ttuhsc-neonatology 9/12/2008
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The Infant of Drug Dependent Mother
Ma. Teresa C. Ambat, MDTTUHSC-Neonatology9/12/2008
Objectives Describe strategies how to identify neonates in whom
substance abuse is suspected Recognize perinatal and long term complications
associated with fetal exposure to major drugs of abuse Recognize signs and symptoms of neonatal abstinence
syndrome Identify treatment strategies for NAS
Question1. The National Household Survey on Drug Abuse: indicated that
45% of women of childbearing age in the United States have used an illicit drug over their lifetime. Of the following, the annual estimate of prenatal exposure to a substance of abuse is highest for:
A. AlcoholB. MarijuanaC. NicotineD. CocaineE. Heroin
Epidemiology Prevalence of gestational use of drugs of abuse varies
ranges from 1% to 27%
Significant number remain regular users, even in the third trimester Tobacco [19.8%], Ethanol [13%], cannabis [9.3%], cocaine
[10%], heroin [1%])
Identification of substance use Maternal self-reports, and few confounders
Identify medical, obstetric, and behavior patterns suggestive of substance use
Obtain history of past and present substance use in a nonjudgmental manner
Questions limited to frequency and amount of specific substances
Patterns suggestive of substance use
Identification of substance use Maternal interview usually underestimates the extent of
exposure
Rates of alcohol and illicit drug use varied with the use of different validated screening instruments: MAST, CAGE, T-ACE
Physicians’ records yielded the lowest prevalence estimates suggesting lack of attention devoted to addiction disorders
Question2. The duration of time for detecting a drug of abuse in the
maternal urine varies, depending on the time of intake, dose and mode of administration, and metabolism of the drug. Of the following, the duration of time after birth for the detection of a drug of abuse in the maternal urine is longest for:
A. AmphetamineB. BenzodiazepineC. MethadoneD. OpiateE. Marijuana
Identification of substance use Indication for toxicology screening
Self-reporting of substance use Multiple characteristics suggesting substance use Compliance requirements with treatment recommendations
Urine is the preferred source for drug testing - easily available and in large quantities
Most substances are measurable in urine for < 72 hours after use, except for marijuana
Identification of substance useTime interval before drug elimination in urine
Drug Detectable in urine
Alcohol <24h
Amphetamines <48h
Barbiturates: Short acting
Long acting
<48h
<7days
Benzodiazepines <72h
Cocaine <72h
Marijuna: Single use
Chronic use
<72h
<30days
Opiates: Morphine, Heroin
Methadone
<48h
<96h
Question3. Various matrices for the detection of fetal exposure to drugs
of abuse have been developed and tested for their sensitivities and specificities. Of the following, the matrix that is most sensitive for the detection of fetal exposure to benzoylecgonine is neonatal:
A. BloodB. Gastric aspirateC. HairD. MeconiumE. Urine
Question4. Testing of neonatal meconium for a drug of abuse depends
on deposition of the drug into the meconium that begins at the commencement of fetal swallowing and continues until after delivery. Of the following, the earliest gestational age at which exposure to cocaine has been detected in meconium in a fetus is:
A. 12 weeksB. 16 weeksC. 20 weeksD. 24 weeksE. E. 28 weeks.
Identification of substance use Meconium testing 93% sensitive (82% PPV) compared
with combined maternal and neonatal urine testing
Meconium and hair analyses - highest sensitivities in detecting use of cocaine and opiates (80-100%),but not cannabis (20%)
Fetal exposure to cocaine detected by meconium testing was documented as early as 16 wks
Other matrices: hair and nail, blood/cord blood, amniotic fluid
Identification of substance use
Perinatal pharmacology Any substance unbound to proteins passes freely from the
maternal compartment placenta fetal compartment
Concentrations in the fetal circulation > the maternal serum
Effects from any substance depend on the gestational timing and the extent of drug distribution
Toxic or teratogenic effects expressed as fetal demise, dysmorphism, growth restriction, or behavioral changes
Except for maternal alcohol, a birth defect syndrome has not been described for other illicit substances
Perinatal pharmacology Substances of abuse may be intentionally or
inadvertently taken at toxic doses
Difficult to ascribe specific effects to a certain drug due to impurity of most illicit drugs and use of multiple substances
Accurate evaluation of dosage and the exact period of exposure are rarely possible
Alcohol Alcohol use during pregnancy: 12.9%, binge drinkers:
4.6%
Difficult to assess by laboratory tests
Alcohol Ethanol - an anxiolytic analgesic with CNS
depressant effect
Impairs placental function Interferes with transport of AA Alters placental expression of EGF and PGF Inhibits DNA and protein synthesis Inhibits phospholipase A2, decreases PGI production,
increases HCG production
Complications of Fetal Alcohol Exposure
Antenatal Intrapartum Neonatal Long term
SAB
Aneuploidy
Stillbirth
Breech
IUGR
Abnormal HR pattern
fetal breathing, movement
Abruptio
Premature labor
Prematurity
LBW, SGA
Abstinence syndrome
FAS
FAE
Abnormal EEG
Post natal growth restriction
Low Bayley/Fagan scores
ADHD
Language problem
Behavior problem
Poor academic performance
Adolescent: difficulty in memory, calculation
Question5. Fetal alcohol syndrome is the leading identifiable
nonhereditary cause of mental retardation and neurologic deficit. Define the 3 specific criteria to qualify for a diagnosis of FAS.
A. growth retardationB. specific mid-facial features, C. non-specific developmental aberrations
Fetal Alcohol Syndrome FAS – leading identifiable nonhereditary cause of
mental retardation and neurologic deficit
Diagnostic criteria: 1. growth retardation, 2. specific mid-facial features, 3. non-specific developmental aberrations
Smooth philtrum, thin upper lip and short palpebral fissure – 100% sensitivity
Diagnostic criteria (FAS and Alcohol related effects
1. FAS + confirmed maternal alcohol exposureA. Confirmed maternal alcohol exposure
B. Characteristic facial anomalies: short palpebral fissures, flat upper lip, flat philtrum, flat midface
C. Growth restriction: LBW/SGA, decelerating weight over time not due to nutrition, disproportional weight to height
D. CNS neurodevelopmental anomalies: decreased HC at birth, structural brain anomalies, neurologic hard or soft signs (impaired fine motor skills, NSHL, poor tandem gait, poor eye-hand coordination)
Diagnostic criteria (FAS and Alcohol related effects
2. FAS without confirmed maternal alcohol exposure
B, C and D as above
3. Partial FAS + confirmed maternal alcohol exposureA. Confirmed maternal alcohol exposure
B. Some components of characteristic facial anomalies
C. C or D as above or
D. Evidence of complex pattern of behavior or cognitive anomalies inconsistent with developmental level and cannot be explained by familial background or environment alone
Diagnostic criteria (FAS and Alcohol related effects
4. Alcohol-Related Birth Defects (ARBD)A. Confirmed maternal alcohol exposure + 1 or more congenital
anomalies (Cardiac, skeletal, renal, ocular, auditory, others)
Every malformation has been described in patients with FAS.
Etiologic specificity to alcohol teratogenesis remains uncertain.
5. Alcohol-related neurologic disorder (ARND)A. Confirmed maternal exposure and D and or E
Tobacco Prevalence during pregnancy: 20%
Nicotine – primary psychoactive chemical
Central effects Binds to nicotinic Ach receptors release of neurotransmitters (Ach,
NE, GABA, glutamate) Dopamine release in mesolimbic dopaminergic pathway
Peripheral effects Releases epinephrine from adrenal cortex physiologic response
flight or fight reaction Suppresses insulin release hyperglycemia, affects appetite
Tobacco Fetal Effects
Poor maternal nutrition affects growth and development Nicotine a vasoconstrictor reduces placental blood flow
decreased fetal O2 hypoxia/ischemia CO + Hb carboxyhemoglobin hinder O2 delivery to
fetus
Nicotine readily crosses placental barrier Nicotine Ach receptors are present early in gestation
affecting brain development (neurotoxic)
Complications of Fetal Exposure to Tobacco
Fetal Intrapartum Neonatal Long termSAB
Stillbirth
Placental decidual necrosis
Abruptio
Premature labor
IUGR
CHD
Deformities of extremities, polycsyctic kidneys, gastroschisis, skull deformities
PPHN
Low test scores (cognitive, language, general academic achievement)
Conduct disorder
Adolescent-onset drug dependence
SIDS
Marijuana Dried material from hemp plant, Cannabis sativa
Smoked in cigarette or pipe passes rapidly into blood rapid high
-9-tetrahydrocannabinol (THC) - primary psychoactive component
THC binds to cannabinoid receptors (CB1) modify release of neurotransmitters
Marijuana Fetal and Neonatal Effects
THC crosses placenta easily and present in amniotic fluid High lipid solubility, slow elimination prolonged fetal
exposure
Cannabinoid receptors present in early gestation modify neurotransmitters (serotonin, dopamine, GABA) altered neuronal growth, maturation and differentiation structural or functional abnormalities
Impact generally subtle, adverse outcomes usually associated with heavy or frequent use
Question6. Children who have been exposed prenatally to substances of
abuse may have physical deformities as well as neurodevelopmental deficits. Of the following, the substance of abuse most associated with intestinal atresia, infarction and necrotizing enterocolitis is:
A. AlcoholB. HeroinC. MarijuanaD. CocaineE. Nicotine.
Complications of Fetal Exposure to Marijuana
Antenatal Intrapartum Neonatal Long term
Precipitous or dysfunctional labor
Meconium stained AF
Prematurity Fine tremors
Disrupted sleep
Poor abstract, visual reasoning, Poor memory and verbal skills
Poor motor skills
Abnormal attention behavior
Small risk for SIDS
Cocaine Alkaloid extracted from leaves of Erythroxylon coca
bush Chemical name: methylbenzoylecgonine
Forms Coca paste – 1st extraction product, 80% cocaine Cocaine HCl – powder soluble in water, can be snorted and
injected Alkaloidal base (free-basing) Crack cocaine – most popular abused form
Cocaine - Pharmacology Affects 3 neurotransmitters: norepinephrine,
dopamine, serotonin
Inhibits reuptake of NE, D accumulation at synapse prolonged stimulation of receptors NE stimulation: tachycardia, HTN, diaphoresis, tremors
Dopamine stimulation: increased alertness, euphoria, enhanced feeling of well-being, sexual excitement, heightened energy
Cocaine - Pharmacology Decreases reuptake of tryptophan affecting
serotonin biosynthesis
Dec serotonin: decreased need for sleep (serotonin regulates sleep-wake cycle)
Cocaine-Pharmacology Low molecular weight, high lipid solubility crosses
placenta by simple diffusion
Elimination of cocaine and metabolites slow increased fetal toxicity
Decreases placental perfusion
Congenital malformation not increased
Complications of Fetal Exposure to Cocaine
Antenatal Intrapartum Neonatal Long termStillbirth
Abortion
Inc uterine vascular resistance
Infection/STD Placental infarcts
IUGR
Abnormal fetal breathing
Abruptio
Premature labor
PROM
Shortened labor
Meconium stained amniotic fluid
PT, LBW, SGA
Small HC
Postnatal growth restriction
CNS: cerebral infarction, seizures, cortical atrophy, IVH
Abnormal EEG and BAER
NECIntestinal perforation
Expressive/ receptive language problem
Low verbal comprehension
Poor recognition, memory, info processing
visual attention
Behavior problem (distractibility, ADHD)
Amphetamines Methyphenyethylamine – stimulant of norepinephrine,
dopamine and serotonin release
Metamphetamine (meth, speed, ice, crystal) – N-methyl homologue of amphetamine Higher CNS stimulation, less PNS and cardiovascular
stimulation
Euphoria, aggressive behavior, arrhythmias, anxiety, seizures, shock, stroke, abdominal cramps, insomnia, death
Complications of Fetal Exposure to Amphetamines / Methamphetamines
Antenatal Intrapartum Neonatal Long termFetal death
Retroplacental hemorrhage
Prematurity
Neonatal death
Drug intoxication (abnormal sleep, tremors, poor feeding, hypertonia, sneezing, high-pitched cry, loose stools, fever, yawning, hyperreflexia, excoriation)
Dec IQ
Aggressive behavior/peer related problems
Poor academic performance
Club drugs Methylene-dioxymethamphetamine or MMDA (ecstasy) Gamma hydroxybutyrate (GHB) Ketamine hydrochloride
Used by young people during all-night dance parties Few data on fetal and neonatal effects One study indicated increased risk of congenital defects
(musculoskeletal, CVS)
Opioids Opiate or narcotic – any natural or synthetic drug
that has morphine like pharmacologic actions
Natural opiates – morphine, codeine
Synthetic opiates – heroin, methadone, propoxyphene, pentazocine, meperidine, oxycodon, hydromorphone, fentanyl
Neonatal Abstinence Syndrome Generally associated with withdrawal from heroin or
methadone Similar signs associated with other narcotics, alcohol,
benzodiazepines and barbiturates
Associated with noradrenergic hyperactivity CNS, respiratory, GI, vasomotor and cutaneous
systems manifestations CNS signs predominate and appear early
Neonatal Narcotic Withdrawal or Abstinence Syndrome Onset within 72 hrs (usually within 24-48 hrs)
Factors influencing onset: amount of narcotics, timing of the last dose before delivery, character of labor, type of analgesia/anesthesia, maturity and nutritional status of infant
Peaks by the 3rd day
Decreases in intensity by 5th – 7th day, but may not completely disappear until 8-16 weeks
Manifestations of Neonatal Narcotic Withdrawal CNS
Hyperactivity, hyperirritability, excessive crying, high-pitched cry, increased muscle tone, exaggerated reflexes, tremors, sneezing, hiccups, yawning, short, non-quiet sleep, fever
Respiratory Tachypnea, excess secretions
Manifestations of Neonatal Narcotic Withdrawal GI
Disorganized sucking, vomiting, drooling, sensitive gag, hyperphagia, diarrhea, abdominal cramps
Vasomotor system Stuffy nose, flushing, sweating, sudden circumoral pallor
Cutaneous Excoriated buttocks, scratches, pressure-point abrasions
Complications of Neonatal Narcotic Withdrawal Abnormalities in serum pH/electrolytes and dehydration Weight loss Aspiration pneumonia Respiratory alkalosis Convulsion
Mortality – 27/1000 LB Causes: immaturity, prematurity, HMD, MAS, PPHN,
congenital malformations
Non-narcotic Hypnosedatives Hypnosedatives
Barbiturates
Non-barbiturate sedatives/tranqulizers Bromide, Chloral hydrate, chlordiaxepoxide, diazepam,
ethchlorvynol, glutethimide, ethanol
Non-narcotic abstinence syndrome Passive addiction even with therapeutic doses (e.g.
phenobarbital)
Manifestations of withdrawal can be intense and life threatening
Convulsion more frequent
Observed 7-10 days after birth as a result of slow clearance
Question7. A 4 day old, SGA presented with generalized tonic, clonic
seizure. There was no prenatal care. On exam, he was found to be irritable, inconsolable, weak suck and swallow and uncoordinated. He was also noted to be hypertonic with tremors. What significant maternal history could have contributed to the above findings?
A. Use of amphetaminesB. Use of marijuanaC. Use of SSRI for depressionD. Maternal seizure disorderE. Use of cocaine
SSRI Prescribed for depression
Inhibits serotonin reuptake at presynaptoic junction increased concentrations at the synaptic cleft potentiates serotonergic transmission
No major birth defects Prenatal exposure and withdrawal associated with
neurobehavioral effects (behavioral changes, altered autonomic activity)
Diagnosis of Neonatal Abstinence Syndrome Scoring tools
Lipsitz scale Finnegan scale Neonatal abstinence score Score at first appearance of NAS symptoms then q3-4 hrs Specific to narcotic withdrawal
Differential diagnoses: hypoglycemia, hypocalcemia, hypomagnesemia, sepsis, meningitis
Treatment of NAS Supportive
Quiet, dimly lit environment, comfortable side lying position, swaddled
Nutrition and fluid and electrolyte balance IV fluids may be required
Pharmacotherapy Average scores >8 over 3 scoring intervals or >12 over 2
scoring intervals Goal: decreased irritability, feeding tolerance, sleeping bet
feeding without sedation
Treatment of NAS Diluted tincture of opium (DTO) – 0.4mg/ml morphine
equivalent Starting dose 0.1ml/kg (2 drops/kg) q4 hrs Increment of 2 drops/kg q3-4 hrs until desired effect Taper gradually after 3-5 days of stabilization
Phenobarbital 2nd line drug Anticonvulsant, NAS by sedatives or hypnotics
Paregoric Deleterious additives: camphor, ethanol, glycerin, benzoic acid,
isoquinolones
Other concerns Maternal support Breast feeding – generally discouraged if noncompliant Drug-dependent mothers as caregivers Social service referral Potential child abuse Follow-up
References Chasnoff IJ. Prenatal Substance Exposure: Maternal Screening
and Neonatal Identification and Management. NeoReviews 4 (9), 2003.
Chan D, Klein J, Koren G. New Methods for Neonatal Drug Screening. NeoReviews 4 (9), 2003.
Rayburn WF. Maternal and Fetal Effects from Substance Use. Clin Perinatol 34, 2007.
Ostrea EM. The infant of drug dependent mother.
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