1 / 54

Parental Substance Abuse and Drug Endangered Children

Parental Substance Abuse and Drug Endangered Children. Walter F. Lambert, MD University of Miami Child Protection Team. Parent Produced Stressors. Low self-esteem Unmet emotional needs Abused as a child Depression Substance abuse Personality disorder or psychiatric illness

moswen
Download Presentation

Parental Substance Abuse and Drug Endangered Children

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Parental Substance Abuse and Drug Endangered Children Walter F. Lambert, MD University of Miami Child Protection Team

  2. Parent Produced Stressors • Low self-esteem • Unmet emotional needs • Abused as a child • Depression • Substance abuse • Personality disorder or psychiatric illness • Ignorance of child rearing-unrealistic expectations • Teenage pregnancy

  3. Triggering Situations • Discipline • Argument/family conflict • Substance Abuse • Acute environmental problem

  4. Drugs of Abuse • Alcohol • Tobacco • Marijuana • Heroin/Methadone • Cocaine • Methamphetamine

  5. Concepts • Exposure • Addiction • Direct effects on fetus/infant/child/adolescent • Effects of parental substance abuse • Reporting to CPS

  6. Drug Endangered Children • Shift in paradigm • Sensationalism • Treatment • Effect of ASFA on case plans

  7. Fetal Alcohol Syndrome • Approximately 10% of women in childbearing years are problem drinkers (up to 6-7 drinks per day) • Alcohol is probably the most common teratogen ingested during pregnancy and most common identifiable cause of intellectual disability (mental retardation)

  8. Acute Perinatal Alcohol Intoxication • Women who are acutely intoxicated may deliver infant who smells of alcohol, has blood alcohol level in the cord blood, has signs/symptoms of intoxication with CNS depression and hypoglycemia • Some infants born to mothers who chronically abuse alcohol may present with withdrawal symptoms (tremors, wakefulness and restlessness, excessive crying, hypertonia, and excessive startling; persist for 72 hours

  9. Fetal Alcohol Syndrome • Constellation of physical, behavioral and cognitive abnormalities • Criteria: specifc craniofacial dysmorphic features, prenatal or postnatal growth deficiency, central nervous system neurodevelopmental findings

  10. Fetal Alcohol Syndrome • Diagnosis requires a history of maternal alcohol use (proven or presumed) and elements of the three primary diagnostic categories • Partial FAS: confirmed facial anomalies and either growth retardation or CNS involvement or other unexplained behavior abnormalities

  11. Fetal Alcohol Syndrome • Characteristic facial anomalies • Short palpebral fissures • Ptosis • Flat midface • Upturned nose • Smooth philtrum • Thin upper lip

  12. Fetal Alcohol Syndrome • Growth Retardation • Low relative birth weight • Growth failure despite adequate nutrition • Low weight relative to height

  13. Fetal Alcohol Syndrome • CNS neurodevelopmental findings • Microcephaly • Structural brain abnormalities (agenesis of the corpus callosum and cerebellar hypoplasia • Other neurological signs (fine motor difficulties, sensorineural hearing loss, poor gait coordination, and poor eye-hand coordination

  14. Fetal Alcohol Syndrome • Unexplained behavioral abnormalities • Learning difficulties • Poor school performance • Poor impulse control • Problems with social perception • Poor language abilities • Poor math skills • Impaired memory and judgement

  15. Fetal Alcohol Syndrome • Birth defects • Congenital heart defects • Skeletal and limb deformities • Anatomic renal abnormalities • Ophthalmologic abnormalities • Hearing loss • Cleft lip or palate

  16. Classification of alcohol-related effects • Fetal alcohol syndrome • Partial FAS • Alcohol-related birth defects (ARBD) • Alcohol-related neurodevelopmental disorder (ARND)

  17. Fetal Alcohol Syndrome • Etiology: • Infrequent binge drinking with occasional high blood alcohol levels • Mild-to-moderate regular drinking with lower peak blood alcohol levels but more continuous fetal exposure

  18. Fetal Alcohol Syndrome • Pathogenesis: • Exposure of the developing fetus to toxic levels of alcohol and its metabolites • Exposure in the 1st trimester affects organogenesis and craniofacial development • Continuing use in later preganancy results in low birth weight and affects postnatal growth • Brain development begins in early pregnancy and undergoes growth spurt with maturation of neurons in second and third trimester

  19. Tobacco • Although prevalence of smoking in US has decreased, up to 20% of pregnant women continue to smoke throughout gestation. • No documented increased risk of birth defects • Major impact is decreased birth weight • Prenatal (and postnatal) smoking is risk factor for SIDS • Secondhand smoke associated with increased risk of respiratory disease

  20. Marijuana • Concern due to fact that marijuana is lipid-soluble and concentrates in fatty tissues (brain) • Older studies did not address long-term issues • Marijuana today much more potent • Anecdotal reports of prenatal marijuana-exposed children with normal IQ, but specific learning disabilities • Cannabis withdrawal syndrome

  21. Heroin • IV use • Recent cultivation in Colombia and Mexico: ability to snort or smoke • Physical dependence of user and neonate • Need to wean infant with use of phenobarbital • Methadone withdrawal longer then heroin

  22. Cocaine • Cocaine powder vs. crack • Intensely stimulates brain’s pleasure centers (not just “buzz”, but euphoria) • “highly addictive”: 16% of people who try cocaine become “hooked” • Binging

  23. Cocaine • Prenatal effects • Prematurity is greatest risk • No perinatal withdrawal syndrome • Post-natal behavior of the drug using parent has greatest effect • Binging • Neglect (physical and emotional) • Economic • Criminal and violence exposure

  24. Methamphetamine:Historical Background • 1887: Amphetamine first synthesized • 1932: Benzathine nasal spray for asthma and rhinitis • 1937: Amphetamine tablet for narcolepsy. A report that year states that intellectual performance can be enhanced via increased wakefulness • 1930’s and 40’s: Abuse of methamphetamine in US and abroad

  25. Methamphetamine Clan Lab

  26. Methamphetamine Clan Lab

  27. Methamphetamine: Crank • Originally transported across the country in the crank cases of motorcycles by biker gangs • Methamphetamine manufacturing: • Large “plants” in California • “Mom & Pop” type spreading from West & Midwest into East Coast and Florida

  28. Chemical Properties • N-methyl homologue of amphetamine • White, odorless, bitter crystalline powder • Color varies with manufacturing process • Street names: pink, quartz, peanut butter speed, crank, tweak, go

  29. The Effects of Methamphetamine • The drug acts on the body in 2 main areas: • Peripherally: Your blood pressure, heart rate, pupil size • Centrally: Your brain function • Some users binge then crash • Others are “weekend” users

  30. Peripheral Effects in Users The mechanism appears to be methamphetamine’s ability to stimulate release of norepinephrine at nerve terminals and of epinephrine from the adrenal medulla and include tachycardia, tachypnea, hypertension, dry mouth, mydriaisis and blurry vision.

  31. Pharmacology • The N-methyl group that differentiates amphetamine from methamphetamine decreases the polarity of the molecule and allows for better penetration of the blood-brain barrier • Half-life ranges from 10-30 hours depending on dosage, form, and urinary pH

  32. Pharmacology • At the cellular level, dopamine is displaced from specific nerve terminals, causing hyperstimulation of dopaminergic receptor neurons in the synaptic cleft • Damage is probably due to excess dopamine • Crash is from dopamine depletion

  33. Acute Central Effects in Users • Irritability, impulsivity, impaired judgment, insomnia, and psychotic behaviors such as hallucinations and paranoia • Methamphetamine can both induce an acute toxic psychosis in previously healthy persons and precipitate a psychotic episode in those with psychiatric illnesses

  34. Chronic Central Effects in Users • Compulsive or repetitive behaviors are manifestations of chronic use. Long term use in humans has resulted in delusional, paranoid behavior, psychosis and violence. The distinguishing feature of the psychosis is its visual or tactile hallucinations, as opposed to generally auditory hallucinations in schizophrenia

  35. Chronic Central Effects in Users • CNS “kindling” phenomenon: • Patients who have used amphetamines over a long period, especially those who have had psychotic episodes from its use, may be pushed into a frank psychosis by even very small amounts of an amphetamine, or by any stimulant including caffeine or nicotine

  36. Chronic Use • Tolerance: The chronic user will progressively increase the dose to obtain desired effects • Methamphetamine abusers may increase their dose 50 to 100 times the initial amount over time: up to several hundred milligrams/day, which would be fatal to the non-user

  37. Chronic Central Effects in Users • Physical detoxification can take weeks, while psychological detoxification can take months. • Unless injecting, it is possible for individuals to take methamphetamine for a period of years before intolerable negative consequences of the drug begin to occur.

  38. Potential Chemical Toxicities • When a clandestine lab is raided, the team wears special protective gear that can weigh up to 30-40 pounds • The most significant health risk related to the production of meth is the acute injury secondary to massive chemical exposure via inhalation or contact to the skin and eyes • The manufacture of 1 pound of meth can produce 5-6 pounds of toxic waste

  39. Potential Chemical Toxicities • These can be corrosive, explosive, flammable, and toxic. • Exposure can occur via skin absorption, inhalation, ingestion, or injection. • The labs can be booby-trapped: A light bulb can be filled with ether so that the mere act of turning on its light switch causes enough friction to cause an explosion.

  40. Reported Toxicities • JAMA 12/6/00: events reported to the Hazardous Substances Emergency Events Surveillance system from 1996-1999 noted 112 methamphetamine-associated events with 155 persons injured. • 51 % were first responders: police officers, EMTs, firefighters, and hospital employees. 54.1 % had respiratory irritation (cough), difficulty breathing, throat irritation • 10.8 % had eye irritation.

  41. What about the Children? • Children breathe faster than adults • Children have a faster heart beat than adults • Children are smaller and closer to the ground than adults • Just imagine their side effects • They have a heavier exposure to the chemicals due to the above

  42. What about the Children? • Their nervous system is still developing • The food they eat is on the same counter as the meth lab • The food in the refrigerator is near the chemicals: meth has been analyzed from food taken from clan meth labs

  43. What about the Children? • Children removed from meth labs have had their urine test positive for methamphetamine • They may have been exposed to the vapors and inhaled it • They may have eaten it or drank it unknowingly

  44. Preliminary Data: TulsaDEC Nurses & Justice Center • 55 children examined Jan 00 - Mar 02 • Majority of children filthy: • 33/55 had either an abnormal physical exam or evidence of neglect • Developmental delays common, especially speech-language delays: 6/55 ages 4-5 years old No consistent abnormal bloodwork

More Related