P020A

P020A

Lecture 5 -

Course Objective #30

• Identify the causative agent and the effects on the fetus in the following maternal infections:– Rubella– Toxoplasmosis– Syphilis– Cytomegalovirus

Development

• Cephalocaudal• Proximal-distal

Rubella• AKA– German Measles

Congenital Rubella Syndrome

• AKA – “Blueberry Muffin Syndrome”

• 1st trimester – 85% affected

• After 20 weeks– Defects rare

Congenital Rubella SyndromeEtiology

• Intrauterine Infection• Critical Time period – 1st trimester

Congenital Rubella SyndromeFYI

• 1941 Australian epidemic– 78 infants w/CRS

• 1964-65 US epidemic – 20.5 M cases of Rubella – 20,000 infants w/CRS

Congenital Rubella SyndromeS&S

• Varied • ID – Normal – severe

• Sensory defects– Deaf*– Blind

Congenital Rubella Syndrome

• S&S– Cardiac defects– Microcephaly– Bone abnormalities– Purpura

Congenital Rubella Syndrome• Treatment• Prevention –Rubella vaccine licensed in

1969•MMR

–2005 Rubella eradicated in US

Rubella Virus Eliminated in the United States

• Washington Post --Monday, March 21, 2005• The invisible "chain of transmission" of rubella virus

has been broken in the United States. With it disappears a disease that a little more than a generation ago struck fear in the heart of every pregnant woman.

• Fewer than 10 people a year in this country now contract the infection known popularly as German measles. Since 2002, all cases have been traceable to foreigners who carried the virus in from abroad.

Congenital Toxoplasmosis

• Toxoplasmosis –Protozoa Parasite–“Transplacental spread” Congenital

Toxoplasmosis

Congenital Toxoplasmosis

• Etiology–Raw, undercooked meat, –Cat feces, –Non-pasteurized milk

Congenital Toxoplasmosis

• Incidence–1:10,000 births

• Prognosis–Many die in 1st month

Congenital Toxoplasmosis

• S&S–Vary widely depending on period of infection

Congenital Toxoplasmosis

• S&S• Triad –Hydrocephalus–Intracranial calcification–Chorioretinitis

Congenital Toxoplasmosis

• Severe ID• Blindness• Epilepsy• Low birth weight• Hepatosplenomegaly –Jaundice

Congenital Toxoplasmosis

•Tx–Antibiotics

Congenital Toxoplasmosis

•Dx–Amniocentesis–Ultrasound

Congenital Syphilis

• Etiology: –Spirochete bacterium –Bacteria!!!!

Congenital Syphilis

•Mom infant –during pregnancy or birth

• Fetus vulnerable –after 18 weeks

Congenital Syphilis

• Incidence–1:100,000 live births (CDC,

2002)• @ 50% die in utero or shortly

before or after birth

Congenital SyphilisS&S

Early stage • Failure to thrive,• Nasal discharge• Blistery rash• No nasal bridge

Congenital Syphilis

• Late stage• Hutchinson’s triad–Hutchinson’s teeth–Keratitis–Deaf

Congenital Syphilis

• Late stage• ID• Bone pain• Vision/hearing loss

Congenital Syphilis

• Treatment–Mom•Prenatal care •Antibiotics

–Delivery•Cesarean

Congenital Cytomegalovirus• Herpes-like infection

Congenital Cytomegalovirus

• Etiology–Transplacental spread

Congenital CytomegalovirusFYI

• Mom may be asymptomatic• 1% all newborns test positive for CMV• 95% asymptomatic• 5% congenitally affected

Congenital cytomegalovirus

• The mother's illness may not have symptoms, so she may be unaware that she has CMV.

Congenital CytomegalovirusS&S

• Inflammation of the retina• Hepatosplenomegaly – Jaundice

• Low birth weight• Petechiae• Seizures• Microcephaly

Congenital CytomegalovirusDx Tests

• Antibody titer against CMV • Bilirubin level • TORCH screen

Congenital CytomegalovirusTx

• Focus on specific problems

Congenital CytomegavirusPrognosis

• Up to 90% of infants who have symptoms of their infection at birth will have neurologic abnormalities later in life. Only about 5 - 10% of infants without symptoms will have these problems.

Congenital CytomegalovirusFYI

-neonatal death is common

Congenital CytomegalovirusPrevention

• CMV is almost everywhere• Wash hands p touching diapers• ⌀ kiss kids < 6 yrs• ⌀ share food c kids• PG ⌀ work with < 2 1/2

Objective #31

• Describe the cause, sequence of events, pathology and preventative factors of erythroblastosis fetalis.

Course Objective #32

• Describe the relationship of the Rh factor disorders and kernicterus

Erythroblastosis Fetalis

• What is erythroblastosis fetalis?

Erythroblastosis Fetalis

• Hemolytic disease–ABO incompatibility–Rh incompatibility

Erythroblastosis Fetalis

• Neonate red blood cell destruction

Erythroblastosis FetalisS&S

• Anemia• Hepatoslenomegaly• Jaundice• Hydrops

Erythroblastosis FetalisDx test

• Complete blood count and immature red blood cell (reticulocyte) count

• Bilirubin level• Blood typing

Erythroblastosis FetalisTreatment

• Phototherapy: –bilirubin breaks down when

exposed to UV light•Blood transfusion

Maternal-Fetal Blood Incompatibilities

-Rh Incompatibility

-ABO Incompatibility

ABO Incompatibility

• Etiology–Mom blood type•O

–Fetus blood type•A •B

ABO Incompatibility

S&S•Mild–Anemia–Jaundice

ABO Compatibility

• Severe –Kernicterus •Brain damage d/t h bilirubin levels

ABO Incompatibility

Treatment• Phototherapy

Rh incompatibility

• Mom blood type – Rh-

• Fetus blood type – Rh+

Rh incompatibility

• Mom develops antibodies to Rh+• Immune response • Destruction of RBC of fetus

Rh incompatibility

•Anemia•h bilirubin

Rh incompatibility

• Neonates Liver can’t adequately metabolizes bilirubin • Kernicterus

Rh incompatibilityS&S - Uterio

• Polyhydramnios• h bilirubin

Rh incompatibilityS&S - neonate

•Mischarge• Jaundice•Hypotonia•Lethargy

Rh incompatibilityTreatment (neonate)

• Phototherapy• Blood transfusions

Rh incompatibilityTreatment

• RhoGAM

Rh incompatibility

• Full recovery is expected for mild Rh incompatibility.

Rh incompatibilityPrevention

• RhoGAM• Prevents development of antibodies

against Rh+ blood• Schedule–2nd trimester –Post deliver

Kernicterus• Neonatal brain damage due to destruction of

RBC in utero • h bilirubin crosses “blood-brain barrier” • Brain damage

KernicterusEtiology

• Rh incompatibility • Drugs• liver anomalies• Blood incompatibilities

KernicterusS&S

• Varied S&S• Characteristic: jaundice

KernicterusS&S

• Choreoathetosis • Spastic paralysis• Hypotonia• Anemia• Hypoxia

Course Objective #33

• Describe the fetal effects from maternal use of the following teratogens– Narcotics– Marijuana– Alcohol– Thalidomide– Anti-convulsants– Tobacco

Drugs and Alcohol(teratogens-potential to produce mutation)

Teratogenspotential to produce mutation

NarcoticsExamples:• Heroin• Methadone

Narcotics

Effect• Retarded fetal growth/low birth weight • Addicted

Narcotic Addicted Neonate

• Withdrawal S&S– Begin @ day 4 four– Last a few weeks :

Narcotic Addicted Neonate

S&S - Withdrawal– Tremors seizures– i swallow– Diarrhea– Tachypnea– h temp diaphoresis

Narcotic

S&S up to 6 mo. • Hyperirritability • Hyperreflexia• Tremulousness• i social responsiveness

Narcotic

S&S up to 6 mo.

• No evidence of congenital abnormalities

Cocaine• Drug type–Stimulant

• Action:–constricts blood vessels –i circulation to brain

Cocaine• Transmission–Transplacental –Lactation

Cocaine

• Effects: –MOM• increased risk of abruptio

placentae

Cocaine

• Effects: • Baby–low birth wt–small –premature

Cocaine

• Withdrawal begins –when cord is cut

Cocaine

• Withdrawal S&S–Tachycardia–Tremors–Hyperirritability–feeding problems–sleep problems –h risk of seizures (lifelong)

CocaineFYI

-by 2 years, 2/3 are developing normally -other 1/3 show difficulty maintaining attention,

interacting with other children, adapting to change

Marijuana• Hallucinogen

Marijuana

• i muscle mass • Tremors• h startle reflex

Alcohol• Type of drug– Depressant

Alcohol• Effects– variable

AlcoholFetal Alcohol Effects

• Less severe

Fetal Alcohol Syndrome

• Severe

Fetal Alcohol Syndrome

Full-blown

Alcohol

•Alcohol • i umbilical blood

circulation•Hypoxia

FAS Characteristics

• i palpebral fissures• Flat nose bridge &

philtrum• Thin upper lips

FAS Characteristics

•Microcephaly• Delayed development• ID• Hyperactivity

FAS: Infancy

• Small w/ Stunted growth • Microcephaly• Tremor• Irritable• i sucking reflex• Failure to thrive

FAS: Early Childhood

• Speech & motor delayed• Short• Hyperactivity• FAS face diminish

FAS: School Age

• ID–2/3 moderate – low/average IQ

• Behavior problems • Hyperactivity & ADD

FAS: Young Adulthood

• Cognitive problems–Memory–Orientation to time, space, – Judgment

• Vulnerable to – alcoholism

FAS: Treatment

• Symptomatic• Prevention

Rx: Thalidomide• Action–Anti-emetic

• Critical time period–First trimester

Thalidomide

Effect on fetus• Limb deformities• Normal intelligence

Anticonvulsants• Rx: Dilantin (Phenytoin)• Effect: –4-7% cleft lip / palate

Anticonvulsants

• Monitor lab values• Risk to benefit • Poly-pharmacy h risk

Nicotine• Type of drug–Stimulant

• Effects–i birth weight

• Critical time period–3rd trimester

Maternal-Fetal Irradiation

AKA: –X-ray

• Effects–Microcephaly

Radiation

• Critical time period–1st & 2nd trimester

Course Objective #34

State the various cause and results to the infant of perinatal asphyxia.

Asphyxia

• Brain injury during delivery caused by prolonged deprivation of fetal O2• Maybe permanent CNS effects

Perinatal

Toxemia / EclampsiaPrematurity Physical TraumaInfection

Toxemia

• Triad S&S (Maternal)–HTN–Edema–Proteinuria

Toxemia

• h B/P • i circulation to the uterus • i O2

Toxemia

• Placenta degenerates • Critical period–3rd trimester

Pre-Eclampsia

• + for 3 S&S of toxemia • Most common in –Primigravida

Eclampsia

• 3 S&S + seizure• h risk –Maternal death –Fetal loss

Complications of Toxemia

• Abruptio placentae• Hemolysis• Cerebral hemorrhage• Pulmonary edema• Renal failure

Toxemia Treatment

• Termination of pregnancy resolves all symptoms!

Prematurity

• Birth weight < 5.5 lbs. OR • Gestational age < 38 wks.

Prematurity

Moms without prenatal care are 3 times more likely to birth early

Prematurity: Risk Factors

• Lack prenatal care• i $• Smoking• Maternal age –< 18–>35

Vulnerabilities of Premature Infants

1. Death2. ID3. i temp regulation

Vulnerabilities of Premature Infants

4. i sucking/swallowing 5. immature liver 6. O2 deprivation

Vulnerabilities of Premature Infants

7. Vision problems8. Cerebral hemorrhage 9. Infection

Infection

Herpes Simplex

Herpes Simplex

• 80% result in death or serious problems–ID–Blind

Herpes Simplex

•Causative agent: –Herpes simplex virus 2 (HSV-2) •Genital

•Prevention–C-section

PostnatalInfectionsCerebral TraumaCerebrovascular AccidentBrain Tumors Poison and Environmental ToxinsMalnutritionCerebral PalsyEpilepsy

Physical Trauma

• Leading cause of death infant–MVA

Physical Trauma

• 2nd leading cause of death - < 2yrs –Abuse

Course Objective #35

• State the symptoms seen in a child suffering from: A. Lead poisoning B. Mercury poisoning

Poisons and Environmental Toxins: Lead

• Source– Paints– Water

Poisons and Environmental Toxins

• Severe effect:• Lead encephalitis • S&S–Stupor – coma–Seizures

Poisons and Environmental Toxins: Lead

• Effect –i IQ –i attention span,–personality changes

Poisons and Environmental Toxins: Lead

• Treatment–Diet –i fat–h iron, Ca, Vitamin C

Poisons and Environmental Toxins

Mercury • Food –TUNA

Poisons and Environmental ToxinsMercury: S&S

• Paresthesia• Vision impairment• Motor problems• Hearing• ID