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93 Cards in this Set
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Fetal Heart Rate Mechanisms
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1. Parasympathetic System (cardiodecelerator)
2. Sympathetic System (cardioaccelerator) 3. Baroreceptors (decrease in fetal heart rate) 4. Chemoreceptors (Respond to a drop in fetal oxygen by increasing HR. If prolonged- decreases HR.) |
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Parasympathetic System for fetal monitoring
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Cardiodecelerator
Vagus nerve is primary nerve As fetus matures PS becomes more dominant (HR decreases) |
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Sympathetic System (for fetal monitoring)
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Cardioaccelerator
Nerve endings are distributed throughout the heart muscle. When stimulated they release norepinephrine. Increases heart rate and strength of cardiac contractions, increasing CO |
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Baroreceptors (for fetal monitoring)
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(decrease in fetal heart rate)
In the carotid arteries and in the walls of the major arteries Fetal BP increases as a result of increase in intervascular volume. Example: Compression of umbilical arteries- stimulates baroreceptors, sends impulse ot vagus nerve causing decrease in heart rate |
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Chemoreceptors (for fetal monitoring)
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Respond to a drop in fetal oxygen by increasing HR. If prolonged- decreases HR.
In medulla oblongata (in brain stem) Respond to changes in pH, O2 and CO2 levels in the blood. Respond to drop in O2 (hypoxia) with an increase in the heart rate as an attempt to get O2 to the brain, but if it continues it stimulates the baroreceptors which then stimulare the vagus nerve decreased in HR |
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Baseline Rate for FHR and how to you get the number
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110-160 bpm
The average FHR during a 10 minutes period, rounded to increments of 5 bpm |
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Internal uterine pressure catheter
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Intran or IUPC
Very accurate about how strong contraction is. Used when not getting a good tracing with the external or if you want to know if contractions are strong enough. Can help monitor effects of pitocin |
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Evaluation of Fetus (how often per stage)
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1st stage: Low Risk- q 30 min High Risk- q 15 min
2nd stage: Low Risk- q 5-15 min High Risk- q 5 min |
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Tachycardia in fetus and causes
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over 160 bpm x 10 min
Can be an ominous signs if w decreased variability, late decels or severe variable decels Reasons: fetal stress and early fetal hypoxia, maternal fever, if mother receives cardiac stimulating drugs (tributiline, atropine) maternal hyperthyroidism (maternal hormones cross placenta) dehydration, anxiety, prematurity, fetal anemia |
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Bradycardia in fetus and causes
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less than 110 bpm x 10 min
Ominous w decreased variability and/or late decels Reasons: Late fetal hypoxia (fetal asphyxia), maternal hypotension, umbilical cord compression (when fetal baroreceptors are stimulated) |
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Baseline Variability (in fetus) breakdowns
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Absent- range undetected
Minimal- range 5 bpm Moderate- range of 6-25 bpm Marked- range greater than 25 bpm Good indicator of fetal cardiac and neurological function |
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Absent Variability in Fetal Monitoring
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range undetected
almost a flat line |
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Minimal Variability in Fetal Monitoring
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A range of 5 bpm
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Moderate Variability in Fetal Monitoring
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Range of 6-25 bpm
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Marked Variability in Fetal Monitoring
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Range greater than 25 bpm
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Sinusoidal pattern
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Smooth wavelike baseline that is equally distributed above and below baseline.
Amplitude is between 5 & 15 Baby is in danger. Associated with sinusoidal pattern Pseudo- if given drugs like morphine or demerol |
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What are the two kinds of accelerations? What are the requirements for < or > 32 weeks?
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Increase in HR ---
Episodic accelerations: with movement or from external stimulation & Periodic accelerations: with UCs These are reassuring signs After 32 weeks gestation- Must be 15 beats above BL for 15 seconds (Less than 32 weeks- 10 beats above BL for 10 seconds) |
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Episodic accelerations
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with movement or from external stimulation
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Periodic accelerations
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with UCs
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Early Decelerations
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from pressure on fetal head
Timing with UCs, greater than 30 seconds to reach nadir (bottom/deepest part). They 'mirror' the contractions Will see with pushing. Pushing on head stimulates vagus nerve |
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Late Decelerations
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uteroplacental insufficiency
Greater than 30 seconds to reach nadir, nadir after peak of UC |
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Variable Decelerations
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umbilical cord compression
15 bpm below BL X 15 seconds, less than 30 seconds to reach nadir. May have 'u' 'v' or 'w' with fast drops Intervention: first try turning the mother |
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Prolonged Decelerations
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FHR decrease is 15 bpm or more and lasts for at least 2 minutes but less than 10 minutes
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Generally- the baby is losing all reserves
Once you go past 10 min- it's just bradycardia |
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Ultrasound
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Sound waves are sent
through maternal abdomen and bounce off of fetal heart valve. Heart rate is interpreted by monitor. Best when placed over fetal back. |
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Internal Fetal Scalp Electrode
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Placed onto fetal scalp
Gives ECG reading Placed by nurse, midwife, or physician |
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Amnioinfusion
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add fluid into the uterus to help get baby up off the cord or sometimes when baby has passed meconium
for cord compression |
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Tocometer
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Pressure sensitive button indicates contraction of uterine muscle
Not useful for determining strength of contraction Best recording often obtained when positioned at fundus (top of uterus) |
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Internal Uterine Pressure Catheter
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Accurately tells us how strong the contractions are
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To calculate Montevideo Units (MVU)
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After IUPC insertion, measure units of pressure above baseline
Multiply units of pressure by number of UC’s in 10 minutes Example: If uterine pressure is 50 mmHg and the patient has 3 UC’s in 10 mins, total Montevideo units (MVUs) would be equal to 150 MVUs. Usually 200 MVUs is considered necessary for adequate labor during the active phase. |
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Scalp Stimulation
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An indirect method of assessing fetal acid base balance when no accelerations on monitor
Stimulation to the fetal scalp with finger Reactivity is associated with fetal well-being Basically a vag exam where you rub the baby's head |
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Fetal Blood Sampling
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Fetus is well oxygenated if pH stays above 7.25
Continue monitoring and resample if pH heads downward and is between 7.25 and 7.20 Below 7.20 shows fetus is acidotic. Prepare for birth |
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Ultrasound
what can u see? 2 types |
High frequency soundwaves
placental location, fetal number, assessment of gestation age, assessment of amniotic fluid (AFI)- how much?, Transabdominal- woman needs to fill bladder before the procedure (drinks water 1-2 hors before appointment Transvaginal- probe goes up vagina, images tend to be more clear, mother may have an empty bladder |
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BPP Test Interpretation and Management
10/10 8/10 |
10/10 Normal nonasphyxiated fetus.
No intervention. Repeat in 1 week. 8/10 With normal fluid: Risk of fetal asphyxia very rare.No intervention. With abnormal fluid: Chronic fetal asphyxia suspected. Induce birth. |
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BPP Test Interpretation and Management
6/10 4/10 |
6/10 Possible fetal asphyxia. If AFV is abnormal, deliver otherwise repeat test.
4/10 Probable fetal asphyxia. Repeat testing same day |
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BPP Test Interpretation and Management
2/10 0/10 |
2/10 Almost certain fetal asphyxia. Induce birth
0/10 Certain fetal asphyxia. Induce birth |
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NonStress Test (NST)
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Reactive NST- 2 or more accelerations, 15 bpm or more, lasting 15 seconds or longer, within a 20 minute period. (If under 32 weeks gestation- an acme of 10 bpm or more, for 10 seconds or longer.)
Nonreactive NST- does not meet the above criteria |
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Contraction Stress Test (CST)
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Evaluates uteroplacental functioning. Typically given after a nonstress test
Need 3 uterine contractions 40-60 secs in duration in 10 min. Use pitocin or strumming technique (strum nipple to release oxytocin) Negative CST- No late decels or significant variable decels after any UCs. Positive CST- Late decels with at least 50% of UCs. |
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Amniocentesis
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Use ultrasound
22 gauge spinal needle Draw up small amount of amnio fluid Chromosomal Biochemical determination AFP alpha fetal protein Lung Maturity |
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AFP- Alfa fetal protein
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protein produced in fetal liver
peaks at about 15 wks in amniotic fluid, found with women who's babies have neural tube defects |
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Lung Maturity Studies
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1. L/S Ratio (Lecithin/Sphingomyelin)
lungs are mature when ratio 2:1 2. PG (Phosphatidylglycerol) |
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L/S Ratio (Lecithin/Sphingomyelin)
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The surfactant is made up of lecithin/sphingomyelin.
When ratio is 2:1 there is high likelihood of maturity @ 20 wks 0.5:1 |
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PG (Phosphatidylglycerol)
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2nd most abundant phospholipid in surfactant
Appears around 36 wks gestation It’s either present or abset. When it’s present the lungs are mature |
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Chorionic Villus Sampling (CVS)
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done for diagnosis of genetic, metabolic or dna studies
done between 10-12 wks gestation Aspirate a small amount of chorionic villus from edge of placenta Can cause bleeding or rupture of amniotic fluid |
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Fetal Development at 8 Weeks
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All body organs are formed
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Fetal Development at 8-12 Weeks
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FHT’s can be heard with doppler
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Fetal Development at 16 Weeks
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Baby’s sex can be seen. Looks like a baby.
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Fetal Development at 20 Weeks
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Quickening, baby develops regular schedule, vernix, head hair, eyebrows, and eyelashes present
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Fetal Development at 24 Weeks
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Weighs 1 lb/10 oz. Activity is increasing.
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Fetal Development at 28 Weeks
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Eyes begin to open and close. Baby is 2/3s its final size.
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Fetal Development at 32 Weeks
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Baby has fingernails and toenails. SQ tissue is being formed. Baby is less wrinkled and red.
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Fetal Development at 38-40 Weeks
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Baby fills total uterus.
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Tobacco effects on Men and Women
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higher infertility rates
Men have impaired sperm concentration and changes in sperm motility Women have difficulties with ovulation and implant disorders (too low in uterus) |
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Tobacco effects on fetus/infants
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Infants have a lower birth weight and a higher incidence of perinatal deaths
Infants born to smokers are more than twice as likely to die from SIDS Increased risk of spontaneous abortion, preterm birth, placenta previa, abruptio placenta, and premature rupture of membranes r/t amount of cigarrettes Nicotine and Carbon Monoxide decrease amount of O2 available for the baby |
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Risks to the Fetus of the Drug Dependent Mother
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Intrauterine anoxia
Intrauterine infection Alterations in birth weight Low Apgar scores |
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The Female Addict
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Problems with criminality (selling self) and physical abuse
stay away from pregnant hookers |
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What happens when mother goes through withdrawal?
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baby does too -causing hyperactivity and you may see cord around neck
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Many drugs during pregnancy increase risk for
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many drugs increase risk for pregnancy induced HTN (PIH) and abruptio placenta that result in placental insuffiency and fetal anoxia
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The Effect (on the fetus) of a Substance is Determined by:
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1. The stage of fetal development
2. The amount of substance taken 3. The type of substance taken |
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Identifying the Substance Abuser- Obstetric History
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In prior pregnancies, a history of:
-Abruptio placenta -Fetal death (after 20 wks) -Low-birthweight infant -Meconium staining -Premature rupture of membranes -Premature labor -Sexually transmitted diseases -Spontaneous abortion |
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What does Cocaine and other Stimulants do to the body?
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Stimulants act at the nerve terminals to prevent the reuptake of dopamine and norepinephrine, which results in vasoconstriction, tachycardia, and hypertension.
Placental vasoconstriction decreases blood flow to the fetus |
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What are the effects of Cocaine and other Stimulants on the fetus?
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Placental abruption
Low birth weight (IUGR) Marked irritability of the newborn Increased risk of SIDS |
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Heroin effects on infant
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Fetal death can occur when addicted mothers stop usage suddenly
Low birth weight Deficits in cognitive and developmental testing The most harmful effect on the newborn is withdrawal- neonatal abstinence syndrome |
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Signs of Neonatal Withdrawal (NAS)
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W - wakefulness
I - irritability T - tremulousness, temperature variation, tachypnea H - hyperactivity, high-pitched cry, hyperreflexia, hypertonus, hiccups D - diarrhea, diaphoresis, disorganized suck R - rub marks on knees, elbows, and face A - apneic spells W - weight loss (or failure to gain weight) A - alkalosis (respiratory) L - lacrimation S - stuffy nose, sneezing, seizures |
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Caring for the Drug-Affected infant
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For Frantic Crying: dark quiet room, swaddle baby, pacifier, rock baby gently
For Tremors: swaddle and hold close, provide firm, gentle touch to tremulous area |
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Fetal Alcohol Syndrome Incidence
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The incidence is between 2-15 cases per 10,000 live births in the United States.
FAS is the leading cause of mental retardation in the western world. The average I.Q. is 74. NO amount of alcohol is safe during pregnancy! FASD= 1 in 100 births in U.S. |
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Clinical Characteristics of Fetal Alcohol Syndrome (FAS)
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Growth Deficiencies
Central Nervous System Involvement Facial Dysmorphology |
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Growth Deficiencies in FAS
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Failure to thrive
Low birth weight Micorcephaly (small head & brain) Short and thin for age |
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Central Nervous System Involvement in FAS
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Developmental delay
Hyperactivity Learning or attention disorders Motor incoordination Mental retardation (need at least 1) |
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Facial Dysmorphology in FAS
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Epicanthal folds
Flat nasal bridge Flat and elongated philtrum (bump between lips and nose) Thin upper lip Short palpebral fissures Upturned nose |
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Intrauterine Growth Restriction (IUGR)
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Advanced gestation and limited fetal growth
Considered an “undergrown newborn” Aka- small for gestational age SGA Baby will be in less than 10% |
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Factors Contributing to IUGR
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Maternal factors- ie low socioeconomic status, lack of prenatal care, and malnutrition
Maternal disease- ie substance abuse, heart disease, preeclampsia Envirnomental factors- ie high altitude, excessive exercise, maternal use of teratogenic drugs Placental factors- ie small placenta, placenta previa Fetal factors- ie congenital infections, chromosome abnormalities (Low socioeconomic- effects health, how they take care of themselves) |
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Symmetric (proportional) IUGR
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caused by long term conditions that affect the fetus (malnutrition, chronic HTN, chronic drug use)
See a shorter lighter baby and small organs and everything.baby is less than 10 |
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Asymmetric (disproportional) IUGR
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later in pregnancy with uteral placental blood flow (preeclampsia) the head circumference and length are appropriate but still under 10%
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Small for Gestational Age (SGA)
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A SGA newborn can be preterm, term, or postterm
Less than 2 standard deviations or less than the 10th percentile for weight |
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Complications of the SGA Newborn
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Chronic Hypoxia (Asphyxia)
Aspiration Syndrome Hypothermia Hypoglycemia Polycythemia |
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Chronic Hypoxia (asphyxia) in SGA Newborn occurs because
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occurs because they don't tolerate labor well.
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Aspiration Syndrome in SGA Newborn occurs because
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Meconium in the amniotic fluid is aspirated at birth
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Hypothermia in SGA Newborn occurs because
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Have less brown fat and less adipose tissue so they lose heat very easily after birth
Brown fat- newborns are born with it in armpits, abdomen and fat, only lasts a few weeks. They don’t have the ability to shiver. So they are born with the brown fat- if they get too cold they metabolize the fat and it heats them up |
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Hypoglycemia in SGA Newborn occurs because
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Because they have less glycogen stores
Because they have increased metabolic rate from heat loss |
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Polycythemia in the SGA Newborn occurs because
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The body starts to produce more red blood cells due to chronic hypoxia in utero.
Can lead to jaundice Do a partial exchange transfusion if it’s pretty significant. So some blood is removed but replaces ml by mL with plasma or plasmanate or 5% albumin (not tested) |
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Compare normal newborn hemoglobin and hematocrit levels to that with polycythemia
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Normal
Hemoglobin- 15-22g/dl Hematocrit - 50%-65% Polycythemia Hemoglobin- greater than 22g/dl Hematocrit- greater than 65%-70% |
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Biggest problem in premature infants
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Respiratory Distress Syndrome
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Respiratory Distress Syndrome in premature infants
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b/c of immaturity of lungs
Before this time they have inability to produce enough surfactant (keeps alveoli open) These babies usually end up in NICU on oxygen Tire out with feeds so you use a gavage tube |
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Loss of Heat
Non-shivering thermogenesis in newborn |
Very little subQ fat.
Baby’s posture makes a difference. Conserve heat when in kind of fetal position Greater risk for aspiration because gag relfex is not developed Thermogenesis- is the break down of the brown fat, which is used up within a few weeks |
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Kernicteris
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what you prevent by treating jaundice. All the bilirubin does into the brain and causes brain damage & mental retardation and nerve damage (irreversible), baby gets lethargic and loses ability to suck, if progresses then see vomiting and loss of moro reflex. Bili level above 20-25 and whole body yellows. Become irritable, hypertonic, and has seizures
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3 Types of Jaundice
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Physiological
Breast Milk Pathologic |
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Physiological Jaundice
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Most common, Always cover eyes. Will see 2-3 days after birth
Caused by destruction of RBC’s and impaired conjugation of bilirubin in the immature liver For the bilirubin to get out of baby’s body it must go through conjugation process. Goes from ‘indirect’ to ’direct’ so it can go out of bowels. Sunlight can do it. If baby has cephalhematoma more concerned with jaundice because the blood must be absorbed into the body- increase of bilirubin that must be processed Forceps baby, bruising on face 50% of full term babys have problem 80% of preterm Do blood draw to get bili level if higher than 12 in term bottle fed baby, 14 in term breastfed baby and 15 in preterm- considered jaundice Starts in head, as number gets high than goes down the rest of the body |
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Breast Milk Jaundice
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Bili levels increase after 1st week of life and peak at 2-3 weeks.
Some women’s breast milk contains more free fatty acids, they complete with bilirubin for the binding sites on albumin Stop breastfeeding for 2-3 days, baby goes on formula to allow break of cycle Then resume breastfeeding |
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Pathologic Jaundice
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Most dangerous
Suspected when the yellow discoloration is visible before 24 hours of life in term infant Before 48 hours in the preterm infant Bilirubin levels are generally above 12 and 14. |
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ABO Incompatability
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Mother Fetus
0 / A or B A / B B / A Hemolytic condition that occurs when the major blood group of the mother is incompatible with that of the fetus. Maternal antibodies are formed against cells of fetus’s blood type Maternal antibodies are found on fetal RBC, those antibodies cause clumping (agglutination) of fetal RBCs the clumps get in small blood vessels where they hemolyze or are broken down and causes an increase in bilirubin Can get severe hyperbilirubinemia or renal failure Clinical Indicators: See neonatal jaundice within 24 hrs of life and get something called Direct Coombs Test, will detect presece of maternal antibodies in neonates blood. If present = positive direct coombs test Tx: phototherapy or exchange transfusion |
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RH Incompatibility
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Causes a hemolytic disease in fetus/newborn
Occurs when mother is Rh neg and baby is Rh positive The fetal red blood cells contain d-antigens, the mother does not They get into the mothers body During the birth there is a mixing and baby’s blood gets into the mother The mother create antibodies that will cross the placenta and attack the next baby if she does not receive Rhogam (destroys RBCs from baby that get into her system) It’s called erythroblastosis fetalis causing fetal anemia If severe- hydrops fetalis: continuation of the erythroblastosis fetalis, baby gets edematis and can cause CHF and multisystem failure and death in utero |
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Diaphragmatic Hernia
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results from defect in baby’s diaphragm. Allows abdominal organs to be displaced so the intestines get into the thoracic cavity cause lungs to remain small. Usually on the left side. Most are discovered with ultrasound. Severe Respiratory Distress at birth.
Will see a scaffoid abdomen (flat or dipped) barrel chest. An x-ray will show loops of intestines Do not bag the baby because air will go into the stomach. You want to put in an endotracheal tube and put the baby on a ventilator.A gastic tube into stomach to relieve any air. Position in High Semi-fowlers position or turn onto affected side. |
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Biophysical Profile (BPP)
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Biophysical Profile
-fetal breathing movements -gross body movements -fetal tone -qualitative amniotic fluid volume -reactive FHR |
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