Maternal Dr. AKhter Flashcards
Stage 1 :Latent
ˆ15%CO
Start L Regular uterine contractions Ends: 4 cm dilatation,
Cx effacement, Cx slowly dilates
Nulli : 6-11hrs
Multi 4-8 hrs
First Stage :Active
ˆ30%CO
Start : 4 cm/ End: 10 cm (complete dilatation)
Regular intense contractions, fetal head descends into pelvis
Nulli 4-6
Multi 2-3
Second Stage of labor
ˆ45% CO
Start: complete Cx dilatation End: delivery of baby
Baby undergoes all cardinal movements : Engagement, Descent, Flexion and Internal rotation, Flexion, External rotation and expulsion
Nulli 1-2hr
Multi : 0.5 - 1 hr
Third Stage
ˆ80% CO
Start:delivery of baby / Ends : delivery of placenta
Placenta detaches from Uterus, Uterus contracts to a establish homeostasis
Nulli 0- 0.5
Multi 0- 0.5
Pain level in First stage labor
Pain is first T11- T12.
Then progress to T10 -T12 and L1.
Visceral Pain from Uterine contraction and Cx dilatation
Spinal Anesthesia needed at level T10-L1
Second stage begins at fully dilated Cx ( 10 cm ) ends at expulsion of fetus. Describe pain
Pain Through the pudendale nerve ( S2-S4)
Somatic pain : by stretching of vagina and perineum by descending fetus.
Spinal anesthesia needed S2- S4
Pain involves T10 to S4 dermatomes
Visceral Pain - what stage of labor and describe
Stage 1.
Visceral pain from contraction of uterus and dilatation of Cx
Pain starts T11-T12 then progress to T10- T12 then L1
Spinal anesthesia needed T10 - L1
Somatic Pain , What Stage, Describe
Stage 2 Somatic pain from stretching of vagina and perineum Pudendal Nerve ( S2-S4) Spinal anesthesia needed S2- S4 Pain involves T10- S4 dermatomes
Third Stage of Labor
ˆ80% CO. Delivery to expulsion of Placenta . Separation and delivery of placenta
Nulli : 0-0.5
Multi : 0-0.5
Pain and temperature from the genitalia are mediated by the
by the autonomic nervous system (not lateral spinothalamic tract)
Cause of pain is uterine contractions and exceeds
25 mmHg pressure ( 25-60mmHg )and dilate Cx.
Visceral pain due to which sympathetic nerves ?
Visceral afferent accompanying sympathetic nerves entering T10, T11, T12 and L1
Pain during late 1st and 2nd stage pain travels through
Pudendal nerve and enter neuraxis S2 S3 S4
Pain due to stretch on vagina and vulva and perineum
What innervate Uterus and Cx
T10 - L1-L2
Pain carried Visceral afferent C fiber
What innervates the perineum
S2 S3 S4
Pain carries by somatic nerve fibers; pudendal nerves
Effects of inhalation anesthetic on uterus
Inhaled anesthetic= Uterine relaxation = increased blood loss
Effects of parent earl agents on labor
Opioids minimally decrease progression of labor
7 reasons reason to use regional anesthesia ( in relations to labor )
1- use of oxytocin
2- Primigravida: pregnant for the first time
3- Prolonged labor
4-Large baby
5- Small Pelvis
6- Fetal malpresentation
7- High requirement for parenteral Opioid
Effects of vasopressors on Uterus
A1– Uterine contraction
B2 - Uterine relaxation
small dosePhenylephrine - Increase BF to uterus by Increasing BP
Use of oxytocin
1) To induce labor
2) prevent postpartum hemorrhage.
Complications with Oxytocin
Fetal Distress Maternal Water retention Hypotension Reflex tachycardia Uterine Tetany
What class of med used for Uterine Atony
Ergot Alkaloids — Bromocriptine ex..
PG F2a used to treat
PPH
What class drugs are used for PPH
Prostaglandins F2a
Use of Magnesium in labor
1) Stop premature contractions
2) Prevent eclamptic seizures
S/E magnesium
Hypotension Heart Block Muscle weakness Sedation Increases blockage for NMB drugs * Cardiac and Respiratory arrest can occur
Treatment for Magnesium OD
1) D/C it
2) Calcium
3) Lasix
Treatment for maternal hypotension
Ephedrine Oxygen Left uterine displacement Fluids Small dose phenylephrine can be used also.
Treatment of Unintentional IV injections
Supine with left uterine displacement
Thiopental and Propofol to stop seizure
Unintentional Intrathecal injection
1) Supine with left uterine displacement
2) Ephedrine and IV fluids
3) Intubation and ventilation in high spinal
Treatment of Post Dural Headache
Bedrest Hydration Oral analgesics Caffeine : 500mg IV *Blood Patch
7 signs of Fetal Distress
1- Oligohydramnios 2- repetitive late deceleration 3- loss of beat-to-beat variability 4- Fetal uterine growth retardation 5- Scalp pH< 7.2 6-Meconium stained amniotic fluid 7- Fetal heart rate < 80 bpm
Obesity is
> 20 % of Ideal body weight
BMI > 30kg/m2
Morbid obesity is
Double of Ideal Body weight
BMI >40kg/M2
PFT of obesity indicates
Restrictive lung disease
Physiological changes of obesity
Decreased chest wall compliance, Decreased ERV, Decrease FRC ( worse supine ) and increase WOB
With morbid obesity : closing capacity > FRC = V/Q mismatch and arterial hypoxemia
Closing capacity exceeds FRC
Obesity effects on drugs volume of distribution
Increased Volume of distribution for lipid soluble drugs
Pickwickian Syndrome aka Obesity-hypoventilation syndrome leads to 10 factors :
1- Hypercapnia 2- Hypoxemia 3- Pulmonary HTN 4- Systemic HTN 5- Pulmonary edema 6- Cyanosis-induced polycythemia 7- Rales 8- LVH/RVH 9-Somnolence;Poor sleep at night 10- Dependant edema 10-
The Fetal circulation has 3 shunts . name them and what is their purpose
1) Ductus Venosus : From umbilical vein to the IVC to bypass liver
2) Foramen Ovale: From the right atrium to the left atrium to bypass the lungs
3) Ductus arteriosus: From the pulmonary artery directly the Aorta then to the head
* the shunt bypass the liver and the lungs
TTN or Transient Tachypnea of the newborn
Benign, self limiting condition present in infant of any gestitional age , present shortly after birth due to delayed clearance of fluid clearance from the lungs .
Preterm neonates and C-section neonates have low catecholamines released which promotes sodium channel transport leading to greater amount of residual liquid in their lungs
Normal Neonate respiratory Rate
30-60 breaths/minute
First breath at 9 seconds— it establishes Neonate FRC.
Breathing should begin at 30 seconds and regular by 90 seconds
Fetal lungs contains
Liquid made of ultrafiltrate plasma of 30 mls. 2/3 expelled from the lungs of the neonate by the time of delivery. 1/3 reabsorbed during labor and delivery.
Residual lung liquid leads to
Difficulty of initiating breath and maintaining normal breathing pattern
Surfactant timeline in the fetus
20 weeks : Present in alveolar lining
28-32 week: within the lumen
34- 38 weeks : Significant amount in the terminal airway
Its production stimulated by chronic maternal stress or corticosteroids
Stress during labor and delivery can lead to
the passage of meconium into the amniotic fluid and gasping efforts by the fetus, which may result in the aspiration of amniotic fluid into the lungs.
Meconium—gasping efforts by fetus—aspiration of amniotic fluid into lungs.
Catecholamines 4 roles
1) production and release of surfactant
2) transition to active sodium transport for absorption of lung fluid
3) preferential blood flow to vital organs during stress of delivery
4) Thermoregulation of the neonate
Explain Non-shivering Thermogenesis of the neonate.
Neonates 1) release Norepinephrine 2) raise their metabolic rate in response to cold = oxidation of brown fat which contains mitochondria. This oxidation leads to the non-shivering thermogenesis. This causes O2 consumption to go up.
Thermal Stress is greater in
Preterm neonates, and infants small for gestational age , due to low fat stores.
Alternative to evaporation heat loss of neonate
Occlusive wrap rather than drying
less than 28 weeks give polythene wrap/bag
Maintain neutral thermal environment 34-35 degree Celsius
Antepartum Risk factors for Resucitation
Maternal Diabetes HTN disorder of pregnancy Chronic HTN Fetal anemia or Isoimmunization Previous fetal or neonatal death Bleeding in 2nd or 3rd trimester Maternal infection Maternal cardiac, pulmonary, thyroid , renal, neurological disease Poly or Oligohydromnios Premature Ruptured membrane Fetal hydrops Post-term gestation Multiple gestation Discrepancy in fetal size and dates ( i.e LMP date ) Drug Therapy : Magnesium, Lithium Carbonate , adrenergic blocking drugs Maternal substance abuse Fetal Malformation Diminished fetal activity No prenatal care Maternal age >35 years.
Meconium is present in the intestinal tract
After 31 weeks and is present in 10-15% of pregnancies
Meconium Aspiration Syndrome (MAS)
Respiratory Distress in a neonate whose airway was exposed to meconium and Chest X-ray showing pulmonary consolidation and atelectasis
Treatment of MAS
Positive Pressure Ventilation ; but risk of pneumothorax to due air leak
Congenital Anomalies that cause upper airway obstruction include:
Micrognathia, macroglossia, laryngeal webs, laryngeal atresia, stenosis , subglottic webs, tracheal agenesis, tracheal rings
Congenital High Airway Obstruction Syndrome ( CHAOS)
Exit procedure .
Intrinsic airway obstruction of the larynx or upper trachea (e.g., laryngeal web, subglottic cyst, tracheal atresia) can lead to retention of bronchial secretions and subsequent pulmonary distention; this constellation of s/s = CHAOS
To reduce the risk for cerebral palsy in surviving infants.
Maternal administration of magnesium sulfate before anticipated early preterm birth
fetal exposure to anesthetic agents may have harmful effects on
neurogenesis and synapse formation in the developing brain.
When pathways leading to orderly brain development are deconstructed, three major events appear critical to the establishment of functional synapses.
1) Neuronal proliferation,
2) migration
3) cellular differentiation
* occur in a preordained fashion to establish early neural circuitry.
neurogenesis starts and peaks at
5 and 25 weeks’ gestation respectively
neuronal migration is completed
between 30 and 36 weeks’ gestation.
a robust and exponential increase in synapse formation (almost 40,000 synapses/min) occurs between
28 weeks’ and term gestation
By ———————the fetus has all the neural machinery necessary to perceive pain.Many clinicians recommend that appropriate measures should be taken to provide fetal analgesia during fetal surgical procedures from this point onward
24 weeks’ gestation,
Although GABA has an inhibitory action in the mature brain, GABA serves——— role during fetal brain development.
an excitatory
Pharmacologic interventions (e.g., ethanol, antiepileptic drugs) that act directly or indirectly on these powerful neuromodulator systems induce long-lasting impairment of fetal brain development, mainly owing to impaired neurogenesis and/or altered neuronal migration.20–22 Alteration of this excitation-inhibition balance is purported to be responsible for an array of childhood neurodevelopmental disorders.
1) impaired neurogenesis
2) altered neuronal migration
fetal blood-brain barrier is morphologically well developed and functionally competent at
Term
Cerebral Palsy first described
In 1861 by Dr, John Little . Called Little’s disease.
Non-progressive CNS disorder
Present at birth , impairment of motor function and posture : may or may not be accompanied by intellectual disability .
Various form exist
Causes are unknown
The only types of cerebral palsy associated with intrapartum hypoxia are
spastic quadriplegia and, less commonly, dyskinesia.
Intellectual disability, learning disorders, and epilepsy should not be ascribed to birth asphyxia unless
accompanied by spastic quadriplegia.
No statements about severity should be made before an affected child is
3 to 4 years of age, because mild cases may improve and dyskinesia may not be evident until then.
Intrapartum hypoxia sufficient to cause cerebral palsy is always accompanied by
neonatal encephalopathy and seizures
Intra-amniotic infection and inflammation show direct evidence of causality between the
intrauterine process and white matter injury.
Elevated maternal temperature is one sign of chorioamnionitis, but alone it is insufficient for the diagnosis. Other signs include, but are not limited to,
maternal and fetal tachycardia,
foul-smelling amniotic fluid
uterine tenderness
maternal leukocytosis.
Chronic placental insufficiency relatively spares the fetal brain compared with other organ systems, although it results in
reduced fetal brain weight.
Unlike the adult brain, the fetal brain can use
ketone bodies and lactate as alternative energy sources.
Meperidine most widely studied opioids
Opioids cross the placenta and enter the fetal circulation.
When you have a non reactive NST you obtain a Biophysical Profile which Includes 5 things
1) NST
2) AFV ( Amniotic Fluid Volume )
3) Fetal Breathing
4) Fetal Tone
5) Fetal Movement
What is a Reactive NST
2 accelerations every 20 minutes
> 32 weeks gestation = HR increase of >15bpm lasting >15 seconds.
<32 weeks gestation + HR increase >10 bpm lasting > 10 seconds.
Early decelerations begin …end…caused by
Early decelerations begin at beginning of contractions and recover at end of contraction. Caused by fetal head compressions
The onset of a late decelaration … and cause
Begins to decrease at the peak of contraction.
Caused by Uteroplacental Insufficiency.
Hypoxia and acidosis : Take blood sample for ABG , If acidotic , ominous sign=head for C-Section.
Variable Decelerations
<30 seconds.
Due to umbilical cord compression.
Sinusoidal Pattern
Due to
Fetal Hypoxia
Fetal Anemia
Hemorrhage
The mean duration of a singleton pregnancy is
280 days/ 40 weeks
Term pregnancy is
37 to 42 weeks and is optimal time for delivery.
Preterm Birth
Before 37 weeks
Early term birth
37 to 38 weeks
Full term is from ..
39-40 weeks
Late term is from …
41 to 42 weeks
Determination of gestational age is most accurate when
Ultrasound Measurements of fetus or embryo are taken in the first trimester; preferably up to and including 14 weeks.
Pregnancies by assisted reproductive technology ( ART) , EDD
Assigned based on age of embryo and date of transfer
Naegele’s rule
Substract 3 month and ass 7 days to first day of last mentrual period
OR : date of assisted reproductive technology
Perception of fetal movement in nulliparous , then Parous at
Nulliparous 18-20 weeks
Parous 16-18 weeks
Fundal height at 20 weeks
20 cm above symphysis pubis ( by umbilicus )
Fetal hear rate with a Doppler can be detected at
10- 12 weeks
Fetal Heart Rate with a non electronic stethoscope at
18 weeks to 20 weeks
Routine US recommended due to its ability to
1) Determine gestational age
2) Viability
3) Placental Location
4) Structural abnormalities in the second trimester
5) Fetal number
Low maternal gestational birth weight
Increased risk for delivery of small-for-gestational age baby or preterm
Higher risk for delivering large for gestitional age baby
Excessive weight gain
Abdominal examination had several limitations especially in the setting of
Small fetus Polyhydromnios Maternal obesity Multiple pregnancy Uterine fibrioids
Abdominal examination is
Safe, well-tolerated, add valuable info on the Antepartum assessment
After 36 weeks( max fundal height week) the fetus
Drops into the pelvis in preparation for labor
Fetal growth restriction is associated with
Intrauterine Demise Neonatal morbidity Neonatal mortality Cognitive Delay in childhood Chronic disease (Obesity, DM type II, CAD, Stroke in adulthood )
Definition of Fetal Growth Restriction is
EFW of a fetus at less than the 10th percentile for gestational age
SGA Small for gestational age
Newborn with birth weight less than the 10th percentile for gestational age
Fetal Growth restriction results from
Suboptimal uteroplacental perfusion and fetal nutrition
Can be classified as Maternal, Fetal, Placental in causes.
Maternal disorders associated with fetal growth restriction
Any that will result in vascular disease: Pregestational Diabetes HTN Antiphospholipid antibody syndrome Renal insufficiency Autoimmune disease Malnutrition Substance abuse
Fetal conditions associated with Fetal Growth Restriction
Teratogen exposure such as certain medications
Intrauterine infection
Aneuploidy ( presence of abnormal number of chromosomes) : Trisommy 13 and 18
Structural malformations;abdominal wall defects, congenital heart defects.
Placental causes for Fetal growth restrictions
Poor placental perfusion : umbilical cord abnormalities ; velamentous or marginal cord insertion.
Fetal Growth restriction is associated with
An increased risk for stillbirth. Less than 10th percentile. 1.5% risk less than 5% percentile 2.5%risk
Risk for stillbirth further increase when Fetal growth restriction occurs in the context of
Oligohydromnios or abnormal diastolic umbilical artery blood flow
Early and acurate diagnosis of fetal growth restriction and …
Appropriate interventions leas to improvement in perinatal outcome. If Fetal growth restriction is suspected clinically and on the basis of US= Thorough evaluation of mother and fetus is warranted
What to do in the setting of FGR?
Serial US to assess amniotic fluid volume and fetal growth
Antenatal surveillance with umbilical artery velocimetry
Antepartum testing : NST and Biophysical Profile
Fetal Macrossomia
Growth beyond and absolute birth weight of 4000 to 4500grams regardless of gestational age .
Large for Gestational age
Birth weight greater than or equal to the 90th percentile for a given gestational age
What is shoulder dystocia ?
Failure of delivery of fetal shoulder after initial attempt at downward traction. It is the most serious consequence of macrosomia .
Most serious consequence of macrossomia
Shoulder dystocia
Perinatal mortality increased with birth weight
> 5000grams
Newborn and Mother morbidity increase with weight
4500-4999 grams
Risk of labor abnormalities increased with weight
4000 to 4999 grams
Fetal injuries associated with shoulder dystocia
Fracture of the clavicle
Nerve injury to brachial plexus paralysis to Erb-Duchenne; most resolve by age 1 year.
Risk of shoulder dystocia at birth weight >4500g is 9 to 14% compared to .2 -3 % with vaginal deliveries and 20-50% in presence of maternal diabetes.
Fetal Macrossomia can be determined 2 ways
Clinically by palpation = Leopold Maneuver
Or by Ultrasound
The rate of prediction is poor false positive >false negative.
EFW measurements are accuracy in Macrossomia
Factors added to macrossomia leading to less accurate measure of EFW are
1) Low amniotic fluid
2) Maternal obesity
3) Fetal position
4) Advancing gestational age
Elective C/S for …
EFW > 4500g in Diabetic mothers and EFW> 5000g in non Diabetic
During labor, decision for C/S if…
EFW >4500g in the setting of prolonged 2nd stage labor or arrest of descent in 2nd stage labor
Fetal movement ( quickening ) present
18- 20 weeks for nulliparous
16-18 weeks for parous
Associated with fetal health
Normal fetus quickening
20- 50 ( scale 0 - 130) per hour
Fewer movements in the day
Larger movement between 9 pm and 1 am
High Risk Pregnancies maternal factors:
Preeclampsia Chronic HTN Diabetes ( including gestational) Chronic Cardiac Disease Chronic Pulmonary Disease Chronic Renal Disease Active thromboembolic disease
High risk pregnancies Fetal Factors
Prior unexplained still birth Isoimmunization Fetal structural anomalies Intra Amniotic infection Fetal Growth restriction Non reassuring Fetal testing ( fetal compromise) Multiple pregnancies
High risk pregnancy Uteroplacental factors
Vasa Previa Placenta Previa Placenta abruptio Unexplained oligohydramnios Prior classic ( high vertical hysterotomy ) Premature rupture of fetal membrane
Fetal NST also called Fetal cardiotocography investigates
Changes in the fetal heart rate pattern with time and reflects the maturity of the fetal autonomic nervous system; for this reason it is less useful in the very preterm <28 weeks gestation.
* Interpretation is largely subjective
Fetal Vibroacoustic stimulation VAS
Response of fetus to vibroacoustic stimulation 82 tp 95 dB applied to the maternal abdomen for 1 -2 seconds. Accelaration of FHR in response to VAS = positive = fetal health
No acceleration in FHR response : do it again up to 3 times with progressive increase in length of time up to 3 seconds
Biophysical Profile when the NST alone not sufficient to determine fetal well-being includes 5 variables : ( BPP)
1) NST
2) Amniotic fluid volume
3) Fetal Tone
4) Fetal movement
5) Fetal Breathing movement
Contraction stress test (CST) aka Oxytocin challenge test (OCT)
Response of FHR to uterine contraction induced by IV oxytocin or nipple stimulation ( release of endogenous oxytocin from neurohypophysis of mother )
Negative CST = no late declarations or severe late decels in response to contractions = healthy well oxygenated fetus .
Doppler Velocimetry
Non invasive, can measure fetal circulation : UA, DV, MCA( umbilical artery , Ductus venosus, middle cerebral artery ) , can measure growth restricted fetus, and growth discordance between twins
Umbilical artery
Frequently evaluated in pregnancy
Has diastolic blood flow
Factors that affect placental resistance
Gestational age
Placental location
Pregnancy complications : abroptio, preeclampsia
Underlining maternal disease : ex maternal Chronic HTN
First , second and third trimester
1st: 1- 12 weeks
2nd: 14- 27 weeks
3rd: 28 weeks - birth
Amniotic Fluid composed of
Water
Lung fluid
Fetal urine
Skin transudate
Aminotic Fluid contains
Electrolytes
Proteins
Desquamated fetal cells called amniocytes
Amniocentesis can be used to
Measure lecithin and sphingomyelin to assess fetal lung maturity
Look for specific pathogenic bacteria when in amniotic fluid infection
To obtain fetal cells for karyotype or genetic analysis
Most common reason for amniocentesis in second trimester
Cytogenetic analysis of fetal cell
* can be done to measure AFP level and acetylcholinesterase level to determine open neural tube defect .
Amniocentesis in the third trimester
1) document pulmonary activity before elective c/s before 39 weeks
2) amnioreduction in pregnancies complicated by polyhydramnios
3) confirm preterm rupture of membrane (PROM)= amnio dye test
4) To exclude amniotic infection .
Fetal Hydrops
Fluid accumulation in more than 1 extra vascular fetal compartment : ascites, Pleural infusion, pericardial effusion, subcutaneous edema, placental edema.
Rho (D) immune globulin decreased immune hydrops
