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Patient Assessment 3 > Fetal Development > Flashcards

Fetal Development Flashcards

1
Q

Embryo

A

<10 Week Gestation

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2
Q

Fetus

A

10 weeks to birth

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3
Q

Pre Term Baby

A

A baby is born <37 weeks gestation

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4
Q

Term Baby

A

A baby born between 38-42 weeks gestation

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5
Q

Post Term Baby

A

Baby is born after 42 weeks gestation

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6
Q

Trimesters

A

1st Trimester: < 12 weeks

2nd Trimester: 13-28 Weeks

3rd Trimester: > 28 Weeks

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7
Q

Process of Fertilization

A
  1. Sperm locates the egg
  2. Fertilization occurs
  3. Zygote travels to uterus
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8
Q

The blastocyst combines with what

A

The blastocyst will combine with tissues from the endometrium to form the chorionic membrane (outermost part of the fetal membrane

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9
Q

How does the amniotic sac form

A

The outer tissue will envelop the embryonic structure to form the amniotic sac

The amniotic sac will surround the entire embryo

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10
Q

Umbilical Stalk

A

The embryo attaches via the umbilical stalk which develops into the umbilical cord

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11
Q

Chorionic Villi

A

The umbilical cord connects to the finger-like projections in the outer lining of the chorion (chorionic villi)

The chorionic vili from the embryonic blastocyte will expand and grow to become the placenta

There will be two parts: Maternal compartement and Fetal Compartment

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12
Q

What are the different germ layers

A

Ectoderm

Mesoderm

Endoderm

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13
Q

Ectoderm

A

Outer layer

Central Nervous System: brain and spinal cord

Peripheral Nervous System: cranial nerves and spinal nerves

Sensory epithelia of the eyes, inner ears, and nose

Glandular Tissues: posterior pituitary gland, adrenal medulla

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14
Q

Mesoderm

A

Middle Layer

Cardiovascular System: Heart and Blood Vessels

Lymphatic system vessels

All Connective Tissue

All Muscle Tissue

Kidneys and ureters, spleen

The three major body cavities: pericardium, left and right pleura, and peritoneum

Serous linings of organs within the body cavities

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15
Q

ENDODERM

A

Innermost layer

Digestive System

Respiratory System: pharynx, lungs, and epithelial lining of the trachea and lungs

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16
Q

Embryonal Stage of Development

A

Will have the development of the trachea and major bronchi

Birth at this stage can result in laryngeal, tracheal, or esophageal atresia or stenosis

The baby will often be trached in order to have the trachea dilated

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17
Q

PSEUDOGLANDULAR PHASE

A

Development of remaining conducting airways

There is the incomplete development of the lungs characterized by an abnormally low number and/or size of bronchopulmonary segments and/or alveoli (hypoplasia) can develop

There will also be lung hypoplasia with diaphragmatic hernia

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18
Q

CANNICULAR PHASE

A

Development of vascular bed and framework of respiratory acini

When the fetus is born premature with inadequate developed airways with a surfactant deficiency (lack type II pneumocytes) will lead to RDS

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19
Q

SACCULAR PHASE

A

Increased complexity of saccules

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20
Q

ALVEOLAR PHASE

A

Development of alveoli

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21
Q

Stages of Human Intrauterine Lung Growth

A
  1. Embryonal
  2. Pseudoglandular
  3. Canalicular
  4. Saccular
  5. Alveolar
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22
Q

Post Birth

A

Alveoli and arterial support will continue to increase in size and number throughout infancy and childhood

More than 80% of the eventual total number of alveoli (~300 million) will form after birth

Alveolar growth will form mostly during the first year and a half

Infants will double in in body weight by 6 months and triple by 1 year

Oxygen uptake will increase proportionally

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23
Q

Factors Affecting Lung Development

A

Glucocoid Steroids

Twins

Maternal Diabetes

Decrease Amniotic Fluid

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24
Q

Factors Affecting Lung Development

Glucocorticoid Steroids

A

Accelerate lung maturation (Type II pneumocytes)

The steroid betamethasone may be given to mom if we are worried about a premature baby

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25
Q

Factors Affecting Lung Development

Maternal Diabetes

A

Slows lung tissue maturation

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26
Q

Pneumocyctes Analysis

A

Amniotic fluid can be analyzed for pneumocytes

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27
Q

Pneumocyctes Type I

A

Lays out the structure

Squamous cells

Thin flat membrane that is permeable to gas

97% of alveolar surface area

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28
Q

Pneumocyctes Type II

A

Surfactant production

Can differentiate and become type I cells

Cuboidal

Will appear ~22-24 weeks gestation

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29
Q

Surfactant Composition

A

Surfactant is composed of phospholipids, neutral lipids, and proteins

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30
Q

Mammalian Fetal Lung Fluid Composition

A
  • 90-95% Lipids
    • 80-85% phospholipids
      • Phophatidylcholine is the most abundant phospholipid (75-80%)
      • Dipalmitoylphosphatidlychoine (50%)
      • 1-palmitoyl-2-oleoyl-phosphatidylcholine
    • 5-10 % proteins

Bovine– BLES- very similar to human surfactant

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31
Q

FETAL LUNG FLUID FUNCTION

A

The presence of fetal lung fluid is essential for normal lung development

Fetal lung fluid will promote lung growth and maintain the shape of airways through keeping them filled with fluid. Allows the patency of potential spaces and the development of FRC.

Fetal airways are not collapsed but filled with fluid from the canalicular period until the delivery and the initation of breathing air

The lungs will have breathing like movements, but there is no function until the first breath of air

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32
Q

FETAL LUNG FLUID AND SECRETION

A

The lungs will secrete fluid from the lower respiratory tract (terminal respiratory units) up the conducting airways into the oropharynx where it will be swallowed or join with the amniotic fluid

The baby will produce ~250-350 mL/day

At tern fetal lung fluid levels will peak at 30 mL/kg which is the equivalence of the volume of FRC

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33
Q

FETAL LUNG FLUID AND AMNIOTIC FLUID

A

The lungs will secrete fluid from the lower respiratory tract (terminal respiratory units) up the conducting airways into the oropharynx where it will be swallowed or join with the amniotic fluid

This is why we can test the amniotic fluid for information about fetal lung fluid

The concentration of phosphatidylglyceroland phosphatidylcholine in amniotic fluid is a sensitive indicator for the state of fetal lung maturity

The fetal lung fluid will have a lower pH than amniotic fluid

The baby will produce ~250-350 mL/day

At tern fetal lung fluid levels will peak at 30 mL/kg which is the equivalence of the volume of FRC

Lung fluid is removed from the lung via decreased production prior to birth (hormones), contractions during labor, and lymphatic absorption after birth

If there is lung fluid retention it can lead to respiratory issues such as transient tachypnea of the newborn

Fluid retention problems can be seen with c-sections

The treatment of TTHN is CPAP and O2 therapy (24 hours)

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34
Q

LUNG FLUID RETENTION

A
  • Lung fluid is removed from the lung via decreased production prior to birth (hormones), contractions during labor, and lymphatic absorption after birth
  • If there is lung fluid retention it can lead to respiratory issues such as transient tachypnea of the newborn
    • The treatment of TTHN is CPAP and O2 therapy (24 hours)
  • Fluid retention problems can be seen with c-sections
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35
Q

Diseases that Effect Surfactant

A

Aspiration Syndrome

Ex. Meconium, blood, amniotic fluid

Meconium can inactivate surfactant as well as decrease the production of surfactant

Pulmonary Hemmorrhage or Edema

Deactivation of surfactant

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36
Q

Pulmonary Hemmorrhage or Edema

Risk Factors

A

PDA is a risk factor

Large differences in systemic to pulmonary vascular pressure between the descending aorta and pulmonary vasculature

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37
Q

Fetal Lung Maturity Tests

A

L/S Ratio

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38
Q

L/S Ratio

A

Looks at the componenets of surfactant

The levels of spingomyelin will remain constant in th eamniotic fluid, whereas the levels of lecithin will increase as the fetal lung matures and produces surfactant

This test will be done through amniocentesis or when mom’s membrane is ruptured

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39
Q

L:S Ratio Values

A

The lecithin/sphingomyelin ration (L:S Ration) is usually 1:1 by week 31-32 and 2:1 by 35 week gestations

  • L:S 2:1 or greater
    • Lungs are mature
  • L:S 1.5-1.9 : 1
    • 50% chance of RDS
  • L:S less than 1.5 : 1
    • High risk of RDS
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40
Q

CARDIOVASCULAR DEVELOPMENT

A

The heart will begin to beat regularly early the fourth week after fertilization

Will be from the mesoderm

The heart is the first organ that will be fully formed

At week 8 the heart will be fully developed

At 21 days there will be the fusion of the tubes

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41
Q

FETAL CIRCULATION AND PVR

A
  • Fetal circulation will be very different from adult circulation as the blood is mostly shunted around the lungs
  • There is highly vascularized resistance in pulmonary circulation in the fetus
    • One of the reason there is high PVR is because of the vasoconstriction in response to PaO2
    • The other reason for high PVR is the fluid in the lungs will be pressing down on the vasculature
  • The pressures will be high in the pulmonary system that blood will back up into the right side of the heart increasing pressures in both the right ventricle and atrium
  • The right ventricle is unable to pump through this resistance so it will go through the foreman ovale
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42
Q

FETAL CIRCULATION AND SVR

A

There is a low vascular resistance in systemic circulation

The placenta is a large surface area/volume with a low resistance

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43
Q

UMBILICAL VEIN

A

Return oxygenation blood from the placenta

Enters the fetal body through the umbilicus to the undersurface of the liver then to the branches (2 or 3) to the liver

Continues on to the ductus venosus

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44
Q

DUCTUS VENOSUS

A

Allows blood (30-50%) returning from the placenta to bypass the liver

Drains into the inferior vena cava which goes into the right atrium

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45
Q

FORAMEN OVALE

A
  • An opening in the septum between the two atriums
    • Blood from the inferior vena cava will be deflected from the right atrium into the left atrium
  • Some of the blood will not be shunted through the foramen ovale and rather will go to the right ventricle then into the pulmonary artery
    • But most blood will not flow into the lungs and will be diverted into the ductus arteriosus
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46
Q

DUCTUS ARTERIOSIS

A

A small vessel that connects the pulmonary artery with the descending (thoracic) aorta

It allows more blood to detour into the systemic circulation without going through the fetal lungs

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47
Q

UMBILICAL ARTERIES

A

There are two umbilical arteries

Extensions of the internal iliac arteries

Will carry deoxygenated fetal blood into the placenta

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48
Q

The Placenta

A

The placenta is the only source of oxygen and nutrient rich blood for the baby. It is also the only way for the baby to remove deoxygenated blood

This occurs via finger like projections in the placenta pool

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49
Q

Pathway of the Placenta to the Right Atrium

A
  • Placenta
  • Umbilical Vein
  • Will branch into two
    • One branch to the liver (venous admixture) and then to the IVC
    • The other branch goes directly to IVC (shortcut via ductus venous) (oxygen rich blood)
  • IVC (venous admixture from legs and PaO2decreases also from the liver)
  • RA
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50
Q

Fetal Circulation Superior Vena Cava

A

The SVC bring deoxygenated blood from the head and arms to the right atrium adding more venous blood into the right atrium and decreasing PaO2

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51
Q

UMBILICAL CORD

A

Contains 3 vessels (2 small arteries and 1 large vein) which will be surrounded by a tough gelatinous material (Wharton’s Jelly)

This jelly will prevent the cord from being squished or bent

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52
Q

Blood from the Umbilical Cord

A
  • Contains hemtopaotic stem cells, which can be frozen and used to treat infant cancers
  • The RTs will run cord blood
    • Respiratory acidosis indicates distress of the fetus and an assessment of the baby is required
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53
Q

Fetal Circulation

Atrial Septum

A

There is a two layered wall in the atrial septum which is composed of the septum secondum and the septum primum

Both walls will have holes in them s when pressure is increase a flap will be created between the holes (Foramen ovale) connecting the two atriums

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54
Q

Basic Fetal Blood Flow

A

Placenta (~SaO290%) - Umbilical vein (~SaO280%) - Ductus venosus (~ SaO270%) âIVC - RA (~SaO255% to 65%) - FO - LA - LV - aorta with some blood, between 13 to 25%, going into pulmonary circulation via

RA - RV - pulmonary trunk - Ductus arteriosus - aorta

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55
Q

AMNIOTIC FLUID

A

Will be continuously produced, used, absorbed, and exchanged throughout pregnancy

A term fetus will swallow about 500 mL of amniotic fluid a day and excretes the same amount of hypotonic urine back into the mis each day

There will be ~30mL of amniotic fluid at 10 weeks

At term there will be 1.5 L

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56
Q

Amniotic Fluid Functions

A

Protect the fetus from injury by acting as a cushion

Controls the thermal environment

Assists in the effacement and dilation of the cervix during labor

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57
Q

Amniotic Fluid Composition

A

Maternal blood products

Amniotic cells

Fetal skin, hair, and urine

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58
Q

What is the gas exchange unit of the fetus

A

the placenta

59
Q

Maternal Blood

A

Maternal blood will have a high PO2 and a low pH

Shifts in the oxyhemoglobin curve to the right decreasing the affinity of maternal Hgb for O2

This allow for easy offloading of oxygen to the fetal blood

The low pH is due to extra CO2and the fact that mom has a big belly and it become harder to breathe (pregnancy is a restrictive lung process)

60
Q

Fetal blood

A

Fetal blood has a low PaO2

Shifts the oxyhemoglobin curve to the left allowing easy uploading of O2 by fetal blood

Fetal hemoglobin has the ability to combine with oxygen to a greater extent than adult hemoglobin

61
Q

PRENATAL CARE

A

Also known as antenatal care, and is medical care recommened for women during pregnancy

Should begin at 6-8 weeks of pregnancy

Purpose: To identify any potential problems [normal/low risk or high risk] and to intervene in a timely manner

62
Q

PRENATAL CARE INCLUDES

A

Maternal history & risk factors: Genetic disorders, infectious disease, etc.

Antenatal assessment

Intrapartum monitoringàex: ultrasound

63
Q

MATERNAL HISTORY & RISK FACTORS

Age

A

Too young = risk of spontaneous abortion or poor prenatal care

Too old = risk of genetic disorders (ex. Down syndrome)

64
Q

MATERNAL HISTORY & RISK FACTORS

Lifestyle

A
  • Tobacco cessation counselling
  • Asthma
    • Due to the hormonal changes during pregnancy women will tend to lose control of their asthma and fear being on corticosteroids thinking it will hurt the baby but research shows it is safe for the baby
  • Acute Care for in case mom gets sick
  • Every mother should have the flu shot
  • Maternal diabetes
  • Drug use
65
Q

VIABILITY OF THE FETUS

A
  • Will be dependent upon the stability and maturity of
  • CNS
    • Including protective mechanisms
  • Circulatory system
  • Respiratory system
  • Musculoskeletal system
    • Integrity of the skin will help determine how susceptible the infant is to infections
66
Q

Ultrasounds (Sonography)

A

The first ultrasound will be done around the 11-14 week mark and used to predict a due date

2nd ultrasound will be done at 18-20 mark and can determine sex of the baby as well as look for any anatomical concerns, viability, and estimate gestational age

67
Q

NUCHAL TRANSLUCENCY SCAN

A

Ultrasound that looks at the nuchal folds in the neck of the fetus

Done at 11-14 week of pregnancy when there is an increase risk in the pregnancy

A wider fold = chromosomal defect

Will have a 70% detection rate of Down Syndrome

68
Q

AMNIOCENTESIS

A

Invasive test where a needle will pierce the amniotic sac to obtain an amniotic fluid sample

done in conjunction with an ultrasound at ~15-18 week

Done when there is something that will make the fetus not viable in order to give mom time to plan if they have to do a late abortion

Can have false positives

Will use a needle to pierce and obtain amniotic fluid sample

69
Q

AMNIOCENTESIS Will Test For

A

Lung Maturity

Gender

Rh isoimmunization

Chromosomal abnormalities [trisomy 21]

Fetal enzyme deficiencies

Certain genetic mutations

Spina bifida

Bleeding disorders

70
Q

Nonstress Test (NST)

A

Assess for spontaneous movement by measuring fetal heart rate

When the fetus move the heart rate will increase

In a 20-30 minute period a reactive (good) test means that the heart rate will increase twice for at least 15 BPM for 15 seconds with maternal perception of fetal movement

Reflect normal uteroplacental function and predicts normal fetal survival

71
Q

Contraction Stress Test (CST)

A

Assess viability of uterus and placenta

Monitors fetal HR during an induced contraction (oxytocin). The contraction is used in order to put stress on the fetus and assess a response

Indicated when there is a lack of movement noted late in the pregnancy

A positive test indicated that more the 50% of contractions result in late decelerations (poor outcomes)

72
Q

BIOPHYSICAL PROFILE [BPP]

A
  • Done at the 26-28 mark
  • Indications: Maternal diabetes, hypertension, low fetal movement
  • Scores
    • 8-10 Normal
    • 6= Uncertain repeat test
    • 0-4= Abnormal
73
Q

BIOPHYSICAL PROFILE [BPP] Measures

A
  • Fetal Breathing: 1 episode of 30 seconds during a 30 minute time
    • Normal: Positive
    • Abnormal:Absent
  • Gross Body Movement: 3 during a 30 minute time
    • Normal: 3 or more
    • Abnormal:2 or less
  • Tone: 1 episode of extension/flexion during a 30 minute time
    • Normal: Positive
    • Abnormal:Absent
  • Reactive NST: 2 episodes of +15 bpm increased in 30 minutes
    • Normal: Yes
    • Abnormal:No
  • Amniotic Fluid: 1 pocket of 1 x 1 cm
    • Normal: Positive
    • Abnormal:Absent
74
Q

CHANGES IN THE MOM During Pregnancy

A
  • Nausea and vomiting at 4-6 weeks gestation
  • Frequent urination
  • Cartilage/joint relaxation and stretching
    • Pregnancy will release relaxin
    • More flexible but more prone to injury
  • Skin changes (acne)
  • Fetal movements as early as 16 weeks
  • Uterine Enlargement (fundal height)
    • Will be determined from ultrasound
  • Effacement and dilation
  • Breast development for milk production
  • Hormonal changes
  • Increased respiratory rate and tidal volume (restrive pattern)
  • Blood volume increase (40-50%)
  • Cardiac output can double or triple by 33 weeks gestation
75
Q

Hyperemesis Gravida

A

Severe nausea and vomitting durign preganancy

76
Q

Fundal height

A

Fundal height measured from pelvis to rib cage

At 36 weeks the uterus should be a few cm under the rib cage

77
Q

Hormonal Changes in Mom during preganacy

A

Increased estrogen progesterone and prostaglandins

Prostaglandin will be used to keep PDA open

78
Q

SPONTANEOUS ABORTION [MISCARRIAGE]

A

If occurs in 1st semester

  • fetal in origin due to faulty development

If occurs in 2nd semester

  • maternal factor (ex. trauma, drugs, cervix not supporting fetus, etc)
79
Q

ECTOPIC PREGNANCY

A
  • Implantation outside uterus
    • Most common in fallopian tubes
  • May lead to tubule ruptue which causes a massive hemmorrhage
  • If it is an ectopic pregancy will have to have an abortion
80
Q

MATERNAL DIABETES MELLITUS

A

Gestational diabetes is abnormal glucose intolerance in pregnancy

Results in greater risk for congenital anomalies, respiratory distress, and electrolyte disorders

With good prenatal care and glycemic control you can expect normal pregnancy outcome

The infant of diabetic mother (IDM) is classically a large plethoric infant (> 4000 gms at birth)

81
Q

Uncontrollable Gestational Diabetes

A

Uncontrolled diabetes = maternal hypertension = can lead to uteroplacental insufficiency and polyhydraminos

82
Q

Diagnosis of Gestation Diabetes

A

Drink glucose drink, test blood glucose

Higher than 9mmol = indicates gestastional diabtetes

83
Q

PREECLAMPSIA

A

Occur after 20 week gestation when >140/90 mmHg or a systolic change >30 mmHg or diastolic >15 mmHg

Unknown etiology

Asmatic women have a higher risk

The ultimate treatment will be the delivery of the baby

84
Q

Preclapsia Triad

A

Hypertension

Proteinuria-Frequent urination

Edema

85
Q

Preclampsia BP

A

systolic change greater 30 mmHg

Dys change of 15 mmHg

Bp greater than 140/90 mmHg= preeclampsia

86
Q

Mild Preeclampsia Treatment

A

Mild preeclampsia may be treated with bed rest, low dose aspirin, salt restrictions, and frequent monitoring

87
Q

Severe Preeclampsia Treatments

A

If severe, MgSO4 is added to lessen risk of seizures and as a smooth muscle relaxant

88
Q

Preeclampsia Major Complications

A

Abruption and HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)

Delivery should be managed quickly with antihypertensive agents in place

89
Q

ECLAMPSIA

A

Eclampsia is a sudden progression of preeclampsia where the patient goes into a coma or convulsive seizures

Can occur post-partum if patient had preeclampsia

90
Q

Eclampsia Treatment

A
  • The routine for preeclampsia
  • Quick delivery of the fetus
  • Treatment of symptoms
91
Q

Oligohydramnios

A
  • An abnormally small amount of amniotic fluid
  • Cause is usually unknown
  • Less room for the fetus to grow
    • Growth retardation/restriction
    • Pul hypoplasia– diaphragmatic hernia
    • Agenesis= malformation of organs
92
Q

OLIGOHYDRAMNIOS Can Lead to

A

Compression of structures as they are growing

Anomalies (limb deformities, pulmonary hypoplasia, renal and urinary defects or agenesis)

IUGR

Compression of the cord

Fetal demise

93
Q

POLYHYDRAMNIOS

A
  • Too much amniotic fluid [>2L]
  • Can over distend the uterus, leading to premature rupture of membranes [PROM]
  • Associated with anomalies like anencephaly (part of skull missing), esophageal atresia, TE fistula, neural tube defects
  • Also associated with multiples, hydrops fetalis, maternal diabetes
  • Cause is usually unknown
94
Q

Hydrops Fetalis

A

abnormal accumulation of fluid in 2 or more units– acites, pl.effusions, pericardial effusions, and skin

95
Q

ABRUPTIO PLACENTAE

A

Premature separation [from a minor separation to complete detachment] of a normally implanted placenta from the uterus

Fetal well being can be seriously compromised

Baby or mom can hemorrhage

C Section may be considered for prompt delivery

Etiology is mostly unknown, with a high correlation to preeclampsia

96
Q

PLACENTA PREVIA

A

Placental implantation over or near the internal os

From partial occlusion/covering to complete obstruction of the os

If the fetus or maternal condition is endangered then a cesarean section [C-sec] is almost always performed to deliver the fetus

If deemed minor with no compromise àbed rest

A C-sec will be done in a total previa

97
Q

PLACENTAL INSUFFICIENCY

A
  • Usually in the post term baby as they have grown so big that the placenta can no longer meets it needs
  • Placental aging usually only affects third trimester or post term growth [> 42 weeks’ gestation]
  • The delivered infant is considered as small for gestational age or intrauterine growth retardation
    • Even though they are post term it is because the placenta cant handle it
  • The younger the babe, the smaller the babe!!
98
Q

IUGR [SGA] & LGA

A

These can give clues for what is happening with the baby

Small for gestational age [SGA] : Birthweight < 10% percentile

Large for gestational age [LGA]: Birth weight > 90% percentile

99
Q

SMALL FOR GESTATIONAL AGE

A

Small for gestational age or intrauterine growth restriction(IUGR) is defined as an infant whose weight is below the 10thpercentile or more than 2 standard deviations below the mean for its’ gestational age

100
Q

SMALL FOR GESTATIONAL AGE

Complications

A
  • Birth asphyxia
    • More prone to be breech
  • Hypoglycemia
  • Polycythemia
    • Not developing as they should
  • Thermal instability
    • Because they are smaller
  • Persistent fetal circulation
    • This includes PDA, foramen ovale, etc
  • Malformations
  • Outcomes are based on severity
101
Q

LARGE FOR GESTATIONAL AGE

A
  • Any infants whose weight for is above the 90th percentile for gestational age
  • Usually associated with infants of diabetic mothers but can be seen in infants with anomalies, large infants from large parents, or infants with hydrops
  • Due to their size these infants are at greater risk of birth trauma
    • Harder to come out of birth cannal
    • HIE more common
    • Umbilical cord around neck more common
  • Complications can include RDS electrolyte imbalances
    • Both are mostly in moms with gestational diabetes
102
Q

CEPHALIC PRESENTATION

A

Normal presentation

Ideal position

Head facing posteriorly

103
Q

BREECH PRESENTATION

A

Coming out feet first due to a failure to turn

Normally this will be identified as a problem before labor

May or may not require c section

104
Q

TYPES BREECH PRESENTATION

A

Frank: butt first, feet near head

Complete: knees are bent, feet near butt

Incomplete or Footling: one or both feet stretched out below butt

105
Q

FACE PRESENTATION

A

The chin presents first in this position with the neck hyper-extended

If the chin is posterior, vaginal delivery is not possible

106
Q

BROW PRESENTATION:

A

Brow presentation usually corrects during pregnancy

Less severe than face presentation

If not, vaginal delivery is not possible

107
Q

TRANSVERSE OR SHOULDER LIE:

A

When the fetus presents with the long axis of it’s body not parallel to the mother’s

They could present as should fisrt and if they can be manipulates so that mom can still give birth vaginally

May present shoulder first or may turn as they proceed down the birth canal

If the fetus can be manipulated, vaginal delivery can be accomplished BUT if not, caesarean is the only option

108
Q

RH (D) ISOIMMUNIZATION

First Pregnancy

A

An Rh(D) Negative mom is impregnated by a Rh(D) + man

The mom will become exposed to fetal RBC which can leak across the placenta and stimulate antibody production

Will not affect the first pregnancy but will affect subsequent pregnancies

109
Q

RH (D) ISOIMMUNIZATION

Detection

A

May be detected on amniocentesis through hyperbilirium

110
Q

RH (D) ISOIMMUNIZATION

Subsequent Pregnancies

A
  • After the 1stsensitization mom’s antibodies will lyse (kill) fetal RBC leading to life threatening anemia in the fetus
  • This hemolytic anemia trigger fetal bone marrow to release erythroblasts into circulation
    • Erythroblastosis
111
Q

RH (D) ISOIMMUNIZATION

Prevention

A
  • Mom can be given Rh(D) immunoglobin (Id D): Rhogam or WinRho immunoglobin
    • Usually given at 28 weeks
    • This is if we identify the problem before the RBC begin to lace
  • Intrauterine transfusions will be given through the umbilicus every 2 weeks
112
Q

RH (D) ISOIMMUNIZATION

A

If there is a suspected isoimmunization, the mom is continually tested for Rh levels

If they rise, amniocentesis will be done to monitor bilirubin levels – high levels indicate impending fetal death

113
Q

RH (D) ISOIMMUNIZATION

Newborns with Erythroblastosis

A

Newborns with Erythroblastosis fetalis will usually have exchange transfusion done after birth

Severe Erythroblastosis fetalis in a newborn results in hyperinsulinism, edema and fluid overload, heart + liver + kidney failure, RDS

114
Q

HYDROPS FETALIS

A

Abnormal accumulation of fluid which can lead to severe life threatening swelling and edema due to blood incompatibility of mom and baby

Abdomen (ascites)

Thorax (pleural effusions)

Pericardiac sac (pleural effusion)

Associated with polyhydramnios (too much amniotic fluid) and placental edema

2 types immune and nonimmune

115
Q

HYDROPS FETALIS

Immune

A

Complication of blood group incompatibility between the mother and baby.

This type of hydrops is uncommon, however, because of the widespread use of Rh immunoglobulin treatment for Rh negative women.

116
Q

HYDROPS FETALIS

Non Immune

A

This is the more common type. It can result when diseases or complications interfere with the baby’s ability to manage fluid.

Severe anemias

Congenital infections (infections present at birth)

Heart or lung defects

Chromosomal abnormalities and birth defects

Liver disease

117
Q

HYDROPS FETALIS

SYMPTONS during Pregnancy

A

Large amounts of amniotic fluid

Thickened placenta

Ultrasound of the fetus shows enlarged liver, spleen, or heart, and fluid buildup surrounding the fetus’ abdomen, heart, and lungs

118
Q

HYDROPS FETALIS

SYMPTONS After Birth

A

Pale coloring

Severe swelling overall, especially in the baby’s abdomen

Enlarged liver and spleen

Respiratory distress (difficulty breathing)

Usualy from the huge abdomine but there are also reason affecting bretahing

119
Q

PREMATURE RUPTURE OF THE MEMBRANES [PROM]

A

Membrane has ruptured prior term

Preterm baby where the water has broke before the baby is ready to come out

Prolonged rupture of membrane (ROM) for more than 24 hours can lead to a greater risk of infection and sepsis

Diagnosis is confirmed if amniotic fluid is observed outside the cervix in conjunction with the maternal history:

Fever, Malaise, reported ROM

120
Q

PREMATURE RUPTURE OF THE MEMBRANES [PROM]

When will Labor be induced

A
  • If the fetus is mature enough (36-38 week), labor will be induced
  • If not, the mom will be restricted to bed rest, given MgSO4 to prevent contractions (tocolytic)and steroids to improve lung growth as well as antibiotics, amnioinfusion may be necessary
    • If they know what they are treating they wll use a specific antibiotic if not it will be a broad spectrum one
121
Q

DYSTOCIA

A

Prolonged difficult labor and delivery which is secondary to uterine, pelvic, or fetal factors

When the 1stand 2ndstages of labor exceed 20 hours

122
Q

DYSTOCIA Causes

A
  • Dysfunction of the uterus
    • Contractions are too weak or too strong (obstructing baby from getting out)
  • Abnormal fetal presentation
    • Breech, brow position, face position
    • Fetal head is too large for maternal pelvic opening
    • Hydrocephalus
    • Abnormalities in size or shape of the birth canal
  • Labor that is too long increases mortality of the fetus due to asphyxia, stress, infection
    • So we will try to quick fix the underlying problem or do an emergency c section
123
Q

SHOULDER DYSTOCIA

A

Can occur in larger infants when the anterior shoulder impinges on the pubic bone (Head is popping out but shoulder is stuck)

Uncommon

Once the head is delivered, the babe is caught by the shoulder and is compressed in the birth canal

Speedy manipulationof the infant and delivery are necessary to prevent further infant stress

Broken collar bones and broken arms are a risk during extraction

124
Q

Helping Labor Along- Amniotomy

A

An amniotomy: The doctor ruptures the amniotic sac during a vaginal exam

Once the membranes are broken, and if the cervix is ready, labor starts in a matter of hours.

125
Q

Induction of Labor

A

Whenlabor is artificially started with either Prostoglandin or Oxytocin– synthetic hormones that start and progress uterine contractions

Indomethathin can also be used

Usually given orally but can also be given vagially

126
Q

Induction of Labor

Prostaglandin

A

Hormone that aids in ripening [soft, thinned out] of the cervix.

A gel inserted into the vagina or a tablet given by mouth.

May be used alone or with oxytocin.

To start the labor

127
Q

Induction of Labor

Oxytocin

A

Hormone given to stimulate contractions.

Administered continuously via an IV

Start low dose and increase as needed until labour is progressing well

Usually used to encourage a labour that is stalling.

128
Q

More than one fetus will increase the risk of

A

Premature labor

Abnormalities

Growth problems

Because they are sharing that space

Problems with the placenta or cord

Mortality increase

129
Q

How are multiple gestation diagnosed

A

But reemmeber not all mom get care duing pregency

Can be diagnosed at the 8-11 week ultrasound

130
Q

vanishing twin

A

Some twin pregnancies will only produce one child, a phenomenon termed as vanishing twin

The fetal compartement is absorbed by the other compartment and mom

131
Q

Multiple Gestation Maternal risk factors

A

Increased maternal risk factors include: preterm labor, hypertension, placental abruption, anemia, and urinary tract infections

132
Q

Multiple Gestation Lung Maturity

A

Prematurity with the average delivery at 32 weeks

Lung maturity is accelerated in multiples

31-32 week gestation twins have the same pulmonary function as average 34-35 week singleton infant

133
Q

Multiple Gestation Fetal Risks

A

Twins weighing less than 2500g also have lower mortality rates than comparable singleton infants

Intrauterine growth retardation is also a complication with an incidence of approximately 50-60%

Congenital anomalies are also more common in multiples than with singletons, mostly in monozygotic twins that developed from a single zygote

Anomalies such as conjoined twins and acardia (absence of a heart) are unique to multiple pregnancies

134
Q

Multiple Gestation

Twin to Twin Transfer

A

Twin to twin transfusion is also unique to monozygotic pregnancies: a vascular anastomosis occurs via the shared placenta, with 1 twin receiving most of the blood flow

Clinically a twin to twin transfusion is diagnosed via US when there is a size and amniotic fluid level difference between twins

135
Q

Dizygotic Twins

A

2/3 are dizygotic (fraternal)

multiple ova, 2 different sperm = 2 zygotes

2 placentas

2 umbilicals

So each baby has its own space

136
Q

Monozygotic Twins

A

1/3 are monozygotic (identical)

single ova, 1 sperm = 1 zygote that will split at the 2 cell stage into 2

1 placenta

2 umbilicals

So the babies are sharing space

137
Q

PREMATUIRTY

A

Any infant less than 37 weeks gestation

In most cases the causes of premature labor or premature rupture of the membranes followed by labor is unknown

It is important to differentiate the preterm infant from the growth retarded

Unknown why one pregnancy ends early and another goes to term

138
Q

Risk factors for premature labor

A

–Low socioeconomic status

–Prior prem birth

–Multiple gestation

–Underlying illness

–Maternal age

–Uterine or vaginal infections

–Stress

–Lifestyles: smoking

–Fertility enhancement

139
Q

Signs of Premature Labor

A
  • Contractions that are regular (unlike Braxton-Hicks-fake contractions)
  • Discharge
  • Pressure or cramping
    • Can also be mistaked for BH
  • Backache
  • Severe cramping
140
Q

Complications are Associated with prematurity

A

Infections due to immaturity of the skin and immune response

Jaundice, anemia

Retinopathy of Prematurity [ROP]

Respiratory Distress Syndrome [RDS] due to immaturity of the lung, then BronchopulmonaryDysplasia [BPD]

Inappropriate feeding responses and apneicspells due to immaturity of the CNS

Thermal instability

NEC, liver, and kidney function problems

IVH and neurological deficits due to an immature CNS

141
Q

Prematurity

Survival Statistics

A

32 + weeks: 98% survival

31 – 28 weeks: 90% survival, high risk of deficits

26 – 23 weeks: 40 – 80% survival dependent on gestational age and birth weight, 50% of survivors have serious debilitating deficits

Less that 5% of all premature births are in this category, but these babes have the most complications and require the most intensive care

Long term chronic issues with survivors include (cerebral palsy (CP), ventilator dependence and CLD, neurodevelopmental challenges

142
Q

Treatment of Premature Labour

A

The best preventive measure against premature labor is good prenatal care

Preterm labor can be stopped in approximately 50% of patients with bed rest and the use of drugs to decrease uterine activity

Tocolytics (also called anti-contraction medications or labor repressants) are medications used to suppress premature labor (from the Greek tokos, childbirth, and lytic, capable of dissolving). They are given when delivery would result in premature birth

143
Q

Tocolysis

A

The process of stopping labor is called Tocolysis

Objective

  • Stop contractions via tocolyticagents like Magnesium Sulfate, Progesterone, Nitrates, and Salbutamol (given via IV)
  • Delay infection via antibiotics
    • Labor > 40 hours( PROM)
  • Encourage lung maturity if labor is not arrested via corticosteroids(Dexamethasoneor Betamethasone) to promote surfactant production and decrease the severity of neonatal respiratory distress
144
Q

Postmaturity

A
  • Any infant born after 42 weeks gestation is postmature
  • The causes of postmaturity are generally unknown
  • Infants will have loose hanging skin on the extremities which can be dry and peeling – caused by decreasing amniotic fluid levels and efficiency of the placenta
  • Placental insufficiency can lead to asphyxia of the fetus during labor
  • Postmature infants are at higher risk for meconium aspiration syndrome (because of the spinctertone they can poop in utero) and hypoglycemia (gestational diabetes)

Patient Assessment 3 (12 decks)

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