Newborn at Risk Flashcards

1
Q

7 Common Complications of Newborns

A

§ Prematurity
§ Thermoregulation
§ Respiratory Distress
§ Hyperbilirubinemia
§ Care of Newborn Exposed to Substances (NAS)
§ Hypoglycemia
§ Sepsis

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2
Q

Survival rates on newborns doubles with:

A

Every week gestation

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3
Q

Having one PTB increases your risk for:

A

Another EARLIER PTB

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4
Q

When does surfactant development begin in gestation?

A

24-26 weeks

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5
Q

Respiratory issues in the premature are due to

A

Lack of surfactant

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6
Q

What respiratory problems arise in premature newborn?

A
  1. RDS (r/t poor gas exchange)
  2. Apnea (r/t poor neurological development)
  3. Bronchopulmonary Dysplasia (secondary to intubation/ventilation)
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7
Q

What cardiovascular problems arise in premature newborn?

A
  1. Patent Ductus Arteriosis
  2. Increased respiratory effort
  3. CO2 retention
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8
Q

What thermoregulatory problems arise in the premature infant?

A
  1. decreased brown/SC fat
  2. poor muscular development to maintain flexed tone
  3. inability to shiver
  4. thin skin
  5. increased BSA
  6. increased exposure during resuscitation
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9
Q

What GI problems arise in the premature infant?

A
  1. small stomach
  2. immature feeding reflexes
  3. NEC
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10
Q

What renal problems arise in the premature infant?

A
  1. decreased ability to concentrate urine
  2. decreased ability to excrete drugs
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11
Q

What hepatic/hematologic problems arise in the premature infant?

A
  1. immature liver - decreased conjugate bilirubin - jaundice
  2. risk for hypoglycemia
  3. anemia - limited iron stores
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12
Q

What neurological problems arise in the premature infant?

A
  1. Peri/Intraventricular Hemorrhage
  2. hydrocephalus
  3. hearing loss
  4. retinopathy of prematurity
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13
Q

Who and how long is delayed cord clamping for?

A

Preterm ( <37) and extremely preterm (<28) for 60-120 seconds

If cannot be deferred for that long, at least 30 seconds

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14
Q

6 Reasons Preterm are at risk for decreased thermoregulation

A
  1. higher BSA
  2. lack of brown fat
  3. thin skin
  4. lack of flexion
  5. increased exposure during resuscitation efforts
  6. ambient temperature of delivery room
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15
Q

2 Guidelines for Preterm Temperature Control

A
  1. Delivery room temperature 25-26
  2. <28 weeks should be placed wet up to their neck in a food grade polyethylene bag

(can’t rub/stimulate babe r/t thin skin)

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16
Q

Gestation of Late Preterm Infant

A

34-38 weeks
Still immature at birth though appear normal size
Have missed 4-6 weeks of 3rd trimester

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17
Q

Brain size of 34-35 week gestation

A

60% of that of infant at termThe

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18
Q

The largest proportion of preterm births are

A

Late preterm (34-36 weeks)

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19
Q

5 Criteria for DC of Preterm Infant

A
  1. 24 hours successful feesing
  2. First time mothers require rooming in experience
  3. Take into account health, parenting/feeding skills, support at home
  4. Post DC assessment in community
  5. Developmental follow up
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20
Q

8 Signs of Respiratory Distress

A

§ Tachypnea ( > 60)
§ Apnea ( > 15 seconds)
§ Cyanosis (circumoral)
§ Grunting/cooing
§ Nasal flaring
§ Retractions/indrawing
§ Poor feeding
§ Accessory muscle use

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21
Q

3 common causes of neonatal respiratory distress

A
  1. Respiratory Distress Syndrome (RDS)
  2. Meconium Aspiration (MSAF, MAS)
  3. Transient Tachypnea of the Newborn (TTN – wet lung syndrome)
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22
Q

RDS accounts for _____ of neonatal deaths in ________

A

20%

First month of life

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23
Q

What is the most common cause of respiratory distress

A

RDS

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24
Q

What is respiratory distress syndrome caused by?

A

Lack of surfactant

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25
When is the onset of RDS
At birth or within a few hours
26
What is a protective factor against RDS
Intrauterine Stress - triggers increased maturation
27
7 Rx Factors for RDS
Ø Prematurity/immaturity of lung – lack of surfactant Ø C/S without labour Ø Males Ø Previous birth with RDS Ø Cold stress Ø Maternal Diabetes Ø Perinatal asphyxia
28
5 Protective Factors for RDS
Ø Prolonged ROM Ø GHTN Ø Donor twin (r/t stress) Ø Any physiological stress experienced by the fetus in utero accelerates surfactant development Ø Use of corticosteroids
29
Management of RDS
1. antenatal steroids 2. synthetic surfactant 3. CPAP 4. PEEP 5. supportive care 6. vitals, BGM, s+s assessment
30
MSAF occurs in ______ of live births
12% (8-20)
31
2 Primary Causes of MSAF
1. Physiologic (breech/post-term) 2. Fetal Compromise (stress, cord compression, hypoxia)`
32
When amniotic fluid is stained, what is first ruled out?
Physiologic reason before suspecting fetal compromise
33
How does fetal compromise cause MSAF?
hypoxia leads to vagal reflex and vasoconstriction, inducing in turn hyperperistalsis and meconium emission also relaxes anal sphincter
34
If the meconium is above vocal cords when aspirated:
Very little chance it is in the lung - risk for impaired gas exchange decreases
35
What % of MFAS develops into MAS?
5%
36
The primary concern with MFAS/MAS is:
Inactivation of surfactant decreasing lung compliance Secondary: pneumonitis
36
Care for Meconium Aspiration
1. prevention (avoid post maturity, suctions as indicated) 2. ventilation 3. synthetic surfactant and steroids 4. observation for RD, crackles, rhonchi
36
Define Transient Tachypnea of Newborn
Excess fluid in the lungs or delayed re-absorption of fetal lung fluid (sometimes called “wet lung syndrome”)
37
Transient Tachypnea is _______ @ birth-develops respiratory distress symptoms in ______
Normal 4-6 hours
38
What is TTN related to:
1. aspiration of amniotic fluid 2. excess secretions/tracheal fluid 3. C/S or preterm
39
When does TTN normally resolve?
12-72 hours PP
40
Periventricular Hemorrhage occurs in ____ of neonates < _______ and/or ____ weeks
50% 1500g 35
41
Why does periventricular hemorrhage occur?
Immature cerebral vascular development and weak ventricular capillaries easily rupture
42
When do most periventricular hemorrhages occur?
Within 72 hours
43
NEC occurs in ____ of neonates
10%
44
Mortality rates of NEC
50%
45
What 4 things are thought to cause NEC
1. ischemic/necrotic injury 2. immature intestinal barrer 3. abnormal colonization 4. formula feedings
46
When does NEC typically present?
3-12 days of life
47
Hyperbilirubinemia
excessive concentration of bilirubin in the blood causes jaundice
48
Jaundice
bile pigment deposited in the skin, mucous membranes and sclera
49
Kernicterus
bilirubin levels rise > accepted levels at a given age or rate of rise is high enough  deposited in brain  encephalopathy Levels rise so high that effects brain – irreversible
50
When bilirubin is broken down, RBCs are broken into:
Heme and Globin
51
What happens to heme in RBC breakdown
Becomes unconjugated bilirubin: metabolized and bound to circulating albumin Can be seen in skin, sclera, and mucous membranes If increased levels can enter brain
52
What happens to the globin in RBC breakdown
Goes to liver and binds with gluconaride and becomes conjugated bilirubin and enters gut Can be excreted or if unable/excess can become unconjugated
53
Conjugated Bilirubin
a water-soluble form of bilirubin that has been processed by the liver, making it easier for the body to excrete in urine and giving it a yellow color
54
Unconjugated Bilirubin
insoluble form of bilirubin that originates from the breakdown of red blood cells and becomes soluble only after being processed by the liver; it can accumulate in tissues, causing a yellowing of the skin and eyes if levels are elevated.
55
What is the most common cause of jaundice?
Physiological Jaundice (50-60% of newborns)
56
4 Mechanisms Leading to Physiological Jaundice
1. Newborns increased RBC volume + decreased life span ... RBC hemolysis increases after birth leading to increased bilirubin load 2. Decreased clearance of bilirubin from plasma 3. Immature livers's decreased ability to excrete conjugated bilirubin 4. immaturity of conjugation at birth
57
When is physiological jaundice seen?
peaks at 3 - 5 days; typically resolved by day 8
58
What causes pathological jaundice?
1. excessive RBC destruction 2. increased extravascular blood 3. polycythemia 4. hereditary conditions
59
Why is jaundice seen in the first 24 hours of life pathological?
Mechanisms that cause physiological jaundice take time to occur and should not be present in 24 hours
60
Describe full assessment of baby with jaundice
1. visual inspection 2. assessment of associated findings 3. TcB 4. TsB 5. Coombs/DAT
61
Describe expected visual inspection of infant with jaundice
o Yellowing of skin and sclera o Cephalocaudal (head  toe) progression o Well lit area, preferably natural daylight o Gentle pressure to blanch skin to reveal underlying color of skin
62
only 50% of babies with a TSB concentration greater than _________ appear jaundiced
128 μmol/L
63
TSB Value Severe Hyperbilirubinemia
> 340 at any time in first 28 days
64
TSB value Critical Hyperbilirubinemia
> 425 any time in first 28 days
65
What is Coomb/s/DAT test?
Tests for blood type (ABO) incompatibility to assess reason for excess RBC breakdown DAT + = hemolytic disease of the newborn mother is -, + attacks newborn's RBC
66
Either TSB or transcutaneous bilirubin (TcB) concentration should be measured in ___ infants between ____________ hours of life, the results plotted on the __________ to determine the __________ to severe hyperbilirubinemia
all 24 and 72 predictive nomogram risk of progression
67
Bilirubin Encephalopathy
Kernicterus Neurological effects of unconjugated bilirubin in the brain may be reversible or permanent
68
How does phototherapy help breakdown bilirubin?
Turns unconjugated (fat soluble) to conjugated (water soluble) bilirubin so it can be excreted in the stool
69
What treatment other than phototherapy is there for jaundice newborns?
1. frequent feedings 2. prevention of dehydration 3. exchange transfusion
70
Why are frequent feedings used for treatment of jaundice?
increase intestinal transit time to assist excretion/removal of conjugated bilirubin through feces & urine
71
Newborns with NAS general present with:
1. neurological irritability (high pitched cry, tremors, hyperactive reflex, increased tone, seizures) 2. increased fluids out of everywhere (vomiting, diarrhea, sweating, tachypnea, stuffiness)
72
Cocaine increases risk of:
* Increased risk of placental problems * Increased Risk of miscarriage * Increased Risk of preterm labor * Increased Risk of SIDS
73
Compared to other substances, cocaine decreases incidence and severity of:
Withdrawal symptoms
74
Considerations of Anti-Depressants in Pregnancy
Benefits may outweigh the risks of use during pregnancy SSRIs are most commonly used Newborns may manifest S & S after exposure in utero
75
How does symptoms of utero exposure to antidepressants present in newborn
* Mild symptoms (neuro-behavioral, respiratory, feeding issues, unstable temp) * May be seen within hours but resolves within 2 weeks
76
Are anti-depressants contraindicated in breast feeding
No
77
What drugs are used to treat withdrawal in NAS?
* Opium * Morphine – primarily given * Methadone * Phenobarbital – seizure prevention o Given as newborn and weaned slowly
78
Why is naloxone contraindicated for NAS withdrawal treatment?
can cause rapid withdrawal and seizures o Given to newborns if mother’s had opioids during labour to prevent fetal respiratory depression NOT for infants who may have NAS
79
3 Points of therapeutic handling/developmental positioning for infant with NAS
1. reduce stimulation 2. swaddling to control tremors 3. C - position
80
Describe the C - position used for NAS
to feed and cuddle – differs from rocking * Hold baby and move up & down carefully with baby held away from person (to reduce stimulation) swaddled in c position
81
Newborn Sepsis Symptoms
1. Subtle behaviour changes "not doing well" 2. Temperature instability 3. tachycardia 4. seizures - hypotonia 5. Poor peripheral circulation 6. respiratory distress 7. hyperbilirubinemia
82
DAT positive meaning
ABO incompatibility reaction between the mother's and baby's blood groups. If your baby's DAT is positive, there is a risk that he/she could develop anaemia (low number of red blood cells) and/or jaundice (yellow colour to the skin).