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Neonatology Flashcards

1
Q

Need to do congenital heart disease LOs

A

Congenital heart disease

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2
Q

What are the clinical features of neonatal sepsis?

A 
Fever or temperature instability or hypothermia 
Poor feeding 
Vomiting 
Apnoea and bradycardia 
Respiratory distress
Abdominal distention 
Jaundice 
Neutropenia 
Hypoglycaemia/hyperglycaemia 
Shock 
Irritability 
Seizures 
Lethargy, drowsiness
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3
Q

How are early and late onset sepsis defined?

A 
Early onset (<48 hours
)Late onset (>48 hours)
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4
Q

What are the risk factors for neonatal sepsis?

A

In colonised mothers the risk factors are:

  • preterm
  • prolonged rupture of the membranes
  • maternal fever during labour
  • maternal chromioamnionitis
  • previously infected infant
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5
Q

How common is group B strep?

A

10-30% of pregnant women have faecal or vaginal carriage of group B strep
Organism causes early and late onset sepsis
- Early - it can causes pneumonia, may also cause septicaemia, and meningitis
- Late - presents with meningitis or occasionally focal infection

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6
Q

How is group B strep managed antenatally?

A

prophylactic intrapartum antibiotics given intravenously to the mother can prevent group B strep infection in the newborn baby
Given if screening has taken place or if there are lots of risk factors

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7
Q

How does early onset sepsis present?

A

pneumonia, respiratory distress, may causes septicaemia and meningitis

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8
Q

How does late onset sepsis present?

A

meningitis, usually by 3/12 may see septic arthritis, osteomyelitis

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9
Q

List common viral and bacterial pathogens causing disease in the newborn

A

group B streptococcal infection
gram-negative infection
herpes simplex virus
hepatitis B

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10
Q

What are the most common viral infections affecting the fetus and newborn

A 
CMV
Rubella
Toxoplasmosis
Parovirus
Varicella Zooster 
Syphilis
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11
Q

What determines the risk and extent of fetal damage in rubella infection

A

mainly determined by gestational age at the onset of maternal infection

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12
Q

What are the consequences of maternal infection with rubella at 8, 13 and 18 weeks?

A

infection <8/40 = deafness, CHD, cataracts
13-16/40 deafness in 30%
After 18 weeks minimal risk

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13
Q

What is the most common congenital infection?

A

CMV

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14
Q

What are the consequences of CMV infection?

A

90% normal
5% heptosplenomegalty and petechiae at birth, usually neurodevelopmental issues e.g. hearing loss 5% develop propblems later e.g. sensorineural hearing loss

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15
Q

What are the consequences of Toxoplasmosis infection?

A

10% clinically affected - retinopathy, cerebral calcification, hydrocephalus
Likely to have long term neurodisabilities

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16
Q

What are the consequences of VZV infection?

A

infection <20/40 small risk of severe scarring, ocular or neurodamage, digital dysplasia infection within 5 days pre/2 days post delivery ~25% have vesicular rash

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17
Q

When does the infant need protection from chickenpox infection?

A

if mother develops chickenpox shortly before or after delivery

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18
Q

What are the clinical features of congenital syphilis?

A

specific to congenital syphilis:

characteristic rash on the soles of the feet and hands and bone lesions

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19
Q

What are the consequences of herpes infection in mothers?

A

localised herpetic lesions on skin or eye or with encephalitis or disseminated disease

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20
Q

How is HIV transmission from mother to baby prevented and managed?

A
  • use of maternal antenatal, perinatal and postnatal antiretroviral drugs to achieve and undetectable maternal viral load at the time of delivery
  • avoidance of breast feeding
  • active management during labour and delivery –> avoid prolonged rupture of membranes
  • pre labour C-section if mothers viral load is detectable close to tie of delivery
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21
Q

What are the differentials for bile stained vomit?

A

intestinal obstruction until proven otherwise

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22
Q

What are the causes of intestinal obstruction?

A

small bowel obstruction:

  • atresia or stenosis of the duodenum/ileum/jejunum
  • malrotation with volvulus
  • meconium ileus
  • meconium plug
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23
Q

How is early onset sepsis treated?

A

antibiotics are started immediately without waiting for culture results - stopped after 36/28 hours if negative culture
broad spectrum abx are given that cover gram positive and negative organisms

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24
Q

How is late onset sepsis treated?

A

most likely acquired flucloxacillin and gentamycin are given as cover most staphylococci and gram-negative organisms if organism resistant that specific abx are given –> vancomycin or broad spectrum abx indicated

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25
Q

What are the risks of prolonged or broad spectrum antibiotics in neonates?

A

predisposes to invasive fungal infections in premature infants

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26
Q

What are the common investigations used in newborns?

A 
chest xray
lumbar puncture 
CRP 
FBC 
Blood cultures
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27
Q

What is IUGR (Intrauterine Growth Restriction)?

A

Baby fails to reach genetically determined growth potential

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28
Q

What are small for gestational age infants?

A

Babies following IUGR with birthweight below the 10th centile for their gestational age

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29
Q

What are the causes of growth restriction in babies?

A

asymmetrical growth restriction:
placental dysfunction secondary to maternal pre-eclampsia, multiple pregnancy, maternal smoking

symmetrical growth restriction: fetal chromosomal disorder or syndrome, a congenital infection, maternal drug or alcohol abuse, chronic medical condition or malnutrition

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30
Q

What is a fetus with IUGR at risk from?

A

intrauterine hypoxia and ‘unexplained’ intrauterine death asphyxia during labour and delivery

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31
Q

What are potential problems at birth in a growth restricted infant?

A

hypothermia - because of their relatively large SA
hypoglycaemia from poor fat and glycogen stores
hypocalcaemia polycythaemia in addition: RDS, NEC, ROP

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32
Q

What are the long term complications of IUGR?

A

increased risk of T2DM, obesity, HTN, dyslipidaemia, insulin resistance (metabolic syndrome) - leads to premature development of CVD

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33
Q

What is respiratory distress syndrome?

A

deficiency of surfactant which lowers surface tension

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34
Q

What are the consequences of surfactant deficiency?

A

widespread alveolar collapse and inadequate gas exchange

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35
Q

How common is RDS?

A

very common in infants before 28 weeks rare at term but may occur in infants with diabetic mothers and very rarely from genetic mutations

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36
Q

How do babies with RDS present at delivery?

A

tachypnoea over 60 breaths/min
laboured breathing with chest wall recession and nasal flaring
expiatory grunting in order to try to create positive airway pressure during expiration and maintains functional residual capacity cyanosis if severe

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37
Q

How are babies with RDS treated?

A

raised ambient oxygen is required
surfactant therapy may be given by instilling surfactant directly into the lungs via the tracheal tube or catheter
additional respiratory support with CPAP or high flow nasal cannula oxygen
mechanical ventilation may also be used if needed

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38
Q

What are the problems preterm infants face?

A
  • need for rescusitation and stabilisation
  • respiratory - RDS, pneumothorax, apnoea, bradycardia
  • hypotension
  • patent ductus arteriousus
  • temperature control
  • metabolic
  • hypoglycaemia, hypocalcaemia, electrolyte imbalance, osteopenia of prematurity
  • nutrition
  • infection
  • jaundice
  • IVH
  • necrotizing enterocoloitis
  • retinopathy of prematurity (ROP)
  • anaemia of prematurity
  • Iatrogenic
  • bronchopulmonary dysplasia
  • inguinal hernias
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39
Q

How common are pneumothorax is preterm infants?

A

10% of patients who are ventilated presents with increased work of breathing and chest movement on affected side is reduced
tension pneumothorax are treated with chest drain insertion

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40
Q

What is NEC?

A

necrotising enterocolitis
bowel of preterm infant is vulnerable ischaemic injury and bacterial invasion are both risk factors less likely to occur if babies are fed breast milk

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41
Q

What are the signs of NEC?

A

feed intolerance and vomiting (may be bile stained)
distended abdomen
pain
stool stained with fresh blood
infant may become shocked and require mechanical ventilation because of ado distension and pain

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42
Q

What are the characteristic signs of NEC on an X-ray?

A

distended loops of bowel

thickening of the bowel wall with intramural gas may be gas in portal venous tract

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43
Q

What are the consequences of NEC?

A

bowel may perforate

20% mortality

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44
Q

What is the treatment for NEC?

A

stop oral feeding
give oral antibiotics to cover both aerobic and anaerobic organisms
parenteral nutrition is required
mechanical ventical
surgery is performed for bowel perforation

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45
Q

Why are preterms at increased risk of infection?

A

IgG is transferred across the placenta in the last trimester and no IgA or IgM is transferred

Infection at cervix is often a reason for preterm labour and may cause infection shortly after birth

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46
Q

What are the consequences of hypothermia in a preterm baby?

A
  • increased energy consumption and may result in hypoxia and hypoglycaemia
  • failure to gain weight
  • increased mortality
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47
Q

Why are preterm infants particularly vulnerable to hypothermia?

A
  • large SA relative to their mass, so there is greater heat loss than heat generation
  • skin is thin and heat permeable, so transepidermal water loss is important in the first week of life
  • little subcutaneous fat for insulation in the first week of life
  • they are often nursed naked and cannot conserve heat by curling up or generate heat by shivering
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48
Q

How are is the temperature managed in preterm babies?

A

incubators which proved overhead radiant heaters and allow ambient humidity to be maintained which reduces transepidermal heat loss

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49
Q

Why are episodes of apnoea/bradycardia and desturation common in very low birth weight infants?

A
  • Common until 32 weeks gestation as immature central respiratory control
  • May occur when infant stops breathing for over 20-30 secs or when when breathing continues against a closed glottis
  • Must exclude an underlying cause (hypoxia, infection, anaemia etc)
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50
Q

How can apnoeas be treated in neonates?

A
  • Gentle physical stimulation usually starts breathing again
  • Treatment with respiratory stimulant caffeine often helps
  • CPAP may be necessary if apnoeic episodes are frequent
51
Q

What causes retinopathy of prematurity?

A

risk increases with uncontrolled use of high concentrations of oxygen

52
Q

What is retinopathy of prematurity?

A
  • affects developing blood vessels at junction of vascular and non vascularised retina
  • there is vascular proliferation which may progress to retinal detachment, fibrosis and blindness
53
Q

How is ROP managed?

A

susceptible preterm infants are screening every week by an ophthalmologist as laser therapy reduces visual impairment

54
Q

How are interventricular haemorrhages recognised?

A

cranial ultrasound scan

55
Q

When do intraventricular hameorrhages occur?

A
  • Occur in 20% of very low birth weight infants
  • Most common in the first 72 hours of life
  • Most common following asphyxia and in infants with severe respiratory distress syndrome
  • Pneumothorax is a significant risk factor
56
Q

How does a large IVH present?

A

may progress to hydrocephalus –> cranial sutures separate –> head circumference increases rapidly –> AF tense this commonly leads to cerebral palsy

57
Q

When are infants mature enough to suck and swallow?

A

35-36 weeks gestational age

58
Q

How are less mature infants fed?

A

Through OG/NG tube breast milk is introduced as soon as possible and may be supplemented with phosphate and may need protein and calorie (BMF) supplementation and calcium

59
Q

How are infants fed who are very premature (under 1kg birthweight)?

A

Parenteral nutrition is required through is PIC or long line

60
Q

What are the important supplements for preterm newborns?

A

phosphate, calcium and vitamin D - preventing osteopenia of prematurity iron - the is mostly transferred in last trimester therefore pre term infants are at a risk of iron deficiency. Sampling of blood and an inadequate erythropoietin response add to this.

61
Q

Why is breast milk important in pre term infants?

A

provides ideal nutrition

protection against infection (respiratory/gastrointestinal etc)

62
Q

What is bronchopulmonary dysplasia (BPD)?

A

previously called - Chronic lung disease

oxygen requirement at a post menstrual age of 36 weeks

63
Q

Why does bronchopulmonary dysplasia (BPD) occur?

A

lung damage is caused from a delay in lung maturation and damage caused by artificial ventilation, oxygen toxicity and infection

64
Q

What are the chest X-ray changes seen in bronchopulmonary dysplasia (BPD)?

A

widespread areas of opacification

cystic changes

65
Q

How is BPD managed?

A

infants requiring artificial ventilation are weaned onto CPAP or high flow nasal cannula therapy followed by additional ambient oxygen

66
Q

What are the consequences of BPD?

A

increased risk of respiratory failure from bronchiolitis and other LRTI

67
Q

What are the neurodevelopment complications of prematurity?

A
  • 5-10% of very low birth weight infants go on to develop cerebral palsy
  • learning difficulties are common
  • presence of cognitive impairment increases with decreasing gestational age
    other developmental problems include:
  • fine motor skills
  • concentration - short span
  • behaviour problems
  • abstract reasoning
  • processing several tasks simultaneously
68
Q

What are the respiratory changes the occur during transition from fetus to newborn?

A
  • in fetus the lungs are filled with fluid
  • fetus relies on delivery of nutrients and oxygen from the placenta
  • before labour lung liquid production is reduced
  • infants chest is squeezed and descent through birth canal and lung liquid is drained
  • multiple stimuli initiate breathing - thermal, tactile, hormonal
  • reabsorption of alveolar fluid
  • remaining lung fluid is absorbed into lymphatic and pulmonary circulation
69
Q

Describe fetal circulation

A
  • blood vessels that supply and drain the lungs are constricted so blood from the right side of the heart bypasses the lungs and flows through the ductus arteriosus into the aorta and some flows across the foramen oval
  • fetal Oxygen saturations are low (35% lower body/65% upper body) and to compensate for this oxygen delivery to the tissues is enhanced by high haemoglobin concentration along with the shift to the left of the oxygen dissociation curve of metal haemoglobin
70
Q

What are the changes to fetal circulation at birth?

A
  • Pulmonary expansion at birth is associated with a rise in oxygen tension and falling pulmonary vascular resistance
  • Pulmonary blood flow increases
  • Increased left atrial filling results in a rise in the left atrial pressure with closure of the foramen ovale
  • Flow of oxygenated blood through the ductus arterioles causes duct closure
71
Q

Why is maternal bonding and breast feeding important?

A

breast feeding can help establish an intimate, loving relationship with their baby (bonding)

72
Q

Why is vitamin K injection given to all newborn infants immediately after birth?

A

to prevent vitamin K deficiency and therefore prevent haemorrhagic disease of the newborn

73
Q

Why does haemorrhagic disease of the newborn occur?

A

it occurs in the first week of life
mostly mild
some suffer intracranial haemorrhage and half of these babies die
breast milk is a poor source of vitamin K so injection is given at birth

74
Q

Why is the newborn exam (within 72 hours) so important?

A
  • detects congenital abnormalities not already identified at birth (e.g. eye abnormalities, congenital heart disease, undescended testis)
  • check for potential problems arising from maternal disease or familial disorders
  • provide an opportunity for parents to ask any questions
75
Q

Why is newborn hearing screening used on every baby?

A

to detect severe hearing impairment

early detection improves speech and language

76
Q

What is the Guthrie test/Biochemical screening test used to test for?

A 
all babies have a heel prick test on day 5-7 of life to test for:
congenital hypothyroidism
haemoglobinopathies 
cystic fibrosis 
six inherited metabolic diseases  
- phenylketonuria 
- MCAD  
- maple syrup urine disease  
- isovaleric academia  
- glutamic acuduria type 1  
- homocystinuria
77
Q

What does antenatal ultrasound screening test for?

A

gestational age
multiple pregnancies
structural malformations can be detected
fetal growth can be monitored
amniotic fluid volume - oligohydramnios and polyhydramnios

78
Q

Why do 50% of newborn infants become visibly jaundiced?

A
  • marked physiological release of haemoglobin from the breakdown of red cells because of of the high haemoglobin concentration at birth
  • red cell lifespan of newborn infants is markedly shorter than that of an adults
  • hepatic bilirubin metabolism is less effective in the first few days
79
Q

Why is neonatal jaundice important?

A

may be sign of another disorder (haemolytic anaemia, infection, inborn error of metabolism, liver disease) unconjugated bilirubin can be deposited in the brain causing kernicterus

80
Q

What is kernicterus?

A

encephalopathy resulting from deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei occurs when the level of unconjugated bilirubin exceeds the albumin binding capacity of bilirubin of the blood free bilirubin is fat soluble so it can cross the blood brain barrier

81
Q

What are the consequences of kernicterus?

A

acutely –> irritability, increased muscle tone, seizures and coma
infants who survive –> cerebral palsy, learning difficulties and sensorineural deafness

82
Q

What are the causes of Jaundice <24 hours of age?

A

usually results from haemolytic disease
Rhesus haemolytic disease
- affected infants are usually detected antenatally and treated ABO incompatibility
- haemolysis can cause jaundice but usually less severe that rhesus disease G6PD deficiency Spherocytosis Congenital infection at birth

83
Q

What are the causes of jaundice at 2 days-2 weeks of age?

A

Physiological jaundice - normal part of transition from fetal life
Breast milk jaundice - jaundice is more common in breast milk fed infants
Dehydration - jaundice can occur when there is a delay establishing breastfeeding
Infection - UTI can present this way as a sign of poor fluid intake, haemolysis, reduced hepatic function

84
Q

What is the management for jaundice?

A

Correct poor milk intake and dehydration
Phototherapy - light converts unconjugated bilirubin into harmless water soluble pigment which can be excreted in the urine
Exchange transfusion - needed if bilirubin are at dangerous levels - blood is removed from baby and replaced with donor blood (risk involved)

85
Q

What is classified as prolonged neonatal jaundice?

A

jaundice in babies lasting over 2 weeks (3 weeks if preterm) KEY FEATURE –> may be caused by biliary atresia

86
Q

Why is it important to detect biliary atresia?

A

delay in surgical treatment adversely affects outcomes

87
Q

When is conjugated hyperbilirubinaemia suggested?

A

pale stools
dark urine
hepatomegaly and poor weight gain and other clinical signs that may be present

88
Q

What are the causes of conjugated hyperbilirubinaemia?

A

neonatal hepatitis syndrome

biliary atresia

89
Q

What is important to note about the presentation timing of jaundice?

A

it often presents in the community setting after discharge from the hospital

90
Q

What is the significance of a mongolian blue spot found in a new born baby check?

A

blue black macular discolouration at the base of the spine
no significance unless undiagnosed bruises
fade slowly over the first few years

91
Q

What is erythema toxic (neonatal urticaria) - found in a new born baby check?

A

common rash appearing at 2-3 days of age

consistent of white pinpoint papule at the centre of an erythematous base lesions come and go at different sites

92
Q

What is capillary haemangioma - found in a new born baby check?

A

“stork bites”

pink macules on the upper eyelids, mid foreheads and nape of the neck are common are arise from distention of dermal capillaries those on the eyelid gradually fade over the 1st year, those on the neck become covered in hair

93
Q

What is cephalhaematoma?

A

Birth injury - soft tissue
Haematoma from bleeding below the periosteum, confined within the margins of the skull sutures - usually involves the parietal bones
Resolves over several weeks

94
Q

When does brachial plexus injury occur?

A

Birth injury
Results from traction of the brachial plexus nerve roots
May occur at breach deliveries or with shoulder dystocia
Upper root palsy (Erb) can resolve completely - if not orthopaedics/plastics referral

95
Q

What is “sticky eye” in neonates?

A

common in newborns as they have narrow tear ducts should resolve after a few weeks when ducts open up ?

96
Q

What is rhesus incompatibility?

A

During birth the mother may be exposed to infants blood and develop antibodies which could effect future Rh+ pregnancies
Rhesus disease can be prevented by treating mother during pregnancy or soon after delivery with an IM injection of anti-RhD immunoglobulin

97
Q

What are the consequences of rhesus incompatibility?

A

affected infants are identified antenatally and monitored and treated if necessary
birth of a severely affect infant with anaemia, hydrops, hydrocephalus is rare

98
Q

What is ABO incompatibility?

A

most ABO antibodies are IgM do not cross the placenta
some group O women have IgG anti - A hameolysin in their blood which can cross placenta and haemolyse the red cells of a group A infant

99
Q

What are the consequences of ABO incompatibility?

A

haemolysis can cause severe jaundice but usually less severe than rhesus disease jaundice peaks at in first 12-72 hours Coomb’s test is positive –> direct antibody test demonstrates antibody on surface of red cells

100
Q

What are the important risk factors for congenital abnormalities of maternal health impacting on these?

A
  • inherited genes
  • anomaly
  • consanguinity (parents are related)
  • ethnic background
  • maternal age
  • infections
  • alcohol/tabacco/radiation
  • nutrition (folate)
101
Q

What are the common craniofacial features in Downs Syndrome?

A 
round face and flat nasal bridge 
unslanted palpebral fissures 
epicanthic fold 
brushfield spots on the iris 
small mouth and protruding tongue 
small ears 
flat occiput and third fontanelle
102
Q

What are the other anomalies in Downs Syndrome?

A 
short neck 
single palmar creases 
incurved fifth finger
short fifth finger 
wide sandal gap 
hypotonia 
congenital heart defects 
duodenal atresia 
Hirschsprung disease
103
Q

What is the VACTERAL association?

A 
a group of malformations 
vertebral anomalies 
anal atresia 
cardiac defects 
trachea-oesophageal fistula 
renal anomalies 
limb defects
104
Q

What is the CHARGE syndrome?

A

an abbreviation for several of the features common in the disorder:
coloboma heart defects, atresia choanae (also known as choanal atresia) growth retardation, genital abnormalities, ear abnormalities

105
Q

What are Patau (trisomy 13) and Edwards syndrome (trisomy 18)?

A

particular constellation of severe multiple abnormalities suggest these diagnoses at birthmost babies die in infancy can be detected by USS in 2nd trimester

106
Q

What is fetal alcohol syndrome?

A

excessive alcohol ingestion during pregnancy is sometimes associated with this clinical features: growth restriction, characteristic face, developmental delay, cardiac defects

107
Q

What are some examples of neural tube defects?

A

anencephaly, encephalocele, spina bifida occulta, meningocele and myelomeningocele and myelomeningocele

108
Q

What are the consequences of NTD (myelomenigocele)?

A

paralysis of the legs dislocation of hips sensory loss neuropathic bladder and bowel scoliosis hydrocephalus Chiari 2 malformation

109
Q

What has reduced the birth prevalence of NTD in the UK?

A

periconceptual folic acid antenatal screening natural decline

110
Q

What is cleft lip and palette?

A

inherited polygenically may be part of a syndrome of multiple abnormalities e.g. chromosomal disorders may be detected antenatally on ultrasound surgical repair of the lip takes place at 3 months and palette tees place at 6-12 months

111
Q

What is gastroschisis?

A

bowel protrudes through a defect in the anterior abdominal wall adjacent adjacent to the umbilicus and there is no covering sac

NOT associated with other congenital abnormalities

112
Q

What is exomphalos?

A

abdominal contents protrude through the umbilical ring covered in a peritoneum often associated with other congenital abnormalities

113
Q

What are one third of duodenal attresia or stenosis of the duodenum associated with?

A

Downs syndrome

114
Q

What are the causes of small bowel obstruction?

A
  • atresia or stenosis of the duodenum
  • atresia or stenosis of the jejunum or ileum
  • malrotation with volvulus
  • meconium ileus, impacted meconium into ileum wall
  • meconium plug
115
Q

How does small bowel obstruction present?

A

Persistent vomiting - while is bile stained unless the obstruction is above the ampulla of vater
Abdominal distention
Diagnosis made on X-Ray

116
Q

What are the causes of large bowel obstruction?

A

Hirschsprung disease - absence of the myenteric nerve plexus in the rectum. More common in boys with Down’s syndrome

Rectal atresia - absence of anus at normal site

117
Q

What is congenital adrenal hyperplasia?

A

several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of mineralocorticoids, glucocorticoids or sex steroids from cholesterol by the adrenal glands (steroidogenesis) conditions involve excessive or deficient production of sex steroids and can alter development of primary or secondary sex characteristics in some affected infants

118
Q

What are the causes of HIE in neonates?

A

most cases occur after a significant hypoxic event immediately before or during labour or delivery including

  • failure of gas exchange across the placenta e.g. placental abruption, prolonged uterine contractions
  • interruption of umbilical blood flow e.g. cord prolapse, cord compression
  • inadequate maternal placental perfusion hypotension or hypertension
  • compromised fetes e.g. IUGR , anaemia
  • failure of cardiorespiratory adaptation at birth e.g. failure to breath
119
Q

What are the clinical features in mild HIE?

A 
infant is irritable 
responds to stimulation 
may have staring of the eyes 
hyperventilation 
hypertonia 
impaired feeding
120
Q

What are the clinical features in moderate HIE?

A

marked abnormalities of movement
hypotonic
cannot feed
may have seizures

121
Q

What are the clinical features in severe HIE?

A

no spontaneous movements or response to pain
tone in limbs may fluctuate
seizures are prolonged are often refractory to treatment
multi-organ failure is present

122
Q

How is HIE managed?

A

skilled resuscitation and stabilisation will minimise neuronal damage may need:

  • respiratory support
  • treat seizures with anticonvulsants
  • fluid restriction because of transient renal impairment
  • treatment of hypotension
  • monitoring and treatment of hypoglycaemia and electrolyte imbalance, especially hypocalcaemia THERAPEUTIC HYPOTHERMIA
123
Q

How can therapeutic hypothermia be used in the management of HIE?

A

mild hypothermia (rectal temp of 33-34 degrees for 72 hours by wrapping infant in a cooling blanket) for infants >36 weeks with moderate or severe HIE reduces brain damage if started within 6 hours of birth

124
Q

What are the long term neurodevelopment risks of HIE

A

mild

  • complete recovery expected moderate
  • if infants haven’t fully recovered by 2 weeks full recovery is unlikely

severe
- mortality - 30-40% neurodevelopmental disabilities can occur including cerebral palsy causes encephalopathy and multi organ dysfunction

Paediatrics (13 decks)

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