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Paediatrics > Neonatal Medicine > Flashcards

Neonatal Medicine Flashcards

1
Q

What is respiratory distress syndrome and who is most at risk

A

Deficiency in surfactant

Prematurity (also babies of DM mothers)

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2
Q

How does respiratory distress occur

A
  1. Insufficient surfactant leads to Atelectasis (lung collapse)
  2. Re-inflation with each breath exhausts baby causing respiratory failure
  3. Hypoxia from respiratory failure leads to decreased CO, hypotension, acidosis and renal failure
  4. Death - major cause of death from prematurity
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3
Q

What are the signs of Respiratory Distress

A 
Increased work of breathing shortly after birth
Tachypnoea
Grunting
Hypoxia/Cyanosis  
intercostal regression 
Nasal flaring
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4
Q

What will be seen on CXR with someone with respiratory distress

A

Diffuse granular appearance (ground glass appearance) +/- air bronchograms

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5
Q

What are two differentials for respiratory distress

A

Transient Tachypnoea of the newborn - due to excess lung fluid usually resolves in 24hrs

Meconium Aspiration

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6
Q

How is respiratory distress prevented

A

Betamethasone/Dexamethasone should be given to all women at risk of premature labour from 23-35 weeks

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7
Q

How is Respiratory Distress Syndrome treated

A
  • Delay cord clamping
  • Give CPAP with a PEEP
  • Persists: intubate with mechanical ventilation and O2 inhalation ( around 90% - 100% is toxic)
  • ET tube administration of artificial surfactant within 2 hours of birth
  • Supportive measures: IV fluid replacement, stabilisation of glucose and electrolyte levels
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8
Q

What is bronchopulmnary dysplasia/chronic lung disease

A

Chronic lung disease primarily found in premature infants who have exposed to prolonged mechanical ventilation and O2 therapy for RDS
(still requiring ventilation at 36 weeks gestation)

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9
Q

How does bronchopulmoary dysplasia occur and how will it present

A

Ventilation causes barotrauma, recurrent infections, pneumothorax, inflammation etc.
Continuance of S/S from RDS

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10
Q

How is BPD diagnosed

A

CXR: fine granular densities
Histology: Necrotizing bronchiolitis, fibrosis and atelectasis

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11
Q

What are the complications of BPD

A

Early: feeding problems, severe RSV bronchiolitis, GORD
Late: lowered IQ, cerebral palsy, pneumothorax

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12
Q

What is meconium aspiration

A

In term/near term infants - when meconium in the fetal colon is passed in utero leading to meconium stained amniotic fluid (MSAF)

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13
Q

What are the two causes of MSAF

A

Fetal maturity

Fetal Distress

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14
Q

What can MSAF lead to

A

meconium aspiration - This leads to respiratory distress in the born infant

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15
Q

What are the complications of meconium aspiration

A

Airway Obstruction
Surfactant disfunction
Pulmonary Vasoconstriction
Infection

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16
Q

What is the Rx for meconium aspiration

A
  • unresponsive neonate with green stained amniotic fluid - Emergency intubation and Endotracheal suctioning
  • Surfactant
  • Ventilation
  • Inhaled NO
  • Abx
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17
Q

what is hypoxic Ischaemic Encephalopathy/ Asphyxia

A

Brain injury secondary to lack of oxygen/blood flow to baby

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18
Q

What may cause hypoxic ischaemic encephalopathy/ Asphyxia

A

Antepartum, intrapartum, postpartum

  • Cord prolapse
  • Maternal Hypoxia e.g eclampisa/epilepsy
  • Placenta Abruption
  • Vasa Praevia
  • Respiratory Distress Syndrome
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19
Q

How may an infant with hypoxic ischaemic encephalopathy present

A

Varies on severity of hypoxia

  • Respiratory Depression
  • Need resuscitation
  • pale blue skin
  • slow/weak pulse
  • acidosis
  • hypotonia
  • Encephalopathy develops within 24hrs of birth
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20
Q

How is encephalopathy managed

A
  • Resuscitation and Ventilation
  • Fluid, Blood pressure and perfusion management
  • Therapeutic Hypothermia - standard in term babies with moderate/severe HIE (reduces death and disability)
  • Monitoring and Treating Seizures e.g general anaesthetic
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21
Q

What are congenital TORCH infections

A

Pathogens transmitted from mother to child during pregnancy or delivery

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22
Q

What are the TORCH infections

A 
T oxoplasmosis 
O thers e.g syphilis, varicella, parvovirus B19
R ubella 
C ytomegaly 
H erpes Simplex Virus
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23
Q

What can the TORCH infections cause

A

Spontaneous abortion
Premature birth
IUGR
CNS, endocrine, skeletal and organ abnormalities

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24
Q

How does Toxoplasmosis present and how is it prevented

A

Classic Triad: Chorioretinitis, diffuse intracranial calcifications and hydrpcephalus
Also may get blueberry muffin rash

Prevention: Avoiding uncooked meat, avoiding handling cat faeces

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25
Q

How does Syphilis present and prevention

A

Jaundice, Hepatosplenomegaly, nasal discharge, maculopapular rash and skeletal deformities (later facial abnormalities)

Prevention: Treat mother with Penicillin

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26
Q

What does Varicella Zoster present with and how is it prevented

A 
IUGR
premature birth 
Cateracts 
Encephalitis 
Pneumonia 
CNS abnormalities

Prevention: active immunisation of mother before pregnancy, passive immunisation with VZIG, Acyclovir

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27
Q

How doe parvovirus B19 present and how is it treated

A

Aplastic Anaemia
Fetal Hydrops

Prvention: Frequent hand washing, avoiding contaminated places e.g schools

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28
Q

What does rubella cause and how is it prevented

A

Petechiae and Purpura (blubbery muffin rash)
Sensorineual Deafness
Cateracts
Heart Defects

Active immunisation before pregnancy

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29
Q

What does the Cytomegaly virus present and how is it prevented

A
  • Jaundice
  • Hepatospelomegaly
  • Sensorineural Deafness
  • Petechiae and Purpura (blueberry muffin rash)
  • Microcephaly

Prevention: Frequent handwashing and avoiding contaminated places, Valacyclovir

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30
Q

How does HSV present and how is it prevented

A
  • Premature birth
  • IUGR
  • Skin, eyes and mouth involvement
  • Meningitis

Prevention: C-section if disease active, Acyclovir

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31
Q

When should live vaccines be given

A

MMR or Varicella should be given 3 months before conception they are contraindicated in pregnancy

32
Q

Why and when does Physiological Hyperbilirubinaemia occur

A

Common! - occurs AFTER 24hrs birth
ALWAYS unconjugated!

  1. Increased bilirubin production due to shorter RBC lifespan
  2. Decreased bilirubin conjugation due to hepatic immaturity
  3. Absence of gut flora impedes elimination of bile pigment
  4. Exclusive Breastfeeding - However continue breastfeeding!
33
Q

What tests should you do for jaundice within 24hrs

A

FBC
Blood Film
Blood groups
Coombs Test - may be +ve in ABO incompatibility

34
Q

What is prolonged jaundice and what are its causes

A 
not fading after 2 weeks term or 3 weeks preterm 
Causes:
- Breastfeeding
- Sepsis (UTIs, TORCH)
- Hypothyroidism 
-  CF
- Biliary Atresia if conjugated and pale stools 
- Galactosemia
35
Q

How is Jaundice treated

A

Phototherapy - light energy converts bilirubin to soluble products that can be excreted without conjugation
Exchange Transfusion

36
Q

What can pathological jaundice be caused by in newborns

A

Conjugated HyperBilirubin

Unconjugated HyperBiliruibn

37
Q

What are the causes of conjugated Hyperbilirubin

A 
Decreased bilirubin excretion
Intrahepatic Cholestasis
- SEPSIS
- Hep A and B
- TORCH 
- CF
- Metabolic 
Extrahepatic Cholestasis 
- Billary Atresia 
- Tumours 
- Prolonged Parenteral Nutrition
- NEC
38
Q

What are the causes of unconjugated Hyperbillirubin

A

Haemolytic

  • Infection or Sepsis
  • Haemolytic Disease of the Newborn e.g Rh disease, ABO incompatibility, RBC defects, G6PD Deficiency

Non Haemolytic

  • Hyperbilirubinemia Syndromes
  • Hypothyroidism
39
Q

What is a complication of prolonged Jaundice

A

Unconjugated Bilirubin is lipid Soluble and can cross blood brain - high levels cause Kernicterus
(Conjugated high levels nothing to worry about)

40
Q

How does Kerictierus Present

A

Acute Bilirubin Encephalopathy

  • Lethargy
  • Poor Feeding
  • Hypotonia (floppy baby)
  • Shrill Cry
  • Apnoea
  • Seizures and Muscle Spasms

Chronic Bilirubin Encephalopathy (yellow staining of brain)

  • Cerebral Paresis,
  • Hearing impairment
  • Vertical gaze palsy
  • Movement disorders
  • Intellectual and Developmental Disability
41
Q

What is oesophageal atresia and what is the most common form

A

congenital defect in which the upper esophagus is not connected to the lower esophagus, ends blindly instead

Esophageal atresia with a fistula connected distally to the trachea is the most common kind of esophageal malformation

42
Q

What are the signs of OA

A

Prenatal:
Polyhydramnios
Small Stomach

Postnatal:
OA: Pooling of scecretions- excessive secretions and foaming from mouth

Tracheoesophageal fistula:

  • Aspiration leading to Aspiration Pneumonia
  • Cough
  • Airway Obstruction
  • Cyanosis
43
Q

How is OA diagnosed

A

Inability to pass catheter into stomach

X-ray - oesophageal pouch, no gas in abdomen

44
Q

How is OA Rx

A

Stop feeding
Continuous Suction of secretions from Oesophageal pouch
Urgent Surgery

45
Q

What is Gastroschisis and Exomphalus

How is it diagnosed

How is it treated

A

Gastroschisis: A birth defect of the anterior abdominal wall just lateral of the umbilical cord in which babies intestines are found outside the babies body
not covered in membrane - exposed to the air

Exomphalus: Abdominal contents protrude through abdominal wall through belly button but are covered in an amniotic sac formed from amniotic membrane and peritoneum (umbilical cord attached to sac)

Most commonly antenatally on US

Cover exposed bowel with clingfilm after delivery
Keep Baby warm and Hydrated
Close defect surgically as soon as possible

46
Q

What is a complication of diabetes in the newborn

A

Hypoglycaemia - can lead to seizures and brain injury if prolonged

Caused by making too much insulin during pregnancy if mother has poorly controlled diabetes

47
Q

How is hypoglycaemia managed

A

Monitoring blood glucose levels
Give formula or glucose water mixture
IV glucose if severe

48
Q

How can Hyperthyroidism during pregnancy affect the fetus

A

High numbers of TSH receptor stimulating autoantibodies can cross placenta cause fetal thyrotoxicosis
(usually mothers with Graves Disease)

49
Q

What can fetal thyrotoxicosis lead to

A 
Fetus:
Premature Delivery (after 24 wks)
Goitre, 
Extended Neck in labour
Fetal Tachycardia

Neonate:
Hyperthyroidism: irritability, restless, tachycardia, hyperphagia, poor weight gain, diffuse goitre, microcephaly

50
Q

How does neonatal thyrotoxicosis usually manifest

A
  • Straight after birth

- 10 days later after transplacental maternal antithyroid medication has worn off!!

51
Q

How is neonatal hyperthyroidism treated and what are complications if left untreated

A

Neonatal Graves disease resolves 1-3 mths
Symptomatic: Propanalol and Methimazole

Cardiac Failure
Intellectual Disability
Hyperactivity

52
Q

Who and why is Neonatal sepsis most common in

A

Premature Babies

Last 3 mths of pregnancy there is active transfer of IgG to fetus if premature they get less of it

53
Q

How is Infection acquired to neonates

A

Transplacentally
Ascent from vagina
During Birth
Environment once born

54
Q

What is sepsis and how does SEPSIS present

A

Dysregulated Host response to infection leading to end organ failure

Common causes: Meningococcal and Streptococcal

Non specific and subtle

  • Temperature
  • Lethargy
  • Poor Feeding
  • Respiratory Distress
  • Collapse
  • DIC - Jaundice
55
Q

What and the RF and common causes of early onset neonatal sepsis

A 
Early onset:
Prolonged ROM
Maternal Infection e.g pyretic, chorioamnionoitis
Mother carrier of group B Strep
Preterm Labour 
Fetal Distress
Breaks in neonatal skin

Causes (aquired from mother): GBS, E.Coli, or Listeria, Herpes, Chlamydia

56
Q

What are RF and common causes for late onset neonatal SEPSIS

A 
Late Onset:
Central lines and Catheters 
Congenital Malformation e.g spina bifida 
Severe Illness
Malnutrition 
Immunodeficiency

Causes (acquired from environment): Coagulase -ve Staphylococci, Staph Aureus, E.coli, GBS, Also BEWARE fungal SEPSIS from Candida should be considered in those who don’t respond to normal therapy

57
Q

How is neonatal SEPSIS managed

A
  • ABCDE
Blood Cultures 
Urine output 
Fluids 
Antibiotics 
Lactate 
Oxygen (94%)
  • Do all these within the hour
  • Appropriate Escalation (ICU)
58
Q

How is Group B Haemolytic Strep transmitted and how does it present

A

Via Mothers vagina
Can present straight away or delayed (up to a month)
Can lead to Meningitis!!!
Give all Mothers high risk of passing GBS or +ve to GBS prophylactic IV BenPen throughout labour

59
Q

What is the most common facial malformation

A

Cleft Lip and Palate

60
Q

How does Cleft lip and palate occur

A

Failure of fusion of maxillary and premaxillary processes (defect runs from lip to nostril)

61
Q

What can cause Cleft Lip and Palate

A

Genes
Benzodiazapines
Antiepileptics
Rubella

62
Q

How can cleft lip and palate be prevented

A

Quit smoking
Folic Acid
Avoidance of anti epileptics

63
Q

How is Cleft Lip and Palate treated

A

MDT: Orthodontist, Plastic surgeon, Oral Surgeon, GP, Paediatrican, Speech Therapist

Unilateral - good cosmetic outcome
Bilateral- will always be some residual deformity

64
Q

What are complications of cleft lip and palate

A

Otitis Media
Aspiration
Poor Speech
Avoid taking to NICU - poor bonding

65
Q

What is retinopathy of prematurity

A

Hyperoxic Insult (risk factors O2 therapy and prematurity)

  • arrests normal vascular growth
  • Fibrous ridge formations
  • Abnormal Vascular proliferation
  • Retinal Haemorrhages
  • Severe: Retinal Detachment, Blindness
66
Q

How is retinopathy of prematurity managed

A

Low risk changes - nothing, regular follow up

High Risk changes - Later Therapy

67
Q

What are the infant benefits of Breast Feeding

A 
Less infection
Less immune driven/allergic disease: Cancer, Eczema, DM, Crohns, MS
Reduced risk of NEC
Reduced GORD
Higher IQ better cognition development
68
Q

What are maternal benefits of Breast Feeding

A

Reduces risk of cancer: Endometrial, Ovarian, Breast
Improved Health: Postpartum Haemorrhage, Post partum depression, Osteoporosis, Child Abuse
Promotes post party weight loss
Less food/medical expense
Delays Fertilty

69
Q

How is feeding managed in premature babies

A

IV fluids and Parenteral Nutrition
Trophic Feeding
Monitor Growth
Suck and Swallow starts 32-34 wks

70
Q

What is Apnoea of prematurity

A

Brain Stem not fully developed baby forgets to breath also associated with bradycardia

71
Q

How is Apnoea managed

A

Made worse by SEPSIS
Physical; NPAP, Stimulation
Drugs: Caffiene

72
Q

What is in the newborn physical examination

A

Eyes - cataracts
Heart - heart murmurs
Testicles - descended?
Hips - check for DDH

73
Q

What is IVH and who is it most common in

A

Bleeding inside or around the ventricles of the brain

Premature babies, VLBW - fragile vessels usually occurring in first 72hrs of life

74
Q

How does IVH present and complications

A
  • Apnoea
  • Bradycardia
  • Cyanosis
  • Seizures
  • Lethargy, Coma
  • Blood clots occlude outflow from ventricles - Hydrocephalus
75
Q

How is IVH managed and what are its complications

A

Supportive care of resuscitation, fluids and oxygen

Hydrocephalus/raised ICP - Surgery for Shunt

76
Q

What is hydrocephalus and how does it present

A

Accumulation of CSF within the ventricles of the brain

  • Raised ICP: vomiting, headache, papilloedema and coma
  • Increased head circumference: skull sutures haven’t fused yet
  • Open anterior fontanel will bulge
  • Severe: Failure of upward gaze (sunsetting eyes)
77
Q

How is hydrocephalus managed

A

Ventriculoperitoneal shunt

Extra Ventricular Drainage - acute and severe

Paediatrics (13 decks)

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