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EOY4 > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What is a strawberry naevus?

A

Hemangioma

Disappears by 2 usually

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2
Q

What are milia?

A

Very very small pearly white papules on the face and forehead due to retained keratin in dermis

Resolves spontaneously

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3
Q

What is erythema toxicum?

A

AKA Neonatal urticaria

  • Appears at 2-3 days
  • Red blotches with central white pustule
  • Found mainly on the trunk
  • Lasts 24h
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4
Q

How does erythema toxicum differentiate to a septic rash?

A

Septic spots are smaller and non-mobile

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5
Q

Why is the skin of neonates more peely?

A

Less vernix (wax) that coats and moisturises their bodies

o Their skin will peel more

  • Olive oil prevents skin from cracking
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6
Q

When are Petechial haemorrhage, facial cyanosis, subconjunctival haemorrhage seen?

A
  • Related to slow birthing trauma of the face
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7
Q

What is neonatal sticky eye and how is it managed?

A

Due to unopened tear duct

Starts on day 3

Saline cleanse and spontaneous resolution

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8
Q

What is ophthalmia neonatal?

A

purulent discharge from the eye in neonates

may be due to bacterial infection (staphylococcal or streptococcal)

Topical chloramphenicol or neomycin

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9
Q

What are two differentials for sticky eye + lid swelling in first 48 hours

A

Gonococcal infection or chlamydia conjunctivis

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10
Q

How should a gonococcal eye infection in first 48 hours be managed? (5)

A

Swab, gram stain and culture urgent

Isolate

Hourly saline lavage

IM or IV ceftriazone

Treat parents

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11
Q

What are the complications of gonococcal eye disease?

A

Risks sight loss and disseminated disease

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12
Q

How does chlamydia conjunctivitis present differently to gonococcal?

A

More delayed presentation (at 1-2 weeks

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13
Q

How should chlamydia conjunctivitis be managed?

A

Regular lavage

Erythromycin PO for 14 days

Treat parents

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14
Q

What are the complications of chlamydia conjunctivits?

A

Pyloric stenosis

Chlamydia in lungs

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15
Q

What are the maternal advantages of breastfeeding?

A

↓ risk T2DM

↓ risk ovarian and breast cancer

Costs less

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16
Q

What are the immediate advantages of breastfeeding? (3)

A

Establishes a relationship/ emotional input from mother

Reduces infection risk e.g. GI, respiratory and otitis media

Protective against necrotising enterocolitis in preterm babies

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17
Q

What are the long term advantages of breastfeeding?

A

Reduces incidence of chronic conditions e.g diabetes, HTN, obesity

Essential nutrition for first 4-6 months

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18
Q

What are are 4 non-medical complications of breastfeeding?

A

Difficult to quantify weight gain

Failure = maternal emotional upset

If preterm, mother has to express until sucking reflex develops (30 weeks)

Multips has risk of not producing sufficient milk

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19
Q

What are 4 medical complications of breastfeeding?

A

Transmission of infection e.g. CMV, HIV

Transmission of drugs e.g. nicotine

Nutritional inadequacy after 6 months

Vitamin k deficiency as insufficient in breast milk

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20
Q

When do the suck reflex, swallow reflex and rooting reflex develop?

A

Suck reflex – 30 weeks gestation

Swallow reflex – 32-34 weeks gestation

Rooting reflex – 3 weeks, disappears at 4 months

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21
Q

Why is infection more common in preterm babies?

A

Maternal IgG is transferred during the 3rd trimester so more immunocompromised

↓ breastmilk = ↓ antibodies

Thymus hypertrophy doesn’t happen until after birth (makes T cells)

Prophylactic abx for sepsis

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22
Q

When is early onset sepsis defined?

A

Within 48 hours.

Anything over is late onset sepsis

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23
Q

What are the risk factors for early onset sepsis? (4)

A

P[P]ROM for >18 hours

Chorioamnionitis

Signs of maternal infection

Foetal distress in preterm lavour

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24
Q

What is the pathophysiology of early onset sepsis?

A

Transplacental Infection (maternal infection that has crossed the placenta)

Environmental Infection (bacterial infection from the birth canal that has entered the amniotic fluid which comes in direct contact with foetal lungs)

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25
Q

What are the most common causative organisms for transplacental infection?

A

Listeria monocytogenes

TORCH viruses

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26
Q

What are the most common causative organisms for environmental infection in early onset sepsis?

A

GBS

E. Coli

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27
Q

What is the pathophysiology of late onset sepsis?

A

Environmental Infection from central lines or endotracheal tubes

Spina bifida

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28
Q

What are the most common causative organisms for environmental infection in late onset sepsis?

A

Gram positive = Staphylococcus epidermidis/aureus or Enterococcus Faecalis

Gram negative = E. coli, Pseudomonas, Klebsiella

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29
Q

What is the definition of preterm birth?

A

Preterm birth as any baby born alive before 37 weeks of pregnancy are completed.

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30
Q

What are the definitions of extremely preterm, very preterm and moderate to late preterm?

A

Extremely preterm = <28 weeks

Very preterm = 28-32 weeks

Moderate to late preterm = 32-37 weeks

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31
Q

What are the CNS complications of preterm birth?

A

Intraventricular Haemorrhage

Retinopathy of prematurity

Poor suck and swallow

↑risk of adverse neurodevelopment outcomes/learning disabilities

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32
Q

What are the CVS complications of preterm birth?

A

↑ risk of PDA + CHD

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33
Q

What are the respiratory complications of preterm birth?

A

Neonatal Respiratory

Distress Syndrome
Chronic lung disease

Apnoea of prematurity

34
Q

What are the GI complications of preterm birth?

A

Necrotising Enterocolitis

Jaundice

Poor milk tolerance

35
Q

Give 3 other complications of preterm birth

A

Hypoglycaemia

Hypothermia

Immunocompromise

36
Q

What is the effect of hypoglycaemia on preterm babies?

A

Defined as <2.6mmol/l

Preterm/ IUGR are more at risk due to poor glycogen stores and ↓ enzyme function

Jittery, drowsy, apnoea ⇢ seizures ⇢ permanent neurological damage if prolonged

Tx = regular monitoring of BMs, milk feed early and often. Can give IV dextrose if really bad

37
Q

What is the effect of hypothermia on preterm babies?

A

Don’t temperature regulate if <1.5kg,

↑SA:Vol, not much subcutaneous fat
Keep warm in incubator, cover baby, heated mattress

↑ energy consumption to keep warm = hypocalcaemia, hypoglycaemia, hypoxia

38
Q

What is intraventricular haemorrhage?

A

Haemorrhage into the ventricular system of the brain, usually happens spontaneously or due to trauma during birth

Usually occurs in first 72 hours of life

39
Q

What are the signs and investigations for intraventricular haemorrhage?

A

Absent moro/drop reflex
Bulging fontanelles
Sleepy

Transfontanelle USS if <32weeks or known IUGR

40
Q

What is the pathophysiology of retinopathy of prematurity?

A

Neonate has immature retinal vessels

Angiogenesis happens in response to an increase in O2

Giving high O2 = rapid and unstructured angiogenesis leading to an inefficient supply to the retina

Leads to a visual impairment

41
Q

What is the management of retinopathy of prematurity?

A

weekly/fortnightly screening from ophthalmologist if premature or low birth weight

Laser photocoagulation/ anti-VEGF injections/ surgery if retinal detachment

42
Q

What is the physiology of surfactant?

A

Surfactant is produced by type 2 pneumocytes and reduces the amount of surface tension within the alveoli by creating a barrier between air and water

Makes alveoli less likely to collapse and easier to inflate

43
Q

When is surfactant produced? Which hormones inhibit and stimulate its production?

A

Surfactant is only produced AFTER 28 WEEKS

Cortisol, thyroxine and prolactin stimulate

Insulin inhibits

44
Q

What is the pathophysiology of Respiratory Distress Syndrome?

A

If baby is born preterm then they have less surfactant so are more susceptible

Insufficient surfactant = ↑ surface tension in the alveoli = ↑ risk of collapse

Diabetic mothers are more prone to having babies with RDS as insulin inhibits surfactant production

45
Q

How does RDS present in neonates?

A

At or within 4 hours of birth:

Tachypnoea - > 60 breaths per minute

Breathing difficulties → subcostal and sternal recessions + nasal flaring

Grunting on expiration → trying to create a positive airway pressure to maintain functional residual capacity!

Cyanosis if really severe

46
Q

What are the bedside investigations for RDS in neonates and why?

A

Pulse oximetry

monitor pO2 and HR

Sats should be maintained at 91-95%

47
Q

What are the blood tests for RDS in neonates and why?

A

Blood gases - Capillary or umbilical? Monitoring for acidosis (Respiratory or metabolic + hypoxia)

U&E - Electrolyte imbalances

Blood culture - Rule out sepsis

LFTs
BM
FBC

48
Q

What imaging should be done for RDS in neonates and why?

A

CXR - changes

Echo - PDA

49
Q

What is the management of RDS in neonates?

A

Oxygen therapy
Can give via high flow cannula or CPAP or mechanically (last resort)

Surfactant
Give steroids to mam if PROM between 28-32 weeks
Surfactant replacement therapy via endotracheal tube

Antibiotics until >3-5 days if blood cultures are negative

Small volume feeds via a tube once breathing is stabilised to stimulate gut development

General supportive therapy

50
Q

What is the normal physiology of bilirubin metabolism?

A

Reticulocytes (RBC precursor) ⇢ Erythrocytes ⇢ Haem + Globin (macrophages in spleen and bone marrow)

Globin → Erythropoeisis

Haem ⇢
Iron → Erythropoeisis

In the liver = Unconjugated Bilirubin → Conjugated Bilirubin

In the terminal ileum = Conjugated bilirubin ⇢ Urobilogen → Stercobilin OR some is reabsorbed using bacterial enzymes from gut flora

51
Q

What are the types of jaundice and how do they come about? Which type of bilirubin is associated?

A

Pre-hepatic
Unconjugated Bilirubin
Anything that ↑ rate of haemolysis e.g. haemaglobinopathies (sickle cell, thalassaemias, G6PD)

Hepatic
Conjugated Bilirubin
Builds up in blood due to ↓ efficiency of liver to break down haemoglobin

Post-hepatic
Conjugated Bilirubin - Bilirubin does not drain into the biliary system via bile

52
Q

When is jaundice normal and not normal in a neonate?

A

First 24 hours = NOT NORMAL

24 hours - 14 days = NORMAL

14+ days = NOT NORMAL

53
Q

Which type of jaundice is present in the first 24 hours and what are the causes?

A

Pre hepatic due to ↑ haemolysis

Sepsis via a congenital infection

Haemolytic Disease of the newborn (ABO incompatibility, Rhesus incompatibility)

Haemaglobinopathy e.g. spherocytosis, sickle cell, thalassaemia, G6PD

54
Q

How does ABO incompatibility lead to haemolytic disease of the newborn?

A

MOther is blood group O

BA-By is blood group A or B

Blood antibodies are usually IgM so can’t cross the placenta but in this case they are IgG so can cross placenta and haemolyse foetal RBCs

55
Q

How does ABO incompatibility present?

A

Severe jaundice that peaks in first 12-72 hours

Normal/slightly ↓ Hb

No hepatosplenomegaly

56
Q

What are the foetal investigations for ABO incompatability?

A

Cord blood samples to find cause

Infection - TORCH screen

Hb (normal or slightly low)

Blood group

Direct Coombs test

LFTs

57
Q

What is the management of ABO incompatibility?

A

Ventilation + high flow + PEEP

Drainage of severe fluid overload e.g. ascites/pleural effusion + IV furosemide if CCF + fluid limitation

Correction of anaemia

IM vitamin K for clotting

58
Q

How does rhesus incompatibility lead to haemolytic disease of the newborn?

A 
Rhesus negative (rr) mother and rhesus positive father (Rr) = Rhesus positive baby 
= baby is incompatible with mother

Blood mixes at birth and maternal immune system becomes sensitised i.e. maternal IgG production in first pregnancy

Problem for later pregnancies is that maternal IgG crosses the placenta causing haemolysis of foetal RBCs

59
Q

How does rhesus incompatibility present?

A

Jaundice - early and more severe than in ABO incompatability + Kernicterus

Hepatospelnomegaly as liver trying to produce more RBCs and liver and spleen taking up more RBCs

Thrombocytopaenia/coagulopathys/hypoalbuminaemia - ↑RBC production at expense of albumin (oedema)

Anaemia → congestive cardiac failure → oedema

Hydrops fetalis

60
Q

What are the maternal investigations for rhesus incompatibility?

A

Maternal blood group, Rhesus status

61
Q

What are the foetal investigations for rhesus incompatibility?

A

Cord blood sampling/ foetal blood

↓ Hb levels, Rh+

62
Q

What is the management of rhesus incompatibility?

A

High risk = intensive phototherapy + extra water

Manage coagulopathy

Daily folic acid for 6 months to ↑RBC

Check for anaemia every 1-2 weeks for 12 weeks - transfuse as packed red cells if Hb <7g/dl or symptomatic. Do audiology screening if transfuse

63
Q

Why is jaundice physiological between 24hours and 14 days?

A

↑ Hb at birth so ↑ breakdown of RBCs (pre-hepatic)

Liver doesn’t fully mature until after 2 weeks (hepatic)

Lack of gut flora to reabsorb conjugated bilirubin/eliminate bile pigments (post-hepatic)

Could also be breast milk jaundice. Cause is unknown but normally resolves around 6 weeks

64
Q

How does prolonged jaundice present?

A

Jaundice after 14 days

Chalky white stools and dark urine that stains the nappy

65
Q

What are the causes of prolonged jaundice with ↑ unconjugated bilirubin?

A

Breast milk jaundice (unknown mechanism) - high unconjugated bilirubin

Infection

Hypothyroidism (↓rate of conjugation)

High GI obstruction e.g. pyloric stenosis

Haemolytic anaemia e.g. spherocytosis

66
Q

What are the causes of prolonged jaundice with ↑ conjugated bilirubin?

A

Biliary atresia is concerning cause
Lumen of biliary tree is absent/blocked leading to an occlusion

Healthy term baby + persistent jaundice + hepatosplenomegaly + high conjugated bilirubin

Diagnose via cholangiogram and needs surgical management + assessment at specialist liver unit

67
Q

What is a general bedside investigation to monitor jaundice?

A

Treatment threshold graph to interpret bilirubin levels (gestation specific as if ↓ gestation then ↓ level of bilirubin for neurological problems).

Has 2 lines: one for phototherapy, one for exchange transfusion and if on/above these lines then have to start the treatment

68
Q

When do you measure serum and transcutaneous bilirubin levels?

A

Measure SERUM BILIRUBIN if in first 24 hours of life OR <35 weeks gestational age

Measure transcutaneously if after 24 hours or if >37 weeks GA

69
Q

What are 6 blood tests to get the cause of jaundice in a neonate and why?

A

Conjugated and unconjugated bilirubin levels

Coombs/ direct antiglobulin test (+ve in antibody mediated anaemias)

FBC + blood film (anaemia + can visualise abnormalities)

TFTs (hypothyroidism is a cause of prolonged jaundice)

U&Es - dehydration?

LFTs - neonatal cirrhosis/damage

70
Q

How does phototherapy work?

A

Light from the blue-green wave converts unconjugated bilirubin to a harmless substance that can be excreted in the urine

71
Q

What are the complications of phototherapy?

A

Not harmful but disrupts care e.g. breastfeeding/cuddles with mum so only start if on or above the treatment line

Baby must be naked except nappy and have eyes covered as bright light is harmful

Also has a risk of temperature disturbance so monitor temperature + macular rash

Stop when bilirubin has fallen below the treatment line (measure serum bill regularly)

72
Q

What is exchange transfusion?

A

Removal of foetal blood through arterial line/umbilical vein and replace with donor blood via peripheral line/umbilical vein

Done if unresponsive to phototherapy

73
Q

What is Kernicterus, a complication of neonatal jaundice?

A

Encephalopathy due to deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei

Happens due to ↑ unconjugated bilirubin to a level that is greater than the albumin binding-capacity

Unconjugated bilirubin is fat soluble so can cross the blood brain barrier

74
Q

How does Kernicterus present acutely?

A

Lethargic/Poor feeding

Irritable

Seizures

Hypertonia + lying with an arched back (opisthotonos)

75
Q

How does chronic Kernicterus present?

A

Choreoathetoid Cerebral Palsy

Learning difficulties

Sensorineural deafness

76
Q

What is necrotising enterocolitis?

A

Preterm bowel is vulnerable to ischaemic insult and bacterial invasion = tissue death

Occurs within first 2-3 weeks of feeding

77
Q

What are the signs of necrotising enterocolitis?

A

Feeding intolerance
Distended abdomen
Bloody stools

78
Q

What are the signs of necrotising enterocolitis on abdominal X-ray?

A

Rigler’s sign (gas in and out of bowel)

Dilated bowel loops

Bowel wall oedema

Pneumoperitoneum

79
Q

Give 4 differentials for tachypnoea in the neonate

A

Acute Respiratory Distress Syndrome

Transient tachypnoea of the newborn (excess fluid in lungs. should resolve within 24hrs)

Meconium Aspiration (resp distress in the neonate born through meconium stained amniotic fluid which cannot be otherwise explained)

Bronchopulmonary dysplasia/Chronic lung disease (need for supplemental O2 28 days after birth)

80
Q

What is Gastroschisis and an omphalocele? How can you differentiate between the two?

A

Defects of the abdominal wall that occur in utero and result in herniation of the gastric contents

There is a lack of a protective sac in gastroschisis which exposes the intestines to amniotic fluid in utero, leading to a thick inflammatory film

81
Q

What is the management of omphalocele?

A

Caesarean to reduce risk of sac rupture

Staged repair (surgery)

82
Q

What is the management of gastroschisis?

A

Vaginal delivery

Go to theatre asap after being born i.e. 4 hours

EOY4 (22 decks)

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