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EOY4 > Neonatology > Flashcards

Neonatology Flashcards

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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
What are the most common causative organisms for transplacental infection?
Listeria monocytogenes TORCH viruses
26
What are the most common causative organisms for environmental infection in early onset sepsis?
GBS E. Coli
27
What is the pathophysiology of late onset sepsis?
Environmental Infection from central lines or endotracheal tubes Spina bifida
28
What are the most common causative organisms for environmental infection in late onset sepsis?
Gram positive = Staphylococcus epidermidis/aureus or Enterococcus Faecalis Gram negative = E. coli, Pseudomonas, Klebsiella
29
What is the definition of preterm birth?
Preterm birth as any baby born alive before 37 weeks of pregnancy are completed.
30
What are the definitions of extremely preterm, very preterm and moderate to late preterm?
Extremely preterm = <28 weeks Very preterm = 28-32 weeks Moderate to late preterm = 32-37 weeks
31
What are the CNS complications of preterm birth?
Intraventricular Haemorrhage Retinopathy of prematurity Poor suck and swallow ↑risk of adverse neurodevelopment outcomes/learning disabilities
32
What are the CVS complications of preterm birth?
↑ risk of PDA + CHD
33
What are the respiratory complications of preterm birth?
Neonatal Respiratory Distress Syndrome Chronic lung disease Apnoea of prematurity
34
What are the GI complications of preterm birth?
Necrotising Enterocolitis Jaundice Poor milk tolerance
35
Give 3 other complications of preterm birth
Hypoglycaemia Hypothermia Immunocompromise
36
What is the effect of hypoglycaemia on preterm babies?
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
What is the effect of hypothermia on preterm babies?
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
What is intraventricular haemorrhage?
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
What are the signs and investigations for intraventricular haemorrhage?
Absent moro/drop reflex Bulging fontanelles Sleepy Transfontanelle USS if <32weeks or known IUGR
40
What is the pathophysiology of retinopathy of prematurity?
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
What is the management of retinopathy of prematurity?
weekly/fortnightly screening from ophthalmologist if premature or low birth weight Laser photocoagulation/ anti-VEGF injections/ surgery if retinal detachment
42
What is the physiology of surfactant?
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
When is surfactant produced? Which hormones inhibit and stimulate its production?
Surfactant is only produced AFTER 28 WEEKS Cortisol, thyroxine and prolactin stimulate Insulin inhibits
44
What is the pathophysiology of Respiratory Distress Syndrome?
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
How does RDS present in neonates?
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
What are the bedside investigations for RDS in neonates and why?
Pulse oximetry monitor pO2 and HR Sats should be maintained at 91-95%
47
What are the blood tests for RDS in neonates and why?
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
What imaging should be done for RDS in neonates and why?
CXR - changes Echo - PDA
49
What is the management of RDS in neonates?
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
What is the normal physiology of bilirubin metabolism?
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
What are the types of jaundice and how do they come about? Which type of bilirubin is associated?
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
When is jaundice normal and not normal in a neonate?
First 24 hours = NOT NORMAL 24 hours - 14 days = NORMAL 14+ days = NOT NORMAL
53
Which type of jaundice is present in the first 24 hours and what are the causes?
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
How does ABO incompatibility lead to haemolytic disease of the newborn?
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
How does ABO incompatibility present?
Severe jaundice that peaks in first 12-72 hours Normal/slightly ↓ Hb No hepatosplenomegaly
56
What are the foetal investigations for ABO incompatability?
Cord blood samples to find cause Infection - TORCH screen Hb (normal or slightly low) Blood group Direct Coombs test LFTs
57
What is the management of ABO incompatibility?
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
How does rhesus incompatibility lead to haemolytic disease of the newborn?
``` 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
How does rhesus incompatibility present?
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
What are the maternal investigations for rhesus incompatibility?
Maternal blood group, Rhesus status
61
What are the foetal investigations for rhesus incompatibility?
Cord blood sampling/ foetal blood | ↓ Hb levels, Rh+
62
What is the management of rhesus incompatibility?
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
Why is jaundice physiological between 24hours and 14 days?
↑ 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
How does prolonged jaundice present?
Jaundice after 14 days Chalky white stools and dark urine that stains the nappy
65
What are the causes of prolonged jaundice with ↑ unconjugated bilirubin?
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
What are the causes of prolonged jaundice with ↑ conjugated bilirubin?
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
What is a general bedside investigation to monitor jaundice?
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
When do you measure serum and transcutaneous bilirubin levels?
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
What are 6 blood tests to get the cause of jaundice in a neonate and why?
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
How does phototherapy work?
Light from the blue-green wave converts unconjugated bilirubin to a harmless substance that can be excreted in the urine
71
What are the complications of phototherapy?
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
What is exchange transfusion?
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
What is Kernicterus, a complication of neonatal jaundice?
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
How does Kernicterus present acutely?
Lethargic/Poor feeding Irritable Seizures Hypertonia + lying with an arched back (opisthotonos)
75
How does chronic Kernicterus present?
Choreoathetoid Cerebral Palsy Learning difficulties Sensorineural deafness
76
What is necrotising enterocolitis?
Preterm bowel is vulnerable to ischaemic insult and bacterial invasion = tissue death Occurs within first 2-3 weeks of feeding
77
What are the signs of necrotising enterocolitis?
Feeding intolerance Distended abdomen Bloody stools
78
What are the signs of necrotising enterocolitis on abdominal X-ray?
Rigler’s sign (gas in and out of bowel) Dilated bowel loops Bowel wall oedema Pneumoperitoneum
79
Give 4 differentials for tachypnoea in the neonate
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
What is Gastroschisis and an omphalocele? How can you differentiate between the two?
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
What is the management of omphalocele?
Caesarean to reduce risk of sac rupture Staged repair (surgery)
82
What is the management of gastroschisis?
Vaginal delivery Go to theatre asap after being born i.e. 4 hours

EOY4 (22 decks)

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