Neonatology Flashcards
(168 cards)
1
Q
What is Jaundice?
A
Condition of abnormal high levels of bilirubin in the blood.
2
Q
What is physiological jaundice in the newborn?
A
There is a high concentration of red blood cells in the neonate and foetus. The red blood cells are more fragile than normal red blood cells and the foetus and neonate also have less developed liver function. Fetal red blood cells break down more rapidly than normal red blood cells and release lots of bilirubin, normally this bilirubin is excreted by the placenta, however at birth the foetus no longer has access to a placenta to excrete bilirubin, this leads to a normal rise in bilirubin shortly after birth which causes a mild yellowing of skin and sclera from 2-7 days of age. Usually it will resolve completely by ten days.
3
Q
What are the causes of jaundice in the first 24 hours?
A
Jaundice in the first 24 hours is always pathological Rhesus haemolytic disease ABO haemolytic disease Hereditary spherocytosis Glucose 6 phosphodehydrogenase
4
Q
If the baby is less than 24hrs and is jaundice, what should you do?
A
They are at high risk of developing severe hyper bilirubin anemia and therefore must have their serum bilirubin urgently (within 2 hours)
5
Q
What investigations should you do if there are still signs of jaundice after 14 days?
A
A jaundice screen is performed, this includes…
Conjugated and unconjugated bilirubin (raised conjugated bilirubin could indicate biliary atresia which requires urgent surgical intervention).
. Direct antiglobulin test (Coombs)
. TFTS
. FBC and blood film
. Urine for MC&S and reducing sugars
. U and Es and LFTS
6
Q
What are the causes of prolonged jaundic3?
A
Biliary atresia Hypothyroidism Galactosaemia UTI Breast milk jaundice Congenital infections-CMV, toxoplasmosis
7
Q
What are the circulation changes during birth?
A
Removal of placenta
Reduced pulmonary vascular resistance
Onset of breathing
Closure of the shunts (ductus venosus, ductus arteriosus, Foramen ovale)
8
Q
What does the heel prick (Guthrie) check for?
A
This on the 5th day of life
It screens got common illnesses (sickle cell anaemia, cystic fibrosis, congenital hypothyroidism, common metabolic defects)
9
Q
What clinical features are assessed in a newborn examination (within 24 hours of life)?
A
Head- red pupil reflex, hard and soft palate, fontanelle, facial dysmorphism, tongue/lip cyanosis.
Breathing- rate, rythm, resp distress?
CVS- rate, murmurs, check femoral pulses (coarctation of aorta)
Neuro- tone, reflexes, baby should be in flexed position, check spine and back for dimples, marks and spina bifida.
Hands and feet- check for palmar crease, talipes, extra digits
Abdomen- palpate for masses, check umbilical cord
Hips- check for developmental dysplasia of the hip
Genitalia
Hearing
Eyes- looking for retinoblastomas (very malignant and can spread to brain) and for cataracts (peripheral blindness within 6 weeks if not treats).
10
Q
Give brief overview of the newborn examination…
A
. Document any birthmarks
. Plot newborn on growth chart
. Get senior input if you Are unsure of any findings
. Ask mum how she is feeling and if she has any concerns.
11
Q
What would be contraindications to vaccinations?
A
Anaphylaxis to previous vaccine or vaccine component
Anaphylaxis to egg (yellow fever and influenza)
Immunocompromised (live attenuated)
12
Q
What is the difference between perinatal and neonatal mortality rate?
A
Perinatal= number of stillbirths and neonatal deaths within the first week of life per 1000 live births
Neonatal= number of deaths per 1000 live births in the first 28 days
13
Q
What are the two types of IUGR and what is meant by them?
A
Symmetrical IUGR= this is where there is a proportionally small head, length and weight
Asymmetrical IUGR= there is a small length and weight but the head circumference is preserved
14
Q
What is the usual causes of symmetrical IUGR?
A
Intrauterine infections and chromosomal abnormalities
15
Q
What are the causes of asymmetrical IUGR?
A
Placental insufficiency/ pre eclampsia
16
Q
What investigations would you do at birth for IUGR?
A
Blood gas is typical on delivery to get a baseline on how unwell the infant is
17
Q
What are the risk factors for prematurity/ IUGR?
A
Multiple pregnancy Maternal illness Placental insufficiency In utero infection Genetic disorder
18
Q
What is meant by prematurity?
A
Any birth before 37/40 weeks gestation.
19
Q
What is meant by IUGR?
A
Failure of the foetus to achieve genetic growth potential.
20
Q
What is meant by SGA?
A
A newborn below a certain centile for that particular gestation, usually the 10th centile.
21
Q
What is LBW?
A
Newborn weighing less than 2500g
22
Q
What is VLBW?
A
Newborn weighing less than 1500g
23
Q
What is a stillbirth?
A
Foetus born after 24/40 that never shows any signs of life.
24
Q
What is neonatal death?
A
Death of a newborn within 28 days of delivery
25
How should you manage premature/SGA babies?
NICU
Very premature often need intubation, ventilation and surfactant.
Often need feeding support and to be closely monitored for complications.
26
Why are neonates susceptible to hypothermia?
They have thin skin
Little adipose tissue
Large body surface area compared to their weight
27
How can you prevent babies from losing heat?
Warm mattress/ skin to skin with Mum (conduction)
Keeping room temperature warm and avoiding droughts (convection)
Wrapping baby including hats and socks (evaporation)
Using incubator as radiant heat source (radiation)
28
What is the blood glucose level in a neonate with hypoglycaemia?
<2.6mmol/l
29
What are the causes of hypoglycaemia?
Decreased glucose production (preterm/metabolic errors)
Increased glucose demands (sepsis/hypothermia)
Hyperinsulinism (diabetic mother)
Endocrine problems
30
What are the symptoms of hypoglycaemia in a neonate?
Jitteriness, hypotonia, apnoeas +/- seizures (if they have seizures it’s severe)
31
What investigations would you do if you were suspecting neonatal hypoglycaemia?
Check blood temp and sugars regularly, if identified then you need to investigate driving cause.
Symptomatic or severe (<1.5mmol/l) hypoglycaemia should prompt a hypo screen which looks for endocrine and metabolic causes.
32
How would you manage an infant with hypoglycaemia?
1.6-2.6mmol/l- feed infant and consider increasing feed frequency and volume, most hypoglycaemic episodes are transient are not sinister.
<1.6mmol/l or asymptomatic- treat immediately with IV dextrose (10%), admit to neonatal unit and monitor blood sugars hourly until stable.
33
What is respiratory distress syndrome?
It is also known as hyaline membrane disease. It is a condition of prematurity caused by insufficient levels of surfactant, it is more prevalent the more premature an infant is. It manifests in a tachypnoea case newborn showing signs of resp distress.
34
What is the pathophysiology behind respiratory distress syndrome?
. Lack of surfactant May be bascule the infant is premature (surfactant is produced in the third trimester) or because the affect of surfactant has been inhibited by asphyxia. Surfactant lowers the alveolar surface tension allowing the lungs to open and close easily without collapsing. The loss of surfactant results in alveolar collapse.
35
What is the cycle of respiratory distress syndrome?
Alveolar collapse due to the surfactant leads to impaired gas exchange, this then leads to hypoxia and acidaemia which further impairs surfactants effect and again leads to alveolar collapse.
36
What are the risk factors for respiratory distress syndrome?
Main one is prematurity
Perinatal asphyxia- difficult birth, meconium aspiration, sepsis, congenital lung anomalies.
Maternal diabetes- lungs are delayed in their maturity.
37
What babies should recieve surfactant treatment?
Surfactant is produced by type 2 pneumocytes which are present from 20/40 gestation however there is an increased number during the final trimester.
All neonates born <28/40 should get surfactant after delivery and maternal antenatal steroids should be given.
Treatment with exogenous surfactant in respiratory distress syndrome reduces the mortality by 40%
38
What are the clinical features of respiratory distress syndrome?
Symptoms- distressed and unwell infant, poor feeding
Signs-
Tachypnoea (>60 breaths per minute)
Hypoxia
Respiratory distress (tracheal tug, head bobbing, nasal flaring, intercostal and subcostal recession)
Grunting (In an attempt to increase airway pressure and open collapsed alveoli).
39
When is the onset of respiratory distress syndrome?
Normally it is less than 4 hours after birth
40
What are the investigations of respiratory distress syndrome which are normally carried out?
Blood gases (they show hypoxia and metabolic acidosis(
CXR (show ground glass infiltrate with air bronchograms and reduced lung volume)
Important to screen for other causes of respiratory exists as so send blood cultures, FBC, U and Es and swabs from both mother and infant.
41
What are the differential diagnoses for respiratory distress syndrome?
```
Sepsis
Complex heart disease
Lung hypoplasia
Pneumothorax
Severe anaemia
```
42
What is the management of respiratory distress syndrome?
Oxygen to improve oxygenation, aiming for pO2 to be between 6 and 10
CPAP and mechanical ventilation to give sufficient pressure to open airways and prevent further lung collapse
Artificial surfactant to increase lung compliance and decrease alveolar surface tension
If possible give antenatal steroids to the mother prior to delivery in at high risk pregnancies
Correct hypothermia, acidaemia and hypoglycaemia.
43
What neurological damage is related to prematurity?
Intra ventricular haemorrhage and periventricular leukomalacia.
44
What is intraventricular haemorrhage?
Alteration in cerebral blood flow (from apnoea, acidaemia, hypotension) this results in bleeding in the fragile germinal matrix, which if severe enough will extend into the ventricles, the germinal matrix disappears in the 3rd trimester and as such is a condition seen in neonates which are born prior to 32 weeks gestation)
45
What is the pathophysiology behind periventricular leukomalacia?
Thought that hypoperfusion and excitotoxic cytokines cause damage to the oligodendroglia, which then results in white matter injury.
46
What are the risk factors for brain injury in a neonate?
```
VLBW (gestation <32 weeks)
Difficult birth
RDS
Cardiovascular instability
Sepsis
Necrotising enterocolitis
```
47
What are the clinical features of brain injury in the neonate?
They are often asymptomatic, especially if the insult is small
Seizures and apnoeas may occur with big bleeds
Significant neurological insult may present as floppy infant and poor feeding
In terms of signs, there may be abnormal movements or tone
A large IVH May present as a hypovolaemia neonate (tachycardia and peripherally shut down).
48
What is the site of injury in IVH?
The germinal matrix
49
What are the risk factors for infection in a neonate?
```
Prematurity
Maternal pyrexia in labour
PROM
LBW
Long lines in situ
Chorioamnionitis
Maternal group B strep colonisation
```
50
What are the differential diagnoses for neonatal infections?
Congenital infections
Respiratory distress syndrome
Congenital heart problems
Necrotising enterocolitis
51
What investigations should be done if your suspecting neonatal infection?
Septic screen(nasal, throat,line swabs, bloods, cultures, urine dip, CXR, lumbar puncture).
52
What is the management of neonatal infections?
Antibiotic treatment should be commenced <1 hour if clinical suspicion of infection, do not delay whilst waiting for investigation!
Specific antibiotic regimens will differ but broadly
<72 hours after birth you should give IV penicillin and IV aminoglycoside
> 72 hours after birth you should give IV flucloxacillin and IV aminoglycosides
Plus acyclovir which covers potential HSV
Proven infections are treated for at least 7 days, 14 days for staph aureus infections and 21 days for meningitis.
53
What is the pathophysiology behind necrotising enterocolitis?
Infection and ischaemia occur in the bowel wall which leads to inflammatory oedema and haemorrhage. Untreated it can lead to bowel necrosis and subsequent perforation
54
What are the risk factors for NEC?
```
Prematurity
Other concurrent illness
Oral feeding
VLBW
IUGR
LBW
Perinatal asphyxia
```
55
How does a neonate with NEC usually present?
```
Usually around 1-2 weeks of age
Classic Hx of abdominal distension and bilious aspirated in a clinically deteriorating neonate with bloody stools.
Fluctuation in temperatures
Neonatal collapse and death
Apnoeas, bradycardia.
```
56
What investigations would you do for a neonate your suspecting of having necrotising enterocolitis?
Bloods (FBC, CRP, coagulation, blood gases (acidosis).
Abdominal x Ray
Screen for other sources of sepsis
57
What would you see on an x Ray of an abdomen in a neonate with NEC?
Pneumatosis intestinalis
58
What are the differentials for NEC?
Other causes of mechanical intestinal obstruction (volvulus)
Congenital bowel malformation
Hirschsprung disease
59
What is the management for NEC?
Keep infant NBM, Feed parenterally(TPN), place NG tube for aspirates.
IV ABx
Replacement off fluid and electrolyte losses, correction of coagulopathy and oxygenate well.
If bowel perforates or is not responsive to conservative management then laparotomy and bowel resection is indicated.
60
What is retinopathy of prematurity?
Eye disease that can happen in premature babies. It causes abnormal blood vessels to grow in the retina and can lead to blindness.
61
What are the risk factors for retinopathy of prematurity?
VLBW (30% of those born <1500g develop ROP)
Hyper oxygenation
Prematurity
62
What infants are screened for Retinopathy of prematurity in the UK?
Infants born <32 weeks gestation or <1500g will be screened in the UK
63
What are the 5 stages of ROP?
1. Mild abnormal vessel growth
2. Moderately abnormal vessel growth
3. Severely abnormal vessel growth
4. Partial retinal detachment
5. Complete retinal detachment
64
What is the differential diagnosis for Retinopathy of prematurity?
Myopia
Congenital cataract
Congenital glaucoma
Cortical blindness
65
What is the management of retinopathy of prematurity?
Keep O2 sats 90-95% and aim to avoid big swings in oxygenation
Stage 1 and 2 will resolve independently
Stage 3+ will need laser treatment of the peripheral retina to prevent further vessel growth.
66
Why is neonatal jaundice important?
High levels of unconjugated bilirubin cross the blood brain barrier and cause permanent damage to neural tissue (kernicterus- bilirubin induced brain damage).
67
When is neonatal jaundice an emergency?
Onset of neonatal jaundice within the first 24 hours should be treated as an emergency.
68
What is bilirubin?
A degradation product of haemoglobin. Initially when bilirubin is broken down it is unconjugated and bound to albumin. It is transported (bound to albumin), to the liver where it is conjugated into conjugated bilirubin.
69
What is meant by conjugated bilirubin?
Direct/ water soluble
70
What happens to the conjugated bilirubin?
Excreted via. The common bile duct into the small intestine, here some is converted to stercobilinogen (colours stool dark) and some is reabsorbed and transported to the kidney where it is excreted as urobilinogen.
71
Why are newborns susceptible to high levels of bilirubin?
1. Their haemoglobin levels at birth are high and foetal haemoglobin lifespan is shorter, leaving a large source of haemoglobin products to be degraded.
2. Hepatic enzymes are immature or fewer in number and not as efficient at conjugating bilirubin, this is especially true of preterm neonates.
3. Slow intestinal transit time causes deconjugation of bilirubin and reabsorption
4. Many medications displace bilirubin from albumin which contributes to jaundice.
72
What are the causes of conjugated neonatal jaundice?
Conjugated (water soluble) causes...
```
. Biliary atresia
. Hepatitis (viral, neonatal, congenital infection)
. CF
. Alpha 1 antitrypsin deficiency
. Lipid storage disease
. TPN
```
73
What are the causes of unconjugated neonatal jaundice?
```
Haemolysis
Breast milk jaundice
Hypothyroidism
Septicaemia
Metabolic disorders- galactosaemia, fructosaemia
Hepatic enzyme defects
Drugs
```
74
What are the risk factors for neonatal jaundice?
Prematurity
Breast fed
Family history
75
What symptoms and signs are important to look out for in the newborn?
Symptoms...
. Look for symptoms suggestive of an infective cause
. Neurological symptoms indicate kernicterus
Signs...
. Yellow skin and sclera
. Hepatosplenomegaly (haemolytic cause)
. Pallor/ pale conjunctiva (if haemolytic cause)
76
What are the causes of haemolytic jaundice?
Haemolytic disease of the newborn (ABO or rhesus incompatibility)
G6PD deficiency
Hereditary spherocytosis
Alpha thalassaemia
77
How does the Coombes test work?
It is positive in antibody mediated haemolytic anaemia (ABO or rhesus incompatibility). Antibodies will bind to erythrocyte surface antigens therefore when Coombes reagent is added the presence of the antibodies make the erythrocytes stick together and give a positive test.
78
How do you investigate babies with jaundice?
Investigate babies who become jaundice within 24 hours of life or those <34 weeks gestation.
Bloods- FBC, U and Es, LFT, split bilirubin and levels, Coombs test, maternal and newborn blood type, TFTs, blood film for red cell morphology.
G6PD screen
Urine dipped for reducing substances
If infection is suspected then swabs, urine, blood and CSF cultures should be taken
79
What is the most common cause of neonatal jaundice?
Breast milk jaundice
Glucuronidases present in the gut and in the breast milk deconjugate bilirubin, allowing more to be reabsorbed enterohepatically in breastfed babies so their serum unconjugated bilirubin increases and jaundice develops.
This can persist past 14 days (persistent jaundice) in 10-20% in infants.
80
How would you manage breast milk jaundice?
Remember breast milk jaundice is not an indication to stop breastfeeding
Those meeting treatment guidelines respond well to phototherapy, poor response to phototherapy suggests an alternative cause.
81
How do you manage neonatal jaundice?
Conservative- most jaundiced babies (especially term) do not require treatment, they can have bilirubin monitored to ensure this does not rise above treatment threshold. They may need support with breastfeeding and dehydration should be addressed.
Phototherapy reduces unconjugated bilirubin. NICE has charts corrected for gestational age to determine at what level treatment is needed.
Exchange transfusion- baby’s blood volume removed and transfused with donor blood, this is used in high potentially toxic bilirubin levels or any signs of kernicterus!
82
What is biliary atresia?
This is congenital absence of part or all of the bile duct system.
83
What is the classic presentation of biliary atresia?
Bleeding/ bruising associated with jaundice developing in the first 1-2 weeks of life
History of pale stools and dark urine
Biliary atresia should be considered in all babies with prolonged jaundice (>2 weeks)
Clinically jaundiced
Persistent cephalohaematomas.
84
What investigations should be done for biliary atresia?
Bloods- LFT, GGT, coagulation, viral and metabolic screen, conjugated bilirubin
USS to look for biliary atresia
Liver biopsy may be indicated
85
How is biliary atresia managed?
Kasai Porto enterostomy or a liver transplant
Babies with conjugated hyperbilirubinaemia need extra vitamin K to avoid haemorrhagic disease of the newborn, their coagulation ability will be impaired.
Once diagnosis is confirmed, urgent discussions with a tertiary paediatric service is needed.
86
What does the term encephalopathy mean?
Damage or disease that affects the brain.
87
What is kernicterus?
Kernicterus is the term used for bilirubin encephalopathy.
88
Why does kernicterus occur?
It occurs as a result of excess, unbound lipid soluble, unconjugated bilirubin crossing the BBB. Any illness which causes systemic acidosis (infection) disrupts the BBB and makes kernicterus more likely.
89
What are the most susceptible parts of the brain?
The most susceptible parts are the metabolically active parts with high blood flow- basal ganglia and midbrain.
90
What are the risk factors for kernicterus?
High unconjugated bilirubin
Sepsis which makes BBB leaky
Acidosis (makes brain more susceptible to damage)
91
How would. Baby present with bilirubin encephalopathy?
Firstly they would have hypotonia, lethargy and poor feeding but eventually having hypertonia, irritability and seizures, progressing to coma and death.
92
How do you manage kernicterus?
Unfortunately kernicterus is not reversible
So treatment is basically preventing it from occurring any signs of kernicterus should be treated with an exchange transfusion.
Also coagulopathy and electrolyte imbalances need correcting.
93
What percentage of babies born weighing <1500g have significant PDA?
50%!!
94
What are the risk factors for PDA?
```
Prematurity
Cyanotic heart lesion
Female sex
Family history
Chromosomal abnormalities
Maternal drug/ alcohol use in pregnancy
```
95
What would you find on examination of someone with PDA?
Continuous machinery murmur loudest below the left clavicle.
Also remember to look for signs of CHF (tachycardia, tachypnoea, hepatomegaly, poor weight gain).
96
What investigations would you do for PDA?
CXR May be normal with a small PDA but a larger shunt will show cardiac enlargement and increased pulmonary vascular markings
ECG- large shunts result in ventricular hypertrophy
Echocardiogram- investigate size of PDA and if any other structural cardiac defects are present.
97
What is the management of PDA?
Treat if PDA is symptomatic or haemodynamically significant
Most PDAs spare closed via. Catheter techniques very successfully
Surgical ligation is reserved for very large PDAs or those that fail to close following catheter techniques.
In premature infants- indomethacin or ibruprofen May be used to medically close the duct.
Medical management of CHF (diuretics)
98
What is meant by single system defects and sequences?
Single system defects: single congenital malformations like spina bifida
Sequence: pattern of multiple abnormalities occurring after one initiating defect. Potter syndrome is an example.
99
What are the clinical features of noonan syndrome?
Characteristic facies
Occasional mild learning difficulties
Short webbed neck with trident hair line
Pectus excavatum
Short stature
Congenital heart disease (pulmonary stenosis, atrial septal defect)
100
What are the clinical features of williams syndrome?
```
Short stature
Characteristic facies
Transient neonatal hypercalcaemia
Congenital heart disease (supravalvular aortic stenosis)
Mild to moderate learning difficulties
```
101
Why is hypoxia really damaging in a neonate?
Normal labour and birth leads to hypoxia, when contractions occur the placenta is unable to carry out normal gaseous exchange which leads to hypoxia. Extended hypoxia leads to anaerobic respiration and a subsequent drop in heart rate (bradycardia). Further hypoxia leads to reduced consciousness and a drop in respiratory effort and eventually hypoxic ischaemic encephalopathy which results in cerebral palsy.
102
What are the principles of neonatal rescuscitation?
Warm the baby
Calculate the APGAR score at 1, 5 and 10 minutes, this is a scoring system which is used to indicate progress over the first minutes of birth
Stimulate the baby- drying vigorously and keeping their head in a neutral position
Inflation breaths can be given when the neonate is gasping or not breathing despite adequate initial simulation.
Two cycles of five inflation breaths can be used to stimulate breathing and heart rate
30 seconds of ventilation breaths if no response
If there is still no response then compressions can be used, co ordinated with ventilation breaths.
103
In neonatal rescucitation what is the compression: ventilation ratio?
Chest compressions are performed at 3:1 ratio with ventilation breaths.
104
Prolonged hypoxia can cause hypoxic ischaemic encephalopathy, if this is suspected can anything be done?
Therapeutic hypothermia with active cooling.
105
What is the APGAR score?
```
This is used in neonatal rescuscitation at 1,5,10 minutes and it is measured out of 10 the lowest score is 0 and the highest is 10. It is based on...
A= appearance
P= pulse
G= grimmace (response to stimulation)
A= activity (muscle tone)
R= respiration
```
106
What is placental transfusion?
In healthy babies there should be at least a minute delay in clamping the cord as this allows some of the significant amount of fetal blood in the placenta to enter the fetal circulation. Delaying cord clamping leads to improved haemoglobin, iron stores and blood pressure and therefore reduces the chance of intraventricular haemorrhage and NEC.
107
What should be done as soon as a baby is born?
```
Skin to skin
Clamp umbilical cord
Dry baby
Label baby
Measure weight and length
Keep baby warm with hat and blankets
```
Vitamin K- should be given in the thigh, this stimulates the baby to cry, helps expand the lungs, prevents bleeding (intracranial, umbilical stump, GI bleeding).
108
What should be done when the baby and mum are out of the delivery room?
. Initiate breast/bottle feeding as soon as baby is alert enough
. Can bath the baby however this can be delayed s few days until baby is warm and stable
. Blood spot test (day 5)
. NIPE (within 72hrs)
. Newborn hearing test
109
What does the blood spot screening test involve?
```
This is a screening test for 9 congenital conditions. It is taken on day 5 (day 8 at the very latest) heel prick is used to provide blood, the screening card requires four separate drops of blood). It screens for 9 congenital conditions...
. Sickle cell
. CF
. Congenital hypothyroidism
. PKU
. Medium chain acetyl coA dehydrogenase deficiency
. Maple syrup urine disease
. Isovaleric acidaemia
. Glutaric aciduria type 1
. Homocystin
```
110
What is the significance of measuring pre ductal and post ductal oxygen saturations?
This means measuring oxygen saturations before and after the ductus arteriosus closes which is around 1-3 days, oxygen sats should be above 96% and there should be no more than a 2% difference. Certain congenital heart conditions are DUCT dependent and rely on the mixing of blood between the pulmonary artery and the aorta, they can rapidly deteriorate when the duct closes. Pre ductal sats can be taken from the right hand and post ductal sats can be taken from either foot.
111
How can haemangiomas be treated?
If they are near the eyes, mouth, affecting the airway then they can be given propanolol
112
What is caput succedaneum (caput)?
This involves fluid collecting on the scalp, outside the periosteum, caput is caused by pressure to a specific area of the scalp during a traumatic, prolonged or instrumental delivery.
113
What is a cephalohaematoma/ traumatic subperiosteal haematoma?
This is caused by damage to blood vessels during a traumatic, prolonged or instrumental delivery
It is a collection of blood between the skull and the periosteum
114
How can you distinguish between cephalohaematoma and caput?
```
Caput= fluid crosses the suture lines
Cephalohaematoma= fluid doesn’t cross suture lines
```
115
What are the risks of cephalohaematoma?
There is a risk of jaundice and anaemia due to the blood that collects within the haematoma and breaks down releasing bilirubin. Baby should be monitored for anaemia, jaundice and resolution of the haematoma.
116
What type of delivery can result in facial nerve palsy and what is the treatment for this?
Forceps delivery, function normally returns normal within a few months.
117
What is Erbs palsy?
This is a result of injury to the C5/C6 nerves in the brachial plexus during birth, it is associated with shoulder dystocia, traumatic or instrumental delivery and a large birth weight.
Damage to the C5/C6 nerves leads fo weakness of shoulder abduction and external rotation, arm flexion and finger extension and leads to the affected arm having a waiters tip appearance.
118
What is a fractured clavicle associated with and how can it be identified?
Associated with shoulder dystocia, traumatic or instrumental delivery, large birth weight.
119
What are the common organisms which cause neonatal sepsis?
```
GBS (harmless to mothers however it can be transferred to baby and cause neonatal sepsis)
E coli
Listeria
Klebsiella
Staph aureus
```
120
What are the risk factors for group B strep?
Vaginal GBS colonisation
GBS sepsis in a previous baby
Maternal pyrexia (sepsis, chorioamnionitis, fever above 38 degrees celsius)
Prematurity
Early (premature) rupture of membranes
PROM prolonged rupture of membranes (18 hours.)
121
What are the clinical features of neonatal sepsis?
```
Fever
Reduced tone and activity
Poor feeding
Resp distress or apnoea
Vomiting
Tachy/brady cardias
Hypoxia
Jaundice within 24 hrs
Seizures
Hypoglycaemia
```
122
What are the red flags of sepsis?
Confirmed or suspected sepsis in the mother
Signs of shock
Seizures
Term baby needing mechanical ventilation
Resp distress starting more than 4hrs after birth
Presumed sepsis in another baby in a multiple pregnancy
123
Antibiotics should be given when there are two or more risk factors or clinical features of sepsis or if there is a single red flag for sepsis, within what time frame should antibiotics be given?
They should be given within an hour.
124
What is a partial septic screen?
FBC
CRP
Blood cultures (whereas full has LP and dipstick)
125
What is the antibiotic choice for neonatal sepsis?
For babies that have not left the hospital it is gentamycin and benzylpenicillin
For babies who have left the hospital and been exposed to more bugs then it is cefotaxime and benzyl
126
What is the ongoing management for sepsis once you have established the baby on Abx?
Blood cultures should be again checked at 36 hours
CRP at 24 hours
Consider stopping the antibiotics if the baby is clinically well, the blood cultures are negative 36 hours after taking them and both CRP levels are less than ten.
Check the CRP again at 5 days if they are still on treatment...
Consider stopping the antibiotics if the baby is clinically well, the lumbar puncture and blood cultures are negative and the CRP is normal at 5 days.
Consider performing a lumbar puncture if any of the CRP results are more than ten.
127
What is hypoxic ischaemic encephalopathy?
```
Hypoxia= lack of oxygen
Ischaemia= restriction of blood flow to the tissues
Encephalopathy= malfunctioning of the brain
```
128
What are the causes of HIE?
Anything that leads to asphyxia (deprovation of oxygen) to the brain...
. Maternal shock
. Intrapartum haemorrhage
. Prolapsed cord
. Nuchal cord (round the neck)
129
What is the management of HIE?
Supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures.
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How does therapeutic hypothermia work?
Babies near or at term considered to have HIE can benefit from therapeutic hypothermia, this involves actively cooling the core temperature of the baby according to a strict protocol, the baby is transferred to neonatal ICU and actively cooled using cooling blankets and a cooling hat, temp is monitored using a rectal probe and should be between 33 and 34 degrees celsius, this is continued for 72 hours after which the baby is gradually warmed to a normal temp over 6 hours
The intention is to reduce the inflammation and neurone loss after the acute hypoxic injury. It reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death.
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What are the classifications of prematurity?
Under 28 weeks: extreme premature
28-32: very preterm
32-37: moderate to late preterm
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What are the associations with prematurity?
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Social deprivation
Smoking
Alcohol
Drugs
Overweight or underweight mother
Maternal co morbidity
Twins
Personal or family history of prematurity
```
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What are the management options for trying to delay birth?
Prophylactic vaginal progesterone (putting a vaginal suppository in the vagina to try and discourage labour)
Prophylactic cervical cerclage (suture in the cervix to hold it closed)
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When preterm labour is confirmed, what can be done for improving the outcome?
. Tocolysis with nifedipine
. Maternal corticosteroids (bedore 35)
. IV mag sulfate (before 34 weeks)
. Delayed cord campling
135
What are the issues in early life for babies who are premature?
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. Learning and behavioural difficulties
. Chronic lung disease of prematurity
. Susceptibility to infections
. Hearing and visual impairment
. Cerebral palsy
```
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What are apnoeas?
Periods where breathing stops spontaneously for more than 20s, or shorter periods with oxygen desaturation and bradycardia. They occur in almost all babies less than 28 weeks gestation, decrease with gestational age and if present at term then they indicate pathology.
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What is apnoea a sign of?
```
Often a sign of a developing illness...
. Infection
. Anaemia
. Airway obstruction
. CNS pathology- seizures or haemorrhage
. Gastro oesophageal reflux
. Neonatal abstinence syndrome
```
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How are apnoeas of prematurity managed?
. Neonatal units attach apnoea monitors to premature babies
. Tactile stimulation is used to prompt baby to restart breathing
. IV caffeine is used to prevent apnoea and bradycardia in babies woth recurrent episodes
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What is retinopathy of prematurity?
Condition affecting preterm and low birth weight babies, mostly affecting those born before 32 weeks
Abnormal blood vessel development in the retina can lead to scarring, retinal detachment and blindness.
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What is the pathophysiology behind retinopathy of prematurity?
Retinal blood vessel development starts around 16 weeks and is complete by 37-40 weeks gestation. The blood vessels grow from the middle of the retina to the outer area. The vessel formation is stimulated by hypoxia therefore when the retina is exposed to higher O2 levels in a premature baby the stimulus for normal blood vessel development is removed.
When the hypoxic environment recurs the retina responds by producing excessive blood vessel development (neovascularisation) as well as scsr tissue. The abnormal blood vessels may regress and leave the retina without a blood supply, scar tissue causes retinal detachment.
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What is the screening for retinopathy of prematurity?
Babies born before 32 weeks or under 1.5kg should be screened
Screening starts at
30-31 weeks gestational age in babies born before 27 weeks
4-5 weeks of age in babies born after 27 weeks
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How do you treat retinopathy of prematurity?
Treatment involves systematically targeting areas of the retina to stop blood vessels developing
First line= transpupillary laser photocoagulation to halt and reverse neovascularisation
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What is necrotising enterocolitis?
A disorder affecting premature babies it is where part of the bowel becomes necrotic, it is a life threatening emergency and death of the bowel tissue can lead to bowel perforation, peritonitis and shock.
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What are the risk factors for NEC?
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Very low birth weight/very premature
Formula feeds
Resp distress and assisted ventilation
Sepsis
PDA and other congenital heart disease
```
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What is the presentation of NEC?
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. Intolerance to feeds
. Vomiting GREEN BILE
. Generally unwell
. Distended tender abdomen
. Absent bowel sounds
. BLOOD IN STOOLS
```
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What investigations do you want to do for NEC?
Blood tests:
FBC for thrombocytopenia and neutropenia
CRP for inflammation
Capillary blood gas which shows metabolic acidosis
Blood culture for sepsis
Abdominal X ray is the investigation of choice for diagnosis
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What would an x ray of NEC show?
Pneumatosis intestinalis
Dilated loops of bowel
Bowel wall oedema
Pneumoperitoneum (indicates perforation)
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What is the management of NEC?
NBM, IV fluids, TPN, antibiotics to stable them, NG tube.
Surgical emergency, an urgent referal to the surgical team is needed,and some neonates can be treated with medical however some need surgical treatment to remove bowel.
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What are the complications of NEC?
```
Perforation and peritonitis
Sepsis
Death
Strictures
Abscess formation
Recurrent
Long term stoma
Short bowel syndrome after surgery
```
150
What is neonatal abstinence syndrome?
This refers to the withdrawal symptoms that happens in neonates that use substances in pregnancy.
151
What substances can cause neonatal abstinence syndrome?
```
Opiates
Methadone
Benzodiazepines
Cocaine
Amphetamines
Nicotine or cannabis
Alcohol
SSRI antidepressants
```
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What are the signs and symptoms of neonatal abstinence syndrome?
CNS- irritability, incesased tone, high pitched cry, not settling, tremors, seizures
Vasomotor/resp- yawning, sweating, unstable temp and pyrexia, tachypnoea (fast breathing)
Metabolic/GI- poor feeding, regurg or vomiting, hypoglycaemia, loose stools with a sore nappy area
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How can you manage Necrotising enterocolitis?
Babies are kept in hospital with monitoring on a NAS chart for at least 3 days to monitor withdrawal symptoms, a urine sample can be collected from the neonate to test for substances.
Medical treatment options for moderate to severe symptoms
Oral morphine sulphate for opiate withdrawal
Oral phenobarbitone for non opiate withdrawal
154
What can drinking alcohol in early pregnancy lead to?
Alcohol in pregnancy can cross the placenta and enter the fetus, where is disrupts fetal development. There is no safe level of alcohol in pregnancy and mothers are encouraged not to drink alcohol at all, however small amounts are less likely to result in lasting effects. The effects are greatest in the first 3 months of pregnancy.
Alcohol in early pregnancy can lead to:
Miscarriage
Small for dates
Preterm delivery
155
What is fetal alcohol syndrome?
```
This refers to certain effects and characteristics that are found in children of mothers that consumed significant alcohol during pregnancy
. microcephaly
. Thing upper lip
. Smooth flat philtrum
. Smooth palpebral fissure
. Learning disability
. Behavioural difficulties
. Hearing and vision problems
. Cerebral palsy
```
156
What is congenital rubella syndrome?
Caused by maternal infection with the rubella virus during pregnancy, the risk is highest during the first 3 months of pregnancy.
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Women planning to become pregnant should ensure they have had the MMR vaccine, if they are in doubt what can be done ?
. They can be tested for rubella immunity
. If they do not have antibodies to rubella they can be vaccinated with 2 doses of the MMR 3 months apart
Pregnant women should not recieve the MMR vaccination as this is a live vaccine, but non immune can be offered the vaccine after giving birth
158
What are the features of congenital rubella syndrome?
Congenital cataracts
Congenital heart disease (PDA and pulmonary stenosis)
Learning disability
Hearing loss
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What is congenital varicella zoster virus?
Chickenpox in pregnancy
Its dangerous in pregnancy as it can lead to...
. More severe cases in the mother, such as varicella pneumonitis, hepatitis, encephalitis
. Fetal varicella syndrome
. Severe neonatal varicella infection if mum is infected around the time of delivery
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If in doubt of whether a pregnant woman has had varicella zoster before but she has been exposed, what can be done?
So IgG for varicella zoster can be tested
161
What should be done when there is exposure to chicken pox in pregnancy?
When the woman has previously had chicken pox then they are safe
When they are unsure then check VZV IgG levels
When they are not immune they can be treated with IV varicella immunoglobulins as prophylaxis against developing chickenpox (should be give within ten days exposure)
When the chickenpox rash starts in pregnancy then if they are more than 20 weeks and present within 24 hours then they can be treated with oral aciclovir.
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What does congenital varicella syndrome present like?
Congenital varicella syndrome occurs in around 1% of cases of chickenpox in pregnancy
Fetal growth restriction
Microcephaly, hydrocephalus and learning disability
```
Scars and significant skin changes following the dermatomes
Limb hypoplasia (underdeveloped limbs)
Cataracts and inflammation in the eye (chorioretinitis)
```
163
What is congenital CMV?
Congenital cytomegalovirus (CMV) infection occurs due to maternal CMV infection during pregnancy. The virus is mostly spread via the infected saliva or urine of asymptomatic children. Most cases of CMV in pregnancy do not cause congenital CMV.
164
What are the features of congenital CMV?
```
Fetal growth restriction
Microcephaly
Hearing loss
Vision loss
Learning disability
Seizures
```
165
What is congenital toxoplasmosis?
Infection with the Toxoplasma gondii parasite is usually asymptomatic. It is primarily spread by contamination with faeces from a cat that is a host of the parasite. When infection occurs during pregnancy it can lead to congenital toxoplasmosis. This risk is higher later in the pregnancy. There is a classic triad of features in congenital toxoplasmosis:
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What is the classic triad of congenital toxoplasmosis?
Intracranial calcification
Hydrocephalus
Chorioretinitis
167
What is congenital zika syndrome?
The zika virus is spread by host Aedes mosquitos in areas of the world where the virus is prevalent. It can also be spread by sex with someone infected with the virus. It can cause no symptoms, minimal symptoms or a mild flu like illness. In pregnancy it can lead to congenital Zika syndrome
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What are the features of congenital zika syndrome?
Microcephaly
Fetal growth restriction
Other intracranial abnormalities, such as ventriculomegaly and cerebellar atrophy
Pregnant women that may have contracted the Zika virus should be tested for the viral PCR and antibodies to the Zika virus. Women with a positive result should be referred to fetal medicine to monitor the pregnancy. There is no treatment for the virus.
