Paediatric Neonatology Flashcards
Surfactant
Surfactant is a fluid produced by type II alveolar cells. It contains proteins and fats. It sits on top of the water in the lungs. It has a hydrophilic side, that faces the water, and a hydrophobic side, that faces the air. The surfactant reduces the surface tension of the fluid in the lungs, essentially providing a barrier that reduces the water molecules tendency to pull towards each other.
The result is that surfactant keeps the alveoli inflated and maximises the surface area of the alveoli. This reduces the force needed to expand the alveoli and therefore the lungs during inspiration. This is known as compliance. Therefore, surfactant increases lung compliance.
Additionally, as an alveolus expands, the surfactant becomes more thinly spread and therefore the surface tension increases, making it more difficult to expand that alveolus further. This stops one alveolus expanding massively whilst another alveolus only expands a little. Therefore, surfactant promotes equal expansion of all alveoli during inspiration.
Type II alveolar cells become mature enough to start producing surfactant between 24 and 34 weeks gestation. Therefore, pre-term babies have problems associated with reduced pulmonary surfactant.
Cardio-respiratory changes at birth
During birth the thorax is squeezed as the body passes through the vagina, helping to clear fluid from the lungs. Birth, temperature change, sound and physical touch stimulate the baby to promote the first breath. A strong first breath is required to expand the previously collapsed alveoli for the first time. Adrenalin and cortisol are released in response to the stress of labour, stimulating respiratory effort.
The first breaths the baby takes expands the alveoli, decreasing the pulmonary vascular resistance. The decrease in pulmonary vascular resistance causes a fall in pressure in the right atrium. At this point the left atrial pressure is greater than the right atrial pressure, which squashes the atrial septum and causes functional closure of the foramen ovale. The foramen ovale then structurally closes and becomes the fossa ovalis.
Prostaglandins are required to keep the ductus arteriosus open. Increased blood oxygenation causes a drop in circulating prostaglandins. This causes closure of the ductus arteriosus, which becomes the ligamentum arteriosum.
Immediately after birth the ductus venosus stops functioning because the umbilical cord is clamped and there is no blood flow in the umbilical veins. The ductus venosus structurally closes a few days later and becomes the ligamentum venosum.
Hypoxia
Hypoxia is central to neonatal resuscitation. Normal labour and birth leads to hypoxia. When contractions happen, the placenta is unable to carry out normal gaseous exchange, leading to hypoxia. Extended hypoxia will lead to anaerobic respiration and a subsequent drop in the fetal heart rate (bradycardia). Further hypoxia will lead to reduced consciousness and a drop in respiratory effort, in turn worsening hypoxia. Extended hypoxia to the brain leads to hypoxic-ischaemic encephalopathy (HIE), with potentially life-long consequences in the form of cerebral palsy.
Other Issues in Neonatal Resuscitations
Babies have a large surface area to weight ratio, and get cold very easily
Babies are born wet, so they loose heat rapidly
Babies that are born through meconium may have this in their mouth or airway
Principles of Neonatal Resuscitation
There is a very helpful neonatal life support algorithm from the UK resuscitation council, available on their website. It is worth learning this, as there may be questions on it in your exams. This section aims to help you understand the principles of this algorithm. When performing neonatal resuscitation always consider whether you need help.
Warm The Baby
Get the baby dry as quickly as possible. Vigorous drying also helps stimulate breathing.
Keep the baby warm with warm delivery rooms and management under a heat lamp
Babies under 28 weeks are placed in a plastic bag while still wet and managed under a heat lamp
Calculate the APGAR Score
This is done at 1, 5 and 10 minutes whilst resuscitation continues
This is used as an indicator of the progress over the first minutes after birth
It helps guide neonatal resuscitation efforts
Stimulate Breathing
Simulate the baby to prompt breathing, for example by drying vigorously with a towel
Place the baby’s head in a neutral position to keep airway open. A towel under the shoulders can help keep it neutral.
If gasping or unable to breath, check for airway obstruction (i.e. meconium) and consider aspiration under direct visualisation
Inflation Breaths
Inflation breaths are given when the neonate is gasping or not breathing despite adequate initial simulation.
Two cycles of five inflation breaths (lasting 3 seconds each) can be given to stimulate breathing and heart rate
If there is no response and the heart rate is low, 30 seconds of ventilation breaths can be used
If there is still no response, chest compressions can be used, coordinated with the ventilation breaths
Technique is very important in delivering effective inflation breaths. Get someone experienced to show you how to perform them. It is essential to maintain a neutral head position and get a good seal around the mouth and nose. Look for a rise and fall in the chest.
When performing inflation breaths, air should be used in term or near term babies, and a mix of air and oxygen should be used in pre-term babies. Oxygen saturations can be monitored throughout resuscitation if there are concerns about the breathing. Aim for a gradual rise in oxygen saturations, not exceeding 95%.
Chest Compressions
Start chest compressions if heart rate remains below 60 bpm despite resuscitation and inflation breaths (see protocol)
Chest compressions are performed at a 3:1 ratio with ventilation breaths
Severe Situations
Time is precious during neonatal resuscitation. Prolonged hypoxia increases the risk of hypoxic-ischaemic encephalopathy (HIE). In severe situations, IV drugs and intubation should be considered. Babies near or at term that have possible HIE may benefit from therapeutic hypothermia with active cooling.
APGAR Score
The APGAR score is measured out of 10. The lowest score is 0 and the highest is 10.
Finding
0
1
2
Appearance (skin colour)
Blue / pale centrally
Blue extremities
Pink
Pulse
Absent
< 100
> 100
Grimmace (response to stimulation)
No response
Little response
Good response
Activity (muscle tone)
Floppy
Flexed arms and legs
Active
Respiration
Absent
Slow / irregular
Strong / crying
Delayed Umbilical Cord Clamping
After birth there is still a significant volume of fetal blood in the placenta. Delayed clamping of the umbilical cord provides time for this blood to enter the circulation of the baby. This is known as placental transfusion. Recent evidence indicates that in healthy babies, delaying cord clamping leads to improved haemoglobin, iron stores and blood pressure and a reduction in intraventricular haemorrhage and necrotising enterocolitis. The only apparent negative effect is an increase in neonatal jaundice, potentially requiring more phototherapy.
Current guidelines from the resuscitation council UK state that uncompromised neonates should have a delay of at least one minute in the clamping of the umbilical cord following birth.
Neonates that require neonatal resuscitation should have their umbilical cord clamped sooner to prevent delays in getting the baby to the resuscitation team. The priority will be resuscitation rather than delayed clamping.
Blood Spot Screening
This is a screening test for 9 congenital conditions. It is taken on day 5 (day 8 at the latest) after consent from the parent. A heel prick is used to provide drops of blood. The screening card requires four separate drops. This screens for nine congenital conditions:
Sickle cell disease
Cystic fibrosis
Congenital hypothyroidism
Phenylketonuria
Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
Maple syrup urine disease (MSUD)
Isovaleric acidaemia (IVA)
Glutaric aciduria type 1 (GA1)
Homocystin
Results take 6-8 weeks to come back.
Caput Succedaneum
Caput succedaneum (caput) involves fluid (oedema) 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. The periosteum is a layer of dense connective tissue that lines the outside of the skull and does not cross the sutures (the gaps in the baby’s skull). The fluid is outside the periosteum, which means it is able to cross the suture lines. There is usually no, or only mild, discolouration of the skin. It does not require any treatment and will resolve within a few days.
Cephalohaematoma
A cephalohaematoma is a collection of blood between the skull and the periosteum. It is caused by damage to blood vessels during a traumatic, prolonged or instrumental delivery. It can be described as a traumatic subperiosteal haematoma.
The blood is below the periosteum, therefore the lump does not cross the suture lines of the skull. This is an important way of distinguishing caput succedaneum from cephalohaematoma. Additionally, the blood can cause discolouration of the skin in the affected area.
Usually a cephalohaematoma does not required any intervention and resolves without treatment within a few months. There is a risk of anaemia and jaundice due to the blood that collects within the haematoma and breaks down, releasing bilirubin. For this reason the baby should be monitored for anaemia, jaundice and resolution of the haematoma.
Facial Paralysis
Delivery can cause damage to the facial nerve. Facial nerve injury is typically associated with a forceps delivery. This can result in facial palsy (weakness of the facial nerve on one side). Function normally returns spontaneously within a few months. If function does not return they may required neurosurgical input.
Erbs Palsy
An Erbs palsy is the 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 large birth weight.
Damage to the C5/C6 nerves leads to weakness of shoulder abduction and external rotation, arm flexion and finger extension. This leads to the affected arm having a “waiters tip” appearance:
Internally rotated shoulder
Extended elbow
Flexed wrist facing backwards (pronated)
Lack of movement in the affected arm
Function normally returns spontaneously within a few months. If function does not return then they may required neurosurgical input.
Fractured Clavicle
The clavicle may be fractured during birth. A fractured clavicle can be associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight.
A fractured clavicle can be picked up shortly after birth or during the newborn examination with:
Noticeable lack of movement or asymmetry of movement in the affected arm
Asymmetry of the shoulders, with the affected shoulder lower than the normal shoulder
Pain and distress on movement of the arm
A fractured clavicle can be confirmed with ultrasound or x-ray. Management is conservative, occasionally with immobilisation of the affected arm. It usually heals well. The main complication of a fractured clavicle is injury to the brachial plexus, with a subsequent nerve palsy.
Neonatal sepsis
Neonatal sepsis is caused by infection in the neonatal period. It potentially results in significant morbidity and mortality for the affected infant, particularly if treatment is delayed. It presents with non-specific signs and requires a high degree of suspicion and a low threshold for starting treatment with broad spectrum antibiotics. This is a brief summary to help your learning, always refer to local and national guidelines and involve seniors when treating patients.
Common causes of neonatal sepsis
Group B streptococcus (GBS)
Escherichia coli (e. coli)
Listeria
Klebsiella
Staphylococcus aureus
TOM TIP: The organism to remember for your exams is group B strep (GBS). This is a common bacteria found in the vagina. It does not cause any problems for the mother, but can be transferred to the baby during labour and cause neonatal sepsis. Prophylactic antibiotics during labour are used to reduce the risk of transfer if the mother is found to have GBS in their vagina during pregnancy.
Risk factors for neonatal sepsis
Vaginal GBS colonisation
GBS sepsis in a previous baby
Maternal sepsis, chorioamnionitis or fever > 38ºC
Prematurity (less than 37 weeks)
Early (premature) rupture of membrane
Prolonged rupture of membranes (PROM)
Clinical Features of Neonatal Sepsis
Fever
Reduced tone and activity
Poor feeding
Respiratory distress or apnoea
Vomiting
Tachycardia or bradycardia
Hypoxia
Jaundice within 24 hours
Seizures
Hypoglycaemia
Red flags for neonatal sepsis
Confirmed or suspected sepsis in the mother
Signs of shock
Seizures
Term baby needing mechanical ventilation
Respiratory distress starting more than 4 hours after birth
Presumed sepsis in another baby in a multiple pregnancy
Treating For Presumed Sepsis
Always check your local policy and consult with experienced paediatricians when treating neonates that potentially have sepsis. Most local policies will follow something similar to the NICE guidelines:
If there is one risk factor or clinical feature, monitor the observations and clinical condition for at least 12 hours
If there are two or more risk factors or clinical feature of neonatal sepsis start antibiotics
Antibiotics should be started if there is a single red flag
Antibiotics should be given within 1 hour of making the decision to start them
Blood cultures should be taken before antibiotics are given
Check a baseline FBC and CRP
Perform a lumbar puncture if infection is strongly suspected or there are features of meningitis (e.g. seizures)
Antibiotic choice for neonatal sepsis
Always check your local antibiotic policy. The NICE guidelines (2012) recommend benzylpenicillin and gentamycin as first line antibiotics.
Alternatively a third generation cephalosporin (e.g. cefotaxime) may be given as an alternative in lower risk babies.
Ongoing management in neonatal sepsis
Check the CRP again at 24 hours and check the blood culture results at 36 hours:
Consider stopping the antibiotics if the baby is clinically well, the blood cultures are negative 36 hours after taking them and both CRP results are less than 10.
Check the CRP again at 5 days if they are still on treatment:
Consider stopping antibiotics if the baby is clinically well, the lumbar puncture and blood cultures are negative and the CRP has returned to normal at 5 days.
Consider performing a lumbar puncture if any of the CRP results are more than 10.
Hypoxic ischaemic encephalopathy
Hypoxic ischaemic encephalopathy (HIE) occurs in neonates as a result of hypoxia during birth. Hypoxia is a lack of oxygen, ischaemia refers to a restriction in blood flow to the brain and encephalopathy refers to malfunctioning of the brain. Some hypoxia is normal during birth, however prolonged or severe hypoxia leads to ischaemic brain damage. HIE can lead to permanent damage to the brain, causing cerebral palsy. Severe HIE can result in death.
Suspect HIE in neonates when there are events that could lead to hypoxia during the perinatal or intrapartum period, acidosis (pH < 7) on the umbilical artery blood gas, poor Apgar scores, features of mild, moderate or severe HIE (see below) or evidence of multi organ failure.
Causes of HIE
Anything that leads to asphyxia (deprivation of oxygen) to the brain can cause HIE. For example:
Maternal shock
Intrapartum haemorrhage
Prolapsed cord, causing compression of the cord during birth
Nuchal cord, where the cord is wrapped around the neck of the baby
Hypoxic-Ischaemic Encephalopathy Grades (Sarnat Staging)
Mild
Poor feeding, generally irritability and hyper-alert
Resolves within 24 hours
Normal prognosis
Moderate
Poor feeding, lethargic, hypotonic and seizures
Can take weeks to resolve
Up to 40% develop cerebral palsy
Severe
Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes
Up to 50% mortality
Up to 90% develop cerebral palsy
Managing hypoxic-ischaemic encephalopathy
Management will be coordinated by specialists in neonatology, on the neonatal unit. This involves supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures. Therapeutic hypothermia is an option in certain circumstances to help protect the brain from hypoxic injury.
Children will need to be followed up by a paediatrician and the multidisciplinary team to assess their development and support any lasting disability.
Therapeutic Hypothermia
Babies near or at term considered to have HIE can benefit from therapeutic hypothermia. Therapeutic hypothermia 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. The temperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe. This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours.
The intention of therapeutic hypothermia 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.
Neonatal jaundice
Jaundice describes the condition of abnormally high levels of bilirubin in the blood. Red blood cells contain unconjugated bilirubin. When red blood cells break down, they release unconjugated bilirubin into the blood. Unconjugated bilirubin is conjugated in the liver. Conjugated bilirubin is excreted in two ways: via the biliary system into the gastrointestinal tract and via the urine.
Physiological Jaundice
There is a high concentration of red blood cells in the fetus and neonate. These red blood cells are more fragile than normal red blood cells. The fetus and neonate also have less developed liver function.
Fetal red blood cells break down more rapidly than normal red blood cells, releasing lots of bilirubin. Normally this bilirubin is excreted via 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, causing a mild yellowing of skin and sclera from 2 – 7 days of age. This usually resolves completely by 10 days. Most babies remain otherwise healthy and well.
