Paeds - Neonatology Flashcards

1
Q

Define Jaundice and describe the simplified physiology?

A

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
- via the urine - ME: gut bacteria convert billirubin to urobilinogen (10% reabsorbed and goes to the kidneys, 90% processed to stercobilin in the GI faeces)

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2
Q

What is physiological jaundice in newborns and what causes it?

What time period of neonatal jaundice is concerning? Why?

A

A mild yellowing of skin and sclera from 2 – 7 days of age. This usually resolves completely by 10 days.

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.

TOM TIP: Jaundice in the first 24 hours of life is pathological. This needs urgent investigations and management. Neonatal sepsis is a common cause - me inflammation impairs liver function. Babies with jaundice within 24 hours of birth need treatment for sepsis if they have any other clinical features or risk factors.

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3
Q

When is neonatal jaundice pathological and what is the top differnetial?

Other causes of Neonatal jaundice - just name a few for each category?

A

TOM TIP: Jaundice in the first 24 hours of life is pathological. This needs urgent investigations and management. Neonatal sepsis is a common cause. Babies with jaundice within 24 hours of birth need treatment for sepsis if they have any other clinical features or risk factors.

The causes of neonatal jaundice can be split into increased production or decreased clearance - see below..

Prematurity: In premature babies, the process of physiological jaundice is exaggerated due to the immature liver. This increases the risk of complications, particularly kernicterus. Kernicterus is brain damage due to high bilirubin levels. Bilirubin levels need to be carefully monitored in premature babies, as they may require treatment.

Breast milk juandice: Babies that are breastfed are more likely to have neonatal jaundice. There are several potential reasons for this. **Components of breast milk inhibit the ability of the liver to process the bilirubin. **Breastfed babies are more likely to become dehydrated if not feeding adequately. Inadequate breastfeeding may lead to slow passage of stools, increasing absorption of bilirubin in the intestines.

Haemolytic disease of the newborn: When there is rhesus incompatibility between the maternal and neonatal red blood cell surface antigens. The most important is the rhesus D antigen. When the mother is Resus D negative, and her child is rhesus D positive, if blood from the babie crosses into the mother’s bload stream the mother’s immune system will produce antibodies to the rhesus D antigen. Thus doesn’t usually cause issues in the first pregnancy, but during subsequent pregnancies the mothers antibodies can cross into the fetus, causes haemolysis of the red blood cells and aneamia, with high billirubin.
///
Others - dont test these!!!
Increased production of bilirubin:

Haemolytic disease of the newborn
ABO incompatibility
Haemorrhage
Intraventricular haemorrhage
Cephalo-haematoma
Polycythaemia
Sepsis and disseminated intravascular coagulation
G6PD deficiency

Decreased clearance of bilirubin:
Prematurity
Breast milk jaundice
Neonatal cholestasis
Extrahepatic biliary atresia
Endocrine disorders (hypothyroid and hypopituitary)
Gilbert syndrome

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4
Q

When is neontal jaundice classed as prolongued and what needs to be done about it?

A

Jaundice is “prolonged” when it lasts longer than would be expected in physiological jaundice. This is:

  • More than 14 days in full term babies
  • More than 21 days in premature babies

Prolonged jaundice should prompt further investigation to look for an underlying cause. These are particularly looking for conditions that will cause jaundice to persist after the initial neonatal period, such as:
- biliary atresia
- hypothyroidism
- G6PD deficiency.

THERE ARE LOADS OF CAUSES TEHY ARE ON THE CARD BEFORE THIS

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5
Q

Ix (7) and Management of neonatal jaundice

A

Investigations
- FBC + blood film for polycythaemia or anaemia
- Conjugated bilirubin: elevated levels indicate a hepatobiliary cause
- Blood type testing of mother and baby for ABO or rhesus incompatibility
- Direct Coombs Test (direct antiglobulin test) for haemolysis
- Thyroid function, particularly for hypothyroid
- Blood and urine cultures if infection is suspected. Suspected sepsis needs treatment with antibiotics.
- Glucose-6-phosphate-dehydrogenase (G6PD) levels for G6PD deficiency

Management
- monitoring of total billibrub on treatment threshold charts. Billrub against age (IN HOURS) - If the total billirubin reaches the threshold then they need to being treatment.
- Phototherapy is usually adequate to correct neonatal jaundice. Term threshold is 350
- Extremely high levels may require an exchange transfusion. Exchange transfusions involve removing blood from the neonate and replacing it with donor blood. Term threshold is 450

**Missed this in the Exam - exchange transfusion was needed. **

Background Phototherapy Mechanism: invovles shining blue light (not UV) on the babies skin, which converts unconjugated bilirubin into isomers than can be execreted in the bile and urine without requiring conjugation in the liver. Billirubin is closely montiored during treatment. Rebound billirubin needs to be measured 12 hours after treatment finnishes to make sure it doesn’t rise again.

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6
Q

Key Complication of neonatal jaundice?

A

Kernicterus is a type of brain damage caused by excessive bilirubin levels. It is the main reason we treat neonatal jaundice to keep bilirubin levels below certain thresholds.

Bilirubin can cross the blood-brain barrier. Excessive bilirubin causes direct damage to the central nervous system. Kernicterus presents with a less responsive, floppy, drowsy baby with poor feeding. The damage to the nervous system is permeant, causing cerebral palsy, learning disability and deafness. Kernicterus is now rare due to effective treatment of jaundice.

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7
Q

NIPE- How do you check the pre-ductal and post-ductal saturations and why is this important?

A

Babies should have their pre-ductal and post-ductal oxygen saturations checked. This measures the oxygen level before and after the ductus arteriosus. Normal saturations are 96% or above. There should not be more than a 2% difference between the pre-ductal and post-ductal saturations.

Pre-ductal saturations are measured in the baby’s right hand. The right hand receives blood from the right subclavian artery, a branch of the brachiocephalic artery, which branches from the aorta before the ductus arteriosus.

Post-ductal saturations are measured in either foot. The feet receive blood traveling from the descending aorta, which occurs after the ductus arteriosus.

Certain congenital heart conditions are duct-dependent, meaning they rely on the mixing of blood across the ductus arteriosus.

Me - actually this makes sense, if the post ductal sats are significantly higher then it shows there might be a congenital heart defect.

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8
Q

Common issues with the NIPE, how are the following abnormalities managed (just one line each)?
- Talipes
- undecended testes
- clicky hips
- skin findings
- haemangiomas near the eyes, mouth or affecting the airway
- port wine stanes
- cephalohaematomas
- boney-injuries (calvicles)
- cardiac murmurs

A

Talipes, also known as clubfoot, is where the ankles are in a supinated position, rolled inwards. It can be positional or structural. Positional talipes is where the muscles are slightly tight around the ankle but the bones are unaffected. The foot can still be moved into the normal position. This requires referral to a physiotherapist for some simple exercises and will resolve with time. Structural talipes involves the bones of the foot and ankle and requires referral to an orthopaedic surgeon.

Undescended testes require monitoring and referral to a urologist if not decended within 6 months

Skin findings generally do not require any action. Many will fade with time.

Haemangiomas near the eyes, mouth or affecting the airway may require referral for treatment with beta blockers (i.e. propranolol). Otherwise they can be monitored and usually resolve with time.

Port wine stains are pink patches of skin, often on the face, caused by abnormalities affecting the capillaries. They don’t fade with time and typically turn a darker red or purple colour. Rarely they can be related to a condition called Sturge-Weber syndrome, where there can be visual impairment, learning difficulties, headaches, epilepsy and glaucoma.

Clicky or clunky hips require referral for a hip ultrasound to rule out developmental dysplasia of the hips.

Cephalohaematomas require monitoring for jaundice and anaemia.

Boney injuries may require an xray to look for fractures (e.g. clavicular fracture).

Soft systolic murmurs of grade 2 or less in otherwise healthy well neonates may be monitored, as these often resolve after 24 – 48 hours. This may be caused by a patent foramen ovale that closes shortly after birth. Any suspicion of heart failure or congenital heart disease requires referral to cardiology for an ECG and echocardiogram. If they are unwell, they require admission to the neonatal unit and immediate management.

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9
Q

Neonatal Respiratory Physiology:
- Which cells produce surfactant and at what gestation?
- What is the function of surfactant?

A

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.

Surfactant 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.

Explanation:
Surface tension is the attraction of the molecules in a liquid to each other, pulling them together and minimising surface area. This is why, in zero gravity, water floats around in a ball rather than diffusing into a mist.

Alveoli are the small sacs where gas collects and diffuses into the blood during inhalation. These are lined with fluid. The molecules of this fluid pull together due to surface tension, in turn pulling the walls of the alveoli towards each-other, attempting to collapse the space in the alveoli.

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10
Q

Cardio-Respiratory Changes at Birth:
- stimulating the baby to breathe
- changes in the heart and lungs
- changes in the ductus arteriosus
- changes in the ductus venosus

A

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.

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11
Q

What are the 3 big issues in neonatal resuscitation (one main one)?

A

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.

Hypothermia - babies have a large surface area to volume ratio and are born wet

Meconium, if present may block the mouth or airway

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12
Q

Steps to the Neonatal Resusitation algorithm?

What score is used?

Threshold for chest compressions?

A

warm the baby - dry them and keep them under a heat lamp, (plastic bag below 28 weeks)

Stimulate breathing - rubbing vigerously with a towel stimulates them to start breathing (often all that is required), keep head in a neutral position, aspirate any meconium that is visualisable

Assess - colour, tone, breathing, heart rate

Calculate the APGAR score are 1,5 and 10 minutes

Ensure an open airway

Inflation breaths (when baby is not breathing/gasping despite adequete inital stimulation) :
- 2x cycles of 5 inflations breaths (3 seconds each) to stimulate breathing and heart rate
- If there is no response and the heart rate is low, 30 seconds of ventilation breaths (1 second each) can be used
- If there is still no response, chest compressions can be used, coordinated with the ventilation breaths

Note - inflation breahes are about expanding the alveoli and pushing out the fluids

chest compressions - used if heart rate remains below 60bpm despite inflation breaths
- 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 ventilation breaths in a 3:1 ratio

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.

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13
Q

Compents of an APGAR score for neonatal resusciation

A

Appearance - pink/ blue extremities/ blue centrally
Pulse - 100+/100-/absent
Grimmance (response to stimulation) - none/ little/ good repsonse
Activity (muscle tone ) - floppy/ flexed/ active
Respiration - abscent/ slow/ strong

each is scored 0-2, giving a maximum score of 10 for an unconcerning baby

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14
Q

Neonatal resucutation - what is the importance of delayed umbilical cord clamping

A

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.

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15
Q

Why are newborns given an injection shortly after birth?

When should baby be fed?

A

Babies are born with a deficiency of vitamin K. Vitamin K is an important part of normal blood clotting. Standard practice is to give all babies an intramuscular injection of vitamin K in the thigh shortly after birth. This can have the helpful side effect of stimulating the baby to cry, which helps expand the lungs. Vitamin K helps to prevent bleeding, particularly intracranial, umbilical stump and gastrointestinal bleeding.

Alternatively, vitamin K can be given orally, however this takes longer to act and requires doses at birth, 7 days and 6 weeks.

Once out of the delivery room, initiate bottle feeding as soon as the baby is alert enough

The blood spot screening test is taken on day 5 of life

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16
Q

What is hypoxic-ischaemic encephalopathy?

4 Key causes?

A

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.

Suspected 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 (cord is then compressed)
17
Q

How is Hypoxic-ischeamic encephalopathy scored?

Management?

A

Sarnat Staging of HIE
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

Management:
- admission to the neonatal unit
- supportive care- ventilation, circulatory support, nutrition, acid-base balance, treatment of seizsures
- Therapeutic hypothermia under certain circumstances for term babies to help prevent hypoxic injurt. 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.

18
Q

What causes respiratory distress syndrome?

CXR shows?

Management?

A

Respiratory distress syndrome affects premature neonates, born before the lungs start producing adequate surfactant. Respiratory distress syndrome commonly occurs below 32 weeks.

Chest xray shows a “ground-glass” appearance. Reticular changes (net) and Air Bronchograms (can see air in broncho against dense lung dissue) - basically all show poorly inflated lungs… CAME UP

Inadequate surfactant leads to high surface tension within alveoli. This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand. This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.

Management:
- Antenatal steroids (i.e. dexamethasone) given to mothers with suspected or confirmed preterm labour increases the production of surfactant and reduces the incidence and severity of respiratory distress syndrome in the baby.
- Intubation and ventilation - if severe
- Endotracheal surfactant - artificial surfactant delivered into the lungs via an endotracheal tube
- Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing
- Supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates

Support with breathing is gradually stepped down as the baby develops and is able to maintain their breathing, until they can support themselves in air.

Complications - not bothered testing but good to know about
Short term complications:

Pneumothorax
Infection
Apnoea
Intraventricular haemorrhage
Pulmonary haemorrhage
Necrotising enterocolitis
Long term complications:

Chronic lung disease of prematurity
Retinopathy of prematurity occurs more often and more severely in neonates with RDS
Neurological, hearing and visual impairment

19
Q

What causes Meconium Aspiration Syndrome?

How does it present?

Management?

A

Meconium is the dark green, sticky and lumpy faecal material produced during pregnancy. It is usually released from the bowels after birth, but in 8-25% of pregnancies, the baby can pass meconium in utero (or during birth), leading to MSAF. Of these, 5-12% of babies can aspirate MSAF and develop MAS. When this happens, MAS can cause the new born to develop respiratory distress which may be life threatening.

In-utero peristalsis occours due fetal hypoxic stress or vagal stimulation due to cord compression. Once aspirated meconium can cause:
- partial or total airway obstruction
- foetal hypoxia
- pulomnary inflammation
- infection
- surfactant inactervation

A clinical diagnosis based on
- confirmed presence of meconium in the maniotic fluid
- newborne shows signs of aspirated fluid - tachypnoea, tachycardia, cynaosis, grunting, nasal flaring, recession

Need to exldue neonatal sepsis
CXR will show increased lung voumes (obstruction), bilateral asymmetric opaccification, pleuraleffusion….
Arterial blood gas often completed.

Rx:
- Oxygen theraoy or CPAP (resp distress)
- antibiotics in infants with signs of infection (assuming fever?)
- surfactant
- inhaled nitric oxide - for pulmonary hypotension

Complications - not for memory
- air leak - air trapping causes alveolar hyperdistention -> pneumothorax or pneumomediastinum
- peristant pulomnary hypertension
- chronic lung disease
- cerebral palsy

20
Q

What is necrotising entercolitis?

How does it present? (6)

Ix? 2 Key Findings?

Rx?

A

Necrotising enterocolitis (NEC) is a disorder affecting premature neonates, where part of the bowel becomes necrotic. It is a life threatening emergency. Death of the bowel tissue can lead to bowel perforation. Bowel perforation leads to peritonitis and shock.

Presentation
- Intolerance to feeds
- Vomiting, particularly with green bile
- Generally unwell
- Distended, tender abdomen
- Absent bowel sounds
- Blood in stools

Ix:
Abdominal X-ray - is diagnosic. It shows:

Xrays can show:
Dilated loops of bowel
Bowel wall oedema (thickened bowel walls)
Pneumatosis intestinalis is gas in the bowel wall and is a sign of NEC (between the layers or the wall, not just the bowel lumen)
Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
Gas in the portal veins

Also Blds - RBC (Neutropenia and thrombocytopenia), CRP, blood gas, Cutlure (sepsis)

Management:
- nil by mouth with IV fluids, total parenteral nutrition and antibiotics
- An NG tube to drain fluid and gas from the stomach and intestines
- Surgical emergency, some recover with medical Rx, some require resection of the necrotic bowel.

21
Q

Classification of prematurity

Management before birth?

Complications?

A

Prematurity is defined as birth before 37 weeks gestation. Many successful and famous people were born prematurely, including Albert Einstein. The more premature the baby, the worse the outcomes. Resuscitation in babies under 500 grams or 24 weeks gestation should be carefully considered, as outcomes are likely to be very poor.

Under 28 weeks: extreme preterm
28 – 32 weeks: very preterm
32 – 37 weeks: moderate to late preterm

Management:
In women with a history of preterm birth or an ultrasound demonstrating a cervical length of 25mm or less before 24 weeks gestation there are two options of trying to delay birth:

Prophylactic vaginal progesterone: putting a progesterone suppository in the vagina to discourage labour
Prophylactic cervical cerclage: putting a suture in the cervix to hold it closed
Where preterm labour is suspected or confirmed there are several options for improving the outcomes:

Tocolysis with nifedipine: nifedipine is a calcium channel blocker that suppresses labour
Maternal corticosteroids: can be offered before 35 weeks gestation to reduce neonatal morbidity and mortality
IV Magnesium sulphate: can be offered before 34 weeks gestation and helps protect the baby’s brain
Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby

Issues In Early Life

Respiratory distress syndrome
Hypothermia
Hypoglycaemia
Poor feeding
Apnoea and bradycardia
Neonatal jaundice
Intraventricular haemorrhage
Retinopathy of prematurity
Necrotising enterocolitis
Immature immune system and infection

Long Term Effects

Chronic lung disease of prematurity (CLDP)
Learning and behavioural difficulties
Susceptibility to infections, particularly respiratory tract infections
Hearing and visual impairment
Cerebral palsy

22
Q

Cleft lip is a congenital condition where there is a split or open section of the upper lip. This opening can occur at any point along the top lip, and can extend as high as the nose. Cleft palate is where a defect exists in the hard or soft palate at the roof of the mouth. This leaves an opening between the mouth and the nasal cavity. Cleft lip and cleft palate can occur together or on their own.

Complications?
Management? (Age at which completed?)

A

Most cases of cleft lip and cleft palate occur randomly, there is some genetic link and 30% are associated with another underlying syndrome

Complications
- signficant problems with feeding, swallowing, and speech
- affects bonding between mother and child
- cleft palates - more prone to hearing problems, ear infections and glue ear (makes sense)

Management - MDT approach
- ensure the baby can eat and drink - specialist bottles and teats, management with specialist nurses to ensure good development
- Surgical correction - Cleft lip at 3 months, Palate at 6-12 months

23
Q

What infections are particularly concerning in pregnancy?

Complicationsd of each?

A

TORCH

-Toxoplasmosis - Toxoplasma gondii (cat feaces) - intracreanial calcificatiin, hydrocephalus, chorioretinitis (chorioid and retina)
- Rubella (deafness, catarcts, heart disease, learning disability)
- Cytomegaly virus (most maternal infections dont cause congenital CMV) - fetal growth restiction, microcephaly, hearing loss and vision loss
- Herpes simplex - high mortality - encephalitis and seizsure, hepatitis, pneumonia, other organs
- HIV- vertical transmission (mode of delivery based on viral load, Zidovudine used for prophalaxis)

Others:
- chickenpox - fetal growth restriction, microcephalus, hydocephalus, limb hypoplasia, chorioretinis - very similar to CMV
- Listeroisis- fetal death or severe neonatal infection
- Parvovirus B19 - severe fetal aneamia leading to hydrop fetalis (fetal heart failure)
- Zika Virus - microcephaly, fetal growth restriction, ventriculomegaly

24
Q

What orgnanisms commonly cause neonatal sepsis? - 5, 1 main one

A

Group B streptococcus (GBS) - Not GA like in older children.
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.

25
Q

Presentation of Neonatal sepsis?

Management?

A
  • PROM and prematurity are risk factors, maternal sepsis
  • fever
  • reduced tone
  • poor feeding
  • respiratory distress - starting more than 4 hours after birth
  • vomitting
  • jaundice within 24 hours of like
  • seizsures - red flag
  • red flag- term baby requiring CPAP

Management:
- blood cultures
- antibiotics -** benzylpenicillin and gentamycin 1st line**
- baseline CRP and FBC
- Lumbar puncture - to check for meningitis (may presents with seizsures or not responding to antibiotics)
- Recheck CRP at 24 hours, and Blood culture at 36, if negative and CRP <10 can stop treatment.

26
Q

What is neonatal hypoglycaemia?

Give 3 risk factors?

Management?

Prophalaxis of neonatal hypoglyceamia in Gestational Diabetes?

A

blood glucose <2.6 mmol/L

Risk factors:
Gestational diabetes (due to fetal hyperinsulinism) - MAIN ONE
Intrauterine growth restriction (IUGR) or preterm birth (reduced glycogen stores)
Sepsis
Delayed feeding
Others…

Note – often asymptomatic but can be hypotonic, tremors…

Ix:
Heel-prick blood tests → blood glucose levels
Persistent or severe hypoglycaemia:
- Insulin levels
- Cortisol
Growth hormone levels

Mx:
- Feeding support, including NG tube
- Dextrose gel
- IV dextrose (symptomatic or severe)

Gestational diabets:
Babies need close monitoring for neonatal hypoglycaemia, with regular blood glucose checks and frequent feeds.
The aim is to maintain their blood sugar above 2 mmol/l, and if it falls below this, they may need IV dextrose of nasogastric feeding.

Complications: Neurological damage, poor neurodevelopmental outcomes, growth failure

27
Q

What is retinopathy of preaturity?

Who is screened for ROP?

A

Retinopathy of prematurity is a condition affecting preterm and low birth weight babies. It typically affects babies born before 32 weeks gestation. Abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment and blindness

Pathophysiology - dont memeorise just be aware:
Retinal blood vessel development starts at 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. This vessel formation is stimulated by hypoxia, which is a normal condition in the retina during pregnancy. When the retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed. When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue - also not good. Cant be too hypoxic or too oxygenated basaically

Screening:
Babies born before 32 weeks or under 1.5kg should be screened for ROP. Screening is performed by an ophthalmologist

Treatment:
involves systematically targeting areas of the retina to stop new blood vessels developing.

First line is transpupillary laser photocoagulation to halt and reverse neovascularisation.

28
Q

Neonatal surgery card - what is:
- gastrroschisis - key antenatal blood test?
- omphalocele
- oesphageal atresia - presentation?
- intestinal atresia - presentation?

A

Gastroschisis is a full-thickness abdominal wall defect in which fetal abdominal organs protrude outside the abdomen with no protective membrane covering them. Direct intestinal exposure to amniotic fluid in utero leads to chemical reactions, creating a thick inflammatory film or peel over the bowel

Alpha-fetoprotein is routinely measured in antenatal screening and typically be elevated in abdominal wall defects

Management:
- A sterile, clear covering over the herniated contents protects the bowel, preventing evaporation, heat loss, and infection.
- The infant is placed on his right side to prevent kinking of mesenteric vessels
- Surgery aims to reduce the protruding organs and close the abdominal wall defect.

Omphalocele – abdominal wall defect presenting with membranous sac covering over abdominal contents, frequently associated with other congenital abnormalities

Oesophageal atresia (OA) - a rare condition where a short section at the top of the oesophagus (gullet or foodpipe) has not formed properly so is not connected to the stomach. It often happens along with another birth defect called a tracheo-oesophageal fistula, which is a connection between the lower part of the oesophagus and the windpipe (trachea).

Inability to swallow often results in poluyhydramnious - diangosed antenatally.

If not, oesophageal atresia (EA) is usually diagnosed shortly after birth when an infant exhibits symptoms such as coughing, choking and turning blue when trying to feed. If the physician is unable to pass a feeding tube all the way into the child’s stomach through the nose or mouth, this is a sign of EA.

**Intestinal atresia - the intestines are not completely connected or blocked (atresia). **

Sx- well at birth but then bowel obstruction symptoms (bilious vomit, distention) and management is surgical repair.

29
Q

What is hydrops fetalis and what causes it?

A

This was a clease for HDN in the mock…

Hydrops fetalis is a severe fetal condition characterized by abnormal accumulation of fluid in at least two fetal compartments, such as:

  • Subcutaneous tissue (skin edema)
  • Pleural space (pleural effusion)
  • Peritoneal cavity (ascites)
  • Pericardial sac (pericardial effusion)

This condition indicates end-stage heart failure or severe fetal distress and often leads to fetal demise if not promptly managed.

Causes:
- the main cause is Haemolytic disease of the newborne (Rh incompatibility) - Haemolytic aneamia → High-output cardiac failure leads to fluid accumulation→ hydrops - This is becomming less common however due to rhesus screening.
There is a long list of non immune causes that all cause fetal heart failure… (wouldnt memorise)

Fetal causes :
- Chromosomal abnormalities: Turner syndrome, trisomies (21, 18, 13).
- Anemia: Alpha-thalassemia, parvovirus B19 infection
- Structural defects: Congenital heart disease, thoracic malformations.
- Metabolic disorders: Lysosomal storage diseases.

Note on parvovirus…Fetal anaemia is caused by parvovirus infection of the erythroid progenitor cells in the fetal bone marrow and liver. These cells produce red blood cells, and the infection causes them to produce faulty red blood cells that have a shorter life span. Less red blood cells results in anaemia. This anaemia leads to heart failure, referred to as hydrops fetalis.

Maternal Causes:
- Infections: TORCH (e.g., CMV, toxoplasmosis).
- Maternal conditions: Diabetes, hyperthyroidism.
- Placental Causes: Twin-to-twin transfusion syndrome (TTTS), Chorioangioma (placental tumor).

30
Q

Brief note of types of birthmarks

A
  • Flat, red or pink areas of skin (salmon patches or stork marks)
  • Raised red lumps (strawberry marks or haemangiomas)
  • Red, purple or dark marks (port wine stains) - very rarely a sign of random syndromes wouldnt worry, normally nothing
  • cafe-au-lait spots - common and not a sign of anythign unless more than 6 i think
  • Blue-grey (Mongolian) - spots are often on the lower back, bottom, arms or legs, more common on darker skin tones and arent a sign of underlying pathology

Basically these arent things to be worried about, in the mock i thought i was missing something….