Neonatal and Newborn 2 Flashcards
What is a cephalohaematoma?
Bleeding between periosteum and skull causes a haematoma, usually in the parietal region and occasionally in the occipital region
Describe the location of a cephalohaematoma
Spread is restricted by suture lines that are adherent so it is limited to the surface of one cranial bone
Don’t cross the midline
What is a risk of a large cephalohaematoma?
Anaemia and potentially hypotension
What can occur as the a cephalohaematoma resolves?
Breakdown of haemoglobin can cause hyperbilirubinaemia that may need urgent treatment
What else may be present with a cephalohaematoma?
Underlying skull fracture
May beed CT / MRI and surgery
What are some RF for developing a cephalohaematoma?
Prolonged or instrumental labour
LGA
Malpresentation
Shoulder dystocia
List some ddx for a cephalohaematoma
Caput succudaneum - can cross midline
Subaponeurotic haemorrhage
What is the management of a cephalohaematoma?
Do not attempt to needle aspirate due to high risk of infection and abscess formation
Phototherapy for jaundice
Exchange transfusion to treat anaemia
What is the prognosis of a cephalohaematoma?
Majority resolve spontaneously within days / weeks however some may calcify
Rarely require surgical removal for cosmetic reasons
What is haemolytic disease of the newborn? What are the two most common causes?
Maternal antibodies react with antigen on the fetal RBC, most commonly:
1) Rhesus incompatibility
2) ABO blood group incompatibility
What is the pathophysiology of rhesus haemolytic disease?
Mother is rhesus negative and fetus is rhesus positive
Mother has been sensitised to rhesus-positive cells in previous pregnancies (during which fetal cells cross into maternal circulation)
Mother develops anti-rhesus antibodies, which cross the placenta and cause haemolysis of fetal RBC
How is rhesus haemolytic disease prevented?
Rhesus negative women are immunised with anti-D antibody at 28wks
This ‘mops up’ fetal RBC before they stimulate maternal IgG production
What is the pathophysiology of ABO haemolytic disease?
The mother is most commonly group O and the baby is most commonly group A
mOther and bAby
The mother’s natural anti-A antibodies react with the fetal cells causing haemolysis and jaundice
Condition cannot be detected antenatally
How does haemolytic disease of the newborn present?
Antenatal:
- Foetal anaemia
- Hydrops foetalis
Postnatal:
- Hydrops foetalis
- Early jaundice (within first 24hrs)
- Kernicterus
- Cutaneous hemopoietic lesions
- Hepatosplenomegaly
- Coagulopathy
- Thrombocytopenia
- Leucopenia
Late:
- Anaemia
- Inspissated bile syndrome
What cause of haemolytic disease of the newborn is more likely to cause RDS?
Rhesus disease
What is the management of haemolytic disease of the newborn?
Aim is to deliver baby before severe haemolysis has occurred and then undertake a serious of exchange transfusions to wash out the antibodies as well as toxic bilirubin
In-utero blood transfusions can now be given via the umbilical cord in severe cases of haemolytic disease
What antenatal investigations are performed for rhesus haemolytic disease?
Indirect Coomb’s test at first antenatal visit
Anetanal USS - detect hydrops fetalis
Fetal blood sampling
- Anaemia
- High reticulocyte count
- If DIC = schistocytes and burr cells can be seen and neutoropenia and thrombocytopenia can occur
What postnatal investigations are performed for haemolytic disease?
Immediately after birth of any baby to a rhesus-negative woman, blood form the umbilical cord or from the baby should be checked for:
- ABO and Rh blood group
- Direct Coomb’s test
- Hb
- Baseline bilirubin
What is hydrops fetalis?
Abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin oedema
List some brain complications of prematurity (4)
1) Intraventricular haemorrhage
2) Posthaemorrhagic hydrocephalus
3) Periventricular leucomalacia
4) Increased risk of cerebral palsy
What is an eye complication of prematurity and how is it managed?
Retinopathy of prematurity due to abnormal vascularisation of the developing retina
Requires laser treatment to prevent retinal detachment and blindness
List some respiratory complications of prematurity (4)
1) RDS - surfactant deficiency
2) Apnoea and bradycardia
3) Pneumothorax
4) Chronic lung disease
List some CV complications of prematurity (2)
1) Hypotension
2) Patent ductus arteriosus
List some GI complications of prematurity (3)
1) Necrotising enterocolitis
2) GOR
3) Inguinal hernias (with high risk of strangulation)
Why do premature babies have problems regulating temperature? (3)
1) Increased SA:V leads to loss of heat
2) Immature skin cannot retain heat and fluid efficiently
3) Reduced SC fat reduces insulation
What metabolic problems do premature babies face?
1) Hypoglycaemia is common:
- Symptomatic hypoglycaemia must be treated promptly
- Blood glucose should be maintained >2.6mmol/L
2) Hypocalcaemia
3) Electrolyte imbalance
4) Osteopenia of prematurity with risk of fractures
What infections are common in prematurity?
1) Increased risk of sepsis - esp group B strep and coliforms
2) Pneumonia is common
3) Infection is a common complication of central venous lines required for feeding
What nutritional requirements may a premature baby have?
May require parenteral nutrition
NG feeds until sucking reflex develops at 32-34wks
NB it is difficult to achieve in utero-growth rates
What blood complications may be associated with prematurity? (2)
1) Anaemia of prematurity
2) Neonatal jaundice
What gestation is defined as:
1) Extremely preterm
2) Very preterm
3) Moderate to late preterm
1) Extremely preterm = <28wks
2) Very preterm = 28-32wks
3) Moderate to late preterm = 32-37wks
What are the most common long-term complications of prematurity?
1) Chronic lung disease = bronchopulmonary dysplasia
- Results from disrupted lung development
- May require long-term oxygen treatment for months / years
2) Neurological sequelae
- Significant risk of hydrocephalus developing secondary to an intraventricular haemorrhage
- Shunt may need to be inserted to relieve pressure
- Hypotension may be sustained which can lead to periventricular leucomalacia. This carries risk of cerebral palsy (esp diplegic type)
3) Blindness
4) Poor growth
- Esp if catch up growth is not achieved
What is periventricular leucomalacia?
White-matter brain injury, characterised by necrosis of white matter near the lateral ventricles
Premature infants are at greatest risk
Leads to problems with motor control and developmental delay, often developing CP or epilepsy later in life
What is the antenatal management of a premature infant?
IM corticosteroids to women expecting delivery <34wks
2 doses, 12-24hrs apart
Betamethasone or dexamethasone
What is the postnatal management of a premature infant?
Most require stabilisation and support (not resuscitation)
<28 weeks need senior paediatrician
Delay cord clamping for 1 min if infant not compromised
Keep warm
Provide resp support if needed:
- Positive end experiratoy pressure = PEEP (CPAP)
- Consider intubation
Monitor and maintain blood glucose
Encourage mother to express breast milk
If ?infection - start broad spectrum abx
What are some causes of respiratory distress syndrome (RDS)? (5)
1) Surfactant deficiency = by far most common
2) Pneumonia
3) Pneumothorax
4) Cardiac failure
5) Congenital lung malformation
What are the risk factors for surfactant deficiency?
- Premature birth - main risk factor
- Genetic predisposition
- Elective C-section - uterine contractions during normal labour increase levels of glucocorticoids that aid lung maturation
- Maternal diabetes - insulin inhibits surfactant synthesis - main cause of RDS in term babies
- Hydrops fetalis
- Multiple pregnancy
How may RDS present?
Tachypnoea - RR > 60 Nasal flaring Intercostal recession Cyanosis Expiratory 'grunting'
What may a CXR show in RDS?
‘Ground glass’ appearance due to alveolar collapse with an air-bronchogram
= bilateral and relatively symmetric diffuse ground glass lungs with low volumes and a bell-shaped thorax
Generalised atelactasis = complete of partial collapse of a lung or lobe of the lung
What is surfactant?
A phospholipid which reduces alveolar surface tension to prevent them from collapsing
Produced by lamellar bodies of type II alveolar cells
When is surfactant production mature?
Surfactant production occurs at 20 weeks’ gestation but distribution throughout the lungs begins around 28-32 weeks and reaches sufficient concentration at 35 weeks
However, the stress of labour usually stimulates production, and thus RDS is usually self-limiting, lasting 5-7 days
What can be administered antenatally to at risk mothers?
24mg IM betamethasone (2 doses of 12mg 24h apart) to stimulate surfactant production
1-7 days before birth
Why do IUGR babies tend to get less severe RDS?
They are physiologically ‘stressed’ and thus tend to get less severe RDS due to endogenous corticosteroid release
What is the management of RDS?
Optimising oxygenation and supporting respiration - either with CPAP via nasal prongs, or by mechanical ventilation
Surfactant can be administered via an endotracheal tube
Abx - penicillin or gentamycin until congenital pneumonia has been excluded (can mimic or coexist with RDS)
Nutrition - IV fluids until stable, then start NG tube feeds
What is a long-term complication of RDS?
What is the prognosis?
20% develop chronic lung disease of prematurity = bronchopulmonary dysplasia
If severe may require home oxygen therapy
Generally good prognosis, 5-10% mortality
What is necrotising enterocolitis (NEC)?
Life-threatening complication in which there is impaired blood flow to the bowel
Mucosal ischaemia allows gut microorgnaisms to penetrate the bowel wall causing severe hemorrhagic colitis
What are some RF and protective factors for necrotising enterocolitis?
Breast milk = protective
But increasing milk feeds (esp formula feeds) too quickly is a risk factor for NEC
Prematurity
How may NEC present?
Acute collapse
Abdo distension
Bilious vomiting
Fresh red blood in stools
What 3 abdo XR views are required to diagnose NEC? What would be seen on AXR
Supine position
Lateral position
Lateral decubitus position
Distended loops of bowel with thickening of bowel wall
Gas in bowel wall = pneumatosis intestinalis
Possible pneumoperitoneum if perforation has occurred
What is the management of NEC?
Gut rest - nil by mouth with IV fluids and TPN and NG tube
Broad spectrum antibiotics - 10 days metronidazole
Laparotomy - surgical emergency
- Resection of dead bowel tissue
- Temporary stoma if significant bowel removed
What can be given antenatally as prophylaxis for NEC?
Erythromycin
What is the management of ROP?
Most cases require no treatment but causes blindness in 1%
Laser ablation to prevent risk of retinal detachment and blindness
What causes ROP?
Proliferation of new blood vessels in an area of relative ischaemia in the developing retina
Oxygen toxicity and genetic predisposition are two causes - at risk infants should be screened by an opthalmologist
What is an intraventricular haemorrhage (IVH)?
A haemorrhage develops in the floor of the lateral ventricle and ruptures into the ventricle
In a small minority the haemorrhage involves the white matter around the ventricle by a process of obstructive venous infarction = high risk of hemiplegic cerebral palsy
Can be asymptomatic and diagnosed by asymptomatic USS
Occurs in 30% of very low birth weight babies
What can occur as a complication of severe IVH?
Posthaemorrhagic hydrocephalus
Occurs in 15% of severe IVH
What is posthaemorrhagic hydrocephalus?
Progressive dilation of the ventricular system
How is posthaemorrhagic hydrocephalusmanaged?
May require insertion of a ventriculo-peritoneal shunt
How common is periventricular leucomalacia (PVL)?
Less common than IVH but is the most common cause of cerebral palsy in surviving infants
What increases risk of PVL?
Chorioamnionitis
Severe hypotension
Monozygotic twins
What worsens the prognosis in PVL?
Cystic change = 80% develop CP
Babies with severe IUGR should be screened for TORCH. What is TORCH?
Toxoplasmosis Other = syphilis Rubella CMV Hepatitis and HIV
What is the risk of over-feeding during infancy?
Excessive weight gain can lead to HTN, IHD and DM later in life
What is a neonatal club foot called?
Tallipes equinovarus
In which group is tallipes more common?
Males 2 x more likely
What % of tallipes are bilateral?
50%
What are the 2 types of talipes?
Talipes equinovarus = club foot - feet are hyper-inverted and plantar-flexed
Talipes calcaneovalgus = ankles are hyperflexed
What are the five deformities in talipes equinovarus?
- Equinus foot position - short Achilles tendon fixes the foot in plantar flexion so dorsiflexion beyond 90 degrees is not possible
- Varus position - supination of calcaneus
- Adductus - medial deviation of the toes
- Supinatus - inversion of forefoot
- Distinct arching of foot
What can tallipes be associated with? (3)
1) Oligohydraminous
2) Uterine anomalies
3) Multiple surgeries
= restrictive uterine environment
Describe the findings when trying to passively move the ankle in an infant with tallipes
The foot cannot be passively everted and dorsiflexed through the normal range
What is the treatment of tallipes?
Ponseti-method - manual correction with serial casting that should be initiated within 24 hours of birth
Foot is manipulated and placed in a long leg plaster cast on repeat occasions - important that the deformity correction is gradual
If this does not work, operations on soft tissues and/or bones may be carried out later (from 2yrs)
What are the main features of congenital rubella?
- IUGR
- Sensorineural deafness
- Bilateral cataracts
- Microcephaly
- PDA
What are the main features of congenital CMV?
- IUGR
- Periventricular calcifications
- Pin point petechial ‘blueberry muffin’ skin lesions
remember CMV infection would have been asymptomatic in the mother so no history of maternal illness
What are the main features of congenital toxoplasmosis?
Classic triad:
1. Chorioretinitis 2. Hydrocephalus 3. Diffuse intracranial calcifications
