Neonatology Flashcards
Prevalence of jaundice in first week of life in neonates
60% of full term babies
80% of pre-term babies
Early jaundice (before 24h)
Unconjugated bilirubin
ALWAYS PATHOLOGICAL, almost always haemolysis
Haemolysis:
- ABO or Rh factor incompatibility
- Red cell shape abnormalities (e.g. spherocytosis)
- Red cell enzyme pathology (e.g. G6PD)
- Sepsis
- Non-haemolytical red cell destruction (polycythaemia, bruising or cephalhaematoma)
Physiological jaundice
Unconjugated
Due to immature liver unable to process and conjugate all the bilirubin
Exaggerated physiological response
Onset >24h
Should resolve within 2 weeks in a term baby (3 weeks in pre-term)
Breast milk jaundice
Prolonged unconjugated hyperbilirubinaemia
Jaundice peaks in second week, resolves very slowly and may last up to 3 months
Healthy, thriving infant
Due to factors in breast milk that increase enteric absorption of bilirubin
Can confirm by improvement of jaundice on temporary interruption of breastfeeding, but this is rarely required
Causes of conjugated hyperbilirubinaemia in neonate
ALWAYS PATHOLOGICAL - requires urgent work up Biliary atresia Neonatal hepatitis - congenital infection - alpha-1 antitrypsin deficiency - idiopathic Metabolic Choledochal cyst
What does yellow sclera indicate
unconjugated hyperbilirubinaemia
Likely causes of neonatal jaundice present at birth
Severe haemolysis
Hepatitis (unusual)
Likely causes of neonatal jaundice presenting within 48 hours of birth
Probably haemolysis
Likely causes of neonatal jaundice presenting after 10 days of life
Hypothyroidism
Biliary atresia
At what bilirubin level does jaundice become clinically apparent
85-120 micromol/L
Non-haemolytic causes of unconjugated hyperbilirubinaemia
Increased haem load: - haemorrhage (e.g. birth trauma) - polycythaemia - swallowed blood Increased enterohepatic circulation - Bowel obstruction or ileus - pyloric stenosis Impaired hepatic uptake and conjugation - Inborn errors of bilirubin metabolism (e.g. Gilbert's disease, galactosaemia) - Endocrine (hypothyroidism, hypopituitarism, drugs) - Inhibitors (breast milk) Mixed - asphyxia - Prematurity - Sepsis - Infants of diabetic mothers
Investigations in all jaundiced infants
Serum bilirubin ratio
CBE + film
Blood group
Coomb’s test
Investigations in systemically unwell jaundiced infants or those with early jaundice (in addition to general ones)
CRP Blood cultures EUC LFT VBG BGL
Investigations in infants with conjugated jaundice
LFT Clotting TFT Septic screen Viral serology Alpha-1 Antitrypsin levels Abdominal USS (+Discuss with gastroenterology team)
Treatment options for neonatal jaundice
Increase hydration (may reduce enterohepatic circulation of bilirubin)
Frequent breast feeding
Phototherapy (photo-isomerises bilirubin into water-soluble forms excreted directly into bile)
Exchange transfusion if bilirubin >340
IVIG if haemolytic disease and rising bilirubin despite phototherapy
Complications of neonatal juandice
Kinicterus:
Unconjugated only - toxic to brain cells - death and yellow staining (particularly grey matter)
Permanent clinical sequelae
Conjugated v unconjugated bilirubin
lipid- v water-soluble
Conjugated is water soluble - hence can be excreted in bile, urine, faeces
Unconjugated is lipid soluble - hence cannot be excreted, and is able to cross the blood brain barrier when not bound to albumin
Enzyme responsible for conjugation of bilirubin in the liver
Glucuronyl transferase (defective in Gilbert’s Disease)
What is the enzyme defective in Gilbert’s disease?
Glucuronyl transferase (responsible for the conjugation of bilirubin in the liver)
Time frame in which biliary atresia must be corrected
Must be corrected within 60 days of life`
Glucuronyl Transferase is defective in which disease
Gilbert’s disease
Causes of respiratory distress in the newborn (5)
Respiratory distress syndrome (Hyaline Membrane disease) Transient tachypnoea of the newborn Pneumonia Meconium aspiration syndrome Pneumothorax/Air leak
+other weird shit like diaphragmatic hernias that are rare and low yield
Definition of respiratory distress syndrome
When a neonate has difficulty breathing due to surfactant deficiency at birth. It is the dominant clinical problem faced by preterm infants
Risk factors for respiratory distress syndrome
Low gestational age
Maternal diabetes
Prenatal asphyxia
Multiple gestation
Clinical presentation of respiratory distress syndrome
Symptoms develop within 6 hours of birth
- grunting
- intercostal recession
- nasal flaring
- cyanosis
- increased oxygen requirement
Chest x-ray findings in respiratory distress syndrome
Diffuse reticulogrannular pattern (ground glass lungs)
Air bronchograms (dark air-filled bronchi made visible by opacification of surrounding alveoli)
Bell-shaped thorax
Hyperinflation excludes RDS unless patient is intubated
Natural history of respiratory distress syndrome
Presents within 6 hours of life
Progressive worsening over first 48-72 hours
Management of Respiratory distress syndrome
ABCs: - Lateral or prone position - Oxygen (warmed, humidified) - intubate (cynaosis, recurrent apnoea, resp failure [pH and pCO2) Thermoregulation Avoid enteral feeding Antibiotics (penicillin + gent after initial investigations) Surfactant administration if intubated
Suction pressure and depth in neonate
maximum 100mmHg
Should be limited to a depth of 5cm below lips
Signs of adequate inflation and ventilation in neonatal resuscitation
increase in HR to 100/minute
Slight rise in chest and upper abdomen with each inflation
Improvement in oxygenation
Steps for BREATHING in neonatal resuscitation
Attend to adequate ventilation BEFORE oxygenation
60/minute
Positive pressure ventilation started initially in air (21% O2) EXCEPT IF GA less than 32 - should be commenced with 30% O2
Aim for oxygen saturations 91-95% by 5-10 minutes
Rate of chest inflation in neonatal resuscitation
60/minute
Normal oxygen saturation at birth
60%, increases to 90% over 5-10 minutes in normal healthy infants
Preferred route of drug administration in neonatal resuscitation
Umbilical venous catheter
Ratio when begin CPR in neonate
3:1
Aim for 90 chest compressions and 30 breaths per minute (2 events per second)
Indications to begin chest compressions during neonatal resuscitation
HR below 60 for over 30 seconds
Determining gestational age postnatally
Dubowitz Ballard Score:
Neuromuscular maturity
- Posture (more flexion = higher GA)
- Square window (wrist)
- Arm recoil (more flexion = higher GA)
- Popliteal angle (smaller = higher GA)
- Scarf sign (should not be able to pull whole arm across chest)
- Heel to ear (closer to achieving = lower)
PHYSICAL MATURITY:
- skin texture, colour, opacity
- Lanugo
- Plantar surface (size and crease)
- Breast (areola and bud?)
- Eye/ear (lids open/fused, curve of pinna, firmness of cartilage)
- Genitals (male - descent of testes + rugae, female - majora:minora:clitoris ratio)
Definition of neonatal hypothermia
Neonate with a temperature less than 36.6
Causes of neonatal hypothermia
Environmental Disorders impairing thermoregulation: - Sepsis - Intracranial haemorrhage - Drug withdrawal
Neonatal septicaemia presentation
WARM SHOCK: wide pulse pressure, rapid capillary refill COLD SHOCK: narrow pulse pressure, prolonged capillary refill \+ fever or hypothermia Tachycardia Hypotension Tachypnoea +/- hypoxia Altered conscious state
Investigations in neonatal septicaemia
Blood cultures Venous gas Blood glucose Lactate (FBE, EUC, coagulation studies as indicated)
Antibiotic therapy to give in neonatal septicaemia
Cefotaxime + benzylpenicillin
Give as an IV push
If no IV access by 30 minutes - IM ceftriaxone while achieving IV access
Management of neonatal sepsis
ABCs
Blood cultures, VBG, BGL (FBE, EUC, coags if easy access)
IV fluids: 20mL/kg bolus push over 10min, consider additional bolus as indicated
IV antibiotics
Inotropes - if no improvement in vital signs/consciousness after fluid boluses
Ventilatory support
Correct any hypoglycaemia, monitor BGL
IF initial lactate higher than 4, repeat after 2 hours, aim for clearance greater than 10%
Inotropes to give in neonatal septicaemia
Warm shock: noradrenaline
Cold shock: dobutamine
Definition of neonatal hypoglyaemia
In infant with risk factors but no clinical signs: BGL less than 2.0
In infants with clinical signs of hypoglycaemia: BGL less than 2.6
In infant on SCN/NICU: total blood glucose less than 2.6 (TBG from blood gas analyser or lab, not from bedside glucometer
Risk factors for hypoglycaemia
Reduced glycogen stores/increased demands - Prematurity - IUGR - Perinatal asphyxia - Hypothermia - Respiratory distress syndrome - Sepsis Hyperinsulinaemic states - maternal DM - Rh isoimmunisation - Persistent hyperinsulinaemia hypoglycaemia of infancy - islet cell hyperplasia - Beckwith-Wiedemann syndrome - Pancreatic tumour Other - Macrosomic infnats - CNS depression or encephalopathy at birth - nil by mouth
Presentation of neonatal hypoglycaemia
Majority are asymptomatic! CNS excitation - jitteriness - high pitch cry - seizures - irritability CNS depression - lethargy - apnoea - cyanosis - poor feeding - hypotonia
Investigations if suspect hyperinsulinism in neonate with hypoglycaemia
Insulin GH Cortisol Free fatty acids Urinary ketones
Prevention of neonatal hypoglycaemia
Early prolonged skin-skin contact and breast feeding
Prevent hypothermia
Commence enteral feeds by 1-2 hours of age if able to tolerate
Feed frequently (2-3 hourly if low risk)
Treatment of neonatal hypoglycaemia
Treat the cause
Feed increased volume of milk if asymptomatic (8-12x per day)
Buccal glucogel
IV glucose - bolus 200-300mg/kg dose, anything higher than 12.5% glucose should be given through umbilical venous catheter
Glucagon for infants with adequate glycogen stores (i.e. hyperinsulinaemic states) with hypoglycaemia despite IV infusion - IM 0.3mg/kg stat
Complications of neonatal hypoglycaemia
Short term: - seizures - apnoea - hypoxia Long term - neurological damage (CP, mental retardation, recurrent seizure activity, developmental delay, personality disorders) -?impaired CVS function
Definition of transient tachypnoea of the newborn
Parenchymal lung disorder characterised by pulmonary oedema resulting from delayed resorption and clearance of foetal alveolar fluid
Risk factors for transient tachypnoea of the newborn
C-section delivery without labour
Maternal diabetes
Maternal asthma
Clinical presentation of transient tachypnoea of the newborn
Immediate onset (within 2 hours, improves within 24 hours) Tachypnoea (over 60) Cyanosis Increased WOB Expiratory grunting AP diameter of chest may be increased Breath sounds typically clear
Chest X ray findings in transient tachypnoea of the newborn
Alveolar and “fluffy” appearance (alveolar oedema)
Effusion (fluid in fissures, costophrenic angle)
Inc. lung volumes with flat diaphragms
Mild cardiomegaly
Prominent vascular markings in sunburst pattern originating at hilum
Management of transient tachypnoea of the newborn
Benign, self-limiting condition
Supportive management
- supplemental O2 if required to maintain saturation over 90%
- nasal CPAP may be required if increased WOB or requiring more than 40% inspired O2
- nutrition via IV or NG if oral feeds not tolerated
- Thermal regulation
Clinical signs for diagnosis of meconium aspiration syndrome
- Evidence of meconium stained amniotic fluid
- Respiratory distress at birth or shortly after
- Characteristic radiographic features
- presence of meconium in the trachea in the setting of requiring intubation
Radiographic features characteristic of meconium aspiration syndrome
Progresses from initially global atelectasis to widespread patchy opacification accompanied by areas of hyperinflation and/or atelectasis
Radiologic changes resolve over 7-10 days
Risk factors for meconium aspiration syndrome
Post-date infants
Small for gestational age
Vaginal breech delivery
Incidence of meconium aspiration syndrome
0.1% of live births
Occurs in 2-10% of infants born through meconium stained amniotic fluid (which is approx 10% of term babies, more post-term)
Prevention of meconium aspiration syndrome
Intrapartum:
- prevent foetal hypoxia
- prevention of delivery later than 41 weeks gestation
Management of meconium aspiration syndrome
ABCs
Most infants will only require O2 therapy and general supportive care
Ventilator/CPAP support when refractory hypoxaemia
Intubation indicated with persistent hypoxaemia despite CPAP or respiratory acidosis
+ General supportive care:
- CVS support (volume and inotrope therapy as required)
- fluid restriction
- Antibiotics until primary bacterial infection is excluded
- IV therapy and nil orally until resp distress resolves
Characteristics of meconium aspiration syndrome
Early onset (within 2h) of respiratory distress and hypoxaemia in a meconium-stained term or near term infant Widespread "wet" inspiratory crackles +/- expiratory noises Tachypnoea, cyanosis and variable hyperinflation
Complications of meconium aspiration syndrome
Persistent pulmonary hypertension
Air leak (pneumomediastinum, pneumothorax, cystic lung disease)
Pulmonary haemorrhage
Complications of asphyxia (encephalopathy, seizures, oliguria, coagulopathy, thrombocytopaenia)
Presence of meconium stained amniotic fluid at preterm delivery raises possibility of which foetal infection in particular
Listeria
Apgar score correlations for later neurodevelopment
At 1 minute does not correlate at all
10 minute apgars between 0-3 much higher risk of cerebral palsy
Single palmar crease in an otherwise normal looking baby - what investigations are warranted
None
Single palmar creases occur normally in 1/30 healthy people
Normal meconium
Odour-free, dark, sterile
Meconium in baby with CF
Thicker, collects in ileum and may present with meconium ileus
Cause of meconium aspiration
Foetal distress leads to passing of meconium in utero, persistent or worsened foetal distress then leads to gasping efforts by baby and aspiration of the meconium in the liqour
Complications in post-term babies
Birth asphyxia secondary to traumatic delivery and meconium aspiration
Hypoglycaemia (depleted glycogen stores)
APGAR score calculation
Appearance: pink = 2, blue peripheries = 1, blue all over= 0
Pulse: more than 100 = 2, less than 100 =1, no HR = 0
Grimace: cough when stimulated = 2, grimace when stimulated = 1
Activity: moving all limbs = 2, some movement = 1, limp = 0
Respiration: Normal, crying = 2, irregular or weak cry = 1 not breathing = 0
