Pead 1 - Neonatology
Pead 1 - Neonatology
Pead 1 - Neonatology
Complications
Hypothermia
Rapid heat loss occurs in premature infants because of their relatively large body surface area and inability
to produce enough heat. Heat is lost by conduction, convection, radiation, and evaporation.
may contribute to metabolic disorders such as hypoglycemia or acidosis
admission temperature inversely related to mortality and late-onset sepsis
Management in delivery room:
o Maintaining the delivery room temperature at a minimum of 26ºC
o Drying the baby thoroughly immediately after birth
o Removal of any wet blankets
o Use of prewarmed radiant heaters if resuscitation is necessary
Once in the NICU, premature infants should be cared for in an incubator or radiant warmer to avoid
hypothermia
Respiratory abnormalities
RDS
Bronchopulmonary dysplasia, also known as chronic lung disease, is a late respiratory complication that
commonly occurs in VLBW infants
o defined as oxygen dependency at 36 weeks postmenstrual age
Apnea of prematurity
Cardiovascular abnormalities
Patent ductus arteriosus
o Symptomatic PDA is common in premature neonates
o Normally →
↑O2 when starting breathing → ↓ prostaglandins leads to DA fibrosis and contraction →
ligamentum arteriousm
Ibuprofen also blocks prostaglandins
o Ibuprofen also however, leads to ↓ blood flow to kidneys → RENAL FAILURE
Monitor renal output
In normal newborns, the DA is substantially closed within 12–24 hours after birth,
and is completely sealed after 3 weeks
Foramen ovale closes due to ↑ LA pressure
First breath → ↑pulmonary vessel diltation as oxygen is most potent vasodilator
o PDA shunts blood flow from left-to-right resulting in increased flow through the pulmonary
circulation and decreased perfusion of the systemic circulation
Pulmonary odema, hypoxia and metabolic acidosis
o Significant shunting may present with a variety of symptoms including apnea, respiratory distress, or
heart failure
Systolic murmur
o Treatment
Ligation, ibuprofen
o MEASURE ALL NEONATAL OXYGEN SATURATION ON RIGHT HAND
Pre-ductal circulation (same as brain)
Blood pressure
o low blood pressure (BP), without evidence of shock, is commonly observed in neonates
o management:
Volume expansion — Both crystalloid (eg, normal saline) and colloid (eg, fresh frozen plasma
and albumin) solutions
Inotropic therapy
Dopamine infusion
Systemic glucocorticoid therapy
Intraventricular hemorrhage
usually occurs in the fragile germinal matrix and increases in frequency with decreasing birth weight
↑risk of bleeding due to immediate change in vascular pressures
o Ultrasound day 1, 2, 7 through anterior fontanelle
o Ultrasound at 1 month for PVS
Periventricular leukomalacia
Scarring of white matter around ventricles
Sign of hypoxia
↑risk CP
Glucose abnormalities
Disorders in glucose supply or metabolism can result in hypoglycemia or hyperglycemia
Necrotizing enterocolitis
2 to 10 percent of VLBW infants
Survivors are at increased risk for growth delay and neurodevelopmental disabilities
10% of preterm infants with NEC will have long-term gastrointestinal difficulties with persistent loose stools
or frequent bowel movements.
Infection
Late-onset sepsis
o >3 days, common in premature
Mainly gram-positive, but also fungal infections
increased likelihood of poor neurodevelopmental outcome and growth impairment.
Retinopathy of prematurity
developmental vascular proliferative disorder that occurs in the incompletely vascularized retina of
premature infants
Due to sudden change in vascular perfusion → ↑O2 → vascular growth in retina → scarring and shrinking →
retinal detatchment
begins about 34 weeks postmenstrual age
should be monitored fortnightly
babies usually adapt in mild cases
Feed volumes
o 60mL first day
o +20mL every day after, until 150mL for term, higher for pre-term
COMMON PROBLEMS
Neonatal Jaundice
very common - 65% of newborns
85 umol/l total serum bilirubin (TSB) in blood to
be visible
look at sclera, mucous membranes, palm creases
Almost always due to unconjugated bilirubin
Risk Factors
prematurity
acidosis
sepsis
hypoalbuminemia
dehydration
Bilirubin
Protects newborn from oxygen toxicity in the first
days of life
is produced by the breakdown of heme (iron
protoporphyrin) in the reticuloendothelial system
and bone marrow
o Heme is cleaved by heme oxygenase to
iron, which is conserved; carbon
monoxide, which is exhaled; and biliverdin, which is converted to bilirubin by bilirubin reductase
o unconjugated bilirubin is bound to albumin and carried to the liver, where it is taken up by hepatocytes
o in the precence of enzyme UDPGT, bilirubin is conjugated to one or two glucuronide molecules
o Conjugated bilirubin is then excreted through the bile to the intestine
o In the presence of normal gut flora, conjugated bilirubin is metabolized to stercobilins and excreted in
the stool
Absence of gut flora and slow GI motility, both characteristic of the newborn, cause stasis of
conjugated bilirubin in the intestinal lumen, where mucosal -glucuronidase removes the
glucuronide molecules and leaves unconjugated bilirubin to be reabsorbed (enterohepatic
circulation)
Low ability to bind to albumin → ↑free bilirubin when drugs, sepsis or acidosis is present
Causes:
< 24 Hours of Age
always pathologic and requires investigation
o blood group, baby’s serum bilirubin (total and
unconjugated), direct Coombs test,
haemoglobin, white cell count, platelets and
peripheral smear, LFTs
o also test mothers red cell antibodies
admit to special care nursery
Mostly caused by haemolysis
o Rh or ABO incompatibility between mother and fetus
o Severe haemolysis → rapid ride in serum bilirubin in over a few hours
o internal hemorrhage
sepsis/congenital infection: TORCH
Further investigate if no haemolysis, or conjugated hyperbilirubinaemia present
Phototherapy should be commenced if the bilirubin level is >150 μmol/L in the first 24h in a term infant
Immediate exchange transfusion if due to rhesus incompatibility and infant anaemia ( Hb <110 g/L)
Frequent monitoring of bilirubin levels is essential as rapid changes may occur
Gilbert Syndrome
This is a common mild autosomal dominant disorder characterized by decreased hepatic UDPGT activity
Affected individuals tend to develop hyperbilirubinemia in the presence of conditions that increase bilirubin
load, including G6PD deficiency.
They are also more likely to have prolonged neonatal jaundice and breast-milk jaundice.
Prematurity
Premature infants often have poor enteral intake, delayed stooling, and increased enterohepatic circulation, as
well as a shorter red cell life.
Infants at 35–36 weeks' gestation are 13 times more likely than term infants to be readmitted for
hyperbilirubinemia.
Even early-term infants (37 weeks' gestation) are four times more likely than term neonates to have TSB greater
than 224 mmol/L.
Bilirubin Toxicity
Unconjugated bilirubin anion is the agent of bilirubin neurotoxicity.
The anion binds to the phospholipids (gangliosides) of neuronal plasma membranes causing injury, which then
allows more anion to enter the neuron.
Intracellular bilirubin anion binds to the membrane phospholipids of subcellular organelles, causing impaired
energy metabolism and cell death.
Risk depends on the duration of hyperbilirubinemia, the concentration of serum albumin, associated illness,
acidosis, and the concentrations of competing anions such as sulfisoxazole and ceftriaxone
Premature infants are at greater risk than term infants because of the greater frequency of associated illness
affecting the integrity of the blood-brain barrier, reduced albumin levels, and decreased affinity of albumin-
binding sites
Treatment
maintain good hydration and normal acid-base status
1st line therapy: phototherapy - photoisomerization (blue light most effective)
exchange transfusion, depending on level of bilirubin, age, weight
treat any underlying cause
do not interrupt breastfeeding in healthy term newborns
Phototherapy
most common treatment for indirect hyperbilirubinemia
Light of wavelength 425–475 nm (blue-green spectrum) is absorbed by unconjugated bilirubin in the skin
converting it to a water-soluble stereoisomer that can be excreted in bile without conjugation
Cover infants eyes
Started electively when TSB > 102 mmol/L
Exchange Transfusion
extreme indirect hyperbilirubinemia
admit to NICU
Albumin (1 g/kg) will aid in binding and removal of bilirubin
Double-volume exchange transfusion (approximately 160–200 mL/kg body weight
invasive, risky, and infrequently performed
o Mortality is 1–5%
o 5–10% risk of serious complications such as necrotizing enterocolitis (NEC), infection, electrolyte
disturbances, or thrombocytopenia
Presentation
tachypnea > 60 / per min
audible expiratory grunting
o Due to closing of glottis to maintain positive pressure on early expiration → PEEP
Increased work of breathing (recession of the lower chest wall and upper abdomen).
o intercostal retractions/indrawing
o Due to negative pressure and softer bones
o Children mainly breath with diaphragm, underdeveloped accessory muscles
nasal flaring
o ↑lumen diameter → ↑flow
duskiness/central cyanosis
decreased A/E on auscultation
tachycardia > 160 / per min
SEND TO NICU if needing >40% O2 to maintain >88% saturation
Diagnosis
chest x-ray
ABG, CBC, blood glucose
blood cultures, Gram stain
Differential Diagnosis
pulmonary
o respiratory distress syndrome (RDS)
o transient tachypnea of the newborn (TTN)
o meconium aspiration (group B strep and others)
o atelectasis
o pleural effusions
o pneumothorax
o congenital lung malformations
cardiac
o congenital heart disease (cyanotic, obstructive, LR shunt)
o persistent pulmonary hypertension (PPHN)
hematologic metabolic
o blood loss o hypoglycemia
o polycythemia o inborn errors of metabolism
infectious neuromuscular
anatomic o CNS damage (trauma, hemorrhage)
o tracheoesophageal fistula o medication (maternal sedation)
o congenital diaphragmatic hernia o anomalies (e.g. Werdnig-Hoffmann
disease)
o drug withdrawal syndromes
Pneumonia
Group B β-haemolytic streptococcus (GBS) is the most common and serious cause of pneumonia and
septicaemia in the newborn
o Acquired at birth from a colonised mother
o Infections usually ascend from the genital tract before or during labor, with the vaginal or rectal flora the
most likely agents
o Therefore consider in infants with prolonged rupture of membranes, chorioamnionitis, or maternal fever
Other organisms such as E.Coli also
presents early with severe and progressive respiratory failure → rapid progression to collapse and death
Later infections → lethargy, temperature instability, poor feeding, respiratory difficulty, apnoea or poor
perfusion
CXR similar to severe RDS, not diagnostic
o Temperature unstable, ↑WBC, neutropenia, ↑CRP
Treat all with broad-spectrum antibiotic penicillin and gentamicin until cause is confirmed
Pneumothorax
May occur spontaneously at birth, or secondary to other lung disease
1% of all deliveries
Risk is increased by manipulations such as positive-pressure ventilation (PPV) in delivery room
Respiratory distress (primarily tachypnoea) is present from birth and typically is not severe
Diagnosis by CXR
main treatment is an intercostal catheter with an underwater drain at low negative pressure
o Asymptomatic pneumothorax usually needs no treatment.
o supplemental O2 and watchful waiting
↑risk of renal abnormalities → consider renal USS
Tension pneumothorax
• This is a medical emergency. There may be no time for a chest radiograph
• If a baby is deteriorating rapidly despite full resuscitation this diagnosis should be considered, particularly if there is
poor air entry on auscultation to one or both sides of the chest.
• In the event of severe deterioration, aspirate the chest using a 25-gauge scalp vein needle attached via a three-way
tap to a 10 mL syringe. The needle is inserted into the second or third intercostal space in the midclavicular line.
Aspirate the chest with the 10 mL syringe. Then insert intercostal catheter
Respiratory care
• A chest radiograph provides the diagnosis in most cases of respiratory difficulty in neonates.
• Monitor cardiorespiratory and blood gas measurements.
• Arterial pH should be maintained at 7.35–7.45. A level of 7.25 (or just under) may be acceptable, depending on the
circumstances.
• Arterial Pco2 should be 40–60 mmHg.
• Arterial Po2.
A low Po2. means the baby is hypoxic. If the pH is also low, the baby may have a metabolic acidosis and a
higher level of inspired oxygen is required. If this does not improve oxygenation, suspect cyanotic heart
disease as a cause
• Arterial bicarbonate should be 22–26 mmol/L. A low level is due to a metabolic acidosis. The pH will also be low
unless the baby has compensated by blowing off CO2.
• Base excess should be between +3 and −3. If low it indicates a metabolic acidosis. A level of −5 is usually tolerated
in small babies without a signifi cant change in pH.
• In ventilated babies with RDS, especially those <30 weeks’ gestation, surfactant should be given via the
endotracheal tube as early as possible.
• The inspired oxygen requirement is initially determined using a pulse oximeter. Aim for an oxygen saturation of
88–95%.
• Arterial blood gases should be measured in babies needing >30% oxygen. Aim for a PaO2 level of 50–80 mmHg.
• Nasal continuous positive airway pressure (CPAP) is effective for treating RDS or apnoea.
• The decision to ventilate a baby is made on the following criteria:
– Apnoea not responding to simple treatment.
– Unsatisfactory arterial blood gases: pH <7.25 with a Pco2 >60 mmHg, or inspired oxygen >60% despite
treatment with CPAP (up to 10 cm H2O).
DIAPHRAGMATIC HERNIA
Posterolateral or Anteromedial
clinical features
o respiratory distress, cyanosis
o scaphoid abdomen
o affected side dull to percussion and breath sounds absent;
may hear bowel sounds instead
o asymmetric chest movements, trachea deviated away from affected side
o may present outside of neonatal period
chest x-ray: portion of GI tract in thorax (usually left side),
displaced mediastinum
treatment: surgical
prognosis: 50% survival overall
o associated with a high incidence of pulmonary vascular
anomalies, hypoplastic lungs
APNEA
Definition
absence of respiratory gas flow for 20 seconds in the preterm infant and 15 seconds in the term infant (less if
associated with bradycardia or cyanosis)
central: no chest wall movement
obstructive: chest wall movement continues
mixed: combination of central and obstructive apnea
Differential Diagnosis
apnea < 24 hrs – strongly associated with sepsis
apnea > 24 hrs – if not pathological, apnea of prematurity
in term infant apnea always requires full W/U CNS
apnea of prematurity presents in the first week of life due to prematurity of CNS and resolves by 36 weeks
GA.
seizures
intracranial hemorrhage
sepsis
GI: GE reflux, esophagitis
metabolic: low glucose, low calcium, low Na
cardiovascular
o low and high blood pressure
o anemia, hypovolemia, PDA
drugs: demerol, morphine
Treatment
correct underlying cause
tactile stimulation, reduce warming of face
monitoring
oxygen, CPAP, ventilation
o medications: methylxanthines (caffeine, theophylline) which stimulate CNS and diaphragm,
• S/E of caffine → tachycardia and hyponatriuemia
o doxapram (direct CNS stimulant) used in some centres
Hypoglycaemia
True blood glucose of <2.5 mmol/L
measured before 1 h of age for infants with the following conditions:
o Infants of diabetic mothers, infants weighing <10th centile, prematurity, large for gestational age,
shock, seizures and infants receiving i.v. infusions.
Risks:
o Maternal diabetes/PET o 90th percintle, <4.5kg
o Drugs o RD, Sepsis, temp
o IUGR o Symdromes
o <2.5kg, <10th percentile o Microphallus
Causes:
o Lack substrate
o Too much insulin
o Enzyme disorders
Clinical features
o Possibly asymptomatic
o apathy, hypotonia, poor feeding, temperature instability, apnoea, jitteriness or
convulsions
Management
o Asymptomatic infants with a true blood glucose of 1.5–2.5 mmol/L: give early,
frequent small milk feeds at 90 mL/kg per day. If no response occurs within 2 h, give
i.v. 10% dextrose
o If the blood glucose is <1.5 mmol/L i.v. dextrose should be given. A bolus of 10%
dextrose, 2 mL/kg, should be followed by an infusion providing 5–10 mg/kg per min
of glucose. The response to therapy should be monitored by frequent blood glucose
measurements.
o Other treatments: Glucagon, diazoxide, steriods
Infection
o 0.7% newborns
o Early onset (<48hrs)
o GBS
o E.Coli
o Listeria monocytogenes
o Late onset (>48hrs)
o Coag negative Staph
o Staph A
o GBS
o Klebsiella
o Pseudomonas
o Gram negative
o Viral → HSV most serious, also RSV
o Always rule out sepsis first
o Risks
o GBS isolated
30% carriage
50% neonatal colonisation
o Chorioamnionitis
o Maternal fever/discagre
o Premature
o PROM
o Neurtopenia
Investigations
Blood culture: arterial or venous, at least 2–4 mL.
Urine: suprapubic aspiration (SPA) under ultrasound imaging if possible. If unsuccessful pass a catheter using
a 5-French gauge tube after adequate preparation of the genitalia
o A bag collection of urine is rarely helpful
Throat and rectal swabs and swabs of any obviously infected lesion.
Cultures or specific PCR for viral infections.
Lumbar puncture if meningitis is suspected. This should always be done in the presence of fever in a
newborn.
Management
Any ill neonate should be admitted to hospital for investigation and treatment.
Start with i.v. benzylpenicillin and gentamicin.
Add i.v. cefotaxime if meningitis is suspected (see Antimicrobial guidelines) and i.v. metronidazole if
abdominal sepsis is suspected.
If there is any possibility that the baby may have HSV (i.e. the mother has active genital herpes), give
aciclovir.
Antibiotics may be subsequently tailored according to culture results
Careful attention to temperature stability, respiratory status, fluid and electrolytes, blood pressure, blood
glucose and haematology is essential.
Neonatal rashes
Naevus flammeus (‘stork-bite’): dilated capillaries, on the nape of the neck and on the bridge of the nose, eyelids
and adjacent forehead. They fade over 6–12 months.
Milia: small white blocked sebaceous glands on the nose. They disappear over the first month.
Miliaria: there are two types – ‘crystallina’ and ‘rubra’.
o Miliaria crystallina are beads of sweat trapped under the epidermis and are most prominent on the
forehead in babies who are overheated.
o Miliaria rubra, also called ‘heat rash’, usually appear after a few weeks of age, fluctuate over 2–3 weeks
and then disappear. They are related to an increasing activity of the sweat glands. They are prominent
on the face, in babies who are overheated.
Erythema toxicum (‘toxic erythema’ or ‘urticaria of the newborn’): these are red ‘urticarial’ spots over the baby’s
trunk that peak at 2–3 days of age and generally resolve by the first week of life, but occasionally runs a
fluctuating course over a few weeks. They are harmless and of unknown cause. New lesions have a broad
erythematous base up to 2–3 cm diameter with a 1–2 mm papule or pustule.
‘Mongolian’ blue spot: this condition results in areas of increased melanin deposition over the lower back and
sacrum. It can be more extensive and is sometimes mistaken for bruising. It is present in most babies born to
dark skinned parents. It gradually lightens over a few years, as the rest of the skin becomes more pigmented.
Dry skin: babies who are post-term have a thicker epidermis and hence drier-looking skin after birth. This dry
skin may occasionally crack and bleed around the hands and feet during the first few days. Emollients will help.
Otherwise the dry skin should be allowed to peel off naturally, which may take up to 1–2 months.
Others:
o Ebsteins pearls
o Pustular melanosis
o Neonatal acne
o Sucking blister
Neonatal seizures
Clinical features
• Subtle: deviation of the eyes, staring, abnormal sucking, lip smacking or cycling movements of the limbs.
• Tonic: stiffening of limbs, frequently associated with apnoea and eye deviation.
• Clonic: movement of one or all limbs that persists despite holding the limb.
• Benign sleep myoclonus: occurs in neurologically normal infants only during sleep. The electroencephalogram
(EEG) is normal and no treatment is necessary. It can be exacerbated by benzodiazepines and usually resolves by 2
months of age.
Aetiology
Causes include:
• Hypoxic ischaemic encephalopathy: seizures occur within 24 h of the hypoxic episode, often within the fi rst 4–6 h.
• Intracranial haemorrhage (subdural, subarachnoid, intraventricular or parenchymal).
• Infection: bacterial or viral meningitis.
• Stroke.
• Metabolic:
– Hypoglycaemia.
– Hypocalcaemia/hypomagnesaemia.
– Hypo- or hypernatremia.
– Kernicterus.
– Inborn errors of metabolism (characterised by intractable seizures, with progressive loss of consciousness,
or metabolic acidosis), including:
Pyridoxine dependency.
Urea cycle disorders.
Non-ketotic hyperglycinaemia.
Fatty acid oxidation defects.
Amino acid/organic acid/hyperammonaemia.
• Drug withdrawal.
• Developmental brain abnormalities.
• Autosomal dominant neonatal seizures.
Investigations
• Bloods:
– Immediately check blood glucose.
– Electrolytes including calcium and magnesium.
– Blood gases.
– Blood cultures.
• Metabolic screen: blood ammonia, lactate, amino acids, carnitine and urinary organic acids.
• Urine analysis including ketones and reducing substances.
• Lumbar puncture and viral investigations.
• Cranial ultrasound.
• Cranial CT scan to exclude intracranial haemorrhage that may warrant neurosurgical intervention.
• MRI brain scan to determine extent of injury in hypoxic–ischaemic encephalopathy (HIE) (usually done around day
5); to exclude stroke where focal seizures are occurring, or for suspected developmental brain abnormality.
• EEG to detect seizure activity and to aid prognosis. Where conventional EEG is not immediately available, bedside
amplitude integrated EEG (aEEG) may be useful in the detection of some seizures.
Management
Admission to a NICU is mandatory for all neonates with seizures.
Attention to normoglycaemia, optimal ventilation, blood pressure control, and fl uid and electrolyte balance is
essential.
Anticonvulsants
• Phenobarbitone: 20 mg/kg i.v. over 30 min
• Phenytoin: 20 mg/kg, i.v. over 1 h.
• Clonazepam: up to 0.25 mg. This may cause apnoea. Careful monitoring and the availability of mechanical
ventilation are essential.
• Pyridoxine: 50–100 mg i.v. or p.o. should be considered for intractable seizures.
Most infants can be weaned from anticonvulsant therapy within a few days of their last seizure.
HEART MURMURS
common in the first days of life and do not usually signify structural heart problems
If a murmur is present at birth, it should be considered a valvular problem until proved otherwise because
the common benign transitional murmurs (eg, patent ductus arteriosus) are not audible until minutes to
hours after birth.
If an infant is pink, well-perfused, and in no respiratory distress, with palpable and symmetrical pulses (right
brachial pulse no stronger than the femoral pulse), the murmur is most likely transitional
o . Transitional murmurs are soft (grade 1–3/6), heard at the left upper to midsternal border, and
generally loudest during the first 24 hours
If the murmur persists beyond 24 hours of age, blood pressure in the right arm and a leg should be
determined. If there is a difference of more than 15 mm Hg (arm > leg) or if the pulses in the lower
extremities are difficult to palpate, a cardiologist should evaluate the infant for coarctation of the aorta
BIRTH TRAUMA
Most associated with difficult delivery
o eg, large fetus, abnormal presenting
position, or fetal distress requiring
rapid extraction
Most common injuries are soft tissue bruising, fractures (clavicle, humerus, or femur), and cervical plexus
palsies
Skull fracture, intracranial hemorrhage (primarily subdural and subarachnoid), and cervical spinal cord injury
can also occur.
Subgaleal hemorrhage into the large potential space under the scalp is associated with difficult vaginal
deliveries and repeated attempts at vacuum extraction
o can lead to hypovolemic shock and death from blood loss and coagulopathy triggered by
consumption of clotting factors and release of thromboplastin from the injured brain
Facial palsy
o May occur in forceps delivery
o Facial asymmetry seen when crying
o Most resolve in a few weeks-months
o If persistent after 12 months, don’t recover
What are the implications of some of these conditions for the child's future?
Neurodevelopmental outcome
Impaired cognitive skills
Motor deficits including mild fine or gross motor delay, and cerebral palsy
Sensory impairment including vision and hearing losses
Behavioral and psychological problems
Growth impairment
o more likely to exhibit poor growth compared to those born full-term
o lighter, shorter, and had a lower body mass index and smaller head circumference
Insulin resistance
o More likely to have insulin resistance and higher blood pressure compared to adults born full-term
Reproduction
o decrease reproduction in adulthood
o preterm women but not men were at increased risk of having preterm offspring.