Paeds Neonatology Flashcards
Newborn Resuscitation
5 steps
- Dry baby and maintain temperature
- Assess tone, RR and HR
- Gasping or No breathing give 5 inflation breaths
- Reasses chest movements
- If HR not improving and below 60bpm then initiate compressions and ventilations at 3:1
inflation breaths are different from ventilation breaths
in a child it is 15:2 ratio (15 compressions 2 breaths)
- check for signs of circulation
- infants use brachial or femoral pulse, children use femoral pulse
- give 5 rescue breaths
in children: compress the lower half of the sternum
in infants: use a two-thumb encircling technique for chest compression
Surfactant deficient lung disease
respiratory distress syndrome
hypoxia, hypercapnia (high CO2) and respiratory distress.
seen in premature infants. It is caused by insufficient surfactant production and structural immaturity of the lungs
- high surface tension in alveoli, leads to atelectasis (lung collapse)
- Difficult for alveoli and lungs to expand, inadequate gaseous exchange
- 4h post birth: Head bobbing, Nasal Flaring, Tracheal tug, subcostal and intercostal recession, Grunting, Tachypnoea, Cyanosis
- Ground glass on X ray with indistinct Heart border
- Antenatal steroids given to mother
- infant gets non invasive ventialatory support.
- Surfactant therapy via endotrachial tube
Other risk factors for SDLD include
* male sex
* diabetic mothers
* Caesarean section
* second born of premature twins
premature birth complication
Bronchopulmonary Dysplasia
lung damage due to delay in maturation
Infants with severe BPD have trouble feeding and gain weight poorly.
- Infants who still have an oxygen requirement at a post-menstrual age of 36 weeks are described as having bronchopulmonary dysplasia (BPD)
- Babies have RDS and reuquire ventillatory support
- Chest x-ray characteristically shows widespread areas of opacification
- Some babies require prolonged artificial ventilation – most weaned onto CPAP or nasal cannula therapy.
Risk of poor neurological development. Recurrent respiratory symptoms
Corticosteroid therapy may facilitate earlier weaning from the ventilator – concerns about side effects in using at such a young age.
Meconium Aspiration Syndrome
Causes Respiratory Distress in newborn
- Meconium in trachea -> RDS
- common in post-term deliveries
- RF: maternal HTN, pre-eclampsia, chorioamnionitis, smoking or substance abuse.
Manage using O2 if required and may require Abx
hypoxic ischaemic encephalopathy pathophysiology
Anything that leads to asphyxia, depriving the brain of oxygen.
- Failure of gas exchange over placenta i.e. excessive uterine contractions, placental abruption, ruptured uterus
- Interruption of umbilical blood flow i.e. cord compression in shoulder dystocia or cord prolapse
- Inadequate maternal placental perfusion, maternal hypertension or hypotension
- Compromised fetus
- Failure to breathe
Hypoxia refers to lack of oxygen at birth, ischaemia refers to restriction of blood flow to the brain and encephalopathy refers to malfunctioning of the brain.
Remains an important cause of brain damage.
COMPLICATIONS
Multi-organ failure can present in a variety of ways.
Can be a cause of significant neuro-disability; leads to cerebral palsy in many cases.
hypoxic ischaemic encephalopathy signs and symptoms
mild moderate severe
- Mild: poor feeding, generally irritability and hyper-alert infant. May have hyperventilation and hypertonia. Generally resolves within 24 hours.
- Moderate: infant shows marked abnormalities of movement, hypotonic, cannot feed and may have seizures. May take weeks to resolve.
- Severe: no normal spontaneous movements or response to pain, tone in the limbs may fluctuate between hypotonic and hypertonic, seizures are prolonged and often refractory to treatment, and multi-organ failure may be present. Reflexes may be absent. There is up to 50% mortality in this stage.
Poor AGPAR score should ring alarm bells
Skilled resuscitation and stabilisation will minimise neuronal damage. Infants may need:
- Respiratory support
- Treatment of seizures with anticonvulsants
- Fluid restriction due to transient renal impairment
- Treatment of hypotension by volume and inotrope support
- Monitoring and treatment of hypoglycaemia and electrolyte imbalance
mainstay treatment: therapeutic cooling
Toxoplasmosis in pregnancy
Transplacental spread from mother to fetus
Neuro damage: Cerebral calcification, Hydropcephalus, Chorioretinitis
Opthal damage: Retionopathy, Cataracts
Picked up on antenatal scan
Infants with toxoplasmosis can be treated with pyrimethamine, an antiparasitic medication, and sulfadiazine, which is an antibiotic. If it is suspected that a mother has toxoplasmosis in the early stages of the pregnancy, spiramycin, an antibiotic and antiparasitic, may be prescribed to prevent transmission to the fetus.
Syphilis in Pregnancy
Syphilis in pregnant women can cause miscarriage, stillbirth, or the baby’s death shortly after birth
a penicillin regimen that is both appropriate for the stage of syphilis and initiated 30 days or more before delivery.
Congenital Syphilis
* Face: Rhinitis (snuffles) with mucopurulent nasal discharge.
* Skin: Jaundice, rash and desquamation.
* Abdomen: Hepatosplenomegaly (enlarged liver and spleen)
* Eye: Chorioretinitis and pigmentary chorioretinopathy (salt and pepper type), glaucoma, cataracts, interstitial keratitis, optic neuritis
VZV in pregnancy treatment
Congenital Varicella Syndrome is an extremely rare disorder in which affected infants have distinctive abnormalities at birth (congenital) due to the mother’s infection with chickenpox (maternal varicella zoster) early during pregnancy (i.e., up to 20 weeks gestation).
Acyclovir can treat VZV
newborns may have a low birth weight and characteristic abnormalities of the skin; the arms, legs, hands, and/or feet (extremities); the brain; the eyes; and/or, in rare cases, other areas of the body.
Parovirus in pregnancy
Hydrops Fetalis
parvovirus B19 in pregnant women can cross the placenta in pregnant women
- severe anaemia due to viral suppression of fetal erythropoiesis
→ heart failure secondary to severe anaemia → the accumulation of fluid in fetal serous cavities (e.g. ascites, pleural and pericardial effusions) - treated with intrauterine blood transfusions
Cytomegalovirus in pregnancy
infected cells have a ‘Owl’s eye’ appearance due to intranuclear inclusion bodies
Congenital CMV infection
* features include growth retardation, pinpoint petechial ‘blueberry muffin’ skin lesions, microcephaly, sensorineural deafness, encephalitiis (seizures) and hepatosplenomegaly
Treatment
- IV ganciclovir is the treatment of choice
over 1/2 BABIES HAVE IT
Neonatal Jaundice Pathophysiology
Breakdown of RBCs releases unconjugated bilirubin into the blood; this is conjugated in the liver which is then excreted two ways: via biliary system to GI tract and via the urine.
Physiological jaundice is common due to marked release of haemoglobin at birth, RBC lifespan of newborns is shorter at 70 days and hepatic metabolism is less efficient in the first few days.
First 24H - Often Pathological: Rhessus, ABO incompatibiltiy, haemorrhage, sepsis G6PD
First 2-14d - Phsiological Jaundice
14+ Days (21 in premature) - Prematurity, blliary atresia (conjugated bilirubin) Breast Milk jaundice, neonatal cholestasis, Gilbert syndrome.
Jaundice can most easily be observed by blanching the skin with a finger. Tends to start on the head and face, and then spread down the trunk and limbs.
Neonatal Jaundice managment & complications
- FBC and blood film – polycythaemia or anaemia
- Conjugated bilirubin – elevated levels indicate hepatobiliary cause
- Direct Coombs Test for haemolysis
- Poor milk intake and dehydration will exacerbate jaundice – need to be corrected.
- phototherapy for unconjugated bilirubin
- Exchange transfusion is required if the bilirubin rises to levels considered potentially dangerous. Blood removed from the baby in small amounts and replaced with donor blood.
Kernicterus is the encephalopathy resulting from the deposition on unconjugated bilirubin in the basal ganglia and brainstem nuclei – occurs when levels exceed the albumin-binding capacity of bilirubin in the blood.
- Acute manifestations are lethargy and poor feeding; in severe cases there is irritability, increased muscle tone causing arched back (opisthotonus) seizures and coma. Can lead to cerebral palsy, learning difficulties and sensorineural deafness.
Leading cause of death in prematures
Necrotising Enterocolitis pathophysiology
Preterm infants who are fed cow’s milk formula are more at risk than if only fed breast milk. others include RDS, Sepsis and PDA
- bowel becomes necrotic. This is a life-threatening emergency as death of the bowel tissue can then lead to bowel perforation.
- feed intolerance and vomiting, which may be bile stained. Abdomen becomes distended and the stool sometimes contains fresh blood.
neonate is very unwell
When perforation occurs, there will be peritonitis and shock.
Necrotising Encolitis Investigations and Management
Xray:
- Thick & distended bowel
- Intramural gas (pneumatosis intstalis)
- Pneumaperitoneum (Perforation)
- Nil by mouth
- TPN
- IV fluids
- Broad spectrum IV Abx
- Surgical referral
