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
Gastroschisis & Exomphalos
Both congenital visceral malformations
Gastroschisis Anterior abdo wall lateral to umbilical cord
- Vaginal delivery may be attempted
- New born go to theatre staright way for repair
Exomphalos (omphalocoele) Abdo contents protrude through anterior abdo wall but covered in amniotic sac and peritoneum (Downs syndrome link)
- C-Section to reduce risk of sac rupture
- staged repair as primary closure difficult due to pressure - forms shell need to wait for infant to grow.
rise in alpha-fetoprotein in the second trimester or as an abnormality on ultrasound scan.
- Abdomen of affected infant should be covered with a clear occlusive wrap to minimise fluid and heat loss.
Usually spotted antenatally
Oesophageal Atresia
Polyhydroaminos during pregnancy
- blind-ending oesophagus ( commonly caused by fistula TOF)
- birth clinical presentation is with persistent salivation and drooling from the mouth. when fed child will choke - aspiration -> cyanosis.
- management is surgery to correct the anatomical abnormality.
If suspected at birth, a wide-calibre feeding tube is passed after birth and checked by x-ray to see if it reaches the stomach.
more common in females than males
Biliary Atresia
a section of the bile duct is either narrowed or absent
Type 1: The proximal ducts are patent, however, the common duct is obliterated
Type 2: There is atresia of the cystic duct and cystic structures are found in the porta hepatis
Type 3: There is atresia of the left and right ducts to the level of the porta hepatis, this occurs in >90% of cases of biliary atresia
- lead to cholestasis, where the bile cannot be transported from the liver to the bowel. Conjugated bilirubin is excreted in the bile - which is unable to be secreted.
- Persistent jaundice in neonate (14+ days)
- Pale stools, Dark urine
- Hepatomegaly
- Leads to faltering growth
- Raised GGT. USS shows no bile duct
- Palliative surgery with a Kasai hepatoportoenterostomy
- must perform within 60 days
- prognosis is good if succesful surgery.
Gestational Diabetes
complicates up to 1 in 20 pregnancies.
- 87.5% have gestational diabetes
- 7.5% have type 1 diabetes
- 5% have type 2 diabetes
Gestational diabetes is the second most common medical disorder complicating pregnancy (after hypertension), affecting around 4% of pregnancies.
RF: BMI 30, heavy baby previous, previous GD, S.Asian
- OGTT Test of choice offered at 24-28wks
- Fasting glucose: 5.6. 2hr Glucose: 7.8
- Refer to antenatal clinic
- Advice given regarding diet
- give target - if not met then excericise, if still not met then insulin (short acting)
Complications: macrosomia or hydramnios
if Insulin over 7mmol/l prescribe insulin
Congenital hypothyroidism
Raised TSH
- Thyroid agenesis: thyroid gland is absent and is the most common cause of sporadic congenital hypothyroidism
- Maldescent of the thyroid: thyroid remains as a lingual mass or a unilobular small gland instead of migrating in early fetal life
- Dyshormonogenesis: inborn error of thyroid hormone synthesis, with autosomal recessive inheritance, occuring in about 10% of cases
- Maternal iodine deficiency: common cause worldwide but rare in the UK
- TSH deficiency: isolated TSH deficiency is rare (<1% of cases) and is usually associated with other features of pituitary dysfunction
Clinical features are difficult to differentiate from normal in the first month of life, but become more prominent with age. These include:
- Reduced feeding
- Faltering growth
- Prolonged jaundice
- Constipation
- Pale, cold, mottled dry skin
- Coarse facies
- Large tongue
- Hoarse cry
- Goitre
- Delayed development
UK screening identifies a raised TSH when blood is taken at 5days
Treatment with thyroxine should be started before 2 weeks of age to reduce the risk of impaired neurodevelopment.
Treatment will be lifelong with replacement of thyroxine in tablet form, titrating the dose to maintain normal growth, and TSH and T4 levels.
neonatal hypoglycaemia
Transient hypoglycaemia in the first hours after birth is common.
Persistent/severe hypoglycaemia may be caused by:
* preterm birth (< 37 weeks)
* maternal diabetes mellitus
* IUGR
* hypothermia
* neonatal sepsis
* inborn errors of metabolism
* nesidioblastosis
* Beckwith-Wiedemann syndrome
Symptoms in the new born are jitteriness, irritability, apnoea, lethargy, drowsiness and seizures. May also have hypothermia and poor muscle tone. Cyanosis may be present.
* Can usually be prevented by early and frequent milk feeding.
Management depends on the severity of the hypoglycaemia and if the newborn is symptomatic
* asymptomatic
encourage normal feeding (breast or bottle)
monitor blood glucose
* symptomatic or very low blood glucose below 2.0 mmol
admit to the neonatal unit
intravenous infusion of 10% dextrose
preterm
Group B strep
most common cause of early-onset severe infection in neonatal period
RF
* prematurity
* prolonged rupture of the membranes
* previous sibling GBS infection
* maternal pyrexia e.g. secondary to chorioamnionitis
- Can lead to early-onset sepsis in term, as well as preterm, infants. It can also lead to late-onset sepsis, that occurs up to 3 months of age.
- infant usually presents within 24 hours with respiratory distress
- if GBS is detected during pregnancy or there are risk factors present, prophylactic intrapartum antibiotics offered.
- an infected child, benzylpenicillin and gentamicin generally recommended as first-line choices
Features of neonatal sepsis include:
- Fever or hypothermia
- Poor feeding
- Apnoea and bradycardia/tachycardia
- Vomiting
- Shock
- Hypoxia
- Jaundice within 24 hours
- Hypoglycaemia
- Irritability
- Seizures
- Lethargy and drowsiness
HSV infection
Neonatal herpes simplex virus infection.
Usually transmitted during passage through an infected birth canal or by ascending infection.
- Presentation is anytime up to 4 weeks of age, with localised herpetic lesions on the skin or eye, or with encephalitis or disseminated disease.
- Disseminated disease has a high mortality, and considerable morbidity with encephalitis.
- accylovir treatement empirically
elective caesarean section at term is advised if a primary attack of herpes occurs during pregnancy at greater than 28 weeks gestation
Cleft lip and palate
most common congenital deformity affecting the orofacial structure
- isolated developmental malformation but they are also a recognised component of more than 200 birth defects.
- maternal antiepileptic use increases risk
- Polygenic inheritance
- cleft lip results from failure of the fronto-nasal and maxillary processes to fuse
- cleft palate results from failure of the palatine processes and the nasal septum to fuse
Problems
* feeding: orthodontic devices may be helpful
* speech: with speech therapy 75% of children develop normal speech
* increased risk of otitis media for cleft palate babies
Management
* cleft lip is repaired earlier than cleft palate, with practices varying from repair in the first week of life to three months
* cleft palates are typically repaired between 6-12 months of age
