Neonatal Teaching: Respiratory Distress In Term Infants, Neonatal And Surgical Emergencies Flashcards
Respiratory distress in newborns
Clinical features:
1. General: cyanosis, perfusion, nasal flaring, grunting
2. Tachypnea: normal RR 40-60
3. Apnoea / Periodic breathing
4. Retraction: Subcostal / Suprasternal
5. Asymmetrical chest expansion / breath sound
6. Mediastinal shifting
7. Added sound on auscultation: crepitations, wheezes etc.
Causes in Term / Preterm:
Common to both:
1. **Sepsis
2. **Congenital pneumonia
3. **Transient tachypnoea of newborn (TTNB) / **Wet lung syndrome
4. ***Congenital disorders: congenital diaphragmatic hernia, lung malformation, congenital heart disease with heart failure, choanal atresia (SpC Paed Grand Round) etc.
5. Pulmonary haemorrhage
6. Air leak (Pneumothorax / Pneumomediastinum)
Specific to Term:
1. **Meconium aspiration syndrome (MAS) (∵ meconium is rarely found in the amniotic fluid prior to 34 weeks)
2. **Persistent pulmonary hypertension of newborn
Specific to Preterm:
1. ***Respiratory distress syndrome (RDS) / Hyaline membrane disease (HMD)
2. Bronchopulmonary dysplasia
Perinatally acquired pneumonia
- Isolated focal infection / Part of sepsis
- X-ray findings + clinical features ***NOT distinguished from other non-infective pulmonary pathology
Common microbiology:
1. **GBS
2. **Gram -ve enteric bacilli
3. **Listeria monocytogenes
4. **STD: Gonorrhoea, Syphilis, Chlamydia
5. ***Viruses: CMV, HSV
6. TB (rare)
Treatment:
- **Penicillin / Ampicillin
+
- **Gentamicin
Transient Tachypnea of Newborn (TTNB) (Wet lung syndrome)
Pathophysiology:
- Transient **pulmonary edema that results from **delayed resorption of fluid
—> Fluid accumulate in interstitial space
—> Bronchiolar collapse
—> Air trapping + Hyperinflation
—> Hypoxaemia + Hypercapnia due to poor alveolar ventilation
Risk factors:
- LSCS (SpC Paedi Cardi website)
Clinical features:
- Term / Near-term infants presents within ***2-6 hrs after delivery
1. Tachypnea
2. Cyanosis
3. Increased AP diameter of chest
- ***Diagnosis of exclusion: need to exclude other causes such as infection
- ***Benign self-limiting condition: typically resolves in 48-72 hrs with clearing of lung fluid
Treatment:
1. Oxygenation
- Supplemental oxygen + occasionally nasal continuous positive airway pressure to prevent hypoxia
2. Feeding
- Consider use of tube feeding to avoid aspiration
3. Fluid restriction
Meconium aspiration syndrome (MAS)
Incidence:
- 9-15% live births
- >30% past 42 weeks gestation
Amount + Thickness of meconium directly related to severity of respiratory s/s
Prevention of aspiration:
1. **Prevention of uteroplacental insufficiency
2. **Suction of mouth + oropharynx before delivery of shoulder
3. ***Direct suctioning from trachea through endotracheal tube by paediatrician
Management of infants with thick meconium stained liquor:
- Infants depressed at birth (in-utero aspiration) + those with meconium retrieved from trachea are at risk
1. Close observation with monitoring of SaO2
2. CXR in those that develop respiratory symptoms
3. Watch out features of perinatal asphyxia
Monitoring:
1. SaO2, blood gases + pH (indwelling arterial catheter), BP
Management of hypoxaemia:
1. **Adequate oxygen
2. **CPAP (may cause air trap + air leaks)
3. **Conventional positive pressure ventilation (PPV) / high frequency ventilation if persistent hypoxaemia + hypercapnia
4. **Surfactant replacement
Complications of MAS:
1. Air leaks
- 10-20% incidence of pneumothorax / pneumomediastinum
Diagnosis:
1. Physical signs
2. Transillumination (high intensity fiberoptic light source)
3. CXR
Treatment: Needle aspiration / Chest drain
Pathophysiology of Meconium aspiration syndrome
Fetal compromise (hypoxia, post-maturity, cord compression)
—> Meconium stained liquor
—> In-utero gasping + Postpartum aspiration
—> Meconium aspiration
- Peripheral airway obstruction
—> Atelectasis
—> VQ mismatch
—> Hypoxaemia + Hypercapnia + Acidosis
—> Ball-valve effect
—> Air trap
—> Air leaks
—> Hypoxaemia + Hypercapnia + Acidosis
- Proximal airway obstruction
—> Hypoxaemia + Hypercapnia + Acidosis - Chemical + Inflammatory pneumonitis
—> Hypoxaemia + Hypercapnia + Acidosis
Fetal compromise (hypoxia, post-maturity, cord compression)
—> Remodelling of pulmonary vasculature
—> PPHN
—> Hypoxaemia + Hypercapnia + Acidosis (and reversibly cause PPHN)
Persistent Pulmonary Hypertension of Newborn (PPHN)
Definition:
- Sustained elevation in pulmonary vascular resistance (PVR) after birth preventing transition to normal extrauterine circulatory pattern (i.e. ***Persistent fetal circulation)
Risk factors:
1. MAS
2. Perinatal asphyxia
3. Pulmonary parenchymal disease
4. Sepsis
Transitional circulation at birth:
- Rapid ↓ PVR with first breath + Rapid ↑ systemic VR with cord clamping
- Functional closure of foramen ovale
- ↑ Arterial oxygen content —> constriction of ductus arteriosus
- Separation of pulmonary + systemic circulations from **parallel to **series circuits
- When PVR > SVR, R to L shunting occurs through foramen ovale + PDA —> severe hypoxaemia
DDx of cyanotic infants:
1. **Uncomplicated pulmonary disease
2. **Sepsis
3. **Congenital heart disease (e.g. coarctation of aorta, cyanotic heart disease)
—> **Hyperoxia test + ***Echocardiogram to differentiate from cyanotic heart disease
Clinical features:
1. Cyanosis
2. Relative mild respiratory distress with markedly low SaO2
3. Difference between simultaneous preductal + postductal SaO2 (i.e. PDA)
Treatment:
1. **Adequate oxygen (hypoxaemia is powerful stimuli to pulmonary vasoconstriction)
2. Prevention + Treatment of acidosis
3. **Maintain high systemic blood pressure
4. Mechanical ventilation
5. ***Nitric oxide therapy (selective vasodilatation of pulmonary vasculature)
(Hyperoxia test (Wiki):
- Measure ABG of patient while they breathe room air —> remeasure ABG after patient has breathed 100% oxygen for 10 minutes
- Pulmonary problem: 100% oxygen will **augment the lungs’ ability to saturate blood with oxygen, and partial pressure of oxygen in the arterial blood will rise (usually >150 mmHg)
- Cyanotic heart disease: 100% oxygen will have **no effect, and partial pressure of oxygen will usually remain <100 mmHg)
Respiratory Distress Syndrome (RDS) (From SpC OG Neonatal Teaching: Fetal Growth Disturbances & Prematurity)
- A disease of ***prematurity mainly
- ***Lack of surfactant —> widespread atelectasis at end expiration
Surfactant system:
- Phosphotidyocholine, Phosphotidyglycerol
- Surface active substance secreted by Type II alveolar cell —> maintain distension of alveoli
- Generally deficient in premature infants ***<30-32 weeks
- Many factors may affect the likelihood of RDS in each particular preterm infants
Predisposing factors:
1. **Prematurity
2. M>F
3. **C-section
- Lack of fetal adrenergic surge
- Associated at gestation <32 weeks less clear
4. ***Maternal DM
5. Familial / Ethnic predisposition (?Chinese less RDS)
6. Twins
7. 2nd coming twin has increase RDS
8. Hypothermia
9. Haemolytic disease of newborn
10. Time of cord clamping
- Early cord clamping —> less placental transfusion —> anaemia may predispose to more RDS
Protective factors:
1. **Intrauterine growth retardation (IUGR) (↑ endogenous surfactant production)
2. **Prolonged rupture of membrane
3. **Maternal drugs + smoking
4. **Heroin (~Glucocorticoids can mature surfactant-synthesising system)
Diagnosis:
- Clinical diagnosis
- Acute illness, usually of preterm infants
- Present within 4-6 hours of delivery
- Signs of respiratory distress:
—> Tachypnoea
—> Intercostal, Subcostal, Sternal retraction
- Expiratory grunting (characteristic)
DDx:
1. Pneumonia
2. Transient tachypnoea of newborn (Wet lung syndrome)
3. Pulmonary air leak (e.g. pneumothorax)
4. Pulmonary haemorrhage
5. Metabolic acidosis, hypothermia
6. Congenital malformation (e.g. diaphragmatic hernia)
CXR:
Features of Diffuse atelectasis
1. Decrease lung volume
2. **Reticulogranular pattern (characteristic, **ground glass appearance)
3. ***Air bronchogram
4. Obliteration of cardiac shadow
Prevention:
1. Prenatal steroid therapy
- significantly ↓ incidence of RDS by 50%
2. Prophylactic surfactant
3. Avoid positive pressure ventilation (e.g. use of early CPAP)
Treatment:
1. Oxygen + Ventilator support
- Non-invasive ventilation: Nasal CPAP / Nasal IMV (Intermittent mandatory ventilation)
- Relieve cyanosis
- Surfactant Replacement Therapy
- Major breakthrough in the treatment of RDS
- ↓ Mortality + Morbidity
- Through ETT tube (SpC OG)
Surgical emergencies in neonates
Respiratory:
1. Diaphragmatic hernia
2. Cystic adenomatoid malformation
3. Tension pneumothorax
GI:
1. Intestinal obstruction
2. Esophageal atresia
3. Gastroschisis / Omphalocele
4. Necrotising enterocolitis (NEC)
CVS:
1. Ductal dependent conditions
2. Pulmonary artery obstruction
3. Aortic outflow obstruction
4. TGA
CNS:
1. Myelomeningocele
2. Hydrocephalus
3. Intracranial haemorrhage
Myelomeningocele
- Neural tube defect
- Commonly at lumbosacral region (but can occur anywhere along the spine)
- Sac-like cystic structure covered by a thin layer of partially epithelialised tissue
- **Paraplegia + **Autonomic dysfunction (depending of level of lesion)
- 80% associated with ***hydrocephalus
- Associated ***chromosomal abnormality
Clinical features:
1. Midline lesion
2. Big head
3. Lower limb deformity
4. Urinary retention
Diagnosis:
1. Antenatal ultrasound
2. Maternal serum / amniotic fluid alpha-fetoprotein (MSAFP) test
3. Postnatal clinical sign
Complications:
1. Infection
2. Hydrocephalus
3. Arnold Chiari malformation
4. Neurological deficit
5. Neurogenic bladder
Management:
Immediate:
1. Covered with sterile dressings, warm saline soaked gauze
2. Semi-elective surgical repair within few days
3. Ventriculo-peritoneal shunt
Long-term:
1. Multidisciplinary approach
Intracranial bleeding
Clinical features:
1. Local scalp trauma
2. Bulging anterior fontanelle
3. Anaemia
4. Abnormal neurological signs
5. Seizure, Coma
Diagnosis:
1. Ultrasound brain
2. CT head
3. Skull X-ray for underlying fracture
Management:
1. Neurosurgical consultation
2. Supportive treatment
Newborn emergencies
- Hypoglycaemia
- Neonatal seizures
- Cyanosis
- Ambiguous genitalia
Newborn hypoglycaemia
- Easily treatable
- Untreated hypoglycaemia —> Severe brain injury
- Can occur in infants who appear well
- Glucose cross placenta by facilitated diffusion, fetal glucose ~2/3 maternal level
- Lack of overt symptoms does NOT rule out CNS injury
Definition of Hypoglycaemia:
- Lack agreement
- Usually 2-2.5 mmol/L (2.2 mmol/L)
- Significance depends on infant’s gestation + chronological age
- No evidence to suggest that premature / young infants are protected from effect of inadequate glucose delivery to brain
- No single value below which brain injury definitely occurs
Causes:
1. Hyperinsulinism
- Infant of DM mother
- Erythroblastosis
- Islet cell hyperplasia
- Beckwith-Wiedemann syndrome
- Insulin producing tumour (Nesidioblastoma, Islet cell dysplasia / adenoma)
- Decreased production / store
- Prematurity
- IUGR
- Inadequate intake - Increased utilisation / decreased production
- Perinatal stress (shock, sepsis, asphyxia, hypothermia)
- Endocrine deficiency
—> **Adrenal insufficiency
—> **Congenital hypopituitarism
—> ***Hypothalamic deficiency
- Carbohydrate metabolism defect
—> Galactosaemia
—> Glycogen storage disease
- Amino acid metabolism defect
—> Organic acidaemia
—> Tyrosenaemia
Clinical features:
1. Lethargy, apathy and limpness
2. Apnea
3. Cyanosis
4. Weak / High pitched cry
5. Seizure, Coma
6. Poor feeding, vomiting
7. Tremor, jitteriness / irritability
8. Some may have no symptoms
Diagnosis:
1. Reagent strips (Dextrostix)
- for screening
- fast
- unreliable often
- but treatment ***should be initiated with low dextrostix
- Confirmatory laboratory glucose
- for documentation
Treatment:
1. Infants at risk should have their blood glucose monitored in first **2 hrs
2. Early **milk feeding (glucose water may cause **rebound hypoglycaemia)
3. **IV glucose in symptomatic infants / cannot tolerate oral feedings
- Bolus dose (~2ml/kg of D10) followed by Infusion (~8mg/kg/min)
4. Critical samples at low serum glucose level
- Blood: **Insulin, **GH, **cortisol, **T4
- Urine ketones (others: urine for organic acid, amino acid)
5. Recheck after initial treatment
Severe / Refractory hypoglycaemia:
- Some infants with hyperinsulinaemia / IUGR may require up to 12-15 mg/kg/min
- **Central venous catheter for infusion of dextrose >12%
- **IV Hydrocortisone: reduce peripheral glucose utilisation, increase gluconeogenesis + increase effect of glucagon
- ***IM Glucagon
