Chronic disease of the neonate Flashcards
Chronic diseases of the neonate
HIE
IVH
BPD
What is HIE?
greatest risk of adverse outcome – severe fetal acidosis (pH 6.7)
major neonatal encephalopathies or seizure – due to perinatal events
Fetal hypoxia may be caused by
inadequate oxygenation of maternal blood from hypoventilation during anesthesia
low maternal BP from acute blood loss, spinal anesthesia, or compression of vena cava by gravid uterus
uterine tetany – inadequate relaxation of uterus for placental filling
abruption placenta
compression or knotting of cord
placental insufficiency from toxemia
after birth
1_ CHD or severe pulmo disease
2. severe anemia (hemorrhagic or hemolytic disease
3. shock (sepsis, blood loss, IVH)
Pathogenesis of HIE
Hypoxia and ischemia»_space; anaerobic metabolism»_space; lactate and inorganic phosphates
Glutamate accumulates in damaged tissue, intracellular edema because of IC Na
Intial response – shnt blood to brain, heart, adrenals
Effects
- congestion and petechiae in pericardium, pleura, thymus, heart, adrenals and meninges
what are the clinical manifestations of HIE?
IUGR with increased vascular resistance – 1st indication of fetal hypoxia
variable or late deceleration pattern
at delivery – meconium stained amniotic fluid – fetal distress
depressed, fail to breathe, remain hypotonic or change to hypertonic state
Pallor, cyanosis, periodic breathing with apnea, slow heart rate and unresponsiveness to stimulation – signs of HIE
Cerebral edema develops next 24 hours – profound brainstem depression»_space; during this time seizures may occur
Heart failure and cardiogenic shock, PPHN< RDS, GI perforation , hematuria»_space; associated with asphyxia due to inadequate perfusion
Diagnosis of HIE
Diff for seizure – IVH, hypocalcemia, hypoglycemia or CNS infection
Diffusion weighted MRI – imaging of choice
CT scan – limited
UTZ – limited in term
aEEG (amplitude integrated EEG) – who is at risk for long term brain injury
what are the complications of HIE?
Ph <6.7 high risk of death and severe neuro impairment
Brain death after HIE
coma unresponsive to pain, auditory or visual stimulation
apnea with PCO2 rising from 40-60mmHg
absence of brain reflexes
what is the treatment of HIE?
Cerebral or body systemic therapeutic hypothermia reduces mortality and major neuro impairment (33.5C within 1st 6 hours after birth)
hypothermia decreases rate of apoptosis, suppresses mediators like glutamate
Phenobarbital (DOC)
Loading dose 20mg/kg)
Additional 5-10mg/kg
Maintenance 3-5mg/kg
Monitor vital signs, prevent hypotension, acid base balance
What is IVH?
-develops spontaneously, or due to trauma and asphyxia, often with preterm infants (IVH)
-can be assoc with fetal alloimmune thrombocytopenia, cerebral hemorrhage, or porencephalic cyst
What is the pathogenesis of IVH?
VLBW infants – IVH and PVL
IVH (preterms) – iccur in the gelatinous subependymal germinal matrix
Immature blood vessels plus poor tissue support
PVL – involves intrauterine and postnatal events
-hypoxia, venous obstruction from IVH, or undetected fetal stress may result in decreased perfusion to the brain, leading to periventricular hemorrhage and necrosis
-risk for PVL increases in infants with IVH or ventriculomegaly
what are the clinical manifestations of IVH?
IVH
-deterioration on 2nd or 3rd day of life
-hypotension, apnea, pallor or cyanosis, poor suck, abnormal eye signs, high pitched shrill cry, convulsions, decreased pmuscle tone,
-metabolic acidosis, shock
-decreased hematocrit or failure to rise after transfusion
Grading
Grade 1 – bleeding isolated to subependymal area
Grade 2 – bleeding within ventricle without ventricular dilatation
Grade 3 – IVH with ventricular dilatation
Grade 4 – IVH with Parenchymal hemorrhage
PVL
usually clinically asymptomatic until neuro sequelae of white matter damage become apparent in later infancy – as spastic motor deficits
may be present at birth but occurs later
Diagnosis of IVH
Preterms <32 weeks evaluated with routine cranial UTZ to check
Infants <1000gms highest risk, UTZ within 3-7th day of life
Ff up at 36-40 weeks AOG to check for PVL
MRI – more sensitive for evaluation of extensive periventricular injury, more predictive of long term outcome
What are the complications of IVH?
Post hemorrhagic hydrocephalus –
Hydrocephalus – 2-4 weeks after
Prognosis
neuro development (CP, mental devt index if <1000gm)
What is the management of IVH?
Antenatal steroids – 24-34 weeks at risk for preterm delivery -> decrease risk IVH
Post hemorrhagic hydrocephalus – ventriculoperitoneal shunt insertion
Symptomatic
Seizures – anticonvulsant drugs
Anemia and coagulopathy – PRBC or FFP
Insert VP shunt
Serial LP and ventricular taps – temporizing but not therapuetic
What is BPD?
-result of lung injury in infants requiring mech vent and supplemental O2
-interference with lung anatomic maturation
-alveolar collapse and volutrauma from mech vent 🡪 lung injury
-free radicals from O2, immaturity, infection, PDA, malnutrition 🡪 contribute to BOD
new BPD
-BW <1000 gms
-<28 weeks AOG
features in new BPD
alveolar hypoplasia
variable saccular wall fibrosis
minimal airway disease
occurrence indirectly proportional to gestational age
Vit A supplementation in VLBW infants reduces risk of BPD