Preterm Infants and Complications Flashcards
Improving outcomes in Preterm Infants
If under 32 weeks: delivery at perinatal center and MgSO4 for neuroprotection
If under 34 weeks: antenatal corticosteroids
Delayed cord clamping
Thermoregulation
pathophysiology of acute respiratory distress syndrome
Path: surfactant deficiency results in non-compliant and stiff lungs: cannot expand, resulting in a bronchiectatic lung and ventilation-perfusion mismatch.
Presentation: increased work of breathing, cyanosis, instability, onset shortly after birth, ground glass appearance on CXR
Natural History: worsens 2-3 days → diuresis → improvement
management of acute RDS
Management: antenatal steroids to increase the development of type II pneumocytes to increase surfactant
ABC, Oxygen
Support airway with CPAP/intubation
Surfactant.
Complications: penumothorax
outline the defintion and blood flow of a patent ductus arteriosus
Definition: arteria to pulmonary vessels: not all the blood goes to the body. Some of the blood from the aorta goes through the ductus arteriosus and into the pulmonary veins (lower pressure), so not all the blood goes to the body– the aortic blood goes to the pulmonary system.
When the ductus arteriosus stays open, blood goes in the opposite direction than it does in the fetus: from the aorta to the lungs. This extra blood, along with the normal flow of blood from the heart to the lungs, can cause a build-up of blood in the baby’s lungs. If the PDA is large, this extra blood flow is too much for the baby to handle and makes it harder for him or her to breathe. Because PDA increases the amount of work for the heart, the baby can have heart failure.
PDA:
Clinical Presentation: ___-like murmur, ___ pulses, ___ pulse pressure, increased precordial activity, tachycardia, feeding intolerance, ventilator dependence, ___ congestions, increased work of breathing.–> can lead to ____ dysplasia
Clinical Presentation: machine-like murmur, bounding pulses, wide pulse pressure, increased precordial activity, tachycardia, feeding intolerance, ventilator dependence, pulmonary congestions, increased work of breathing.–> can lead to bronchopulmonary dysplasia
Treatment: NSAIDS, surgical ligation, catheter device
treatment of PDA
NSAIDS, surgical ligation, catheter device
outline the three presentations types of intraventricular hemorrhage
Presentation:
Silent
Saltatory: apnea, bradycardia, hypotonia
Catastrophe deterioration: met acidosis, hypotension, bulging fontanelle, sudden drop in hematocrit, posturing, seizures
prevention of IVH
- antenatal steroids
- cardiovascular stability
- minimal handling, midline head position,
Co2 targets
no hyperteonic solutions
supportive therapy for IVH
correct the metabolic acidosis
- blood transfusion
correction of coagulopathies
- monitor for hydrocephalus
Most common cause of cerebral palsy in chidlren surviving a preterm birth
Intraventricular hemorrhage!
Natural History/sequelae: the higher grade, the worse the outcome.
Post haemorrhagic ventricular dilation can lead to hydrocephalus
Long- term motor and mental disabilities
Most severe and frequent cause of cerebral palsy and NDI in children surviving preterm birth
NEC:
Presentation: gastric residuals, distention, abdominal wall discoloration, vomiting, blood in stool, worsening of apneas, temperature instability
key XR finding of necrotizing enterocolitis?
AXR: air in liver (pneumatosis is hallmark of nec), dilated bowel loops.
Staging: via Bell’s Staging Criteria
management for NEC
Management: EBM, GDM, early colostrum and slowly increase the milk they are receiving, possible use for probiotics.
NPO, gastric decompression
Antibiotics
Surgery
Complications: short bowel surgery, poor growth, cholestasis, NDI
key bugs responsible for early onset sepsis
microbiology: E.Coli, GBC, listeria.
treat: ampicillin
key bugs for late onset sepsis
LOS is hospital acquired after 72 horus of life
- microbiology is coagulase negative staph
