Preterm baby Flashcards

1
Q

What are four problems that pre-term babies have

A
  • get cold faster
  • fragile lungs
  • breathe ineffectively
  • fewer reserves

-pulse oximetry is often indicated and many preterm babies need help with transition to air breathing

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2
Q

What is different about cord clamping in pre-term babies?

A
  • if baby = ok and can be kept warm

- pause for at least 1 min to allow placental transfusion to take place

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3
Q

How are pre-term babies kept warm?

A

-place immediately, while still wet, in a suitable plastic bag and then later under a radiant heater

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4
Q

What does mechanical ventilation in pre-term babies predispose to? what is seen on CXR?

A

-lungs are fragile and this pre-disposes to bronchopulmonary dysplasia AKA chronic lung disease of prematurity
=oxygen dependence at 36 weeks gestation as the working definition for BPD.

The most common clinical scenario is of a 23- to 26-weeks of gestation baby who over a period of 4-10 weeks progresses from needing ventilation to CPAP through to requiring supplemental oxygen. They commonly have initial RDS and needed ventilation/CPAP.

CXR:
CXR changes with development of diffuse haziness and coarse interstitial pattern which reflects atelectasis, inflammation and/or pulmonary oedema. Areas of gas trapping may alternate with areas of atelectasis.

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5
Q

Why is thermal regulation ineffective in babies?

A
  • low BMR
  • minimal muscular activity
  • high ratio s/a to body mass
  • negligable subcut fat insulation
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6
Q

what methods are used to increase body temperature of babies?

A
  • wraps/bags
  • transwarmer mattress
  • skin to skin care
  • pre-warmed incubator
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7
Q

What is gestatational correction?

A

40 - gestational age baby = x weeks premature

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8
Q

What is the difference in organisms that cause:

  • early onset sepsis
  • Late onset sepsis
A
early onset (EOS)
mainly due to bacteria acquired before and during delivery
late onset (LOS)
	acquired after delivery 
	(nosocomial or community sources
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9
Q

What organisms typically cause neonatal sepsis?

A

ν Group B streptococcus (GBS)

ν Gram negative organisms
♦ Klebsiella, Escherichia coli, Pseudomonas, and Salmonella

ν Gram positive organisms
♦ Staphylococcus aureus, Coagulase negative staphylococci (CONS), Streptococcus pneumoniae, Streptococcus pyogenes

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10
Q

What is included in the prevention of neonatal sepsis?

A
ν	Prevention
ν	Hand washing
ν	Super vigilant and infection screening
ν	Judicial use of Antibiotics 
ν	Optimum supportive measures
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11
Q

What is the cause and clinical features of RDS?

A
  • Grunting
  • Tachypnoea
  • Intercostal recessions
  • Nasal flaring
  • Cyanosis

Cause: surfactant deficiency

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12
Q

What is the management of RDS?

A

ν Maternal steroid
ν Surfactant
ν Ventilation
o Invasive / non invasive ventilation

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13
Q

What is a patent ductus arteriosis? what condition does this exacerbate?

A

ν Premature infants at risk
ν Duct does not respond to “close” signals
ν Leads to symptoms of congestive heart failure
ν Oxygen requirements are high
ν Exacerbates RDS

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14
Q

What type of intracranial haemorrhage can preterm infants get?

A

Interventricular haemorrhage:
ν a form of intracranial haemorrhage that occurs in preterm infants, which begins with bleeding into the germinal matrix.
ν 80% of cases the GMH leads to an intraventricular bleed.

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15
Q

What are the 2 major risk factors for intraventricular haemorrhage in preterm infants?

A

Inverse relationship between the incidence and gestational age at birth

There are 2 major risk factors:
Prematurity – GM is still present and cerebral autoregulation is immature
Respiratory distress syndrome – hypoxia, acidosis and hypotension makes it more likely to have an unstable cerebral circulation

Most occurs in the first day of life,
up to 90% of neonates who will get GMH-IVH, the insult is present by 72 hours.

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16
Q

How is intraventricular haemorrhage in the pre-term baby prevented?

A
♦	antenatal steroids 
♦	prompt and appropriate resuscitation 
♦	avoid hemodynamic instability 
♦	avoid 
ν	hypoxia, 
ν	hypercarbia, 
ν	hyperoxia, and 
hypocarbia
17
Q

Necrotising entererocolitis:

  • is this common?
  • what is this?
  • where is the highest incidence?
A

ν Most common neonatal surgical emergency
ν Widespread necrosis in the small and large intestine
ν High incidence in the most premature infants

18
Q

What is the clinical picture for necrotising enterocolitis?

A
  • usually after recovering from RDS
  • early signs: lethargy and gastric residuals
  • Bloody stool, temperature instability, apnoea and bradycardia