Wk 5: Respiratory distress and neonatal sepsis Flashcards

1
Q

What are some signs of respiratory distress and wha are they signaling?

A

Tachypnoea- a compensatory reaction to hypoxia

Chest wall restraction, grunting, poor air entry-> due to lung mechanics

Central cyanosis- L) to R) cardiopulmonary shunting

Peripheral cyanosis beyond 24hrs of life-> poor tissue oxygenation due to acidosis, heart failure, shock or hypothermia

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2
Q

How is grunting created?

A

caused by the neonate partially closing their epiglottis at the end of each breath in order to maintain positive pressure in their lungs. It’s essentially the neonate trying to maintain his own functional residual capacity (FRC).

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3
Q

What are some differential diagnoses of resp distress in newborn?

A
  • Mec aspiration syndrome
  • Respiratory distress syndrome
  • Neonatal pneumonia
  • Transient tachynea of the newborn
  • Persistent pulmonary hypertehsion of the newborn
  • Pneumotherax
  • Congenital heart disease
  • Congenital diaphragmatic hernia
  • Pulmonary congenital defects
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4
Q

What is transient tachypnea of the new born?

A

= tachypnoea as a result of pulmonary odema due to excess fluid in the lungs that wasn’t cleared at birth.
aka wet lung

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5
Q

What are some risk factors for TTN?

A
  • Infants <39wks
  • Infants born via c/s without labour
  • Male infants
  • Infants born to mother with GDM
  • excessive fluid administration to mother during labour
  • precip
  • second twin
  • LGA or SGA
  • cord prolapse
  • DM
  • asthma (maternal)
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6
Q

What are some symptoms of TTN?

A
  • tachypnea= >60 breaths/min
  • Nasal flaring
  • Grunting
  • Retractions
  • Clear lung fields or crackles
  • cyanosis
  • Cyanosis which resolves with O2 administration of <40%
  • Barrel chest in some neonates (symetrical hyperinflation)
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7
Q

How does TTN resolve?

A
  • usually its self over time
  • usually resolves in 24- 48 hours of age, though for some neonates up to 72 hours of age.
  • if resolves in 2-6 hours may be considered ‘delayed transition’
  • As symptoms are due to slow absorption of lung fluid
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8
Q

Define neonatal pneumonia

A

= transfer of infection from mother though infected amniotic fluid that the baby practice breaths with or transplacenta though the blood.

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9
Q

What are some risk factors for neonatal pneumonia?

A
  • prem
  • maternal chorioamnionitis
  • ROM >18hrs
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10
Q

What can cause neonatal pneumonia?

A

GBS
Herpies simplex virus
Kelebsiella
E. coli

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11
Q

What are some symptoms of neonatal pneumonia?

A
  • Respiratory distress
  • Poor feeding
  • Apnea
  • Tachycardia
  • Poor perfusion
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12
Q

What are some key points of late onset pneumonia?

A

Often hospital acquired

Major risk factors: receipt of respiratory support

Chlampdia which as long incubation person and causes infection around 4 wks

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13
Q

Define respiratory distress syndrome

A

= deficiency of pulmonary surfactant in the immature lung
*surfactant production commences in labour

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14
Q

What is a risk factor for RDS?

A
  • <37 weeks
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15
Q

What are some symptoms of RDS?

A
  • Tachypnea >60
  • Nasal flaring
  • Grunting-> create positive pressure so alveoli stay open
  • Retractions
  • Cyanosis
  • General increased WOB
  • Apnoea
  • Cyanosis
  • Increased oxygen requirements of >60% to maintain target Sp02 is not uncommon and therefore transfer to tertiary neonatal unit is common
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16
Q

What is the management of RDS?

A
  • can be reduced with pre birth maternal corticosteroids
  • can be given surfactant via NGT
  • manage thermoregulation
  • oxygenation
    enteral feed should be avoided with infants with RDA requirements >35%
  • FBC and cultures
  • IM antibiotics in these circumstances
  • minimal handelig
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17
Q

Define meconium aspiration syndrome (MAS)

A

=clinical diagnosis when a neonate has birthed through meconium stained liquor and has respiratory distress, appearances on chest x-ray of MAS and no other diagnosis for respiratory distress.

  • Release of cytokines and proinflammatory factors
  • Obstruction of air ways
  • Distal gas trapping
  • Alveoli rupture
  • Deactivation and decreased synthesis of surfactant
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18
Q

What are some symptoms of MAS?

A
  • Tachynea
  • Retractions
  • Grunting
  • Nasal flaring
  • Cyanosis
    *develop immediately after birth
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19
Q

Explain some of the key pathological points of RDS

A
  • Surfactant is produced and stored by the epithelial lining of the alveoli from approximately 22 weeks gestation
  • it reduces alveoli tension and keeps them open.
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20
Q

What may exacerbate RDS?

A
  • sepsis (most common)
  • Cold stress
  • Hypoxia
  • Acidosis
  • Disease causing secondary surfactant deficiencies e.g. meconium aspiration syndrome, pneumonia, infant of diabetic mother
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21
Q

Explain the pathophysiology of MAS

A

How mec is released
- In utero hypoxia and acidosis can cause a vagal response leading to increased peristalsis and a relaxed anal sphincter resulting in meconium passage.
- Intra-uterine distress (at any time in gestation) may initiate gasping in utero -> may result in amniotic fluid and particulate matter to be inhaled into the large airways.

When a mec particle is aspirated
1. physical obstruction of airway-> Chemical pneumonitis-> surfactant dysfunction and inflammation-> further leads to parenchymal disease
2. Mec causes a ball valve effect in airways resulting in complete obstruction-> collapse or atelecatasis or over expansion due to trapping and air leak.
3. Air leaks from being trapped in alveoli and into plural space-> Pneumomediastinum.
4. Pneumonitis: inflammation of lungs
5. Inactivation of surfactant-> stoped it from working
6. Infection potential-> provides potential for infection breeding

Mec is potential activator of inflammatory mediators which not only leads to lung dysfunction (pneumonitis) but also causes systemic inflammatory response.

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22
Q

What are the complictions of MAS?

A
  • the initial reason the baby was stressed
  • resp distress or hypoxia
  • PPH
  • infection
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23
Q

What are some risk factors for MAS?

A
  • post dates (Due to or in the presence of placental insufficiency syndrome= stress and the older placenta cant meet the needs of the older baby)
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24
Q

What is the risk of MAS?

A

3-12% of the neonates born with meconium stained liquor will develop Meconium Aspiration Syndrome

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25
Q

What are some clinical presentations of MAS?

A
  • Early onset of respiratory distress, often within 2 hours in a meconium stained neonate.
  • Tachypnoea
  • Cyanosis
  • Grunting with nasal flaring
  • Retraction with a hyper inflated chest (barrel shaped chest)
  • Course breath sound/’wet inspiratory crackles on auscultation
  • Occasionally expiratory noises suggesting a ‘ball-valve’ airway obstruction
  • Swings in O2 saturations due to intra/extra pulmonary shunting (see diagram below)
  • Poor perfusion due to impaired cardiac function often due to right-left shunting at the ductus arteriosis and foramen ovale, a ECG is attended to exclude cyanotic heart disease
26
Q

What is the management of MEC?

A
  • oxygen therapy w/ target sats of 91-95%
  • nasal CPAP
  • IPPV
  • surfactant therapy
  • suctioning (no longer reccomended however may be needed later in resus)
  • NGT and evacuate stomach contents
  • IV therapy
  • fluid restriction
27
Q

Define persistent pulmonary hypertension that occcurs due to MEC

A
  • the neonate fails to transition from fetal ot normal newborn circulation.
    = acidosis contributes to PPHN resulting in right to left shunting of blood causing severe hypoxemia.
  • Hypoxemia contributes to ventricular dysfunction and complicates PPHN.
28
Q

What are some key points of management when caring for a neonate on O2 therapy?

A
  • check and document O2 every 2-3 hours, at hand over, hourly if on CPAP or ventilated
  • resite O2 sat every 4-6 hours.
29
Q

Why are neonates at an increased risk of sepsis?

A
  • immature system
30
Q

Define neonatal sepsis

A

= a syndrome of clinical signs associated with sepsis, with or without positive blood cultures.

31
Q

What are some risk factors for neonatal sepsis?

A
  • LBW
  • prem
  • known congenital abnormalities/medical conditions
  • babies of socially disadvantaged families
32
Q

What are some maternal related risk factors for neonatal sepsis?

A
  • PROM >18 hours
  • prolonged labour >24hrs
  • multiple VEs
  • chorio
  • Mec stained liquor
33
Q

What are some neonatal related risk factors for neonatal sepsis?

A
  • prem
  • LBW
  • need for resus
  • need for CPAP
  • need for IV
  • arterial lines
  • BBA
34
Q

What are some clinical manifestations of neonatal sepsis?

A
  • Requires positive pressure ventilation resuscitation at birth
  • apnoea
  • poor skin perfusion
  • abnormal feeding behaviour e.g. not interested in feeding for 8 hours after birth or the last feed
35
Q

What is the management for sepsis?

A
  • commence antis asap
36
Q

How do we diagnose neonatal sepsis?

A
  • Positive blood culture (the gold standard)
  • Isolation of pathogen without presence of infection
  • Inability to identify pathogen does not rule out infection
  • Lumbar puncture (LP) should be performed where there is high susicipion of meingitis e.g. altered conscious state, sezuires
    *if blood cultures can not be attained, antibitoics should not be delayed.
37
Q

What are some causes of neonatal sepsis?

A
  • GBS
  • E coli
  • Listeria
38
Q

Define early onset sepsis

A

= within the first 48hrs.

39
Q

What are some causes of early onset sepsis?

A
  • transplacental or vertical transmission of organisms primarily from the mother’s birth canal acquired during the intrapartum period.
  • Occasional transmission may occur via the blood stream e.g. Listeria
  • Over 80% of early onset sepsis in the neonate is due to Group B Streptococcus (GBS) and Gram negative bacteria
40
Q

what are some risk factors for early onset sepsis?

A
  • PROM >18hrs
  • fetal distress
  • maternal pyrexia >38c
  • multiple obstetric procedures
  • pre term birth
  • history of GBS
41
Q

What are some clinical manifestations of early onset sepsis?

A
  • pneumonia
  • high or low temp
42
Q

Define late onset sepsis

A
  • onset after 48hours
  • infection is acquired either around or at the time of birth or in hospital
42
Q

What is vertical and horizontal transmission of sepsis?

A

Vertical transmission- colonise and cause infection later on.

Horizontal transmission/Hospital acquired (nosocomial)- infection from environment/care givers e.g. IV cannula, SCN/NICU environment

43
Q

What are some risk factors of late onset spesis?

A

Prolonged hospitalisation e.g. preterm neonate in SCN/NICU

Presence of cannula/tubing insitu e.g. IV cannula, Endotracheal tubes

Cross infection from staff/parents

Congenital malformations e.g. urinary tract anomalies, neural tube defects.

44
Q

What are the perinatal viris’?

A

T- Toxomplasmosis gondaii (protozoan parasite)
o- other
R- Rubella
C- Cytomegalovirus
H- Herpes Simplex Virus
E- Enterovirus
S- Syphilis (Treponema pallidium - spirochaete)
C-Chickenpox (VZV - Varicella Zoster virus)
L- Lyme disease
A- AIDS
P- Parovirus B19 (fifth disease, “slapped cheek” or erythema infectiosum)

45
Q

What are some clinical manifestations of perinatal infection?

A
  • SGA
  • myocarditis, CDH
  • Pneumonititis
  • Hepatosplenomegaly, conjugated jaundice
  • Haemolytic anaemia
  • Petechiae, purpura
  • Microcephaly, hydrocephaly, meningoencephalitis, intracranial calcifications
  • chorioretinitis, glaucoma, cataracts, keratoconjunctivitis
46
Q

What is the managemt of perinatal infections?

A
  • careful observation
  • ?sepsis and monitor for it
47
Q

What is CMV?

A

= a viral disease resulting from the common Herpes Virus family.
- passed from mother to baby

48
Q

What are risk factors for CMV?

A
  • most people will be exposed during their life.
49
Q

What are clinical manifestations of CMV?

A
  • flu like symptoms (hence why must go unknown)
  • in the neonate mostly it is silent.
50
Q

How is CMV transmitted?

A

saliva
urine
nasal mucous
tears
blood
breastmilk
vaginal secretions
Semen

51
Q

What is primary CMV

A
  • This is a 1st time contact, infection and development of CMV disease
  • Once you have CMV you are infected for life however most of the time CMV lays dormant/inactive
  • CMV infection may result in up to 30% ris of transmission to the fetus.
52
Q

What is non primary CMV

A

This is a situation where the dormant/inactive CMV reactivates OR the person has been re-infected with a new strain of CMV to the primary CMV infection.

53
Q

What are some complications of CMV?

A

Disability
Hearing loss
Vision loss
Cerebral palsy
Developmental delay
Learning problems
Epilepsi
Death *in rare cases

54
Q

Who do we screen CMV for?

A
  • not everyone
  • thocse abnormal fetal ulrasound findings
  • IUGR
  • microcpephaly
55
Q

How can CMV be prevented?

A
  • good hygiene, hand washing, not sharing food utensils
  • a conversation to promote awareness
56
Q

How does GBS manifest?

A
  • resp symptoms
  • speticaemia
  • shock with or without meningitis
57
Q

Who is at risk of GBS? and gets antibitoics?

A
  • women with GBS colonised
  • ATSI
  • preterm
  • PROM >18hrs
  • maternal fever
  • previous baby of GBS
  • GBS in pregnancy
58
Q

What is the does of BENZYLPENICILLIN?

A

60mg/kg/dose IV 12 hourly
120mg/kg/dose 12 hourly if suspected meningitis

59
Q

What is the does of gentamicine for sepsis?

A

5mg/kg/dose IV or IM *organisational

60
Q

What is the management of giving antibitoics

A

Separate administration by 1 hour of each drug

OR if not possible

Ensure IV lines suitably flushed with 0.9% Sodium Chloride before and after administration of each antibiotic