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C2 Modules CLINICAL > Neonatal hypoxia Ischemia > Flashcards

Neonatal hypoxia Ischemia Flashcards

1
Q

What is Neonatal hypoxia ischaemia?

A

most common cause of death and disability in human neonates, and is often associated with persistent motor, sensory, and cognitive impairment

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2
Q

What causes hypoxic ischemic brain injury?

A
  1. Maternal factors
  2. Cord factors
  3. Placemtal factors
  4. Uterine factors
  5. Neonatal postnatal events such as shock, respiratory or cardiac arrest
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3
Q

What are factors which influence damage?

A
  1. Etiology
  2. Degree and duration of hypoxia ischaemia
  3. Maturational stage of brain
  4. Regional changes in cerebral blood flow
  5. General health of the infant prior to injury
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4
Q

What is Neonatal encephalopathy (NE)?

A

Descriptive term for clinical constellation of neurological dysfunction

  1. Difficulty with initiating and maintaining respiration
  2. Depression of tone and reflexes
  3. Subnormal level of consciousness
  4. Seizures
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5
Q

What is a specific terminology related to hypoxic ischemic injury?

A

Hypoxic Ischemic Encephalopathy (HIE)

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6
Q

What is Neonatal encephalopathy?

A
  1. Major cause of global mortality
  2. 4 million children die each year - 1/4th from HI injury
  3. 85% in SE asia & SS Africa
  4. One of the highest numbers of DALY’s
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7
Q

What is the incidence of neonatal encephalopathy?

A

15-20/1000 (SS Africa)
1-3/1000 in high income countries

1/4th from HI injury

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8
Q

What is the outcome following perinatal HI at term?

A
  1. 10-15% of affected infants die in the first few days [studies come from developed countries]
  2. 15% of survivors develop cerebral palsy [motor problems, one or both side weakness]
  3. 40% of survivors, other significant problems:
    - Deafness
    - Blindness
    - Epilepsy
    - Global developmental delay [cognitive problems]
    - Autism
    - Problems with cognition, memory and fine motor skills
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9
Q

Mortality in children < 5 years

[WHO]

A
  1. 2.6 million deaths, ~46% of all < 5 deaths, occurred during neonatal period
  2. ~7000 newborn death everyday
  3. Majority of neonatal deaths are on first day [relative to HI]
  4. ~1 million die on first day
    other 1 million die within the next 6 days
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10
Q

What does mitochondria help to produce?

A

NADH
Which goes into the ETC
produce energy in the form of ATP

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11
Q

What can MRS help to identify?

A

The concentration of different chemicals in the brain

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12
Q

Phosphorus Magnetic Resonance spectroscopy (neonatal - preclinical work)

A

Direct information about the energy

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13
Q

Proton magnetic resonance

A

Direct information about the brain lactate

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14
Q

Broadband NIRS

A

Information about what is happening in the ETC

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15
Q

What are some examples of metabolites of the 1H MRS?

A
  1. Choline
  2. Creatine
  3. NAA
  4. Lactate
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16
Q

Choline

A

Cell membrane

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17
Q

Creatine

A

Energetics

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18
Q

NAA

A

Marker of neuronal/axonal density and viability

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19
Q

Lactate

A

Marker of failed oxidative phosphorylation

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20
Q

What can be used for biomarker?

A
  1. NAA

2. Lactate

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21
Q

What are the phases of brain injury following HI?

A
  1. Primary phase (mins)
  2. Latent phase (hours)
  3. Secondary phase (days)
  4. Testing phase (weeks, years)
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22
Q

What is primary phase?

A

Cerebral hypoxia

Ischemia of sufficient severity to deplete tissue energy reserves

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23
Q

What is the latent phase?

A

Repurfusion and re-oxygenation + restoration of glucose use and high energy phosphates

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24
Q

What is secondary phase?

A

Decrease in high energy phosphate in parallel with cell injury

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25
Q

What is testing phase?

A

Long term cell regeneration and repair

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26
Q

What are the key milestone leading to Therapeutic Hypothermia as routine therapy

A
  1. Piglet model
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27
Q

What is the piglet model

A
  1. Hypothermia ameliorates brain energy decline on MRS
  2. 1997 - Gunn colleagues show that 75% hypothermia is safe and effective in reducing cytotoxic oedema
  3. 2005 - cooling reduces mortality without increasing disability in survivors of perinatal hypoxia ischaemia
  4. 2012- NICE- therapeutic hypothermia become standard treatment of moderate to severe neonatal encephalopathy
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28
Q

What are the effect of cooling on conventional brain MRI?

A

Cooled infants more likely to have normal scans

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29
Q

What did cooling reduce the incidence of lesions in?

A
  1. Basal Ganglia
  2. White matter
  3. Abnormal posterior limb of internal capsule
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30
Q

What is insult severity associated with?

A

Shortening of the subsequent latent-phase, worse secondary energy failure and more severe cortical damage

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31
Q

How do we assess injury?

A
  1. alpha EEG/EEG
  2. CRUSS
  3. MRI/1H MRS

Future modalities

  1. Broadband NIRS
  2. 31P MRS
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32
Q

What is alpha EEG/EEG?

A

The most promising test: amplitude integrated electroencephalography sensitivity and specifity

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33
Q

What does cooling alter?

A

Predictive value of alpha EEG

34
Q

What is the most quantitiative MR biomarker for predicting neurodevelopmental outcome after NE?

A

Deep grey matter Lac/NAA

-Lac/NAA < 0.3 indicates good outcome

35
Q

Near Infrared Spectroscopy

A

Information regarding cerebral heamodynamics and oxygenation

36
Q

What did Barkovich and others describe for injury on conventional MRI?

A
  1. Watershed (white matter loss at the boundaries of territories of 3 major cerebral arteries)
  2. Basal Ganglia and thalamic lesions
  3. Total cortical loss
37
Q

What is the sudden profound hypoxia ischaemia?

A
  1. placenta separates from uterine wall
  2. Blood pressure falls
  3. Decrease in oxygenated blood supply to fetus via umbilical cord
  4. Blood oxygenation concentration falls
38
Q

What is the cool aid trial?

A

Large, multicentre trial, international trial

- glucose control is not optimal , chance of injury increases

39
Q

What happens if the baby has no facility to get cooling treatment?

A

The baby has to be stabilised

and picked up by transport team

40
Q

Time to start treatment from the incidence

A

Important factor for the outcome

41
Q

What is intrapartum?

A

What happens around the time of the birth

42
Q

What is the risk determined by?

A

Where you are born

43
Q

How many births are in the high income group?

A

11 million births

They have full intensive care

44
Q

How many births are in the middle income group?

A

34 million births

There are some unit intensive care and some degree of support

45
Q

What does low income have?

A

Facility birth

40m

46
Q

In what group are there more home birth?

A

Low income group

highest: 50 million birth

47
Q

What do the survivors have?

A

Significant neurodevelopmental disability

Significant burden to family and society and country

48
Q

What happened in 1 in 4 deaths?

A

Problems with adequate staffing and resources

49
Q

What do we need to produce energy?

A

Glucose

50
Q

What is the process of cerebral metabolism?

A
  1. Glucose goes through the glycolysis
  2. If oxygen present, pyruvate goes to Acetyl-coA and goes into Kreb’s cycle and produces NADH and a little of FADH which is transferred to ETC which produces ATP
  3. In the absence of oxygen, lactate is produced and little bit of energy
51
Q

How can you monitor the brain?

A
  1. proton magnetic resonance sprectoscopy
  2. Electron transport chain - there are 4 different complexes from lungs - when electron flows through cytochrome oxidase - there is a chain of reaction -broadband near spectroscopy
52
Q

How can you confirm the energy state of the brain?

A

phosphorus magnetic resonance spectroscopy and identify it

- Gives background and main understanding of pathogenic mechanism of this condition

53
Q

What does PCr tell you?

A

The energy of the brain

54
Q

What is lactate by NA?

A

The most sensitive and specific biomarker used clinically

55
Q

What happens in severe injury?

A

Latent phase is small

Goes to secondary energy failure

56
Q

What does cooling treatment help?

A

Can prevent secondary energy failure

Biggest culprit which causes brain damage

57
Q

What is cooling?

A

Neurprotective therapy

58
Q

Therapeutic hypothermia in clinical practice

A
  1. Connect baby to several controlled machine
  2. Temperature on the machine: 33.5
  3. Bring the temperature by 3.5 points
    37-3.5=33.5
  4. Maintain that over 72 hours
  5. Gradually warm it over 14 hours
  6. Take baby to MRI to see the extent of damage
59
Q

What responds to cooling treatment?

A

moderate-to-severe encephalopathy

60
Q

How can you prevent 1 death of disability?

A

NNT 6 babies=moderate encephalopathy

NNT 7 babes = severe

61
Q

How many adults need to take a statin to prevent 1 cardiac arrest?

A

Around 8-100

62
Q

Why is deep grey matter important?

A

Area of highest metabolic rate in the brain

63
Q

Why is the temperature 33.5 hours and why is the temperature 72?

A

look at brain structures after deeper cooling and see what happens without cooling = pretty much the same

it has the best outcome

64
Q

What is the standard assessment for injury?

A
  1. electrical lead on the head and monitor with EEG
65
Q

What is alpha EEG/EEG?

A

Semi-logarithmic compressed version of EEG
small period - see larger duration of the study and quickly identify if there is a problem
- very sensitive and specific before the start of the cooling

66
Q

What is normal for aEEG?

A

Amplitude integrated EEG

Thinning and thickening of the amplitude integrated bands

67
Q

What does lactate nA have?

A

100% sensitivity

about 97% specifity to predict motor outcome

68
Q

What are the biomarkers after therapeutic hypothermia following HI?

A
  1. Motor outcome
  2. Cognitive outcome
  3. Language outcome
69
Q

What is near infrared spectroscopy?

A

Information regarding cerebral haemodynamics and oxygenation

70
Q

Watershed injury

A

White matter looks bright

71
Q

What is the watershed predominant pattern?

A
  1. Parasagittal

2. Borderzone

72
Q

What are the watershed predominant pattern characterstics

A

Lesion of the cerebral cortex and subcortical white matter with a characteristic distribution over the superomedial aspects of the cerebral convexities

Necrosis of the cortex and the immediately adjacent white matter, affecting mainly parieto-occipital regions

73
Q

What are acute total hypoxia ischaemia?

A

Basal Ganglia and Thalamus uterine rupture, cord prolapse, placental abruption
Infants usually require major resuscitation
Apgar score < 5 at 5 mins
Associated with Cerebral Palsy
preserved intelligence if focal
quadriplegic CP if widespread

74
Q

What is partial prolonged asphyxia

A

WatershedInfants usually do not require major resuscitation at birth
Apgar scores > 5 at 5 mins
Extensive white matter involvement predicts cognitive deficits

75
Q

What are the therapeutic agent

Adjunct therapy with cooling?

A
  1. Noble gasses
  2. Xenon
  3. Argon
  4. Melatonin
  5. Remote ischaemic post conditioning
  6. Stem cell therapies
  7. Epo
  8. Allopurinol (Albino studies)
76
Q

Noble gases

A

One clinical trial completed

Pre-clinical studies completed

77
Q

Melatonin

A

New formulation

Pre-clinical studies – promising result

78
Q

Remote ischaemic post conditioning

A

Pre-clinical studies completed

Further studies with cooling/therapeutic wind

79
Q

Stem cell therapies

A

Pre-clinical studies and clinical trials

80
Q

EPO

A

Phase 1 study

Phase 2 study starting in the US

81
Q

Allopurinol (albino study)

A

Horizon 2020 study. 14 European centres 2016-2020

C2 Modules CLINICAL (26 decks)

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