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Neo Pathophys 2 > Asphyxia/HIE > Flashcards

Asphyxia/HIE Flashcards

1
Q

T/F: there are many reasons for encephalopathy

A

True

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2
Q

In HIE, encephalopathy is caused by either a lack of _______ or oxygen delivery to the brain.

A

Perfusion

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3
Q

Encephalopathy is a clinical syndrome w/abnormal _____ function as manifested by: (4 things)

A 
CNS function:
Abnormal LOC
Seizures
Tone
Reflexes
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4
Q

HIE is abnormal neurologic behavior following _____ _____ or ischemia.

A

perinatal hypoxia

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5
Q

What are the 2 ways the brain is deprived of oxygen?

A

Hypoxia: diminished O2 to the brain
Ischemia: diminished amount of blood perfusing the brain

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6
Q

What 3 types of insults should alert you to possible HIE and which group is the most susceptible?

A
  1. Maternal
  2. Utero-Placental (most susceptible)
  3. Fetal
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7
Q

During what periods do most HIE events occur? What is the %.

A

Antepartum and Intrapartum periods just before or during delivery
Accounts for 35% of HIE

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8
Q

HIE incidence in the developed world =

A

1-2 per 1000 live term births

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9
Q

Is HIE higher/lower in the developing world?

A

Higher

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10
Q

HIE is the most _______ cause of neurologic dz in the neonatal period.

A

common

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11
Q

HIE can result in what disorders?

6 things

A
  1. Hearing loss
  2. Learning disability
  3. Mild motor dysfunction
  4. CP
  5. Severe motor dysfunction
  6. Death
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12
Q

The hypoxic event is followed by what?

A

Reperfusion injury

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13
Q

What are the 2 phases of injury/damage to the brain?

What phase is in between?

A

Early/primary: cerebral hypoxia (no oxygen/no blood to brain)
Late/Secondary: Reperfusion injury

Latency phase: our opportunity betwen 6-15 hours to intervene to try to avoid Secondary/reperfusion injury

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14
Q

Which phase is characterized by failure to create ATP as a result of decreased blood flow to the brain?

A

Primary/early phase

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15
Q

During the early phase, cells are _______ –>lots of necrosis of brain tissue itself.

A

exploding

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16
Q

When there are low ATP levels, there is ______ in cell integrity and ____ pumps and mechanisms to maintain low intracellular ____.

A

breakdown
Na/K
Ca++

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17
Q

When _______ pumps fail–>delpolarizes cell membranes—>____________ release—>binds to _____ receptors—>____ influx into cell—>cerebral edema, ischemia, microvascular damange w/resultant necrosis

A

Na/K
Glutamate release
NMDA
Ca++

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18
Q

T/F: there is normal cerebral metabolism during the Latency phase.

A

True

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19
Q

Secondary phase is characterized by (4 things)

A
  1. Ongoing energy failure (supply can not meet demand)
  2. Excitotoxicity injury (glutamate-excitatory AA–ok in regulated amts)
  3. Cytokine injury
  4. Oxidative stress
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20
Q

_______ is the primary type of cell death in the secondary phase.

A

Apoptosis

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21
Q

T/F: In the secondary phase during excitotoxicity injury, Glutamate binds w/NMDA receptor which worsens Ca++ influx into cells.

A

True

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22
Q

Ca++ influx–> inflammatory process in the ______.

A

brain

23
Q

Free radicals are formed in the breakdown of the ____ ________.

A

cell membranes

24
Q

What are free radicals?

A

Molecules w/unpaired electrons–they initiate reactions that cause cell damage

25
Q

T/F: Free radicals can cause breakdown of the BBB?

A

True

26
Q

T/F: Free radicals can affect blood cells including platelets so clotting doesn’t work as well. WBC’s accumulate in the brain instead of circulating the site of injury.

A

True

27
Q

What 3 things do free radicals do?

A
  1. Leakage of BBB
  2. Change platelet function
  3. Neutrophil accumulation
28
Q

WHat 3 proinflammatory cytokines are activated and have nuerotoxic properties?

A

TNF Alpha
IL1B
IL8

29
Q

What is Apoptosis?
When does it occur?
Characterized by?

A

Programmed cell death
Following the injury days-weeks
Cell shrinking, preservation of cell membrane, death w/o inflammation

30
Q

T/F: when in development HIE occurs matters

A

True

31
Q

In term infants with HIE, the _______ (functional cells of the brain) and gray nuclei are most vulnerable.

A

Neurons

32
Q

In preterm infants with HIE, the ___________ are vulnerable to hypoxic injury –> white matter dz–>____.

A

Oligodendrocytes

PVL

33
Q

If you have HIE at < 20 wks, you can have what?

A

Abnormal migration of brain tissue

34
Q

If you have HIE at 26-36 wks GA, you will have what?

A

PVL

35
Q

If you have HIE >36 wks, you will have what?

A

Deep gray matter/watershed areas injured

36
Q

What area of the brain has the most tenuous blood supply?

A

Watershed areas—needs the most optimal blood flow to be perfused

37
Q

The _____ ______ along with ____ _____ controls motor

A

Basal ganglia

Motor Cortex

38
Q

Communication run via the ______________

A

Thalamus

39
Q

There is a ____ hr window for initiating hypothermia.

A

6

40
Q

Cooling tx of HIE works to: 4 things

A
  1. decrease tissue metabolic demand
  2. Decrease calcium influx into neuronal cells
  3. Reduce free radicals
  4. Attenuates pro-inflammatory cascade
41
Q

You can see what VS change in a baby with increasingly severe HIE

A

Bradycardia

42
Q

What is important to assess in a baby w/HIE?

A

Primitive reflexes (they are preserved even in the presence of severe injury)

43
Q

The optimal Rectal/core temp during cooling=?

A

33-34 degrees C

44
Q

What is the minimum age for cooling?

A

36 wks GA

45
Q

How do you decide who to cool?

A
  • > 36 wks
  • APGAR <5 at 10 min
  • Continued need for resuscitation: ETT/PPV at 10 min
  • Acidosis (pH <7, Base def >16 w/in 60 min birth)
  • Mod-severe HIE w/altered LOC (lethargy/stupor/coma) AND 1 of: Hypotonia, abnormal reflexes, weak/absent suck, clinical seizures
  • EEG for 20 min shows abnormal background or seizures
46
Q

What are contraindications to cooling? 6 things

A
  • <36 wks GA
  • > 6 hrs life
  • coagulopathy w/ACTIVE bleeding
  • Prenatal dx of syndrome/do not compatible w/life
  • head trauma/ICH
  • BW <1800 gms
47
Q

What labs to obtain pre-cooling:

A
  • ABG and cord gas
  • BMP (follow lytes and renal fxn)
  • Troponin (heart)
  • AST/ALT (liver)
  • PT/PTT (coags)
  • CBC
  • Ammonia (r/o underlying metabolic dz)
48
Q

What is very common and a Hallmark of HIE?

A

End organ dysfunction

-up to 70% have renal impairment

49
Q

What imaging would you want pre-cooling

A
  1. HUS (critical to r/o big bleed 1st)

2. CXR

50
Q

What would you want during cooling?

A

EEG to monitor for subclinical seizures (entire 72 hrs so you can tx if needed)
Neurology consult
Medication metabolism (may be altered)
Hyperglycemia
QT prolongation (w/bradycardia, check this out)
Coagulation abnormalities

51
Q

How fast do you re-warm?

A

0.5 degrees/hr

52
Q

Why do you want slow vs. fast re-warm?

A

Fast is not good for cellular functioning

53
Q

What imaging do you want 1 wk after cooling?

A

MRI

Neo Pathophys 2 (20 decks)

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