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Neo Pathophys 2 > Asphyxia/HIE > Flashcards

Asphyxia/HIE Flashcards

(53 cards)

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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 ______.

23
Q

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

Study These Flashcards
A

cell membranes

24
Q

What are free radicals?

Study These Flashcards
A

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

25
T/F: Free radicals can cause breakdown of the BBB?
True
26
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.
True
27
What 3 things do free radicals do?
1. Leakage of BBB 2. Change platelet function 3. Neutrophil accumulation
28
WHat 3 proinflammatory cytokines are activated and have nuerotoxic properties?
TNF Alpha IL1B IL8
29
What is Apoptosis? When does it occur? Characterized by?
Programmed cell death Following the injury days-weeks Cell shrinking, preservation of cell membrane, death w/o inflammation
30
T/F: when in development HIE occurs matters
True
31
In term infants with HIE, the _______ (functional cells of the brain) and gray nuclei are most vulnerable.
Neurons
32
In preterm infants with HIE, the ___________ are vulnerable to hypoxic injury --> white matter dz-->____.
Oligodendrocytes | PVL
33
If you have HIE at < 20 wks, you can have what?
Abnormal migration of brain tissue
34
If you have HIE at 26-36 wks GA, you will have what?
PVL
35
If you have HIE >36 wks, you will have what?
Deep gray matter/watershed areas injured
36
What area of the brain has the most tenuous blood supply?
Watershed areas---needs the most optimal blood flow to be perfused
37
The _____ ______ along with ____ _____ controls motor
Basal ganglia | Motor Cortex
38
Communication run via the ______________
Thalamus
39
There is a ____ hr window for initiating hypothermia.
6
40
Cooling tx of HIE works to: 4 things
1. decrease tissue metabolic demand 2. Decrease calcium influx into neuronal cells 3. Reduce free radicals 4. Attenuates pro-inflammatory cascade
41
You can see what VS change in a baby with increasingly severe HIE
Bradycardia
42
What is important to assess in a baby w/HIE?
Primitive reflexes (they are preserved even in the presence of severe injury)
43
The optimal Rectal/core temp during cooling=?
33-34 degrees C
44
What is the minimum age for cooling?
36 wks GA
45
How do you decide who to cool?
- >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
What are contraindications to cooling? 6 things
- <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
What labs to obtain pre-cooling:
- 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
What is very common and a Hallmark of HIE?
End organ dysfunction | -up to 70% have renal impairment
49
What imaging would you want pre-cooling
1. HUS (critical to r/o big bleed 1st) | 2. CXR
50
What would you want during cooling?
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
How fast do you re-warm?
0.5 degrees/hr
52
Why do you want slow vs. fast re-warm?
Fast is not good for cellular functioning
53
What imaging do you want 1 wk after cooling?
MRI

Neo Pathophys 2 (20 decks)

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