hypoxic-ischemic encephalopathy Flashcards

1
Q

What s HI/ perinatal asphyxia

A

characterized by clinical and laboratory evidence of acute or subacute brain injury due to asphyxia caused by systemic hypoxia or reduced cerebral blood flow

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2
Q

How does HIE occur (PP)

A

1) Systemic hypoxia d/2 a primary insult causing PRIMARY ENERGY FAILURE
- -insuff o2 to mitochondria in the subependyman germinal matrix d/2 immaturity and high E demands=> insuff ATP=> ion imbalances=> Na+ influx for AP’s =>Intracellur calcium accum=> toxic build up NT’s (glutamate) => NECROTIC cell death

2)REPERFUSION & TRANSIENT RECOVERY
causes the following compensatory mechanisms
-redistribution of cardiac output to essential organs, brain, heart, and adrenal glands.
-A blood pressure (BP) increase due to increased release of epinephrine further enhances the increased CO

2) persistent hypoxia => reduced BF // loss of compensation// overshoot of compensatory increased Cerebral blood flow causes loss of cerebral auto regulation & CBF decreases =>ISCHEMIC BRAIN INJURY causing SECONDARY ENERGY FAILURE
- brain hypoxemia and acidosis
- caspase cascade occurs=>APOPTOTIC cell death
- oxidative injury
- inflammation

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3
Q

What is cerebral autoregulation

A

CBF is maintained at a constant level despite a wide range in systemic BP. This phenomenon is known as the cerebral autoregulation, which helps maintain cerebral perfusion

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4
Q

BP range at which CBF is maintained in Adults:

A

is 60-100 mm Hg.

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5
Q

BP range at which CBF is maintained in

A

between 10-20 mm Hg

Narrower range so HIE is more likely as CBF is easily disrupted

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6
Q

Types of clinical CNS presentation of Achile

A

Mild hypoxic-ischemic encephalopathy

Mod severe hypoxic-ischemic encephalopathy

SEVERE hypoxic-ischemic encephalopathy

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7
Q

Clinical presentation of Mild hypoxic-ischemic encephalopathy

A

Muscle tone slightly increased

deep tendon reflexes brisk in the first few days

Transient behavioral abnormalities, such as poor
feeding, irritability, or excessive crying or sleepiness

Typically resolves in 24h

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8
Q

Clinical presentation of Moderately severe hypoxic-ischemic encephalopathy

A

The infant is lethargic,
significant hypotonia and diminished deep tendon reflexes

The grasping, Moro, and sucking reflexes may be sluggish or absent

occasional periods of apnea

Seizures occur early within the first 24 hours after birth

Full recovery within 1-2 weeks is possible

associated with a better long-term outcome than the others

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9
Q

Clinical presentation of Severe hypoxic-ischemic encephalopathy

A

Seizures:
severe // initially resistant to conventional treatments.
generalized,
increased frequency during the 24-48 hours after onset.

Stupor or coma.

Breathing may be irregular. // Apnea

Generalized hypotonia and depressed deep tendon reflexes are common.

Neonatal reflexes (eg, sucking, swallowing, grasping, Moro).

Disturbances of the eyes:
skewed eyes, nystagmus, bobbing, and loss of conjugate gaze
Pupils may be dilated, fixed, or poorly reactive to light
.
Irregularities of heart rate and blood pressure are common.

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10
Q

lab Dg

A

Serum electrolyte levels

Renal & liver function studiesd/2 MODS

Cardiac and liver enzymes - Assess the degree of hypoxic-ischemic injury to the heart and liver

Coagulation system - Includes prothrombin time, partial thromboplastin time, and fibrinogen levels

Arterial blood gas - Blood gas monitoring is used to assess acid-base status and to avoid hyperoxia and hypoxia, as well as hypercapnia and hypocapnia

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11
Q

Imaging for dg of HIE

A

MRI of the brain- check for
Cranial ultrasonography- for interventricular hemorrhages
Echocardiography- reduced CO worsens/causes HIE

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12
Q

Addition confirmatory dgstics

A

Electroencephalography (EEG)- to monitor assyx seizures!
Hearing test – There is an increased incidence of deafness
Retinal and ophthalmic examination

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13
Q

How is HIE MANAGED

A

Adequate ventilation

Perfusion and blood pressure management w/ Inotropic agents
- mean blood pressure (BP) above 35-40 mm Hg to avoid decreased cerebral perfusion

Careful fluid management

Avoidance of hypoglycemia and hyperglycemia

Avoidance of hyperthermia

Treatment of seizures:
Anticonvulsants, Anxiolytics, Benzodiazepines

Therapeutic hypothermia (33º-33.5ºC for 72h) followed by slow and controlled rewarming for infants with moderate to severe HIE
-EEG 48 hrs after rewarming to check for seizures
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14
Q

Inotropic Agent’s

A

Dopamine

Dobutamine

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15
Q

Anticonvulsant

A

Phenobarbitals

Phenytoin

Lorazepam

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16
Q

criteria for HIE

A

Early onset encephalopathy

MODS

Metabolic acidosis w/ cord pH below 7

17
Q

when is HIE most common

A

PRETERM births especcially those that require —resuscitations & are cyanotic
-low apgar scors

18
Q

complications

A
neonatal seizures- no1 cause
cerebral palsy
MODS
hearing deficits
interventricular hemorrhages
19
Q

what are caspases

A

Caspases (cysteine-aspartic proteases, cysteine aspartases or cysteine-dependent aspartate-directed proteases) are a family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation.