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Hypoxic Ischemic

Encephalopathy

Prof. Saad S Al-Ani


Senior Pediatric Consultant
Head of Pediatric Department
Khorfakkan Hospital . Sharjah
saadsalani@yahoo.com

Definitions

Anoxia
is a term used to indicate the consequences of complete lack of oxygen as a
result of a number of primary causes

Hypoxia
refers to an arterial concentration of oxygen that is less than normal

Ischemia
refers to blood flow to cells or organs that is insufficient to
maintain their normal function
Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic resonance
imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:461

05/26/2010

Khorfakkan Hospital Pediatric


Department

Hypoxic-ischemic encephalopathy
Is an important cause of permanent
damage to CNS cells that may result in
neonatal death or be manifested later
as cerebral palsy or mental deficiency
Nelson Textbook of Pediatrics 19th ed.2010 . pages 566 - 568

05/26/2010

Khorfakkan Hospital Pediatric


Department

Fifteen to 20% of infants with hypoxicischemic encephalopathy die in the neonatal


period

25-30% of survivors are left with permanent


neurodevelopmental abnormalities (cerebral
palsy, mental retardation).

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes after


newborn encephalopathy. Pediatrics 2002;109:26-33

05/26/2010

Khorfakkan Hospital Pediatric


Department

Effects of Asphyxia
System Effect

I. Central nervous system

II.Cardiovascular

1.Hypoxic-ischemic encephalopathy

1.Myocardial ischemia

2.Infarction

2. Poor contractility

3. Intracranial hemorrhage

3. Cardiac stun

4.Seizures

4. Tricuspid insufficiency

5. Cerebral edema

5. Hypotension

6. Hypotonia

7. Hypertonia
Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain
lesions in term infants with neonatal encephalopathy. Lancet 2003;361:73642.
05/26/2010

Khorfakkan Hospital Pediatric


Department

Effects of Asphyxia
System Effect (cont.)

V. Adrenal

III. Pulmonary
1. Pulmonary hypertension

Adrenal hemorrhage

2. Pulmonary hemorrhage
3. Respiratory distress syndrome

VI. Gastrointestinal
1. Perforation

IV. Renal
Acute tubular or cortical
necrosis

2. Ulceration with hemorrhage


3. Necrosis

Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain


lesions in term infants with neonatal encephalopathy. Lancet 2003;361:73642.
05/26/2010

Khorfakkan Hospital Pediatric


Department

Effects of Asphyxia
System Effect (cont.)

VII. Metabolic
1. Inappropriate secretion of antidiuretic hormone
2. Hyponatremia
3. Hypoglycemia
4. Hypocalcemia
5. Myoglobinuria

VIII. Integument
Subcutaneous fat necrosis

IX. Hematology
Disseminated intravascular coagulation
Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain
lesions in term infants with neonatal encephalopathy. Lancet 2003;361:73642.

05/26/2010

Khorfakkan Hospital Pediatric


Department

Asphyxia
is considered in infants with:
1.

Fetal acidosis (pH <7.0)

2.

A 5-min Apgar score of 0-3

3.

Hypoxic-ischemic encephalopathy:
i. Altered tone
ii. Depressed level of consciousness
iii. Seizures

And
4. Other multiorgan system signs
Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of
infants treated with head cooling and mild hypothermia after perinatal
asphyxia. Pediatrics 2001;107:480

05/26/2010

Khorfakkan Hospital Pediatric


Department

Causes Of Fetal Hypoxia


(1)Inadequate oxygenation of maternal blood
as a result of:

I. Hypoventilation during anesthesia


II. Cyanotic heart disease
III. Respiratory failure
IV. Carbon monoxide poisoning

(2) low maternal blood pressure


as a result of the hypotension that may:
I. Complicate spinal anesthesia
II. Result from compression of the vena cava and aorta by the gravid
uterus
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Khorfakkan Hospital Pediatric


Department

Causes Of Fetal Hypoxia (cont.)

(3) Inadequate relaxation of the uterus


to permit placental filling as a result of uterine tetany caused by the
administration of excessive oxytocin

(4) Premature separation of the placenta

Johnson MV: MRI for neonatal encephalopathy in full-term


infants. Lancet 2003;361:713-4
05/26/2010

Khorfakkan Hospital Pediatric


Department

10

Causes Of Fetal Hypoxia (cont.)

(5) Impedance to the circulation of blood


through the umbilical cord as a result of compression or knotting of
the cord

(6) Uterine vessel vasoconstriction by cocaine


(7) placental insufficiency

from numerous causes

including toxemia and postmaturity.

Johnson MV: MRI for neonatal encephalopathy in full-term


infants. Lancet 2003;361:713-4
05/26/2010

Khorfakkan Hospital Pediatric


Department

11

Fetal hypoxia

Abnormal Doppler velocimetry.


On an umbilical artery Doppler flow velocity waveform
The umbilical placental impedance is so high that the diastolic component
shows flow in a reverse direction. This finding is an indication of severe
intrauterine hypoxia and intrauterine growth restriction .
Nelson Textbook of Pediatrics (on 20 November 2003) 2003 Elsevier

05/26/2010

Khorfakkan Hospital Pediatric


Department

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Causes of after birth hypoxia

(1)Anemia severe enough to lower the oxygen content of the blood to


a critical level, as after severe hemorrhage or hemolytic disease

(2) Shock severe enough to interfere with the transport of oxygen to vital
organs as a result of
i. Overwhelming infection
ii. Massive blood loss
iii. Intracranial or adrenal hemorrhage

05/26/2010

Crowley P: Prophylactic corticosteroids for preterm birth. Cochrane


Database Syst Rev 2002;Issue 1. De Felice C, Toti P, Laurini RN, et al:
Early neonatal
brain Pediatric
injury in histologic chorioamnionitis. J Pediatr
Khorfakkan
Hospital
2001;138:101
Department
13

Causes of after birth hypoxia (cont.)


(3) Deficit in arterial oxygen saturation
from failure to breathe adequately postnatally because of
i. Cerebral defect
ii. Narcosis
iii. Injury

(4) Failure of oxygenation of an adequate amount of


blood as a result of severe forms of cyanotic congenital heart disease or
pulmonary disease

Crowley P: Prophylactic corticosteroids for preterm birth. Cochrane


Database Syst Rev 2002;Issue 1. De Felice C, Toti P, Laurini RN, et al:
Early neonatal brain injury in histologic chorioamnionitis. J Pediatr
2001;138:101
Khorfakkan Hospital Pediatric
05/26/2010

Department

14

Pathophysiology
Within minutes of the onset of total fetal hypoxia:
1.Bradycardia
2. Hypotension
3. decreased cardiac output
4. severe metabolic as well as respiratory acidosis occur

The initial circulatory response of the fetus


* is increased shunting through the ductus venosus, ductus
arteriosus, and foramen ovale

* with transient maintenance of perfusion of the brain, heart, and


adrenals in preference to the lungs (because of pulmonary
vasoconstriction), liver, kidneys, and intestine.
05/26/2010

Khorfakkan Hospital Pediatric


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Patterns of periodic fetal heart rate (FHR)


deceleration

A shows early deceleration occurring during the peak of uterine


contractions as a result of pressure on the fetal head

. Hon EH: An Atlas of Fetal Heart Rate Patterns. New Haven,


CT, Harty Press, 1968.)

05/26/2010

Khorfakkan Hospital Pediatric


Department

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Patterns of periodic fetal heart rate (FHR)


deceleration (cont.)

B, Late deceleration caused by uteroplacental insufficiency

. Hon EH: An Atlas of Fetal Heart Rate Patterns. New Haven,


CT, Harty Press, 1968.)

05/26/2010

Khorfakkan Hospital Pediatric


Department

17

Patterns of periodic fetal heart rate (FHR)


deceleration (cont.)

C, Variable deceleration as a result of umbilical cord compression

. Hon EH: An Atlas of Fetal Heart Rate Patterns. New Haven,


CT, Harty Press, 1968.)

05/26/2010

Khorfakkan Hospital Pediatric


Department

18

Clinical Manifestations
Hypoxic-Ischemic Encephalopathy in Term Infants
Signs:

Stage 1

Stage 2

Stage 3

Stuporous

coma

Hypotonic

Flaccid

Flexion

Decerebrate

I. Level of consciousness
Hyperalert , Lethargic

II. Muscle tone


Normal
III. Posture

Normal

05/26/2010

Biagioni E, Mercuri E, Rutherford M, et al: Combined use of


electroencephalogram and magnetic resonance imaging in full-term
neonates with acute encephalopathy. Pediatrics 2001;107:461
Khorfakkan Hospital Pediatric
Department
19

Clinical Manifestations
Hypoxic-Ischemic Encephalopathy in Term Infants
(cont.)

Signs:

Stage 1

Stage 2

Stage 3

Hyperactive

Absent

IV. Tendon reflexes


Clonus ,Hyperactive

V. Myoclonus
Present

Present

Absent

Weak

Absent

VI. Moro reflex

Strong

05/26/2010

Biagioni E, Mercuri E, Rutherford M, et al: Combined use of


electroencephalogram and magnetic resonance imaging in full-term
neonates with acute encephalopathy. Pediatrics 2001;107:461
Khorfakkan Hospital Pediatric
Department
20

Clinical Manifestations
Hypoxic-Ischemic Encephalopathy in Term Infants
(cont.)

Signs:

Stage 1

Stage 2

Stage 3

Mydriasis

Miosis Unequal

Poor light reflex

VII. Pupils

VIII. Seizures
None

Common

Decerebration

IX. Electroencephalographic

Normal

Low voltage changing


to seizure activity

05/26/2010

Burst suppression
to isoelectric

Biagioni E, Mercuri E, Rutherford M, et al: Combined use of


electroencephalogram and magnetic resonance imaging in full-term
Khorfakkan
Pediatric
neonatesHospital
with acute
encephalopathy. Pediatrics 2001;107:461
Department
21

Clinical Manifestations
Hypoxic-Ischemic Encephalopathy in Term Infants
(cont.)

Signs:

Stage 1

Stage 2

Stage 3

X. Duration
<24 hr

if progresses; otherwise,

Days to weeks

may remain normal24 hr to 14 days


XI. Outcome
Good

Variable

Death, severe deficits

Biagioni E, Mercuri E, Rutherford M, et al: Combined use of


electroencephalogram and magnetic resonance imaging in full-term
neonates with acute encephalopathy. Pediatrics 2001;107:461

05/26/2010

Khorfakkan Hospital Pediatric


Department

22

Treatment
Therapy is supportive and directed at the organ system manifestations

Careful attention to:

Ventilatory status and adequate oxygenation

Blood volume,

Hemodynamic status
Acid-base balance
Possible infection
is important

05/26/2010

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental


outcomes after newborn encephalopathy. Pediatrics
2002;109:26-33.
Khorfakkan Hospital Pediatric
Department
23

Treatment

(cont.)

No established effective treatment is available for the brain tissue injury,


although many drugs (phenobarbital, allopurinol, calcium channel blockers)
and procedures (total body or local cranial hypothermia) are under study

Aggressive treatment of seizures is critical and may necessitate


continuous electroencephalographic monitoring.

05/26/2010

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental


outcomes after newborn encephalopathy. Pediatrics
2002;109:26-33.
Khorfakkan Hospital Pediatric
Department
24

Treatment

(cont.)

Seizure activity may be severe and refractory to the usual doses of


anticonvulsants
Phenobarbital, the drug of choice, is given with an intravenous loading
dose (20 mg/kg); additional doses of 10 mg/kg (up to 40-50 mg/kg total)
may be needed.
Phenobarbital levels should be monitored 24 hr after the loading dose
and maintenance therapy (5 mg/kg/24 hr) are begun
Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may
be needed for refractory seizures.
Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental
outcomes after newborn encephalopathy. Pediatrics
2002;109:26-33.
Khorfakkan Hospital Pediatric
05/26/2010

Department

25

Prognosis
The outcome of hypoxic-ischemic encephalopathy ranges from complete
recovery to death

The prognosis depending on :


1.Whether the metabolic and cardiopulmonary complications
(hypoxia, hypoglycemia, shock) can be treated
2. Infant's gestational age
(outcome is poorest if the infant is preterm)
3. Severity of the encephalopathy
Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants
treated with head cooling and mild hypothermia after perinatal asphyxia.
Pediatrics 2001;107:480.

05/26/2010

Khorfakkan Hospital Pediatric


Department

26

Prognosis (Cont.)
Severe encephalopathy characterized by :
1.Flaccid coma
2.Apnea
3.Absence oculocephalic reflexes
4. Refractory seizures
Is associated with a poor prognosis

Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants


treated with head cooling and mild hypothermia after perinatal asphyxia.
Pediatrics 2001;107:480.

05/26/2010

Khorfakkan Hospital Pediatric


Department

27

Prognosis (Cont.)
1. A low Apgar score at 20 min
2. Absence of spontaneous respirations at 20 min of age
3. Persistence of abnormal neurologic signs at 2 wk of age
predict death or severe cognitive and motor deficits

Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants


treated with head cooling and mild hypothermia after perinatal asphyxia.
Pediatrics 2001;107:480.

05/26/2010

Khorfakkan Hospital Pediatric


Department

28

Prognosis (Cont.)

Brain death
after neonatal hypoxic-ischemic encephalopathy is diagnosed by:
1. Clinical findings of coma unresponsive to pain, auditory, or visual stimulation
2. Apnea with Pco2 rising from 40 to over 60 mm Hg
3. Absent brainstem reflexes

(pupil, oculocephalic, oculovestibular, corneal, gag, sucking)

Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants


treated with head cooling and mild hypothermia after perinatal asphyxia.
Pediatrics 2001;107:480.

05/26/2010

Khorfakkan Hospital Pediatric


Department

29

Thank you

05/26/2010

Khorfakkan Hospital Pediatric


Department

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