hypoxic ischemic encephalopathy

Hypoxic Ischemic Hypoxic Ischemic EncephalopathyEncephalopathy

Prof. Saad S Al-AniProf. Saad S Al-AniSenior Pediatric ConsultantSenior Pediatric Consultant

Head of Pediatric DepartmentHead of Pediatric DepartmentKhorfakkan Hospital . SharjahKhorfakkan Hospital . Sharjah

[email protected]@yahoo.com

05/26/201005/26/2010 Khorfakkan Hospital Pediatric DKhorfakkan Hospital Pediatric Departmentepartment

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Ischemia refers to blood flow to cells or organs that is insufficient to maintain their normal function

DefinitionsAnoxia

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

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


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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


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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

Fifteen to 20% of infants with hypoxic-ischemic encephalopathy die in the neonatal period


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Effects of Asphyxia

System Effect

I. Central nervous system

1.Hypoxic-ischemic encephalopathy

2.Infarction

3. Intracranial hemorrhage

4.Seizures

5. Cerebral edema

6. Hypotonia

7. Hypertonia

II.Cardiovascular

1.Myocardial ischemia

2. Poor contractility

3. Cardiac stun

4. Tricuspid insufficiency

5. Hypotension

Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet

2003;361:736-42.


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Effects of Asphyxia

System Effect (cont.)

III. Pulmonary

1. Pulmonary hypertension

2. Pulmonary hemorrhage

3. Respiratory distress syndrome

IV. Renal

Acute tubular or cortical necrosis

V. Adrenal

Adrenal hemorrhage

VI. Gastrointestinal

1. Perforation

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;361:736-42.


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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;361:736-42.


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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


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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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Causes Of Fetal Hypoxia (cont.)

(4) Premature separation of the placenta

Johnson MV: MRI for neonatal encephalopathy in full-

term infants. Lancet 2003;361:713-4

(3) Inadequate relaxation of the uterus to permit placental filling as a result of uterine tetany caused

by the administration of excessive oxytocin


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Causes Of Fetal Hypoxia (cont.)

(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

(5) Impedance to the circulation of blood

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

the cord


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Fetal hypoxia

Nelson Textbook of Pediatrics (on 20 November 2003) 2003

Elsevier

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 .


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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 hemorrhageCrowley 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


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Causes of after birth hypoxia (cont.)

(4) Failure of oxygenation of an adequate amount of blood as a result of severe forms of cyanotic congenital heart disease or pulmonary disease

(3) Deficit in arterial oxygen saturation

from failure to breathe adequately postnatally because of

i. Cerebral defect

ii. Narcosis

iii. Injury

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


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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.

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


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. Hon EH: An Atlas of Fetal Heart Rate Patterns. New Haven, CT, Harty Press, 1968.)

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


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Patterns of periodic fetal heart rate (FHR) deceleration (cont.)

B, Late deceleration caused by uteroplacental insufficiency


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Patterns of periodic fetal heart rate (FHR) deceleration (cont.)

C, Variable deceleration as a result of umbilical cord compression


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Clinical Manifestations

Hypoxic-Ischemic Encephalopathy in Term Infants Signs: Stage 1 Stage 2

Stage 3

I. Level of consciousness

Hyperalert , Lethargic Stuporous coma

II. Muscle tone

Normal Hypotonic Flaccid

III. Posture

Normal Flexion Decerebrate

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


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Hypoxic-Ischemic Encephalopathy in Term Infants (cont.) Signs: Stage 1 Stage 2 Stage 3

IV. Tendon reflexes

Clonus ,Hyperactive Hyperactive Absent

V. Myoclonus

Present Present Absent

VI. Moro reflex

Strong Weak Absent




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VII. Pupils

Mydriasis Miosis Unequal Poor light reflex

VIII. Seizures

None Common Decerebration

IX. Electroencephalographic

Normal Low voltage changing Burst suppression

to seizure activity to isoelectric




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X. Duration

<24 hr if progresses; otherwise, Days to weeks

may remain normal24 hr to 14 daysXI. Outcome

Good Variable Death, severe deficits




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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 importantDixon G, Badawi N, Kurinczuk JJ, et al: Early

developmental outcomes after newborn

encephalopathy. Pediatrics 2002;109:26-33.


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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.

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



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Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for refractory seizures.

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

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



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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.


2727

Severe encephalopathy characterized by : 1.Flaccid coma 2.Apnea

3.Absence oculocephalic reflexes

4. Refractory seizures

Is associated with a poor prognosis

Prognosis (Cont.)




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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

Prognosis (Cont.)




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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)

Prognosis (Cont.)




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