hypoxicischemicencephalopathy-100526095658-phpapp02.ppt

8/10/2019 hypoxicischemicencephalopathy-100526095658-phpapp02.ppt

1/30

Hypoxic Ischemic

Encephalopathy

Prof. Saad S Al-AniSenior Pediatric Consultant

Head of Pediatric DepartmentKhorfakkan Hospital . Sharjah

[email protected]


2/30

05/26/2010Khorfakkan Hospital Pediatric

Department 2

Ischemia

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

Definitions

Anoxia

is a term used to indicate the consequences of complete lack of oxygen as aresult 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. Pediatrics2001;107:461


3/30

05/26/2010Khorfakkan Hospital Pediatric

Department 3

Hypoxic-ischemic encephalopathy

Is an important cause of permanent

damage to CNS cells that may result inneonatal death or be manifested lateras cerebral palsy or mental deficiency

Nelson Textbook of Pediatrics 19thed.2010 . pages 566 - 568


4/30

05/26/2010 Khorfakkan Hospital PediatricDepartment 4

25-30%of survivors are left with permanentneurodevelopmental abnormalities (cerebralpalsy, mental retardation).

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes afternewborn encephalopathy. Pediatrics2002;109:26-33

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


5/30


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 contractility3. Cardiac stun

4. Tricuspid insufficiency

5. Hypotension

Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brainlesions in term infants with neonatal encephalopathy. Lancet 2003;361:736-

42.


6/30


Effects of Asphyxia

System Effect (cont.)

III. Pulmonary

1. Pulmonary hypertension

2. Pulmonary hemorrhage3. Respiratory distress syndrome

IV. Renal

Acute tubular or corticalnecrosis

V. Adrenal

Adrenal hemorrhage

VI. Gastrointestinal

1. Perforation

2. Ulceration with hemorrhage3. Necrosis


42.


7/30


Effects of Asphyxia

System Effect (cont.)

VII. Metabolic

1. Inappropriate secretion of antidiuretic hormone

2. Hyponatremia3. Hypoglycemia

4. Hypocalcemia

5. Myoglobinuria

VIII. Integument

Subcutaneous fat necrosis

IX. HematologyDisseminated intravascular coagulation


42.


8/30


Asphyxia

is considered in infants with:1. Fetal acidosis (pH


9/30


Causes Of Fetal Hypoxia

(1)Inadequate oxygenation of maternal bloodas a result of:

I. Hypoventilation during anesthesia

II. Cyanotic heart disease

III. Respiratory failureIV. 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


10/30


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 uterusto permit placental filling as a result of uterine tetany caused by the

administration of excessive oxytocin


11/30


Causes Of Fetal Hypoxia(cont.)

(6) Uterine vessel vasoconstrictionby cocaine

(7) placental insufficiency from numerous causesincluding 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


12/30


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 componentshows flow in a reverse direction. This finding is an indication of severe

intrauterine hypoxia and intrauterine growth restriction.


13/30


Causes of after birth hypoxia

(1)Anemiasevere enough to lower the oxygen content of the blood to

a critical level, as after severe hemorrhage or hemolytic disease

(2) Shocksevere 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

Crowley P: Prophylactic corticosteroids for preterm birth. CochraneDatabase Syst Rev2002;Issue 1. De Felice C, Toti P, Laurini RN, et al:

Early neonatal brain injury in histologic chorioamnionitis. J Pediatr2001;138:101


14/30


15/30


The initial circulatory responseof 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


16/30


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

Patterns of periodic fetal heart rate (FHR)deceleration

Ashows early deceleration occurring during the peak of uterinecontractions as a result of pressure on the fetal head


17/30



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

B, Late deceleration caused by uteroplacental insufficiency


18/30



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

C, Variable deceleration as a result of umbilical cord compression


19/30


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. PostureNormal Flexion Decerebrate

Biagioni E, Mercuri E, Rutherford M, et al: Combined use ofelectroencephalogram and magnetic resonance imaging in full-term

neonates with acute encephalopathy. Pediatrics2001;107:461


20/30

05/26/2010

Khorfakkan Hospital Pediatric

Department 20


Hypoxic-Ischemic Encephalopathy in Term Infants(cont.)


IV. Tendonreflexes

Clonus ,Hyperactive Hyperactive Absent

V. Myoclonus

Present Present Absent

VI. Moro reflexStrong Weak Absent




21/30

05/26/2010


Department 21




VII. Pupils

Mydriasis Miosis Unequal Poor light reflex

VIII. Seizures

None Common Decerebration

IX. ElectroencephalographicNormal Low voltage changing Burst suppression

to seizure activity to isoelectric




22/30

05/26/2010


Department 22




X. Duration


23/30

05/26/2010


Department 23

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 infectionis important

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmentaloutcomes after newborn encephalopathy. Pediatrics

2002;109:26-33.


24/30


25/30

05/26/2010


Department 25

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

Treatment (cont.)

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

Phenobarbital, the drug of choice, is given with an intravenous loadingdose (20 mg/kg); additional doses of 10 mg/kg (up to 40-50 mg/kg total)

may be needed.

Phenobarbital levelsshould be monitored 24 hr after the loading doseand maintenance therapy (5 mg/kg/24 hr) are begun

Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmentaloutcomes after newborn encephalopathy. Pediatrics

2002;109:26-33.


26/30

05/26/2010


Department 26

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 infantstreated with head cooling and mild hypothermia after perinatal asphyxia.

Pediatrics2001;107:480.


27/30

05/26/2010


Department 27

Severe encephalopathycharacterized by :

1.Flaccid coma

2.Apnea

3.Absence oculocephalic reflexes

4. Refractory seizures

Is associated with a poor prognosis

Prognosis (Cont.)




28/30

05/26/2010


Department 28

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.)




29/30

05/26/2010


Department 29

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.)




30/30

05/26/2010


Department 30

Thank you

Documents

hypoxicischemicencephalopathy-100526095658-phpapp02.ppt