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Asphyxia

Objectives: To define asphyxia and hypoxic ischemic encephalopathy and other related terms including the criteria To discuss the risk factors, causes and pathophysiology including affected organs To discuss the clinical manifestations and staging of HIE. To discuss diagnostics, treatment, and newer modalities.

Asphyxia
I. Definition of terms

A. - Asphyxia is also termed as Hypoxic-Ischemic Encephalopathy (HIE)

AAP and ACOG recommend using HIE because this term accurately describes the clinical condition, encephalopathy from asphyxia, without implying the time of brain injury

Asphyxia
I. Definition of terms

A. Hypoxic-Ischemic Encephalopathy - Condition of impaired blood gas exchange during the intrapartum period which may lead to progressive hypoxemia and hypercapnea with metabolic acidosis.
-This is an important cause of permanent damage to CNS tissues that may result to neonatal death or manifest later as developmental delay.

Asphyxia
I. Definition of terms B. Hypoxemia Refers to decreased arterial concentration of oxygen

C. Hypoxia Refers to decreased oxygenation to cells or organs. D. Ischemia Refer to blood flow to cells or organs that is insufficient to maintain normal function.

Asphyxia
Criteria
1. Evidence of metabolic acidosis (pH < 7.0 BE > 12mmol/L 2. Early onset of severe/moderate encephalopathy 3. Apgar 0-3 at 5 minutes of life 4. Multi organ involvement

Asphyxia
20-30% of HIE cases are in the neonatal period 33-50% of the survivors are left with permanent neurodevelopmental abnormalities (cerebral palsy, mental retardation). Greatest risk factors:
(ABG) pH of < 6.7 has 90% mortality and/or impairment (ABG) base deficit > 25 mmol/L has 72% mortality

Risk factors
Antepartum :
Maternal diabetes Pregnancy induced hypertension Chronic hypertension Previous Rh sensitization Previous stillbirth Bleeding in second or third trimester Maternal infection Polyhydramnios or oligohydramnios post-term gestation multiple gestation size-dates discrepancy maternal drug abuse maternal age >35 or<16 no prenatal care

Risk factors
Intrapartum :
Elective or emergency c/s Precipitous labour, prolonged labour Prolonged second stage of labour Premature labour Abnormal presentation Rupture of membranes > 24 hours Foul-smelling amniotic fluid Non reassuring fetal heart rate patterns Use of general anesthesia Prolapsed cord

Asphyxia
II. Causes and Pathophysiology The main cause of asphyxia is decreased in O2 supply resulting to hypoxia and ischemia. Fetal hypoxia may to caused by the following mothers conditions: a. Hypotension due to acute blood loss spinal anesthesia, or compression of veno cava b. Inadequate maternal oxygenations due to cyanotic heart disease, anesthesia, or respiratory failure.

Asphyxia
II. Causes and Pathophysiology c. inadequate relaxation of uterus to permit placental filling d. Premature separation of the placenta e. impedance to the circulation of blood through the umbilical cord f. placental insufficiency

Asphyxia
II. Causes and Pathophysiology Postnatal causes of hypoxia a. Failure of oxygenation as a result of severe cyanotic CHD or severe pulmonary disease b. Severe anemia c. Shock

Multiorgan Systemic Effects of Asphyxia

SYSTEM Central nervous system Cardiovascular Pulmonary Renal Adrenal Gastrointestinal Metabolic Integument Hematology

EFFECT Hypoxic- ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia, hypertonia Myocardial ischemia, poor contractility, cardiac stun, tricuspid insufficiency, hypotension Pulmonary hypertension, pulmonary hemorrhage respiratory distress syndrome Acute tubular or cortical necrosis Adrenal hemorrhage Perforation, ulceration with hemorrhage necrosis Inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia, hypocalcemia, myoglobinuria Subcutaneous fat necrosis Disseminated intravascular coagulation

Asphyxia
III. Clinical Manifestations Fetal period: 1. Fetal heart rate slows and beat to beat variability declines. 2. Deceleration pattern of fetal monitoring
A. Early B. Late C. Variable

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.)

Patterns of periodic fetal heart rate (FHR) deceleration

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.)

Patterns of periodic fetal heart rate (FHR) deceleration

B, Late deceleration caused by uteroplacental insufficiency

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

Asphyxia
III. Clinical Manifestations Post natal Period: 1. depressed and may fail to breath spontaneously 2. hypotonic or may change to hypertonic state (* may also remain normal) 3. Pallor, cyanosis, apnea, bradycardia

Asphyxia
III. Clinical Manifestations Post natal Period: 4. Brain edema may develop - seizure - any change in sensorial activity 5. Multi organ failure Ex. Acute tubular necrosis, necrotizing enterocolitis, myocardial infarction.

Topography of Brain Injury in terms infants with hypoxic ischemic encephalopathy and clinical correlates
Area of Injury
Selective neuronal necrosis

Location of Injury
Entire neuroaxis, deep cortical area, brainstem and pentocubicular

Clinical Correlate
Stupor or coma Seizures Hypotonia Oculomotor abnormalities Suck/swallow abnormalities

Long term sequelae


Cognitive delay Cerebral palsy Dystonia Seizure disorder Ataxia Bulbar and pseudobulbar palsy Spastic quadriparesis Cognitive delay Visual and auditory processing Difficulty Hemiparesis Seizures Cognitive delays

Parasagittal injury

Cortex and subcortical white matter Parasagittal regions, esp. posterior Cortex and subcortical white matter Vascular injury (usually MCA distribution) Injury to motor tracts, especially lower extremity

Proximal limb weakness Upper extremities affected greater than lower extremities

Focal ischemic necrosis

Unilateral findings Seizures common and typically focal

Periventricular injury

Bilateral and symmetric weakness in lower extremity More common in preterm infants

Spastic diplegia

Hypoxic-ischemic encephalopathy in term infants


Signs
Level of consciousness Muscle tone Posture Tendon reflexes/clonus Myoclonus Moro reflex Pupils Seizures

STAGE I
Hyperalent Normal Normal Hyperactive Present Strong Mydriasis None

STAGE II
Lethargic Hypotonic Flexion Hyperactive Present Weak Miosis Common

STAGE III
Stuporous, coma Flaccid Decerebrate Absent Absent Absent Unequal, poor light reflex Decerebration

Electroencephalographic

Normal

Low voltage changing to seizure activity


24 hr. to 14 days

Burst suppression to isoelectric


Days to weeks

Duration

<24 hr. if progresses; otherwise, may remain normal Good

Outcome

Variable

Death, severe deficits

Asphyxia
IV. Diagnosis
Cord arterial blood gas - to determine pH, pCO2, ACO3, and base excess/deficit Neuroimaging - CT scan or cranial ultrasound, usually used in late stage, evaluates cortical neuronal injury - MRI - preferred imaging at the early stage on injury because of its increased sensitivity/specificity early in the process and its ability to outline the topography of the lesion.

Asphyxia
IV. Diagnosis

Electroencephalogram (EEG) - provides information of the severity of asphyxial injury through electrocerebral activity.

Asphyxia
IV. Treatment
1. Immediate resuscitation 2. Maintenance of adequate ventilation - to maintain physiologic levels of pCO2 pCO2 intracerebral acidosis and impair cerebrovascular autoregulation pCO2 associated and preventricular leukomalacia (Preterm) and sensory hearing loss (Term)

Asphyxia
IV. Treatment

3. Maintenance of adequate oxygenation 4. Control seizures

Treatment
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.

Asphyxia
IV. Diagnosis and Treatment

Potential New Modality:


Hypothermia (33.5C)
- Cerebral cooling - whole body cooling - lowers the incidence of cortical neuronal injury

Asphyxia
Principle of Hypothermia as Treatment for HIE:
Hypothermia decrease rate of apoptosis and suppresses production of mediators: reducing glutamates, free radicals, lactates which can be neurotoxic.

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.

Prognosis
Severe encephalopathy characterized by :

1.Flaccid coma
2.Apnea 3.Absence oculocephalic reflexes 4. Refractory seizures

These are 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.

Prognosis
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.

Prognosis
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.

Thank you

Multiorgan Systemic Effects of Asphyxia

SYSTEM Central nervous system Cardiovascular Pulmonary Renal Adrenal Gastrointestinal Metabolic Integument Hematology

EFFECT Hypoxic- ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia, hypertonia Myocardial ischemia, poor contractility, cardiac stun, tricuspid insufficiency, hypotension Pulmonary hypertension, pulmonary hemorrhage respiratory distress syndrome Acute tubular or cortical necrosis Adrenal hemorrhage Perforation, ulceration with hemorrhage necrosis Inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia, hypocalcemia, myoglobinuria Subcutaneous fat necrosis Disseminated intravascular coagulation

Topography of Brain Injury in terms infants with hypoxic ischemic encephalopathy and clinical correlates
Area of Injury
Selective neuronal necrosis

Location of Injury
Entire neuroaxis, deep cortical area, brainstem and pentocubicular

Clinical Correlate
Stupor or coma Seizures Hypotonia Oculomotor abnormalities Suck/swallow abnormalities

Long term sequelae


Cognitive delay Cerebral palsy Dystonia Seizure disorder Ataxia Bulbar and pseudobulbar palsy Spastic quadriparesis Cognitive delay Visual and auditory processing Difficulty Hemiparesis Seizures Cognitive delays

Parasagittal injury

Cortex and subcortical white matter Parasagittal regions, esp. posterior Cortex and subcortical white matter Vascular injury (usually MCA distribution) Injury to motor tracts, especially lower extremity

Proximal limb weakness Upper extremities affected greater than lower extremities

Focal ischemic necrosis

Unilateral findings Seizures common and typically focal

Periventricular injury

Bilateral and symmetric weakness in lower extremity More common in preterm infants

Spastic diplegia

Hypoxic-ischemic encephalopathy in term infants


Signs
Level of consciousness Muscle tone Posture Tendon reflexes/clonus Myoclonus Moro reflex Pupils Seizures

STAGE I
Hyperalent Normal Normal Hyperactive Present Strong Mydriasis None

STAGE II
Lethargic Hypotonic Flexion Hyperactive Present Weak Miosis Common

STAGE III
Stuporous, coma Flaccid Decerebrate Absent Absent Absent Unequal, poor light reflex Decerebration

Electroencephalographic

Normal

Low voltage changing to seizure activity


24 hr. to 14 days

Burst suppression to isoelectric


Days to weeks

Duration

<24 hr. if progresses; otherwise, may remain normal Good

Outcome

Variable

Death, severe deficits

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