Asphyxia

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


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


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 post-term gestation

Pregnancy induced hypertension multiple gestation

Chronic hypertension size-dates discrepancy

Previous Rh sensitization maternal drug abuse

Previous stillbirth maternal age >35 or<16

Bleeding in second or third trimester no prenatal care

Maternal infection

Polyhydramnios or oligohydramnios

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


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


• 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 EFFECT

Central nervous system Hypoxic- ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia, hypertonia

Cardiovascular Myocardial ischemia, poor contractility, cardiac stun, tricuspid insufficiency, hypotension

Pulmonary Pulmonary hypertension, pulmonary hemorrhage respiratory distress syndrome

Renal Acute tubular or cortical necrosis

Adrenal Adrenal hemorrhage

Gastrointestinal Perforation, ulceration with hemorrhage necrosis

Metabolic Inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia, hypocalcemia, myoglobinuria

Integument Subcutaneous fat necrosis

Hematology 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

. 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



C, Variable deceleration as a result of umbilical cord compression



B, Late deceleration caused by uteroplacental insufficiency

Asphyxia


• 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


• 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 Location of Injury Clinical Correlate Long term sequelae

Selective neuronal necrosis

Entire neuroaxis, deep cortical area, brainstem and pentocubicular

Stupor or comaSeizuresHypotoniaOculomotor abnormalitiesSuck/swallow abnormalities

Cognitive delayCerebral palsyDystoniaSeizure disorderAtaxiaBulbar and pseudobulbar palsy

Parasagittal injury Cortex and subcortical white matterParasagittal regions, esp. posterior

Proximal limb weaknessUpper extremities affected greater than lower extremities

Spastic quadriparesisCognitive delayVisual and auditory processingDifficulty

Focal ischemic necrosis

Cortex and subcortical white matterVascular injury (usually MCA distribution)

Unilateral findingsSeizures common and typically focal

HemiparesisSeizuresCognitive delays

Periventricular injury Injury to motor tracts, especially lower extremity

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

Spastic diplegia

Hypoxic-ischemic encephalopathy in term infants

Signs STAGE I STAGE II STAGE III

Level of consciousness Hyperalent Lethargic Stuporous, coma

Muscle tone Normal Hypotonic Flaccid

Posture Normal Flexion Decerebrate

Tendon reflexes/clonus Hyperactive Hyperactive Absent

Myoclonus Present Present Absent

Moro reflex Strong Weak Absent

Pupils Mydriasis Miosis Unequal, poor light reflex

Seizures None Common Decerebration

Electroencephalographic Normal Low voltage changing to seizure activity

Burst suppression to isoelectric

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

24 hr. to 14 days Days to weeks

Outcome Good 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

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

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 (33.5°C)- 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.

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

3.Absence oculocephalic reflexes

4. Refractory seizures

“These are associated with a poor prognosis”

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”

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)

Prognosis



Thank you

Multiorgan Systemic Effects of Asphyxia

SYSTEM EFFECT

Central nervous system Hypoxic- ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia, hypertonia

Cardiovascular Myocardial ischemia, poor contractility, cardiac stun, tricuspid insufficiency, hypotension

Pulmonary Pulmonary hypertension, pulmonary hemorrhage respiratory distress syndrome

Renal Acute tubular or cortical necrosis

Adrenal Adrenal hemorrhage

Gastrointestinal Perforation, ulceration with hemorrhage necrosis

Metabolic Inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia, hypocalcemia, myoglobinuria

Integument Subcutaneous fat necrosis

Hematology Disseminated intravascular coagulation

Topography of Brain Injury in terms infants with hypoxic ischemic encephalopathy and clinical correlates

Area of Injury Location of Injury Clinical Correlate Long term sequelae

Selective neuronal necrosis

Entire neuroaxis, deep cortical area, brainstem and pentocubicular

Stupor or comaSeizuresHypotoniaOculomotor abnormalitiesSuck/swallow abnormalities

Cognitive delayCerebral palsyDystoniaSeizure disorderAtaxiaBulbar and pseudobulbar palsy

Parasagittal injury Cortex and subcortical white matterParasagittal regions, esp. posterior

Proximal limb weaknessUpper extremities affected greater than lower extremities

Spastic quadriparesisCognitive delayVisual and auditory processingDifficulty

Focal ischemic necrosis

Cortex and subcortical white matterVascular injury (usually MCA distribution)

Unilateral findingsSeizures common and typically focal

HemiparesisSeizuresCognitive delays

Periventricular injury Injury to motor tracts, especially lower extremity

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

Spastic diplegia

Hypoxic-ischemic encephalopathy in term infants

Signs STAGE I STAGE II STAGE III

Level of consciousness Hyperalent Lethargic Stuporous, coma

Muscle tone Normal Hypotonic Flaccid

Posture Normal Flexion Decerebrate

Tendon reflexes/clonus Hyperactive Hyperactive Absent

Myoclonus Present Present Absent

Moro reflex Strong Weak Absent

Pupils Mydriasis Miosis Unequal, poor light reflex

Seizures None Common Decerebration

Electroencephalographic Normal Low voltage changing to seizure activity

Burst suppression to isoelectric

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

24 hr. to 14 days Days to weeks

Outcome Good Variable Death, severe deficits

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Asphyxia