Mohd Maghayreh Asphyxia

Post -resuscitation management of an asphyxiated neonate

Dr Mohd Maghayreh

PRTH

Perinatal asphyxia Common neonatal problem Contributes significantly to neonatal morbidity & mortality Second most important cause of neonatal death Accounts for 25 % of neonatal deaths

Perinatal asphyxia

Insult to the fetus / newborn

Lack of oxygen - hypoxia &/or Lack of perfusion – ischemia

Effect of ischemia & hypoxia – inseparable Both contribute to tissue injury

ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIA Prolonged metabolic or mixed acidemia (pH < 7.00) on an

umbilical cord arterial blood sample

Persistence of an Apgar score of 0-3 for > 5 minutes

Clinical neurological manifestations e.g. seizure, hypotonia, coma or hypoxic-ischaemic encephalopathy in the immediate neonatal period

Evidence of multiorgan system dysfunction in the immediate neonatal periods

Incidence

1. Perinatal asphyxia is about 1%-1.5% of life births.

2. It is inversely related to gestational age and birth weight .

3. It occur in (o.5%(of live born infants with gestational age >36wk

4. It account for 20% of perinatal deaths

Risk factors

Ante partum events (20%) Maternal: cardiac arrest, hemorrhage, diabetes ,pre

eclamptic toxemia, fetal: IUGR, congenital anomalies

Intrapartum events (35%) birth trauma, abruption, uterine rupture, uteroplacental

insufficiency Ante partum and Intrapartum (35%) Postpartum events (10%)

apnea, bradycardia, septic shock, pulmonary disease, some CHD (LVOT obstr), PDA (premie

FACTORS

Mat. Oxygenation

Blood flow mother to placenta

Gas Exchange across placenta or fetal tissue

Fetal O2 Req.

PATHOPHYSIOLOGY

Hypoxia

Diving seal reflex

Away from lungs, kidney gut & skin

Shunting of blood to brain adrenals & heart

CEREBRAL CORTICAL LESIONS

PATHOPHYSIOLOGYAsphyxia continues

Shunting within the brain

Anterior Circulation

Suffers

Posterior Circulation Maintained

PNA is produced by the interaction of one of the following

factors: 1- Impaired maternal oxygenation. 2- Decreased blood flow from mother to placenta

or placenta to fetus 3- impaired gas exchange across the placenta or

at the fetal tissue.

4- 4- Increase fetal O2 requirementsIncrease fetal O2 requirements..

Circulatory depressionRespiratory depression

Hypoxemia

Hypercarbia

Respiratory acidosis

Low cardiac output

Decreased tissue perfusion

Ischemia

Metabolic acidosis

Capillary leak, edema

Multi-organ dysfunction

PATHOLOGY Target organs of perinatal asphyxia

Kidneys 50%

Brain 28 %

Heart 25%

Lung 23%

Liver, Bowel, Bone marrow < 5%

Clinical consequences of perinatal asphyxia Brain ( Hypoxic Ischemic Encephalopathy,

HIE ) Altered sensorium Irritability, lethargy, deeply comatose Tone disturbances - Hypotonia of proximal girdle muscles (lack of head control & weakness of

shoulder muscle in term infants )

Clinical consequences of perinatal asphyxia (contd.) Brain ( Hypoxic Ischemic

Encephalopathy,HIE ) Autonomic disturbances eg. hypotension,

increase salivation, abnormal pupillary reflex Altered neonatal reflexes -Moro’s, sucking , swallowing Seizures

PATHOLOGY

At cellular level

Cerebral O2

Substrate supply

Synaptic inactivation (Reversible)

Energy failure

Memb. pump failure

ROS Release

ISCHEMIA AND REPERFUSION INJURY

Ischemia ATP depletio

n

Calcium influx

Phospholipase activation

Arachidonic acid release

Prostaglandins Proteases, lipases

VasodilationMicrovascular permeabilityReperfusion

MECHANISM

RESUSCITATION ATP ASPHYXIA

HYPOXANTHINE

XANTHINE

URIC ACID

Oxygen

Oxygen free radicals

Oxygen

Oxygen free radicals

BLOCKED

BLOCKED

EFFECT OF ROS

ROS

DNA strand

breakage

Lipid peroxidation

Neutrophil accumulation

Release of proteases,

myeloperoxidase, prostaglandins

Tissue damage

Phagocytosis

PMN plugging of capillaries

Ischemia

Membrane damage

Cell death

Fetal and neonatal assessment

1. A- Fetal Heart rate monitoring

2. B- Passage of Meconium

3. C- Failure to establish spontaneous respiration

4. D- low Apgar Scores

5. E- Hypoxic - Ischemic Encephalopathy

6. F- Multi organ Involvement

CLINICAL MANIFESTATIONS OF HIE Altered consciousness Tone problems Seizure activity Autonomic disturbances Abnormalities of peripheral and stem reflexes

Principles of management

Prevent further organ damage Maintain oxygenation, ventilation & perfusion Correct & maintain normal metabolic & acid

base milieu Prompt management of complications

CLASSIFICATION OF HIE (LEVENE)

Mild Moderate

Consciousness

Tone

Seizure

Sucking / Resp.

Irritable

Hypotonia

No

Poor Suck

Lethargy

Marked

Yes

Unable to suck

Feature Severe

Comatose

Severe

Prolonged

Unable to sustain

spont. Resp.

Grade 1 (mild)Grade2 (moderate)Grade 3 (severe)

Level of consciousnessIrritable/hyperalertLethargyComa

Muscle toneNormal or hypertoniaHypotoniaFlaccid

Tendon reflexesIncreasedIncreasedDepressed or absent

SeizuresAbsentFrequentFrequent

Complex reflexesNormalweakAbsent

PrognosisGoodVariableHigh mortality and neurologicl disability

Sarnat staging of hypoxic-ischemic encephalopathy.

According to Sarnat classification of severity

stage 1 100 % normal

stage 2 80 % normal

stage 3 50 % death 50 % major sequalae

Initial management

Admit in nursery,if -Apgar score <3 at 1 minute -Babies requiring intubation, chest compressions

or medications Nurse in thermo-neutral temperature to maintain skin

temperature at 36.5oC Secure IV line , fluids 2/3 rd of maintenance Fluid bolus if CRT > 3 secs or blood pressure low Inj vit k Stomach wash

Clinical monitoring

HR, RR, colour, CRT, O2 saturation, BP & temperature Assessment of neurologic status

Tone, seizures, consciousness, pupillary size & reaction, sucking, swallowing

Abdominal circumference Urine output

Biochemical monitoring

Blood gases & pH Bedside blood sugar by Dextrostix Hematocrit S. electrolytes ( Na, K) S. calcium BUN, creatinine

Other investigations

Sepsis screen & blood culture to exclude in- utero or acquired infection during resuscitation

X-ray chest to look for pneumothorax, malformations, cardiac enlargement

Other investigations contd..

Neuroimaging CT scan -brain edema as suggested by small

compressed ventricles -hemorrhage Ultrasound -small compressed ventricles -intraventricular hemorrhage EEG

Aims of specific management

Maintain temperature, perfusion, oxygenation, ventilation & normal metabolic state Temperature 36.5 C – 37.5 C Perfusion:

BP Mean 40-60 mm Hg ( Term) CRT maintain < 3 sec

Oxygen PaO2 60-80mmHg saturation 90-93 %

CO2 35-45 mm of Hg Glucose 70-110 mg/dl Calcium 9-11 mg/dl

Specific management

Maintain perfusion Normal blood pressure CRT < 3 secs Normal urine output ( >1ml/kg/hr) Absence of metabolic acidosis

Specific management

Maintain perfusion Maintain mean arterial pressure and CRT by giving

slow bolus of crystalloid 10 ml/kg over 20 minutes. Repeat one more time , if still does not improve

Use vasopressors Dopamine and /or Dobutamine to increase BP

Sodium bicarbonate 1-2 ml/kg diluted in 5 % dextrose can be used for babies with documented acidosis after establishing respiration

SUBSEQUENT MANAGEMENT

Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure

Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure

TREATMENT OF SEIZURESTREATMENT OF SEIZURES

Correction of hypoglycemia, hypocalcemia & electrolyte

Prophylactic Phenobarbitone ?

Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance)

Lorazepam – 0.05 – 0.1 mg / kg

Diazepam to be avoided

Correction of hypoglycemia, hypocalcemia & electrolyte

Prophylactic Phenobarbitone ?

Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance)

Lorazepam – 0.05 – 0.1 mg / kg

Diazepam to be avoided

Predictors of poor neuro-developmental outcome Failure to establish resp. by 5 minutes Apgar score of 3 or less at 5 minutes Onset of seizures with in 12 hours Refractory seizures Inability to establish oral feeds by 1 wk Abnormal EEG, neuro-imaging

Preventing asphyxia

Perinatal assessment Regular antenatal check ups High risk approach Anticipation of complications during labour Timely intervention ( eg. LSCS)

Perinatal management Timely referral Management of maternal complications