Paediatric Radiology · Neonatal neuroimaging · Original Sarnat staging with modified-examination context

Sarnat staging of neonatal hypoxic–ischaemic encephalopathy

Clinical and electroencephalographic staging of neonatal encephalopathy into mild, moderate and severe categories. It supports early severity assessment and selection for further evaluation for therapeutic hypothermia.

Purpose

To grade the clinical severity of neonatal encephalopathy following suspected perinatal hypoxic–ischaemic injury using consciousness, activity, tone, reflexes, autonomic function, seizures and electroencephalographic findings.

StageConsciousness and activityTone, posture and reflexesAutonomic signs and seizuresEEG and usual implication
Stage I — mildHyperalert; normal or increased spontaneous activityNormal or increased tone; mild distal flexion; brisk stretch reflexes; strong, low-threshold Moro; suck normal or mildly impairedPredominantly sympathetic features may occur, including mydriasis and tachycardia; seizures absentEEG usually normal; classical stage lasts less than 24 hours and usually has a favourable short-term course
Stage II — moderateLethargic; decreased spontaneous activityHypotonia; prominent distal flexion or extension; weak suck; incomplete MoroMiosis, bradycardia and periodic or irregular breathing; seizures common and may be focal or multifocalAbnormal background with discontinuity or periodic activity; requires urgent assessment for therapeutic hypothermia when other eligibility criteria are met
Stage III — severeStupor or coma; absent spontaneous activityFlaccidity; intermittent decerebrate posture may occur; absent suck and Moro; depressed or absent stretch reflexesPupils may be deviated, dilated or poorly reactive; variable heart rate and apnoea; clinical seizures may be uncommon because of profound cerebral depressionMarkedly suppressed, periodic or inactive EEG background; associated with a high risk of death or major neurodevelopmental impairment

How to use it

Common mistake

Do not equate neonatal encephalopathy automatically with hypoxic–ischaemic encephalopathy. Sarnat staging grades encephalopathy severity but does not establish its cause, and sedatives, anticonvulsants, paralysis, hypothermia and systemic illness can alter the examination.

Exam pearl

Stage II is the classic seizure-prone stage; seizures may become clinically inconspicuous in Stage III because cerebral activity is profoundly suppressed.

Viva questions

What is Sarnat staging?
It is a clinical and electroencephalographic system that grades neonatal encephalopathy as Stage I mild, Stage II moderate or Stage III severe.
What are the three Sarnat stages?
Stage I is mild encephalopathy, Stage II is moderate encephalopathy and Stage III is severe encephalopathy.
What are the characteristic findings of Stage I encephalopathy?
The neonate is hyperalert with normal or increased activity and tone, brisk reflexes and no seizures. The EEG is usually normal.
What are the characteristic findings of Stage II encephalopathy?
The neonate is lethargic with decreased activity, hypotonia, weak suck, incomplete Moro and periodic breathing. Seizures are common and the EEG background is abnormal.
What are the characteristic findings of Stage III encephalopathy?
The neonate is stuporous or comatose, with absent activity, flaccidity, absent primitive reflexes, autonomic instability and a markedly suppressed or inactive EEG.
Why may clinical seizures be uncommon in Stage III encephalopathy?
Profound cerebral dysfunction may prevent an organised clinical seizure despite severe brain injury. Continuous EEG is therefore important for detecting electrographic seizures.
How does Sarnat staging influence therapeutic hypothermia?
Moderate or severe encephalopathy supports eligibility for therapeutic hypothermia when the infant also meets the required perinatal, biochemical, gestational-age and treatment-window criteria.
Does Sarnat staging establish that neonatal encephalopathy was caused by hypoxia–ischaemia?
No. It grades the severity of encephalopathy but does not prove its aetiology; metabolic, infectious, genetic, vascular and drug-related causes must be considered.

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