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Sarnat staging
Sarnat staging
Sarnat staging
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Sarnat staging
SynonymsSarnat Classification
Purposeclassification for hypoxic-ischaemic encephalopathy of newborn

Sarnat staging, Sarnat Classification or the Sarnat Grading Scale is a classification scale for hypoxic-ischaemic encephalopathy of the newborn (HIE), a syndrome caused by a lack of adequate oxygenation around the time of birth which manifests as altered consciousness, altered muscle tone, and seizures.[1] HIE is graded based on the infant's clinical presentation, examination findings, the presence of seizures and the duration of illness. Sarnat staging is used alongside electroencephalogram (EEG) findings to provide information about the prognosis for the infant. Mild HIE, according to the scale, usually has a normal outcome, whereas in severe HIE the mortality rate is 75%, and 80% of survivors have neurological sequelae.[2]

UK Resuscitation Council guidelines on newborn life support recommend that a baby who received significant resuscitation at birth and who goes on to show signs of encephalopathy should be assessed by Sarnat Staging between 24 and 48 hours from birth.[3]

Staging

[edit]
Grade I Mild Grade II Moderate Grade III Severe
Alertness Hyperalert Lethargy Coma
Muscle tone Normal or increased Hypotonic Flaccid
Seizures None Frequent Uncommon
Pupils Dilated, reactive Small, reactive Variable, fixed
Respiration Regular Periodic Apnoea
Duration < 24 Hours 2 - 14 Days Weeks

Adapted from [2]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sarnat staging

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Sarnat staging is a clinical classification system developed to assess the severity of hypoxic-ischemic encephalopathy (HIE) in term newborns, categorizing the condition into three progressive stages based on findings and electroencephalogram (EEG) patterns. First described by pediatric neurologists Harvey B. Sarnat and Margaret S. Sarnat in their 1976 study of 21 neonates with , the system identifies evolving clinical features following an acute hypoxic-ischemic insult, distinguishing it from chronic or progressive encephalopathies. This staging tool remains a cornerstone for diagnosing HIE, predicting neurodevelopmental outcomes, and determining eligibility for interventions such as therapeutic . The original Sarnat staging delineates three stages of postanoxic , each with characteristic clinical and EEG correlates that reflect the temporal evolution of brain injury. Stage 1, or mild , typically lasts less than 24 hours and features hyperalertness, uninhibited Moro and suck reflexes, , and dominance (e.g., pupil dilation, ), accompanied by a normal EEG. Stage 2, moderate , involves obtundation, with distal flexor posturing, weak or absent , multifocal seizures, and parasympathetic effects (e.g., , ), with EEG showing low-voltage continuous delta and activity or a periodic pattern. Stage 3, severe , manifests as or , flaccid tone, absent reflexes and seizures initially, suppressed and autonomic functions, and an isoelectric or suppressed-burst EEG pattern, often persisting for days to weeks. In the original cohort, infants who did not progress beyond stage 1 or resolved stage 2 within five days generally had normal outcomes, while prolonged stage 2 or any stage 3 correlated with high risks of death or neurological impairment. Over the decades, modifications to the Sarnat system have been proposed to enhance its practicality in clinical settings, particularly by simplifying assessments or incorporating additional signs without relying on EEG, which may not always be immediately available. For instance, the modified Sarnat score, widely used in therapeutic trials, evaluates six domains—level of , spontaneous activity, posture, tone, , and autonomic function—assigning points to classify severity, and has demonstrated strong prognostic value for 2-year neurodevelopmental outcomes even when performed early after birth. These adaptations maintain the core principles of the original while improving and applicability in neonatal intensive care units. Despite variations, Sarnat staging continues to inform management strategies, with moderate to severe classifications (stages 2 and 3) indicating a need for aggressive neuroprotective therapies to mitigate long-term disabilities such as or cognitive deficits.

Background

History and Development

The Sarnat staging system was developed by pediatric neurologists Harvey B. Sarnat and Muriel S. Sarnat in , based on a prospective study of 21 term infants ( greater than 36 weeks) who experienced acute leading to hypoxic-ischemic (HIE). The research focused on newborns with a well-defined episode of fetal distress, excluding those with chronic intrauterine hypoxia or other etiologies, to isolate the effects of acute on neurological function. The system's foundational work was published in the Archives of Neurology under the title "Neonatal Encephalopathy Following Fetal Distress: A Clinical and Electroencephalographic Study" (Volume 33, Issue 10, pages 696–706). In this seminal paper, the authors correlated evolving clinical signs of with contemporaneous electroencephalographic (EEG) patterns and long-term neurodevelopmental outcomes, demonstrating that milder or shorter-duration abnormalities were associated with normal recovery, while persistent severe features predicted impairment or mortality. For instance, infants without progression to the most severe stage and with moderate signs resolving within five days typically achieved normal outcomes, whereas prolonged moderate beyond seven days or non-normalizing EEGs were linked to adverse results. The initial purpose of the Sarnat staging was to establish a standardized, clinically observable classification for the severity and progression of postnatal in asphyxiated newborns, facilitating more precise and beyond vague terms like "birth ." This framework has since informed therapeutic strategies, such as therapeutic , by enabling risk stratification in HIE management.

Context in Neonatal Encephalopathy

Neonatal encephalopathy refers to a syndrome of dysfunction in newborns, characterized by altered consciousness, , seizures, and difficulties with feeding and respiration, typically manifesting within the first week of life. This condition encompasses a range of etiologies, but the most common is hypoxic-ischemic encephalopathy (HIE), resulting from that deprives the of oxygen and blood flow. HIE affects approximately 1 to 8 per 1,000 live term births worldwide, with higher rates in low-resource settings due to variations in prenatal and intrapartum care. The pathophysiology of HIE involves a biphasic injury process initiated by acute hypoxia-ischemia, leading to primary energy failure and subsequent reperfusion injury. This triggers excitotoxicity from excessive glutamate release, mitochondrial dysfunction, oxidative stress, and inflammatory cascades, culminating in neuronal apoptosis and necrosis. Vulnerable brain regions, such as the basal ganglia, thalami, and watershed zones between major arterial territories, are particularly susceptible to these insults, resulting in selective patterns of injury depending on the timing and severity of the hypoxic event. Early assessment and staging of HIE are critical for risk stratification, enabling timely initiation of neuroprotective interventions like therapeutic , which must begin within the first 6 hours after birth to mitigate secondary brain injury and improve neurodevelopmental outcomes. Sarnat staging serves as a foundational clinical tool for classifying the severity of HIE based on neurological findings in this critical window.

Clinical Parameters

Neurological Examination Components

The neurological examination in the modified Sarnat staging systematically assesses six core clinical domains to evaluate the extent of in term neonates following perinatal hypoxic-ischemic events. These domains—level of , spontaneous activity, posture, , , and autonomic function—provide a structured framework for identifying abnormalities in function, drawing from observations and targeted maneuvers during the exam. The original Sarnat staging uses a more descriptive approach to these and related findings. Seizures are assessed separately through clinical observation and often confirmed with EEG. Level of consciousness is evaluated through the neonate's and to stimuli, such as , , or touch. In typical assessments, it ranges from hyperalert or normal to (drowsy but arousable), and further to or (unarousable with minimal or no response). This parameter serves as a primary indicator of cortical involvement. Spontaneous activity is observed without provocation, focusing on the and of movements in the limbs and trunk. Normal activity involves vigorous, coordinated motions, while abnormalities manifest as mildly or markedly decreased movements, or complete absence, reflecting potential subcortical or dysfunction. Posture is assessed with the neonate at rest, noting the position of the limbs and trunk. Normal posture appears relaxed, but deviations include mild distal flexion (suggesting ) or more pronounced flexed or flaccid states, which may indicate evolving neurological impairment. is tested using maneuvers such as ventral suspension (holding the prone by the trunk) or traction (pulling the arms upward). Responses are graded from normal resistance to (reduced resistance) or flaccidity (no resistance), highlighting disruptions in neuromuscular control. Primitive reflexes, including the Moro (startle), suck, and grasp reflexes, are elicited and graded for strength and symmetry. These are typically intact and brisk in healthy neonates but may appear weak (diminished response) or absent (no elicitable response), signaling immaturity or suppression of brainstem-mediated arcs. Autonomic function is evaluated by signs such as pupil size and reactivity, , respiration, and gastrointestinal activity. Normal findings include midposition reactive pupils, >100 bpm, and spontaneous respiration; abnormalities progress to constricted or dilated fixed pupils, , apnea, or other disruptions indicating involvement. The presence or absence of seizures is determined through clinical observation of rhythmic movements, eye deviations, or autonomic changes, with subclinical events often confirmed via (EEG). These domains collectively contribute to classifying into mild, moderate, or severe stages based on the constellation of findings.

Evaluation Methods

The Sarnat is typically initiated within the first 24 hours of life in infants suspected of having , with serial assessments performed to monitor the progression or resolution of symptoms. This timing aligns with the critical window for therapeutic interventions like , where early evaluation helps determine eligibility and tracks dynamic changes in severity. The examination follows a standardized protocol conducted by trained neonatologists or pediatric neurologists to ensure accurate assessment of the infant's responses. Each generally lasts 10-15 minutes and involves observing and eliciting responses across six key clinical parameters: level of , spontaneous activity, posture, tone, , and autonomic function. Serial exams by the same or consistent examiners enhance reliability in detecting subtle improvements or deteriorations. In the original descriptive approach, findings are categorized into stages based on the constellation of clinical signs rather than a numeric total. Some modified versions grade each of the six parameters on a 0-3 scale (0 indicating normal function and 3 the most severe abnormality), allowing for a summed score to quantify severity, though the core staging remains qualitative. This grading facilitates objective tracking but emphasizes clinical judgment over strict summation. The exam is often supplemented with adjunct tools such as (EEG) to confirm and detect subclinical seizures, which may not be apparent on clinical assessment alone. Continuous or amplitude-integrated EEG is particularly valuable during the first 72 hours, providing complementary data on brain activity that refines staging accuracy. Studies on demonstrate moderate to high agreement when exams are performed consistently by experienced clinicians, with values ranging from 0.6 to 0.8 across parameters and overall staging. Reliability improves with rater and , particularly for subjective elements like tone and reflexes, underscoring the importance of standardized for reproducible results.

Staging System

Stage 1: Mild

Stage 1 of the Sarnat staging system represents mild in neonates following , characterized by transient and self-resolving symptoms that typically do not progress to more severe forms. This stage usually lasts less than 24 hours, often resolving spontaneously without intervention, distinguishing it from the prolonged deficits observed in higher stages that may influence eligibility for therapies like . Clinically, infants in Stage 1 exhibit hyperalertness or in , with normal to increased spontaneous movements and normal contributing to features such as tremors or jitteriness. Posture is normal, while reflexes remain normal or exaggerated, including uninhibited Moro and stretch responses, and there are no seizures. Sympathetic autonomic effects, such as and dilated pupils, may accompany these signs, alongside sparse bronchial and salivary secretions and normal or decreased gastrointestinal motility. Electroencephalogram (EEG) findings in Stage 1 are generally normal, though mild abnormalities such as theta activity can occasionally be observed, reflecting minimal disruption to function. The prognosis for these infants is excellent, with near-normal neurodevelopment reported in the majority of cases, as evidenced by long-term follow-up studies of affected neonates.

Stage 2: Moderate

Stage 2 of the Sarnat staging system, known as moderate , typically persists for 2 to 14 days following in term neonates, during which clinical signs may gradually resolve or, if untreated, progress to Stage 3 severe . This stage often evolves from Stage 1 mild or presents directly after the initial hypoxic-ischemic insult, reflecting ongoing neuronal dysfunction without complete recovery. Infants in this stage exhibit with responsiveness to vigorous stimuli, distinguishing it from the hyperalertness of Stage 1 and the coma of Stage 3. Key clinical features include in the limbs, decreased spontaneous movements, weak or absent (such as grasp and suck), and a characteristic decorticate posturing (flexion of arms and extension of legs). Seizures occur occasionally, manifesting as focal or generalized clonic activity, further indicating moderate cerebral involvement. Electroencephalographic (EEG) findings correlate with these clinical signs, showing moderate abnormalities such as periodic patterns, low-voltage continuous delta and theta activity, or intermittent voltage suppression, which typically improve over the stage's duration but persist longer in cases of poor . This stage plays a critical role in selecting neonates for therapeutic , as moderate qualifies infants for this neuroprotective intervention when initiated within 6 hours of birth.

Stage 3: Severe

Stage 3 represents the most severe form of in the Sarnat staging system, characterized by profound and persistent neurological impairment that typically persists indefinitely, often exceeding 72 hours with minimal or no signs of improvement. This stage is distinguished by a deep level of , where infants are stuporous or comatose and remain unarousable even to painful stimuli, reflecting extensive cerebral dysfunction. In contrast to milder stages that may resolve more readily, the lack of responsiveness in stage 3 underscores the need for immediate differentiation to guide urgent intensive care. Key clinical features include flaccid with profound , absence of spontaneous movements, and dependent limb positioning, often accompanied by a decerebrate posture indicative of involvement. Primitive reflexes such as the Moro, sucking, and rooting are entirely absent, and functions are suppressed, manifesting as dilated and fixed pupils, ptosis, and irregular respirations. Seizures are frequent and notoriously difficult to control pharmacologically, further complicating the clinical picture. Electroencephalographic (EEG) findings in stage 3 correlate with the severity of , typically showing severe suppression such as an isoelectric pattern or burst-suppression activity, which signifies widespread neuronal depression. This EEG profile contrasts sharply with the more variable patterns seen in earlier stages and provides objective evidence of the extensive . Common associations with stage 3 include multi-organ failure, involving renal, hepatic, and cardiovascular systems, which exacerbates the overall critical condition and contributes to a high of mortality. These systemic complications arise from the underlying hypoxic-ischemic insult and amplify the neurological devastation.

Applications and Implications

Use in Therapeutic Interventions

Sarnat staging serves as a critical diagnostic tool to identify neonates with moderate (Stage 2) or severe (Stage 3) hypoxic-ischemic encephalopathy (HIE) who are eligible for , specifically whole-body cooling initiated within 6 hours of birth. This staging, based on findings such as level of consciousness, tone, reflexes, and seizures, helps confirm encephalopathy severity alongside indicators. Standard inclusion criteria for cooling include of at least 36 weeks, an of 5 or less at 10 minutes, umbilical cord arterial less than 7.0 (or base deficit of 16 mmol/L or greater), and confirmation of Stage 2 or 3 encephalopathy on Sarnat assessment. The therapeutic hypothermia protocol involves maintaining core body temperature at 33–34°C for 72 hours, followed by gradual rewarming at 0.5°C per hour, which has been shown to reduce the risk of death or major neurodevelopmental . This approach is supported by evidence from the Total Body Hypothermia for (TOBY) and the National Institute of Child Health and Human Development (NICHD) Neonatal Research Network , where demonstrated a 24% (RR 0.76, 95% CI 0.69–0.84) in death or at 18–24 months, with greater benefits (up to 32% reduction) observed in moderate cases. These findings underpin the 2014 American Academy of (AAP) guidelines recommending therapeutic as the standard of care for eligible infants with HIE. Beyond , Sarnat staging guides additional interventions, such as initiating for clinical or electrographic , which are more prevalent in Stages 2 and 3. Common agents include or , selected based on characteristics confirmed via amplitude-integrated EEG (aEEG) in conjunction with staging. Furthermore, higher-stage classifications inform intensified (NICU) monitoring levels, including continuous vital signs, serial neurological exams, and to optimize supportive care.

Prognostic Value

The Sarnat staging system offers significant prognostic value in predicting neurodevelopmental outcomes for neonates with , particularly in the context of hypoxic-ischemic injury. For stage 1 (mild encephalopathy), more than 90% of infants achieve normal neurodevelopmental outcomes at 18 to 24 months of age, with minimal risk of long-term disabilities. In the pre-therapeutic hypothermia era, stage 2 (moderate encephalopathy) was associated with 20% to 30% mortality, and among survivors, 30% to 50% developed , cognitive delays, or other neurodevelopmental impairments; stage 3 (severe encephalopathy) carried the poorest , with mortality rates of 50% to 75%, and survivors frequently exhibiting severe disabilities, including quadriplegia, , and profound intellectual impairment. With the integration of therapeutic as standard care since the , these risks have been substantially reduced, with meta-analyses showing a 24–28% relative reduction in death or major disability overall (e.g., combined rates of ~45–55% for treated moderate-to-severe cases at 18–24 months as of 2023 data). Greater relative benefits are seen in stage 2 compared to stage 3, though higher stages still predict worse outcomes, with recent studies reporting stage 2 mortality around 5–15% and stage 3 around 20–30%. Several factors influence the prognostic accuracy of Sarnat staging beyond the initial classification. The duration of is critical; shorter durations in stage 2 correlate with better recovery, while prolonged symptoms predict worse outcomes. (EEG) findings, such as or low-voltage patterns in severe cases, enhance predictive power when combined with staging. Similarly, (MRI) patterns provide additional context, with and thalamic injuries commonly observed in stage 3 cases and linked to adverse neurodevelopment. Long-term follow-up studies underscore the reliability of Sarnat staging for outcome prediction. In the original cohort of 21 infants, stage 1 cases showed full recovery, while stages 2 and 3 had increasing rates of impairment at 3 to 15 months. Modern registries, such as those from therapeutic hypothermia trials, confirm these patterns of relative risk, demonstrating strong correlations between staging and Bayley Scales of Infant and Toddler Development scores at 18 to 24 months, where higher stages predict lower cognitive and motor composite scores despite overall improvements from treatment. Despite its utility, Sarnat staging has limitations in prognostic precision, performing best for severe cases while showing more variability in mild to moderate due to overlaps with risks like or preterm complications. Integration with therapeutic has been shown to modify outcomes favorably in stages 2 and 3, reducing mortality and rates in treated cohorts.

Limitations and Variations

Criticisms of the Original System

The original Sarnat staging system, introduced in , has been criticized for its heavy reliance on subjective clinical judgment, which introduces significant inter-observer variability in assessments such as grading or level of . This subjectivity stems from the descriptive nature of the criteria, where examiners must interpret qualitative signs like or reflexes without standardized thresholds, leading to inconsistencies across providers. For instance, studies have highlighted challenges in reliably assigning stages based on fluctuating neurological signs in the early hours post-birth. A key limitation is the lack of quantification in the original framework, which uses categorical descriptions rather than numerical scores, complicating direct comparisons across studies or serial evaluations of disease progression. This descriptive approach hinders precise tracking of evolution and limits its utility in settings requiring objective metrics. The system's scope is also narrow, primarily developed for term infants with hypoxic-ischemic (HIE) and failing to account for preterm neonates or alternative causes of , such as metabolic disorders. Furthermore, as it predates advancements in like MRI and refined EEG techniques, it often misses subtle brain injuries that these tools can detect, particularly in mild cases where clinical signs may be absent or ambiguous. Validation concerns further undermine the original system's reliability, with its development based on a small cohort of only 21 neonates, raising questions about generalizability and lacking subsequent validation in independent populations. Modern reviews from the 2010s have noted its poor sensitivity for mild , where up to 33% of cases may progress to more severe stages undetected early on, potentially delaying interventions.

Modified Versions

The Thompson Scoring System, introduced in 1997, represents an early numeric adaptation of the Sarnat staging framework for assessing hypoxic-ischemic encephalopathy (HIE) in newborns. This system quantifies severity using a score ranging from 0 to 22 across nine clinical parameters, including tone, , seizures, posture, , grasp reflex, suck, respiration, and , graded from 0 to 3 (with some parameters up to 2), providing a more objective and quantifiable alternative to the original categorical stages for use in clinical trials and outcome prediction. Higher scores, such as 15 or above, demonstrate a 92% positive predictive value for abnormal neurodevelopmental outcomes. In the 2000s, modified versions of the Sarnat system emerged to enhance precision in the therapeutic era, incorporating explicit grading of seizures and integration of (EEG) data alongside traditional clinical signs. These adaptations, often termed the expanded or modified Sarnat exam, evaluate abnormalities in categories such as level of , tone, reflexes, respiration, pupils, and seizures, classifying moderate or severe if three or more categories are affected, and have been standardized for eligibility in hypothermia trials. The National Institute of Child Health and Human Development Neonatal Research Network (NICHD NRN) further refined this approach by incorporating amplitude-integrated EEG (aEEG) for objective detection and background pattern assessment, allowing real-time monitoring of evolution during cooling therapy. This modification improves identification, as clinical exams alone detect only about 30% of electrographic seizures, and correlates aEEG patterns with Sarnat stages for better prognostic accuracy in term infants. International adaptations, particularly in European settings, have extended these modifications by integrating brain (MRI) for staging confirmation beyond the initial 72 hours, combining clinical and neurophysiologic data with to assess patterns like or watershed involvement. For instance, protocols in trials such as the Total Body Hypothermia for (TOBY) study utilize modified Sarnat exams with aEEG during acute phases and MRI for later verification, enhancing applicability across diverse populations. These modified systems offer advantages including improved , with kappa values greater than 0.72 for overall staging in trained examiners, and greater suitability for preterm infants or those undergoing therapeutic cooling where traditional parameters may be confounded. In the 2020s, clinical practice guidelines from international organizations and consortia recommend a combined approach integrating clinical modified Sarnat assessments with neurophysiologic tools such as aEEG or full EEG to optimize HIE , monitoring, and intervention timing.

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