Rungta institute of pharmaceutical sciences
This part is a clinical syndrome which in new born characterized by disturbed neurological function, which include altered consciousness, difficulty initiating or maintaining respiration, abnormal tones or reflexes, & often seizures. While the most common cause is hypoxic-ischemic encephalopathy (HIE) resulting from oxygen deprivation or reduced blood flow to the brain—NE may also arise from infections, metabolic disorders, trauma, or genetic conditions. During the 1800s, obstetrics became a more formalized field, and complications during labour were increasingly linked to poor neonatal outcomes. Physicians began recognizing the effects of prolonged labour and mechanical trauma on newborns. Clinicians may perform , Clinical Diagnosis: History taking- Maternal history Infections (e.g.chorioamnionitis, TORCH infections). Complications during pregnancy (e.g.,preeclampsia, diabetes, placental abruption), Prolonged rupture of membranes. Perinatal history Apgar scores at 1, 5, and 10 minutes , Need for resuscitation at birth (e.g. intubation, chest compression). Monitoring and Imaging - Neurological Examination Evaluate seizures, tone, reflexes, and degree of awareness, EEG/aEEG- Keep an eye out for seizures in brain activity. Imaging- Initial screening with cranial ultrasonography, Brain MRI to find patterns to brain damage (best at 5-7 days).
Neonatal encephalopathy (NE) is a term that describes a spectrum of neurological conditions in newborns, characterized by a decrease in neurological function due to various underlying causes. This condition is primarily recognized in the first few days of life and can lead to significant long-term consequences, including cognitive and motor impairments. Understanding NE is essential for timely intervention and improved outcomes for affected infants.While the most common cause is hypoxic-ischemic encephalopathy (HIE)—resulting from oxygen deprivation or reduced blood flow to the brain—NE may also arise from infections, metabolic disorders, trauma, or genetic conditions.
The severity of NE can vary, ranging from mild and transient symptoms to severe outcomes such as developmental delays, cerebral palsy, or death. Diagnosis often involves clinical assessment, neuroimaging, and EEG, with treatment tailored to the underlying cause, including supportive care and interventions like therapeutic hypothermia for HIE.
Ancient times- Physician like Hippocrates and Galen made early references to newborns with poor outcomes with difficult deliveries. They observed symptoms like lethargy, abnormal cries, and convulsions, which likely correspond to what we now call neonatal encelopathy. These conditions were attributed to humoral imbalances or birthing difficulties, with little understanding of the role of oxygen deprivation or brain injury. Medieval and Renaissance- Newborn deaths or neurological impairements were often seen as acts of fate or divine will. Limited knowledge about childbirth complications and neonatal care hindered progress 19th century: The Birth of Neonatal Medicine – During the 1800s, obstetrics became a more formalized field, and complications during labour were increasingly linked to poor neonatal outcomes. Physicians began recognizing the effects of prolonged labour and mechanical trauma on newborns. Terms like “birth asphyxia” began to emerge, describing infants who failed to breathe immediately after birth. 20th century : Emergence of Neonatal Encelopathy - Advance in the Neonatal care (Early 1900s) The inventions of devices like forceps for assisted deliveries aimed to reduce trauma but occasionally caused unintended brain injury, Studies started connecting birth asphyxia to long term conditions like cerebral palsy. Hypoxia- Ischemia Recognized (Mid 1900s): In the 1950s and 1960s, researchers identified the brains vulnerability to oxygen deprivation during childbirth. This period marked the early understanding of Hypoxic-ischemic Encelopathy (HIE) as a major cause of NE. The development of foetal monitoring techniques (e.g. foetal heart rate monitoring) highlighted the role of intrapartum events in brain injuries. Neuroimaging and EEG (1970s-1980s): The introduction and technologies like computed tomography (CT), magnetic resonance imaging (MRI), and electroencephalography (EEG), allowed doctors to visualize brain injuries and measure electrical activity in newborns. Researchers developed systems, such as sarnat staging system (1976), to classify the severity of encephalopathy. Therapeutic hypothermia (Late 1990): Studies demonstrated that cooling a newborn’s brain could reduce the extent of brain damage after hypoxic events. The discovery revolutionized the treatment of NE, particularly in case of HIE. 21st century: Modern understanding : NE is recognized as a syndrome caused by a variety of factors beyond hypoxia, including infections, metabolic conditions, and genetic abnormalities. Precision Medicine: Advantages in genetics and molecular biology have improved the diagnosis of rare metabolic and genetic cause of NE.
Key Historical Milestones: 1960s-1970s: Recognition of perinatal asphyxia as a major contributor to neonatal brain injury, 1976: Introduction of the slant staging system for assessing Hypoxic-ischemic encephalopathy, 1990s: Implementation of therapeutic hypothermia as a standard element, 2000s-present: Expansion of understanding to include other causes (e.g., infections, genetic condition) and the use of advanced neuroimaging and biomarkers.
The clinical presentation of NE can the condition. Common symptoms may include:
Altered level of consciousness: Infants may exhibit lethargy, poor feeding or conversely, excessive irritability. Abnormal muscle tone: This can present as either hypotonia (decreased muscle tone) or hypertonia (increased muscle tone), affecting the infant’s ability to move normally. Seizures: Seizures may occur in some cases, manifesting as twitching, jerking movements, or abnormal posturing. Feeding difficulties: Poor feeding can result from diminished alertness or abnormal swallowing reflexes. Difficulty breathing : Observed in more severe cases, especially when associated with other underlying conditions. Early identification of these symptoms is critical, as timely medical intervention can significantly influence outcomes
Fig. No.- 1 Brain injury (Hypoxia ischemia)
4.Diagnosis:
Diagnosing Neonatal Encelopathy typically involves a combination of clinical evaluation and diagnostic testing. Clinicians may perform , Clinical Diagnosis: History taking- Maternal history Infections (e.g.chorioamnionitis, TORCH infections). Complications during pregnancy (e.g.,preeclampsia, diabetes, placental abruption), Prolonged rupture of membranes. Perinatal history Apgar scores at 1, 5, and 10 minutes , Need for resuscitation at birth (e.g. intubation, chest compression). Foetal heart rate abnormalities during labour . Neurological Examination: Level of consciousness (alertness, lethargy, stupor or coma). Muscle tone (hypotonia or hypertonia), Reflexes (e.g. sucking, Moro, and grasp reflexes), Seizures (subtle, clonic , tonic, or myoclonic movements).
Abnormal respiratory patterns. Investigations, Neuroimaging: Cranial ultrasound Useful for detecting intraventricular hemmorrhage or gross structural abnormailities. )Magnetic resonance imaging (MRI): Preffered for assessing the extent of brain injury, Diffusion-weighted imaging helps identify areas of acute hypoxic-ischemic injury, Computed tomography (CT): Limited use due to radiation exposure but may be used for hemorrhagic lesions. Electroencelography (EEG): Monitors brain activity and detect seizures or abnormal patterns, Amplitude-integrated EEG (aEEG) can provide continuous monitoring in NICUs. Echocardiography: Assesses cardiac function, which may be impaired in severe hypoxic-ischemic cases.
4.1 Supportive Diagnostic criteria:
Sarnat and Sarnat staging (for Hypoxic-Ischemic Encelopathy-HIE): Stage I (Mild): Hyperalertness, irritability, and mild hypotonia, normal EEG, Stage II (Moderate): Lethargy, Hypotonia, siezures, abnormal EEG, Stage III (Severe): Stupor/coma, flaccid tone, absent reflexes, severly abnormal EEG. Modified {Appearance, Pulse, Grimace, Activity and Respiration (APGAR)} score, Correlates with severity and likelihood of NE, if the score remains slow despite resuscitation. Management of Neonatal Encelopathy: The main goals of managing newborn Encelopathy (NE) are to cure the underlying causes, provide supportive care, and stop more brain damage. Hypoxic Ischemic Encelopathy (HIE) which is brought on by a reduction in blood or oxygen supply to the brain after birth, is frequently linked to NE.
Supportive care: Assistance with Respiration Ensure proper ventilation and oxygenation, Blood gases and oxygen saturation (SpO2) are continuously monitored, As required, administer more oxygen or ventilation (invasive or non-invasive). Support for the heart- Keep an eye on and maintain perfusion and blood pressure, To prevent fluid excess, use fluids sparingly, If necessary, give vasopressors (such as dopamine or dobutamine) to treat hypotension. Control of Temperature- Steer clear of hyperthermia since it can worsen brain damage. Keep your core temperature at a reasonable level (neutral thermal environment). Metabolic support & nutrition- First, administer parenteral nourishment, To avoid hypoglycemia or hyperglycemia, keep an eye on and control blood glucose level, Address electrolyte abnormalities, (such as calcium and sodium). Seizure management- Neonates with encelopathy are at risk for seizures, Monitor for clinical and sub-clinical seizures using amplitude-integrated EEG (aEEG) or continuous EEG, Treat seizures with antiepileptic drugs (e.g. phenobarbital, levetiracetam).
Fig. NO.- 2 Brain Seizure
Therapeutic Hypothermia (Cooling Therapy):The usual treatment for moderate to severe newborn Encelopathy bought on by hypoxic-ischemic damage is therapeutic hypothermia. Recommended for infants who are term or near-term (>36 weeks) and exhibit moderate to severe Encelopathy and perinatal asphyxia, To achieve the best neuroprotection, cooling must begin within six hours of delivery. Two Approaches- Head cooling that is selective (helmet based cooling). Identification and management of underlying causes- Infections: Treat with empiric antibiotics (e.g. ampicillin, gentamicin) if sepsis is suspected. Metabolic disorders: Screen and correct metabolic disturbances, Congenital anomalies: Evaluate structural abnormalities of the brain via imaging (e.g. MRI). Monitoring and Imaging - Neurological Examination Evaluate seizures, tone, reflexes, and degree of awareness, EEG/aEEG- Keep an eye out for seizures in brain activity. Imaging- Initial screening with cranial ultrasonography, Brain MRI to find patterns to brain damage (best at 5-7 days).
Because it can both have short-long term effects, Neonatal Encelopathy (NE) is a serious clinical illness that possess a substantial challenge in neonatal care. Although it has several different causes, the most prevalent one is Hypoxic ischemic encelopathy (HIE). To reduce neurological damage and enhance results, the problem need to be identified quickly and managed thoroughly. The ability to lessen brain damage in afflicted neonates has greatly improved because to development in diagnostic techniques like neuroimaging and electroencephalography as well as therapeutic measures like therapeutic hypothermia. Disparities in care still exist, nevertheless especially in low-resource environments where access to specialized newborn is still restricted. The severity of the illness, the underlying etiology, and the time and caliber of therapies all affect the long-term prognosis of newborn encelopathy. Optimizing neurodevelopmental outcomes requires early therapy interventions and multi-disciplinary follow up.
REFERENCES
Dewanjali Rathore*, Aryan Sahu, Shubham Deshmukh, Vivek sahu, Aditya kumar, Prince Suryavanshi, Understanding Neonatal Encephalopathy: Causes Symptoms, and Management, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 6, 1064-1070. https://doi.org/10.5281/zenodo.15605425