Hypoxic-ischemic encephalopathy (HIE) is brain injury caused by lack of oxygen and blood flow around the time of birth. It can cause death or long-term disabilities like cerebral palsy. Diagnosis is based on clinical presentation and lab/imaging findings. Cranial ultrasound and MRI are useful imaging modalities. HIE is characterized by Sarnat stages ranging from hyperalert to stuporous. Prognosis depends on severity - mild cases often have no complications while severe cases have high mortality or serious disabilities.
Neonatal encephalopathy is a clinical syndrome in newborns associated with hypoxic-ischemic injury to the brain near the time of birth. It is characterized by difficulties with maintaining respiration, hypotonia, altered consciousness, depressed reflexes, and sometimes seizures. Risk factors include complications of pregnancy, issues during labor and delivery, and problems with the placenta or umbilical cord. An evaluation includes the baby's history and exam findings as well as imaging studies, EEG, and laboratory tests to assess organ function and rule out other conditions. Management focuses on treatment of seizures and supportive care, with cooling therapy in moderate to severe cases aiming to reduce brain injury.
This document summarizes asphyxia neonatorum (hypoxic-ischemic encephalopathy), which can result from a lack of oxygen before, during, or after birth and cause permanent brain damage or death. Risk factors include fetal distress, cord compression, and respiratory failure after birth. Effects involve multiple organ systems. Diagnosis involves assessing factors like Apgar scores, MRI, and EEG. Treatment focuses on resuscitation, therapeutic hypothermia to reduce neurotoxicity, and careful management to prevent secondary issues. Prognosis depends on severity factors like initial pH and neurologic exam, with more severe cases having higher risks of death or impairment.
1) Hypoxic-ischemic encephalopathy (HIE) is brain injury caused by lack of oxygen and blood flow before, during, or after birth. It remains a serious condition that can cause death or long-term disabilities like cerebral palsy or intellectual impairment.
2) The document discusses the definition, risk factors, pathophysiology, clinical features based on the Sarnat staging system, diagnosis using imaging and EEG, and treatment approaches for HIE including supportive care, perfusion management, anti-seizure medications, and therapeutic hypothermia.
3) The goal of treatment is to prevent further brain injury by maintaining appropriate oxygenation, blood pressure, glucose levels, and treating seizures
Perinatal asphyxia refers to progressive hypoxia, hypercarbia and acidosis during birth. It can cause multi-organ dysfunction in neonates. The essential criteria for diagnosis are prolonged acidemia on cord blood, low Apgar scores for over 5 minutes, and neurological or multi-organ issues in the newborn period. Asphyxia is caused by factors that limit oxygen delivery to the fetus, such as placental insufficiency, cord accidents, difficult delivery, or postnatal cardiac or respiratory issues. The brain, heart, kidneys and lungs are most commonly affected. Treatment involves resuscitation, controlling seizures, avoiding hyperthermia, and therapeutic hypothermia within 6 hours of birth to reduce neurological
1) Birth asphyxia and hypoxic ischemic encephalopathy occur when there is impaired gas exchange or insufficient blood flow to the baby's brain during birth, leading to brain injury.
2) The document discusses the definitions, causes, effects on multiple organ systems, investigations, management including supportive care and therapeutic hypothermia, and long-term outcomes like cerebral palsy and developmental delays.
3) The goal of treatment is to maintain the baby's vital functions, optimize cardiac output and cerebral perfusion, control seizures, and use interventions to protect the brain such as therapeutic hypothermia.
This document provides an outline and overview of asphyxia management. It begins with definitions of related terms like anoxia, hypoxia, and discusses perinatal asphyxia. It then covers clinical features like signs seen in mild, moderate and severe hypoxic-ischemic encephalopathy. Investigations discussed include MRI, CT, ultrasound and EEG. Management involves supportive care, anticonvulsants, fluid management, glucose control and therapeutic hypothermia to reduce secondary brain injury.
Perinatal asphyxia, also known as birth asphyxia, is a common cause of neonatal mortality and morbidity worldwide. It occurs due to impaired gas exchange leading to hypoxemia and hypercarbia during labor or delivery. In India, 250,000-350,000 infants die each year due to birth asphyxia within the first three days of life. It can result in hypoxic-ischemic encephalopathy (HIE), a type of neonatal brain injury. The pathogenesis of HIE involves energy failure, excitotoxicity from glutamate, oxidative stress, and cell death mechanisms like necrosis and apoptosis. Specific patterns of brain injury seen in HIE include selective neuronal necrosis, parasagittal cerebral
Neonatal encephalopathy is a clinical syndrome in newborns associated with hypoxic-ischemic injury to the brain near the time of birth. It is characterized by difficulties with maintaining respiration, hypotonia, altered consciousness, depressed reflexes, and sometimes seizures. Risk factors include complications of pregnancy, issues during labor and delivery, and problems with the placenta or umbilical cord. An evaluation includes the baby's history and exam findings as well as imaging studies, EEG, and laboratory tests to assess organ function and rule out other conditions. Management focuses on treatment of seizures and supportive care, with cooling therapy in moderate to severe cases aiming to reduce brain injury.
This document summarizes asphyxia neonatorum (hypoxic-ischemic encephalopathy), which can result from a lack of oxygen before, during, or after birth and cause permanent brain damage or death. Risk factors include fetal distress, cord compression, and respiratory failure after birth. Effects involve multiple organ systems. Diagnosis involves assessing factors like Apgar scores, MRI, and EEG. Treatment focuses on resuscitation, therapeutic hypothermia to reduce neurotoxicity, and careful management to prevent secondary issues. Prognosis depends on severity factors like initial pH and neurologic exam, with more severe cases having higher risks of death or impairment.
1) Hypoxic-ischemic encephalopathy (HIE) is brain injury caused by lack of oxygen and blood flow before, during, or after birth. It remains a serious condition that can cause death or long-term disabilities like cerebral palsy or intellectual impairment.
2) The document discusses the definition, risk factors, pathophysiology, clinical features based on the Sarnat staging system, diagnosis using imaging and EEG, and treatment approaches for HIE including supportive care, perfusion management, anti-seizure medications, and therapeutic hypothermia.
3) The goal of treatment is to prevent further brain injury by maintaining appropriate oxygenation, blood pressure, glucose levels, and treating seizures
Perinatal asphyxia refers to progressive hypoxia, hypercarbia and acidosis during birth. It can cause multi-organ dysfunction in neonates. The essential criteria for diagnosis are prolonged acidemia on cord blood, low Apgar scores for over 5 minutes, and neurological or multi-organ issues in the newborn period. Asphyxia is caused by factors that limit oxygen delivery to the fetus, such as placental insufficiency, cord accidents, difficult delivery, or postnatal cardiac or respiratory issues. The brain, heart, kidneys and lungs are most commonly affected. Treatment involves resuscitation, controlling seizures, avoiding hyperthermia, and therapeutic hypothermia within 6 hours of birth to reduce neurological
1) Birth asphyxia and hypoxic ischemic encephalopathy occur when there is impaired gas exchange or insufficient blood flow to the baby's brain during birth, leading to brain injury.
2) The document discusses the definitions, causes, effects on multiple organ systems, investigations, management including supportive care and therapeutic hypothermia, and long-term outcomes like cerebral palsy and developmental delays.
3) The goal of treatment is to maintain the baby's vital functions, optimize cardiac output and cerebral perfusion, control seizures, and use interventions to protect the brain such as therapeutic hypothermia.
This document provides an outline and overview of asphyxia management. It begins with definitions of related terms like anoxia, hypoxia, and discusses perinatal asphyxia. It then covers clinical features like signs seen in mild, moderate and severe hypoxic-ischemic encephalopathy. Investigations discussed include MRI, CT, ultrasound and EEG. Management involves supportive care, anticonvulsants, fluid management, glucose control and therapeutic hypothermia to reduce secondary brain injury.
Perinatal asphyxia, also known as birth asphyxia, is a common cause of neonatal mortality and morbidity worldwide. It occurs due to impaired gas exchange leading to hypoxemia and hypercarbia during labor or delivery. In India, 250,000-350,000 infants die each year due to birth asphyxia within the first three days of life. It can result in hypoxic-ischemic encephalopathy (HIE), a type of neonatal brain injury. The pathogenesis of HIE involves energy failure, excitotoxicity from glutamate, oxidative stress, and cell death mechanisms like necrosis and apoptosis. Specific patterns of brain injury seen in HIE include selective neuronal necrosis, parasagittal cerebral
HIE has been one of the problems facing newborns due to birth asphyxia caused by variety of conditions during child birth or after childbirth, i hope the readers will learn something from the slides
Neonatal hypoxic-ischemic encephalopathy (HIE) occurs when the brain is damaged due to a lack of oxygen before, during, or after birth. It can cause long-term complications such as cerebral palsy, intellectual disability, epilepsy, or death. The document discusses the causes, clinical presentation, treatment, and prognosis of HIE, noting that outcomes depend on the severity of the brain injury and may include permanent neurological deficits or death. Imaging studies and supportive care aim to prevent further brain damage while treatments for seizures and cerebral edema can help reduce complications. Factors like abnormal clinical findings persisting over a week suggest a poor prognosis.
The document summarizes neonatal hypoxic-ischemic encephalopathy (HIE), including its causes, effects on organ systems, clinical manifestations at different stages of severity, imaging findings, treatment of seizures, and supportive care. HIE is caused by a lack of oxygen during birth and can lead to long-term neurological impairments or death. Clinical manifestations range from mild abnormalities to coma and seizures, depending on the severity of the injury. Imaging studies like MRI are useful for assessment. Treatment involves controlling seizures, maintaining oxygenation and blood pressure through supportive care.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can lead to death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful for showing patterns of brain injury. HIE management aims to prevent further brain damage through measures like temperature control and treating seizures, while newer treatments target excitotoxicity and oxidative stress.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can cause death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful to detect brain injury patterns. HIE management aims to prevent further brain damage through temperature control, seizure treatment, and potentially neuroprotective drugs. The condition remains a major cause of newborn mortality and morbidity.
Hypoxic ischemic insult, by prof Ayman Galhom, ass prof neurosurgery, Suez ca...mohamed osama hussein
This document discusses hypoxic ischemic brain injury in newborns. It begins by defining terms like HIE, hypoxia, ischemia and asphyxia. It then notes the problem magnitude, with HIE affecting 1-5/1000 term newborns and being a major cause of neonatal death and cerebral palsy. The document reviews investigation techniques like EEG, ultrasound, CT and MRI and their findings. It discusses cell death mechanisms and neuroprotective strategies like hypothermia, magnesium sulfate, xenon, and antioxidants. Overall, the document provides an overview of hypoxic ischemic brain injury in newborns, including causes, effects, diagnostic tools, and potential treatment strategies.
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord pH <7.0, 5-minute Apgar score of 0-3, or evidence of
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord pH <7.0, 5-minute Apgar score of 0-3, or evidence of
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord blood pH <7.0, Apgar score of 0-3 for more than 5 minutes,
Hypoxia-mediated selection leads to cells with diminished apoptotic potential. Cancer cells can die through either necrosis or apoptosis. Necrosis is unregulated cell death, while apoptosis is a regulated process of cell suicide. Apoptosis is triggered when DNA damage cannot be repaired. Bcl-2 proteins help determine whether a cell undergoes apoptosis or survives under hypoxic conditions. Diminished apoptotic potential allows cancer cells to survive hypoxia and evade cell death.
A 62-year-old hypertensive man collapsed after an argument and was unresponsive. He received CPR and defibrillation, regaining spontaneous circulation after 15 minutes. On examination, he showed extensor posturing and a Glasgow Coma Scale of 4. The likely diagnosis is hypoxic ischemic encephalopathy resulting from prolonged cardiac arrest. HIE causes acute global brain injury from reduced blood flow and oxygen. Neuroimaging may show injury to basal ganglia, thalami, cortex and cerebellum due to their susceptibility. The prognosis based on the neurologic exam is poor due to the severity of findings.
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis. It is diagnosed based on an umbilical cord blood pH less than 7.0.
2) Hypoxic ischemic encephalopathy (HIE) is the term used for abnormal neurological behavior in newborns caused by birth asphyxia. It can lead to neonatal death or long term complications like cerebral palsy or developmental delays.
3) Management of severe HIE includes therapeutic hypothermia within 6 hours of birth to reduce the infant's temperature to 33.5°C, as well as
Perinatal asphyxia is caused by lack of oxygen or poor perfusion to organs in fetuses or newborns. It is defined by criteria like low umbilical cord pH, low Apgar scores, seizures or multiorgan dysfunction in newborns. It can cause neurological injuries like selective neuronal necrosis or periventricular leukomalacia. Management involves maintaining normal temperature, oxygenation, blood pressure, blood glucose and treating seizures. Outcomes are predicted by factors like lack of breathing at birth or severe hypoxic ischemic encephalopathy.
This case discusses a 22-month-old female patient diagnosed with asymmetric dyskinetic cerebral palsy. MRI images show bilateral cystic necrosis of the lateral putamen and globus pallidus, likely due to perinatal hypoxia/ischemia. This resulted in an extrapyramidal form of cerebral palsy. Cerebral palsy is caused by nonprogressive brain defects or lesions early in development. Perinatal factors cause 70-80% of cases. Basal ganglia injury can result in dyskinetic cerebral palsy phenotypes.
This document discusses asphyxia of the newborn. It defines asphyxia and lists its incidence and risk factors. It describes methods to detect infants at risk and the potential consequences of asphyxia, which can include death, organ dysfunction, or long-term neurological effects. The prediction of outcome is difficult, though grading of encephalopathy and EEG abnormalities provide guidance. Interventions discussed include appropriate resuscitation and monitoring, as well as treatments for complications. Hypothermia treatment is proven to help decrease the severity of hypoxic ischemic encephalopathy.
Metabolic disoders internal medicine and neuroscienceNeilVincentDeAsis
This document discusses acquired metabolic disorders of the nervous system that result from failure of other organ systems. It focuses on hypoxic-ischemic encephalopathy, where lack of oxygen and blood flow to the brain causes global disturbance of cerebral function. The main causes are discussed as well as the clinical features and progression from confusion to stupor and coma. Laboratory tests that can help identify potential causes are also outlined.
Hepatic encephalopathy is a syndrome characterized by personality changes, impaired intellect, and depressed consciousness that occurs in patients with cirrhosis of the liver. An important prerequisite is the diversion of portal blood into systemic circulation through portosystemic shunts. Subtle signs are seen in 70% of cirrhosis patients, with symptoms debilitating in 24-53% of those with portosystemic shunt surgery. Triphasic waves seen on EEGs are nonspecific but classic for hepatic encephalopathy. While commonly caused by hepatic or renal failure, triphasic waves can result from various toxic, metabolic, or structural abnormalities.
Clinically, more term babies suffered from hypoxic ischemic encephalopathy (HIE) than premature babies. However, pathologically, more premature babies suffered from HIE than term babies. HIE manifests clinically as symptoms of consciousness changes that can be excitatory like seizures or depressing like coma. Treatment of HIE focuses on monitoring, controlling seizures, maintaining circulation and glucose levels, with therapies like hypothermia and investigates like amplitude integrated EEG shown to improve outcomes. The prognosis depends on the severity of brain damage and treatment, with mild cases often having a full recovery but severe cases having a high risk of mortality or neurological sequele like cerebral palsy.
HIE has been one of the problems facing newborns due to birth asphyxia caused by variety of conditions during child birth or after childbirth, i hope the readers will learn something from the slides
Neonatal hypoxic-ischemic encephalopathy (HIE) occurs when the brain is damaged due to a lack of oxygen before, during, or after birth. It can cause long-term complications such as cerebral palsy, intellectual disability, epilepsy, or death. The document discusses the causes, clinical presentation, treatment, and prognosis of HIE, noting that outcomes depend on the severity of the brain injury and may include permanent neurological deficits or death. Imaging studies and supportive care aim to prevent further brain damage while treatments for seizures and cerebral edema can help reduce complications. Factors like abnormal clinical findings persisting over a week suggest a poor prognosis.
The document summarizes neonatal hypoxic-ischemic encephalopathy (HIE), including its causes, effects on organ systems, clinical manifestations at different stages of severity, imaging findings, treatment of seizures, and supportive care. HIE is caused by a lack of oxygen during birth and can lead to long-term neurological impairments or death. Clinical manifestations range from mild abnormalities to coma and seizures, depending on the severity of the injury. Imaging studies like MRI are useful for assessment. Treatment involves controlling seizures, maintaining oxygenation and blood pressure through supportive care.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can lead to death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful for showing patterns of brain injury. HIE management aims to prevent further brain damage through measures like temperature control and treating seizures, while newer treatments target excitotoxicity and oxidative stress.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can cause death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful to detect brain injury patterns. HIE management aims to prevent further brain damage through temperature control, seizure treatment, and potentially neuroprotective drugs. The condition remains a major cause of newborn mortality and morbidity.
Hypoxic ischemic insult, by prof Ayman Galhom, ass prof neurosurgery, Suez ca...mohamed osama hussein
This document discusses hypoxic ischemic brain injury in newborns. It begins by defining terms like HIE, hypoxia, ischemia and asphyxia. It then notes the problem magnitude, with HIE affecting 1-5/1000 term newborns and being a major cause of neonatal death and cerebral palsy. The document reviews investigation techniques like EEG, ultrasound, CT and MRI and their findings. It discusses cell death mechanisms and neuroprotective strategies like hypothermia, magnesium sulfate, xenon, and antioxidants. Overall, the document provides an overview of hypoxic ischemic brain injury in newborns, including causes, effects, diagnostic tools, and potential treatment strategies.
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord pH <7.0, 5-minute Apgar score of 0-3, or evidence of
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord pH <7.0, 5-minute Apgar score of 0-3, or evidence of
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis as evidenced by an umbilical cord arterial blood pH <7.0.
2) It can cause hypoxic ischemic encephalopathy (HIE) and multi-organ damage in newborns. Long term sequelae of birth asphyxia include cerebral palsy, cognitive delays, seizures, and visual/auditory processing difficulties.
3) Diagnosis is based on criteria such as an umbilical cord blood pH <7.0, Apgar score of 0-3 for more than 5 minutes,
Hypoxia-mediated selection leads to cells with diminished apoptotic potential. Cancer cells can die through either necrosis or apoptosis. Necrosis is unregulated cell death, while apoptosis is a regulated process of cell suicide. Apoptosis is triggered when DNA damage cannot be repaired. Bcl-2 proteins help determine whether a cell undergoes apoptosis or survives under hypoxic conditions. Diminished apoptotic potential allows cancer cells to survive hypoxia and evade cell death.
A 62-year-old hypertensive man collapsed after an argument and was unresponsive. He received CPR and defibrillation, regaining spontaneous circulation after 15 minutes. On examination, he showed extensor posturing and a Glasgow Coma Scale of 4. The likely diagnosis is hypoxic ischemic encephalopathy resulting from prolonged cardiac arrest. HIE causes acute global brain injury from reduced blood flow and oxygen. Neuroimaging may show injury to basal ganglia, thalami, cortex and cerebellum due to their susceptibility. The prognosis based on the neurologic exam is poor due to the severity of findings.
1) Birth asphyxia, also known as perinatal asphyxia, refers to impaired gas exchange during birth that leads to hypoxemia, hypercarbia, and fetal acidosis. It is diagnosed based on an umbilical cord blood pH less than 7.0.
2) Hypoxic ischemic encephalopathy (HIE) is the term used for abnormal neurological behavior in newborns caused by birth asphyxia. It can lead to neonatal death or long term complications like cerebral palsy or developmental delays.
3) Management of severe HIE includes therapeutic hypothermia within 6 hours of birth to reduce the infant's temperature to 33.5°C, as well as
Perinatal asphyxia is caused by lack of oxygen or poor perfusion to organs in fetuses or newborns. It is defined by criteria like low umbilical cord pH, low Apgar scores, seizures or multiorgan dysfunction in newborns. It can cause neurological injuries like selective neuronal necrosis or periventricular leukomalacia. Management involves maintaining normal temperature, oxygenation, blood pressure, blood glucose and treating seizures. Outcomes are predicted by factors like lack of breathing at birth or severe hypoxic ischemic encephalopathy.
This case discusses a 22-month-old female patient diagnosed with asymmetric dyskinetic cerebral palsy. MRI images show bilateral cystic necrosis of the lateral putamen and globus pallidus, likely due to perinatal hypoxia/ischemia. This resulted in an extrapyramidal form of cerebral palsy. Cerebral palsy is caused by nonprogressive brain defects or lesions early in development. Perinatal factors cause 70-80% of cases. Basal ganglia injury can result in dyskinetic cerebral palsy phenotypes.
This document discusses asphyxia of the newborn. It defines asphyxia and lists its incidence and risk factors. It describes methods to detect infants at risk and the potential consequences of asphyxia, which can include death, organ dysfunction, or long-term neurological effects. The prediction of outcome is difficult, though grading of encephalopathy and EEG abnormalities provide guidance. Interventions discussed include appropriate resuscitation and monitoring, as well as treatments for complications. Hypothermia treatment is proven to help decrease the severity of hypoxic ischemic encephalopathy.
Metabolic disoders internal medicine and neuroscienceNeilVincentDeAsis
This document discusses acquired metabolic disorders of the nervous system that result from failure of other organ systems. It focuses on hypoxic-ischemic encephalopathy, where lack of oxygen and blood flow to the brain causes global disturbance of cerebral function. The main causes are discussed as well as the clinical features and progression from confusion to stupor and coma. Laboratory tests that can help identify potential causes are also outlined.
Hepatic encephalopathy is a syndrome characterized by personality changes, impaired intellect, and depressed consciousness that occurs in patients with cirrhosis of the liver. An important prerequisite is the diversion of portal blood into systemic circulation through portosystemic shunts. Subtle signs are seen in 70% of cirrhosis patients, with symptoms debilitating in 24-53% of those with portosystemic shunt surgery. Triphasic waves seen on EEGs are nonspecific but classic for hepatic encephalopathy. While commonly caused by hepatic or renal failure, triphasic waves can result from various toxic, metabolic, or structural abnormalities.
Clinically, more term babies suffered from hypoxic ischemic encephalopathy (HIE) than premature babies. However, pathologically, more premature babies suffered from HIE than term babies. HIE manifests clinically as symptoms of consciousness changes that can be excitatory like seizures or depressing like coma. Treatment of HIE focuses on monitoring, controlling seizures, maintaining circulation and glucose levels, with therapies like hypothermia and investigates like amplitude integrated EEG shown to improve outcomes. The prognosis depends on the severity of brain damage and treatment, with mild cases often having a full recovery but severe cases having a high risk of mortality or neurological sequele like cerebral palsy.
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3. Background
• Despite major advances in monitoring technology and knowledge of
fetal and neonatal pathologies, perinatal asphyxia or, more
appropriately, hypoxic-ischemic encephalopathy (HIE), remains a
serious condition that causes significant mortality and long-term
morbidity.
• Hypoxic-ischemic encephalopathy is characterized by clinical and
laboratory evidence of acute or subacute brain injury due to asphyxia
(ie, hypoxia, acidosis). Most often, the exact timing and underlying
cause remain unknown.
4. Definition
• Anoxia
is a term used to indicate the consequences of complete lack of oxygen as a
result of a number of primary causes
• Hypoxia
refers to an arterial concentration of oxygen that is less than normal
• Ischemia
refers to blood flow to cells or organs that is insufficient to maintain their
normal function
Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic
resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:461
5. • Hypoxic-ischemic encephalopathy
Is an abnormal neurobehavioral state in which the predominant pathogenic
mechanism is impaired cerebral blood flow that may result in neonatal
death or be manifested later as cerebral palsy or mental deficiency.
1996 guidelines from the AAP and ACOG for hypoxic-ischemic encephalopathy
(HIE)
• Profound metabolic or mixed acidemia (pH < 7) in an umbilical artery blood
sample, if obtained
• Persistence of an Apgar score of 0-3 for longer than 5 minutes
• Neonatal neurologic sequelae (eg, seizures, coma, hypotonia)
• Multiple organ involvement (eg, kidney, lungs, liver, heart, intestines
Nelson Textbook of Pediatrics 19th ed.2010 . pages 566 - 568
6. Epidimiology
• Frequency
a) Birth asphyxia is the cause of 23% of all neonatal deaths worldwide.
b) It is one of the top 20 leading causes of burden of disease in all age
groups by the World Health Organization.
c) It is the fifth largest cause of death of children younger than 5 years (8%)
d) More than a million children who survive birth asphyxia develop
problems such as cerebral palsy, mental retardation, learning
difficulties, and other disabilities.
Bryce J, Boschi-Pinto C, Shibuya K, Black RE. WHO estimates of the causes of death in
children. Lancet. Mar 26-Apr 1 2005;365(9465):1147-52.
7. • Mortality/Morbidity:
a) In severe hypoxic-ischemic encephalopathy, the mortality rate is
reportedly 25-50%.
b) As many as 80% of infants who survive severe hypoxic-ischemic
encephalopathy develop serious complications, 10-20% develop
moderately serious disabilities, and as many as 10% are healthy.
c) The infants who survive moderately severe hypoxic-ischemic
encephalopathy, 30-50% may have serious long-term complications, and
10-20% have minor neurological morbidities.
d) Infants with mild hypoxic-ischemic encephalopathy tend to be free from
serious CNS complications.
Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head cooling with mild systemic
hypothermia after neonatal encephalopathy: multicenter randomised trial. Lancet.
2005;365:663-70.
8. • Race
No predilection is noted.
• Sex
No predilection is observed.
• Age
Most often, the condition is noted in infants who are term at birth.
van Handel M, Swaab H, de Vries LS, Jongmans MJ. Long-term cognitive and
behavioral consequences of neonatal encephalopathy following perinatal asphyxia: a
review. Eur J Pediatr. Jul 2007;166(7):645-54
12. Fetal response to asphyxia illustrating the initial redistribution of blood
flow to vital organs. With prolonged asphyxial insult and failure of
compensatory mechanisms, cerebral blood flow falls, leading to ischemic
brain injury.
13. Pathophysiology of hypoxic-
ischemic brain injury in the
developing brain. During the
initial phase of energy
failure, glutamate mediated
excitotoxicity and Na+/K+
ATPase failure lead to necrotic
cell death. After transient
recovery of cerebral energy
metabolism, a secondary
phase of apoptotic neuronal
death occurs. ROS = Reactive
oxygen species.
14. Clinical features- Sarnat Staging System
Stage 1 Stage 2 Stage 3
Level of
conciousness
Hyperalert Lethargic/obtunded Stuporous
Neuromuscular control
Muscle tone Normal Mild hypotonia Flaccid
Posture Mild distal flexion Strong distal flexion Intermittent
decerebration
Stretch reflex Overactive Overactive Decreased/absent
Segmental
myoclonus
Present Present Absent
Complex Reflexes
Suck Weak Weak/absent Absent
Moro Strong, low
threshold
Weak; incomplete,
high threshold
Absent
Oculovestibular Normal Overactive Weak/absent
Tonic neck Slight Strong Absent
15. Autonomic
function
Generalised
sympathetic
Generalised
parasympathetic
Both systems
depressed
Pupils Mydriasis Miosis Variable;ofetn
unequal;poor light
reflex
Heart rate Tachycardia Bradycardia Variable
Bronchial &
salivary secretions
Sparse Profuse Variable
GI motility Normal/decreased Increased,diarrhea Variable
Seizures None Common; focal /
multifocal
Uncommon
EEG Normal Early : low voltage
continuous delta &
theta.
Later: periodic
pattern
Seizures: focal 1 Hz
spike and wave
Early: periodic with
isopotential phases.
Later: totally
isopotential
Duration 1-3 days 2-14 days Hours . weeks
16. Diagnosis
• There are nor specific tests to confirm or exclude a diagnosis of hypoxic-
ischemic encephalopathy (HIE) because the diagnosis is made based on
the history, physical and neurological examinations, and laboratory
evidence.
• Laboratory studies include :-
Study
Serum electrolyte Markedly low serum sodium, potassium, and chloride levels in
the presence of reduced urine flow and excessive weight gain
may indicate acute tubular damage or (SIADH) secretion,
particularly during the initial 2-3 days of life.
Renal function Serum creatinine levels, creatinine clearance, and BUN levels
Cardiac & liver enzymes Assess the degree of hypoxic-ischemic injury to other organs
Coagulation system Prothrombin time, partial thromboplastin time, and fibrinogen
levels.
ABG Assess acid-base status and to avoid hyperoxia and hypoxia as
well as hypercapnia and hypocapnia.
17. Imaging studies:-
Cranial US:
a) Convenient, noninvasive, relatively low-cost
and non –radiation screening examination
of the hemodynamically unstable neonate
at the bedside.
b) Doppler study and resistive index (RI)
provide additional information on cerebral
perfusion.
c) RI decreases with increasing gestational
age, and thus correlation with gestational
age is necessary for accurate interpretation
of RI results.
d) Decreased RI is abnormal & is postulated to
be caused by impairment in cerebral
autoregulation.
e) Sustained asphyxia & ICH or diffuse cerebral
edema results in increased RI and is
indicative of a poor outcome.
PV-cysts (swiss cheese
appearance)
18. Cranial CT:
a) CT technology provides a
rapid mode of screening for
ICH & hydrocephalus in a sick
neonate without the need for
sedation.
b) CT is the least sensitive
modality for evaluation of HIE
because of poor parenchymal
contrast resolution due to:
high water content in the
neonatal brain.
high protein content of the
cerebrospinal fluid, which
result in.
CT has the inherent
disadvantage of radiation
exposure.
Unenhanced CT scan shows diffuse cortical swelling
and hypoattenuation in the white matter relative to
areas of preserved cortex, A small amount of
extraaxial hemorrhage adjacent to the left frontal
lobe is also seen (arrow).
19. Cranial MRI
a) The most sensitive and
specific imaging technique
for examining infants with
suspected hypoxic-
ischemic brain injury.
b) Hypoxic-ischemic injury
(deep grey
matter,cortex)demonstrat
es characteristic T1
hyperintensity and
variable T2 intensity.
c) Ischemic injury generally
results in T1 hypointensity
&T2 hyperintensity (white
matter)due to ischemia-
induced edema.
relatively subtle increases in signal intensity in the perirolandic
regions, posterior aspect of the putamen, lateral aspects of the
thalamus, and corpus callosum.
Bottom: show diffuse abnormally high signal intensity in the
supratentorial parenchyma in comparison with the superior
aspect of the cerebellum, which has normal signal intensity.
20. Histological findings
Bilateral acute infarctions of the frontal lobe are shown.
The infarctions depicted in the figure (arrows) are
consistent with watershed infarctions secondary to global
hypoperfusion.
presence of pyknotic and hyperchromatic
nuclei, the loss of cytoplasmic Nissl
substance, and neuronal shrinkage and
angulation (arrow). These alterations begin to
appear approximately 6 hours following hypoxic-
ischemic insult.
21. Reactive astrocytosis is evident approximately
24-48 hours after the primary hypoxic-ischemic
event.
Periventricular leukomalacia is depicted.
Note the extensive hemorrhage within the cystic space as well
as the hemosiderin-laden macrophages around the lesional
rim.
22. Other studies
Amplitude-integrated electroencephalography (aEEG)
a) The abnormalities seen in infants with moderate-to-severe hypoxic-
ischemic encephalopathy include the following:
b) Discontinuous tracing characterized by a lower margin below 5 mV and
an upper margin above 10 mV
c) Burst suppression pattern characterized by a background with minimum
amplitude (0-2 mV) without variability and occasional high voltage bursts
(>25 mV)
d) Continuous low voltage pattern characterized by a continuous low
voltage background (< 5 mV)
e) Inactive pattern with no detectable cortical activity
f) Seizures, usually seen as an abrupt rise in both the lower and upper
margin
23. Standard EEG
Generalized depression of the background rhythm and
voltage, with varying degrees of superimposed seizures, are
early findings. EEG characteristics associated with abnormal
outcomes include
a) background amplitude of less than 30 mV.
b) interburst interval of more than 30 seconds.
c) electrographic seizures.
d) absence of sleep-wake cycle at 48 hours.
24. Treatment
Medical care
a) Initial Resuscitation and Stabilization-
• Delivery room management follows standard Neonatal Resuscitation
Program (NRP) guidelines. Close attention should be paid to appropriate
oxygen delivery, perfusion status, and avoidance of hypoglycemia and
hyperthermia.
• A lot of attention is currently focused on resuscitation with room air
versus 100% oxygen in the delivery room. Several clinical trials indicate
that room air resuscitation for infants with perinatal asphyxia is as
effective as resuscitation with 100% oxygen.
• International Liaison Committee on Resuscitation (ILCOR)
recommendations include initiating neonatal resuscitation with
concentrations of oxygen between 21-100%
Guideline] Ten VS, Matsiukevich D. Room air or 100% oxygen for
resuscitation of infants with perinatal depression. Curr Opin Pediatr. Apr
2009;21(2):188-93
25. b) Supportive Care in Patients with Hypoxic-ischemic
Encephalopathy
• Most infants with severe hypoxic-ischemic encephalopathy need
ventilatory support during first days of life.
• The role of mechanical ventilation is to maintain the blood gases and
acid-base status in the physiological ranges and prevent
hypoxia, hyperoxia, hypercapnia, and hypocapnia.
• Infants with hypoxic-ischemic encephalopathy are also at risk for
pulmonary hypertension and should be monitored. Nitric oxide (NO) may
be used according to published guidelines.
[Guideline] American Academy of Pediatrics. Committee on Fetus and Newborn. Use of
inhaled nitric oxide. Pediatrics. Aug 2000;106(2 Pt 1):344-5.
26. c) Perfusion and Blood Pressure Management
• A mean blood pressure (BP) above 35-40 mm Hg is necessary to avoid
decreased cerebral perfusion.
• Hypotension is common in infants with severe hypoxic-ischemic
encephalopathy and is due to myocardial dysfunction, capillary leak
syndrome, and hypovolemia; hypotension should be promptly treated.
• Dopamine or dobutamine can be used to achieve adequate cardiac
output in these patients. Avoiding iatrogenic hypertensive episodes is also
important.
27. d) Fluid and Electrolytes Management
• Prophylactic theophylline, given early after birth helps in reducing renal
dysfunction
• A single dose of theophylline (5-8 mg/kg) given within 1 hour of birth resulted in
(1) decreased severe renal dysfunction (defined as creatinine level >1.5 mg/dL for 2
consecutive days);
(2) increased creatine clearance;
(3) increased glomerular filtration rate (GFR); and
(4) decreased b2 microglobulin excretion.
• Avoid hypoglycemia and hyperglycemia because both may accentuate brain
damage.
Jenik AG, Ceriani Cernadas JM, Gorenstein A, et al. A randomized, double-blind, placebo-controlled trial of
the effects of prophylactic theophylline on renal function in term neonates with perinatal
asphyxia.Pediatrics. 2000;105:E45
28. e) Treatment of Seizures
• Hypoxic-ischemic encephalopathy is the most common cause of seizures
in the neonatal period.
• Current therapies available to treat neonates with seizures include
phenobarbital, phenytoin, and benzodiazepines.
• Phenobarbital has been shown to be effective in only 29-50% of cases,
• Phenytoin only offers an additional 15% efficacy.
• Benzodiazepines, particularly lorazepam, may offer some additional
efficacy
Boylan GB, Rennie JM, Chorley G, et al. Second-line anticonvulsant treatment of neonatal
seizures: a video-EEG monitoring study. Neurology. Feb 10 2004;62(3):486-8.
30. f) Hypothermia Therapy
• Mild hypothermia (3-4°C below baseline temperature) applied within a few hours
(no later than 6 h) of injury is neuroprotective. Possible mechanisms include
(1) reduced metabolic rate and energy depletion;
(2) decreased excitatory transmitter release;
(3) reduced alterations in ion flux;
(4) reduced apoptosis due to hypoxic-ischemic encephalopathy; and
(5) reduced vascular permeability, edema, and disruptions of blood-brain barrier
functions.
• Therapeutic hypothermia when applied within 6 hours of birth and maintained for
48-72 hours is a promising therapy for mild-to-moderate cases of hypoxic-ischemic
encephalopathy.
Best Evidence] Azzopardi DV, Strohm B, Edwards AD, et al. Moderate hypothermia to treat
perinatal asphyxial encephalopathy. N Engl J Med. Oct 1 2009;361(14):1349-58.
31. h) Diet
• In most cases, the infant is restricted to nothing by mouth (NPO) during
the first 3 days of life or until the general level of alertness and
consciousness improves.
• In addition, infants undergoing hypothermia therapy should remain NPO
until rewarmed. Enteral feeds should be carefully initiated and the use of
trophic feeds is initially advisable (about 5 mL every 3-4 h).
• Infants should be monitored carefully for signs and symptoms of
necrotizing enterocolitis, for which infants with perinatal asphyxia are at
high risk.
33. Surgical care
• In cases of posterior cranial fossa hematoma, surgical
drainage may be lifesaving if no additional pathologies are
present.
Further Inpatient Care
• Close physical therapy and developmental evaluations are
needed prior to discharge in patients with hypoxic-ischemic
encephalopathy (HIE).
34. Further Outpatient Care
• The goal of follow-up is to detect impairments and promote early
intervention for those infants who require it.
• Growth parameters including head circumference should be closely
monitored in all infants with hypoxic-ischemic encephalopathy.
• In infants diagnosed with moderate-to-severe hypoxic-ischemic
encephalopathy with either abnormal neurologic examination findings or
feeding difficulties, intensive follow-up is recommended. include follow-up
by developmental pediatrician and pediatric neurologic.
• In infants with moderate hypoxic-ischemic encephalopathy but no feeding
difficulties and normal neurologic examination findings, routine care is
appropriate.
35. Prognosis
• Lack of spontaneous respiratory effort within 20-30 minutes of birth is
almost always associated with death.
• The presence of seizures is an ominous sign.
• Abnormal clinical neurological findings persisting beyond the first 7-10
days of life usually indicate poor prognosis.
• EEG at about 7 days that reveals normal background activity is a good
prognostic sign.
• Persistent feeding difficulties, which generally are due to abnormal tone of
the muscles of sucking and swallowing, also suggest significant CNS
damage.
• Poor head growth during the postnatal period and the first year of life is a
sensitive finding predicting higher frequency of neurologic deficits.
Patel J, Edwards AD. Prediction of outcome after perinatal asphyxia. Curr Opin Pediatr. Apr
1997;9(2):128-32.