HYPOXIC ISCHEMIC Encephalopathy

Hypoxic-ischemic encephalopathy (HIE)

A brain injury caused by oxygen deprivation, also known as intrapartum asphyxia.

Primary energy failure

The initial phase of hypoxic-ischemic injury occurring 0-6 hours after the insult, resulting in compromised cardiac contractility and energy metabolism.

Secondary energy failure

A phase occurring 7 to 72 hours after the hypoxic-ischemic insult, featuring increased neurotransmitter release and mitochondrial dysfunction.

Tertiary phase

The phase occurring 72 hours after hypoxic-ischemic injury, lasting from days to months, with possible recovery or continued deterioration.

Therapeutic hypothermia

A neuroprotective treatment involving controlled cooling of the body temperature to reduce metabolic rates and protect brain tissue post-injury.

Excitatory amino acids (EAA)

Chemical messengers released during hypoxic conditions that can lead to neurotoxicity, particularly glutamate.

Cerebral blood flow (CBF)

The amount of blood that flows through the brain's blood vessels, significantly affected by hypoxic-ischemic events.

Apoptosis

A form of programmed cell death that can be triggered in neurons following hypoxic-ischemic injury.

Metabolic acidosis

A condition where the body has an excess of acid, often seen in severe hypoxic-ischemic injury.

Apgar score

A quick test performed on newborns soon after birth to assess their physical condition; low scores can indicate severe conditions like HIE.

What occurs during hypoxic-ischemic encephalopathy (HIE)?

HIE is a brain injury caused by a lack of oxygen, often seen during birth.

What is the initial phase of hypoxic-ischemic injury called?

The initial phase is known as primary energy failure, occurring within the first 6 hours.

What happens during secondary energy failure?

This phase occurs 7 to 72 hours post-injury, marked by neurotransmitter release and mitochondrial dysfunction.

How long does the tertiary phase last after hypoxic-ischemic injury?

The tertiary phase can last from days to months and may result in recovery or ongoing deterioration.

What is the purpose of therapeutic hypothermia?

Therapeutic hypothermia reduces metabolic rates to protect brain tissue following an injury.

What are excitatory amino acids (EAA)?

EAA are neurotransmitters, such as glutamate, that can cause neurotoxicity during hypoxic conditions.

How does cerebral blood flow (CBF) change during hypoxic-ischemic events?

CBF decreases significantly during hypoxic-ischemic events, impacting brain function.

What triggers apoptosis in neurons?

Apoptosis can be triggered in neurons following hypoxic-ischemic injury.

What is metabolic acidosis?

Metabolic acidosis is an excess of acid in the body, commonly seen in severe hypoxic-ischemic injury.

What does a low Apgar score indicate?

A low Apgar score in newborns can indicate severe conditions such as hypoxic-ischemic encephalopathy (HIE).

What is the primary cause of hypoxic-ischemic encephalopathy (HIE)?

The primary cause of HIE is oxygen deprivation during birth.

What time frame is considered for the primary energy failure phase?

The primary energy failure phase occurs within the first 0-6 hours after injury.

Which neurotransmitter is primarily associated with neurotoxicity during hypoxia?

Glutamate is the primary neurotransmitter associated with neurotoxicity during hypoxia.

What physiological changes occur in CBF during a hypoxic-ischemic event?

Cerebral blood flow (CBF) significantly decreases during a hypoxic-ischemic event.

What is a common symptom of severe metabolic acidosis?

Common symptoms of severe metabolic acidosis include rapid breathing and confusion.

What role does mitochondrial dysfunction play in secondary energy failure?

Mitochondrial dysfunction during secondary energy failure leads to impaired cellular energy production.

How can therapeutic hypothermia benefit a patient with HIE?

Therapeutic hypothermia can prevent further brain injury by reducing metabolic demand.

What is the significance of the Apgar score in newborns?

The Apgar score assesses the newborn's physical condition and determines the need for immediate medical intervention.

What is the expected outcome during the tertiary phase of HIE?

The tertiary phase may lead to either recovery or continued neurological deterioration.

What are the potential long-term effects of HIE?

Potential long-term effects of HIE include cognitive impairments and motor skill delays.

What are common diagnostic methods for HIE?

Common diagnostic methods include clinical examination, imaging, and monitoring Apgar scores.

How does hypoxia affect the neuronal cell membrane?

Hypoxia can lead to changes in ion permeability of the neuronal cell membrane, disrupting normal function.

What interventions are recommended immediately after birth for HIE?

Immediate interventions may include resuscitation and monitoring vital signs.

What is the role of excitatory amino acids in the brain during hypoxia?

Excitatory amino acids can lead to overstimulation of neurons, causing cell injury.

How is HIE typically diagnosed?

HIE is typically diagnosed through clinical assessment combined with imaging studies.

In what ways can early intervention improve outcomes for patients with HIE?

Early intervention can improve brain function and reduce long-term disabilities.

What is the therapeutic target of hypothermia in treating HIE?

The therapeutic target of hypothermia is to lower the brain's metabolic rate.

What is meant by programmed cell death in the context of HIE?

Programmed cell death refers to apoptosis triggered by the brain injury in HIE.

What types of monitoring are used in the management of HIE?

Monitoring may include neurological assessments and imaging to track brain health.

What is the relationship between glucose levels and HIE outcomes?

Low glucose levels during HIE can worsen outcomes and brain injury.