<aside>

Hypoxic-ischemic encephalopathy (HIE) is a type of global brain injury resulting from reduced oxygen (hypoxia) and impaired cerebral perfusion (ischemia). It most commonly affects neonates following perinatal asphyxia, but also occurs in adults (e.g., post-cardiac arrest, near-drowning, asphyxiation).

</aside>

https://www.youtube.com/watch?v=s9SXf3nSeOw

Etiopathology

![Schematic Overview of the Pathophysiological Features of Hypoxic-Ischemic Encephalopathy

Douglas-Escobar M, Weiss MD. Hypoxic-Ischemic Encephalopathy. JAMA Pediatrics. 2015;169(4):397-397. doi:https://doi.org/10.1001/jamapediatrics.2014.3269](attachment:aae06288-0522-4708-9190-3e046edd5d5b:image.png)

Schematic Overview of the Pathophysiological Features of Hypoxic-Ischemic Encephalopathy

Douglas-Escobar M, Weiss MD. Hypoxic-Ischemic Encephalopathy. JAMA Pediatrics. 2015;169(4):397-397. doi:https://doi.org/10.1001/jamapediatrics.2014.3269

Neonatal HIE Adult HIE
• Perinatal asphyxia
• Placental abruption
• Umbilical cord prolapse/compression
• Uterine rupture
• Maternal hypotension or hypoxia • Cardiac arrest (most common)
• Near-drowning
• Hanging/strangulation
• Carbon monoxide poisoning
• Hypoglycemia or severe hypotension

Pathophysiology:

![Schematic illustration of pathophysiology of HIE in relation to hypoxic ischemic (HI) insult resulting in primary (acute phase) and secondary energy failure (secondary phase) in the brain. Brain damage (tertiary phase) continues to occur months to years after the injury resulting in decreased plasticity and reduced number of neurons. Latent period following resuscitation is ideal for interventions to decrease the impact of secondary energy failure. However, strategies are developed to attenuate tertiary brain damage which will expand the therapeutic window, substantially increasing the beneficial effects of neuroprotection in these infants and hence its impact on long-term outcomes. CBF—cerebral blood flow; ATP—Adenosine tri phosphate; NT—neurotransmitters.

Nair J, Kumar VHS. Current and Emerging Therapies in the Management of Hypoxic Ischemic Encephalopathy in Neonates. Children. 2018; 5(7):99. https://doi.org/10.3390/children5070099](attachment:03918718-820e-4a16-95a6-475ec0ea06b2:children-05-00099-g001.png)

Schematic illustration of pathophysiology of HIE in relation to hypoxic ischemic (HI) insult resulting in primary (acute phase) and secondary energy failure (secondary phase) in the brain. Brain damage (tertiary phase) continues to occur months to years after the injury resulting in decreased plasticity and reduced number of neurons. Latent period following resuscitation is ideal for interventions to decrease the impact of secondary energy failure. However, strategies are developed to attenuate tertiary brain damage which will expand the therapeutic window, substantially increasing the beneficial effects of neuroprotection in these infants and hence its impact on long-term outcomes. CBF—cerebral blood flow; ATP—Adenosine tri phosphate; NT—neurotransmitters.

Nair J, Kumar VHS. Current and Emerging Therapies in the Management of Hypoxic Ischemic Encephalopathy in Neonates. Children. 2018; 5(7):99. https://doi.org/10.3390/children5070099

Histopathology:

![Comparison of brain areas between normal and damaged brains.

She H-Q, Sun Y-F, Chen L, Xiao Q-X, Luo B-Y, Zhou H-S, Zhou D, Chang Q-Y and Xiong L-L (2023) Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities. Front. Neurosci. 17:1136500. doi: 10.3389/fnins.2023.1136500](attachment:cf95adde-5202-41ee-8b11-deaf5c433bac:fnins-17-1136500-g006.webp)

Comparison of brain areas between normal and damaged brains.

She H-Q, Sun Y-F, Chen L, Xiao Q-X, Luo B-Y, Zhou H-S, Zhou D, Chang Q-Y and Xiong L-L (2023) Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities. Front. Neurosci. 17:1136500. doi: 10.3389/fnins.2023.1136500

Clinical features

Neonatal HIE: Sarnat and Sarnat Clinical Staging

Stage Clinical Features
I (Mild) Hyperalert, jittery, normal EEG
II (Moderate) Lethargy, hypotonia, seizures, abnormal EEG
III (Severe) Stupor, flaccidity, brainstem dysfunction, burst suppression or flat EEG

Hypoxic Ischemic Encephalopathy (HIE).jpg

Detailed Sarnat staging:

![The Sarnat chart for the staging of the severity of hypoxic ischemic encephalopathy as introduced by Sarnat H.B and Sarnat M.S. in 1976.

https://doi.org/10.1371/journal.pone.0122116.t002](attachment:9c4e9e43-932d-4e1d-9c37-52b2b6d74bf0:pone.0122116.t002.png)

The Sarnat chart for the staging of the severity of hypoxic ischemic encephalopathy as introduced by Sarnat H.B and Sarnat M.S. in 1976.

https://doi.org/10.1371/journal.pone.0122116.t002

Radiology