Related Experiment Video
Updated: May 14, 2026
09:09
Cryosectioning and Immunostaining Mouse Inner Ear Tissue: From Embryonic to Adult Stages
Published on: April 11, 2025
Hypoxic Ischemic Encephalopathy: Hearing Impairment and Related Risk Factors
Francesca Serrao1, Simonetta Frezza1, Guido Conti2
1Neonatal Unit, Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168 Rome, Italy.
Journal of Clinical Medicine
|May 13, 2026
Summary
Newborns with hypoxic-ischaemic encephalopathy (HIE) treated with therapeutic hypothermia (TH) have a 2.7% rate of permanent hearing loss. Early audiological screening is crucial for timely intervention and management in these high-risk infants.
Area of Science:
- Neonatology
- Audiology
- Pediatric Neurology
Background:
- Hypoxic-ischaemic encephalopathy (HIE) is a serious condition in newborns.
- Therapeutic hypothermia (TH) is a standard treatment for HIE.
- Infants with HIE are at increased risk for hearing impairment.
Purpose of the Study:
- To compare the incidence of hearing loss in HIE infants treated with TH to literature values.
- To identify risk factors for audiological impairment in this cohort.
- To track changes in hearing thresholds during the first year of life.
Main Methods:
- Retrospective observational cohort study.
- Inclusion of 149 newborns with HIE treated with TH.
- Audiological screening and diagnostic evaluation at 3 months, with follow-up for 1 year.
Main Results:
- Hearing loss identified in 4.0% at 3 months.
- Permanent bilateral sensorineural hearing loss (SNHL) prevalence of 2.7%.
- Gestational age was a protective factor against SNHL (OR 0.49).
Conclusions:
- Audiological screening is effective for early detection and intervention.
- Infants with HIE require vigilant audiological and neonatological management.
- Individualized management based on risk factors, including gestational age, is recommended.
Related Concept Videos
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
01:19Encephalitis l: Introduction
Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
01:21Cytotoxic Edema: Pathophysiology
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
01:29Increased Intracranial Pressure ll: Pathophysiology
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
01:15Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...