Hypoxic-Ischemic Encephalopathy (HIE): Diagnostic, And Therapeutic Strategies: Clinical review

Abstract

Hypoxic-ischemic encephalopathy (HIE) is one of the main causes of morbidity and mortality in neonates. On account of high groupings of sensitive immature cells, metal-catalyzed free radicals, non-saturated fatty acids, and low concentrates of antioxidants enzymes, the brain requires elevated degrees of oxygen supply and is, in this manner, very sensitive to hypoxia. Solid proof shows that oxidative stress assumes a significant part in pathogenesis and progression. Following hypoxia and ischemia, reactive oxygen species (ROS) production rapidly increments and overpowers antioxidant defences. A large excess of ROS will straightforwardly change or degenerate cell macromolecules, like membranes, proteins, lipids, and DNA, and lead to a cascading inflammatory reaction, and protease secretion. These derivatives are engaged with a complex interplay of numerous pathways (e.g., inflammation, apoptosis, autophagy, and necrosis) which at last lead to brain injury. In this review, we feature the molecular mechanism for oxidative stress in HIE, sum up current research on therapeutic methodologies used in combating oxidative stress, and attempt to explore novel potential clinical methodologies.

Mental disorder as an example of sequelae of cerebral hypoxia-ischemia in case of acute blood loss in forensic medicine

“…Considering the stability of hemodynamics during the operation, sufficient cardiac output, and sinus rhythm, cardiac arrest was reflexive in nature due to forced traction of the myocardium. Reperfusion is considered the main pathological stage of hypoxic-ischemic encephalopathy, which is an integral part of post-resuscitation disease Hypoxic-ischemic encephalopathy has been reported to have either a favorable outcome with recovery following mild to moderate hypoxia of short duration or an adverse outcome following severe injury, including coma or persistent vegetative state, dementia, extrapyramidal syndrome, and cognitive deficits [11] . Some examples of successful treatment of post-resuscitation illness with complete restoration of motor, sensory, cognitive functions within a year or with minimal neurological impairment are given [2] .…”