Can a baby's brain damage be cured?

Don't think that only adults often suffer from brain damage due to physical injuries. Many infants may also suffer from brain damage. For example, they stay in the abdomen for too long or have a lack of amniotic fluid, which increases the intracranial pressure and causes brain damage. Infant brain damage can be recovered, but if the rescue is not timely, it will leave sequelae, which can be recovered slowly the day after tomorrow.

Nonsurgical

Resuscitation of blood pressure and oxygen saturation

A large amount of data shows that the early occurrence of hypotension [systolic blood pressure (12kPa)] and hypoxia [asphyxia or cyanosis or PAO2 (8kPa)] after injury greatly increases the incidence and mortality of secondary brainstem injury after severe craniocerebral injury.

Control of increased intracranial pressure

The use of mannitol 20% mannitol injection can drain water from the normal brain and the edema part of the brain, effectively reducing intracranial pressure, which is the main method for treating patients with craniocerebral injury. The initial dosage is 0.5 g/kg. Adjust according to the effect on intracranial pressure and cerebral perfusion pressure.

Hyperventilation therapy: 40% of patients with severe craniocerebral injury have cerebral edema and progressive increased intracranial pressure, and uncontrollable increased intracranial pressure is the most common cause of disability and death. Hyperventilation reduces intracranial pressure by causing vasoconstriction and subsequent reduction in cerebral blood flow. Hyperventilation plays a role in the management of severe head injury because it can rapidly reduce intracranial pressure.

Many drugs are used in traumatic brain injury with the aim of interfering with the molecular, biochemical, cellular and microvascular processes involved in traumatic brain injury. Increased awareness of traumatic and ischemic brain injury has noted the severity of the mechanism of action, such as increased intracellular calcium ions, excess oxygen free radicals, excitotoxic lipid peroxides of glutamate and other excitatory amino acids.

The use of nimodipine in the acute phase of craniocerebral injury is still controversial. Some scholars believe that the acute use of nimodipine injections can cause cerebral vasodilation, which may aggravate cerebral edema and cause cerebral hemorrhage. Recent studies suggest that nimodipine injections relieve cerebral vasospasm and reduce cerebral edema through calcium antagonism, thereby reducing morbidity and mortality. It is suggested that the best effect is achieved when used as early as possible (12 hours) after craniocerebral injury.

The prognostic evaluation of craniocerebral injury proposed the Glasgow prognostic classification of five levels: moderate disability, severe disability, vegetative state and death. After severe craniocerebral injury, 10% to 20% of people suffer severe disability for 6 months or longer. During this period, only 1% to 3% remain in a vegetative state.

There is considerable controversy regarding the efficacy of rehabilitation for traumatic brain injury. However, there is evidence that intensive care provided by neurologists soon after trauma is beneficial and that certain therapies such as hyperbaric oxygen can promote awakening from coma and help neurological recovery. It has certain therapeutic effects on the recovery period, sequelae period and brain trauma syndrome.