What Are the Most Common Dehydration Effects?

Acute brain failure is caused by a variety of etiologies or lesions, and it is an acute critical clinical pathological condition mainly manifested by disturbance of consciousness. The serious consequences of its development are the formation of intracranial hypertension and cerebral hernia, which can often be the cause of death. Critical illness that must be treated urgently clinically.

Acute brain failure

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Acute brain failure is caused by a variety of etiologies or lesions, and it is an acute critical clinical pathological condition mainly manifested by disturbance of consciousness. The serious consequences of its development are the formation of intracranial hypertension and cerebral hernia, which can often be the cause of death. Critical illness that must be treated urgently clinically.

nickname

Acute brain failure

English name

Acute brain failure

Common locations

Brain

Common symptoms

Symptoms and signs of acute disturbance of consciousness, limited or diffuse brain damage, and increased intracranial pressure.

Contagious

No infection

Brain failure refers to the development of brain damage to a severe stage or the involvement of the brain by primary diseases of other organs and systems, resulting in serious brain damage, thereby causing brain dysfunction, and gradually losing the ability to compensate, and finally develops To brain failure. According to the rate of occurrence and development of brain failure, brain failure can be divided into acute brain failure and chronic brain failure. Chronic brain failure often manifests as progressive dementia, eventually entering a coma, and acute brain failure is mainly manifested by acute coma. Clinically, the so-called brain failure mostly refers to acute brain failure. The causes of acute brain failure are diverse, and the clinical status of brain failure caused by brain damage varies widely. The causes of brain failure are basically divided into two categories: intracranial lesions and systemic diseases. The pathology and pathophysiology of acute cerebral failure are very different according to their pathogenesis, mainly manifested by increased intracranial pressure, cerebral edema and cerebral hernia.

The clinical manifestations of acute brain failure, in addition to the various clinical manifestations of the primary disease, are mainly symptoms and signs of acute conscious disturbance, localized or diffuse brain damage, and increased intracranial pressure, which can be accompanied by seizures And disorders of respiratory function. EEG and brain evoked potential monitoring can produce corresponding potential changes, which are of great significance to the diagnosis and prognosis of patients. CT and MRI examinations can identify most causes.

The treatment of acute brain failure is multi-faceted, mainly including active treatment of primary diseases, reduction of intracranial pressure, hyperbaric oxygen therapy, hibernation therapy, symptomatic treatment and management of complications, while applying brain protective agents and nutritional support therapy. The prognosis of acute brain failure mainly depends on the cause of brain failure and the severity of brain damage caused by it.

The principle of treatment should be based on different etiology, and effectively adopt a comprehensive treatment plan to control and reverse the development of acute brain failure, minimize brain damage, and enable patients to restore normal functions.

(1) Etiology treatment: timely and effective treatment for the cause is the key to rescue brain failure, such as intracranial tumors, traumatic hematomas and large hematomas of hypertensive cerebral hemorrhage. Surgery should be performed as soon as possible; Respiratory and circulatory disorders, hypoxia and metabolic disorders and other systemic diseases caused by it should maintain good respiratory and circulatory function; patients with water-electrolyte and acid-base balance disorders must be actively corrected; those with diabetic ketotoxicity should be treated with insulin And rehydration; those who are acutely poisoned must take effective measures to remove poisons and perform detoxification treatment.

(2) General treatment: keep the airway open, regularly sputum, give oxygen to prevent the root of the tongue from falling back, closely observe and maintain vital signs such as breathing, blood pressure, pulse, etc., rehydration, and strengthen nursing.

(3) Control of cerebral edema: Cerebral edema is an important pathological basis for brain failure. Therefore, eliminating cerebral edema and reducing intracranial pressure is an important measure for brain function recovery. The most commonly used dehydration therapy is the use of hypertonic dehydrating agents such as mannitol, urea, and glycerol; diuretics such as furosemide can also be used; adrenocortical hormones and dimethylsulfoxide can also be used. Pay attention to fluid therapy while dehydrating. If the drug can not be controlled, you can choose cerebral decompression or ventricular drainage.

(4) Prevention and treatment of comorbidities: such as prevention and treatment of gastrointestinal bleeding and acute renal failure, correction of water-electrolyte disorders and acid-base balance disorders, prevention of infection, and anticonvulsions.

(5) Cryoprotective therapy: Reduce brain metabolism through hypothermia, reduce hypoxia and cerebral edema, and provide the possibility for the recovery of brain function. The main methods of cooling are:

a, head cooling: using an ice trough, ice cap and ice bag.

b. Cooling of the body surface: Mostly place ice packs on large blood vessels on the body surface, such as the neck, underarms, and groin, or use alcohol and water for a systemic scrub bath.

c, body cooling: ice water enema or ice water for gastric lavage. Cooling should be completed before the peak of cerebral edema, usually the brain temperature should be reduced to 28 ° C, and maintain a sufficient low temperature time until the condition is stable, usually 3-7 days, if necessary, 2-3 weeks, the shortest time is not less than 48 hours . The cooling process should be smooth. To prevent chills and control convulsions, a small amount of muscle relaxant or sedative can be used. Re-warming must be carried out gradually. Remove the ice pack from the bottom up first. It should be maintained that the body temperature rises 1-2 ° C every 24 hours.

(6) Brain protective agents: Apply anti-free radical drugs, calcium channel blockers, and reduce brain metabolism to prevent irreversible changes in brain cells and achieve protective effects on brain tissue. These drugs include:

a. Barbiturates: can inhibit brain metabolism; scavenge free radicals and have membrane stabilization; it can also reduce intracranial pressure and reduce cerebral edema. Generally, barbiturates with ultra-short-term effects are used. Often, thiophenal sodium 30 mg / kg body weight, thiopentabarbital sodium 20 mg / kg body weight, and pentobarbital sodium 1 mg / kg body weight are often used.

b. Adrenocortical hormone, non-glucocorticoid 21-aminosteroid, etc.

c. 20% mannitol: slow intravenous drip has anti-free radical effect.

d. Excitatory amino acid antagonists.

e. Calcium channel blocker: it has the effect of inhibiting vasoconstriction, anti-free radical, and inhibiting platelet aggregation. By acting on calcium channel-related neuron receptors and cerebrovascular receptors, it protects and stabilizes neuron function, increases cerebral blood perfusion, and improves tolerance to ischemia. Nimodipine 40mg can be used orally 3 times a day; Nimodipine 4-8mg or Nimodon 10mg can be added to 500ml of 5% glucose solution slowly intravenously.

f, phenytoin sodium; can reduce brain oxygen consumption, reduce lactic acid production, improve resistance to cerebral ischemia and cerebral hypoxia, stabilize cell membranes, etc .; usually add 500% to 500-750mg 10% glucose solution in 500-750ml slow vein Drip.

g. Nidazolid fumarate: It has extremely significant brain protective effects, which can reduce brain metabolism by 20% -30%; it has the functions of scavenging free radicals, anti-oxidation, and stabilizing biofilms; it has the effect of antithrombin A2; Promote prostacyclin production. The usual dosage is 5-10mg, intravenous infusion 2-3 times a day for 5 days. Because there is no anesthetic effect and respiratory depression of barbiturates, it is easy to be widely used in clinical practice.

(7) Brain Nutrition Metabolism Agents and Awakening Agents:

a. Peptides: Participate in improving cell metabolism, promoting protein synthesis and restoring brain cell function. Such drugs commonly used in clinical practice include nerve growth factor, cerebrolysin, and Aiweizhi. The commonly used amount of Cerebrolysin is an intravenous infusion of 250 ml of normal saline 10 to 30 ml each time, once a day, and a course of 2-3 weeks. The commonly used amount of Aiweizhi is 400-800mg each time by adding 250ml of physiological saline into a intravenous drip, once a day, 2-3 weeks as a course of treatment. No significant side effects have been found.

b. Other brain nutritional metabolism agents: citicoline, adenosine triphosphate, cytochrome C, coenzyme A, etc.

c. L-dopa: Dopamine is an important neurotransmitter in the CNS. Because it cannot pass the blood-brain barrier, it is clinically supplemented with dopamine precursor substance, that is, levodopa that can pass the blood-brain barrier. L-dopa enters nerve cells and is converted into dopamine and norepinephrine, which can expel the pseudo-neurotransmitter out of nerve endings, thereby restoring normal nerve conduction. It is mainly used for hepatic coma, but also for dementia caused by cerebral cortex and brain surgery. Usually 50-150mg, intravenous drip; or 3-5g / d orally.

d. Kenao fans: The active thiol group that can be released in the body has strong oxidizing ability, has a promoting effect on brain metabolism, and can accelerate the recovery of brain function. 1g is usually added to 500ml of 5% glucose solution slowly intravenously, 7-10 days as a course of treatment. There may be side effects such as rash, phlebitis, and anaphylactic shock, which are contraindicated in patients with coronary heart disease.

e. Chloroester awakening: It can promote the redox process of brain cells, reduce the awakening response threshold of the cerebral cortex and hippocampus, and have a wake-up effect. It is usually injected intravenously at 250mg intramuscularly or 250ml with 5% glucose solution, 1-2 times a day. Its effect is slow, often need to be maintained for a period of time may have curative effect, hypertension and obvious infection are contraindicated.

f. Thyroid-stimulating hormone (TRH): It has an anti-central nervous system inhibitory effect and has a good effect on improving the disturbance of consciousness. Generally, intramuscular injection or intravenous drip of 0.5 mg of TRH tartrate is given once a day for 10 days as a course of treatment.

g. Xingnao Injection (An Gong Niuhuang Injection): It has the effect of regaining spasm and injecting 2 to 4 ml intramuscularly or 4 to 8 ml with 25% glucose solution and 40 ml intravenously once or twice daily. Other traditional Chinese medicines such as Niuhuang Qingxin Pill, Zhibao Dan and Zixue Pill are also available.

h. Other drugs that can be tried: ganglioside, -aminobutyric acid, acetylglutamine, inosine, fructose phosphate, Duxil, Naoxin and Naoxukang, etc.