The purpose of the treatment of hepatic encephalopathy basis for the treatment of liver disease and the promotion of awareness of recovery. Has entered a coma early treatment period than the effect as well. Because of its complex pathogenesis, there are multiple factors are involved, should be for different types of causes and clinical focus on choice of treatment.
(A) early identification and correct or remove the incentive for
Most often can be found in the pathogenesis of HE incentives first step to correct or remove the treatment incentives. Only by removing the incentive for some patients without the need to take further measures to improve the condition can be reversed or HE. Such as the timely control of gastrointestinal bleeding and remove intestinal hemorrhage; prevent or correct the water, electrolyte and acid-base balance; active infection control; caution or disable the sedative drugs, such as patients with mania, should promethazine, chlorobenzene that sensitive place of sedatives such as antihistamines. If the rhythm sleep disorders may oral melatonin at bedtime to correct the disorder of the circadian clock; attention to prevention and treatment of intractable constipation.
(B) reduction and removal of intestinal nitrogen generation and absorption of toxic
1. Limit the intake of protein
~ in patients with intestinal protein supplement should be banned from the coma more than 2 to 3 days should be supplemented with intravenous amino acid s
olution (70g / d). ~ patients started a few days of the protein should be limited, controlled 20g / d within. As symptoms improve, increase every 2 to 3 days l0-20g protein, but HE does not occur for the degree. Increasing protein intake in patients tolerated until the 60-80g / d, in order to maintain positive nitrogen balance in patients with essential. Plant protein than animal protein, plant protein production due to less ammonia; to increase the non-absorbent fiber content in order to increase the combination of fecal bacteria and nitrogen removal; plant protein is the acid production of intestinal bacteria glycolysis excluded in favor of ammonia. It should be noted that for patients with chronic HE, encourage small meals often (5 to 6 times / day), protein intake should be individualized, and gradually increase the total protein, protein can not be limited way to prevent the occurrence of HE, otherwise it would deterioration in nutritional status.
2. Clean the intestinal tract
Particularly from the gastrointestinal bleeding and hepatic encephalopathy caused by constipation, by enema or cathartic bowel cleansing measures to reduce the intestinal absorption of ammonia has a useful role. Adopt the following measures: oral or nasal feeding laxatives such as lactulose, milk pear alcohol, 25% magnesium sulfate; an enema with normal saline or weak acid solution, on the one hand discharge volume of blood, on the other hand to maintain the acidic intestinal condition, not conducive to the absorption of ammonia.
3. Oral nonabsorbable disaccharide lactulose
After oral administration of lactic acid bacteria in the colon are anaerobic bacteria such as lactic acid and acetic acid decomposition, lower colon pH, the acidic lumen, thereby reducing the formation and absorption of ammonia; its laxative effect of toxic substances contribute to intestinal nitrogen discharge; intestinal acidification, the promotion of lactic acid bacteria and other large population of beneficial bacteria and inhibit bacterial growth and ammonia production, decreased production of ammonia. Dose of 30ml, 3-4 times a day orally, but also nasal feeding. Lactulose non-toxic, common side effects for the fullness, and sometimes abdominal pain, nausea and vomiting. Pear milk alcohol (p galactose sorbitol) is a similar disaccharide lactulose its role and the same. HE effect of improving the same with lactulose, but the sweetness of low milk pear alcohol, good taste, abdominal distension, abdominal pain and other adverse reactions less than lactulose. Dose of 30-45g / d, orally 3 times.
Intestinal absorption of oral antibiotics can not easily inhibit the intestinal bacteria produce urease, reduction of ammonia production.
Recent Meta-analysis showed that the antibiotic is superior in improving the oral administration of HE does not absorb disaccharides. Commonly used neomycin, metronidazole, vancomycin, rifaximin (rifaximin) and so on. Long-term use of neomycin may occur hearing or renal damage, metronidazole, or the efficacy of rifaximin and neomycin similar. However, due to the potential toxicity of these drugs and lead to dangerous drug-resistant strains, currently do not advocate long-term use.
Taking some of urease does not produce beneficial bacteria such as Lactobacillus, Enterococcus, Bifidobacterium, Bacillus butyricum and so on, can inhibit the growth of bacteria produce urease and acidification intestine, preventing the absorption of ammonia and toxic substances have a role in ;
(C) to promote the removal of ammonia in vivo
1. Ornithine ornithine aspartate ornithine aspartate is a mixture of preparation and aspartic acid, can activate a key enzyme in the synthesis of urea, urea generation and provision of glutamine synthetase reaction substrate ornithine and aspartic acid, glutamine increased urea synthesis and the promotion of generation, and thus clear the portal blood ammonia in the liver. To prevent overloading of acute HE at the time of ammonia nitrogen levels effective. The intravenous infusion of glucose solution by adding 20-40g / d.
2. Zinc preparations
Zinc supplementation on urea cycle enzymes involved must be coenzyme, and in cirrhosis of the liver due to excessive excretion of urine and malnutrition, the body''s zinc is often inadequate. It has been reported to add 600mg of zinc daily can reduce blood ammonia levels in patients with HE.
3. Other drugs
Such as glutamic acid, arginine, sodium benzoate, etc., of limited use in clinical practice is rarely used.
(D) against nerve toxin on the inhibition of neurotransmitter
1.GABA/BZ composite receptor antagonist flumazenil (flumazenil) for the BZ receptor antagonists, endogenous BZ derivatives can lead to inhibition of nerve conduction are short-term improvement. Flumazenil may be some benefit in patients with acute hepatic encephalopathy. Usage lmg / times, intravenous drug use.
2. Branched-chain amino acids
Oral or intravenous infusion of branched-chain amino acids to the amino acid-based mixture of amino acid metabolism can correct imbalances in theory, provide energy, suppression of false neurotransmitters in the brain to form, but portal-systemic shunt encephalopathy there controversial. For those who can not tolerate protein food supplement branched-chain amino acids undoubtedly help to improve the nitrogen balance in patients.
3. Other drugs
Such as L-carnitine, manganese drive drugs EDTA and sodium salicylate on the amino-opioid receptor antagonist naloxone and naltrexone, 5-HT receptor antagonist, a so on. Its efficacy needs to be further verified.
(E) temporary liver support
Commonly used in acute liver failure caused by HE, as a temporary waiting for liver transplantation or liver regeneration support measures to win time. Previously used plasma exchange, the current number of molecular adsorbent recirculating system (-tem, MARS) toxin removal and albumin, bilirubin. Biological artificial liver support system in cultured liver cells and other biological material, provides support for liver function, is still in the testing stage. Also in the pilot phase of liver cells and bone marrow stem cell transplantation, but has been shown for fulminant hepatic failure (fulminanthepaticfailure, FHF) induced liver necrosis substitution can improve the survival rate will be the direction of future research.
(F) liver transplantation
Liver transplantation is an effective measure to save the lives of patients, surgical indications and grasp how to choose the timing of surgery on long-term survival after transplantation is important. Where no brain edema in HE or FHF and above 5 in the following 3 or 3 above, there are indications for emergency liver transplantation arterial blood pH <7.3; aged <10 years 40 years; appear jaundice before encephalopathy 7 days; prothrombin 50 seconds; year survival rate was 65% after liver transplantation.
(Vii) symptomatic treatment
Of fulminant hepatic failure patients, treatment directed against multiple organ failure and damage liver function support. Patients should be placed in the intensive care unit. HE with severe tracheal intubation when necessary to reduce the risk of respiratory arrest. Strengthen the protection of brain cell function and prevention of cerebral edema, cerebral edema secondary to intracranial hypertension, is the stage , a common complication in patients with HE can lead to death or irreversible brain damage, attention to early identification and treatment.