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镇静药物中毒急救进展 2010

2011-09-13 9页 pdf 79KB 27阅读

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镇静药物中毒急救进展 2010 1 Toxicity, Sedative- Hypnotics 复旦大学 Background Sedative-hypnotics are a group of drugs that cause CNS depression.  Benzodiazepines (BZD)  barbiturates  nonbarbiturate nonbenzodiazepine sedative- hypnotics (NBNB) the most commonly used agents ...
镇静药物中毒急救进展 2010
1 Toxicity, Sedative- Hypnotics 复旦大学 Background Sedative-hypnotics are a group of drugs that cause CNS depression.  Benzodiazepines (BZD)  barbiturates  nonbarbiturate nonbenzodiazepine sedative- hypnotics (NBNB) the most commonly used agents Background  acute sedative-hypnotics poisoning  withdrawal syndrome 2 Etiology Benzodiazepines (BZD) • Long acting (half life >30h): chlordiazepoxide (利眠宁) diazepam(地西泮、安定) flurazepam (氟安定) • Short acting (half life 6-30h): alprazolam(阿普唑仑) • Ultrashort acting : triazolam(三唑仑) Etiology  Barbiturates  Ultrashort acting  Methohexital (Brevital甲己炔巴比妥)  thiopental (Pentothal硫喷妥那)  Short acting  pentobarbital (Nembutal戊巴比妥)  secobarbital (Seconal司可巴比妥)  Intermediate acting  Amobarbital (Amytal异戊巴比妥)  butalbital (Fioricet, Fiorinal异丁巴比妥)  Long acting  Phenobarbital (Luminal鲁米那) Nonbarbiturate, nonbenzodiazepine sedative-hypnotics (NBNB) Chloral hydrate (水合氯醛) Ethchlorvynol (乙氯维诺) Glutethimide (导眠能) Methyprylon (甲乙哌酮) Meprobamate (眠尔通) Etiology 3 一、Pharmacokinetics : 1、Pharmacokinetics of the BZD • Most BZD are extensively metabolized by the liver. • Some are metabolized to products which are active and may have a much longer half life than the parent drug. • The major route of metabolism is N-demethylation. in the elderly Cimetidine Pathogenesis Pathogenesis 2、Pharmacokinetics of Barbiturates  Barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys. ie phenobarbital(苯巴比妥).  Barbiturates with high lipid solubility are metabolized to more polar compounds in the liver before being excreted via the kidneys. ie thiopental (硫喷妥). 3、Pharmacokinetics of NBNB  Most NBNB are extensively metabolized by the liver Pathogenesis 4  BZD In the CNS, benzodiazepines exert their clinical effect by enhancing the activity of the inhibitory neurotransmitter GABA. (The clinical effects of GABA release and GABA-gated chloride channels include sleep induction and excitement inhibition)  Barbiturates in prolongation of the duration of opening of GABA-gated chloride channels, leading to hyperpolarization of the membrane and suppression of neurotransmission. 。 NBNB similar to the action of Barbiturates 二、 The mechanism of action Pathogenesis BZD GABA chloride channel Cl- Cl- ++ + + +- - --- hyperpolarization Clinical  Benzodiazepine  blurred vision, dizziness, confusion, drowsiness, anxiety, agitation, and unresponsiveness or coma.  BZD overdose in itself is remarkably safe. most patients with benzodiazepine overdose can be managed in the ED and released home after appropriate care.  When combined with other sedatives (most frequently alcohol), patients with benzodiazepine overdose can present with profoundly depressed levels of consciousness. . 5 Clinical  Barbiturates  Mild intoxication is characterized by ataxia, incoordination, nystagmus, slurred speech, and altered level of consciousness.  Moderate poisoning leads to respiratory depression and hyporeflexia.  Severe poisoning leads to flaccid areflexic coma, apnea, and hypotension.  Occasionally, hyperreflexia, rigidity, clonus, and Babinski signs are present.  Miosis is common, but mydriasis may be present with certain agents. Generally, 10 times the hypnotic dose produces severe toxicity.  Chloral hydrate  Mild intoxication is characterized by ataxia, lethargy  Severe poisoning leads to stupor, coma, pinpoint pupils, hypotension, slow or rapid and shallow respiration, hypothermia, areflexia, and muscle flaccidity.  Arrhythmias Clinical Clinical  Glutethimide (Doriden)  Loss of brainstem reflexes  Flaccidity  Anticholinergic effects  Delayed gastric emptying  May cause hyperthermia or heatstroke 6  Methaqualone (Quaalude)  Resembles barbiturate poisoning  Has more pronounced motor problems (eg, ataxia) and is known as wallbanger because of this phenomenon.  Can lead to severe muscular hypertonicity and seizures Clinical Lab Studies  Obtain a complete blood count (CBC), arterial blood gas (ABG), glucose, chemistry,  Imaging Studies:  Obtain an abdominal x-ray. Chloral hydrate is radiopaque.  Other Tests:  Obtain an electrocardiogram (ECG); Co-ingested drugs may have direct cardiac effects (eg, tricyclic antidepressants).  Quantitative serum drug concentrations are recommended for patients with serious toxicity  Barbiturates: For short-acting drugs, the lethal dose is 3 g or a serum concentration higher than 3.5 mg/dL. For long-acting drugs, the lethal dose is 5-10 g or a concentration higher than 8 mg/dL.  Chloral hydrate: The lethal dose is 10 g and a concentration higher than 100 mg/mL is toxic Lab Studies 7 Diagnosis  History  Symptom and sign  serum drug concentrations Differentials  Toxicity, Alcohols  Hypoglycemia  Diabetic Ketoacidosis  Neoplasms, Brain Treatment  Emergency Department Care  Establish ABCs, obtain IV access, provide oxygen  Ensure adequate airway and ventilation. Do endotracheal intubation if necessary.  Fluid resuscitation and anti-shock  Naloxone is recommended to the patients with comma. 8  Prevention of absorption  Gastric lavage may be performed if the patient presents obtunded within 2hour of ingestion  Activated charcoal is recommended for sedative- hypnotic overdoses. Multi-dose activated charcoal (20-50 g q4h) is recommended for overdoses with barbiturates, glutethimide, and meprobamate. Treatment  Elimination enhancement  Alkaline diuresis enhances elimination of phenobarbital and other long-acting barbiturates. It is recommended for all symptomatic patients with long-acting barbiturate toxicity.  Consider hemodialysis or hemoperfusion in glutethimide, methyprylon, phenobarbital, meprobamate, and chloral hydrate poisoning. Treatment  Detoxicant Flumazenil  Flumazenil competitively and reversibly binds benzodiazepine receptors (ie, GABA).  The use of flumazenil for suspected benzodiazepine overdoses is controversial. If used, it should be administered slowly (0.2 mg/min up to 3-5 mg) because large doses cause agitation and withdrawal.  This drug is contraindicated in patients with increased intracranial pressure (ICP) or closed head injury (CHI), those with a history of epilepsy, or those known to have ingested a tricyclic antidepressant (TCA) agent Treatment 9 Treatment of complication  Pneumonia  Arrhythmias  Acute renal failure Prognosis prophylaxis
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