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1、ASRA recommendations on systemic toxicity of local anestheticsThe American Society of Regional Anesthesia (ASRA has developed a series of recommendations addressing the systemic toxicity of local anesthetics. The AAOS Council on Research, Quality Assessment and Technology reviewed the recommendation

2、s, and the AAOS Board of Directors, at its meeting on June 12, 2008, agreed to publish them inAAOS Now.Prevention of systemic local anesthetic toxicityBe vigilant. Monitoring electrocardiogram, blood pressure, and arterial oxygen saturation is recommended.Communicate frequently with the patient to q

3、uery for symptoms of toxicity. Limit local anesthetic (LA dose based on site of injection, hypercapnia, advanced age, poor cardiac function, ischemic heart disease, cardiac conduction abnormalities (see notes, metabolic (especially mitochondrial disease, or abnormally low plasma protein concentratio

4、n.Aspirate syringe prior to each injection observing for blood or cerebrospinal fluid.Inject small volumes (5 mL, incrementally (4560 sec intervals observing for signs and symptoms of toxicity between each injection.Use a pharmacologic marker (e.g., epinephrine 5 mcg/mL of LA. Know the expected r es

5、ponse, onset, duration, and limitations of “test dose” in identifying intravascular injection.Monitor the patient after completion of injection as peak blood concentrations may not occur for up to 30 minutes.Detection of systemic LA toxicityBe aware. The signs, symptoms, and timing of local anesthet

6、ic systemic toxicity are unpredictable. Because there is a potential antidote to this life-threatening event, the most important step in treating local anesthetic toxicity is to consider the diagnosis in any patient with altered mental status or cardio vascular instability following a regional anest

7、hetic.Central nervous system (CNS symptoms are often subtle or absent;cardiovascular signs, particularly hypotension or bradycardia, are often the only manifestation of severe local anesthetic toxicity; and the toxic syndrome can occur an hour or more after injection. CNS excitation (agitation, conf

8、usion, twitching, seizure, depression (drowsiness, obtundation, coma, or apnea, or nonspecific neurologic symptoms (metallic taste, circumoral paresthesias, diplopia, tinnitus, dizziness are each typical of LA toxicity. Progressive hypotension and bradycardia, leading to asystole are typical of seve

9、re cardiovascular toxicity. Ventricular ectopy, multiform ventricular tachycardia, and ventricular fibrillation are also frequently seen.Treatment of systemic LA toxicityBe prepared: The ASRA strongly advises anesthesiology departments to establish a plan for managing systemic local anesthetic toxic

10、ity at their facility. This should include stocking 20 percent lipid emulsion and the means for its rapid delivery close to every site where local anesthetics are used. Having a Local Anesthetic Toxicity Kit is encouraged.Get help and call for lipid or an LA Toxicity Kit, then focus attention on the

11、 following:1. Airway management2. Seizure suppression and, if needed,3. Cardiopulmonary resuscitation4. Alert the nearest facility having cardiopulmonary bypass capability. Administer 20 percent lipid emulsion (values in parenthesis are for 70kg:1. Bolus 1.5 mL/kg intravenously over 1 minute (100mL2

12、. Continuous infusion 0.25 mL/kg/min (500 mL over 30 minutes3. Repeat bolus Q 5 minutes for persistent cardiovascular collapse.4. Double infusion rate if blood pressure returns but remains low.5. Continue infusion for a minimum of 30 minutes.Notes on preventionSedative hypnotic drugs reduce seizure

13、risk but even light sedation may abolish the patients ability to recognize rising LA concentrations.Patients with severe cardiac dysfunction, particularly very low ejection fraction, severe conduction abnormality, or ongoing ischemia, may not be good candidates for plexus or peripheral nerve block o

14、r epidural anesthesia (blocks requiring larger doses of LA. Despite the prejudice that regional anest hesia is safer and that such patients might be too sick for general anesthesia, they could be more susceptible to irreversible cardiovascular collapse with local anesthetic exposure (even with nonli

15、pophilic LA than with inhalational exposure. Consider alternatives such as spinal or small dose field block (subcutaneous injection.Notes on treatmentArguably the most important factor in treating LA toxicity is aggressive airway management to avoid hypoxia, hypoventilation, and tissue acidosis, whi

16、ch all exacerbate LA-induced cardiovascular depression.Timing of lipid infusion in the LA toxic syndrome is controversial. The most conservative approach would be to wait until American Heart Association/Advanced Cardiovascular Life Support has proven unsuccessful in returning adequatecirculation. T

17、his seems unreasonable given the many reports of early reversal of toxicity, suggesting that progression to cardiovascular collapse can be stopped by early intervention. An aggressive strategy would be to infuse lipid at the earliest sign of systemic toxicity. This may result in the unnecessary trea

18、tment of many patients given that only a fraction are expected to progress to cardiovascular collapse. The most reasonable approach at this time, lacking rigorous datasupporting one extreme over the other, is somewhere in between. The clinical context, severity, and rate of progression of clinical signs of toxicity should guide the use of lipid therapy.Propofol should not be used when the patient exhibits signs of cardiovascular instability. There is considerable confusion about this point given that propofol is typically