The current recommendations regarding maximum doses of local anesthetics presented in textbooks, or by the responsible pharmaceutical companies, are not evidence based (ie, determined by randomized and controlled studies). Rather, decisions on recommending certain maximum local anesthetic doses have been made in part by extrapolations from animal experiments, clinical experiences from the use of various doses and measurement of blood concentrations, case reports of local anesthetic toxicity, and pharmacokinetic results. The common occurrence of central nervous system toxicity symptoms when large lidocaine doses were used in infiltration anesthesia led to the recommendation of just 200 mg as the maximum dose, which has remained unchanged for more than 50 years. In most cases, there is no scientific justification for presenting exact milligram doses or mg/kg doses as maximum dose recommendations. Instead, only clinically adequate and safe doses (ranges) that are block specific are justified, taking into consideration the site of local anesthetic injection and patient-related factors such as age, organ dysfunctions, and pregnancy, which may influence the effect and the pharmacokinetics of the local anesthetic. Epinephrine in concentrations of 2.5 to 5 microg/mL should be added to the local anesthetic solution when large doses are administered, providing there are no contraindications for the use of epinephrine. As a rule, conditions (eg, end-stage pregnancy, high age in epidural, or spinal block) or diseases (uremia) that may increase the rate of the initial uptake of the local anesthetic are indications to reduce the dose in comparison to one normally used for young, healthy, and nonpregnant adults. On the other hand, the reduced clearance of local anesthetics associated with renal, hepatic, and cardiac diseases is the most important reason to reduce the dose for repeated or continuous administration. The magnitude of the reduction should be related to the expected influence of the pharmacodynamic or pharmacokinetic change.

Interscalene brachial plexus anesthesia for shoulder surgery routinely includes sensory anesthesia of the fourth and fifth cervical nerves. The authors reasoned that some degree of diaphragm paralysis should result from interscalene blocks that produce surgical C3-C5 sensory anesthesia. In this investigation, ultrasonography was used to study the incidence of ipsilateral hemidiaphragmatic paresis during routine interscalene block, as it is a practical, sensitive, and low-risk method for diagnosing hemidiaphragmatic function without radiation exposure. Thirteen healthy patients received interscalene blocks using a paresthesia technique with 34-52 mL 1.5% mepivacaine with added epinephrine and bicarbonate. All developed cervical sensory anesthesia. Data were collected before and 2, 5, and 10 min after injection, and, when possible (11 of 13 patients), at hourly intervals after surgery. Changes from normal to paradoxical motion of the ipsilateral hemidiaphragm were seen in all 13 patients during sniff and Mueller maneuvers within 5 min (in 11 of 13 patients at 2 min). Diaphragmatic motion returned to normal in 10 of 11 patients between 3 and 4 h after injection and in the remaining patient by the fifth hour after injection. Diaphragmatic paresis appears to be an inevitable consequence of interscalene brachial plexus block when providing anesthesia sufficient for shoulder surgery.

We studied the effects of unilateral hemidiaphragmatic paresis caused by interscalene brachial plexus block on routine pulmonary function in eight patients. In an additional four patients, we studied changes in chest wall motion during interscalene block anesthesia by chest wall magnetometry. Ipsilateral hemidiaphragmatic paresis, as diagnosed by ultrasonography, developed in all patients within 5 min of interscalene injection of 45 mL of 1.5% mepivacaine with added epinephrine and bicarbonate. Large decreases in all pulmonary function variables were measured in every patient. Forced vital capacity and forced expiratory volume at 1 s decreased 27% +/- 4.3% and 26.4% +/- 6.8%, respectively (P = 0.0001). Peak expiratory and maximum midexpiratory flow rates were also significantly reduced. Interscalene block caused changes in pulmonary function and chest wall mechanical motion that were similar to those published in previous studies on patients with hemidiaphragmatic paresis of pathological or surgical etiology. Interscalene block probably should not be performed in patients who are dependent on intact diaphragmatic function and in those patients unable to tolerate a 25% reduction in pulmonary function.

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