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We experienced a case of accidental pilsicainide poisoning suspected as the cause of pacing failure leading to cardiac arrest. The patient was a 36-year-old woman with a history of refractory multifocal supraventricular tachycardia who had previously undergone multiple cardiac ablations requiring placement of a pacemaker. Upon her arrival on the day of dental treatment, the patient's condition deteriorated rapidly, with a heart rate of approximately 30 beats/min, pacing failure, and an idioventricular rhythm upon electrocardiographic

mucosa during phase I was significantly longer in the LvE group than in the LiE group. This finding indicates that the drug transfer into the blood during the early phase after dosing is lower when levobupivacaine rather than lidocaine is administered in combination with 1:80,000 epinephrine. This difference is probably attributable to the fact that levobupivacaine has vasoconstrictive actions while lidocaine has vasodilatory actions. The concomitant administration of epinephrine is expected to reduce the incidence of poisoning by the local anesthetic. Furthermore

Carabine , U. A. , P. M. C. Wright , and J. Moore . Preanesthetic medication with clonidine: a dose-response study. Br J Anaesth 1991 . 67 : 79 – 83 . 63 Kappagoda , C. , D. N. Schell , R. M. Hanson , and P. Hutchins . Clonidine overdose in childhood: implications of increased prescribing. J Paediatr Child Health 1998 . 34 : 508 – 512 . 64 Heidemann , S. M. and A. P. Sarnaik . Clonidine poisoning in

perioperative period: a proposal for a guideline in elective surgery . Psychosomatics . 2006 ; 47 : 8 – 22 . 10 Thanacoody HK, Thomas SH. Tricyclic antidepressant poisoning: cardiovascular toxicity . Toxicol Rev . 2005 ; 24 : 205 – 214 . 11 Morgan GE

B, Schwarz F, et al . Impact of dental implant surface modifications on osseo integration . Biomed Res Int . 2016 ; ID6285620 P16 . 15 Soejima T. A experimental study in the bone marrow: second report: leukocyte migration in the bone marrow by poison of autonomic nerves . J Okayama Med Assoc . 1954 ; 66 : 705 – 718

Complications of SCh with little-to-no clinical relevance include increases in intragastric, intraocular, and intracranial pressures. 12 Other less common complications associated with SCh administration include malignant hyperthermia, anaphylaxis, and myoglobinuria. Pathophysiology of PChE Deficiency The natural physiologic purpose of PChE is unknown; however, it is thought that it may be protective against AChE inhibitors and inhaled poisons. 13 Clinically, PChE quickly degrades the depolarizing neuromuscular blocker SCh and the rapid

injections of long-acting, depot preparations (generally every 2 weeks). These are particularly useful for delusional paranoid patients who frequently believe that “medicines are poison.” Exemplary antipsychotic agents are summarized in Table 4 . Dosages for antipsychotic agents can be quite variable and must be titrated to the individual patient. Notice from the Table that the more potent conventional agents, ie, those requiring <50 mg/day, produce the greatest incidence of extrapyramidal effects, while those having less potency are more likely to produce sedation and

oxide release is responsible for its vasodilating effects. Sodium nitroprusside acts primarily on the arterial vasculature, while nitroglycerin has its most prominent effect on venous capacitance vessels. 23 Hydralazine is a direct systemic arterial vasodilator that produces baroreceptor reflex stimulation with resulting increases in heart rate and myocardial contractility. 9 Anesthetic Implications Sodium nitroprusside can cause cyanide and thiocyanate poisoning, especially in those with renal failure or reduced renal perfusion. 22

is usually short onset (several hours to 24–48 hours). 32 , 33 Agents producing hepatitis are generally toxins and poisons that are converted to toxic metabolites. 33 , 34 , 36 Clinical manifestations are highly variable, ranging from asymptomatic with elevated liver enzymes to fulminant hepatic failure. Acetaminophen can cause fulminant hepatic failure after an overdose and can also induce chronic hepatic injury in analgesic doses to those who have chronic alcoholism and existing impaired liver function/liver damage. 33 , 34 Ethanol has been show to induce the