Journal of The Association of Physicians of India ■ Vol. 64 ■ March 201692

Table 1: The distribution frequencies of all reported signs of CNS toxicity among published cases of local anaesthetics systemic toxicity

Seizures 68%CNS Perioral numbness

DizzinessLight HeadacheDysarthriaConfusionObtundation

18%

CVS ArrhythmiaTachycardiaWide QRSVentricular ectopyVT,VF

50%

Bradycardia or asystole 27%Hypotension 18%

Local Anesthetics Systemic ToxicityR Jayanthi1, KSGA Nasser2, K Monica3

AbstractLidocaine Hydrochloride is an amide ester, which is widely used local anesthetic agent that is well tolerated but what is less known is the occurrence of systemic toxicity which manifests in the central nervous and cardiovascular systems. We report here 3 cases of Lidocaine associated Seizures.

1Professor of Medicine, Stanley Medical College, Chennai, Tamil Nadu; 2Principal, Tamil Nadu Govt. Dental College; 3Resident, Dept of Internal Medicine, Stanley Medical College, Chennai, Tamil NaduReceived: 23.08.2014; Revised: 22.12.2014; Accepted: 27.12.2014

Introduction

Li d o c a i n e d i s c o v e r y i n 1 9 4 8 , r e v o l u t i o n i z e d a n e s t h e t i c

management of minor surgeries. Amino Amides like Mepivacaine, Prilocaine and Bupivacaine all used in modern day dent is t ry were developed in 1963.1 1969 saw the dawn of Articaine which with its potency and safety profile is the most common LA for dental procedures in most of Europe.2 Lidocaine, though widely used local anesthetic, is associated with systemic toxicity which manifests in myriad ways ranging from simple confusion to CNS depression and even death.

Case Reports

Three otherwise healthy individuals with no previous history of seizure d i s o r d e r d e ve l o p e d t o n i c c l o n i c seizures almost instantly after LA administration for dental extraction. Two were males 22 and 19 years old and one 48 years female . Al l three had maxillary tooth extracted under Lidocaine hydrochloride with

adrenaline 1 in 100,000. In all the patients except for drowsy state other general and systemic examination was normal. In all the patients routine laboratory investigations, CT scan brain and EEG were normal. All were managed conservatively with nasal oxygen and intravenous diazepam. All the patients recovered completely.

Discussion

Lidocaine’s main effects are due to decreased conductance of sodium channels which cause nerve blockade and ant i arrhythmic e f fec t . 3 I t i s hepatically metabolized and excreted via kidneys. Lidocaine toxici ty is primari ly found in CNS and CVS (Table 1). CNS toxicity is biphasic, the ear l ier manifestat ion are due to excitation resulting in seizures followed by CNS depression causing loss of consciousness, respiratory depression or arrest, this is because LA first blocks CNS inhibitory pathways. CVS effects are seen with higher serum concentration. Timing of symptoms is variable. Onset of systemic toxicity occurs within 50 seconds in half of the cases and in the rest is delayed by 5 mins or more. Acid-base status plays an important role in the setting of local anesthetic toxicity. Acidosis and hypercarbia amplify the CNS effects of local anesthetic overdose and exacerbate cardiotoxicity

Because of wide usage and under reporting, the reported incidence of lidocaine toxicity may be inaccurate. One study, estimated a prevalence rate of 0.2% after epidural anesthesia and

1.45% following brachial plexus block.T h e C N S t o x i c i t y i s d i r e c t l y

c o r r e l a t e d w i t h l o c a l a n e s t h e t i c potency. Light headedness, dizziness, headache, perioral paraesthesia, visual disturbances, sedation, dysarthria, metallic taste, hypersalivation, muscle twitching and tremors, consti tute the early manifestation.4 Tonic clonic seizures, eventually unconsciousness and coma are delayed and serious manifestation.

Lidocaine levels in blood can be assayed which co-relates with toxicity. Imaging studies such as CT Brain or EEG may be helpful to rule out other causes of seizures.

If toxicity is suspected then stop the injection immediately. Ensure adequate oxygen by face mask. Benzodiazepines is the drug of choice for seizure control. I.C.U care, monitoring, vasopressors, defibrillation may be useful in CVS toxicity. One important but less known modality is “Intravenous lipid infusions of 20% lipid emulsions”.

Prevention any day better than cure, it is useful to adopt few useful strategies.• Use l owes t concen t ra t ion o f

volume of LA with strict adherence to dosage protocol to give good result.

• Adrenalineinratioof1:200,000inLA, reduces toxicity by slowing vascular uptake.

• A careful injectionmethod is ofprime importance namely perform high volume i.e., more than 5 ml Inj. Slowly in 3 ml increments and stop to aspirate after every 3 ml. It is good practice to maintain verbal contact with the patient which help in detecting subtle symptoms early.

In conclusion, local anesthetics are widely used in offices of general practitioners, dentists and surgeons. Non-anesthesiologists use LA more

Journal of The Association of Physicians of India ■ Vol. 64 ■ March 2016 93

than anesthesiologists do. The incidence of systemic toxicity, eventhough rare, is a definite entity. Early recognition of symptoms, t imely intervention, careful selection of patient and safe practice procedures will go a long way in preventing unpleasant experience to both patient and doctors alike.

remember local anesthetic systemic toxicity as the first thing, before you infiltrate every patient with LA.

References1. Brown DL, Ransom DM, Hall JA, et al. Regional anesthesia

and Local anesthetic induced systemic toxicity; seizure frequency and accompanying Cardiovascular changes.

Anesthesia and Analgesia 1995; 81:321-328.

2. Di Gregorio G. Clinical Presentation of Local Anesthetic Systemic Toxicity- A review of published cases 1979-2009. Regional Anesthesia Pain Medicine 2010; 35:2.

3. Zenouz AT. The incidence of intravascular needle entrance during inferior alveolar nerve block injection Research Dental Clinics, Dental Prospects 2008; 2:1.

4. Weinberg GL. Treatment of Local Anesthetic Systemic Toxicity (LAST). Regional Anesthesia Pain Medicine 2010; 35: 183-193.