The Way to Safe Local Anesthesia

Dr. Mohamed Sayedalahl, MD

Mansoura University, Egypt

Ass.Consultant, KAMC

Monday, February 23, 2015

Wide spread use of LA

Toxicity is prevalent

Lack of awareness

Why This Subject ?

Wide spread use of LANurses, General surgeons, Plastic surgeons, ENT surgeons, Orthopedic surgeons, Obstetricians & Gynecologists, Dentists, Ophthalmologists, Radiologists, Cardiologists, ER physicians, Anesthetists.

Why This Subject ?

Toxicity is prevalent

Why This Subject ?

Lack of awarenessRecent survey in UK, 2010

Less than 50%→ Calculate dose

Less than 25%→ Recommended safe dose

Less than 7% → Intralipid

Less than 3% → Initial dose of Intralipid

Why This Subject ?

Retaining consciousnessNo need for Airway securingLess risk of AspirationLess hemodynamic variationsLess MedicationsLess need for complex MonitoringSuperior Pain controlFaster smooth Recovery & DischargeLess risk of perioperative complicationsLess Cost

Why WE prefer LA ?

1860 cocaine isolated Albert Niemann

1884 Carl Koller, local anesthesia, glaucoma patient

200 cases systemic toxicity & 13 deaths

1904 Novocaine (procaine) by Alfred Einhorn

1943 Lidocaine by Lofgren & Lundquist

1957 Bupivacaine by Ekenstam

1979, 5 reports of cardiac arrests, prolonged unsuccessful CPR.

1983, FDA , 49 cases of cardiac arrests, 0.75% bupivacaine.

Historical Perspective of LA

Historical Perspective of LA

Concurrently, UK, Bupivacaine prohibited in IVRA, 5 deaths

1996, Ropivacaine, safest long acting LA

Levobupivacaine, more potent, less cardiotoxic

N

Lipophilic Head

(Benzene Ring)

Hydrophilic Tail

(Amine)

Intermediate Chain

(Hydrocarbon)Ester

(-CO-)

Amide

(-NHC-)

R

R

H+

Pharmacology

Pharmacology

Lidocaine

Bupivacaine

Etidocaine

Mepivacaine

Prilocaine

Ropivacaine

Chloroprocaine

Cocaine

Procaine

Tetracaine

Block Na+ channels with loss of nerve conduction

Ropivacaine → cardiac K channels

Ropivacaine & Bupivacaine →Ca channels

Pharmacology

- Different pharmacological agents- Only 2-3% enters nerves- Degree of systemic absorption(Intravenous > tracheal > intercostal > caudal > paracervical > epidural> brachial plexus > sciatic > subcutaneous)

- Carried by alpha-1-acid glycoprotein- Metabolize by the liver- Renal dysfunction- cardiac- Elderly- Pediatrics- pregnancy

Toxicity-related pharmacokinetic considerations

Mechanism of LAST

- Blocking neuronal and cardiac NA channels

- Blocking K & Ca channels

- Interference with ATP generation

Contributing Factors

- Where you inject

- How you inject

- What you inject (LA, volume& conc.)

- Who you inject (Body weight & Comorbidities)

Local Anesthetic Systemic Toxicity (LAST)

CNS toxicity of LARelated to the plasma conc. of LAInitially: Circumoral numbness, dizziness, blurring of vision, muscle twitching → tonic-clonic convulsions.Higher plasma conc.:Reduced level of consciousness and eventually coma

Local Anesthetic Systemic Toxicity (LAST)

Cardiac toxicity of LA

Initially: ↑ BP & tachycardia

Higher Conc.: conduction delay, ↑ PR, wide QRS,

ventricular arrhythmia, profound contractile dysfunction → cardiovascular collapse.

Possible contributory mechanisms :

direct –ve intotropic effect

Vasoactivity of LA:Lidocaine

Bupivacaine & levobupivacaine

Ropivacaine

Local Anesthetic Systemic Toxicity (LAST)

Toxicity profile of common LA

Lidocaine Vs Bupivacaine

Order of safety:

Lidocaine˃Ropivacaine˃Levobupivacaine˃Bupivacaine.

Peditric: Cardiac toxicity; 1st.

Local Anesthetic Systemic Toxicity (LAST)

Intralipid20%

FK, 200 gms purified soya bean, 12 gmpurified egg phospholipids, 22 gmanhydrous glycerol, omega 3 & omega 6 FA.

Discovered by chance

↑ bupivacaine cardiac toxicity # protective against toxicity.

Experimental & case reports proof.

Approved: FDA, ASRA, AHA, AAGBI

Intravenous Lipid Emulsion(ILE) Intralipid

Mechanism of action

lipid sink theory: extract lipophilic LA

Metabolic theory: supply FA substrate

Risks :Anaphylaxis

Why Intralipid100% long chain FA # Medialipid & Structolipid

Intravenous Lipid Emulsion(ILE) Intralipid

Treatment of LAST

Be Prepared:Plan for management, LA toxicity KitBe sensible (Risk Reduction)- Use least dose, do not exceed max. dose

- Factors influencing plasma level- Use pharmacologic marker- Aspirate prior to each injection- 5 ml increments- UltrasoundBe Vigilant (Detection)- Standard Monitors, Monitor patient during & after injection,

communicate with the patient frequently, suspect LAST with the early signs, sedatives

Prevention of LAST

- Get help

crash cart

Trained personnel

Monitors & IV access

- Initial Focus

Airway securing

Seizure suppression (avoid propofol)

Alert nearest facility having CPB capability

New 2012 ASRA Guidelines

- Manage Cardiac arrhythmia

Modified ACLS

Consider lower doses of epinephrine(˂1u/kg)

Prepare for prolonged effort

Avoid vasopressin, beta blocker, CCB, LA

Amiodarone

- Obtain Intralipid

New 2012 ASRA Guidelines

- Bolus 1.5 mL/kg IV over 1 minute (~100mL for 70 Kg BW)

- Continuous infusion 0.25 mL/kg/min (~18 mL/min for 70 Kg BW)

- Repeat bolus once or twice

- Double the infusion rate to 0.5 mL/kg/min

- Continue infusion for at least 10 minutes

- Recommended maximum dose 10 ml/kg over the first 30 minutes

New 2012 ASRA GuidelinesIntralipid

- Local anesthetic toxicity is a life threatening complication.

- Early detection & treatment is necessary for good patient outcome.

- 2012 ASRA Guidelines include: Monitoring, Emergency equipment, modified ACLS protocols & familiarity with the lipid emulsion.

Summary