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Local Anaesthesia
 DEFINITION: Local anaesthesia is drug-induced reversible
  local blockade of nerve conduction in a specific part of
  the body that does not alter consciousness.
Prosperities of ideal LA
   Reversible action.
   Non-irritant.
   No allergic reaction.
   No systemic toxicity.
   Rapid onset of action.
   Sufficient duration of action.
   Potent.
   Stable in solutions.
   Not interfere with healing of tissue.
   Have a vasoconstrictor action or compatible with VC.
   Not expensive
structural classification of local
            anaesthetics
•Examples of
amides include
lidocaine,
bupivacaine and
prilocaine.
Examples of esters
include cocaine,
procaine and
amethocaine.
Esters vs Amides
 The ester linkage is more easily broken so the ester drugs
  are less stable in solution and cannot be stored for as long
  as amides.
 Amide anaesthetics are also heat-stable.
 The metabolism of most esters results in the production
  of para-aminobenzoate (PABA) which is associated with
  allergic reaction.
 Amides, in contrast, very rarely cause allergic
  phenomena. For these reasons amides are now more
  commonly used than esters.
The mechanism of action of local
           anaesthetics
 Disruption of ion
  channel function via
  specific binding to
  sodium channels,
  holding them in an
  inactive state.
 Disruption of ion
  channel function by
  the incorporation of
  local anaesthetic
  molecules into the cell
  membrane .
Demonstrating video
 Small nerve fibres are more sensitive than large nerve
 fibres

 Myelinated fibres are blocked before non-myelinated
 fibres of the same diameter.

 Thus the loss of nerve function proceeds as loss of
 pain, temperature, touch, proprioception, and then
 skeletal muscle tone. This is why people may still feel
 touch but not pain when using local anaesthesia.
LA and pH
 All local anaesthetic agents are weak bases, meaning that
  they exist in two forms: unionised (B) and ionised (BH+).

 The pKa of a weak base defines the pH at which both
  forms exist in equal amounts.

 As the pH of the tissues differs from the pKa of the
  specific drug, more of the drug exists either in its charged
  or uncharged form.
Local anaesthetics and infection
 The relevant feature of infected tissue is
  that it tends to be a more acidic
  environment than usual.
 As the pH is reduced the fraction of
  unionised local anaesthetic is reduced
  and consequently the effect is delayed
  and reduced.
 Infected tissue may also have an
  increased blood supply and hence more
  anaesthetic may be removed from the
  area before it can affect the neurone.
Physicochemical characteristics of
  a local anaesthetic affect its
            function
 The aromatic ring structure and hydrocarbon chain length
  determine the lipid solubility of the drug.

 The more lipid soluble drug penetrates the cell
  membrane more easily to exert its effect.

 Thus bupivacaine – which is highly lipid soluble – is
  approximately four times more potent than lidocaine.
The duration of action
 The duration of action of the drug is also related to the
  length of the intermediate chain joining the aromatic and
  amine groups.

 Protein binding , Procaine is only 6% protein bound and
  has a very short duration of action, wherease bupivacaine
  is 95% protein bound. bupivacaine have a longer duration
  of action .
Absorption and distribution
 Some of the drug will be absorbed into the systemic
  circulation: how much will depend on the vascularity of
  the area to which the drug has been applied.

 The distribution of the drug is influenced by the degree of
  tissue and plasma protein binding of the drug. the more
  protein bound the agent, the longer the duration of
  action as free drug is more slowly made available for
  metabolism.
Metabolism and excretion
 Esters (except cocaine) are broken down rapidly by
  plasma esterases to inactive compounds and
  consequently have a short half life. Cocaine is hydrolysed
  in the liver. Ester metabolite excretion is renal.

 Amides are metabolised hepatically by amidases. This is a
  slower process, hence their half-life is longer and they can
  accumulate if given in repeated doses or by infusion.
Adverse Effects
 CNS: excitation followed by depression
  (drowsiness to unconsciousness and
  death due to respiratory depression.

 Cardiovascular System: bradycardia,
  heart block, vasodilation (hypotension)

 Allergic reactions: allergic dermatitis to
  anaphylaxis (rare, but occur most often
  by ester-type drugs).
Mechanism
•Block nerve conduction reversibly.



   Two groups                         amide
Procaine,chloroprocaine,tetracaine    Lidocaine,prillocaine,mepivocaine,bubi
                                      vacaine,ropivacaine

Less common                           More common
Plasma cholinestrase                  Metabolized at liver
More side effect                      less
Uses:
 Local anesthesia.


 Ventricular arrhythmia.


 Decrease haemodynamic response to tracheal intubation
  also decrease cough.

 Treatment of epileptic fits.
Advantage of using adrenaline:
•Epinephrine vasoconstricts arteries reducing bleeding and also delays the
resorption of lidocaine, almost doubling the duration of anaesthesia.



•Bupivacaine has caused several deaths when the epidural anaesthetic
has been administered intravenously accidentally.
Treatment of overdose: lipid rescue

 There is animal evidence that Intralipid, a commonly
  available intravenous lipid emulsion, can be effective in
  treating severe cardiotoxicity secondary to local
  anaesthetic overdose.
Contraindications
 Heart block, second or third degree (without pacemaker)
 Severe sinoatrial block (without pacemaker).
 Serious adverse drug reaction to lidocaine or amide local
  anaesthetics.
 Concurrent treatment with quinidine, flecainide,
  disopyramide, procainamide (Class I antiarrhythmic
  agents).
 Prior use of Amiodarone hydrochloride.
 Hypotension not due to Arrhythmia.
 Bradycardia.
 Accelerated idioventricular rhythm.
Six Placement Sites

Surface/topical   Local infiltration   Peripheral nerve
  anesthesia                                block



 Bier block (IV       Epidural         Spinal anesthesia
   regional          anesthesia
 anesthesia)
Topical/Surface anesthesia
  For Application to mucous membranes:
  Nose- Mouth- Esophagus- Tracheobronchial tree-
     Genitourinary tract.

  Commonly used drugs:
     Cocaine (4%-10%).

     > 50% of rhinolaryngologic cases (USA).

        Unique pharmacological property: produces
        localized vasoconstriction as well as
        anesthesia.
        Localized vasoconstriction:
          less bleeding.

          improved surgical field visualization.
Cocaine substitution:
 lidocaine (Xylocaine) -oxymetazoline
  (Afrin) combinations.
 tetracaine (pontocaine)-
  oxymetazoline (Afrin) combinations.
 Tetracaine (pontocaine) (1%-2%).
 Lidocaine (Xylocaine) (2%-4%).


Ineffective agents:
 Procaine (Novocain) & chloroprocaine
   (Nesacaine): poor mucous membrane
   penetration.
 Nebulized lidocaine (Xylocaine)--
  surface anesthesia

  •   Upper & lower respiratory tract
      prior to bronchoscopy or fiber-
      optic Laryngoscope.
  •   Treatment for intractable cough.
  •   Normal subjects: No effect on
      airflow resistance (they produce
      some bronchodilation).
  •   Patients with asthma: nebulized
      lidocaine (Xylocaine) may increase
      airflow resistance
      (bronchoconstriction)-- concern if
      bronchoscopy is intended for this
      patient group.
 Systemic concentration following nebulized lidocaine (Xylocaine)
     Following mucosal absorption: systemic.
     concentration may be similar to IV injection.

  Reasons:
   Large surface area.

   Significant vascularity of tracheobronchial region.
Skin Surface Application
Barrier: keratinized skin layer
    Higher local anesthetic
      concentrations required:

      o    5% lidocaine (Xylocaine)-
          prilocaine (Citanest) cream
          {2.5% lidocaine (Xylocaine)
          & 2.5% prilocaine
          (Citanest)}
            no local irritation.

            even absorption.

            no systemic toxicity.
Combination of local anesthetic:
Definition: eutectic mixture of local anesthetics (EMLA) .
General definition: eutectic--said of a mixture which has the lowest melting
  point which it is possible to obtain by the combination of the given
  components.
Melting point of combined drug is lower then either lidocaine (Xylocaine) or
  prilocaine (Citanest) alone.
Clinical uses of EMLA applications-- pain relief for:

   Venipuncture


   Lumbar puncture


   Arterial cannulation
Special uses
          In combination with nitroglycerin ointment -- makes venous
           cannulation easier by causing vasodilation.
          EMLA use in blood sampling: no effect on blood analysis.




Factors affecting EMLA analgesia time to onset, duration of action, & efficacy

            Skin blood flow.
            Epidermal/girl thickness.
            Application duration.
            Presence of pathology.
Contraindications/Concerns

   EMLA cream not recommended for mucosal application
   due to faster lidocaine (Xylocaine)/prilocaine (Citanest)
   absorption.

   EMLA cream not recommended for application to skin
   wounds (wound infection risk, increased)

   EMLA cream: contraindicated in patients are allergic to
   amide local anesthetics
Local Infiltration
 Definition: Extravascular placement of the local anesthetic in the region to
  be anesthetized.
    Example: subcutaneous local anesthetic injection in support of
     intravascular cannula placement.

 Preferred local anesthetics for local infiltration:
     Most common: lidocaine (Xylocaine).
     Other choices: 0.25% Ropivacaine (Naropin) or Bupivacaine (Marcaine)
      (effective for pain management at inguinal operative location),
 Duration of action:

   Duration extended by 2x using 1:200,000 epinephrine.


   Caution: Epinephrine-containing local anesthetic solution should not be
    injected intracutaneously (intradermal) or into tissues supplied by
    "end-arteries" such as ears, nose, fingers because vasoconstriction may
    be sufficiently severe to produce tissue ischemia and gangrene.
Peripheral Nerve Block
 Procedure: local anesthetic injection into tissues around individual nerves
  or nerve plexuses (e.g. brachial plexus).

 Mechanism:
    Local anesthetic diffusion path: nerve outer surface (mantle) to the
     nerve core [driving force: concentration gradient].
    Anesthetized first: mantle fibers (innervating more proximal
     structures).
    Anesthetized last: core fibers (innervating more distal anatomy)
      Explanation of why anesthesia develops proximately first.

      Recovery in the opposite direction (sensation returns proximally first;
        lastly the distal anatomy).
•The median nerve is blocked
by inserting the needle
between the tendons of the
palmaris longus and flexor
carpi radialis. The needle is
inserted until it pierces the
deep fascia. Three to 5 mL of
local anesthetic is injected.
Although the piercing of the
deep fascia has been described
to result in a fascial "click", it is
more reliable to simply insert
the needle until it contacts the
bone. The needle is then
withdrawn 2-3 mm and the
local anesthetic is injected.
 Mixed peripheral nerves: (motor/sensory)


    Sequence of onset & recovery (motor anesthesia first or sensory
     anesthesia first): dependent on anatomical locations within the nerve
     fiber.

 Not recommended: Tetracaine (pontocaine): slow onset & more likely to
  cause systemic toxicity; not recommended for peripheral nerve block or for
  local infiltration.
Duration of action-dependencies

  • Prolongation of drug effect:
    safer with added vasoconstrictor (e.g. epinephrine) than
      by increasing local anesthetic dose.

   Example: bupivacaine (Marcaine) + epinephrine:
    peripheral nerve block may last 14 hours (in some
    reports).
Intravenous Regional Anesthesia
            (Bier Block)
Procedure:
   Local anesthetic injection into an
      extremity isolated by tourniquet.
   Result: rapid anesthesia onset; skeletal
      muscle relaxation.
Duration of anesthetic action:
   Dependent on how long the tourniquet
      is kept inflated.
   Following tourniquet deflation: rapid
      recovery as blood dilutes local
      anesthetic concentration.
Probable Mechanism:
   Drug action on nerve endings & nerve
      trunks.
Lidocaine                     Prilocaine
                      Higher                lower plasma prilocaine
                                           (Citanest) concentrations
                                              following tourniquet
                                             deflation, compared to
                                                    lidocaine
                       Less                          Safer

Agents not recommended:
      Chloroprocaine (Nesacaine) -- High incidence of thrombophlebitis.



          Bupivacaine (Marcaine) -- More likely than other local anesthetic to
          cause cardiotoxicity upon tourniquet deflation.

          Ropivacaine (Naropin)-Might also cause cardiotoxicity upon
          tourniquet deflation (less likely than with bupivacaine (Marcaine)).
Indications for local anesthesia
 Most frequent use: regional anesthesia.


 Analgesic espescially post operative pain.


 Lidocaine (Xylocaine) also reduces blood pressure response to direct
  laryngoscopic tracheal intubation, an effect probably secondary to
  generalized cardiovascular depression.

 Treatment of intractable cough.
1-Causes.
2-Factors reducing toxicity.
3-Signs and symptoms.
4-Treatment of toxicity.
Causes :
 Accidental rapid
  intravenous injection

 Rapid absorption, such as
  from a very vascular site
  ie mucous membranes.

 Overdose .
Factors reducing toxicity:

 Decide on the concentration of the local anaesthetic that
  is required for the block to be performed. Calculate the
  total volume of drug that is allowed according to the
  table below
 Use the least toxic drug available


 Use lower doses in frail patients or at the extremes of
  ages

 Always inject the drug slowly (slower than 10ml /minute)
  and aspirate regularly looking for blood to indicate an
  accidental intravenous injection

 Injection of a test dose of 2-3ml of local anaesthetic
  containing adrenaline will often (but not always) cause a
  significant tachycardia if accidental intravenous injection
  occurs
 Add adrenaline (epinephrine) to reduce the speed of
  absorption. The addition of adrenaline will reduce the
  maximum blood concentration by about 50%. Usually
  adrenaline is added in a concentration of 1:200,000, with
  a maximum dose of 200 micrograms.

 Make sure that the patient is monitored closely by the
  anaesthetist or a trained nurse during the administration
  of the local anaesthetic and the following surgery.
Signs and Symptoms of Local
         Anaesthetic Toxicity:
1-CNS toxicity :

 Early or mild toxicity: light-headedness, dizziness,
  tinnitus, circumoral numbness, abnormal taste, confusion
  and drowsiness.

 Severe toxicity: tonic-clonic convulsion leading to
  progressive loss of consciousness, coma, respiratory
  depression, and respiratory arrest.
2-CVS toxicity:

 Early or mild toxicity: tachycardia and rise in blood
  pressure. This will usually only occur if there is adrenaline
  in the local anaesthetic. If no adrenaline is added then
  bradycardia with hypotension will occur.

 Severe toxicity: Usually about 4 - 7 times the convulsant
  dose needs to be injected before cardiovascular collapse
  occurs. Collapse is due to the depressant effect of the
  local anaesthetic acting directly on the myocardium.
Essential Precautions:
 Secure intravenous access before injection of any dose
  that may cause toxic effects
 Always have adequate resuscitation equipment and drugs
  available before starting to inject.
Treatment of Toxicity:
Treatment is based on the A B C D of Basic Life Support :
 A. Ensure an adequate airway, give oxygen in high
  concentration if available

 B.  Ensure that the patient is breathing adequately.
  Ventilate the patient with a self inflating bag if there is
  inadequate spontaneous respiration. Intubation may be
  required if the patient is unconscious and unable to
  maintain an airway.
C    Treat circulatory failure with intravenous fluids and
 vasopressors such as ephedrine (10mg boluses) if
 hypotension occurs. Adrenaline may be used cautiously
 intravenously in boluses of 0.5 - 1ml of 1:10,000 (1mg in
 10ml) if ephedrine is either not available or not effective
 in correcting the hypotension. Treat arrhythmias
D     Drugs to stop fitting such as Diazepam 0.2-0.4mg/kg
  intravenously slowly over 5 minutes repeated after 10
  minutes if required, or 2.5mg - 10 mg rectally.
  Thiopentone 1-4 mg/kg intravenously may also be used in
  theatre

 Treatment of local anaesthetic toxicity is likely to have a
  good outcome if toxicity is recognised and basic
  resuscitation is started early. Monitor patients closely
  when using local anaesthetics. If a reaction occurs.
Advantages of local anaesthesia
 Non inflammable.

 Excellent muscle relaxant effect.

 During local anesthesia the patient remains conscious.

 It requires less skilled nursing care as compared to other
  anesthesia like general anesthesia.

 Maintains his own airway.
 Less pulmonary complication.s

 Aspiration of gastric contents unlikely.

 Less nausea and vomiting.

 Contracted bowel so helpful in abdominal and pelvic surgery.

 Postoperative analgesia.

 There is reduction surgical stress.

 Earlier discharge for outpatients.
 Suitable for patients who recently ingested food or fluids.

 Local anesthesia is useful for ambulatory patients having
  minor
 procedures.

 Ideal for procedures in which it is desirable to have the patient
  awake and cooperative.

 Less bleeding.

 Expenses are less.
Disadvantages of local anaesthesia
 There are individual variations in response to local anesthetic
  drugs.

 Rapid absorption of the drug into the bloodstream can cause
  severe, potentially fatal reactions.

 Apprehension may be increased by the patient's ability to see
  and hear. Some patients prefer to be unconscious and
  unaware.
 Direct damage of nerve.


 Post-dural headache from CSF leak.


 Hypotension and bradycardia through blockade of the
  sympathetic nervous system.

 Not suitable for extremes of ages.


 Multiple needle bricks may be needed.
Introduction
 Spinal anesthesia also
  called spinal analgesia or
  sub-arachnoid block (SAB),
  is a form of regional
  anesthesia involving
  injection of a local
  anesthetic into the
  subarachnoid space,
  generally through a fine
  needle.
Difference from epidural anesthesia
 Epidural anesthesia is a technique whereby a local
  anesthetic drug is injected through a catheter placed into
  the epidural space. This technique has some similarity to
  spinal anesthesia, and the two techniques may be easily
  confused with each other.
Differences include:
 The involved space is larger for an epidural, and
  consequently the injected dose is larger, being about 10–
  20 mL in epidural anesthesia compared to 1.5–3.5 mL in a
  spinal.
 In an epidural, an indwelling catheter may be placed that
  avails for additional injections later, while a spinal is
  almost always a one-shot only.
 The onset of analgesia is approximately 15–30 minutes in
  an epidural, while it is approximately 5 minutes in a
  spinal.
Injected substances
 Bupivacaine (Marcaine) is the local anaesthetic most
  commonly used, although lignocaine (lidocaine),
  tetracaine, procaine, ropivacaine, levobupivicaine and
  cinchocaine may also be used.
 Sometimes a vasoconstrictor such as epinephrine is
  added to the local anaesthetic to prolong its duration.
Mechanism
 Regardless of the anesthetic agent (drug) used, the
  desired effect is to block the transmission of afferent
  nerve signals from peripheral nociceptors.

 Sensory signals from the site are blocked, thereby
  eliminating pain.

 The degree of neuronal blockade depends on the amount
  and concentration of local anesthetic used and the
  properties of the axon.
Limitations
 Spinal anesthetics are typically limited to procedures
  involving most structures below the upper abdomen.

 To administer a spinal anesthetic to higher levels may
  affect the ability to breathe by paralyzing the intercostal
  respiratory muscles, or even the diaphragm in extreme
  cases (called a "high spinal", or a "total spinal", with
  which consciousness is lost).
Indications
 This technique is very useful in patients having an irritable
  airway (bronchial asthma or allergic bronchitis),
  anatomical abnormalities which make endotracheal
  intubation very difficult (micrognathia), borderline
  hypertensives where administration of general anesthesia
  or endotracheal intubation can further elevate the blood
  pressure, procedures in geriatric patients.
Contraindications
 Non-availability of patient's consent, local infection or
  sepsis at the site of lumbar puncture, bleeding disorders,
  space occupying lesions of the brain, disorders of the
  spine and maternal hypotension.
Operations
All surgical interventions below the umbilicus, is the general
  guiding principle:
 Abdominal & vaginal hysterectomies
 Laparoscopy Assisted Vaginal Hysterectomies (LAVH)
    combined with general anesthesia
   Caesarean sections
   Hernia (inguinal or epigastric)
   Piles fistulae & fissures
   orthopaedic surgeries on the pelvis, femur, tibia and the ankle
   nephrectomy
Complications
  Can be broadly classified as immediate (on the operating
  table) or late (in the ward or in the P.A.C.U. post-anesthesia
  care unit):
 Spinal shock.

 Cauda equina injury.

 Cardiac arrest.

 Hypothermia.

 Broken needle.

 Bleeding resulting in hematoma, with or without subsequent neurological
  sequelae due to compression of the spinal nerves.
 Infection: immediate within six hours of the spinal anesthetic
  manifesting as meningism or meningitis or late, at the site of
  injection, in the form of pus discharge, due to improper
  sterilization of the LP set.

 PDPH: Post dural puncture head ache or post spinal head ache.
Epidural anesthesia
Mechanism
 Direct action on nerve
  roots and spinal cord
  following local anesthetic
  diffusion across the dura.

 Diffusion of local
  anesthetic into
  paravertebral region.
 Onset of action:15-30
  minute delay .

 Choice of local anesthetics:
    Lidocaine (Xylocaine):
     frequently used; diffuses
     well for tissues.
    Bupivacaine (Marcaine)
     & Ropivacaine (Naropin)
     (0.5%-0.75%).
Epidural anathesia                  Spinal anathesia


Site of injection    In the epidural space               Subarachnoid space


Onset and duration   Slow onset and continous duration   Rapid onset and limited
                     (use catheter)                      duration

advantages           Can be used in analgesia            Not used


Needle               Curved,longand blunt (touhy)        Small and sharp
dose                 10_30ml                             1_4ml

space                Any space usually lumber            lumber


Quality of sensory   less                                More liable
and motor nerve
block
toxicity             Hypotention gradual                 Sudden
                     total spinal +++                    +
                     systemic toxicity +++               +
 Indications:
  1-Pain relief:
  a)Post operative
  b)Labour pain
  c)Cancer

  2-Operations in perineum lower limb
  lower abdomen.

  3-Expected difficult intubation.

 An epidural injection may be
  performed anywhere along the
  vertebral column (cervical, thoracic,
  lumbar, or sacral).
Contra indications:
 A)absolute:
 1-Hypovolemia.
 2-Refusal of patient.
 3-Coagulopathy.
 4-Local and systemic sepsis.

 B)relative:
 - Increase intra cranial pressure deformity of vertebral
 column.
Complications

A)during operation:

   1)Hypotension
   2)Bradycardia
   3)Cardiac arrest
   4)Nausea ,vomiting
   5)Failed spinal
   6)Total spinal
   7)Broken needle
   8)Hypothermia
 B)Post operative:


  1)Post dural puncture
  headache.
  2)Back pain.
  3)Meningitis and
  neurological sequalae.
  4)Haematoma.
  5)Urine retention.

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Local anaesthesia

  • 1.
  • 2. Local Anaesthesia  DEFINITION: Local anaesthesia is drug-induced reversible local blockade of nerve conduction in a specific part of the body that does not alter consciousness.
  • 3. Prosperities of ideal LA  Reversible action.  Non-irritant.  No allergic reaction.  No systemic toxicity.  Rapid onset of action.  Sufficient duration of action.  Potent.  Stable in solutions.  Not interfere with healing of tissue.  Have a vasoconstrictor action or compatible with VC.  Not expensive
  • 4. structural classification of local anaesthetics •Examples of amides include lidocaine, bupivacaine and prilocaine. Examples of esters include cocaine, procaine and amethocaine.
  • 5.
  • 6. Esters vs Amides  The ester linkage is more easily broken so the ester drugs are less stable in solution and cannot be stored for as long as amides.  Amide anaesthetics are also heat-stable.  The metabolism of most esters results in the production of para-aminobenzoate (PABA) which is associated with allergic reaction.  Amides, in contrast, very rarely cause allergic phenomena. For these reasons amides are now more commonly used than esters.
  • 7. The mechanism of action of local anaesthetics  Disruption of ion channel function via specific binding to sodium channels, holding them in an inactive state.  Disruption of ion channel function by the incorporation of local anaesthetic molecules into the cell membrane .
  • 9.  Small nerve fibres are more sensitive than large nerve fibres  Myelinated fibres are blocked before non-myelinated fibres of the same diameter.  Thus the loss of nerve function proceeds as loss of pain, temperature, touch, proprioception, and then skeletal muscle tone. This is why people may still feel touch but not pain when using local anaesthesia.
  • 10. LA and pH  All local anaesthetic agents are weak bases, meaning that they exist in two forms: unionised (B) and ionised (BH+).  The pKa of a weak base defines the pH at which both forms exist in equal amounts.  As the pH of the tissues differs from the pKa of the specific drug, more of the drug exists either in its charged or uncharged form.
  • 11.
  • 12. Local anaesthetics and infection  The relevant feature of infected tissue is that it tends to be a more acidic environment than usual.  As the pH is reduced the fraction of unionised local anaesthetic is reduced and consequently the effect is delayed and reduced.  Infected tissue may also have an increased blood supply and hence more anaesthetic may be removed from the area before it can affect the neurone.
  • 13. Physicochemical characteristics of a local anaesthetic affect its function  The aromatic ring structure and hydrocarbon chain length determine the lipid solubility of the drug.  The more lipid soluble drug penetrates the cell membrane more easily to exert its effect.  Thus bupivacaine – which is highly lipid soluble – is approximately four times more potent than lidocaine.
  • 14. The duration of action  The duration of action of the drug is also related to the length of the intermediate chain joining the aromatic and amine groups.  Protein binding , Procaine is only 6% protein bound and has a very short duration of action, wherease bupivacaine is 95% protein bound. bupivacaine have a longer duration of action .
  • 15.
  • 16. Absorption and distribution  Some of the drug will be absorbed into the systemic circulation: how much will depend on the vascularity of the area to which the drug has been applied.  The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. the more protein bound the agent, the longer the duration of action as free drug is more slowly made available for metabolism.
  • 17. Metabolism and excretion  Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal.  Amides are metabolised hepatically by amidases. This is a slower process, hence their half-life is longer and they can accumulate if given in repeated doses or by infusion.
  • 18. Adverse Effects  CNS: excitation followed by depression (drowsiness to unconsciousness and death due to respiratory depression.  Cardiovascular System: bradycardia, heart block, vasodilation (hypotension)  Allergic reactions: allergic dermatitis to anaphylaxis (rare, but occur most often by ester-type drugs).
  • 19. Mechanism •Block nerve conduction reversibly. Two groups amide Procaine,chloroprocaine,tetracaine Lidocaine,prillocaine,mepivocaine,bubi vacaine,ropivacaine Less common More common Plasma cholinestrase Metabolized at liver More side effect less
  • 20. Uses:  Local anesthesia.  Ventricular arrhythmia.  Decrease haemodynamic response to tracheal intubation also decrease cough.  Treatment of epileptic fits.
  • 21. Advantage of using adrenaline: •Epinephrine vasoconstricts arteries reducing bleeding and also delays the resorption of lidocaine, almost doubling the duration of anaesthesia. •Bupivacaine has caused several deaths when the epidural anaesthetic has been administered intravenously accidentally.
  • 22. Treatment of overdose: lipid rescue  There is animal evidence that Intralipid, a commonly available intravenous lipid emulsion, can be effective in treating severe cardiotoxicity secondary to local anaesthetic overdose.
  • 23. Contraindications  Heart block, second or third degree (without pacemaker)  Severe sinoatrial block (without pacemaker).  Serious adverse drug reaction to lidocaine or amide local anaesthetics.  Concurrent treatment with quinidine, flecainide, disopyramide, procainamide (Class I antiarrhythmic agents).  Prior use of Amiodarone hydrochloride.
  • 24.  Hypotension not due to Arrhythmia.  Bradycardia.  Accelerated idioventricular rhythm.
  • 25.
  • 26. Six Placement Sites Surface/topical Local infiltration Peripheral nerve anesthesia block Bier block (IV Epidural Spinal anesthesia regional anesthesia anesthesia)
  • 27. Topical/Surface anesthesia For Application to mucous membranes: Nose- Mouth- Esophagus- Tracheobronchial tree- Genitourinary tract. Commonly used drugs:  Cocaine (4%-10%).  > 50% of rhinolaryngologic cases (USA).  Unique pharmacological property: produces localized vasoconstriction as well as anesthesia.  Localized vasoconstriction:  less bleeding.  improved surgical field visualization.
  • 28. Cocaine substitution:  lidocaine (Xylocaine) -oxymetazoline (Afrin) combinations.  tetracaine (pontocaine)- oxymetazoline (Afrin) combinations.  Tetracaine (pontocaine) (1%-2%).  Lidocaine (Xylocaine) (2%-4%). Ineffective agents:  Procaine (Novocain) & chloroprocaine (Nesacaine): poor mucous membrane penetration.
  • 29.  Nebulized lidocaine (Xylocaine)-- surface anesthesia • Upper & lower respiratory tract prior to bronchoscopy or fiber- optic Laryngoscope. • Treatment for intractable cough. • Normal subjects: No effect on airflow resistance (they produce some bronchodilation). • Patients with asthma: nebulized lidocaine (Xylocaine) may increase airflow resistance (bronchoconstriction)-- concern if bronchoscopy is intended for this patient group.
  • 30.  Systemic concentration following nebulized lidocaine (Xylocaine)  Following mucosal absorption: systemic.  concentration may be similar to IV injection. Reasons:  Large surface area.  Significant vascularity of tracheobronchial region.
  • 31. Skin Surface Application Barrier: keratinized skin layer  Higher local anesthetic concentrations required: o 5% lidocaine (Xylocaine)- prilocaine (Citanest) cream {2.5% lidocaine (Xylocaine) & 2.5% prilocaine (Citanest)}  no local irritation.  even absorption.  no systemic toxicity.
  • 32. Combination of local anesthetic: Definition: eutectic mixture of local anesthetics (EMLA) . General definition: eutectic--said of a mixture which has the lowest melting point which it is possible to obtain by the combination of the given components. Melting point of combined drug is lower then either lidocaine (Xylocaine) or prilocaine (Citanest) alone.
  • 33. Clinical uses of EMLA applications-- pain relief for:  Venipuncture  Lumbar puncture  Arterial cannulation
  • 34. Special uses  In combination with nitroglycerin ointment -- makes venous cannulation easier by causing vasodilation.  EMLA use in blood sampling: no effect on blood analysis. Factors affecting EMLA analgesia time to onset, duration of action, & efficacy  Skin blood flow.  Epidermal/girl thickness.  Application duration.  Presence of pathology.
  • 35. Contraindications/Concerns  EMLA cream not recommended for mucosal application due to faster lidocaine (Xylocaine)/prilocaine (Citanest) absorption.  EMLA cream not recommended for application to skin wounds (wound infection risk, increased)  EMLA cream: contraindicated in patients are allergic to amide local anesthetics
  • 36. Local Infiltration  Definition: Extravascular placement of the local anesthetic in the region to be anesthetized.  Example: subcutaneous local anesthetic injection in support of intravascular cannula placement.  Preferred local anesthetics for local infiltration:  Most common: lidocaine (Xylocaine).  Other choices: 0.25% Ropivacaine (Naropin) or Bupivacaine (Marcaine) (effective for pain management at inguinal operative location),
  • 37.  Duration of action:  Duration extended by 2x using 1:200,000 epinephrine.  Caution: Epinephrine-containing local anesthetic solution should not be injected intracutaneously (intradermal) or into tissues supplied by "end-arteries" such as ears, nose, fingers because vasoconstriction may be sufficiently severe to produce tissue ischemia and gangrene.
  • 38. Peripheral Nerve Block  Procedure: local anesthetic injection into tissues around individual nerves or nerve plexuses (e.g. brachial plexus).  Mechanism:  Local anesthetic diffusion path: nerve outer surface (mantle) to the nerve core [driving force: concentration gradient].  Anesthetized first: mantle fibers (innervating more proximal structures).  Anesthetized last: core fibers (innervating more distal anatomy)  Explanation of why anesthesia develops proximately first.  Recovery in the opposite direction (sensation returns proximally first; lastly the distal anatomy).
  • 39. •The median nerve is blocked by inserting the needle between the tendons of the palmaris longus and flexor carpi radialis. The needle is inserted until it pierces the deep fascia. Three to 5 mL of local anesthetic is injected. Although the piercing of the deep fascia has been described to result in a fascial "click", it is more reliable to simply insert the needle until it contacts the bone. The needle is then withdrawn 2-3 mm and the local anesthetic is injected.
  • 40.
  • 41.
  • 42.  Mixed peripheral nerves: (motor/sensory)  Sequence of onset & recovery (motor anesthesia first or sensory anesthesia first): dependent on anatomical locations within the nerve fiber.  Not recommended: Tetracaine (pontocaine): slow onset & more likely to cause systemic toxicity; not recommended for peripheral nerve block or for local infiltration.
  • 43. Duration of action-dependencies • Prolongation of drug effect: safer with added vasoconstrictor (e.g. epinephrine) than by increasing local anesthetic dose.  Example: bupivacaine (Marcaine) + epinephrine: peripheral nerve block may last 14 hours (in some reports).
  • 44. Intravenous Regional Anesthesia (Bier Block) Procedure: Local anesthetic injection into an extremity isolated by tourniquet. Result: rapid anesthesia onset; skeletal muscle relaxation. Duration of anesthetic action: Dependent on how long the tourniquet is kept inflated. Following tourniquet deflation: rapid recovery as blood dilutes local anesthetic concentration. Probable Mechanism: Drug action on nerve endings & nerve trunks.
  • 45.
  • 46. Lidocaine Prilocaine Higher lower plasma prilocaine (Citanest) concentrations following tourniquet deflation, compared to lidocaine Less Safer Agents not recommended:  Chloroprocaine (Nesacaine) -- High incidence of thrombophlebitis.  Bupivacaine (Marcaine) -- More likely than other local anesthetic to cause cardiotoxicity upon tourniquet deflation.  Ropivacaine (Naropin)-Might also cause cardiotoxicity upon tourniquet deflation (less likely than with bupivacaine (Marcaine)).
  • 47. Indications for local anesthesia  Most frequent use: regional anesthesia.  Analgesic espescially post operative pain.  Lidocaine (Xylocaine) also reduces blood pressure response to direct laryngoscopic tracheal intubation, an effect probably secondary to generalized cardiovascular depression.  Treatment of intractable cough.
  • 48.
  • 49. 1-Causes. 2-Factors reducing toxicity. 3-Signs and symptoms. 4-Treatment of toxicity.
  • 50. Causes :  Accidental rapid intravenous injection  Rapid absorption, such as from a very vascular site ie mucous membranes.  Overdose .
  • 51. Factors reducing toxicity:  Decide on the concentration of the local anaesthetic that is required for the block to be performed. Calculate the total volume of drug that is allowed according to the table below
  • 52.
  • 53.  Use the least toxic drug available  Use lower doses in frail patients or at the extremes of ages  Always inject the drug slowly (slower than 10ml /minute) and aspirate regularly looking for blood to indicate an accidental intravenous injection  Injection of a test dose of 2-3ml of local anaesthetic containing adrenaline will often (but not always) cause a significant tachycardia if accidental intravenous injection occurs
  • 54.  Add adrenaline (epinephrine) to reduce the speed of absorption. The addition of adrenaline will reduce the maximum blood concentration by about 50%. Usually adrenaline is added in a concentration of 1:200,000, with a maximum dose of 200 micrograms.  Make sure that the patient is monitored closely by the anaesthetist or a trained nurse during the administration of the local anaesthetic and the following surgery.
  • 55. Signs and Symptoms of Local Anaesthetic Toxicity: 1-CNS toxicity :  Early or mild toxicity: light-headedness, dizziness, tinnitus, circumoral numbness, abnormal taste, confusion and drowsiness.  Severe toxicity: tonic-clonic convulsion leading to progressive loss of consciousness, coma, respiratory depression, and respiratory arrest.
  • 56. 2-CVS toxicity:  Early or mild toxicity: tachycardia and rise in blood pressure. This will usually only occur if there is adrenaline in the local anaesthetic. If no adrenaline is added then bradycardia with hypotension will occur.  Severe toxicity: Usually about 4 - 7 times the convulsant dose needs to be injected before cardiovascular collapse occurs. Collapse is due to the depressant effect of the local anaesthetic acting directly on the myocardium.
  • 57.
  • 58. Essential Precautions:  Secure intravenous access before injection of any dose that may cause toxic effects  Always have adequate resuscitation equipment and drugs available before starting to inject.
  • 59. Treatment of Toxicity: Treatment is based on the A B C D of Basic Life Support :  A. Ensure an adequate airway, give oxygen in high concentration if available  B. Ensure that the patient is breathing adequately. Ventilate the patient with a self inflating bag if there is inadequate spontaneous respiration. Intubation may be required if the patient is unconscious and unable to maintain an airway.
  • 60. C Treat circulatory failure with intravenous fluids and vasopressors such as ephedrine (10mg boluses) if hypotension occurs. Adrenaline may be used cautiously intravenously in boluses of 0.5 - 1ml of 1:10,000 (1mg in 10ml) if ephedrine is either not available or not effective in correcting the hypotension. Treat arrhythmias
  • 61. D Drugs to stop fitting such as Diazepam 0.2-0.4mg/kg intravenously slowly over 5 minutes repeated after 10 minutes if required, or 2.5mg - 10 mg rectally. Thiopentone 1-4 mg/kg intravenously may also be used in theatre  Treatment of local anaesthetic toxicity is likely to have a good outcome if toxicity is recognised and basic resuscitation is started early. Monitor patients closely when using local anaesthetics. If a reaction occurs.
  • 62. Advantages of local anaesthesia  Non inflammable.  Excellent muscle relaxant effect.  During local anesthesia the patient remains conscious.  It requires less skilled nursing care as compared to other anesthesia like general anesthesia.  Maintains his own airway.
  • 63.  Less pulmonary complication.s  Aspiration of gastric contents unlikely.  Less nausea and vomiting.  Contracted bowel so helpful in abdominal and pelvic surgery.  Postoperative analgesia.  There is reduction surgical stress.  Earlier discharge for outpatients.
  • 64.  Suitable for patients who recently ingested food or fluids.  Local anesthesia is useful for ambulatory patients having minor  procedures.  Ideal for procedures in which it is desirable to have the patient awake and cooperative.  Less bleeding.  Expenses are less.
  • 65. Disadvantages of local anaesthesia  There are individual variations in response to local anesthetic drugs.  Rapid absorption of the drug into the bloodstream can cause severe, potentially fatal reactions.  Apprehension may be increased by the patient's ability to see and hear. Some patients prefer to be unconscious and unaware.
  • 66.  Direct damage of nerve.  Post-dural headache from CSF leak.  Hypotension and bradycardia through blockade of the sympathetic nervous system.  Not suitable for extremes of ages.  Multiple needle bricks may be needed.
  • 67.
  • 68. Introduction  Spinal anesthesia also called spinal analgesia or sub-arachnoid block (SAB), is a form of regional anesthesia involving injection of a local anesthetic into the subarachnoid space, generally through a fine needle.
  • 69. Difference from epidural anesthesia  Epidural anesthesia is a technique whereby a local anesthetic drug is injected through a catheter placed into the epidural space. This technique has some similarity to spinal anesthesia, and the two techniques may be easily confused with each other.
  • 70. Differences include:  The involved space is larger for an epidural, and consequently the injected dose is larger, being about 10– 20 mL in epidural anesthesia compared to 1.5–3.5 mL in a spinal.  In an epidural, an indwelling catheter may be placed that avails for additional injections later, while a spinal is almost always a one-shot only.  The onset of analgesia is approximately 15–30 minutes in an epidural, while it is approximately 5 minutes in a spinal.
  • 71. Injected substances  Bupivacaine (Marcaine) is the local anaesthetic most commonly used, although lignocaine (lidocaine), tetracaine, procaine, ropivacaine, levobupivicaine and cinchocaine may also be used.  Sometimes a vasoconstrictor such as epinephrine is added to the local anaesthetic to prolong its duration.
  • 72. Mechanism  Regardless of the anesthetic agent (drug) used, the desired effect is to block the transmission of afferent nerve signals from peripheral nociceptors.  Sensory signals from the site are blocked, thereby eliminating pain.  The degree of neuronal blockade depends on the amount and concentration of local anesthetic used and the properties of the axon.
  • 73. Limitations  Spinal anesthetics are typically limited to procedures involving most structures below the upper abdomen.  To administer a spinal anesthetic to higher levels may affect the ability to breathe by paralyzing the intercostal respiratory muscles, or even the diaphragm in extreme cases (called a "high spinal", or a "total spinal", with which consciousness is lost).
  • 74. Indications  This technique is very useful in patients having an irritable airway (bronchial asthma or allergic bronchitis), anatomical abnormalities which make endotracheal intubation very difficult (micrognathia), borderline hypertensives where administration of general anesthesia or endotracheal intubation can further elevate the blood pressure, procedures in geriatric patients.
  • 75. Contraindications  Non-availability of patient's consent, local infection or sepsis at the site of lumbar puncture, bleeding disorders, space occupying lesions of the brain, disorders of the spine and maternal hypotension.
  • 76. Operations All surgical interventions below the umbilicus, is the general guiding principle:  Abdominal & vaginal hysterectomies  Laparoscopy Assisted Vaginal Hysterectomies (LAVH) combined with general anesthesia  Caesarean sections  Hernia (inguinal or epigastric)  Piles fistulae & fissures  orthopaedic surgeries on the pelvis, femur, tibia and the ankle  nephrectomy
  • 77. Complications Can be broadly classified as immediate (on the operating table) or late (in the ward or in the P.A.C.U. post-anesthesia care unit):  Spinal shock.  Cauda equina injury.  Cardiac arrest.  Hypothermia.  Broken needle.  Bleeding resulting in hematoma, with or without subsequent neurological sequelae due to compression of the spinal nerves.
  • 78.  Infection: immediate within six hours of the spinal anesthetic manifesting as meningism or meningitis or late, at the site of injection, in the form of pus discharge, due to improper sterilization of the LP set.  PDPH: Post dural puncture head ache or post spinal head ache.
  • 79.
  • 81. Mechanism  Direct action on nerve roots and spinal cord following local anesthetic diffusion across the dura.  Diffusion of local anesthetic into paravertebral region.
  • 82.  Onset of action:15-30 minute delay .  Choice of local anesthetics:  Lidocaine (Xylocaine): frequently used; diffuses well for tissues.  Bupivacaine (Marcaine) & Ropivacaine (Naropin) (0.5%-0.75%).
  • 83. Epidural anathesia Spinal anathesia Site of injection In the epidural space Subarachnoid space Onset and duration Slow onset and continous duration Rapid onset and limited (use catheter) duration advantages Can be used in analgesia Not used Needle Curved,longand blunt (touhy) Small and sharp dose 10_30ml 1_4ml space Any space usually lumber lumber Quality of sensory less More liable and motor nerve block toxicity Hypotention gradual Sudden total spinal +++ + systemic toxicity +++ +
  • 84.  Indications: 1-Pain relief: a)Post operative b)Labour pain c)Cancer 2-Operations in perineum lower limb lower abdomen. 3-Expected difficult intubation.  An epidural injection may be performed anywhere along the vertebral column (cervical, thoracic, lumbar, or sacral).
  • 85. Contra indications: A)absolute: 1-Hypovolemia. 2-Refusal of patient. 3-Coagulopathy. 4-Local and systemic sepsis. B)relative: - Increase intra cranial pressure deformity of vertebral column.
  • 86. Complications A)during operation: 1)Hypotension 2)Bradycardia 3)Cardiac arrest 4)Nausea ,vomiting 5)Failed spinal 6)Total spinal 7)Broken needle 8)Hypothermia
  • 87.  B)Post operative: 1)Post dural puncture headache. 2)Back pain. 3)Meningitis and neurological sequalae. 4)Haematoma. 5)Urine retention.