PHYSIOLOGY OF PAIN AND LOCAL ANESTHESIA

Pain

“ an unpleasant feeling often caused by intense or damaging stimuli, such as

stubbing a toe, burning a finger, putting alcohol on a cut, and bumping the "funny

bone.”-Wikipedia

“Pain is the psychical adjunct of an imperative protective reflex.”-According to Sheringhton (1906)

“Pain as an unpleasant sensory experience evoked by stimuli that injures”

-Mountcastle (1968)

“ Pain as an unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damage”

-International association for the study of pain IASP (1979)

ORIGIN OF PAIN: Pain from external sources

-from mechanical, chemicals and thermal sources, withdrawal is possible Pain from internal sources

-Mainly from chemical sources, usually dull, may be referred, last long Pain from lesions of nervous system

- Last long, localization may be faulty, withdrawal is impossible Pain from idiopathic sources

-It’s associated with psychological, social &/or environmental factors

PURPOSE OF PAIN It warns against tissue damage The negative effects associated with pain

serve as an effective re-inforcement for learned avoidance.

Deep pains (e.g. joint sprains, muscle stress) tell us that it is time to rest

As useful as pain may be, the extreme pain suffered by people with chronic illnesses such as cancer is a protective mechanism gone awry- Patton et al,

PAIN TERMINOLOGIES

Somatogenic pain o Nociceptive

 caused by stimulation of peripheral nerve fibers that respond only to stimuli approaching or exceeding harmful intensity (nociceptors)

o Neuropathic  caused by damage or disease affecting any part of the

nervous system involved in bodily feelings (the somatosensory system)

Hyperpathia• A painful syndrome characterized by an

abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold.

Allodynia• Pain due to a stimulus that does not normally

provoke pain. Analgesia

• Absence of pain in response to stimulation which would normally be painful

Hyperalgesia• Increased pain from a stimulus that normally

provokes pain. Phantom

•  pain felt in a part of the body that has been lost or from which the brain no longer receives signals

Psychogenic•  also called psychalgia or somatoform pain, is

pain caused, increased, or prolonged by mental, emotional, or behavioral factors

Breakthrough pain• pain that comes on suddenly for short periods

of time and is not alleviated by the patients' normal pain management.

Incident pain•  pain that arises as a result of activity, such as

movement of an arthritic joint, stretching a wound, etc. 

Referred pain• Pain experienced at a site far away from the site of

injury.Neurogenic pain

• Sharp, burning and intense. Maybe constant or intermittent

Vascular pain• Difficult to localize; diffuse

Muscle pain• Dull and limited to area of origin; movement of the

affected part worsens the pain.

THEORIES ABOUT PAIN1. Specific Theory (Rene Descartes in 1644)

Transmission of pain via “straight through” channels from the skin to the brain

Modified by: a. Johannes Muellens- via sensory nerve

b. Maximillian Von Frey- specific cutaneous receptors for the mediation of touch, pain, pressure, heat, cold.

- also postulated about the idea of pain “center” w/in the brain.

2. Pattern theory ( Golddscheider in 1894)• Proposed that stimulus intensity and central

summation are critical determinants of pain. • Suggested that particular patterns of

impulses that evoke pain are produced by a summation of sensory input w/in the dorsal horn of the spinal cord. Pain results when total output exceeds a critical level.

• E.g. TOUCH + PRESSURE + HEAT= PAIN

3. Gate Control Theory (Ronald Melzack and Patrick D. Wall in 1965)

Postulated the following:a. The transmission of the nerve

impulses from afferent fibers to spinal cord transmission (T) cells is modulated by a spinal gating mechanism in the dorsal horn.

b. The spinal gating mechanism is influenced by the relative amount of activity in larger diameter (L) and small diameter (S) fibers. Activity in large fibers tend to inhibit transmission (close the gate) while small fiber activity tends to facilitate transmission (open the gate)

c. The spinal gating mechanism is influenced by nerve impulses that descends from the brain.

d. a specialized system of large diameter, rapidly conducting fibers (central control trigger) activates selective cognitive processes that then influence, by way of descending fibers, the modulating properties of the spinal gating mechanism.

e. When the output of the spinal cord transmission (T cells) exceed critical level, it activates the action system those neural areas that underlie the complex, sequential patterns of behavior and experience he characteristics of pain.

SUBSTANCIA GELATINOSA The control system composed of lamina II and

III. Intentional stimulation of fast conducting large

diameter fibers result in inhibition transmission of pain by small nerve fibers.

Trnsmission of impulses is prevented from reaching the T cells (2nd order neurons that transmit impulses to higher nervous system centers)

When T-cells stimulation succeeds a critical level, the action system is activated.

ACTION SYSTEM Subserver emotions Involves the RAS, limbic system, thalamus

and hypothalamus.a. Sensory Discriminative Components

It knows where the pain is coming from. Rapidly transmit spatiotemporal information

about the stimuli Responsible for the phantom limb

b. Motivational- affective system Associate pain with misery/ suffering Regulates vasomotor and autonomic functions Can be altered with the effects of narcotics.

c. Activation of motor mechanism Responsible for individual’s overt reaction to pain An affective aspect of painful experience Its is a series of responses seen in an individual.

1. Startle response2. Flexion response3. Postural

readjustment4. Vocalization5. Reorientation in

an individual

6. Evocation of past experiences

7. Prediction of the consequences

8. Other patterns of behavior aimed in reducing the sensation.

d. Descending control Facilitates neural transmission location

within PAG (periaqueductal Gray matter) of the midbrain.

Results in profound analgesia Can be activated by pharmacological and

psychological factors.

TYPES OF PAIN

Based on where in the body the pain is felt:  Somatic Visceral Neuropathic

• Pain of all three types can be either acute or chronic.• Somatic, visceral, and neuropathic pain can all be felt at the

same time or singly and at different times. The different types of pain respond differently to the

various pain management therapies. Somatic and visceral pain are both easier to manage

than neuropathic pain.

Nociceptive Pain  arises from the stimulation of specific

pain receptors. These receptors can respond to heat,

cold, vibration, stretch and chemical stimuli released from damaged cells.

Non Nociceptive Pain arises from within the peripheral and

central nervous system. Specific receptors do not exist here,

with pain being generated by nerve cell dysfunction.

Somatic Pain Caused by the activation of pain receptors in

either the cutaneous (body surface) or deep tissues (musculoskeletal tissues).

Deep somatic pain When it occurs in the musculoskeletal tissues

• Common causes of somatic cancer pain include metastasis in the bone (an example of deep somatic pain) and postsurgical pain from a surgical incision (an example of surface pain).

• Deep somatic pain is usually described as dull or aching but localized.

• Surface somatic pain is usually sharper and may have a burning or pricking quality.

Somatic Pain Source - tissues such as skin, muscle, joints,

bones, and ligaments - often known as musculo-skeletal pain.

Receptors activated - specific receptors (nociceptors) for heat, cold, vibration, stretch (muscles), inflammation (e.g. cuts and sprains which cause tissue disruption), and oxygen starvation (ischaemic muscle cramps).

Characteristics - often sharp and well localised, and can often be reproduced by touching or moving the area or tissue involved.

Useful Medications - may respond to combinations of Paracetamol, Weak Opioids OR Strong Opioids, and NSAIDs

Visceral Pain

"Viscera" refers to the internal areas of the body that are enclosed within a cavity.

It is caused by activation of pain receptors resulting from infiltration, compression, extension, or stretching of the thoracic (chest), abdominal, or pelvic viscera.

Common causes of visceral pain include pancreatic cancer and metastases in the abdomen.

It is not well localized and is usually described as pressure-like, deep squeezing.

Visceral Pain

Source - internal organs of the main body cavities. There are three main cavities - thorax (heart and lungs), abdomen (liver, kidneys, spleen and bowels), pelvis (bladder, womb, and ovaries).

Receptors activated - specific receptors (nociceptors) for stretch, inflammation, and oxygen starvation (ischaemia).

Characteristics - often poorly localised, and  may feel like a vague deep ache, sometimes being cramping or colicky in nature. It frequently produces referred pain to the back, with pelvic pain referring pain to the lower back, abdominal pain referring pain to the mid-back, and thoracic pain referring pain to the upper back.

Useful medications - usually very responsive to Weak Opioids and Strong Opioids. 

Acute pain

Sudden onset, lasting for hours to days and disappears once the underlying cause is treated. 

Acute pain has a clear cause. It could result from any illness, trauma, surgery or any painful medical procedures.

It is beneficial to the patient because if there’s no pain, the individual will ignore his illness resulting in complications and even death.

Acute pain signals that there is something wrong and motivates the person to get help.

Acute Pain

Short lasting and usually manifests in ways that can be easily described and observed.

It may, for example, cause sweating or increased heart rate. It can last for several days, increasing in intensity over time (subacute pain), or it can occur intermittently (episodic or intermittent pain).

Chronic pain  Starts as an acute pain and continues

beyond the normal time expected for resolution of the problem or persists or recurs for various other reasons It is not therapeutically beneficial to the patient.

In acute pain, attention is focused to treat the cause of pain whereas in chronic pain, the emphasis is laid upon reducing the pain to give relief, limit disability and improve function.

Chronic pain is defined as pain lasting for more than 3 months. It is much more subjective and not as easily described as acute pain. Effectively treating chronic pain poses a great challenge for physicians. This kind of pain usually affects a person's life in many ways. It can change someone's personality, ability to function, and quality of life.

SPECIAL TYPES OF PAIN

Neuropathic Results from damage or disease affecting

the somatosensory system. It may be associated with abnormal sensations

called dysesthesia, and pain produced by normally non-painful stimuli (allodynia).

May have continuous and/or episodic (paroxysmal) components.

Common qualities include burning or coldness, "pins and needles" sensations, numbness and itching. 

Cause Central neuropathic pain is found in spinal cord injury,

multiple sclerosis, and some strokes. Aside from diabetes and other metabolic conditions,

the common causes of painful peripheral neuropathies are herpes zoster infection, HIV-related neuropathies, nutritional deficiencies, toxins, remote manifestations of malignancies, immune mediated disorders and physical trauma to a nerve trunk. 

Neuropathic pain is common in cancer as a direct result of cancer on peripheral nerves (e.g., compression by a tumor), or as a side effect of chemotherapy radiation injury or surgery.

Neuralgia  Pain in one or more nerves caused by a

change in neurological structure or function of the nerves rather than by excitation of healthy pain receptors.

Neuralgia falls into two categories: central neuralgia - the cause of the pain

is located in the spinal cord or brain peripheral neuralgia.

Neuralgia • This unusual pain is thought to be linked to

four possible mechanisms: ion channel gate malfunctions; the nerve fibers become mechanically sensitive and create an ectopic signal; signals in touch fibers cross to pain fibers; and malfunction due to damage in the brain and spinal cord.

Pain Receptors The pain receptors in the skin and other

tissues are all free nerve endings.

Stimuli Mechanical Thermal Chemical

Bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, proteolytic enzymes, substance P, prostaglandin

Pain Fibers A-delta or Aδfibers C-fibers

A-delta fibers Thinly myelinated 1-5 µm in diameter Stimulation is

interpreted as fast pain

Respond to stimuli such as cold and pressure

C-fibers Unmyelinated 0.2-1.5 µm in

diameter Stimulation is

interpreted as slow pain

React to stimuli that are thermal, mechanical, and chemical in nature

4 Distinct Processes of Pain1. Transduction2. Transmission3. Modulation4. Perception

1. Transduction• Noxious stimuli are translated into

electrochemical impulses at sensory nerve endings

• Afferent nerve endings participate in translating noxious stimuli

2. Transmission3. Modulation4. Perception

1. Transduction2. Transmission

• Impulses are sent to the dorsal horn of the spinal cord, and then along the sensory tracts to the brain

3. Modulation4. Perception

1. Transduction2. Transmission3. Modulation

• Process of dampening or amplifying the pain related neural signals

• Transmission is altered by the influence of discreet pathways containing analgesic neurotransmitters

4. Perception

1. Transduction2. Transmission3. Modulation4. Perception

• Conscious awareness of the experience of pain

• Subjective and emotional experience of pain is created

Pain receptors

Spinal Nerve

Brain Stem

Paleospinothalmic pathway

Neospinothalmic pathway

Hypothalamus

Thalamus

Spinal cord

Limbic forebrain To cerebral cortex

Cerebrum

Nociceptive stimuli

A-delta(fast)

C-fiber(slow)

Spinal cord and dorsal horn*Pain modulating circuits

Thalamus (sensation)Somesthetic nuclei

Limbic cortex*(emotional experience)

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Pale

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Primary touch fibers

Pharmacologic and non pharmacologic Treatment

of Pain

Pharmacological Therapy (Medication)

• Nonopioid pain relievers (e.g. aspirin and ibuprofen)

• Opioids (e.g. vicodin and morphine)• Adjuvant medications (drugs whose

primary purpose is not for pain but rather for other conditions; e.g. antidepressants and anticonvulsants)

• Topical treatments (drugs that are applied directly to the skin)

Non-Pharmacological Treatment

Less invasive options:• Physiatric Approaches• Non-invasive Stimulatory Approaches• Psychological Approaches• Alternative ApproachesMore invasive options:• Anesthesiologic Approaches• Invasive Stimulatory Approaches• Surgical Approaches

Physiatric Approaches:1. Therapeutic Exercise options help: Strengthen weak muscles Mobilize stiff joints Restore coordination and balance Promote a sense of well-being Decrease anxiety and stress Maintain an appropriate weight

2. Heat Therapy• Heat therapy reduces pain, especially pain from

muscle tension or spasms. Heat helps with pain because heat increases the blood flow to the skin, dilates blood vessels, increasing oxygen and nutrient delivery to tissues, and decreases joint stiffness by increasing muscle elasticity.

 3. Cold Therapy• Cold therapy constricts blood vessels near the

skin and helps relieve the pain of muscle tension or spasms. It also helps reduce the swelling of an injury.

Non-Invasive Stimulatory Approaches:1. Transcutaneous Electrical Nerve

Stimulation (TENS): a method of applying a gentle electric current to the skin to relieve pain. It is a small box-shaped device that patients can put in their pocket and it transmits electrical impulses through wires to electrodes taped to the skin in the painful area. However, TENS can become less effective at relieving pain over time.

Psychological Approaches:1. Cognitive Behavioral Techniques• Deep breathing – the patient focuses on breathing

deeply. This may shift attention away from the pain.• Progressive muscle relaxation – patients contract,

then relax, muscles throughout the body, group by group. This helps patients relax the muscles in their body.

• Imagery – patients focus on pleasant thoughts, such as waves crashing onto a beach. The patient may also be told to think of an image that represents pain and then imagine it changing into an image representing a pain-free state.

• Meditation – the individual aims to empty the mind of thoughts and focus on breathing and the rhythms of the body.

• Biofeedback Therapy – individuals learn to reduce their body’s unproductive responses to stress which decreases their sensitivity to pain.

• Distraction – a pain management technique in which patients focus their attention on something other than their pain and negative emotions, by doing thing such as singing, listening to music, watching TV, or talking to friends.

Psychotherapy and Social Support

• Psychotherapy: a one-on-one approach that may be useful for anyone whose pain is difficult to manage, who has developed clinical depression, or who has a history of psychiatric illnesses. The goals of psychotherapy include teaching new coping skills, establishing a bond to decrease patient’s sense of isolation, and fostering a sense of self-worth.

• Group Approaches: an approach where individuals with the same conditions get to together for support. This approach helps the patient maintain a social identity and shows the patient how others are coping.

Alternative Approaches1. Acupuncture: an ancient method for relieving

pain and controlling disease. Thin metal needles that are gently twirled for ten to twenty minutes can be used to stimulate acupuncture points, which relieve pain in specific parts of the body. It is effective for some patients with chronic pain.

2. Massage: works by stimulating blood flow, relaxing muscles that are tight or in spasm, and promoting a feeling of well-being. Massage should not be used on swollen tissue.

Local Anesthesia

TERMINOLOGIES ANESTHESIA – It is a condition wherein

there is loss modalities of sensation.

ANALGESIA – It is the deadening or absence of the sense of pain without loss of consciousness.

LOCAL ANESTHESIA – It is an anesthesia without the involvement of the CNS and a condition wherein the patient remains conscious.

GENERAL ANESTHESIA – It is an anesthesia wherein there is an elimination of all the sensations, accompanied by the loss of consciousness.

LOCAL ANESTHETICS – These are agents that are used to eliminate the different modalities of sensation.

GENERAL ANESTHETICS – These are agents that produces loss of sensation and loss of consciousness.

Local anesthesia loss of sensation in a circumscribed area

of the body by a depression of excitation in nerve endings or an inhibition of the conduction process in the peripheral nerves.

In clinical practice a localized loss of pain sensation is desired. Although the terms dental anesthesia and dental analgesia are used synonymously in dentistry, local analgesia is more accurate.

Local anesthesia can be achieved by a number of mechanisms including mechanical trauma, anoxia, and use of neurolytic agents in addition to traditional local anesthetic drugs. However, clinically only reversible local anesthetic agents and other reversible techniques such as temperature reduction or electronic stimulation are useful to prevent pain.

Properties of an ideal local anesthetic Specific action Reversible action Rapid onset of action Suitable duration of action Active whether applied topically or injected Nonirritant Causes no permanent damage No systemic toxicity High therapeutic ratio Chemically stable and a long shelf life Ability to combine with other agents without loss of properties Sterilizable without loss of properties Nonallergenic Nonaddictive

Local anesthetic agents can be classified in several ways:

Chemical structure local anesthetics are classified usually as

either esters or amides. Duration of action

local anesthetics maybe classified as short acting, intermediate-acting, or long-acting.

General constituents of a dental cartridge of anesthetic solution

Local anesthetic agent Vasoconstrictor

this is sometimes included to delay the removal of the anesthetic from the tissues by decreasing the blood flow through adjacent blood vessels. A vasoconstrictor produces the following advantages: (a) longer duration of local anesthetic action, (b) reduced bleeding of a surgical site, and (c) reduced systemic effects. The most commonly used vasoconstrictors are epinephrine (adrenaline) and octapressin (felypressin). Only epinephrine is available in the United States.

Reducing agent this prevents oxidation of the vaso constrictor and

acts by competing with the vasoconstrictor for oxygen available in the solution. The most commonly used reducing agent is sodium metabisul-fite.

Preservative a bacteriostatic preservative prolongs the shelf life

of the solution, but since preservatives can provoke allergic reactions, they are no longer contained in dental local anesthetic cartridges in the United States. The typical shelf life of an anesthetic without preservative is approximately 18 months to 2 years.

Fungicide Thymol is used occasionally as a

fungicide. Carrier solution

an acidic aqueous solution dissolves the local anesthetic salt and maintains it at an acceptable pH.

The injectable local anesthetics used in dentistry have a common core structure consisting of

Hydrophilic amino terminal Intermediate chain Lipophilic aromatic terminal

Hydrophilic portion consists of a substituted secondary or

tertiary amine. Solubility in water is essential for 2

reasons to allow for the dissolution in a solvent to

permit injection to allow penetration through interstitial

fluid following administration. 

Intermediate chain Consists of either an amide or ester

linkage. Allows spatial separation of the hydrophilic

and lipophilic components of the molecule. The older agents, procaine and cocaine,

are ester-based drugs but are no longer widely used as dental anesthetics due to their unwanted side effects, such as toxic or allergic reactions

Lipophilic part an aromatic residue that is essential for

its ability to penetrate fatty tissue such as the lipid sheath of nerves in order to gain access to the nerve cell membrane to reach its site of action.

Theories of regional anesthesia Acetylcholine Theory Calcium Displacement Theory Surface Charge Theory Specific Receptor Theory Membrane Expansion Theory

Acetylcholine theory Acetylcholine, aside from its role as a

neurotransmitter at nerve synapses, is also involved in nerve conduction

There is no evidence that proves that acetylcholine is involved in neural transmission along the body of the neuron

Calcium Displacement Theory Local anesthetic nerve block is produced

due to displacement of Calcium ions that control the membranes permeability to sodium

Surface charge theory “repulsion theory” Local anesthetics acted by binding to the nerve

membrane and changing the electrical potential at the membrane surface

The electrical potential at the membrane surface becomes more positive, decreasing the excitability of the nerve by increasing the threshold potential

This theory cannot explain the activity of uncharged LA such as benzocaine in blocking nerve impulses

Specific Receptor Theory Local anesthetics act by binding to

specific receptor binding site present on the sodium channels. Specific receptor sites are present on either the external or internal surface of the sodium channels

Nerve conduction is interrupted once the local anesthetics gain access to the receptors

Specific Receptor Theory External receptor site

Two naturally occurring biotoxins, tetrodotoxin and saxitoxin block sodium influx by acting on the external receptor

Internal receptor site Local anesthetics may act by competitive

action with calcium for the same receptor

Displacement of calcium ions from the sodium channel receptor site

Binding of the local anesthetic molecule to the receptor site

Blockade of the sodium channel

Decrease in sodium conductance

Depression of rate of electrical depolarization

Failure to achieve threshold potential level

Lack of development of propagated action potentials

Classification of Local Anesthetics according to biological site and mode of action

Agent acting at receptor site on external surface of nerve membrane

Agents acting on receptor site on internal surface of nerve membrane

Agents acting by a receptor independent physic-chemical mechanism

Agents acting by combination of receptor and receptor-independent mechanism

Membrane Expansion Theory States that local anesthetic agents

penetrate the lipid portion of the cell membrane which causes its expansion and decreases the diameter of sodium channels. This causes the inhibition of flux of sodium ions and nerve impulse generation

Na+

+ + + + + +

Na+

Mechanism of Action Its mechanism of action is related to the

ion channels, nerve, and depolarization Local anesthetics block the conduction

of impulse in peripheral nerves that inhibits the nerves from being excited and thus create anesthesia

Factors Affecting the Reaction of Local Anesthetics1. Lipid solubility All local anesthetics have weak bases.

Increasing the solubility leads to faster nerve penetration, block sodium channels, and speed up the onset of action

The more tightly local anesthetics bind to the protein, the longer the duration of onset of action

2 forms of local anesthetics: Ionized Non-ionized

2. pH influence Decrease in pH shifts equilibrium

towards the ionized form, delaying the onset of action

Lower pH : more acidic : slower onset of action

3. Vasodilation Lower rate of vasodilation leads to a

slower absorption of local anesthetics agent, and longer duration of its action

Duration of Local Anesthetics Long-acting

180 minutes or more 0.5% Bupivacaine with 1:200,000 epi 0.5% to 1.5% Etidocaine with 1:200,000

epi Medium-acting

90 to 150 minutes 4% Prilocaine with 1:200,000 epi

Duration of Local Anesthetics Short-acting

45 to 75 minutes 4% Prilocaine when used for nerve block 2% Procaine with 0.45 Ppropoxycaine used as

a vasoconstrictor Ultra-short acting

Less than 30 minutes Procaine w/o a vasoconstrictor 2% Lidocaine w/o a vasoconstrictor

Procedures requiring local anesthesia Root canal treatment Removal of teeth Deep dental fillings Periodontal gum surgeries Cosmetic dentistry procedures Crown and bridge work Implants Oral surgical procedure

Groups of Local Anesthesia ESTER GROUP

Benzoic acid esters Cocaine Benzocaine

Para-aminobenzoic acid esters Procaine Tetracaine Propoxycaine 2-chloroprocaine

NON-ESTER GROUP Anilide

Bupivacaine (Marcaine)

Etidocaine (Duranest)

Mepivacaine (Carbocaine)

Lidocaine (Xylocaine) Prilocaine (Citanest)

Amides Amide link between secondary or

tertiary amine and aromatic ring Undergoes biotransformation primarily

in the liver by microsomal enzymes End products of metabolism are

excreted by the kidneys

Esters Ester link between secondary or tertiary

amine and aromatic ring Inactivated by hydrolysis which occurs

in the plasma Catalyzed by the enzyme plasma

cholinesterase

Factors in selecting the method of induction Area to be anesthetized Profoundness required Duration of anesthesia Presence of infection Age of patient hemostasis

Indications and contraindications for regional anesthesia Indication: when it is necessary for the

patient to remain in the conscious state Contraindications:

Fear or apprehension on the side of the patient Presence of infection Allergy to various local anesthetics Patient is below age of reason Mental deficiencies History of major oral surgery Presence of anomalies

TOXICITY Is the peak circulation levels of local

anesthetics Levels of LA concentration administered to

patients are varied according to age, weight and health

Maximum dose for an individual is usually between 70mg to 500mg

The amount of dose also varied bassed on the type of solution used and the presence of vasoconstrictor

Common toxic effects Light headedness Shivering or twitching Seizures Hypotension Numbness

COMPLICATIONS OF LOCAL ANESTHETICSArising from drugs/ chemical

used Soft tissue injury Sloughing of the tissue Toxicity Allergy Infection caused by contaminated

solution

Arising from injected technique Needle breakage Hematoma Failure to obtain local anesthesia Post- injections herpetic lesions

Arising from both Pain on injection Burning of the

injection Trismus Blanching of the

skin Edema Persistent

paresthesia

Infection Persistent pain Neurological

symptomsfacial paralysisvisual

disturbances

Soft tissue injury Self inflicted trauma to lips and tongue while still

numb Seen in children which are mentally and physically

disabled. Soft tissue anesthesia last longer than the pulpal.

Sloughing of tissuei. Epithelial desquamation

Topical anesthetic for prolong period Hightened sensitivity of tissue to LA reactions in area of

topical anesthetics.

ii. Sterile abscess prolonged Ischemia due to vasoconstrictions Develops on hard palate

Needle breakage PRIMARY CAUSE: unexpected movement of the patient SECONDARY CAUSE:

Inaapropriate thickness of the needle Previously bent Redirection of needle once inserted inside tissue Manufacture defect (rare) Forcing needle against resistance Needle engaging the periosteum

PREVENTION:o Inform the patiento Avoid multiple penetrationo Use proper gauze needleo Use presterilized disposable needleo Entire length should not be insertedo Stabilization of the jaw

Hematoma effusion of blood into extravascular space can

result from inadvertently nicking of blood vessels during the insertion of LA

• CAUSE:Nick blood effusion from the vessels until extravascular pressure exceeded intravascualar clotting occurs

• PREVENTION: Use the appropriate length of the needle Minimize no. of penetration Do not use needle as probe

Failure to obtain local anesthesia CAUSES:

o Operator dependent LA agent (type, dose) Improper surgical technique Injection of wrong solution

o Patient dependent Anatomical- additional innervation Psychological- uncooperative movement Pathological- infection

Pain on injection• Careless technique• Blunt needle• High temperature of solution• Rapid insert of LA solution

Burning sensation• Rapid injection• Contaminated needle cartridge• High temperature of LA solution can alter the ph of

solution

Infection• Contamination of needle• Improper preparation of the site• Needle passing through an area of infection• LA solution deposited under pressure.

Edema• Trauma• Infection• Hemorrahage• Allergy

Injection of irritating solutionTissue blanching• Trauma to blood vessels by needle• I.V administration

Trismus