A local anesthesia (LA) is a drug that causes the absence of a pain sensation, although other senses are also frequently affected. Also, when used on certain neural pathways (nerve block of local anesthesia), paralysis (loss of muscle strength) can also be achieved.
The LA clinic belongs to one of two classes: aminoamide and local aminoester anesthesia. The synthetic LA is structurally linked to cocaine. They differ from cocaine primarily because they have very low abuse potential and do not produce hypertension or (with few exceptions) vasoconstriction.
They are used in a variety of local anesthetic techniques such as:
- Topical (surface) anesthesia
- Application of a topical anesthetic cream, gel, ointment, or spray of anesthetic is dissolved in DMSO or other solvent/carrier for deeper absorption
- Infiltration
- Brachial plexus block
- Epidural block (extradural)
- Spinal anesthesia (subarachnoid block)
- Iontophoresis
Video Local anesthetic
Medical use
Acute pain
Acute pain may occur due to trauma, surgery, infection, blood circulation disorders, or many other conditions in which tissue injury occurs. In medical settings, pain reduction is desirable when the warning function is no longer needed. In addition to improving patient comfort, pain therapy can also reduce the harmful physiological consequences of untreated pain.
Acute pain can often be managed using analgesics. However, conduction anesthesia may be preferred because of superior pain control and fewer side effects. For the purpose of pain therapy, LA drugs are often given with repeated injections or continuous infusions through a catheter. Low doses of LA drugs can be sufficient so that muscle weakness does not occur and patients can be mobilized.
Some typical uses of conduction anesthesia for acute pain are:
- Labor pain (epidural anesthesia, pudendal nerve block)
- Postoperative pain (peripheral nerve block, epidural anesthesia)
- Trauma (peripheral nerve block, intravenous regional anesthesia, epidural anesthesia)
Chronic pain
Chronic pain is a complex and often serious condition requiring diagnosis and treatment by an expert in pain medication. LA can be applied repeatedly or continuously for a long time to relieve chronic pain, usually in combination with drugs such as opioids, NSAIDs, and anticonvulsants.
Surgery
Almost every part of the body can be anesthetized using conduction anesthesia. However, only a limited number of techniques are commonly used in clinics. Occasionally, conduction anesthesia is combined with general anesthesia or sedation for patient comfort and ease of operation. Typical surgeries performed under conduction anesthesia include:
- Dentistry (surface anesthesia, infiltration anesthesia or intraligamentary anesthesia during restoration or extraction operations, and regional nerve blocks during extraction and surgery)
- Podiatrists (cutaneous, nail avulsion, matricectomy, and other podiatric procedures)
- Eye surgery (surface anesthesia with topical anesthesia or retrobulbar block)
- ENT surgery, head and neck surgery (infiltration anesthesia, field block, or peripheral nerve block, plexus anesthesia)
- Shoulder and arm surgery (plexus anesthesia or intravenous regional anesthesia)
- Cardiac and pulmonary surgery (epidural anesthesia combined with general anesthesia)
- Abdominal surgery (epidural anesthesia/spinal anesthesia, often combined with general anesthesia)
- Gynecological, obstetrical and urological surgery (spinal/epidural anesthesia) Bone and pelvic, hip, and leg joint surgery (spinal/epidural anesthesia, peripheral nerve block, or intravenous regional anesthesia)
- Skin and peripheral blood surgery (topical anesthesia, field block, peripheral nerve block, or spinal/epidural anesthesia)
Other uses
Topical anesthesia, in the form of lidocaine/prilocaine (EMLA) is most commonly used to activate relatively painless venipuncture (blood collection) and intravenous cannula placement. It may also be suitable for other types of punctures such as asites drainage and amniocentesis.
The surface anesthesia also facilitates some endoscopic procedures such as bronchoscopy (visualization of the lower airway) or cystoscopy (visualization of the inner surface of the bladder).
Maps Local anesthetic
Side effects
Localized side effects
Local adverse effects of anesthetic agents include neurovascular manifestations such as prolonged anesthesia (numbness) and paresthesia (tingling, pin and needle feeling, or odd sensations). This is a symptom of local neurological damage or nerve damage. Of particular note, the use of topical anesthesia to relieve eye pain can cause severe corneal damage.
Risk
The risk of temporary or permanent nerve damage varies between different locations and types of nerve blocks.
Recovery
Permanent nerve damage after peripheral nerve block is rare. Symptoms will likely disappear within a few weeks. Most of those affected (92% -97%) recovered within four to six weeks; 99% of these people have recovered within a year. It is estimated that one in 5,000 to 30,000 neural blocks produces some degree of permanent persistent nerve damage.
Symptoms may continue to improve for up to 18 months after the injury.
Cause
The causes of local symptoms include:
- neurotoxicity due to an allergic reaction
- excess fluid pressure in confined spaces
- decide on nerve fibers or support tissues with needles/catheters
- an injection site hematoma that puts pressure on the nerve
- infection of the injection site resulting in inflammatory pressure on the nerve and/or necrosis
Common side effects
A common systemic side effect is due to the pharmacological effects of the anesthetic agent used. Electrical impulse conduction follows the same mechanisms in peripheral nerves, central nervous system, and heart. Therefore, local anesthetic effects are not specific to signal conduction in peripheral nerves. Side effects on the central nervous system and heart can be severe and potentially fatal. However, toxicity usually occurs only at rare plasma levels if appropriate anesthetic techniques are followed. High plasma levels may appear, for example, when doses intended for administration of epidural or intrasupport tissues are inadvertently sent as intravascular injection.
Central nervous system
Depending on the local concentration of local anesthetic tissue, the effects of excitatory or depressant on the central nervous system may occur. Early symptoms indicate some form of central nervous system stimulation such as ringing in the ear (tinnitus), metallic taste in the mouth, or tingling or numbness in the mouth. As the concentration increases, a relatively selective inhibitory neuron depression results in cerebral excitation, which may lead to further symptoms including a twitching motor in the periphery followed by a grand mal seizure. Deep depression of brain function occurs at higher concentrations that may lead to coma, respiratory arrest, and death. The concentration of the tissue may be due to extremely high plasma levels after large doses of intravenous injection. Another possibility is direct exposure of the central nervous system through cerebrospinal fluid, ie, overdose in spinal anesthesia or inadvertent injection to subarachnoid space in epidural anesthesia.
Cardiovascular system
Cardiac toxicity associated with an intravascular injection overdose of local anesthesia is characterized by hypotension, atrioventricular conduction delays, idioventricular rhythms, and eventually cardiovascular collapse. Although all local anesthetics have the potential to shorten the period of myocardial refractories, bupivacaine actively blocks the heart's sodium channel, making it most likely to precipitate malignant arrhythmias. Even levobupivacaine and ropivacaine (single-derived enantiomers), developed to improve cardiovascular side effects, still retain the potential for disrupting cardiac function.
Hypersensitivity/allergy
Side effects on local anesthesia (especially esters) are not uncommon, but real allergies are very rare. Allergic reactions to esters are usually due to sensitivity to their metabolites, para-aminobenzoic acid, and do not cause cross allergies to the amide. Therefore, the amide may be used as an alternative to the patient. Nonallergic reactions can mimic allergies in their manifestations. In some cases, skin tests and provocative challenges may be necessary to establish an allergy diagnosis. Also cases of allergy to paraben derivatives occur, which are often added as preservatives to local anesthetic solutions.
Methemoglobinemia
Methemoglobinemia is a process in which iron in hemoglobin is altered, reducing the ability to carry oxygen, resulting in cyanosis and hypoxic symptoms. Benzocaine, lidocaine, and prilocaine all produce this effect, especially benzocaine. The systemic toxicity of prilocaine is relatively low, but its metabolite, o-toluidine, is known to cause methemoglobinemia.
Overdose treatment: "Lipid rescue"
This method of treatment of toxicity was discovered by Dr. Guy Weinberg in 1998, and has not been widely used until after the first successful rescue published in 2006. The evidence suggests that Intralipid, the available intravenous lipid emulsion, can be effective in treating severe secondary cardiotoxicity. for overdose of local anesthesia, including successful human case reports in this way (lipid rescue). However, evidence at this time is still limited.
Although most reports to date have used Intralipid, generally available intravenous lipid emulsions, other emulsions, such as Liposyn and Medialipid, have also been shown to be effective.
Self supporting animal evidence and human case reports show successful use in this way. In the UK, efforts have been made to publicize this use more widely and lipid rescue has now been formally promoted as a treatment by the British and Irish Anesthesia Association. One published case has been reported about the success of refractory heart stopping treatment in bupropion and overdose of lamotrigine using a lipid emulsion.
The design of a homemade lipid rescue kit has been described.
Although the lipid rescue mechanism of action is not fully understood, lipids added in the bloodstream can act as a sink, allowing to remove lipophilic toxins from the affected tissue. This theory is compatible with two studies on lipid rescue for clomipramine toxicity in rabbits and with clinical reports on the use of lipid rescue in veterinary medicine to treat puppies with moxidectin toxicosis.
Action mechanism
All LA is a membrane stabilizer; they reversibly lower the rate of depolarization and favorable membrane repolarization (such as nociceptors). Although many other drugs also have membrane stabilizing properties, not all are used as LA (propranolol, for example). LA drugs act primarily by inhibiting the entry of sodium through sodium-specific ion channels in nerve cell membranes, especially so-called voltage-gated sodium channels. When the sodium influx is disrupted, the action potential can not arise and the conduction signal is inhibited. Receptor sites are considered to be in the cytoplasm (in) sodium channel. Local anesthetic drugs more easily bind the sodium channel in the active state, so the onset of neuronal blockade is faster in fast-paced neurons. This is called a state-dependent blockade.
LA is a weak base and is usually formulated as a hydrochloride salt to make them water soluble. At a pH equal to protonated base pKa, ionized (unionized) and un-stimulated (unionized) molecules form in an ecimolar amount, but only unstabilized bases that diffuse easily across the cell membrane. Once inside the cell, the local anesthetic will be in equilibrium, with the formation of ionized (ionized) form, which can not be directly out of the cell. This is called an "ion trap". In protonated form, the molecules bind to the LA binding sites on the inside of the ion channel near the cytoplasmic end. Most LA works on the membrane's internal surface - the drug must penetrate the cell membrane, which is best achieved in an unionized form.
Acidosis as caused by inflammation of the wound partially reduces the LA action. This is partly because most of the anesthetics are ionized and therefore can not cross the cell membrane to reach its cytoplasmic action site on the sodium channel.
All nerve fibers are sensitive to LA, but because of the combination of diameter and myelination, the fibers have different sensitivity to the LA blockade, called differential blockade. Type B fibers (sympathetic tones) are most sensitive followed by type C (pain), type A delta (temperature), gamma type A (proprioception), type A beta (touch and sensory pressure), and type A alpha (motor). Although the B-type fibers are thicker than the C-type fibers, the myelin fibers are blocked in the presence of C fibers that are not mely and thin.
Technique
Local anesthesia can block almost every nerve between the peripheral nerve endings and the central nervous system. The most peripheral technique is topical anesthesia on the skin or other body surfaces. Small and large peripheral nerves can be anesthetized individually (peripheral nerve block) or in anatomy nerve bundles (anesthetic plexus). Spinal anesthesia and epidural anesthesia combine into the central nervous system.
LA injection is often painful. A number of methods can be used to reduce this pain, including buffering the solution with bicarbonate and heating.
Clinical techniques include:
- Surface anesthesia is an LA spray application, solution, or cream to the skin or mucous membranes; the effect is short and limited to the contact area.
- Infiltration anesthesia is the infiltration of LA into the tissue to be anesthetized; surface anesthesia and infiltration are collective topical anesthesia
- The field block is LA subcutaneous injection in the area adjacent to the field to be anesthetized.
- The peripheral nerve block is a LA injection around peripheral nerves to anesthetize the neural innervation area.
- Plexus anesthesia is a LA injection around the nerve plexus, often within the tissue compartment that limits the diffusion of the drug away from the intended site. The anesthetic effect extends to the neural area of ​​some or all of the nerves originating from the plexus.
- Epidural anesthesia is LA injected into the epidural space, where it acts primarily on the spinal cord roots; depending on the injection site and the injected volume, an anesthetized area varies from the abdomen or chest area to a large body area.
- Spinal anesthesia is LA injected into cerebrospinal fluid, usually in the lumbar spine (in the lower back), where it acts on the spinal cord roots and part of the spinal cord; The resulting anesthesia usually extends from foot to stomach or chest.
- Intravenous regional anesthesia (Bier block) is when the blood circulation of the extremity is disturbed by using a tourniquet (a device similar to a blood pressure cuff), a large volume of LA is injected into the peripheral vein. This drug fills the vein system of the extremities and diffuses into the tissues, where the peripheral nerves and nerve endings are drugged. The anesthetic effect is limited to the area removed from the blood circulation and disappears rapidly once the circulation recovers.
- Local anesthesia in the body cavity includes intrapleural anesthesia and intra-articular anesthesia.
Transcision (or transwound) catheter anesthesia using multilateral catheters is inserted through an insision or injury and aligned through it on the inside due to incisions or closed wounds, granting continuous local anesthesia throughout the incision or wound.
Type
Local anesthetic solutions for injections usually consist of:
- The local anesthetic agent itself
- Vehicles, which are usually water based or just sterile water
- The vasoconstrictor may (see below)
- Reducing agents (antioxidants), e.g. if epinephrine is used, then sodium metabisulfite is used as a reducing agent
- Preservatives, e.g. methylparaben
- Buffer
Esters tend to produce allergic reactions, which may require the use of amides. The names of each local clinical anesthetic have a "-caine" suffix. Most LA esters are metabolized by pseudocolinesterase, whereas LA amides are metabolized in the liver. This may be a factor in choosing agents in patients with liver failure, although since cholinesterases are produced in the liver, physiologists (eg very young or very old individuals) or pathologists (eg cirrhosis) liver metabolic disorders are also considered when using amides.
Sometimes, LA is combined, for example:
- Lidocaine/prilocaine (EMLA, eutectic mixture of local anesthesia)
- Lidocaine/tetracaine (Rapydan)
- TAC
LA solutions for injection are sometimes mixed with vasoconstrictors (combination drugs) to increase the duration of local anesthesia by constricting blood vessels, thus securely concentrating the anesthetic agent for extended duration, as well as reducing bleeding. Because the vasoconstrictor temporarily reduces the level of systemic circulation that removes local anesthesia from the injection area, the maximum dose of LA in combination with the vasoconstrictor is higher than that of the same LA without the vasoconstrictor. Occasionally, cocaine is given for this purpose. Examples include:
- Prilocaine hydrochloride and epinephrine (trade name Citanest Forte)
- Lidocaine, bupivacaine, and epinephrine (recommended final concentrations of 0.5, 0.25, and 0.5%, respectively)
- Iontocaine, consisting of lidocaine and epinephrine
- Septocaine (trade name Septodont), a combination of articaine and epinephrine
One combination product of this type is used topically for surface anesthesia, TAC (5-12% tetracaine, 1 / 2000 (0.05%, 500 ppm, Ã, ½ per mille) adrenaline, 4 or 10% cocaine).
Using LA with a vasoconstrictor is safe in the area supplied by the end arteries. The usual belief that LA with a vasoconstrictor can cause necrosis of the extremities such as the nose, ears, fingers and toes (due to late artery narrowing), is invalid, since no cases of necrosis have been reported since the introduction of commercial lidocaine. with epinephrine in 1948.
Esther Group
- Benzocaine
- Chloroprocaine
- Cocaine
- Cyclomethycaine
- Dimethocaine/Larocaine
- Piperocaine
- Propoxycaine
- Procaine/Novocaine
- Proparacaine
- Tetracaine/Amethocaine
Amide Groups
- Articaine
- Bupivacaine
- Cinchocaine/Dibucaine
- Etidocaine
- Levobupivacaine
- Lidocaine/Lignocaine
- Mepivacaine
- Prilocaine
- Ropivacaine
- Trimecaine
Naturally downgraded
- Saxitoxin
- Neosaxitoxin
- Tetrodotoxin
- Menthol
- Eugenol
- Cocaine
Naturally occurring local anesthetics do not originate from cocaine, usually neurotoxins, and have a toxo-ending in their name. [1] Unlike cocaine that produces local anesthetics that have intracellular effects, saxitoxin, neosaxitoxin & amp; tetrodotoxin binds to the extracellular side of the sodium channel.
History
In Peru, the ancient Inca are believed to have used coca leaf as a local anesthetic in addition to its stimulant properties. It was also used for the payment of slaves and was thought to play a role in the destruction of Inca culture after the Spaniards realized the effects of chewing coca leaves and taking advantage of it. Cocaine was isolated in 1860 and was first used as a local anesthetic in 1884. The search for a less toxic and less addictive substitute led to the development of the local aminoester anesthesia stadium in 1903 and procaine in 1904. Since then, several synthetic local anesthetic drugs have been developed and put into clinical use, especially lidocaine in 1943, bupivacaine in 1957, and prilocaine in 1959.
Shortly after the first use of cocaine for topical anesthesia, blocks of peripheral nerves have been described. Brachial plexus anesthesia with percutaneous injections through axillary and supraclavicular approaches developed in the early 20th century. The search for the most effective and least traumatic approach to plexus anesthesia and peripheral nerve blocks continues to this day. In recent decades, continuous regional anesthesia using catheters and automatic pumps has evolved as a method of pain therapy.
Intravenous regional anesthesia was first described by August Bier in 1908. This technique is still used and is very safe when low systemic toxicity drugs such as prilocaine are used.
Spinal anesthesia was first used in 1885, but was not put into clinical practice until 1899, when August Bier subjected himself to a clinical experiment in which he observed the effects of anesthesia, but also the typical side effects of postpunctural pain. Within a few years, spinal anesthesia became widely used for surgical anesthesia and was accepted as a safe and effective technique. Although atraumatic (noncutting-tipped) cannulae and modern medicine are used today, this technique has changed very little over several decades.
Epidural anesthesia with a caudal approach was well known in the early twentieth century, but a well-defined technique using lumbar injection was not developed until 1921, when Fidel PagÃÆ' Â © published his article "Anesthesia MetamÃÆ' Â © rica". This technique was popularized in the 1930s and 1940s by Achile Mario Dogliotti. With the advent of thin, flexible catheters, continuous infusions and repeated injections have become possible, making epidural anesthesia is still a very successful technique. In addition to many uses for surgery, epidural anesthesia is very popular in obstetrics for the treatment of labor pain.
See also
- Amylocaine
- Anesthesia
- General anesthesia
- List of cocaine analogs
- List of local anesthesia
References
External links
- The American Society of Regional Anesthesia
- Regional Anesthesia and Pain & amp; Medicine
- Lipid Rescue
Source of the article : Wikipedia
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