 Hello everyone welcome back to another session in dentistry and more so today's topic in oral surgery is local anesthesia this is a huge topic this will be dealt in three or four sessions so today's session is about the mechanism the repolarization depolarization and action potential mechanism and the basic things of local anesthesia. So next session we have the theories of local anesthesia and then we have the properties the local anesthetic solution and its classification so all will be covered in future sessions. So today's session is about the mechanism that is a action potential mechanism across a nerve membrane how the polarization is happening the resting potential and how it is getting changed and what is a role of local anesthetic in this polarization so all this will be dealt in so let's start learning local anesthesia. The loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves so it is going to act on the nerves either on the nerve endings or the conduction process okay either it depress the excitation of nerve endings or it inhibits the conduction process in peripheral nerves that is how it is creating the anesthesia so it is a loss of sensation without inducing loss of consciousness there is no loss of consciousness like general anesthesia so we have lots of method to produce this local anesthesia such as low temperature, mechanical trauma, anoxia, neurolytic agents such as alcohol or phenols and the chemical agents such as local anesthetics so these are the other methods for producing local anesthesia so not just local anesthetics does anesthesia we have local low temperature mechanical trauma anoxia neurolytic agents such as alcohol and phenols so all can produce the effect of local anesthesia so what are the properties of local anesthesia so the properties we have instead synonym I4 non-irritating okay non-irritating because it should not be irritating due to issues to which it is applied then it is related to nerve it should not cause any permanent alteration of the nerve structure then the systemic effect should be very low because anyway it is going to enter in the blood circulation so it not it should not create any systemic toxicity then the time of onset should be short time of onset should be short then it should be effective effective regardless of whether it is injected into the tissue or applied locally to mucus membranes it should be effective and the duration of action so it should be long enough to permit the completion of procedure that is a duration so we need to have proper local anesthetic effect so that we can complete the surgical procedure so it should be non-irritating should not create any permanent damage to nerve structure the systemic toxicity should be very low and it should be having very low or short time of onset and should be effective irrespective of if it is injecting or if we are applying it on the mucus membrane and we should have enough duration of action and also it should have the potency sufficient to give complete anesthesia without the use of harmful concentration solutions and it should be free from producing allergic reactions and it should be free in solution and relatively undergo bio transformation in the body it should be either sterile or capable of being sterilized by heat without deterioration so these are the properties of local anesthesia now let's learn the electrophysiology of nerve conduction so this is important part electrophysiology so what exactly is happening at the nerve membrane where the local anesthetic going to work so we have a nerve membrane here let this be the nerve membrane okay and this is inside the nerve membrane and this is outside the nerve membrane this is outside this is inside okay so usually the outside the nerve membrane we have positive charges okay so this is positively charged and inside we have usually negatively charged we have negative charged inside so this is our now membrane and there will be always a electric charge across the membrane so that is known as membrane potential okay membrane potential so this membrane potential is also known as resting potential which is equal to minus 70 milliwatt that is the resting potential so without any excitation without any changes in the cell this will be the electric wall to which is existing between or the membrane surface so we learned what is membrane potential now let's learn what is action potential okay so action potential is nothing but when this membrane potential is going to change under stimulation or fiber excitation okay so this is outside and this is inside outside we have positively charged and this is negatively charged so this minus 70 milliwatt is because of the gradient okay so we have lots of positive charge and lots of negative charge so the change in concentration gradient across the membrane is resulting minus 70 milliwatt so when there is an action potential before we have all the channels or the sodium potassium channels are closed at resting potential so when this nerve fiber is excited or stimulated what happens is the sodium channel will be opened okay so this is the inside area this is the outside area so from outside there will be influx of sodium ions so lots of sodium ions will be entering okay so sodium ions will be entering into the cell membrane so once this sodium ions enters from outside to inside this process will be takes place this is known as de-polarization that is a polarity is going to changed so the sodium channel closes once it enters and it reaches level the minus 70 will be become plus 20 that is de-polarization happened okay so this minus become positive because of the influx of sodium ions so the sodium channel will be closed because it is de-polarized okay so we have sodium channel closed so after that what happens is the nerve membrane or the nerve tries to go back to its original position or original state that is a resting potential to maintain the equilibrium so again one more channel will be opened that is not the sodium it is potassium okay so from inside there is out flex of potassium okay until it reaches minus 70 millivolt okay so resting potential we have de-polarization and this is known as re-polarization because we revert the polarity okay before it was de-polarized now it is re-polarized because we revert back so that is minus 70 MP we went back to the resting potential so once it is reached minus 70 what happens is this channel also will be closed so it is like resting potential where sodium and potassium channels are closed so during de-polarization sodium channel open and it enters it reaches plus 20 that is de-polarization then potassium going outward and balancing to reach the minus 70 millivolt so this voltage gradient along axon causing a current okay this causes configurational change in sodium channel in the next segment and the conduction process is happening so this is how the electro reaction happening in nerve endings or in nerve membrane okay that is a de-polarization and repolarization mechanism so what exactly happening with respect to the two types of nerve membrane so we have two types of nerve membrane one we know myelinated and the second one is unmyelinated so it differs from myelinated and unmyelinated so this impulse spread from one segment to another segment because a de-polarized segment impulse will be spread to the next segment so the propagated impulse travels along the nerve membrane towards the CNS okay the spread of impulse the rate of speed is differ in myelinated and unmyelinated so first let's take unmyelinated nerve fibers so unmyelinated nerve fiber it doesn't have a myelin sheath so because of this it has high resistance cell membrane and extracellular media it produce a rapid decrease in density of current within a short distance of de-polarized segment so it doesn't have a myelin sheath so it will be producing a rapid decrease in density of current so what happens is the spread of impulses characterized as a slow forward creeping process slow forward creeping process it cannot propagate in a very fast manner so the conduction rate is very slow 1.2 meter per second and it goes like this so if we have a nerve membrane here we have this impulse so just go like this okay so the impulse moves forward by sequential de-polarization of short adjoining membrane segments okay but whereas on the myelinated nerve fiber so in myelinated nerve fiber it's a different story so the current leaps from nodes to nodes is happening not the sequential de-polarization so here the impulse goes like this from nodes to nodes here it was sequential de-polarization so the impulse moves forward by sequential de-polarization of short adjoining membrane segments okay but here it is impulse leaps forward from one node to another one so the myelinated nerve fiber process the nerve impulse from nodes to nodes forward movement is known as salt-air trick conduction so it is more rapid in thicker nerves because of increase in thickness of myelin sheath and increase in distance between the adjacent nodes of ran wear so this is the nodes of ran wear so if conduction of impulse is blocked at one node of you know the local current will skip over that node and prove adequate to raise that membrane potential at next node to its firing potential and produce de-polarization so that the process will not be stopped if there is blockage at one node so it will jump to the next one it will skip that particular node and jump to the next one so the conduction here it was just 1.2 meter per second but here it is almost 120 meter per second almost 100 times faster in myelinated nerve fibers and now we are going to learn the basic mechanism of local anesthesia so far we finished our electro physiology of the nerve fiber how the repolarization depolarization is happening now the local anesthetic action so this local anesthetic agent interferes with the excitation process so it can be done in many ways the first one is changing the resting potential of nerve membrane so we know what is resting potential so the first mechanism of this local anesthetic is changing the resting potential then changing the threshold potential so this local anesthetic will increase the threshold potential so it will remain repolarized so there will be less chances of depolarization so ultimately local anesthetic is increasing the rate of repolarization that is it is not allowing depolarization so increasing the rate of repolarization and decreasing depolarization so repolarization is the process happened when we apply local anesthesia because there is no depolarization or it prolongs the repolarization or decrease the depolarization so that's all about local anesthesia so we can say it as a part one where we discussed about the action potential the membrane potential the sequential depolarization the solitary conduction and local anesthesia mechanism that is changing the resting potential threshold potential or increasing the repolarization or decreasing the depolarization the electrophysiology so this is the introduction part of local anesthesia so the next session is about the various theories of local anesthesia so we have many theories such as acetylcholine theory calcium displacement theory surface charge theory membrane expansion theory then specific receptor so all these theories we are going to learn in next session okay so I'll come back with the theories of local anesthesia in my next session thank you everyone welcome back to another session in dentistry and more we are continuing our local anesthesia sessions so this session is about theories of mechanism of action of local anesthetics so there are various theories which has been put forward over the years to explain the mechanism of action of local anesthetics the first one was acetylcholine theory acetylcholine theory which stated that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses so it is basically a nerve synapse neurotransmitter but it has got a role in local anesthesia that is what this theory is saying but there is no scientific evidence to prove that acetylcholine is involved in neurotransmission so it was rejected in its first place so the second theory was calcium displacement theory so this theory states that the nerve block or local anesthetic nerve block was produced by displacement of calcium from some membrane site which controlled permeability of sodium so sodium is the key element which is involved in local anesthesia because we have seen in our last session how sodium is involved in depolarization and repolarization so when the sodium enters to cell membrane the depolarization starts so sodium is a key element so calcium displacement theory highlighting the involvement of sodium and next theory we have surface charge repulsion theory surface charge or repulsion theory so it says that local anesthetics acted by binding to nerve membrane and changing the electric potential at the membrane surface so if you have the nerve membrane so it has positive outside and negative inside okay so let it be the outside and this be the inside so negative charge is inside and positive charge on outside so this local anesthetics will bind to the nerve membrane and changing the electrical potential at the membrane surface so the cationic membrane cationic molecules that is the cationic drug molecules align at the membrane water interface okay so we have this lmm positive charges which is aligned here so since the cationic drug molecules aligned at the membrane interface so some of the local anesthetic molecule carried a net positive charge they made the electrical potential at the membrane surface more positive so what happens when it become more positive it decreases excitability of nerve by increasing the threshold potential so when we have more more positive charge here it increases the threshold potential that means the action potential needs more depolarization potential so it will be in that repolarization phase but the problem is there is no such evidence which indicate that resting potential of nerve membrane is affected by LA molecules so this theory was rejected okay so there is no concept scientific evidence says that there is changing in threshold potential by the LA molecules so it was not accepted one whereas the fourth one is membrane expansion theory membrane expansion theory membrane expansion theory it states that local anesthetic molecule diffuse to hydrophobic regions of membranes and produce a disturbance in the bulk membrane structure and expand the membrane and preventing increasing the permeability to sodium ions this is the membrane so what happens is there is the LA molecules enters and this will be changed to different shape okay or it expands so it prevents the increase in permeability to sodium ions so lipid soluble LA solutions can easily penetrate through the lipid portions of cell membrane changing the configuration of this lipoprotein matrix of nerve membrane which results in decreased diameter of sodium channel so you know we have channels sodium channels we have learned in our first session sodium channels where sodium enters to the cell membrane and causes depolarization so sometimes as per this membrane expansion theory it decreases the sodium channel diameter or it expands the membrane and preventing an increase in permeability of sodium ions so ultimately there will be inhibition of sodium conduction and thereby novel excitation so the ultimate aim is to prevent the entry of sodium into nerve membrane okay so that is the key thing when sodium enters to this what happens is there is depolarization so that is a membrane expansion theory and the most accepted theory is specific receptor theory okay so this is a entirely different mechanism compared to all the four other theories so this theory says that local anesthetics act by binding to specific receptors in the sodium channel okay so we know what is sodium channel so sodium channel will be having a receptors a specific receptor where the local anesthetic molecules will get binded to so that is the mechanism okay so not the acetylcholine or calcium displacement or surface charge or membrane expansion so this is a real mechanism how the LA works so there will be a receptors which is present on the sodium channel where the LA molecules get attached to okay so it is not mediated by any change in the general properties of cell membrane but the action of drug is very direct not changing by membrane potential or expanding or anything that sort of this is direct action directly attaching to this receptors which is on the sodium channel and doing the LA action so once it is attached to this there will be biochemical and electrophysiological changes happening and the mechanism is very simple once the molecule LA molecule is attached to the specific receptors the permeability to sodium ion is decreased okay so only when the sodium ions enters into the cell membrane the depolarization happens so what we want is repolarization the prolonged repolarization we don't want depolarization we just want continuous repolarization state so it is not letting the sodium ions to enter into this membrane so the permeability to sodium ion is decreased or eliminated and the nerve conduction is interrupted okay so that is a mechanism so this is the most acceptable one specific receptor theory so we learned this class was about the theories acetylcholine calcium displacement surface charge membrane expansion and the most acceptable one that is specific receptor theory so hope you understood this concept of theories of local anesthesia mechanism so i'll come up with next topic there is a properties or the components of local anesthesia what are the components which is present in local anesthesia and its function so i'll come up with that topic thank you hello everyone welcome back to another session in dentistry and more so we are continuing our local anesthetic sessions so this session is about local anesthetic agent components so what are the components and its function in a local anesthetic agent so we'll start straight away so we have the basic local anesthetic agent can be xylokane or lignokane the second one is vasoconstrictor commonly used one is adrenaline which is in the dilution of 1 is to 80000 and the third one is reducing agent which is a product used is sodium meta by sulphate and preservative is methyl paraben then fungicide is thymone and vehicle can be either distilled water or sodium chloride so the first component is a basic local anesthetic agent the commonly used in dentistry xylokane and lignokane so it is 2 percentage so it is a dilution factor there's nothing but 2 gram in 100 ml so that is a weight by volume measurement so this is the component which produces local anesthesia the next thing is vasoconstrictor so what is the role of vasoconstrictor so from the name we get the idea it is to constrict the vessels so commonly used is adrenaline or epinephrine it is to counteract the vasodilatory action by constricting the blade vessels so what it does is it decreases the blade flow to the injection area and the absorption of the local anesthetic into the cardiovascular system is slowed which results in lower anesthetic level and thereby minimizing the risk of local anesthesia toxicity so it also increases the duration of anesthesia by allowing the local anesthesia to remain around the nerve for a longer period of time so on a short it does three jobs one is decrease the blade flow decrease the blade flow to the injection area then decrease the toxicity because it slows the absorption into cardiovascular system and also increases the duration so that it stays around the nerve for a longer period of time so what is the role of vasoconstrictor we learned so what is the over dosage resultant so if we use more vasoconstrictor more concentration of vasoconstrictor what happens is it will taken up to the bloodstream which causes increase in the systolic and diastolic blood pressure at it increases the cardiac output and stroke volume so these actions lead to an overall decrease in cardiac efficiency so always when we do local anesthesia for a cardiac patient or someone with cardiac disease we should always remove the adrenalin from the local anesthetic agent we give just plain local anesthesia to avoid the side effects of vasoconstrictor with respect to such patients and regarding the dilution factor so this is one is to 80,000 that means one gram per 80,000 milliliter or we can say 0.8 milligram per ml that is the amount per unit volume okay so that is the dilution factor so that much diluted quantity we are using in LA agent that is the adrenalin or epinephrine so the next component is reducing agent or antioxidants the product is sodium metabolisulfate so this vasoconstrictor has one problem because it is very unstable in solution and may oxidize especially on prolonged exposure to sunlight so once it is oxidized the color will become brown and that is an indication that the solution must be discarded so we need to prevent that so in order to prevent that we add sodium metabolisulfate as a reducing agent okay so this reducing agent will compete for this available oxygen and the shelf life of the local anesthesia or local anesthetic solution will increase so reducing agent are compounds which donates electron because it is very highly reactive compounds so which donates electrons and become reduced and oxidizing agents which accept electrons and oxidized so hope you all remember that redox reaction the oxidation and reduction reduction so reduction where it is donating electron oxidation where it is accepting electron so reducing agent we add this to increase the shelf life okay because this will compete for available oxygen oxygen is very bad for this vasoconstrictor next we have preservative preservative is medial paraben or capryl hydro cuprino toxin so modern la solutions are very stable basically and often have a shelf life of two years or more so their sterility is maintained by the inclusion of small amount of preservatives such as medial hydro cuprino toxin and also we have another one which is a medial paraben but it has some disadvantages that is it is producing some allergic reaction for few people next we have fungicide fungus in the past the some solutions it tended to become cloudy due to the proliferation of minute fungus so in order to avoid that most of the solutions nowadays add a little bit of thymol which is a fungicide to prevent the occurrence of this fungal cloudy and vehicle which is distilled water of sodium chloride so this anesthetic agent and the additives referred to all the additives are dissolved in distilled water and sodium chloride so this isotonic solution minimizes the discomfort during injection and there will be also presence of sodium hydroxide to adjust the pH and the last component is nitrogen bubbles so there will be nitrogen bubbles within the cartridge it is to put to avoid the entrapment of oxygen so if oxygen is there the problem is with vasoconstrictor so oxygen will destroy the vasoconstrictor that is adrenaline or epinephrine so to avoid that there will be nitrogen bubble presence in the cartridge so these are the components of local anesthetic agent the basic component is xylokine or lignokine 2 percentage then we have vasoconstrictor that is adrenaline and 1 is to 80 000 that is a dilution it decreases the blood flow to the site decreases our systemic toxicity and increases the duration of action then the reducing agent which is antioxidant which is complete for the oxygen and get reduced which is sodium metabysulfate then we have preservative methyl paraben and capril hydro kupnotoxin then fungicide thymol and all this will be added in the vehicle distilled water and sodium chloride and we add sodium hydroxide to adjust pH and nitrogen bubble to prevent the entrapment of oxygen it's a very commonly asked uh short essay or short not in oral surgery exam so i'll come up with the next part of local anesthesia hope you understood this small concept thank you everyone welcome back to another session in dentistry and more so we are continuing local anesthesia part four so this session is about classification and the concept of dissociation of local anesthetic and the most important hunter's and hasselback equation okay so let's start with the classification so the first classification category is biological site and mode of action so biological site of action so in this category we have abcd so the class a so agents acting at receptor sites on external surface of nerve membrane so this is acting on the external surface so the most common example is uh biotoxins so which is acting on the external surface so the class b okay so this is class a class b class c and class d so in class b so it is the acting agents which is acting on receptor sites on internal surface of nerve membrane internal surface example is lidocaine and scorpion venum lidocaine lidocaine is quaternary ammonium analogs of lidocaine whereas a class c so the agents acting by receptor independent of physiochemical mechanism which is benzocaine which is the receptor independent of physiochemical mechanism and class d agents acting by combination of receptors and receptor independent mechanism so most common examples are the lidocaine prilocaine and mypivocaine so here also we have one lidocaine that is nothing but quaternary ammonium analogs so this is class abcd based on the biological site and mode of action next we have based on the source so from where it is obtained that is natural synthetic and others okay next based on the mode of application it can be topical or injectable next is based on the duration of action so ultra short it is very very lesser duration then short then medium and long so based on the onset of action short we have intermediate and long so that's all about classification now let's see what is dissociation of local anesthetics so local anesthetics are available as salts usually hydro chlorides for clinical use so the salts both water soluble and stable is dissolved in either sterile water or saline so in this solution it exists simultaneously as unchanged molecule so this is an unchanged molecule without any charge which is called as base and positively charged molecule which is known as cations so this is a equation so the relative concentration of each ionic form in the solution varies in the pH of the solution or surrounding tissues so in the presence of high concentration of hydrogen ion that is low pH we have very high concentration of hydrogen ions so what happens is the equilibrium shifts to left and most of the anesthetic solution exists in cationic form so this will become there will be shifting equilibrium shifting to left okay whereas the hydrogen ion concentration decreases that is a higher pH when this is decreases that means high pH the equilibrium shift towards a free base form that is more number of free base form will be available so that is depending upon the pH so when there is a low pH the more of cationic form will be present when there is high pH more of base form will be available so the relative proportion of this ionic form also depends on the dissociation constant which is known as dissociation dissociation constant that is pKa so this pKa is nothing but measure of molecules affinity for H plus ions what is the affinity towards H plus ions is what meant by pKa so when the pH of the solution has the same value as pKa of local anesthetics exactly half of the drug will exist as RNH plus and the other half will be in RN form okay so this RNH will be equal to RN that is when pH of the solution pH of the solution has the same value as pKa of the local anesthetic this ionic form will be equal to as base form when pH is equal to pKa of that is a dissociation constant of local anesthetic so the percentage of drug exist in either form can be determined so in which form the drug or percentage of drug existing in the solution can be determined by an equation which is known as Handterson-Hasselbach equation okay so this equation actually determines how much of a local anesthetic will be in a non-ionized versus ionized form based on the tissue pH and the pKa of local anesthetic so the injectable local anesthetics are weak basis so injectable local anesthetic weak basis though dissociation constant will be around 7.5 to 9.5 so when a local anesthetic is injected into tissues it is neutralized and part of the ionized form is converted to non-ionized so part of the ionized form will be converted to non-ionized and this non-ionized base is what diffused into the nerve so this is what diffused into nerve okay so when we inject the local anesthetics into the tissues it is neutralized and part of the ionized form is converted to non-ionized form and the non-ionized base is what diffuses into nerve so hence if the tissue is infected so many cases we might face a patient has infection okay in that case why the LA is not working properly because when the tissue is infected the pH is lower the pH is very low because it is more acidic because it has infection so according to this equation there will be less of the non-ionized form okay the presence of this non-ionized form will be very less when there is an infection so this RN is very less to cross the nerve membrane okay so now the less number of non-ionized form of local anesthetic tract to cross into the nerve membrane so the LA will be less effective so that is why in acidic condition or in infection cases the LA won't work that is the reason because if the infection is there it will be more acidic the pH is very low and as per the equation there will be very less amount of non-ionized form to cross the nerve membrane so this is what actually crossing the nerve membrane so less number of RN or the base form to cross the membrane that will be less effective so next part is mechanism of action of local anesthetic LA mechanism okay so we already learned it so LA mechanism so these are the sequence the first thing is displacement of calcium ion from the sodium channel receptor site so we have this receptor site okay so this is a receptor site receptor site this is sodium channel sodium channel so what happens is the calcium ion is displaced from sodium channel receptor site so calcium ions will be displaced from this receptor site so the binding of local anesthetic molecule to this receptor site so the our RN molecule will be binding here first thing is calcium displacement then the RN molecule the local anesthetic molecule binds to the receptor site so it blocks the sodium channel so what it does is it blocks the sodium channel okay so that is the ultimate aim so once the sodium enters there will be depolarization but we want repolarization so there will be decreased sodium conductance so it depress the rate of electrical depolarization and there will be failure to achieve the threshold potential level because there is no sodium going inside and lack of propagated action potential and there will be conduction blockade conduction blockade so this is what is happening okay so from receptor site calcium will be displaced the LA molecule will be attached to this receptor site the sodium channel the conduct the conduction will be reduced the sodium channel will be blocked and there will be decrease sodium conductance decrease rate of electrical depolarization and failure to achieve threshold potential level and lack of development of propagated action potential so that is what is happening the sodium ion channel is blocked in pain neurons okay so that is all about this session so we discussed the classification of local anesthesia then about the dissociation how the LA molecule is changing from cation to base form and famous equation and finally the mechanism how the LA molecules blocks the sodium channel so i'll come up with another topic in all surgery thank you and welcome back to another session in dentistry and more today's topic in local anesthesia we'll be learning about the complications so the local complications and systemic complications so this is a part five of our local anesthesia sessions so moving on local complications of anesthesia that is first one is needle breakage then the ocular complications paracetia facial nerve paralysis chrismas soft tissue injury hematoma pain on injection infection edema whereas on systemic complications we have overdose and allergy so we'll start with the local complications the first one is needle breakage so this is quite rare because of using disposable needles but if it happens it is due to mainly because of bending of needles if you are trying to bend the needle for any purpose the chances of breakage then it could be due to sudden unexpected movement of the patient or sometimes the entire length of the needle inserted into the soft tissue and we suddenly move or the patient tries to move there are chances of breakage and use of smaller needles that is 40 gauge needles we are using there are chances of breakage so how do we prevent this the first thing is always use large gauge needles especially for ianb and posterior superior alveolar nerve block and use always long needles and do not insert the needle into tissues to its hub so completely we should not insert into tissue and do not redirect a needle once it is inserted into tissue so the redirecting is always comes with our ianb so it should be done cautiously because there are chances of breakage so we can manage it because if the needle breakage is visible we need to keep the patient calm and instruct the patient not to move and keep his mouth open and it can be removed using a hemostat or a intubation forceps if it is not visible we can refer the patient to for the surgically removing this and before that we can take a nexary and confirm it that is needle breakage the second one is ocular complications so there are chances of temporary blindness, pupillary dilation, droopy islet or double vision because of this local anesthesia and the cause is orbital injunction that is the injection into the orbit through the inferior orbital fissure so it is causing damage and there are chances of ocular complications so prevention we need to aspirate before the injection and we need to inject very slowly so if any complications either we can treat it by telling the patient that this is a transient this is a temporary problem and cover the affected eye with gauze dressing and refer the patient to an ophthalmologist and we need to keep a regular follow-up the third one is paracetia paracetia the main causes trauma to the nerve while giving a block or injection so local anesthesia sometimes contaminated by alcohol or sterilizing solution and with this contaminated solution we give anesthesia and it results in edema and increased pressure in the region of the nerve ending which leads to paracetia we should not insert the needle inside a foramen and sometimes hemorrhage with the presence of hemorrhage there will be increased pressure that also create paracetia so prevention is proper care and handling handling to injection control and cartridge so how do we manage paracetia first thing is most paracetia will get resolved within eight weeks without any treatment the first part is always reassuring the patient that it is a transient problem then we need to follow up the patient for every two months so if sensory deficit is still more than one year consultation with a neurologist or oral surgeon next we have the facial nerve paralysis so this is we learned in our previous session how facial nerve paralysis is happening that is while giving IA and B if the bone resistance is not obtained and if we are injecting the solution into the parotid gland where the nerve fibers of facial nerve is present so that time if we are injecting on to the facial nerve okay branches of facial nerve that will cause facial nerve paralysis that also temporary or transient problem so it is mostly associated with inferior alveolar nerve block or the wazirani echinocinor block so we can prevent it by proper care and handling of injection and give by doing in a proper way with all the landmarks and other proper criteria so managing is reassure the patient and if sometimes the patient might be using contact lens that should be remote so an eye patched should be applied to affected eye or manually close the lower eyelid periodically to keep the conia lubricated next we have trismus trismus is a pain and difficulty of opening often after the posterior alveolar or inferior alveolar nerve block so it is one to six days after the treatment it is most commonly seen causes are the trauma to the muscles or blood vessels in the infratemporal forza so local anesthetic solution contaminated by alcohol or any other sterilizing solution produce irritation to the muscle and there will be also a low-grade infection so we can prevent it by using sharp sterile or disposable needle and proper care of proper care and handling of this cartridge and always try to do the procedure as a traumatic so management trismus management we can with heat therapy warm saline drinks we can give analgesics like aspirin then muscle relaxants if necessary such as diazepam then 10 milligram twice a day then physiotherapy for five minutes every three to four hours if there is infection we can give antibiotics for seven days improvement start within two to three days and recovery will be done in a range of four to 20 weeks so surgical intervention might be required in some cases so next we have the soft tissue injury so that is trauma to lip or the tongue caused by biting or chewing these tissues while still anesthetized especially with children so it is most commonly seen when ianb nerve block where the tongue and lip will be anesthetized and patient won't realize it so always keep a constant role between the lips and teeth one the patient and self-healer and warning sticker should be given for the parents to notice it soft tissue injury we can manage it by providing analgesics for pain and antibiotics if there is any infection warm saline drinks to aid in decrease the swelling and petroleum chili to cover the lesion and minimize the irritation then we have hematoma so hematoma is a effusion of the blood into extra vascular spaces which can result from damaging of a blood vessel so caused by piercing to artery or vein when giving the injection so most commonly occur with ianb and posterior superior alveolar nerve block so the hematoma will be seen 7 to 14 days so prevention is understanding the proper anatomy of a nerve and its surrounding structures use shorter needles for posterior superior alveolar nerve then minimize the number of needle penetration never use a needle as a probe in the tissue and management we can give direct pressure on the site of bleeding apply cold moist towels to affected area each 20 minutes and advice the patient about soreness and limitation of the mouth opening possibly so we should educate the patient regarding the complications and next we have the pain on injection so pain on injection causes by the careless injection of the palatal injection is always painful and dull dullness of the needle because of the multiple injection also create pain and rapid deposition also will result in pain so always we should adhere to proper techniques and always we should use sharp needles that is nowadays there is no reuse age of needles we are using only disposable syringes and needles we can use topical anesthetics before giving injection inject slowly next we have infection infection the main causes the contamination of the needle now it is very rare because as I said it is disposable needles are being used nowadays the usage of needles is almost not there in any of the dental clinics so before that we had disposable needle and glass cartridge that time this was a common thing infection so if infection is there we can manage it with antibiotics such as penicillin and last one in local complication the edema the main causes trauma infection allergy hemorrhage injection of injection of irritating solution that is alcohol or cold solution we can manage it by just giving analgesics for pain and if the large edema is there we can prescribe antibiotics now let's move on to systemic complication first one is overdose so overdose reaction is occurring when the drug access to the circulatory system so normally there is constant absorption of the drug from its site of administration into the circulatory system and a steady removal from the blood by the liver but if overdose is happening there will be symptoms in the body so what are the predisposing factors so patient factors and drug factors are there patient factors we have age weight medications gender presence of disease genetics mental attitude so regarding age the function of absorption metabolism and excretion are diminished in older age okay old age that is a problem so the increasing the half life of the drug in circulation of blood and weight greater body weight we require larger dose and people who are under medication are also should be considered before giving injection such as finitoin, quinidine such thing has a effect on our local anesthetic then regarding the gender so renal functions during pregnancy may impaired leading to increased local anesthesia blood level so we need to be careful when giving injection for pregnant women then presence of any kind of disease such as hepatic renal heart failure so in this case there are chances of increase in anesthesia blood level and genetics also is there some of the deficiency of enzymes such as pseudo-colonial stress and mental attitude patient who are fearful they need large dose and in such patients we need to make the patient first relax and then provide the dosage regarding the drugs so we were talking about the patient factors in our dosage the predisposing factors so in drug factors we have first thing is vasoactivity that is the vasodilating properties of LA so short duration of clinical anesthesia and increased blood level of local anesthesia will create vasodilation and concentration lower concentration should be given and dose smallest dose should be given so in the drug factors the first one is vasoactivity so vasodilating properties of LA leads to shorter duration of clinical anesthesia and increased blood level of LA and concentration lower concentration should be given dose smallest dose should be given so root of administration should be careful about the intra vascular injection so rate of injection should be slow and vasoconstrictors which decrease the absorption of the drug if vasoconstrictor is not there will be rapid uptake so how do we prevent it use of aspiration syringe need use a needle no smaller than 25 gauge aspirate in at least two planes before injection and always give slow injection so clinical manifestation will be the apprehension there will be slurred speech there will be excitability sweating vomiting failure to follow commands elevated blood pressure heart rate and respiratory rate there are chances of tonic clonic seizure cns depression or myocardial depression and cardiac arrest is also there so management for mild onset and severe onset we can manage it differently so the basic emergency management is first thing is proper positioning this is a synonym PCAPD that is positioning circulation airway breathing and definite care so for mild overdose for mild overdose we need to give PCAB that is first reassure the patient administer oxygen then monitor and record the vital signs we can give IV anti convulsions such as diazepam it is an optional and we can go for emergency medical assistance so in cases of mild overdose that is patient is conscious and it is low onset that is greater than five minutes so in that case we need to reassure the patient and administer oxygen via nasal canal monitor and record vital signs and we can give IV anti convulsions that is diazepam five milligram per minute but only if required it is optional and if it is greater than 15 minutes that is a onset this very slow onset reassure the patient then oxygen the same procedure oxygen via nasal canal monitor the vital signs but the IV anti convulsions is mandatory and before discharging we can take for medical assistance severe overdose that is patient is unconscious so in that case that is rapid onset within one minute we need to first protect the patient then we need to immediate ask for the emergency medical assistance we need to start the VLS that is a basic life support and IV anti convulsions should be given immediately then if the severe overdose where patient is unconscious with slow onset that is five to 15 minutes first of all we need to give anti convulsions that is through IV diazepam or midazolam and ask for medical assistance VLS and also along with we should give vasopressors and IV fluids that is first one overdose age now we have the allergy allergy that is hypersensitive state acquired through exposure to a particular allergen so allergic reactions cover a broad spectrum of clinical manifestation ranging from mild and delayed response occurring as long as 48 hours after exposure to allergen or to immediate and threatening reaction developed within seconds of exposure so what are the predisposing factors so predisposing factors could be the first one is sodium bisulfate sodium bisulfate could be a allergic predisposing factor and epinephrine epinephrine then latex so these could be predisposing factors so the clinical manifestation basically there will be articaria and angioedema articaria and angioedema will be there then clinical manifestation there will be bronchospasm such as dyspnea, wheezing, fleshing, sinosis, perspiration, tachycardia and respiratory distress sometimes extension of edema to the larynx it could be a life-threatening emergency for generalized anaphylaxis there will be skin reactions smooth muscle spasm of GIT and bronchospasm will be there respiratory distress cardiovascular collapse so management skin reaction we can expect a delayed reaction or immediate reaction for respiratory reaction there will be bronchospasm and laryngeal edema for skin reaction if it is a delayed one our PCAB will be like first oral histamine blocker 50 milligram di phenyl hydrene or chlorphenamen should be given and observe the patient for one hour then medical consultation and if patient is drowsiness not allowed to leave the clinic as a patient to rest for a while so for immediate reaction so we should first administer epinephrine 0.3 milligram intramuscularly then intramuscular histamine blocker then we can ask for medical consultation and observe for one hour and prescribe oral histamine blocker for three days so for respiratory problem we should administer oxygen then epinephrine and similarly the histamine blocker and prescribe oral histamine for three days for laryngeal edema also we should follow this epinephrine histamine blocker and sometimes we need Crico thyrotomy that is very rare cases and generalized NFL axis if the patient is unconscious we should follow this epinephrine oxygen checking vital signs and intramuscular histamine blocker and corticosteroids uh that is all about uh complications of local anesthesia so we learned the complications in two category one is a local complication and second one is systemic complications local complications we have needle breakage oculocomplications paracetia facial nerve paralysis trismus soft tissue injury hematoma pain on injection infection and edema whereas in systemic we have just two overdose and allergy but you need to explain it in detail overdose and allergy uh how to manage it how to prevent it what are the uh drugs used and should follow this uh PCAP uh code so in overdose there will be predisposing factors uh that is drug factors and patient factors and also uh we have clinical manifestations and manage in different category that is a mild overdose and severe overdose in mild overdose we have slow onset that is uh more than five minutes and more than 15 minutes and rapid onset is also there within one minute and five to 15 minutes and we need to write about the management and regarding the allergy uh we have the clinical manifestations and also the skin reaction respiratory and generalized nalaphylaxis and also the uh management accordingly so this is very commonly asked question uh it could be as a short assay or a long assay so hope you understood the complications of local anesthesia so i'll come up with a new topic in all surgery thank you