Risks And Complications Of local Anesthesia In The Dental Office.

Complications of local anesthesia in the dental daily issues are usually few, because the concentrations of anesthetic solutions and the volumes used are scarce, however, any procedure, even the most banal, is not without risk and is mandatory the professional is trained to prevent, recognize and, in most cases, treat.

The morbidity with local anesthesia is very low even though this assertion is true, there are described some cases in which death occurred for reasons local anesthetics. It is known Massachusetts experience: after treating 1.5 million patients in the dental office after five years, not a single death. The most common complication was syncope, which occurred in one of every 142 patients who received local anesthesia.
The incidence of most minor side effects associated with dental anesthesia is 4.5%, 7.6 to 23.2% compared to general anesthesia and 0.2 to 19.6% for regional anesthesia. Such side effects were observed, two in 5.7% of patients at risk, compared with 3.5% of patients without risk (ASA I). Patients who self-medicate with a significantly increased risk of developing side effects (9.1%). Additionally, self-medicated patients require reinjection most frequently (28.6%) and received higher doses of local anesthetic (3.4 ml). In addition, patients using NSAIDs, analgesics, aspirin or antibiotics have insufficient depth of anesthesia, requiring higher doses, and are more likely to suffer more commonly psychogenic reactions. It also recommended that treatment for any patient at high risk, should be limited to 30 minutes, since there is a significant increase in the incidence of complications, treatments from 2.9 to under 20 minutes, to 15% for treatments that reach 90 minutes or more.
The cornerstone of prevention of complications is the realization of an accurate and complete medical history.
It is recommended, therefore:
* Appropriate medical history
* Dose relative to weight and not to exceed the maximum dose. In this regard it is important to adjust the dose in children weighing less than 50 kg
* Anesthetic with the lowest possible dosage of epinephrine as sympathomimetic effects are minimized.
* Individualize anesthesia for each patient: type and duration of procedure and risk factors.
Failures of anesthesia
There are few standards on data latency, duration and other effects of anesthesia that are related to each anesthetic product, each anesthetic technique and as the place to be anesthetized. In general terms, the key to success lies in the anesthesia tank enough anesthetic product as close as possible to anesthetize nerve.
Objective signs of anesthesia are well known, whatever the territory of the oral cavity and to which we refer, when these are not present, it is thought that the anesthetic objective has failed.
Anesthesia failure percentages vary by the author consulted. Amounts to about 10% in cases of alveolar nerve block mandibular and 7% in general anesthesia in general dental practice.
It is known that the more local anesthesia fails is in cases of root canals and incision and drainage of abscesses. When present infection and inflammation, anesthetic intravascular resorption is accelerated and low pH adversely affects their diffusion. Repeated application of anesthesia can induce the phenomenon of tachyphylaxis or acute tolerance manifested by decreased response to a standard dose of local anesthetic, requiring increasing the dosage to maintain the same analgesic effect, this is a phenomenon that interferes use when long local anesthetics in clinical practice. While this effect has been attributed to the pH has not been shown in all instances.
Anesthesia little flaw in the infraorbital nerve block, something more infiltrative anesthesia and is high in mandibular nerve block.
Sistematizaremos then causes anesthesia failure.
A) Technical incorrect.
Generally this section refers to the fact of depositing the anesthetic in the wrong place. This is in connection with an imperfect understanding of the anatomy of the region. Especially in the alveolar nerve anesthesia mandibular should inject a sufficient amount of anesthetic solution as close to the spine of Spix or maybe something above and behind her. Moles1 Keetley and studied the success of 580 punctures to the alveolar nerve anesthesia mandibular succeeded in finding that 91.9% (533) and that the failures were simply due to poor technique by the dentist himself.
Specifically, in the case of anesthesia mandibular alveolar nerve in the mandibular foramen there atener details that are important to note:
1) Needle: a) The direction of the needle (too low, too this, too later, parallel to the ramus, medial ligament pterygopalatine jaw, very high, too domestic, too high and too far back). b) Needle length: just use 38 mm needles, because although it is flexible, does not break and also with a long needle will reach the near and the far. c) Some authors recommend intramuscular needle type, being stiff as a failure of anesthesia, especially nerve-mandibular alveolus is related to the deflection of the needle during the puncture. Hochman and Friedman2 found that this deviation is one of the elements which may reduce the accuracy and predictability of alveolo-lock mandibular nerve, demonstrating that the use of an insertion technique minimizes bending bidirectional rotation of the needle .
2) The ascending limb abnormalities anteroposterior orientation or width.
3) The opening of the dental canal. The child is placed lower than in adults, so be punctured at a lower height or tilt the needle down. In toothless, by contrast, is higher with respect to the remaining alveolar process, which in the adult dentate.
4) Changes in nerve. The most important of this section are the peripheral nerves, for example, nerve anastomosis, as in the central regions of both jaws, where there anastomosis with the same nerves, but on the opposite side. In recent years there have been revisions that update some details about the distribution of the trigeminal nerve branches.
To lower nerve anesthesia by the conventional technique described three possible failure of anesthesia ipsilateral lower teeth fully anesthetized (already explained the possible mediation collecting mylohyoid nerve sensitivity), the third molar ipsilateral lower is sometimes incompletely anesthetized (citing that sometimes, there is a branch of the inferior alveolar nerve aberrant that emerges above the mandibular foramen and would take one to anterosuperior branch, running its own conduit, collecting sensitivity of the third molar), incomplete anesthesia of all ipsilateral mandibular teeth (this is explained by a possible position of the mandibular foramen higher than usual).
The bifurcation of the mandibular nerve, rarely mentioned in the literature may be due to inadequate anesthesia in a small percentage of cases. There come aberrant innervation posterior superior alveolar nerve, auriculotemporal or lingual nerve branches, one branch or aberrant retromolar can mandibular nerve innervates the third molar, suggesting places while additional injections as buccal or sublingual injection, other blocking techniques other than the spine of Spix intraligamentosas or injections. Little attention has been given to a bifid mandibular alveolar canal with a second located inferiorly than usual. This branch can not be anesthetized by blocking traditional Spix's spine.
The Gow-Gates technique has, in this regard, some advantages over the conventional technique of anesthesia mandibular alveolar nerve in the mandibular foramen.
Advantage
* Deep anesthesia of the mandibular pulp, gums and alveolar mucosa, since the third molar to central incisor with a single injection.
* Uncommon intravascular injection (seems to be the deposit of anesthesia in the mandibular neck anterolateral side because to get to this position, the needle passes lateral to the usual position of the internal maxillary artery, inferior alveolar and middle meningeal artery, and less than masseteric artery). The number of positive aspirations, ranges from 1.6 to 1.9%, whereas the traditional block are between 10 and 15%.
* Low trismus casuistry that with the conventional technique.
* High degree of success.
* References anatomical constants (intertragiano groove).
* Rare problems finding partial or incomplete anesthesia of mandibular posterior region.
* With anesthesia anesthesia Gow-Gates is also the mylohyoid nerve, so yes this nerve contribute to the innervation somewhere in the mandibular arch, would be blocked by this technique.
* Rare presentation of adverse events (syncope, fainting).
* Vasoconstrictors unnecessary anesthetic.
* Lack of facial paresis.
Disadvantages
* Lack of buccal nerve anesthesia, probably due to the buccal nerve is more distant from the site where the anesthetic is deposited in what is believed and treated describing what anatomic, since when deposited mouth anesthesia with very open (opening of the actual anesthetic technique), is separated from the place of deposit for the external pterygoid muscle and its fascia. It has also been attributed to the oral anesthesia would require more material anesthetic, or the patient should be supine, it seems that the former is more definitive for success, that the position of the patient.
* Long latency period (5-7 minutes).
* A degree of suspicion by the dentist during the learning period (1-2 weeks). With the experience and, in some cases, perseverance, you get a success rate of 95%.
It is necessary to recall the area of ​​anesthesia is the anterolateral condylar neck, and anteromedial area. This error did not contribute to bone contact and to produce auriculotemporal nerve anesthesia, associated with a poor buccal nerve block.
5) Great bone density, as a cause of failure infiltrative techniques.
6) We have already cited the anatomic arrangement of the ascending branch block technique for conventional dental alveolar nerve.
7) Great bulking muscle.
8) Great adipose tissue.
B. Dependents of the individual
Anesthesia also can fail by factors related to the individual or the ground.
Anesthesia may fail in very anxious patients or patients with suboptimal anesthesia experience. Stew cols3 Moya and studied the behavior of patients and found a significant relationship between dental anxiety, poor oral hygiene, pain intensity to local anesthesia and efficiency of routine dental procedures.
For sensitivity anesthetic which, apart from the allergic problems, lead to a failure of anesthesia.
If the buffering action of the fabric is decreased or if the pH is lower than normal (for example, in the acidic environment of inflammation) is available then fewer free base for diffusion through tissue, and Accordingly, the local anesthetic has less activity.
Others think that inflammation modifies the activity of peripheral sensory nerves. Inflammation produces a primary hyperesthesia area mediated by chemicals that reduce the threshold of sensory receptors. Since the hyperesthesia induced inflammation, a stimulus given an increased sensitivity occurs. This neural response is increased less effectively blocked by a given amount of anesthesia. This problem can be solved simply by increasing the concentration (not necessarily volume) of anesthetic to reduce the action potential of the nerves.
C. Dependent Product
With regard to the anesthetic, anesthesia can also fail because the product may be old or in poor condition. Other reasons for failure are: hipodosificación anesthetic, inadequate heating and contamination of the anesthetic solution. Although they have tried to find enhancers anesthetic action, only vasoconstrictors have fulfilled this function. It was once thought that hyaluronidase, when added to the anesthetic would produce greater extent and tissue penetration.
Choosing the right product is essential. If a product is chosen poorly in relation to the type and duration of the intervention, the result may be a failure, but overall, maybe so partial. Parameters such as latency, depth, duration, tolerance and absence of side effects are especially valued when selecting a local anesthetic, but this selection does not seem to have anything to do with the type of nerve block.
The long-term anesthetics have proven effective in suppressing intra-and postoperative pain especially in surgical procedures and with few side effects when used at appropriate doses. However, they have some potential effects, such as, for example, bupivacaine which may cause cardiac depression and dysrhythmias, or etidocaine that produces less effect on the cardiovascular system as above but in exchange, their use is associated with difficulty intraoperative control of bleeding.
PDL anesthesia can be very useful, not only when they fail nerve block techniques, but in other circumstances. It may be convenient to use and intraseptal intraligamentous anesthesia for patients with hemophilia or other bleeding disorders and children as well as physically or mentally disabled may appear in greater risk of infection after trauma of the lower lip or tongue. Also may be indicated to control pain in isolated regions of the jaw for short procedures or in one or two teeth without having to anesthetize the entire quadrant or soft tissue. Some states that the use of anesthesia endodontic intraligamentous in diagnosis can be invaluable. Anesthesia is thought to exert its effect intraligamentous extending through the same channels as the intraosseous and the damage induced by the injection needle and / or the anesthetic solution (injected under high pressure) is of inflammatory type, but localized, smaller and reversible, probably in relation with the small amount of anesthetic injected and rapid infiltration into the cancellous bone spaces.
Sometimes, the doubling the dose of anesthetic causes postoperative pain, and as described Jorkjend Skoglund4.
There anesthetic methods have limitations, such as EMLA and electronic dental anesthesia. According to McMillan and cols5 point, the EMLA (eutectic mixture of lidocaine and prilocaine) topical anesthetic agent is more effective than lidocaine gel isolated, although the duration of action is relatively short, it is suitable for minor operations in the gum.
Accidents and local complications
A) immediate Accident
1. Pain
The injection pain persists co-mo a frequent source of anxiety for some patients. Amide anesthetics, such as lidocaine and bupivacaine, are known for their propensity to cause discomfort when infiltrators.
The pain during the administration of anesthetic liquid can be produced for different reasons: the puncture of a particular nerve injury cause pain that persist hours or days, the tearing of the gingival tissues and the periosteum is mainly because of postoperative discomfort intensity variable postanesthesia these pains are to be distinguished from postoperative pain.
The level of pain, especially in some areas, for example in the upper lip region may be obscured by any distracting maneuver, such as the traction thereof. We have tested the effects of distraction on pain control in children aged 3 to 7 years, found that certain techniques, such as deep breathing and blowing the air, have some advantages over the administration of local anesthetic in children (minors torso and hand movements, arching eyebrows lower and lower expression of pain).
The most requested by patients to avoid the pain, topical anesthesia.
It has been shown that the puncture pain is slightly smaller when the product is slowly injected anesthetic, but not eliminated altogether.
Some professionals use and recommend the use of buffered anesthetic to reduce pain, the anesthetic solution diluted 1:10, that is part of NaHCO3 for 10 standard lidocaine or bupivacaine (with or without epinephrine), particu-larly in patients particularly squeamish or children.
Subperiosteal injection causes tearing of the periosteum, and the resulting pain.
Some authors describe their techniques to not cause pain to puncture the palatal region, as Aslin6.
Another issue to consider is the role of postoperative pain in the anesthetic solution. Skoglund4 Jorkjend and conducted a study on postoperative pain after the completion of a bilateral gingivectomy depending on the amount of anesthetic used. On one side is a standard volume of injected solution containing lidocaine 2% with epinephrine 1/80.000 and on the other side twice the volume, found that in the place where he had doubled the dose, the intensity of acute postoperative pain ( between 2 and 8 hours) increased after gingivectomy.
Cited smaller diameter than the needle puncture less pain.
2. Rupture of the injection needle
The breakage of the puncture needle, when present, may be considered an outstanding accident. The late withdrawal of a broken needle that disappeared inside the tissues, is downright difficult and will be always under radiological guidance and radiopaque objects.
It is imperative, therefore, to use good quality needles, the patient does not make sudden movements unexpected, we use proper technique, we do not lose sight of the puncture site, we try to remove it as soon as possible, that the patient's informed accident and that, if we can not remove it, send the patient to the hospital, where decide whether or not to prompt removal or otherwise, defer. In any case, the extraction is usually, usually laborious.
Within this exceptional, the most common place is in the spinal fracture in the mandible, particularly in anesthesia alveolar nerve inferior alveolar, although there are reported cases of rupture in the posterior maxilla, moreover, was followed the area of ​​infection.
3. Hematoma
Sometimes during the puncture of the anesthetic, vascular injuries occur and torn vessels, but this accident is rare. The simple puncture of a blood vessel causes blood output variable intensity according to the injected region, and patient characteristics. You may have bruising, especially when the patient has a disorder of hemostasis, which drain following the natural ways either to the genial region, submandibular cell or into the neck.
It is well known intraligamentous recommendation anesthetic injection in all patients suffering from haemophilia. Thus, do not show the dreaded complications of bleeding or hematoma formation and provides a good quality without requiring anesthetic administration missing factor.
Epidemiologically, is especially common in women, very white skin and blonde.
In retrotuberositarias injections, the hematoma is usually instantaneous and alarming. The spill blood takes days to its resolution. No consequence, unless your infection.
4. Facial paralysis
When the inferior alveolar nerve anesthesia has been penetrated with the needle behind the ramus, are injected into the parotid gland. This facial paralysis appears to last as long as the duration of anesthesia, but it is certainly a frightening crash for the patient. This is a downright weird accident. Keetley and Moles1, however, after 580 punctures after mandibular foramen to the alveolar nerve anesthesia mandibular found an incidence of facial paralysis much higher than expected: 0.3%.
The examples are cited related facial paralysis, most par-te with the anesthesia the alveolo-mandibular nerve. The paralysis can be immediate or delayed, in the immediate type paralysis occurs in the first few minutes after injection, when the function recovering anesthetic effects have disappeared at approximately 3 hours or less. In the delayed type, onset of paralysis may appear several hours or several days after injection. Recovery may occur after 24 hours to 6 weeks depending on the degree of nerve damage. It seems that the cause of paralysis is the same anesthetic solution.
In the immediate type, the anesthetic solution affects the facial nerve retromandibular space or within the parotid fascia. Nerve involvement by the anesthetic solution is therefore unique and can only be explained by individual anatomical variations. Otherwise, it is necessary that the injection point is positioned very high and close to the rear edge of the ramus. However, the facial nerve is outside the scope of the longer needle, so that this accident is attributable to the penetration of liquid inside the gland, affecting the nerve by diffusion.
In the delayed type solution stimulates the sympathetic nerve probably connected with the external carotid artery, which in turn is in communication with the overlying artery plexus estilomastoidea. This sympathetic stimulation causes a reflex spasm of the vasa nervorum facial nerve, leading to ischemic neuritis and edema secondary.
5. Paralysis of the soft palate
If the puncture and deposit the anesthetic solution is made in the area behind the posterior palatal canal or locks the middle and posterior palatine nerves discomfort occur deglutition and phonatory by anesthesia of the soft palate, likewise, will occur from anesthesia estafilinos paralyzed muscles of the soft palate and phonatory disorders and breathing.
6. Ischemia of the skin of the face
Sometimes anesthesia following any noticeable on the skin of the patient's face pallor areas of ischemia due to this region.
Bleaching usually occurs at the moment of injection, usually in the upper jaw and especially in the punctures of posterior superior alveolar nerve or anterior palatine nerve.
There are three theoretical explanations:
* The anesthetic solution epinephrine causes vasoconstriction along branches of vessels near the site of injection.
* The anesthetic is injected into a vessel and taken to the periphery where due to epinephrine and vasoconstriction, whitening skin appear.
* Needle damage or excite sympathetic fibers associated with arterial injection site, inducing a reflection terminating in the peripheral branches of a given vessel, the excitation leads to vasoconstriction localized cutaneous peripheral vessels.
Often orbital pain is associated, and in these instances the patient is profoundly alarm, the duration of this pain is usually short.
Bleaching is solved, usually before the disappearance of the anesthetic effect.
7. Injection of anesthetic solutions in neighboring organs
It's a freak accident.
The liquid can be injected into the nostrils during anesthesia nasopalatine nerve, causing a little bleeding, no more problems, but usually alarm the patient.
Injection into the orbit during anesthesia for dental nerves prior or maxilla diplopia and strabismus can lead what lasting anesthetic effect.
We have referred above to the injection into the parotid.
8. Eye accidents
Accidents related ocular techniques for dental anesthesia are extremely rare and literature exhibits some publications.
There are several theories to explain this problem.
The description of the double vision (diplopia) following nerve anesthesia mandibular alveolar-has long been described in the literature. The generally accepted explanation to this phenomenon is that the anesthetic solution inadvertently injected directly into the inferior alveolar artery and, due to the injection rate appeared retrograde flow of the anesthetic solution. The proposed flow through the first division of the maxillary artery superiorly and then reaches the middle meningeal artery enters the skull. It accepts the connection between the artery and the middle meningeal artery tear through the superior orbital fissure through lagrinal recurrent branch. The proposed mechanism of double vision, therefore, is related to vasoconstriction affecting branches rectus muscle. In addition, there is a rich anastomosis between the recurrent lacrimal branch of the ophthalmic artery branches.
It is also proposed another mechanism. There is a trauma to the sympathetic plexus surrounding the common carotid, external and internal carotids and all its branches when the anesthetic needle inadvertently irritates the lining of an artery. In the case of anesthesia inferior alveolar artery, inferior alveolar be involved. In the case of an infiltration jaw, would be involved posterior superior alveolar arteries. In both instances the trauma could cause a boost that would travel along the maxillary artery in the pterygopalatine fossa. From there, the momentum would pass along sympathetic nerve deep petrosal internal carotid plexus, then along the internal carotid artery and finally to the ophthalmic artery in the orbit. Because the secondary response to traumatic injury decreases sympathetic activity policy, then the parasympathetic its action would be increased with consequent signs of lacrimation, salivation and bleaching of fabrics.
Diago and Sanchís Peñarrocha Bielsa7 **, published a series of 14 ophthalmic complications after intraoral anesthesia posterior superior alveolar nerve. Symptoms usually found were diplopia, mydriasis, ptosis and abduction difficulties of the affected eye. In all cases, these effects occurred minutes after anesthetic injection, followed by complete resolution without sequelae ceased once the anesthetic effect. They suggest, as the mechanism, a possible spread of the anesthetic solution into the orbital region.
9. Intravascular injection
The intravascular injection of an accident undesirable application of local anesthesia, the adverse reactions that occur in this method can be serious.
When it is necessary to inject into a blood vessel (for example, during intravenous sedation) is essential aspirate blood into the syringe to check that are in a vein. For the same reason, when you try to be extravascular injection, one would aspire to ensure no blood enters the cartridge before administration of the drug. Well, this argument, which is used routinely by doctors and nurses, is not universally accepted by dentists before administration of local anesthesia.
There may be false negatives. The self-priming syringe Evers is, in our experience, a secure suction and is not related to a particular brand of local anesthetic.
The frequency of positive aspirations is somewhat variable according to the author consulted and cited figures reach 8.9%, or 67.2% of children between 8 and 10 years. The most common place is aspiration during anesthesia in the mandibular foramen.
The incidence of clinically observed reactions to intravascular injection amounts to a reaction every 450 injections, but some authors suspect an even higher incidence, especially in children. It is estimated that increases the intravascular injection to 200 times the toxicity of local anesthetics.
It is very important to be vigilant when suctioning, as if blood is aspirated blood and therefore enters the cartridge to much pressure, blood red color can be perceived more difficulty if the venous blood enters the cartridge at a lower pressure.
Research into the extent of anesthetic solutions intraligamentous managed, conflicting findings have revealed. Some studies show that the anesthetic reaches the ridge, delves beneath the periosteum and into the cancellous bone along the vascular channels, vascular penetration happening. There seems to be a universal input in vessels, more than a simple diffusion in the alveolar tissue. This finding is clinically significant, since it is well documented that transient toxic reactions may occur even with low levels of local anesthetics in blood.
The presence of epinephrine (1:100.000) in solutions which are administered anesthetic intraosseous, and intravenous intraligamentous cause rapid but transient hypotension and tachycardia periods are likely significant. Since the film is really hard alveolar bone cribriform type, it seems logical that the solutions injected into the periodontal space under pressure can flow quickly to adjacent marrow spaces containing venules which anastomose with the vessels of the periodontal ligament space. High pressures can force the fluid into the microcirculation before vascular smooth muscle can react to epinephrine. It is clearly demonstrated that epinephrine is the causative agent of systemic responses to these injections. Thus, anesthetic solutions containing catecholamines should not be used in a medically compromised patients intraosseous.
10. Other immediate complications.
Facial paralysis can be accompanied by changes in taste in the anterior part of the tongue, indicating involvement of the chorda tympani, which is an anastomosis between the facial and lingual infiltration of the chorda tympani could be responsible for this anesthesia.
There intraligamentous bacteremia after injection and infiltration anesthesia.
Described a case of factitious gingival after topical anesthetic.

B) Accident mediate
1. Persistence of anesthesia:
It can occur after nerve injury in the puncture. The nerve regenerates slowly and after a variable time period is retrieved sensitivity.
Pogrel and Thamby8, conclude that the incidence is between 1:26.762 and 1:160.571. Anesthetic agents used, prilocaine seems to be most frequently involved in this study. In most cases only partial damage, but the recovery is incomplete.
As Haas and Lermon9 published, the Canadian Responsibility Program between 1973 and 1993 included 143 cases of paresthesia not associated with surgery. No significant differences with respect to the patient's age, sex or used needle. All cases involving anesthesia mandibular arch, being the most symptomatic tongue, lip followed. It was accompanied by pain in 22% of cases. In 1993 alone there were 14 cases of paresthesia not associated with surgery, which projected yields an incidence of 1:785.000 injections. The products involved in more anesthetic paresthesia were the articaine and prilocaine. Articaine was responsible for 10 of those cases and prilocaine from the other four. These results suggest that local anesthetics themselves have some potential neurotoxicity.
2. Infection at the site of puncture.
The risk of introducing microorganisms in deeper tissues is indeed increased in the oral cavity, where sterilization is impossible and where a range of potentially pathogenic microorganisms constitute the normal flora of the mouth. Pathogenic microorganisms can be inoculated when the drug is being administered, causing infection in tissue that has been introduced "puncture culture."
The bacteria that causes infection of the needle tract can come from three sources: the same substance that is injected, the environment and the dental patient's own microflora.
The development of infection from the needle tract depends on the status of the defense mechanisms of the patient and the number and virulence of the inoculated bacteria. Symptoms of infection ranging from prolonged myalgia and muscle dysfunction in acute infection and septicemia tissue spaces.
3. Pain.
This phenomenon usually occurs when the periosteum is injured, the typical example is subperóstica anesthesia or when without being so in infiltrative anesthesia supraperiosteal gets misplaced the needle bevel.
There may be pain also anesthetic injection in the muscles.
The injury of the nerve trunks of the needle tip may cause neuritis also persistent.
4. Necrosis.
This is a freak accident, but once not uncommon. The necrosis was more typical of the palatal fibromucosa in connection primarily with the use of a particular anesthetic product (butanilicaine phosphate) or with the injection of excessive amount of solution that also contained a high concentration of vasoconstrictor. The scar (sometimes alarming) follows in a few days, depending on the extent and postenormente, begins a long process of granulation by secondary intention.
5. Frey syndrome.
Syndrome aetiology is uncertain, by irritation of the inner jaw, which causes signs of sweating, heat and redness in the region auriculotemporal upon ingestion.
6. Irritation ionic contamination.
When the syringe remains charged for a long time before the injection, anesthetic solution can become contaminated with copper ions inside the needle, with the clinical manifestation of edema after two or three days or abnormally long persistence of the effects anesthetics.
7. Automordeduras
It is relatively frequent, especially in children, automordedura lips, usually the bottom, but also on the buccal mucosa and tongue or scratches on the skin even during the time in which these areas are unaffected following administration of a solution local anesthetic.
Sufficient that the child is informed of the problem and that parents be vigilant during the duration of the feeling of numbness.
8. Trismus and muscle involvement
The appearance of trismus is rare, but it occurs more when alveolodentario block and lingual nerves and infiltrates the posterior maxilla. It is known that lidocaine with epinephrine, chloroprocaine and piperocaine produce muscle fiber damage and also to the vasculature and bupivacaine only causes damage primarily to the muscle fibers.
The administration of multiple injections increase the risk of muscle bleeding or blood vessel damage.
The hematoma may in turn lead to the formation of fibrous tissue, the trismus appears after a latency period of 24 hours, is usually painless and may persist for several weeks.
As noted above, muscle trauma or blood vessels in space infatemporal is the most common etiologic factor after dental injections. In the acute phase, the bleeding pain leads to muscle spasm and limitation of movement. Yes the treatment is not instituted, there will be a progression to chronic limitation of motion, this is secondary to hypomobility organizing hematoma with subsequent fibrosis and contracture scarring. Hematoma infection in space can also contribute to infatemporal hypomobility due to increased pain and finally more and scar tissue reaction. Early treatment must be directed toward prevention of chronic hypomobility (heat, analgesics and muscle relaxants), thereby preventing the organization, fibrosis and contraction. If the patient, after 48 hours, no response and the pain continues, there may be an infection infatemporal space. To all the above treatment should be added antibiotics. We also have to make a study of CT and MRI to verify that there is in any different than expected. Once chronic mandibular hypomobility develops, surgery is required.
When the concentration of epinephrine is high, muscle damage can be attributed to it due to local muscle ischemia. Additionally it is known that epinephrine depressed and increases muscle glycogen oxygen consumption. These effects combined with the ischemia can induce muscle necrosis. When epinephrine also joins the local anesthetic may have an additive effect. There is a significant increase in serum creatine phosphokinase (CPK) between 8 and 48 hours after a single intramuscular injection of 10% lidocaine.
9. Alveolitis
With no anesthesia intraligamentous most dry sockets with truncal infiltrative anesthesia or normal. However, it is reported that the incidence of dry socket is significantly higher after use of lidocaine and prilocaine as compared to the use of repeated injections or intraligamentosas techniques increases the likelihood of this problem painful post-extraction.
10. Other late complications
As a local tissue reactions are described cases of thrombophlebitis following administration of lidocaine and histological changes in skeletal muscles using lidocaine, mepivacaine, prilocaine, bupivacaine and etidocaine but always reversible, with complete muscle regeneration in two weeks.
Systemic complications
Systemic effects of local anesthetic agents can be divided into three broad categories: drug toxicity, allergic reactions and psychogenic reactions. The majority of systemic reactions are related with drug or psychogenic in nature.
1) Systemic reactions
A) Toxicity
Despite the high security provided by these agents, there is evidence of adverse reactions ranging from 2.5 to 11%. The majority of adverse reactions to the injection occurring immediately or within the first two hours after it. For cols10 Kaufman, most adverse reactions occur within the first two hours following injection.
Under standard conditions, and for administration of local anesthetic solutions in the appearance of toxic symptoms must exceed usually widely recommended therapeutic doses, so that the toxic reactions are extremely rare. These complications usually occur when due to overdose, intravascularly administered at therapeutic doses, or conversely, typical dose used in sensitive patients.
One of the conditions of an ideal anesthetic is their low systemic toxicity and free of undesirable side effects. If two anesthetics have the same general toxicity, but one of them is more effective at lower concentrations, it provides a greater margin of safety. Even when an anesthetic is toxic when its concentration passes a certain level in blood, addition of a vasoconstrictor allows the administration of a higher dose of anesthetic and safer. This is because, as already known, a vasoconstrictor which retards the absorption of anesthetic from its site of application, and therefore, the anesthetic concentration in the circulating blood can not get to a high level. However, if the local anesthetic is injected intravascularly accidentally, the presence of the vasoconstrictor can not reduce their toxicity.
A greater vascularization (speed venous and lymphatic drainage) of the area where anesthetic is deposited, faster absorption, so that their action is of short duration and in the plasma concentration will be high, increasing, therefore, toxicity. Consequently, the same dose may be securely in place, but dangerous in another.
Another factor known to affect the absorption of the local anesthetic is the acidity, which causes vasodilation and consequently, the effects are not predictable when injections are applied in local tissue acidosis.
The nature of tissue vascularization addition is also important in the absorption of a local anesthetic. The adipose tissue requires liposoluble agents, reducing vascular absorption rate. Thus, the duration of the nerve block can be prolonged when nerves are found in adipose tissue.
Local anesthetics are excreted in the urine, mainly as metabolites, but also as unchanged. Therefore, patients with impaired renal function may accumulate these products and must, precautoriamente to avoid toxicity, reduce the dose limit of anesthetics. Acidifying the urine facilitates removal of local anesthetic, suggesting that absorption takes place by diffusion tubular nonionic.
The amino ester local anesthetics are hydrolyzed by plasma cholinesterase. Obviously any factor that could contribute to a decrease in the activity of this enzyme would allow an increase in serum concentrations of local anesthetics ester bond, raising systemic toxicity. The most frequent cause of the deficient activity of plasma cholinesterase is the use echothiophate iodide chronic treatment for glaucoma, and genetic deficiency (atypical cholinesterase) which is associated with extremely low activity of plasma cholinesterase. Whenever possible be avoided the use of local anesthetics amino ester when suspected cholinesterase activity is poor (for example, myasthenia gravis).
The amino-amide local anesthetics are mainly metabolised in the liver to microsomal enzymes.
The amide local anesthetic that is rapidly metabolized prilocaine, which partly explains its low systemic toxicity.
Bupivacaine, the most potent amino-amide local anesthetic, is the slower metabolism. This, along with its proven power, explains the relatively high systemic toxicity of bupivacaine.
Hepatic metabolism of anesthetics of amide bond may be affected by any factor that impairs liver function. This may include, from liver disease to drugs that affect hepatic blood flow, or an alteration of hepatic enzyme activity. For example, cimetidine increases the plasma half-life of lidocaine in rats up to 38%.
The danger is directly proportional to the concentration of anesthetic in circulation, which depends on the agent administered, dosage, administration site and anesthetic technique. So when there overdosage, inadvertent intravascular injection or rapid absorption, may appear any adverse pharmacological action. In any case, the incidence and severity of these effects, it is usually much more frequent the longer the anesthetic potency of the drug. Unlike most drugs, which produce their therapeutic effect once it reaches the systemic circulation, the analgesic action of local anesthetics according to the drug decreases disappears at the point of injection and passes into general circulation. Therefore, these undesirable effects usually appear within several minutes after being administered. They produce high arterial concentrations of the anesthetic of from 10 to 25 minutes after the injection, so that the individual monitoring must be done mainly in the first half hour after administration.
In dentistry, the number of adverse reactions, particularly toxic reactions, is extraordinarily low. There are cases in which the toxic reaction to the fogging occurs transoral / transfaríngea preoperatively with lidocaine during preparation for general anesthesia.
The anesthetic overdose in dental practice is rare, but can occur and in some cases can be fatal. Normally the use of a good technique that uses small amounts of solution, limiting toxicity. Moreover, a good story can help us discover past problems.
It is recommended not to exceed the dose of 25 ml (500 mg) of lidocaine 2% with epinephrine 1:80,000 for a healthy adult. The recommendations are: 1. - In mixtures of two pharmacologically active drugs (dual formulations), the basis of the safety limit is lidocaine circulating levels, rather than the amount of adrenaline contained in the injected volume. 2. - The suggested upper limit is four and a half rounds of lidocaine with epinephrine (180-198 mg lidocaine or 2.57 to 2.82 mg / Kg.) 3. - For some medically compromised patients, minimum dose should be used lidocaine with epinephrine (about a cartridge) and you have to pay attention to the possible reaction to exogenous adrenaline in this dual formulation. 4. - For both children and adults, the dose should be adapted to the body size and you have to pay attention to other forms of topical anesthetic such as pastes, creams or sprays. The doses of anesthetic should be the minimum necessary to perform the procedure provided, if necessary, it is best to quote the patient several times, to inject a large amount of anesthetic and perform all the treatment in one visit.
Lidocaine security is increased by the addition of epinephrine which inhibits systemic absorption of lidocaine preparation. It should be noted that epinephrine may also have toxic effects. In the volume and concentration of the anesthetic usually used in dentistry, overdoses not have to happen. However, excessive levels in plasma can also result from rapid absorption due to an inadvertent intravascular injection or injection too fast.
Topical lidocaine (rinses) for the treatment of oral mucositis in patients who have had bone marrow transplantation fact be minimally systemically absorbed.
Factors that influence toxicity are the site of injection (intravascular or extravascular) and rates of absorption, distribution, metabolism and excretion, but there are a number of situations that can modify and increase the toxicity of local anesthetics: drugs that can compete with them, states hypoproteinemia, renal or cardiac hypothermia states and factors that modify the rate of absorption.
2) Central nervous system
The reactions can produce CNS excitation and / or depression ranging from nervousness to respiratory arrest.
It is believed that the stimulation produced by successive depression and local anesthetics in the CNS, are actually the result of neuronal depression and stimulation would be the consequence of CNS depression selective inhibitory neurons. Reactions in principle be pacing, if the blood concentration is increasing is appearing affect excitatory central depression.
Clinical symptoms of intoxication may appear immediately or a few minutes after administration as delayed reaction. It begins with disorientation, incoherent words, ringing in the ears, headache, nausea, vomiting and muscle tremulación. You can then unconsciousness occur with a chronic seizure state that alternates with periods of tonic contracture. Breathing is insufficient and ineffective and the patient becomes cyanotic. This phase, lasting one or two minutes, you can stop the patient's death by asphyxia or cardiovascular depression.
If you exceed this CNS arousal phase is passed to a phase of depression, in which the unconscious patient shows areflexia and muscle relaxation with low blood pressure, tachycardia, soft pulse, irregular breathing and sometimes faint gasps. Finally can de-sembocar in respiratory arrest, in part because there has been excessive central stimulation resulting in depression of the respiratory center, and partly because respiration can not take place if the intercostal muscles and diaphragm are in convulsive status .
The excitement phase can be treated by administering intravenous diazepam (0.1 mg / kg., Or 5-10 mg, IV, not to exceed 5 mg / mm; may be repeated at intervals of 10-15 minutes if not budge, even a maximum dose of 30 mg, keeping an eye on the constant respiratory) or barbiturates (thiopental, 25-50 mg). Hypercapnia and acidosis may facilitate the development of seizures, while oxygen administration is beneficial, but not abolish its administration. Muscular manifestations can be suppressed with succinylcholine (0.5-1 mg / kg, IV) or suxamethonium. In fact, in presence of severe convulsions, tracheal intubation combined with the administration of succinylcholine and artificial respiration and prevent pulmonary aspiration facilitate hyperventilation. Studies of primates, advise the use of diazepam to alleviate seizures without respiratory depression produced by barbiturates. Although succinylcholine, muscular blocking agent short acting muscle contractions can control and facilitate ventilation, inducing respiratory paralysis may be more dangerous than the attack itself.
The epidural injection may be a frequent cause of accidents in the dental chair, and has received little attention in the literature. The perineurium of peripheral nerves is a continuation of the pia and arachnoid membrane surrounding the spinal cord. If a fine needle is inserted into the perineurium of the peripheral nerves, the fluid travels in-jected centripetally towards the neuraxis. Perhaps, then, by this means that small amounts of local anesthetics can reach the brain. This can occur in human clinic, if very thin needles are used to block nerves that are relatively fixed, such as the inferior alveolar nerve in the vicinity of the mandibular foramen. In this case, even with small amounts, such as 2 cc of lidocaine 2% or 40 mg, may cause a transient blockage, medullary and midbrain.
At high doses, to block nerve conduction, can inhibit both the sympathetic and the parasympathetic system.
The central nervous system is more susceptible to the cardiovascular effects of systemic local anesthetic. However, in the case of lidocaine most common toxic effect is stimulation of the central nervous system followed by depression, or depression only. Deaths attributed to overdose of lidocaine are usually due to the effects of central nervous system depressants.
3) Cardiovascular system
Toxic effects on the cardiovascular system will occur roughly in the following order: depressed contractility, excitability and conduction velocity, decreased volume / minute, mild to moderate hypotension, peripheral vasodilation, hypotension, bradycardia sinus and cardiovascular collapse.
Reactions on the cardiovascular system range from slight changes in blood pressure to cardiac arrest. Almost all local anesthetic agents having a vasodilating action in vitro except prilocaine and mepivacaine, but this apparently contributes little to produce hypotension.
The actions on the cardiovascular system occur only at relatively high and are a primary type quinidinico on the myocardium to cause a decrease in excitability, conduction velocity of, the refractory period and the inotropic effects which can be visualized in The EGG.
Antiarrhythmic drugs are behaving as membrane stabilizers, suppressing reentry by bidirectional block. Procaine, procainamide and lidocaine have been used intravenously by quinidinicos effects to control cardiac arrhythmias.
A vascular level produce arterial vasodilation and hypotension, both by direct action and by blocking vascular conduction of nerve impulses and sympathetic ganglionic transmission.
Although cardiodepresores effects appear only at higher concentrations have been observed in rare cases, small concentrations of anesthetic may cause circulatory collapse and death. This could be due to the activity stop sinus or ventricular fibrillation. This risk increases after intravascular administration of the anesthetic and in particular the ventricular fibrillation if used anesthetic with adrenaline.
Bupivacaine exerts a decrease in systolic dose-dependent, but not cause other significant cardiovascular changes.
Stabile and cols11 found that most patients receiving an intraosseous injection etidocaine have a transient increase in heart rate. Most patients receiving an intraosseous inye-ction lidocaine-epinephrine experience a transient increase in heart rate, a fact which does not occur when applied 3% mepivacaine by the same route.
Cols12 Replogle and studied the cardiovascular effects of intraosseous injection and found that most patients receiving an intraosseous injection of lidocaine, epinephrine experience a transient increase in heart rate, a fact which does not occur when applied 3% mepivacaine the same route.
The dose Felypressin safety for patients suffering from essential hypertension is approximately 0.18 UI. Although not noticed ischemic effect, caution is recommended in patients with severe hypertension, which may develop myocardial ischemia.
A systolic blood pressure greater than 200 mm Hg and diastolic BP greater than 115 mm Hg is an absolute contraindication for any dental procedure.
The information obtained from conventional monitoring, such as the measurement of blood pressure and heart rate and electrocardiography, is inadequate to explain the pathophysiological changes occurring in the dental patient has heart disease. However, echocardiography, a noninvasive method of cardiac examination, provides excellent information on the functional changes of the heart.
The use of EMLA topically to the gum can be chosen for short and minor surgical procedures, the maximum analgesia after application of 4 mg of anesthetic is reached at 14 minutes, 30 minutes later, the gingival sensation returns to normal. The duration of analgesia is similar to that obtained with topical lidocaine spray 10% (200 mg). High concentrations have been associated with toxic symptoms of CNS or cardiovascular system. In patients with liver disease or heart failure, EMLA should be used with caution.
4) reactions due to the use of vasoconstrictors
Toxic effects caused by vasoconstrictors often develop before the local anesthetic toxicity and thus may be a factor limiting the total dose of anesthetic supplied. The dose of epinephrine and levonordefrin should be limited to 3 micrograms per kg and not exceed 0.2 mg for patients in good health.
The local effects produced by a vasoconstrictor depend on the type of tissue into which it is injected. For example, epinephrine produces local vasodilatation when injected into skeletal muscle because it contains predominantly beta-adrenergic receptors. In this case epinephrine may activate the systemic absorption of the local anesthetic, thereby increasing the possibility of occurrence of undesirable systemic side effects. The vasoconstrictor activity is reduced, as we said above, in acidotic environments (sites of infection or inflammation). It exact mechanism of inactivation of the sympathomimetic amine with a low pH.
The only absolute contraindication to the use of vasoconstrictors occurs in patients with thyrotoxicosis. This may occur in patients with primary or secondary hyperthyroidism or induced excessive thyroid supplementation. Sympathomimetic amines administered exogenously or endogenously released in response to stress can precipitate a crisis whose results would be hypertension, delirium and vasomotor collapse eventually. The mortality rate associated with this acute crisis may be as much as 70%.
Adrenaline is the prototype of adrenergic vasoconstrictors. Adrenergic agents act by stimulating two separate pharmacological receptor systems: the alpha and beta adrenergic receptors. The stimulation of alpha-adrenergic receptors produces the desired vasoconstrictive effects. Stimulation of beta-adrenergic receptors is responsible for the cardiac stimulant and bronchodilator action showing many agents these drugs. Adrenergic drugs individually vary in their ability to stimulate these two receiver systems from pure alpha stimulating action of phenylephrine, through the action drugs mixed alpha and beta (adrenaline, noradrenaline and levonordefrin not) to the stimulating beta Pure isoproterenol.
If you are rapidly absorbed into the circulatory system, adrenergic agents produce several important cardiovascular actions. The effects of beta-adrenergic stimulation on the heart are most often greater contraction intensity, the higher driving speed and increased irritability. The submucosal administration of a local anesthetic cartridge containing epinephrine 1:100,000 cardiac output increases by approximately 10%. The systemic effect of alpha adrenergic stimulation is constriction of the smooth muscle of blood vessels, thereby increasing blood pressure.
Following intraoral submucosal injection of a local anesthetic solution containing epinephrine, alpha-adrenergic effects dominate locally and produces vasoconstriction. This effect is immediate and normally lasts about 30 to 90 minutes after injection. Gradually, the local tissue concentration of epinephrine decreases to a level that no longer produces alpha-adrenergic effect (vasoconstriction) and predominantly beta-adrenergic response (vasodilation). The local blood flow increases and the hemostatic effects of epinephrine disappear. The hyperaemic effect can be maintained for two hours.
While the action of noradrenaline predominant cause increased blood pressure, increased heart rate adrenalin, which is a side effect safer.
Furthermore inflamed tissues in tissue blood flow increases which induces a systemic absorption may occur vasoconstrictor and unwanted systemic side effects (cardiovascular stimulation).
Stress and pain can cause an increase in endogenous adrenaline levels to a degree dangerous to the patient, and it is best to apply a local anesthetic that substance, which prevents pain during the treatment session, this includes patients with cardiac known as the opinion of a special committee of the Association of New York Cardiology.
Norepinephrine is less effective as the adrenalin vasoconstrictor, although vasoconstriction is longer. The total dose of norepinephrine, should not exceed 0.34 mg. Currently, due to the number of adverse reactions, its use has been rejected.
Phenylephrine, like adrenaline and also has sympathomimetic actions, is very stable, low pressor action, lacks central effects of adrenaline and is quite safe, although its toxicity is similar to that of adrenaline. It is used in concentrations of 1:2500. Possibly replace the routine adrenaline as a vasoconstrictor.
Calatayud and cols13 ** make an excellent review of the use of vasoconstrictor in dentistry in Spain.
There have been many attempts to discover safer than vasoconstrictor sympathomimetic amines, adrenaline and noradrenaline, studying the vasopressin (hormones of the posterior lobe of the pituitary) among which include: vasopressin, and ornipressin Felypressin.
To treat a patient with ischemic heart disease in the consultation is recommended:
* Pain Control by good anesthetic technique, as it constitutes one of the main reasons of stress during dental treatment. It will use a local anesthetic with vasoconstrictor, since the risk of angina attack is increased by endogenous release of epinephrine secondary to stress that it is the small amount of vasoconstrictor used in local anesthetics.
* You must be sought for a deep and prolonged anesthesia with the lowest possible dose of vasoconstrictor. It is recommended not to exceed 0.04 mg of epinephrine in one visit (a maximum of 2 or 3 carpules with a concentration of 1:100,000 epinephrine), although no objective data to support an absolute limit dose. Generally, the use of higher concentrations of epinephrine at 1/100.000 is considered risky. Anesthesia was administered slowly and with regular intake.
* Long lasting anesthetics such as bupivacaine or etidocaine, are available with reduced amounts of vasoconstrictor (1/200.000) and may be useful in long procedures or those which cover large areas of the oral cavity. In contrast to other authors would not be given this type of anesthetic, as they believe that a higher power greater anesthetic toxicity.
* Some authors contraindicate the use of PDL and intraosseous anesthesia, and the use of gingival retraction cords impregnated with epinephrine, while others believe that would only be a relative contraindication.
* The use of small amounts of vasoconstrictor is controversial. Some authors contraindicate its use in these patients, as they believe that while a minimum surge in plasma epinephrine in healthy patients have a negligible effect in patients with unstable angina may lead to serious consequences, as it increases oxygen consumption Myocardial. Other authors, however, have a treatment protocol of high risk cardiac patients using as local anesthetic lidocaine 2% with epinephrine 1:100,000, performing an incremental therapy for anxiety and prevent the possible occurrence of angina , these patients were administered 10 mg of oxazepam or diazepam 5 mg orally the night before and one hour before the dental treatment and the same was done during sedation with nitrous oxide or intravenous sedation with midazolam was administered plus 5 mg of sublingual nitroglycerin inhalation or preventively.
In cases of Marfan syndrome, anesthetics containing epinephrine should be handled with care as they cause heart disturbances.
Perusse and cols14 **, understand that the absolute contraindications to vasoconstrictors in connection with heart disease are: unstable angina, recent myocardial infarction (6 months), recent surgery for coronary bypass, refractory arrhythmias, severe hypertension uncontrolled and untreated or failure Untreated heart failure or uncontrolled. As a relative contraindication related to the heart cite those patients taking non-selective beta-blockers.
The use of a local anesthetic containing vasoconstrictor should be avoided in patients taking beta-blocker medication due to possible adverse drug reaction. However, when a vasoconstrictor is indicated by its hemostatic action, the anesthetic solution should be administered slowly and in small quantities, monitoring the pulse and blood pressure. The patient should be warned that the duration of anesthesia may be prolonged.
When a patient is being medicated with nonselective beta blockers there are several options to avoid interactions:
ª l) If hemostasis is not essential, consider using local anesthetic without vasoconstrictor.
2nd) Consult with your doctor and ask if the medication can be stopped one day before the procedure and restored immediately after.
3rd) Managing a cartridge and retake voltage and pulse after 3-4 minutes, repeating this protocol for each cartridge.
Mask15 says that epinephrine should be used with caution in patients with pacemakers or defibrillators because of the possibility of occurrence of refractory arrhythmia, should be discussed with the patient's cardiologist.
The time of day that epinephrine causes more effect on cardiovascular variables coincides with the time when the highest elevations in blood pressure occurred at eight in the morning and the lowest elevations happened at two in the afternoon.
Meechan and cols16, publish that heart transplant patients experiencing significant tachycardia 10 minutes before the injection of a solution containing epinephrine. No significant change was found in heart rate after injection of a solution without epinephrine. Hence it can be concluded that the cardiovascular responses to local dental anesthesia in heart transplant patients is governed by the injected solution.
It is known that accelerates healing after extraction using an anesthetic without vasoconstrictor, nor the use of epinephrine is not only not prolonged, but seems to promote wound healing.
Cols17 Meechan and studied the arterial pressure changes in children when lidocaine with epinephrine is used for restorative procedures, so that influence hemodynamic response itself so that the diastolic pressure dropped 20 minutes after injection.
Niwa and cols18, measured hemodynamic responses to intraoral injection of 1.8 ml of lidocaine 2% with epinephrine 1:80,000-cardiogarfia impedancio by concluding that the solution of lidocaine and epinephrine is safe and causes few hemodynamic consequences patients with cardiovascular disease.
Cols19 Gallatin and show that 3% mepivacaine has minimal effect on heart rate and that can be used in patients in which epinephrine is contraindicated.
The combination prilocaine-Felypressin seems to have little effect on cardiac performance.
Career and cols20, study some cardiovascular parameters using 4% articaine 1:200,000 epinephrine, 3% mepivacaine without vasoconstrictor and prilocaine 3% with the 1:1,850,000 Felypressin concluding that patients were more stable with articaine plus epinephrine 1 : 200,000, but none of the three solutions studied cause significant hemodynamic changes relative to baseline values ​​when administered to healthy patients subject to surgery for removal of the third molar.
Besides contraindications expressed above, ** cols14 Perusse and insist that vasoconstrictors should be avoided absolutely in patients with hyperthyroidism uncontrolled, uncontrolled diabetes, sensitivity to sulfites, steroid-dependent asthma, and pheochromocytoma. Relative contraindications would be in: patients taking tricyclic antidepressants, patients taking phenothiazine compounds, patients taking MAOIs and cocaine addicts.
However, this issue is very controversial, and not everyone agrees and some think that local anesthetics formulated with epinephrine or norepinephrine as a vasoconstrictor be used without special reserve in patients taking MAO inhibitors or phenothiazines. Epinephrine is a vasoconstrictor adrenergic option in patients taking tricyclic antidepressant medication, but prudence suggests that the dosage should be reduced maxima.
It is well known that epinephrine can cause hypokalemia.
The first consideration in the treatment of systemic toxic reaction is permeable maintain airway by assisted or controlled ventilation with oxygen and treating the signs of CNS excitation with diazepam (5-10 mg IV) or a fast-acting barbiturate, thiopental sodium (50 mg IV to cessation of seizures). A depolarizing muscle relaxant succinylcholine-type (1 mg / kg), may be indicated if seizures do not yield to the above measures, requiring endotracheal intubation.
We must correct the hypotensive states: elevation of the lower limbs, fluid therapy, vasopressors (methoxamine, ephedrine, etc.). If there bradycardia, applying atropine (0.6 mg IV).
B) Allergic reactions
Although allergic reactions to local anesthetics are rare, apparently there is a large number of patients who claims to be allergic to these agents.
Allergic reactions occur mainly with ester anesthetics (procaine, dibucaine, tetracaine) and range from dermatitis to anaphylactic response reactions, when they do appear are often extremely serious. The typical clinical signs include erythema, pruritus, urticaria or exfoliative dermatitis, oral edema, facial or circunorbitario, a quarter of cases present with respiratory distress and possible death may have seizures, gastrointestinal symptoms, shock and coma. Suspect allergy exists if any of the symptoms noted-two is presented below for the administration of local anesthetics, but not normal in his absence.
To recall, the hypersensitivity to procaine involves hypersensitivity to other ester local anesthetics and other derivatives of PABA.
Many of the amide type local anesthetic solutions have contained methylparaben as preservative. The methylparaben is an alkyl ester of parahydroxybenzoic acid and is therefore structurally similar to PABA. This similarity suggests that the methyl paraben may also cause hypersensitivity. The FDA requires methylparaben removal of anesthetics containing a single dose, as dental cartridges. Lidocaine prepared for topical use can also contain preservatives such as methylparaben or chlorocresol that lead to sensitization.
It must be emphasized that the test can not provide intracutáneos reliability hypersensitivity to local anesthetics, because false reactions were observed, both positive and negative.
Sometimes, in the body, they trigger exaggerated immune reactions against a particular particle considered strange and potentially dangerous. This reaction, known hypersensitivity can occur in four ways according to Gell and Coombs (1963, 1975). The most dangerous is the anaphylactic reaction.
As specified Bourrain21, accidents related allergic to local anesthetics may occur are usually of type IV and I. The type IV hypersensitivity reactions are cell mediated delayed. The prototype is the Mantoux reaction.
All these inflammatory reactions or "hypersensitivity" have in common the fact of being initiated by an immune response against an antigen and occur in a sensitized individual (ie, are the result of antigenic restimulation in a person who has already developed a response cellular immune against said antigen).
In the case of local anesthetics usually expressed in skin eczema. Symptoms appear with a delay, ranging from a few hours to 48 hours, mostly near the site of application, but when the allergen is injected lesions may appear remote. Manifest as erythematous, vesicular and usually itchy. The cure is slow, lasting several days and is accelerated by the application of a dermocorticoid.
This type of allergy was mainly due to ester anesthetics. Allergy amide anesthetics is very rare for there some, in any case, most often manifested after application of creams and gels and rarely when injected.
The major problem is that occur in case of allergy, it is possible the existence of cross-sensitivities. Sometimes allergy is to lidocaine and simultaneously, a mepivacaine, prilocaine and bupivacaine. By contrast, the risk of cross-reactions of lidocaine with articaine seems less possible and esters absent.
Type I. Immediate hypersensitivity or atopic allergy. Inflammatory reactions are immediate onset, although sometimes semirretardada caused by the massive release of inflammatory mediators (histamine, tryptase, prostaglandins and leukotrienes) for basophil leucocytes and mast cells. These mediators are responsible for the clinical manifestations, which, according to the path and the degree of dissemination of intracorporeal allergen, may adopt a localized form-as rhinitis or asthma-or general-as anaphylactic reactions triggered by medications, insect stings or certain foods.
The identification of specific allergens regarding local anesthetics may represent a particular challenge in the dental clinic. Pseudoallergic allergies and reactions can be associated with all kinds of drugs used in dental practice.
Rood22, like many authors consulted, also believes that most of the time the adverse reactions are psychogenic reactions.
It's hard to know exactly how often are hypersensitivity reactions as normal would not all cases were published. Another problem is that the signs and symptoms observed during an adverse reaction are generally nonspecific and may lead to misdiagnosis and erroneously labeling a patient is allergic.
We agree with Wilson and cols23, in which a detailed history is essential to avoid risks to a patient with an agent to which there is proven intolerance. True allergy to local anesthetics are rare, but common diagnosticarías wrong and think that any serious adverse event is an allergic reaction. The most common causes are preservatives, antioxidants, metabolic, and not exactly the same anesthetic. Cols24 Campbell and emphasize the need for dentists and general dentists perform correct diagnosis in these situations.
Cols25 and Brown, show a case of a patient with different local anesthetic regimens always presented dermal erythema and pruritus, approximately 36 hours after treatment.
Another side effect is the idiosyncrasy. The idiosyncrasy to lidocaine is rare. The most common manifestations are tachycardia and hypertension with small amounts of drugs. Another form of adverse reaction is intolerance or decreased tolerance. Factors such as myocardial disease, acidosis, anemia or variation in the activity of a specific enzyme system may be responsible for diminished tolerance to local anesthetics. Intolerance to a local anesthetic is usually characterized by circulatory depression rather than the central nervous system depression, as shown in toxic reactions.
There is described a case of allergy to articaine. The patient tolerated the treatment well with lidocaine.
Malamed26, suggests that when the patient is unable to safely provide information on whether or not allergic to an anesthetic, the dentist or dentist can try talking to the previous dentist involved. If this fails, there are two options: 1) you can use an antihistamine (diphenhydramine) as a local anesthetic or 2) can refer the patient to an allergist to perform a challenge test. Often (in America), the most practical option is to use diphenhydramine. The pharmacist may prepare a 1% solution containing diphenhydramine 1:100,000 epinephrine without preservative. This solution induces anesthesia about 30 minutes long and can be used by infiltration or block injection. When used in a mandibular block, it takes 1-4 ml of solution. Some patients have noticed a burning sensation, swelling or erythema following a mandibular block with diphenhydramine 1%, but these effects were not severe and disappeared in 1-2 days. Should not be given more than 50 mg of diphenhydramine in a single session.
The dentist or dentist may prefer to refer the patient to an allergist for evaluation and perform the necessary tests, which are usually skin tests and provocation tests (PP). Most researchers agree that only perform skin tests to local anesthetics has little interest because they are frequent false positives, so the allergist also make PP. It is very useful also for testing send specific samples of their usual anesthetics without vasoconstrictor.
When given an anesthetic alternative to a patient with a history of allergy to local anesthetics, the dentist or dentist must follow these steps:
1) Inject slowly, aiming first to be sure not to administer the drug in a glass.
2) Inject a drop of the solution into the tissues.
3) Remove the needle and wait 5 minutes waiting to occur or not a reaction. If not an allergic reaction, can be deposited the amount of anesthetic necessary. We must be sure to vacuum before the second injection.
Anaphylactic shock is characterized by the sudden onset of clinical manifestations in the respiratory tract, cardiovascular system, skin and digestive tract, with bronchospasm, hypotension, urticaria, angioedema, vomiting and diarrhea, as complete medical. Symptoms occur immediately (5-20 minutes) after exposure to the allergen or trigger agent. The patient feels itching, profound malaise, anxiety, rhinitis and conjunctivitis, chest tightness, vomiting and diarrhea. Symptoms may progress and appear laryngeal edema, bronchospasm and hypotension.
The clinical diagnosis is absolutely, settling sometimes when symptoms and refer. No laboratory data that can be obtained quickly anaphylaxis is specific. When hypotension with no demonstrations, no diagnostic problems arise, especially if there is an immediate predecessor of administration of a drug or other form of exposure to an allergen or other suspect triggering agent. When hypotension occurs as isolated manifestation, problems of differential diagnosis with other circumstances can cause a sudden hypotension.
This is a potentially very serious, if not promptly treated properly, can cause death.
Kemp and Lockey27, based on the literature, recommend the following treatment of anaphylactic shock, we transcribed and summarized in a modified form:
a) Immediate intervention:
- Basic Life Support (ABC).
- Administer epinephrine 1:1000 aqueous dilution, 0.3-0.5 ml (0.01 mg / kg body weight in children, maximum dose, 0.3 mg), intramuscular, arm (deltoid) every five minutes, as often as necessary until control symptoms and blood pressure. However, and even cited the shot in the arm, intramuscular administration into the anterolateral thigh (vastus medialis) produces more rapid high plasma levels in the arm and will be the venue of choice.
- Administer epinephrine 1:1000 aqueous, 0.1-0.3 ml in 10 ml of saline (dilution between 1:100,000 and 1:33.000) intravenously. Could be repeated if there is no response. Continuous hemodynamic monitoring is essential.
b) General measures:
- Supine position with legs elevated
- Establish and maintain the airway (endotracheal tube or tracheostomy cricotiroidectomia).
- Managing 6-8 oxygen ratio L / min.
- Take one and administer intravenous saline for fluid replacement. If there is severe hypotension, administer plasma expanders if necesanos.
c) Specific actions:
- Diphenhydramine, 50 mg or more, orally or intravenously, with a daily maximum of 300 mg for children and 400 mg for adults.
- Other measures: ranitidine or cimetidine, albuterol, aminophylline, glucagon, glucocorticoids.
In all cases, therefore, management should start with the standard ABC standard and supplemental oxygen. The duration of action of epinephrine is relatively short (10-30 minutes) and that is biotransformed soon and doses may need to be repeated if symptoms recur.
In the dental literature repeatedly mentions the possible use of the floor of the mouth or tongue to administer epinephrine.
C) psychogenic reactions
Psychogenic reactions are probably the most common adverse reactions associated with the administration of local anesthetics. Because of the insidious nature of these reactions, often mistakenly attributed to toxicity or hypersensitivity reactions.
The source of such reactions is in treating anxiety or puncture anesthetic.
As psychogenic reactions usually occur two tables:
1) The vasodepressor syncope vasovagal syncope or psychogenic reaction is the most common and is characterized by prodromal signs such as sweating, pallor, nausea, mental confusion, dizziness, tachycardia, hypotension and sometimes tonic-clonic contractions.
This table responds well to measures postural (supine with elevated legs). You have to monitor vital signs and also to maintain the air traffic will be given 100% oxygen, which is essential to correct the acidosis would exacerbate the toxicity of local anesthetics: therefore also be injected intravenous bicarbonate, continuing in this way the liquid infusion (Ringer lactate, plasma expanders, etc.) according to the state of the blood pressure. The treatment of hypotension is usually done with direct-acting sympathomimetic amines such methoxamine, 10-15 mg IM or IV, which is stimulating specific alpha, without action on the heart muscle, ephedrine or phenylephrine. Also useful may be a corticosteroid administration parenterally.
It also advises on vasodepressor reactions, atropine, 0.3 to 05 mg (0.02 mg / kg) subcutaneously every 10 minutes (maximum dose, 2 mg to 1 mg for adults and children) 27.
2) hyperventilation syndrome precipitate is excessive anxiety and characterized by a shallow, rapid breathing. This leads to a reduction in carbon dioxide tension of blood and can cause a decrease in cerebral oxygenation and unconsciousness. Treatment should be aimed at restoring normal levels of blood carbon dioxide. This can be achieved by having patients breathe again its own carbon dioxide in a paper bag.
D) Methemoglobinemia
Methemoglobin is normally present in the blood at levels less than 1%. The levels can be toxic when hemoglobin is oxidized to methemoglobin after being administered anesthetics benzocaine and prilocaine.
The maximum permissible dose varies according to the authors consulted. The maximum dose for a child of 22 kg should not exceed 150-200 mg and the maximum dose for an adult is between 450 and 600 mg. This corresponds approximately to 7 cartridges with 4% prilocaine for a 70 Kg weight.
A dose of 500 mg of 5% prilocaine become hemoglobin in metahemogloblina. In healthy individuals this is insignificant, however, a reduction of 5% of the oxygen-carrying capacity may be very harmful for patients with cardiopulmonary reserve limitation, sickle cell anemia or deficiency-6-phosphate dehydrogenase.
Cited a case of cyanosis under general anesthesia due to methemoglobinemia, because of the topical application of benzocaine in the pharynx and trachea. It solves the problem by means of oxygen and administration of 1.5 mg / kg of methylene blue slowly in 5 minutes, although ascorbic acid can also be used to reverse the situation. It is recommended that methylene blue is in the dentist's emergency kit, especially if used regularly prilocaine.
E) Other systemic complications
It has been reported the appearance of severe dermatomyositis in a child of 11 years just days after injection of a local anesthetic, which already had happened to her grandmother by the same mechanism when he was 34.
5) Other actions
For cols28 Nakamura, administration of local anesthesia and tooth extraction resulting activated adrenals increased serum glucose level in normotensive patients.
Action on the fetus. Most local anesthetics cross the placenta by passive diffusion concentrating especially in the liver, brain and fetal myocardium so seizures and arrhythmias may occur following its use in obstetrics. Felypressin not be used in pregnant patients, because it has a moderate oxytocic effect can prevent placental circulation by blocking the uterine tone. This contraindication is doubly valid since Felypressin usually available with prilocaine, which passes the placental barrier and, as we know, a high dose can cause fetal methemoglobinemia.
The monoetilglicinexilidina, a major metabolite of lidocaine, has power equal to 1/80 of that of the parent compound. Sedation is often observed at the termination of dental procedures that require multiple injections of lidocaine, can be depressed due to the effect that this has on the active metabolite CNS.
Chronic poisoning occurs mainly with the addition to cocaine (cocaine addiction) leading to impaired emotional, mental and physical, the cocaine addict becomes a social misfit. Cocaine, on the other hand, is controlled prescription.
On occasion cited antithrombotic properties of the lidocaine, by inhibition of thrombus formation, has also been reported that the leukocyte adhesion is reduced in the presence of lidocaine, which is thought to have anti-inflammatory effects.
In pregnancy and lactation, as we mentioned above, it is preferable not to administer local anesthetics, especially in the first three months. In any case be avoided if prilocaine and is associated with Felypressin.