<unk> ized side effects Edema of tongue, pharynx and<unk> rynx may develop as a side effect of<unk>  anaesthesia. This could be caused by a variety of reasons including trauma during injection, infection, an allergic reaction, haematoma or injection of irritating solutions such as cold-sterilisation solutions. Usually there is tissue swelling at the point of injection. This is due to puncturing of the vein which allows the blood to flow into loose tissues in the surrounding area. Blanching of the tissues in the area where the<unk>  is deposited is also common. This gives the area a white appearance as the blood flow is prevented due to vasoconstriction of arteries in the area. The vasoconstriction stimulus gradually wears off and subsequently the tissue returns to normal in less than 2 hours. The side effects of inferior alveolar nerve block include feeling tense, clenching of the fists and moaning. The duration of soft tissue anaesthesia is longer than pulpal anaesthesia and is often associated with difficulty eating, drinking and speaking. Risks The risk of temporary or permanent nerve damage varies between different<unk> ions and types of nerve blocks. There is risk of accidental damage to<unk>  blood vessels during injection of the<unk>  solution. This is referred to as Haematoma and could result in pain, trismus, swelling and/or discolouration of the region. The density of tissues surrounding the injured vessels is an important factor for Haematoma. There is greatest chance of this occurring in a posterior superior alveolar nerve block or in a pterygomandibular block. Giving<unk>  anaesthesia to patients with liver disease can have significant consequences. Thorough evaluation of the disease should be carried out to assess potential risk to the patient as in significant liver dysfunction, the half-life of amide<unk>  agents may be drastically increased thus increasing the risk of overdose.<unk> s and vasoconstrictors may be administered to pregnant patients however it is very important to be extra cautious when giving a pregnant patient any type of drug. Lidocaine can be safely used but bupivacaine and mepivacaine should be avoided. Consultation with the obstetrician is vital before administrating any type of<unk>  to a pregnant patient. Recovery Permanent nerve damage after a peripheral nerve block is rare. Symptoms are likely to resolve within a few weeks. The vast majority of those affected (92%–97%) recover within four to six weeks; 99% of these people have recovered within a year. An estimated one in 5,000 to 30,000 nerve blocks results in some degree of permanent persistent nerve damage. Symptoms may continue to improve for up to 18 months following injury. Potential side effects General systemic adverse effects are due to the pharmacological effects of the<unk>  agents used. The conduction of electric impulses follows a similar mechanism in peripheral nerves, the central nervous system, and the heart. The effects of<unk> s are, therefore, not specific for the signal conduction in peripheral nerves. Side effects on the central nervous system and the heart may be severe and potentially fatal. However, toxicity usually occurs only at plasma levels which are rarely reached if proper<unk>  techniques are adhered to. High plasma levels might arise, for example, when doses intended for epidural or intrasupport tissue administration are accidentally delivered as intravascular injection. Emotional reactions When patients are emotionally affected in the form of nervousness or fear, it can lead to vasovagal collapse. This is the anticipation of pain during administration that activates the parasympathetic nervous system while inhibiting the orthosympathetic nervous system. What results is a dilation of arteries in muscles which can lead to a reduction in circulating blood volume inducing a temporary shortness of blood flow to the brain. Notable symptoms include restlessness, visibly looking pale, perspiration and possible loss of consciousness. In severe cases, clonic cramps resembling an epileptic insult may occur. On the other hand, fear of administration can also result in accelerated, shallow breathing, or hyperventilation. The patient may feel a tingling sensation in hands and feet or a sense of light-headedness and increased chest pressure. Hence, it is crucial for the medical professional administrating the<unk>  anaesthesia, especially in the form of an injection, to ensure that the patient is in a comfortable setting and has any potential fears alleviated in order to avoid these possible complications. Central nervous system Depending on<unk>  tissue concentrations of<unk> s, excitatory or depressant effects on the central nervous system may occur. Initial symptoms of systemic toxicity include ringing in the ears (tinnitus), a metallic taste in the mouth, tingling or numbness of the mouth, dizziness and/or disorientation. At higher concentrations, a relatively selective depression of inhibitory neurons results in cerebral excitation, which may lead to more advanced symptoms include motor twitching in the periphery followed by grand mal seizures. It is reported that seizures are more likely to occur when bupivacaine is used, particularly in combination with chloroprocaine. A profound depression of brain functions may occur at even higher concentrations which may lead to coma, respiratory arrest, and death. Such tissue concentrations may be due to very high plasma levels after intravenous injection of a<unk> rge dose. Another possibility is direct exposure of the central nervous system through the cerebrospinal fluid, i.e., overdose in spinal anesthesia or accidental injection into the subarachnoid space in epidural anesthesia. Cardiovascular system Cardiac toxicity can result from improper injection of agent into a vessel. Even with proper administration, it is inevitable for some diffusion of agent into the body from the site of application due to unforeseeable anatomical idiosyncrasies of the patient. This may affect the nervous system or cause the agent to enter into general circulation. However, infections are very seldom transmitted. Cardiac toxicity associated with overdose of intravascular injection of<unk>  is characterized by hypotension, atrioventricular conduction delay, idioventricular rhythms, and eventual cardiovascular collapse. Although all<unk> s potentially shorten the myocardial refractory period, bupivacaine blocks the cardiac sodium channels, thereby making it most likely to precipitate malignant arrhythmias. Even levobupivacaine and ropivacaine (single-enantiomer derivatives), developed to ameliorate cardiovascular side effects, still harbor the potential to disrupt cardiac function. Toxicity from<unk>  combinations is additive. Endocrine Endocrine and metabolic systems only have slightly adverse effects with most cases being without clinical repercussions. Immunologic allergy Adverse reactions to<unk> s (especially the esters) are not uncommon, but legitimate allergies are very rare. Allergic reactions to the esters is usually due to a sensitivity to their metabolite, para-aminobenzoic acid, and does not result in cross-allergy to amides. Therefore, amides can be used as alternatives in those patients. Nonallergic reactions may resemble allergy in their manifestations. In some cases, skin tests and provocative challenge may be necessary to establish a diagnosis of allergy. Also cases of allergy to paraben derivatives occur, which are often added as preservatives to<unk>  solutions. Methemoglobinemia Methemoglobinemia is a process where iron in hemoglobin is altered, reducing its oxygen-carrying capability, which produces cyanosis and symptoms of hypoxia. Exposure to aniline group chemicals such as benzocaine, lidocaine, and prilocaine can produce this effect, especially benzocaine. The systemic toxicity of prilocaine is comparatively low, but its metabolite, o-toluidine, is known to cause methemoglobinemia. Second-generation effects Application of<unk> s during oocyte removal during in vitro fertilisation has been up to debate. Pharmacological concentrations of<unk>  agents have been found in follicular fluid. Clinical trials have not concluded any effects on pregnant women. However, there is some concern with the behavioral effects of lidocaine on offspring in rats. During pregnancy, it is not common for<unk> s to have any adverse effect on the fetus. Despite this, risks of toxicity may be higher in pregnancy due to an increase in unbound fraction of<unk>  and physiological changes increase the transfer of<unk>  into the central nervous system. Hence, it is recommended that pregnant women use a lower dose of<unk>  to reduce any potential complications. Treatment of overdose: "Lipid rescue" This method of toxicity treatment was invented by Dr. Guy Weinberg in 1998, and was not widely used until after the first published successful rescue in 2006. Evidence indicates Intralipid, a commonly available intravenous lipid emulsion, can be effective in treating severe cardiotoxicity secondary to<unk>  overdose, including human case reports of successful use in this way (lipid rescue). However, the evidence at this point is still limited. Though most reports to date have used Intralipid, a commonly available intravenous lipid emulsion, other emulsions, such as Liposyn and Medialipid, have also been shown effective. Ample supporting animal evidence and human case reports show successful use in this way. In the UK, efforts have been made to publicise this use more widely and lipid rescue has now been officially promoted as a treatment by the Association of Anaesthetists of Great Britain and Ireland. One published case has been reported of successful treatment of refractory cardiac arrest in bupropion and<unk> motrigine overdose using lipid emulsion. The design of a 'homemade' lipid rescue kit has been described. Although lipid rescue mechanism of action is
Local anesthetic
Muscle relaxant
Equianalgesic
Inhalational anesthetic
General anaesthetic
Querulant
Analgesic
Local anesthesia