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 large 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 local anesthetic is characterized by hypotension, atrioventricular conduction delay, idioventricular rhythms, and eventual cardiovascular collapse. Although all local anesthetics potentially shorten the myocardial refractory period, bupivacaine blocks the cardiac sodium channels, thereby making it most likely to precipitate malignant arrhythmias.
Presence of systemic health problemsILI utilization is expected to increase because dental patients prefer fewer soft tissue anesthesia and dentists aim to reduce administration of traditional inferior alveolar nerve block (INAB) for routine restorative procedures.Injection methodology: The periodontal ligament space provides an accessible route to the cancellous alveolar bone, and the anesthetic reaches the pulpal nerve via natural perforation of intraoral bone tissue.Advantages of ILI over INAB: rapid onset (within 30 seconds), small dosage required (0.2-1.0 mL), limited area of numbness, lower intrinsic risks such as neuropathy, hematoma, trismus/jaw sprain and self-inflicted periodontal tissue injury, as well as decreased cardiovascular disturbances. Its usage as a secondary or supplementary anesthesia on the mandible has reported a high success rate of above 90%.Disadvantages: Risk of temporary periodontal tissue damage, likelihood of bacteriemia and endocarditis for at-risk populations, appropriate pressure and correct needle placement are imperative for anesthetic success, short duration of pulpal anesthesia limits the use of ILIs for several restorative procedures that require longer duration, postoperative discomfort, and injury on unerupted teeth such as enamel hypoplasia and defects. Technique description:

All plaque and calculus to be eradicated, optimally before the operative visit to assist gingival tissue healing. Before injection, disinfect gingival sulcus with 0.2% chlorhexidine solution. Administration of soft tissue anesthesia is recommended prior to ILI administration. This helps to enhance patient comfort. Needle gauges of sizes 27-gauge short or 30-gauge ultra-short needle are usually utilized.