Hypochlorite accident during wndodontic therapy with nerve damage - A case report.

Endodontic therapy is a routinely practised clinical procedure with few reported complications but, as a bleaching agent, inadvertent spillage of sodium hypochlorite beyond the root canal system may result in extensive soft tissue or nerve damage, and even airway compromise. Although very rare, complications arising from hypochlorite extrusion beyond the root apex are described. NaOCl causes oxidation of protein and lipid membrane and causes necrosis, hemolysis and dermal ulcerations (2-4). Neurological complication are very rare. Paraesthesia and anaesthesia may affect the mental, inferior dental and infra-orbital branches of the trigeminal nerve and normal sensation may take many months to  completely resolve (6, 7). Nerve damage (the buccal branch) was described in 2005 by Witton et al. (8) and patients exhibited a loss of the naso-labial groove and a down turning of the angle of the mouth and the motor function was regained after several months. We present a case in which the extrusion of NaOCl solution during endodontic therapy led to important destructive effects on soft tissues and nerves. The arisen medico legal issues are discussed.

Before you reach for the bleach...

Sodium hypochlorite (bleach) is advocated as an irrigant for use in endodontic therapy for its bacteriocidal and tissue dissolving properties. Extrusion of hypochlorite into the surrounding soft and hard tissues, however, can lead to severe complications, as illustrated in our four case reports. This article considers the risk benefit ratio of the different materials available and advises dental practitioners to ensure patients are aware of the potential risks of the materials used when seeking informed consent. It also aims to provide some guidance on prevention, identification and management of incidents.

Neurological deficit of the facial nerve after root canal treatment.

Here we report the unusual case of a patient who suffered neurological deficit of the facial nerve as a complication of a root canal treatment. During the canal treatment, 3% hydrogen peroxide and 90% ethanol rinses were performed. The present case demonstrated rinse toxicity to vital tissue as evidenced by severe clinical damage. Chlorhexidine can be used instead of potentially toxic rinses with good antimicrobiological results. Furthermore, special attention should be paid to determination of the root canal length and the integrity of the canal system before rinsing. Also irrigation should be applied at a low pressure.

Articaine and paresthesia: epidemiological studies.

Permanent paresthesia following a local anesthetic injection is a possible adverse event. Epidemiological studies have suggested that the 4% solutions used in dentistry, namely prilocaine and articaine, are more highly associated with this occurrence. This article reviews the epidemiological evidence regarding articaine and paresthesia.

Silver nitrate injury in the rat sciatic nerve: a model of facial nerve injury.

BACKGROUND: An unpublished communication of a permanent facial paralysis secondary to silver nitrate application in a postoperative mastoid cavity with a dehiscent facial nerve raises concern regarding its neurotoxicity. This study was performed to examine functional neural injury and the morphology of nerve injury due to silver nitrate contact with a peripheral motor nerve. METHODS: Sprague-Dawley male rats were assigned to a sham surgery group or to a group where silver nitrate was applied directly to a surgically exposed sciatic nerve for 1, 5, or 10 seconds. Individual walking track data were collected on postoperative days (POD) 1, 4, 7, and 14, and the Sciatic Functional Index (SFI) was calculated to assess neural function. On POD 14, the cauterized nerve was harvested, and the histologic axon loss of each specimen was graded. RESULTS: In all experimental groups, the most severe functional loss was noted on POD 1. At POD 14 the greatest neural recovery was observed in the 1-second group, whereas the 5- and 10-second cautery groups demonstrated a significantly worse deficit. A moderate or greater degree of axon loss was observed in 50% of animals injured for 1 second and nearly all animals injured for 5 or 10 seconds. CONCLUSION: Functional and neuropathologic data demonstrate that silver nitrate causes significant injury to the rat sciatic nerve. A 5-second cautery causes greater functional impairment and more severe axonal loss than a 1-second injury.