Australian Dental Journal
The official journal of the Australian Dental Association
Australian Dental Journal 2013; 58: 522–525 doi: 10.1111/adj.12120
Superficial skin necrosis and neurological complications following administration of local anaesthetic: a case report N Pattni* *General dental practice, Birmingham, United Kingdom.
ABSTRACT Local anaesthesia is used routinely throughout dentistry. Complications are, however, relatively uncommon. A unique case of superficial skin necrosis and neurological symptoms following administration of local anaesthesia for dental treatment is reported and the possible mechanisms behind this unusual presentation are discussed. Awareness of this possible complication and its mechanism helps clinicians diagnose and manage patients with similar problems appropriately. Keywords: Complications, local anaesthetic. (Accepted for publication 3 March 2013.)
INTRODUCTION Administration of local anaesthesia is one of the commonest procedures undertaken in dentistry. It is an effective and safe means of pain control that allows routine procedures to be undertaken. Although uncommon, adverse local and systemic reactions to local anaesthetic occur. They are usually multifactorial in origin and are related to toxic drug overdose, rapid absorption, intravascular injection, cardiovascular, central nervous system, psychogenic or idiosyncratic reactions; allergy is rare.1 Complications include postoperative trismus, palpitations and diaphoresis; however, transient amaurosis, sudden unilateral deafness and cranial nerve palsies have also been reported.1–4 A previously unreported case of cutaneous and neurological complications following suspected intra-arterial injection of local anaesthetic solution is presented and the possible mechanisms of this unusual presentation are discussed. CASE REPORT A fit and well 22-year-old patient attended the dental surgery requiring restoration of a carious left mandibular molar; the patient had never received dental treatment nor local anaesthetic previously. A conventional left inferior dental block (lateral to the pterygomandibular raphe, medial to the temporalis tendon, approximately 1 cm above the occlusal surface of the mandibular molars and angulated so that the syringe 522
is overlying the contralateral premolars) using 2.2 ml of 2% lignocaine with 1:80 000 adrenaline (Septodont) was administered. The 27 gauge 35 mm needle was advanced until bone contact was made, withdrawn a few millimetres and the cartridge injected over approximately 10 seconds. Aspiration was not performed as the syringe was a non-aspirating syringe. Quintessentially, the administration of local anaesthetic was undertaken unremarkably with no difference to any other inferior alveolar nerve block. Restoration of the tooth was undertaken uneventfully and the patient left the clinic. The patient returned three hours later complaining of a burning sensation in her mouth and an area of her chin appeared burnt and blistered. Upon examination an area of superficial skin erosion was noted in the cutaneous distribution of the left inferior alveolar artery. No utricaria nor airway obstruction was reported. She denied a self-inflicted injury. The patient was reassured and scheduled for a follow-up appointment the next day. Prior to returning to the clinic for this appointment the patient presented to her GP the following morning complaining of neurological symptoms overnight. Approximately 10 hours following administration of the local anaesthetic she developed systemic tremors and numbness, especially of her peripheries. She was unable to perform simple motor functions, stating she dropped dishes whilst washingup and was unable to get into bed without assistance. The GP liaised with the local neurology department who recommended close follow-up and allergy testing; no in-patient or out-patient arrangements were made. © 2013 Australian Dental Association
Local anaesthetic complications Although it was not possible to determine whether the patient’s symptoms were neurological or physiological, both clinicians felt the presentation was consistent with systemic complications from the local anaesthetic. Upon returning to the clinic approximately 24 hours after administration of local anaesthetic the patient reported her systemic and oral symptoms had begun to subside with an area of crusting where the cutaneous lesion was observed (Fig. 1); 72 hours later the lesion showed evidence of healing (Fig. 2) and the systemic symptoms had resolved entirely. Following one month the lesion had healed entirely with no scarring or altered pigmentation in the area (Fig. 3). The patient underwent immunological testing using lignocaine and prilocaine skin prick challenges; both were negative. The patient underwent restoration of other carious teeth using an alternative anaesthetic agent uneventfully.
Fig. 1 Clinical photograph illustrating crusting over the cutaneous distribution of the left inferior alveolar artery 24 hours following administration of local anaesthetic.
Fig. 2 Clinical photograph illustrating healing of the lesion over the cutaneous distribution of the left inferior alveolar artery 72 hours following administration of local anaesthetic. © 2013 Australian Dental Association
Fig. 3 Clinical photograph illustrating resolution of the lesion with no cutaneous pigmentation or scarring approximately 1 month following administration of local anaesthetic.
DISCUSSION Although uncommon, the majority of complications following use of local anaesthesia in dentistry are well known. A recent study by Sambrook et al.1 analysed serious adverse reactions to dental local anaesthetics which have been reported to the Office of Product Review of the Therapeutics Goods Administration in Australia over a 35-year period; a similar case to ours was not reported. Of the 221 reported cases, neurological complications represented 16% of all adverse systemic reactions and was the second most common reaction after syncope. Neurological complications occur after a toxic level of local anaesthetic solution crosses the blood brain barrier. Early signs include slurred speech, muscle twitching, visual disturbances and disorientation, while later with increased dose convulsions and seizures can occur.5 This may represent the patient’s psychological state or a direct effect of the local anaesthetic or both. This study also showed 70% of all reported reactions were related to prilocaine; only 2% were attributed to articaine. Reactions to lignocaine accounted for 28% of adverse reactions; however only 10 cases of neurological complications after lignocaine administration were reported. Given how commonly used lignocaine is, this demonstrates not only how safe it is but also how rare adverse reactions to it are. It has been shown that a higher concentration of local anaesthetic solution is related to a higher rate of complications; however, in our case the dosage and volume of local anaesthetic used was minimal.6 A review of the literature revealed only two similar cases occurring following administration of an inferior dental block. Torrente-Castells et al.7 reported a case involving a 10-year-old girl who received an inferior alveolar nerve block using one cartridge of 4% articaine with 1:200 000 adrenaline. After the procedure she developed pallor of the ipsilateral lower lip and chin that subsequently evolved into surface ulceration which healed 15 days later. 523
N Pattni Kruger and Nehs8 reported the case of a 30-yearold woman who received an inferior alveolar nerve block and infiltration of the mental nerve for dental treatment. A total of three cartridges of 4% articaine with 1:100 000 adrenaline were administered. Crusting was observed on the ipsilateral lower lip, with transient sensory alteration of the area innervated by the ipsilateral mental nerve branch. They also observed a haematoma in the vestibular mucosa at the left canine/premolar region. In this case the authors acknowledge it is not possible to ascertain whether the inferior dental block or the mental nerve block was the cause of the patient’s signs and symptoms. Both of these cases present a similar cutaneous presentation to that observed in our case; however, the significant difference is that neither case presents the patient also experiencing neurological symptoms. Also, the local anaesthetic agent used in these cases was articaine whereas in our case lignocaine was used. The mechanism behind the complications seen in our case are likely to be related to intra-arterial injection involving the maxillary artery and viral activation within the inferior alveolar nerve. Anatomy The maxillary artery is the terminal branch of the external carotid artery that typically originates posterior to the neck of the mandible. It courses forward between the ramus of the mandible and sphenomandibular ligament, passing either deep or superficial to the lateral pterygoid running towards the pterygopalatine fossa to supply the deep structures of the face. Cadaveric dissection studies have shown when the maxillary artery courses superficial to the lateral pterygoid it loops inferiorly 88% of the time,9 passing as close as 4 mm to the mandibular foramen.10 The inferior alveolar artery braches from the first portion of the maxillary artery. It courses along with the corresponding nerve to enter the mandibular foramen to supplying the mandible, teeth and the ipsilateral lower lip and chin. Therefore, within the pterygomandibular space the maxillary or inferior alveolar may be encountered or penetrated whilst administering an inferior dental block. Vascular injection Contact between a needle and artery may result in vasospasm, causing a transient ischaemia of the inferior alveolar artery which would manifest as discomfort and blanching. Furthermore, a perivascular injection may lead to sympathetic nerve stimulation and subsequent vessel vasospasm, which again may 524
lead to peripheral tissue necrosis. However, immediate blanching was not observed in our case which would have occurred if contact was made with the artery, or if sympathetic nerves were stimulated. Alternatively, inadvertent intra-arterial administration of local anaesthetic containing a vasocontrictor may result in stimulation of a-adrenergic receptors with contraction of smooth muscle within the arterial wall.9 This may lead to transient ischaemia of the structures distal to the injection site supplied by the vessel, which if prolonged may result in tissue necrosis. This may account for the superficial necrosis of the skin of the chin seen in our patient. Therefore, it is important to aspirate when administering an inferior alveolar block to ensure local anaesthetic solution is not injected intra-arterially. An intra-arterial injection also explains the systemic symptoms the patient reported. An intra-arterial injection may circulate in a retrograde fashion reaching the carotid bifurcation where it may be distributed to the central nervous system via the internal carotid artery; this is the proposed mechanism for visual and auditory disturbances following inferior dental blocks.4 This phenomenon of reverse carotid flow was proposed and demonstrated in animal studies by Aldrete et al.11 Malamed12 considered retrograde flow is only possible with injections administered faster than one cartridge in 30 seconds. This would help account for the systemic neurological symptoms observed in our patient. The elimination half-life of lignocaine is approximately 1.5–2.0 hours; however, studies have shown an increased toxicity of lignocaine when administered with adrenaline which may account for the prolonged neurological toxicity observed in our case. The reason for this is not fully understood but it is proposed that the adrenaline alters the distribution of lignocaine by its effects on the cardiovascular system and direct interaction of the drug.13 Viral activation Various viruses, including herpes simplex and herpes zoster, are ubiquitous in the population.14 Following infection and local replication viruses enter nerve endings and are transported by retrograde axonal transport to the neuronal cell bodies. Here they remain in a latent state and can be reactivated by a range of factors including stress, ultraviolet light and immunosupression.15 Trauma can also result in viral reactivation and has been implicated in herpes zoster oticus, facial palsy and mental nerve neuropathy following dental treatment.14 Therefore, in our case the administration of local anaesthesia may have induced trauma to the inferior alveolar nerve, resulting in intracellular viral activation and subsequent cutaneous manifestations. © 2013 Australian Dental Association
Local anaesthetic complications CONCLUSIONS This case highlights the need for a careful technique when administering local anaesthesia in the oral and maxillofacial region. Nevertheless, complications may still occur and clinicians should be aware of these in order to diagnose and manage patients appropriately. REFERENCES 1. Sambrook PJ, Smith W, Elijah J, Goss AN. Severe adverse reactions to dental local anaesthetics: systemic reactions. Aust Dent J 2011;56:148–153.
8. Lacouture C, Blanton P, Hairston E. The anatomy of the maxillary artery in the infratemporal fossa in relationship to intraoral injections. Anat Rec 1983;205:104A. 9. Berini-Aytes L, Gay-Escoda C. Anestesia Odontol ogica. 3rd edn. Madrid, Spain: Ediciones Avances, 2005. 10. Ruocco I, Cuello AC, Parent A, Ribeiro-da-Silva A. Skin blood vessels are simultaneously innervated by sensory, sympathetic, and parasympathetic fibers. J Comp Neurol 2002;448: 323–336. 11. Aldrete JA, Narang R, Sada T, Liem ST, Miller GP. Reverse carotid blood flow–a possible explanation for some reactions to local anesthetics. J Am Dent Assoc 1977;94:1142–1145. 12. Malamed SF. Handbook of Local Anaesthesia. 3rd edn. St Louis: Mosby-Year Book, 1990:160–218, 245–257.
2. Meechan JG. Local anaesthesia: risks and controversies. Dent Update 2009;36:278–280, 282–283.
13. Yagiela JA. Intravascular lidocaine toxicity: influence of epinephrine and route of administration. Anesth Progr 1985; 32:57–61.
3. Kaufman E, Goharian S, Katz Y. Adverse reactions triggered by dental local anesthetics: a clinical survey. Anesth Prog 2000; 47:134–138.
14. Maini S, Preece M. Herpes zoster oticus following mandibular block. J Laryngol Otol 2000;114:212–213.
4. Crean SJ, Powis A. Neurological complications of local anaesthetics in dentistry. Dent Update 1999;26:344–349.
15. Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features. J Oral Pathol Med 2008;37:107–121.
5. Subramaniam S, Tennant M. A concise review of the basic biology and pharmacology of local analgesia. Aust Dent J 2005;50 (4 Suppl 2):S23–30. 6. Kingon A, Sambrook P, Goss A. Higher concentration local anaesthetics causing prolonged anaesthesia. Do they? A literature review and case reports. Aust Dent J 2011;56:348–351. 7. Torrente-Castells E, Gargallo-Albiol J, Rodrıguez-Baeza A, Berini-Aytes L, Gay-Escoda C. Necrosis of the skin of the chin: a possible complication of inferior alveolar nerve block injection. J Am Dent Assoc 2008;139:1625–1630.
© 2013 Australian Dental Association
Address for correspondence: Dr Neeraj Pattni 1 Fieldfare Green Luton LU4 0YA United Kingdom Email: [email protected]
525
The official journal of the Australian Dental Association
Australian Dental Journal 2013; 58: 522–525 doi: 10.1111/adj.12120
Superficial skin necrosis and neurological complications following administration of local anaesthetic: a case report N Pattni* *General dental practice, Birmingham, United Kingdom.
ABSTRACT Local anaesthesia is used routinely throughout dentistry. Complications are, however, relatively uncommon. A unique case of superficial skin necrosis and neurological symptoms following administration of local anaesthesia for dental treatment is reported and the possible mechanisms behind this unusual presentation are discussed. Awareness of this possible complication and its mechanism helps clinicians diagnose and manage patients with similar problems appropriately. Keywords: Complications, local anaesthetic. (Accepted for publication 3 March 2013.)
INTRODUCTION Administration of local anaesthesia is one of the commonest procedures undertaken in dentistry. It is an effective and safe means of pain control that allows routine procedures to be undertaken. Although uncommon, adverse local and systemic reactions to local anaesthetic occur. They are usually multifactorial in origin and are related to toxic drug overdose, rapid absorption, intravascular injection, cardiovascular, central nervous system, psychogenic or idiosyncratic reactions; allergy is rare.1 Complications include postoperative trismus, palpitations and diaphoresis; however, transient amaurosis, sudden unilateral deafness and cranial nerve palsies have also been reported.1–4 A previously unreported case of cutaneous and neurological complications following suspected intra-arterial injection of local anaesthetic solution is presented and the possible mechanisms of this unusual presentation are discussed. CASE REPORT A fit and well 22-year-old patient attended the dental surgery requiring restoration of a carious left mandibular molar; the patient had never received dental treatment nor local anaesthetic previously. A conventional left inferior dental block (lateral to the pterygomandibular raphe, medial to the temporalis tendon, approximately 1 cm above the occlusal surface of the mandibular molars and angulated so that the syringe 522
is overlying the contralateral premolars) using 2.2 ml of 2% lignocaine with 1:80 000 adrenaline (Septodont) was administered. The 27 gauge 35 mm needle was advanced until bone contact was made, withdrawn a few millimetres and the cartridge injected over approximately 10 seconds. Aspiration was not performed as the syringe was a non-aspirating syringe. Quintessentially, the administration of local anaesthetic was undertaken unremarkably with no difference to any other inferior alveolar nerve block. Restoration of the tooth was undertaken uneventfully and the patient left the clinic. The patient returned three hours later complaining of a burning sensation in her mouth and an area of her chin appeared burnt and blistered. Upon examination an area of superficial skin erosion was noted in the cutaneous distribution of the left inferior alveolar artery. No utricaria nor airway obstruction was reported. She denied a self-inflicted injury. The patient was reassured and scheduled for a follow-up appointment the next day. Prior to returning to the clinic for this appointment the patient presented to her GP the following morning complaining of neurological symptoms overnight. Approximately 10 hours following administration of the local anaesthetic she developed systemic tremors and numbness, especially of her peripheries. She was unable to perform simple motor functions, stating she dropped dishes whilst washingup and was unable to get into bed without assistance. The GP liaised with the local neurology department who recommended close follow-up and allergy testing; no in-patient or out-patient arrangements were made. © 2013 Australian Dental Association
Local anaesthetic complications Although it was not possible to determine whether the patient’s symptoms were neurological or physiological, both clinicians felt the presentation was consistent with systemic complications from the local anaesthetic. Upon returning to the clinic approximately 24 hours after administration of local anaesthetic the patient reported her systemic and oral symptoms had begun to subside with an area of crusting where the cutaneous lesion was observed (Fig. 1); 72 hours later the lesion showed evidence of healing (Fig. 2) and the systemic symptoms had resolved entirely. Following one month the lesion had healed entirely with no scarring or altered pigmentation in the area (Fig. 3). The patient underwent immunological testing using lignocaine and prilocaine skin prick challenges; both were negative. The patient underwent restoration of other carious teeth using an alternative anaesthetic agent uneventfully.
Fig. 1 Clinical photograph illustrating crusting over the cutaneous distribution of the left inferior alveolar artery 24 hours following administration of local anaesthetic.
Fig. 2 Clinical photograph illustrating healing of the lesion over the cutaneous distribution of the left inferior alveolar artery 72 hours following administration of local anaesthetic. © 2013 Australian Dental Association
Fig. 3 Clinical photograph illustrating resolution of the lesion with no cutaneous pigmentation or scarring approximately 1 month following administration of local anaesthetic.
DISCUSSION Although uncommon, the majority of complications following use of local anaesthesia in dentistry are well known. A recent study by Sambrook et al.1 analysed serious adverse reactions to dental local anaesthetics which have been reported to the Office of Product Review of the Therapeutics Goods Administration in Australia over a 35-year period; a similar case to ours was not reported. Of the 221 reported cases, neurological complications represented 16% of all adverse systemic reactions and was the second most common reaction after syncope. Neurological complications occur after a toxic level of local anaesthetic solution crosses the blood brain barrier. Early signs include slurred speech, muscle twitching, visual disturbances and disorientation, while later with increased dose convulsions and seizures can occur.5 This may represent the patient’s psychological state or a direct effect of the local anaesthetic or both. This study also showed 70% of all reported reactions were related to prilocaine; only 2% were attributed to articaine. Reactions to lignocaine accounted for 28% of adverse reactions; however only 10 cases of neurological complications after lignocaine administration were reported. Given how commonly used lignocaine is, this demonstrates not only how safe it is but also how rare adverse reactions to it are. It has been shown that a higher concentration of local anaesthetic solution is related to a higher rate of complications; however, in our case the dosage and volume of local anaesthetic used was minimal.6 A review of the literature revealed only two similar cases occurring following administration of an inferior dental block. Torrente-Castells et al.7 reported a case involving a 10-year-old girl who received an inferior alveolar nerve block using one cartridge of 4% articaine with 1:200 000 adrenaline. After the procedure she developed pallor of the ipsilateral lower lip and chin that subsequently evolved into surface ulceration which healed 15 days later. 523
N Pattni Kruger and Nehs8 reported the case of a 30-yearold woman who received an inferior alveolar nerve block and infiltration of the mental nerve for dental treatment. A total of three cartridges of 4% articaine with 1:100 000 adrenaline were administered. Crusting was observed on the ipsilateral lower lip, with transient sensory alteration of the area innervated by the ipsilateral mental nerve branch. They also observed a haematoma in the vestibular mucosa at the left canine/premolar region. In this case the authors acknowledge it is not possible to ascertain whether the inferior dental block or the mental nerve block was the cause of the patient’s signs and symptoms. Both of these cases present a similar cutaneous presentation to that observed in our case; however, the significant difference is that neither case presents the patient also experiencing neurological symptoms. Also, the local anaesthetic agent used in these cases was articaine whereas in our case lignocaine was used. The mechanism behind the complications seen in our case are likely to be related to intra-arterial injection involving the maxillary artery and viral activation within the inferior alveolar nerve. Anatomy The maxillary artery is the terminal branch of the external carotid artery that typically originates posterior to the neck of the mandible. It courses forward between the ramus of the mandible and sphenomandibular ligament, passing either deep or superficial to the lateral pterygoid running towards the pterygopalatine fossa to supply the deep structures of the face. Cadaveric dissection studies have shown when the maxillary artery courses superficial to the lateral pterygoid it loops inferiorly 88% of the time,9 passing as close as 4 mm to the mandibular foramen.10 The inferior alveolar artery braches from the first portion of the maxillary artery. It courses along with the corresponding nerve to enter the mandibular foramen to supplying the mandible, teeth and the ipsilateral lower lip and chin. Therefore, within the pterygomandibular space the maxillary or inferior alveolar may be encountered or penetrated whilst administering an inferior dental block. Vascular injection Contact between a needle and artery may result in vasospasm, causing a transient ischaemia of the inferior alveolar artery which would manifest as discomfort and blanching. Furthermore, a perivascular injection may lead to sympathetic nerve stimulation and subsequent vessel vasospasm, which again may 524
lead to peripheral tissue necrosis. However, immediate blanching was not observed in our case which would have occurred if contact was made with the artery, or if sympathetic nerves were stimulated. Alternatively, inadvertent intra-arterial administration of local anaesthetic containing a vasocontrictor may result in stimulation of a-adrenergic receptors with contraction of smooth muscle within the arterial wall.9 This may lead to transient ischaemia of the structures distal to the injection site supplied by the vessel, which if prolonged may result in tissue necrosis. This may account for the superficial necrosis of the skin of the chin seen in our patient. Therefore, it is important to aspirate when administering an inferior alveolar block to ensure local anaesthetic solution is not injected intra-arterially. An intra-arterial injection also explains the systemic symptoms the patient reported. An intra-arterial injection may circulate in a retrograde fashion reaching the carotid bifurcation where it may be distributed to the central nervous system via the internal carotid artery; this is the proposed mechanism for visual and auditory disturbances following inferior dental blocks.4 This phenomenon of reverse carotid flow was proposed and demonstrated in animal studies by Aldrete et al.11 Malamed12 considered retrograde flow is only possible with injections administered faster than one cartridge in 30 seconds. This would help account for the systemic neurological symptoms observed in our patient. The elimination half-life of lignocaine is approximately 1.5–2.0 hours; however, studies have shown an increased toxicity of lignocaine when administered with adrenaline which may account for the prolonged neurological toxicity observed in our case. The reason for this is not fully understood but it is proposed that the adrenaline alters the distribution of lignocaine by its effects on the cardiovascular system and direct interaction of the drug.13 Viral activation Various viruses, including herpes simplex and herpes zoster, are ubiquitous in the population.14 Following infection and local replication viruses enter nerve endings and are transported by retrograde axonal transport to the neuronal cell bodies. Here they remain in a latent state and can be reactivated by a range of factors including stress, ultraviolet light and immunosupression.15 Trauma can also result in viral reactivation and has been implicated in herpes zoster oticus, facial palsy and mental nerve neuropathy following dental treatment.14 Therefore, in our case the administration of local anaesthesia may have induced trauma to the inferior alveolar nerve, resulting in intracellular viral activation and subsequent cutaneous manifestations. © 2013 Australian Dental Association
Local anaesthetic complications CONCLUSIONS This case highlights the need for a careful technique when administering local anaesthesia in the oral and maxillofacial region. Nevertheless, complications may still occur and clinicians should be aware of these in order to diagnose and manage patients appropriately. REFERENCES 1. Sambrook PJ, Smith W, Elijah J, Goss AN. Severe adverse reactions to dental local anaesthetics: systemic reactions. Aust Dent J 2011;56:148–153.
8. Lacouture C, Blanton P, Hairston E. The anatomy of the maxillary artery in the infratemporal fossa in relationship to intraoral injections. Anat Rec 1983;205:104A. 9. Berini-Aytes L, Gay-Escoda C. Anestesia Odontol ogica. 3rd edn. Madrid, Spain: Ediciones Avances, 2005. 10. Ruocco I, Cuello AC, Parent A, Ribeiro-da-Silva A. Skin blood vessels are simultaneously innervated by sensory, sympathetic, and parasympathetic fibers. J Comp Neurol 2002;448: 323–336. 11. Aldrete JA, Narang R, Sada T, Liem ST, Miller GP. Reverse carotid blood flow–a possible explanation for some reactions to local anesthetics. J Am Dent Assoc 1977;94:1142–1145. 12. Malamed SF. Handbook of Local Anaesthesia. 3rd edn. St Louis: Mosby-Year Book, 1990:160–218, 245–257.
2. Meechan JG. Local anaesthesia: risks and controversies. Dent Update 2009;36:278–280, 282–283.
13. Yagiela JA. Intravascular lidocaine toxicity: influence of epinephrine and route of administration. Anesth Progr 1985; 32:57–61.
3. Kaufman E, Goharian S, Katz Y. Adverse reactions triggered by dental local anesthetics: a clinical survey. Anesth Prog 2000; 47:134–138.
14. Maini S, Preece M. Herpes zoster oticus following mandibular block. J Laryngol Otol 2000;114:212–213.
4. Crean SJ, Powis A. Neurological complications of local anaesthetics in dentistry. Dent Update 1999;26:344–349.
15. Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features. J Oral Pathol Med 2008;37:107–121.
5. Subramaniam S, Tennant M. A concise review of the basic biology and pharmacology of local analgesia. Aust Dent J 2005;50 (4 Suppl 2):S23–30. 6. Kingon A, Sambrook P, Goss A. Higher concentration local anaesthetics causing prolonged anaesthesia. Do they? A literature review and case reports. Aust Dent J 2011;56:348–351. 7. Torrente-Castells E, Gargallo-Albiol J, Rodrıguez-Baeza A, Berini-Aytes L, Gay-Escoda C. Necrosis of the skin of the chin: a possible complication of inferior alveolar nerve block injection. J Am Dent Assoc 2008;139:1625–1630.
© 2013 Australian Dental Association
Address for correspondence: Dr Neeraj Pattni 1 Fieldfare Green Luton LU4 0YA United Kingdom Email: [email protected]
525
