Emboli Cutis Medicamentosa After Root Canal Treatment Review PDF
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Maharaja Ganga Singh Dental College & Research Centre
Beena J Dev, Devendra Chaudhary, Shweta Sharma, Harmeet Singh
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This review article examines Emboli cutis medicamentosa, or Nicolau syndrome, a rare adverse reaction that can occur after root canal treatment. It discusses the causes, clinical features, and potential treatment strategies associated with this complication. The review highlights the importance of understanding and managing the potentially hazardous effects of calcium hydroxide.
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Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research REVIEW ARTICLE Emboli cutis medicamentosa after root canal treatment: a review Beena J Dev1, D...
Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research REVIEW ARTICLE Emboli cutis medicamentosa after root canal treatment: a review Beena J Dev1, Devendra Chaudhary2, Shweta Sharma3, Harmeet Singh3 Abstract Calcium hydroxide used in RCT when pushed beyond apex through pressure syringe system causes tissue necrosis and other hazardous effects of adjacent supporting structures. Similar conditions were also observed in the injection of various drugs including NSAIDS, corticosteroids, antibacterial agent, chlorphineramine maleate etc. In 1924 first case with similar symptoms was reported after the injection of bismuth for syphilis in the gluteal area by Freudenthal and named it as Nicolau syndrome (Emboli cutis medicamentosa). The aim of the review article is to bring out the thorough knowledge in understanding and managing the adverse effects and consequences of Nicolau syndrome in root canal treatment. Keywords: Calcium hydroxide, Emboli cutis medicamentosa, Nicolau syndrome, Skin necrosis. Calcium hydroxide paste can result in necrosis and INTRODUCTION degenerative changes in animal models by intense Calcium hydroxide has been used successfully in root canal inflammatory responses. Its pH is around 12; it has very low therapy for many years. solubility at body temperature and will remain in the tissue for considerable time and therefore cannot be considered However, it can cause Nicolaus syndrome, if it is inadvertently biocompatible4. displaced into surrounding vital structures, resulting in thrombosis if displaced into blood vessel, damaging CLINICAL FEATURES connective tissue, and causing skin necrosis1. Clinical features of NS are presented by three typical phases7, The case of the adverse reaction to intra canal medicament calcium hydroxide was published in 2000. Although it has been considered as a safe agent2, a few reports dealt with the negative side effects of CaOH2 including bone necrosis and continuing inflammatory response in repaired mechanical perforations, the neurotoxic effect of root canal sealers, cytotoxicity on cell cultures, damaged epithelium with or without a cellular atypia when applied on hamster cheek pouches and cellular damage following early CaOH2 dressing of avulsed teeth3. Some authors have reported deleterious effects if the material is extruded under a high pressure during endodontic treatment4. 1 Post graduate student 2. Principal & Head of the Department 3. Professor Department of Conservative Dentistry and Endodontics, Corresponding Author: Beena J Dev, post graduate student Ph. 9747446130, Email:[email protected], Department of Conservative Dentistry and Endodontics, Maharaja Ganga Singh Dental College & Research Centre, Sri Ganganagar, Rajasthan. 7 www.cdronline.org Official Publication of Kothiwal Dental College & Research Centre. Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research PATHOGENESIS Pathogenesis of Nicolau syndrome is not clear but a vascular origin is the most reasonable hypothesis. Acute vasospasm, inflammation of arteries and thromboembolic occlusion of arteriole are the key mechanisms5. The leakage of around artery and neural space has been suggested as cause of intense pain. Moreover, sympathetic nerve stimulation and vasospasm lead to ischemic change and skin necrosis. Unintended intravascular injection of drugs also has been proposed as causing inflammation or thromboembolic occlusion of the arterioles. These may cause arterial intimal necrosis, destruct the arterial membrane and induced subsequently cutaneous necrosis6. Fig.1 Skin necrosis in the left infraorbital area after 2 weeks following endodontic treatment of tooth 141 NICOLAU SYNDROME AFTER ENDODONTIC TREATMENT The reaction inadvertent calcium hydroxide extrusion into the soft tissue or blood vessels can vary from a simple inflammatory reaction to serious damage. In some cases where the canal bleed profusely during the root canal therapy, the bleeding might be explained by the proximity of the apices of the root to vascular structure. Immediately after the injection of intra canal calcium hydroxide, pain and ischemia in skin extra orally occur7. BRIEF REVIEW OF REPORTED CASE Fig.2 The appearance of the skin after endodontic treatment1 De Bruyne et al. reported gingival necrosis after extrusion of Ca (OH)2 paste (La Maison Dentaire, Balzers, Switzerland) through a root perforation of maxillary central incisor3. They treated the necrotic gingival zone with rinses of hydrogen peroxide 3% and chlorhexidine 2% and daily application (BID) of chlorhexidine di gluconate 10 mg/g gel and concluded that as long as Ca (OH)2 does not come into direct contact with surrounding soft tissues, problems either do not occur or are of a mild transient nature 4. Fig.3 Three-dimensional construction of the cone-beam computed tomographic scan showing a contrast material in Sharma et al. described two severe cases of iatrogenic the route of the infraorbital artery1 extrusion of Ca(OH)2 Nordiska Dental, Angelholm, Sweden) on upper and lower molar tooth causing extensive necrosis in the scalp, skin, and mucosa in the first case and infraorbital nerve paraesthesia and palatal mucosal necrosis in second case8. Both patients reported severe pain immediately after Ca(OH)2 Injection. A computerized tomography (CT) scan with 3- dimensional (3-D) reconstruction in second case confirmed the intravascular distribution of the material. Authors explained that an exposure of Ca (OH)2 to blood resulted in crystalline precipitation and the consequent ischemic tissue necrosis. Their patient underwent thrombolytic, steroid and antibiotic therapies to maintain tissue reperfusion, limit inflammatory responses, and Fig.4 CBCT image showing the presence of opaque material prevent infections, respectively4. in the root of the posterior superior alveolar artery1. 8 www.cdronline.org Official Publication of Kothiwal Dental College & Research Centre. Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research Lindgren et al. reported a case of Ca(OH)2 (Calasepts, Nordiska Dental, Angelholm, Sweden) injection into the root of a lower second molar, the inferior alveolar and farther maxillary and external carotid artery, causing necrosis of the ear lobe and superficial necrosis of the cheek skin9. When the paste was applied with a syringe in the distal canal, the patient experienced severe local pain. Angiogram showed a number of vascular occlusions in the right external carotid artery branches4. Bramante et al. reported a case of Ca (OH)2 therapy for root resorption control in a maxillary lateral incisor10. Three days after Ca (OH)2 placement (Biodinâmica, Ibiporã, PR, Brazil), an irregular zone of necrosis was observed on buccal mucosa. Careful curettage was performed around the region for removal of necrotic tissue and extruded Ca (OH)2; healing was observed at a 15-day follow-up4. Ahlgren et al. showed paraesthesia and changes in surrounding bone after a mishap with Ca (OH)2 extrusion (Calasept Nordiska Dental, Angelholm, Sweden) through the apex of a mandibular premolar tooth11. They surgically excavated the excessive paste from the spongious bone and after six months, patient was symptom free4. Four cases of seven patients reported moderate to severe pain immediately after Ca (OH)2 injection. Blurred vision occurred in two cases, anesthesia or paresthesia in four, swelling in three, facial palsy or weakness in two, and mucosal ulceration Fig. 5 Photomicrographs of biopsy specimen showing in six cases. In two cases, angiogram or computerized foreign material surrounded by necrotic tissues tomography scanning revealed vascular obstruction. In five of the above cases, pressure syringe system was the culprit; however, two cases did not use a pressure syringe system for DIAGNOSIS the application of Ca (OH)2 4 Clinical Diagnosis of Nicolau Syndrome is done mainly by: HISTOPATHOLOGY Skin biopsy shows necrotic changes caused by The tissue sections were stained with H & E and examined by ischemia12. light microscopy for histopathological changes. Ultra-sonography of the skin Histopathological analysis revealed areas of degenerative Magnetic resonance imaging help in delineating the changes and necrosis in the tissues in direct contact with the extent of damage13. injected paste. Granulomatous tissues containing numerous giant cells and macrophages with engulfed particles in their TREATMENT cytoplasm were also observed in contact with the extruded material. The aggregation of macrophages and giant cells There is no consensus of treatment of Nicolau syndrome so around Ca (OH)2 particles in the absence of other far. However we suggest the treatment of Nicolau syndrome inflammatory cells such as neutrophils, lymphocytes, and step by step as the three phases. Phasic treatments depend on plasma cells suggests that the paste induced a typical foreign the extent of the necrotic lesion and ranges from medication to body reaction4. surgical debridement6. Initial phase: Because of severe pain, conservative pain control with analgesics and dressings is usually recommended. 9 www.cdronline.org Official Publication of Kothiwal Dental College & Research Centre. Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research And differential diagnosis is most important in the initial phase. Ice pack application increases the acute focal vasospasm and can aggravate the disaster14, 15. Until cellulitis of affected site is ruled out, systemic antibiotics are suggested. After any signs of cellulitis ruled out such as fever, elevated white blood cell count, C-reactive protein and erythrocyte sedimentation rate, prophylactic antibiotics might be useful6. Acute phase: Hypothesis of vascular origin and inflammatory sequelae is most reasonable. For this reason systemic steroid and anticoagulant agent are usually used 16, 17. Hyperbaric oxygen treatment was given to patient with the assumption of Fig.7 Discolored cortex due to an ischemia and decreased micro arterial thrombi as well as heparin and blood supply4. pentoxyphilline18. Subcutaneous injection of heparin 5000 to 10000 U b.i.d.17 and intravenous infusion of betamethasone diphosphate 24 mg/d induce improving symptom within 2d. Patient responses rapidly to methylprednisolone 1g IV q.d. or dexamethasone 32 mg intravenous injection for three days and pentoxifylline 400 mg PO t.i.d.. Warm intermittent compression is also recommended6.Necrotic phase: The patients with NS undergo surgical debridement of the affected skin, subcutaneous tissue and muscle in case of clinical and radiographic evidence of tissue necrosis6. And after the ulcerative necrotic lesion was filled with healthy granulation, Fig.8 Removal of foreign material and necrotic tissues around split-thickness skin graft or reconstructive surgery were the roots4. performed. Finally the wound healed well and uneventfully with atrophic skin scar or wound contraction19. CONCLUSION Nicolau syndrome is rarely occurring side effect of injectable drugs. Post signs and symptoms of injectable drugs should be considered as wake-up call in nicolau syndrome, so that the complications can be treated at the earliest. Proper and efficient health care is mandatory from the licensed professionals for the awareness. REFERENCE 1. Fatima Al-sheeb BDS et al: Nicolau syndrome after Endodontic Treatment: A Case Report. Journal of Endodontics 2022 Feb. 2. Lindgren P, Eriksson KF, Ringberg A: Severe facial ischemia after endodontic treatment. J Oral Maxillofac Surg. 2002; 60(5):576-9. 3. De Bruyne MA, De Moor RJ, Raes FM: Necrosis of the gingiva caused by calcium hydroxide: a case report. Int Endod J. 2000; 33(1):67-71. 4. Arash Shahravan et al: Oveextension of Nonsetting Calcium Hydroxide in Endodontic Treatment: Literature Review and Case Report. Iranian Endodontic Journal 2012;7(2):102-108 5. Luton K, Garcia C, Poletti E, Koester G: Nicolau Fig.6a Radiographs showing radiopaque CaOH2 paste Syndrome: three cases and review. Int J Dermatol 2006. surrounding root of the premolars4 Fig.6b, Radiograph showing 6. Kwang-Kyoun Kim et al: Nicolau syndrome A Literature the tracing of gingival detachment by gutta-percha4 Review. World J Dermatol 2015; 4(2): 103-107. 10 www.cdronline.org Official Publication of Kothiwal Dental College & Research Centre. Chronicles of Dental Research, Dec2023, Vol 12, Issue1 Chronicles of Dental Research 7. Dr.Ruchi paharia : Nicolau syndrome saraswati dental college and 14. Cherasse A, Kahn MF, Mistrih R, Maillard H, Strauss J, hospital 26 may 2023. Tavernier C. Nicolau’s syndrome after local glucocorticoid 8. Sharma S, Hackett R, Webb R, Macpherson D, Wilson A: injection. Joint Bone Spine 2003; 70: 390-392 [PMID: Severe tissue necrosis following intra-arterial injection of 14563471 DOI: 10.1016/S1297-319X(03)00137-4] endodontic calcium hydroxide: a case series. Oral Surg 15. Stricker BH, van Kasteren BJ. 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