sodium hypochlorite extrusion: an atypical case of massive soft tissue necrosis

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J Oral Maxillofac Surg69:1776-1781, 2011

Sodium Hypochlorite Extrusion:An Atypical Case of Massive Soft

Tissue NecrosisJulie Lee, DMD,* Dorothy Lorenzo, DMD,†

Therese Rawlins, DDS,‡ and Vito A. Cardo, Jr, DDS§

Sodium hypochlorite, although commonly used inendodontic practices, has the potential for detrimen-tal consequences. Sodium hypochlorite is recognizedas an antibacterial solvent with excellent tissue-dis-solving and lubricating capabilities. This agent has along shelf life, is relatively inexpensive, and is readilyavailable. Its low viscosity allows for easy introduc-tion into the canal system. For these reasons, sodiumhypochlorite is an attractive adjunctive agent in den-tistry. However, inadvertent introduction of sodiumhypochlorite beyond the root apex into periradiculartissues can be extremely destructive and caustic.There is potential for soft tissue necrosis, nerve dam-age, and possible airway compromise.1

There are few studies reported in the literaturepertaining to complications using this agent. Uniqueto this case report is root canal treatment rendered inthe operating room under general anesthesia. Al-though most patients can verbalize symptoms andalert the clinician to terminate treatment, this was notpossible in the present case.

The following presentation describes a case of severesoft tissue inflammatory reaction secondary to sodium

*Former Resident, Caritas Health Care; Present Chief Resident in

Oral and Maxillofacial Surgery, Medisys Health Network at Brook-

dale University Hospital, Brooklyn, NY.

†Former Resident, Caritas Health Care; Present Chief Resident in

Oral and Maxillofacial Surgery, Medisys Health Network at Brook-

dale University Hospital, Brooklyn, NY.

‡Former General Practice Resident, Caritas Health Care; Private

practice.

§Former Chairman of the Department of Dental Medicine and

Oral/Maxillofacial Surgery, Caritas Health Care; Present Director of

the Oral and Maxillofacial Training Program, Medisys Health Net-

work at Brookdale University Hospital, Brooklyn, NY.

Address correspondence and reprint requests to Dr Lee: Oral

and Maxillofacial Surgery, Medisys Healthnetwork at Brookdale

Hospital, One Brookdale Plaza, Brooklyn, NY 11212; e-mail:

[email protected]

© 2011 American Association of Oral and Maxillofacial Surgeons

278-2391/11/6906-0069$36.00/0

oi:10.1016/j.joms.2010.07.041

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hypochlorite extrusion. The purpose of this report is todescribe clinical signs and symptoms, present a treat-ment option, discuss pertinent implications, and encour-age clinicians to be cognizant of its use.

Report of a Case

A 25-year-old, mentally handicapped woman presented toMary Immaculate Hospital Dental Clinic (Queens, NY) fororal rehabilitation and treatment planning. After evaluationby the dental practitioners, she was recommended to un-dergo full mouth oral rehabilitation under general anesthe-sia due to her behavioral management disorder. In additionto her neurologic and behavioral deficits, she was diagnosedwith bipolar disorder and urinary incontinence and wasnonverbal. She was taking olanzapine, fluoxetine, clomip-ramine and desmopressin. Her allergies included diphenhy-dramine and codeine.

Consent for treatment was obtained from her legal guard-ian. The patient was taken into the operating room andplaced in a supine position. General anesthesia was admin-istered through a nasoendotracheal tube. A lead apron wasplaced on the patient. A periapical radiograph of the max-illary left central incisor revealed an apical radiolucent le-sion (Fig 1). The dental team agreed that salvaging the toothwith endodontic therapy was ideal. Lingual access wasmade with a handpiece. A working length of 24 mm wasestablished using a digital radiograph. K files of subsequentsizes 15, 20, 25, 30, and 35 were used to instrument andshape the canal. Each file was coated with R-C preparationbefore instrumentation. There was intermittent irrigation ofthe canal with sodium hypochlorite and saline betweeneach step.

A backfilling technique was used while irrigation with so-dium hypochlorite and saline was introduced throughout therecapitulation of the master apical file. The gutta percha wassealed and the composite was condensed. A final radiographrevealed adequate therapy (Fig 2). The patient was extubatedatraumatically in the operating room and transferred to therecovery room. The total amount of irrigating solution usedwas sodium hypochlorite approximately 6 mL and saline 6 mL.

In recovery, it was noted that the patient had a suddenonset of unilateral swelling and mild ecchymosis of the lefteye (Fig 3). The oral and maxillofacial surgery service wasconsulted immediately after exacerbation of the periorbitaledema. The patient was given dexamethasone 8 mg intra-venously, promethazine 12.5 mg intravenously, and pen-icillin 1 million U intravenously by the recovery roomstaff at the request of the oral and maxillofacial surgicalteam. She was subsequently admitted to the hospital for
observation and pharmacologic intervention. An ophthal-
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LEE ET AL 1777

mology consultation was requested to rule out orbitalinvolvement and intraocular insult. The ophthalmologyexamination was limited because the patient was unco-operative and in a hyperexcitable state due to pain anddiscomfort from the swelling. Although it was a limited

FIGURE 1. Periapical radiograph of the maxillary left centralincisor with associated periapical radiolucent pathologic lesion.

Lee et al. Sodium Hypochlorite Extrusion. J Oral Maxillofac Surg2011.

FIGURE 2. Completed root canal therapy of the maxillary leftcentral incisor.

Lee et al. Sodium Hypochlorite Extrusion. J Oral Maxillofac Surg
2011.
examination, anterior segment globe pathology was ruledout. To complete the evaluation of the patient’s condition,an infectious disease consultation was called. The recom-mendations from this service were to start the patient onampicillin and sulbactam 3 g intravenously every 6 hoursalong with an immediate dose of hydrocortisone 100 mgintravenously. The recovery room staff administered thesemedications.

Although the patient remained afebrile overnight, the leftperiorbital and buccal edema were progressively increasingwith complete obliteration of the nasolabial fold. The buc-cal edema had also spread inferiorly to the mandibularborder and continued to spread at an alarming rate (Figs 4,5). Although a subjective assessment could not be obtaineddue to the patient’s nonverbal status and combative state,the patient was observed to be clearly uncomfortable andprotective of any foreign contact with her face. Although anacute inflammatory reaction to sodium hypochlorite israrely reported, the oral and maxillofacial surgical teamagreed surgical intervention was appropriate to drain anddebride the area in question.

The patient was brought to the operating room and undergeneral anesthesia with nasoendotracheal intubation, a sur-gical incision was made in the left anterior maxillary vesti-bule. A full mucoperiosteal flap was raised, exposing theperiapical area of the maxillary left central incisor. Nopurulent exudate was evident. Upon exposure of the max-illary alveolus, a 1- � 1-cm buccal plate perforation wasobserved apical to the left maxillary central incisor (Fig 6).The apex of the maxillary left central incisor was clearlyvisible with associated radicular granulation tissue. An over-extended gutta percha point was noted approximately 2mm beyond the apex. An aggressive curettage and irrigationwas performed. After this, an apicoectomy was completedwith a round bur and an amalgam retrofill. All associatedsurgical tissues from the pathologic defect were excisedand sent for pathologic evaluation (Fig 7). Blunt dissectionwas carried into the canine space and surrounding areas.

FIGURE 3. Photograph immediately after extubation shows signif-icant left periorbital edema and ecchymosis.


The surgical site was irrigated with copious amounts of

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1778 SODIUM HYPOCHLORITE EXTRUSION

saline irrigation. A 5-cm Penrose drain was placed horizon-tally into the surgical site and passively secured by reap-proximating the apical and coronal margins of the maxillaryvestibule (Fig 8).

FIGURE 5. Twenty-four hours after initial therapy with increasingleft facial edema and spread to mandibular inferior border.


FIGURE 4. Twenty-four hours after initial therapy with rapidly pro-gressing buccal and periorbital edema.


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The patient was continuously given hydrocortisone 20mg intravenously every 6 hours and promethazine 12.5mg intravenously every 6 hours. Twelve hours after theincision and drainage, the patient showed remarkableimprovement with subsidizing edema and ecchymosis ofthe left face (Fig 9). At 24 hours after surgery, buccaledema had also decreased dramatically with no evidenceof swelling inferior to the mandibular border. She wascomfortable and appeared to be in minimal pain (Fig 10).The patient was discharged home the following day withamoxicillin and clavulanic acid and ibuprofen. A 1-weekfollow-up revealed facial symmetry with complete reso-lution of facial swelling (Fig 11).

Discussion

Sodium hypochlorite is a potent oxidizing agentwith a pH of approximately 11 to 12.2 It reacts withatty acids, amino acids, and intracanal pathogensesulting in the dissolution of these tissues andicrobes. Sodium hypochlorite also acts to osmot-

cally draw fluid out of tissues.3 These propertiesre especially beneficial to performing a successfuloot canal treatment. However, when this agent isxposed beyond the apex of the teeth, these prop-rties can cause potential harm.There is no universally accepted concentration of

odium hypochlorite among dentists and endodon-ists. It is known that the bactericidal and tissueissolution qualities increase with increasing con-entrations. Clancy et al3 found in a study examin-ng the toxicity of sodium hypochlorite that at aoncentration of 0.025% the solution was bacteri-idal and nontoxic. However, at a concentration of.25% the solution became severely toxic to tissues.

FIGURE 6. Surgical exploration revealing a 1- � 1-cm buccalplate perforation in the apex of the maxillary left central incisor andassociated periapical granulation tissue.


ven at a low dilution of 1:1,000 this agent causes

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complete hemolysis of red blood cells with poten-tial hematoma formation.3

The general dental team reported that during theremoval of the surgical drapes and at the time ofextubation of the patient, a mild swelling wasnoted. After this finding, the patient was transferredto the recovery room, where the facial swellingrapidly progressed over a short period. The oral andmaxillofacial surgical team was then called for con-sultation. The rationale for the rapid facial swellingis likely a result of high-pressure sodium hypochlo-rite irrigation. Because the patient’s face was cov-ered and under general anesthesia and could not bevisualized or respond to unusual pain, this adversereaction went unnoticed.

This supposition proved to be true during thesurgical exploration. It was evident that the buccalbone perforation seen at this time allowed a path-way for sodium hypochlorite extrusion into sur-rounding tissues. The solution traveled through thecanine and buccal fascial spaces causing tissuebreakdown on contact. The resulting inflammatory

FIGURE 7. Surgical ti

ee et al. Sodium Hypochlorite Extrusion. J Oral Maxillofac Surg

ssue from pathologic defect.

response correlated with the clinical presentation

FIGURE 8. Penrose drain placement into left maxillary vestibuleafter surgical exploration, debridement, and curettage.

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1780 SODIUM HYPOCHLORITE EXTRUSION

of swelling and erythema. The periorbital ecchymo-sis was a result of massive hemolysis of red bloodcells underlying the thin delicate epithelium sur-rounding the orbital structures. The rapid progres-

FIGURE 9. Twelve hours after exploration and debridement withsubsiding edema and ecchymosis.


FIGURE 10. Twenty-four hours after surgical exploration and debride-ment with marked decrease of left periorbital and buccal edema.

Lee et al. Sodium Hypochlorite Extrusion. J Oral Maxillofac Surg 2011.

sion of this toxic clinical presentation was of majorconcern, resulting in an immediate response with adefinitive treatment plan.

The rationale for this treatment was based on theclinician’s knowledge of foreign body reactions.The goal of treatment is to address the inflamma-tion, control pain, and prevent infection. The initialtreatment was to administer appropriate medica-tions as described earlier. The decision for surgicalintervention stemmed from the rapid progressiveswelling that continued despite the pharmacologicintervention. An incision and drainage was per-formed to expel any hematoma formation and toflush and debride the involved tissue spaces. Thegoal was to stop the spread of toxic reaction andallow for more rapid recovery. A Penrose drainremained in place to prevent hematoma formationand facilitate irrigation and drainage. The patientwas administered intravenous hydrocortisone forits anti-inflammatory effects and empiric intrave-nous ampicillin and sulbactam to prevent possibleinoculation of the necrotic tissue.

Although the risk of this reaction is minimal, extraprecaution by the dental clinician can facilitate itsprevention. The syringe needle should never engagethe canal but should be loosely positioned within.Sodium hypochlorite solution should always be ad-ministered with slow, gentle, controlled pressure to

FIGURE 11. Seven days after surgical exploration and debride-ment with complete resolution of left facial swelling.


prevent extrusion through the apex. Luer-Lock sy-

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ringes and side venting syringes can be used to pre-vent such high pressures.1 A radiograph before irriga-tion using a file and apex marking can reassure theclinician of the canal integrity and proper measure-ment before insertion of the irrigating needle andcanal lavage. The use of an apex locator will assist inthe prevention of overinstrumentation and in the de-tection of canal perforation.4

Recent studies have suggested alternatives to so-dium hypochlorite and its use as an intracanal medi-cament. Brandt et al4 concluded that chlorhexidineluconate was more effective than sodium hypochlo-ite because of its greater antimicrobial activity.owever, it possesses no tissue-dissolving proper-

ies. Therefore, to combine both effects, these in-estigators suggest alternating between dilute so-ium hypochlorite and chlorhexidine gluconate.ven the use of normal saline lavage after irrigationith sodium hypochlorite may decrease the de-

cribed risks. Electrochemically activated water haseen marketed in endodontic therapy to have effi-ient cleaning properties comparable to sodiumypochlorite. However, further investigation ob-erved nearly no antimicrobial effect and its use inndodontic therapy is questionable.4

It is clear that treatment in the operating roomunder general anesthesia with full surgical draping didhave an effect on the development of these compli-cations. Previous studies have reported root canaltreatment under local anesthesia, when clinicianswere promptly notified of pain, resulting in cessationof treatment and prevention of similar complications.This particular case was further complicated by thefact that the patient was nonverbal and unable to
express her pain.
In conclusion, sodium hypochlorite, although amainstay for treatment of intracanal pathology, haspotential complications when used without cautionas evidenced in the present case. Several suggestionshave been reviewed to assist the clinician in futuretreatment and care. Although sodium hypochloriteand its use are justified in dentistry, several modifica-tions can be made, such as dilution, substitutions, andradiographic verification. The present findings of alarge apical lesion contributed significantly to thepathologic process. This cavity became a containerfor this toxic solution preventing drainage backthrough the canal, causing extrusion into the sur-rounding tissues. It is our recommendation that animmediate apicoectomy should follow root canaltherapy in these clinical presentations. Most impor-tantly, the clinician should be astute to the signs andsymptoms of sodium hypochlorite toxicity in theevent this occurs after a routine root canal treatment.It is suggested that in the event of these occurrences,immediate aggressive surgical intervention should beundertaken by the proper surgical specialist.

References1. Brennan PA, Ike V, Spencer HR: Review: The use of sodium

hypochlorite in endodontics—Potential complications and theirmanagement. Br Dent J 202:555, 2007

2. Medical Toxicology Unit, International Programme of ChemicalSafety: Sodium hypochlorite. London, UK, December 1997.Available at: http://www.inchem.org/documents/pims/chemical/pim495.htm

3. Clancy D, Mehra P, Wu J: Formation of a facial hema-toma during endodontic therapy. J Am Dent Assoc 131:67,2000

4. Brandt M, Eppendorf K, Gernhardt CR, Kozlowski A: Toxicity ofconcentrated sodium hypochlorite used as an endodontic irri-
gant. Int Endod J 37:272, 2004
http://www.inchem.org/documents/pims/chemical/pim495.htm

http://www.inchem.org/documents/pims/chemical/pim495.htm

sodium hypochlorite extrusion: an atypical case of massive soft tissue necrosis

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