the oral implications of caustic soda ingestion in children

6
The oral implications of caustic soda ingestion in children Fiona Ryan, MFDS RCSE (Eng), a Helen Witherow, FDS, FRCS (Eng), FRCS OMFS (Eng), b Jack Mirza, MFDS RCSE (Eng), a and Peter Ayliffe, FDS, FRSC (Eng), FRCS OMFS (Eng), c London, UK GREAT ORMOND STREET HOSPITAL The morbidity related to caustic soda (sodium hydroxide) ingestion is well described in the literature. The majority of publications have concentrated on the effects to the trachea and gastrointestinal tract, with little reference to the oral and peri-oral areas. Accidental ingestion of sodium hydroxideecontaining substances is fortunately rare; however the consequences can be devastating. Three cases of children who drank caustic substances are described. Treatment included fitting splints, injecting steroids, local surgical procedures, and the use of dynamic appliances to maintain mouth opening. Despite these interventions, all patients developed severe scarring, resulting in stenosis of the oral musculature and extra-articular ankylosis. There is perhaps a role for further investigation of early use of antiproliferative agents to prevent scaring, more aggressive surgery, and long-term physiotherapy appliance use. These patients require lifelong follow-up. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:29-34) Ingestion of caustic substances carries significant mor- bidity, and occasional mortality. It has both acute and chronic implications for the patient, and often lifelong sequelae. Ingestion of these substances is fortunately relatively rare. The US poison control centers reported 26 000 cases annually, with more than 65% occurring in children, 1 the majority of whom are between the ages of 2 and 3. While the effects on the trachea and esophagus are well described, there is little in the literature with respect to the oral and dental implications of caustic ingestion. The pathology of caustic soda ingestion and the early management are described. Three case reports are discussed and the literature reviewed. TOXICITY Caustic soda (sodium hydroxide) is commonly found in drain cleaners, oven cleaners, and dishwasher products. It is very hazardous, especially in the liquid form. 2 A 30% solution will cause full-thickness necrosis of the esophagus after a 1-second exposure in experi- mental animals. 2 Caustic soda causes liquefaction necrosis. It com- bines with tissue proteins to form proteinates, and with fats to form soap and water. These products favor further penetration of the soda and increase its solubility, leading to full-thickness injuries. 3 There is direct relationship between the quantity, duration, and concentration and the severity of the in- jury. 4,5 Ingestion of more then 60 grams, ie, 3 table- spoons, is generally agreed to be fatal. 3 PATHOGENESIS The physiopathological process occurs in stages. First is eosinophilic necrosis with edema and intense hemorrhagic congestion, 6 the tissues ranging from white, to sloughy grey, to black (Fig. 1). Ten days later, granulation tissue begins to replace the necrotic slough, and by week 3 there is fibroblastic proliferation and scarring, and formation of strictures commences. A late complication may be malignant transformation at the stricture site. 7 PRESENTATION Features on early presentation include oropharyngeal pain, dysphagia, vomiting, drooling and excessive salivation, ulcerative mucosal burns, dyspnea, stridor, shock, and skin burns. EARLY MANAGEMENT A history including as much detail as possible on the substance ingested including formulation, granules or liquid, and quantity should be obtained. A thorough examination should be undertaken. Immediate man- agement should be directed at securing an airway, relieving pain, and replacing lost fluid. Oral intake a Senior House Officer, Oral and Maxillofacial Surgery, Dental and Maxillofacial Department, Great Ormond Street Hospital, London, UK. b Specialist Registrar, Oral and Maxillofacial Surgery, Dental and Maxillofacial Department, Great Ormond Street Hospital, London, UK. c Consultant, Oral and Maxillofacial Surgery, Dental and Maxillofa- cial Department, Great Ormond Street Hospital, London, UK. Received for publication Jan 16, 2005; returned for revision Apr 25, 2005; accepted for publication Apr 25, 2005. 1079-2104/$ - see front matter Ó 2006 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2005.04.025 29

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Page 1: The oral implications of caustic soda ingestion in children

The oral implications of caustic soda ingestion in children

Fiona Ryan, MFDS RCSE (Eng),a Helen Witherow, FDS, FRCS (Eng), FRCS OMFS (Eng),b

Jack Mirza, MFDS RCSE (Eng),a and Peter Ayliffe, FDS, FRSC (Eng), FRCS OMFS (Eng),c

London, UKGREAT ORMOND STREET HOSPITAL

The morbidity related to caustic soda (sodium hydroxide) ingestion is well described in the literature. The majority

of publications have concentrated on the effects to the trachea and gastrointestinal tract, with little reference to the oral and

peri-oral areas.

Accidental ingestion of sodium hydroxideecontaining substances is fortunately rare; however the consequences can

be devastating. Three cases of children who drank caustic substances are described. Treatment included fitting splints, injecting

steroids, local surgical procedures, and the use of dynamic appliances to maintain mouth opening. Despite these interventions,

all patients developed severe scarring, resulting in stenosis of the oral musculature and extra-articular ankylosis.

There is perhaps a role for further investigation of early use of antiproliferative agents to prevent scaring, more

aggressive surgery, and long-term physiotherapy appliance use.

These patients require lifelong follow-up. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:29-34)

Ingestion of caustic substances carries significant mor-bidity, and occasional mortality. It has both acute andchronic implications for the patient, and often lifelongsequelae. Ingestion of these substances is fortunatelyrelatively rare. The US poison control centers reported26 000 cases annually, with more than 65% occurring inchildren,1 the majority of whom are between the ages of2 and 3. While the effects on the trachea and esophagusare well described, there is little in the literature withrespect to the oral and dental implications of causticingestion. The pathology of caustic soda ingestion andthe early management are described. Three case reportsare discussed and the literature reviewed.

TOXICITYCaustic soda (sodium hydroxide) is commonly found

in drain cleaners, oven cleaners, and dishwasherproducts. It is very hazardous, especially in the liquidform.2 A 30% solution will cause full-thickness necrosisof the esophagus after a 1-second exposure in experi-mental animals.2

aSenior House Officer, Oral and Maxillofacial Surgery, Dental

and Maxillofacial Department, Great Ormond Street Hospital,

London, UK.bSpecialist Registrar, Oral and Maxillofacial Surgery, Dental

and Maxillofacial Department, Great Ormond Street Hospital,

London, UK.cConsultant, Oral and Maxillofacial Surgery, Dental and Maxillofa-

cial Department, Great Ormond Street Hospital, London, UK.

Received for publication Jan 16, 2005; returned for revision Apr 25,

2005; accepted for publication Apr 25, 2005.

1079-2104/$ - see front matter

� 2006 Mosby, Inc. All rights reserved.

doi:10.1016/j.tripleo.2005.04.025

Caustic soda causes liquefaction necrosis. It com-bines with tissue proteins to form proteinates, and withfats to form soap andwater. These products favor furtherpenetration of the soda and increase its solubility,leading to full-thickness injuries.3

There is direct relationship between the quantity,duration, and concentration and the severity of the in-jury.4,5 Ingestion of more then 60 grams, ie, 3 table-spoons, is generally agreed to be fatal.3

PATHOGENESISThe physiopathological process occurs in stages.

First is eosinophilic necrosis with edema and intensehemorrhagic congestion,6 the tissues ranging fromwhite, to sloughy grey, to black (Fig. 1). Ten dayslater, granulation tissue begins to replace the necroticslough, and by week 3 there is fibroblastic proliferationand scarring, and formation of strictures commences. Alate complication may be malignant transformation atthe stricture site.7

PRESENTATIONFeatures on early presentation include oropharyngeal

pain, dysphagia, vomiting, drooling and excessivesalivation, ulcerative mucosal burns, dyspnea, stridor,shock, and skin burns.

EARLY MANAGEMENTA history including as much detail as possible on

the substance ingested including formulation, granulesor liquid, and quantity should be obtained. A thoroughexamination should be undertaken. Immediate man-agement should be directed at securing an airway,relieving pain, and replacing lost fluid. Oral intake

29

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30 Ryan et al. January 2006

should be prohibited. Gastric lavage and emesis arecontraindicated due to the reintroduction of the toxicsubstance to the esophagus and mouth. Neutralizingchemicals are also contraindicated because the reactionis exothermic and this compounds any damage.8

Early flexible endoscopy is recommended to assessthe extent of the injury. Parenteral antibiotics andhigh-dose steroids are usually administered, but arecontroversial.

Early maxillofacial intervention is essential to helpprevent oral stenosis and extra-articular ankylosis inan effort to preserve oral function. This is attemptedby fitting soft acrylic splints and oral screens as soonas possible and the use of physiotherapy devices toincrease mouth opening. The role of injecting anti-fibrotic agents such as mitomycin C into the formingscar has been used with treatment of achalasia ofthe cardia with some success. These anti-proliferativeagents act by interfering with RNA synthesis andthereby inhibiting fibroblast proliferation.9 It hasbeen shown experimentally in a laminectomy modelin rats to decrease fibrosis and does not induce sideeffects.10

Fig. 1. Early appearance of patient 1: 2 days post-injury.

CASE REPORTSCase 1

An 18-month-old girl was admitted to the pediatricintensive care unit following ingestion of drain cleaner. Thepatient was drooling and examination showed several areas oforal hemorrhage. Following elective intubation, she under-went an examination of the pharynx under general anesthetic,esophagoscopy, microlaryngoscopy, bronchoscopy, and tra-cheostomy. There was evidence of severe caustic burns to themouth, lips, buccal cavity, and larynx, and a small trachealburn at the carina (Fig. 2). Upper gastrointestinal (GI)endoscopy showed circumferential damage to the esophagealmucosa down to the gastro-esophageal junction and a nor-mal stomach. A percutaneous endoscopic gastrostomy tubewas placed at this time. Upper and lower dental impressionswere taken. Chlorhexidine gluconate mouthwash via a spongeand topical 1% hydrocortisone cream to the lips was com-menced.

Four days later lower soft acrylic mouth guards and an oralscreen were fitted under anesthesia in an attempt to preserveas much oral aperture as possible, maintain the sulci, and toprevent ankylosis. Examination under anesthesia revealed thedevelopment of thick, fibrous bands in the retromolar region.Over the following months, new oral splints were made andthese managed to preserve some sulcus depth. However,severe tethering of the tongue was already present and mouthopening was limited to 0.5 cm. Upper and lower applianceswith reverse springs were fitted, designed to give somemechanical force for the muscles towork against (Fig. 3). Overa 6-month period, bilateral commisureplasties, Z- plasties, andthe use of the buccal fat pads had temporary beneficial effects.However, fibrosis continued to re-form, restricting mouthopening and tongue mobility.

At 6 months, both microlaryngoscopy and esophagoscopyshowed a normal esophagus and trachea. Continued extra-articular ankylosis has prevented decannulation, and thepatient continues to be gastrostomy dependent.

Case 2A 17-month-old boy was transferred to pediatric intensive

care unit following ingestion of caustic soda granules. Onpresentation, burns to the lips, mouth, and tongue wereapparent. He was electively intubated and laryngoscopyrevealed black lips and tongue, but a pink epiglottis. Therewere circumferential burns involving the esophagus, and theunderlying mucosa was friable and bleeding. The patient wasstarted on high-dose steroids and antibiotics. He wasextubated, and underwent elective tracheostomy 3 days lateras there were concerns regarding his airway secondary toincreasing inflammation in the supraglottic region. A gastros-tomy was also performed.

Over the next few months he underwent numerous surgicalprocedures under general anesthesia including commisur-plasty, sulcoplasty, full-thickness skin grafting to the upperand lower labial and buccal sulci from the abdomen,commisurectomy, steroid injection to fibrous bands, and fittingof upper and lower oral splints. However, he developed severescarring leading to a reduction in the size of his oral aperture(Fig. 4), and reduced mouth opening. In an attempt to maintain

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Volume 101, Number 1 Ryan et al. 31

Fig. 2. Early endoscopic view showing intense hemorrhagic congestion to mouth, epiglottis, and pharynx.

mouth opening, a dynamic extra-oral device was fitted using aHalo Frame and elastics (Fig. 5). Initial results were encour-aging after each surgical episode, but mouth opening relapsedwhen the dynamic frame was removed.

Case 3A 4-year-old boy was referred 2 years following caustic

soda ingestion. The patient had been managed abroad prior tohis presentation. At time of initial injury, he sustainedaspiration injury and major burns of the mouth and chestwall. Tracheostomy and gastrostomy were performed. High-dose steroids were commenced. The patient suffered severeperioral contracture. Attempts to surgically release this failed.Again oral splints were placed. Following referral furthersurgical procedures were undertaken, including sulculoplasty,commisurplasty, vestibuloplasty, tongue release, and skingrafting (Fig. 6 and Fig. 7). Triamcinolone steroid was injectedbilaterally into the buccal mucosa. Finally, a Halo Frame wasfitted in conjunction with oral appliances.

Fig. 3. Upper and lower acrylic appliances with extension forelastic placement.

Again, short-term mouth opening results were good withinter-incisal distance increasing from 3 mm to 15 mm mouth,but relapse to 5 mm following removal of the dynamicappliances.

DISCUSSIONAlthough ingestion of caustic substances is re-

latively rare, the effects are debilitating. Mortality islow, but morbidity is high, with up to 33% of patientsdeveloping long-term problems secondary to strictureformation.11 This may lead to obliteration of the lingualand buccal sulci and failure of normal tongue movementwith resultant difficulty with oral hygiene, speech, andmastication. Severe fibrosis of the alveolar mucosa andsoft tissue envelope may lead to abnormal development

Fig. 4. Severe microstomia secondary to scarring in patient 2.

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32 Ryan et al. January 2006

of the secondary dentition and subsequent problemswith facial growth.

Initial management is well described with respect tosupportive measures. However, the importance of insti-gating preventive measures in the early days followinginjury to minimize stricture formation has not beendescribed from a maxillofacial viewpoint (see Fig. 8).The use of parenteral high-dose steroids and antibioticsto decrease inflammation and therefore scar formationremains controversial. However, there is a general trendtoward their implementation, as their use has beenproven in animal and in vivo studies.12,13

Oral intervention consists of construction and place-ment of custom-made soft acrylic splints with full sulcusextension as soon as possible. Fitting an oral screen alsois advisable to prevent lip contracture.

Future advancement in the treatment of the fibrosisproduced by caustic soda ingestion may lie in chemo-therapeutic research. Methods of inhibiting fibroblastproliferation in the very early stages of inflammationmay reduce scaring and fibrosis. Studies in the rabbitand rat model have demonstrated that intra-operativeexposure of 5-fluorouracil (5-FU) and mitomycin-Cdelays fibroblast outgrowth and reduces scaring.14,15

5-FU acts as a metabolic blocker via its metabolites

Fig. 5. Halo frame in situ following commisurectomy inpatient 2.

by inhibiting thymidylate synthesis and hence DNAsynthesis, and by incorporation into RNA.

Sodium butyrate has also been used with somesuccess in inhibiting fibroblast proliferation. Howeverit was observed that fibroblast proliferation occurredrapidly when treatment with sodium butyrate wasstopped, whereas a more prolonged effect on thefibroblasts was observed following treatment with 5-FU. Sodium butyrate affects the expression of variouscellular genes by affecting proteins (histones) that bindDNA. It nonspecifically inhibits cellular proliferation.15

Topical use and injection of mitomycin-C and 5-FUhave been used with beneficial results in reducingfibroblasts locally both in the short- and long-term andanimal studies on rabbits show that intra-operativeexposure to 5-FU, and mitomycin-C inhibited fibroblastproliferation limited to the treatment area.10 However,although experimental research on the dose and fre-quency of administration of these cytotoxic agents hasbeen undertaken,14-16 the optimum dose has yet to bedetermined. Too high a dose results in apoptosis and

Fig. 6. Sulcoplasty performed prior to skin graft placement.

Fig. 7. Full-thickness abdominal skin graft sutured into labialsulcus.

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Volume 101, Number 1 Ryan et al. 33

Fig. 8. The possible maxillofacial treatment of caustic soda ingestion.

failure of tissue healing, while too low a dose achievesonly temporary reduction in fibroblast proliferation withdelayed scar formation.16 The use of these cytotoxicagents in the early management of caustic soda inges-tion at the acute inflammatory stage may be extremelyuseful. However, more research is required to achievethe optimal dose and frequency of treatment. Thebenefits of use must also be weighed against thepotential long-term complications.

Following conventional treatment, all 3 patientssuffered perioral contracture with associated loss offunction. Surgical intervention with multiple Z-plasties,skin grafts, reconstruction with the buccal fat pad,sulcoplasty, and commisureplasty have been used withlimited success. These patients, whowill require severalmore procedures under general anesthesia, present asignificant difficulty with intubation due to trismus.They also have problems with swallowing and clearingsecretions due to limited tongue mobility. Therefore,they currently require permanent tracheostomy andgastrostomy. Controversially there may be a role in theearly management for radical surgical resection of thescarred tissue and reconstruction with free vascularizedtissue, as has been used with success in the treatment ofadult patients with oral submucous fibrosis. Encourag-ing results at moderate-term follow-up using radialforearm free flaps to reconstruct the defect, have advo-cated this more aggressive surgical approach at anearlier stage in these patients.17 Of course, radial fore-arm flaps have limitations with respect to size inchildren, and harvesting of sufficient tissue may not bepossible to replace the defect. There may be a role forusing jejenal free vascularized flaps.

Packaging and labeling legislation is confusing.Successful lobbying by the medical profession hasreduced the concentration of sodium hydroxide inhousehold cleaning products from a maximum of 30%to 5%. However, as can be readily seen in the abovecases, this percentage is potentially still extremelydangerous. Despite this fact, in the United States, thesesubstances are only classified as ‘‘dangerous’’ if theycontain more than 10%. The Poison Prevention Pack-aging Act requires all caustic soda- containing sub-stances to be packaged in child-resistant containers ifthey are re-sealable. However, this means that certain

products, for example dishwasher tablets, can continueto be packaged in containers that are not childproof.Gaps in the legislation like this can have catastrophicimplications.

LONG-TERM EFFECTSThe oral effects of caustic soda ingestion can be

debilitating. Severe scarring can lead to stenosis of theoral musculature and extra-articular ankylosis, leadingto microstomia and trismus. This can have deleteriouseffects on oral hygiene and the erupted dentition.Speech and feeding can also be affected secondary todecrease in tonguemobility. In the cases studied, it is tooearly to ascertain the effect of the scarring on mandib-ular and maxillary growth and on the developingdentition. However, it is reasonable to assume that thesemay exhibit disordered development.

Another long-term complication of caustic ingestionis malignant transformation at the stricture site. The riskof progression to cancer has been estimated as 10.8%.3

Andreoni et al.18 suggested that the incidence is 3000times higher in patients with caustic soda burns thanamong the population at large. All patients thereforerequire lifelong follow-up.

CONCLUSIONSOur series has shown that despite early intervention

and surgery there is as yet no effective treatment for thedamage that caustic ingestion causes. Treatment there-fore should be aimed at prevention, with all sodiumhydroxideecontaining substances kept in childproofcontainers out of the reach of children.

REFERENCES1. Anderson KD, Rouse TM, Randolph JG. A controlled trial of

corticosteroids in children with corrosive injury of the esopha-gus. N Engl J Med 1990;323:637-40.

2. Gumaste VV, Dave PB. Ingestion of corrosive substances byadults. Am J Gasterenterol 1992;87:1-5.

3. Mamede RC, de Mello Filho FV. Ingestion of caustic substancesand its complications. Sao Paulo Med J/Rev Paul Med 2001;119(1):10-5.

4. Krey H. The treatment of corrosive lesions in the esophagus.Acta Otolaryngol 1952;s102:9-49.

5. Holinger LD. Caustic ingestion, oesophageal injury and stricture.Paediatric laryngology and bronchoesophalogy. Philadelphia:Lippincott-Raven; 1997. p. 295-303.

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6. Hugh TB, Kelly MD. Corrosive ingestion and the surgeon. J AmColl Surg 1999;189:508-22.

7. Eaton H. Squamous carcinoma of the stomach followingcorrosive acid burns. Br J Surg 1972;59:382-7.

8. Bates N. Alkali Injury: Clinical features and management.London: National Poisons Information Service (London), De-partment of Health; 2003.

9. Afzal NA, Albert D, Thomas AL, Thomson M. A child withesophageal strictures. Lancet 2002;359(9311):1032.

10. Lee JY, Stenzel W, Ebel H, Wedekind C, Ernestus RI, Klug N.Mitomycin C in preventing spinal epidural fibrosis in alaminectomy model in rats. J Neurosurg 2004;100:52-5.

11. Thirlwall AS, Friedman N, Leighton SEJ, Saunders M, Jacob A,Kangesu L. Caustic soda ingestion—a case presentation andreview of the literature. Int J Pediatr Otorhinolaryngol 2001;59:129-35.

12. Bautista R, Tojo R, Varela R, Estevez E, Villanueva, Cadranel S.The effects of prednisolone and dexamethasone on alkali burnsof the esophagus in rabbit. J Pediatr Gastroenterol Nutr 1996;22:275-83.

13. Bautista A, Varela R, Villanueva A, Estevez E, Tojo R, CadranelS. Effects of prednisolone and dexamethasone in children withalkali burns of the oesophagus. Eur J Pediatr Surg 1996;6:198-203.

14. Khaw PT, Sherwood MB, Doyle W, Fran Smith M, Grierson I,McGorray S, et al. Intraoperative and post-operative treatmentwith 5-fluorouracil and mitimycin-c: long-term effects in vivo onsubconjunctival and scleral fibroblasts. Int Ophth 1992;16:381-5.

15. Ferguson B, Gray SD, Thibeault S. Time and dose effects ofmitomycin C on extracellular matrix fibroblasts and proteins.Laryngoscope 2005;115:110-5.

16. Khaw PT, Ward S, Porter A, Grierson I, Hitchins RA, Rice SC.The long-term effects of 5-fluorouracil and sodium butyrate ofhuman Tenon’s fibroblasts. Invest Ophth Visual Sci 1992;33(6):2043-52.

17. Wei F, Chang Y, Kildal M, Tsang W, Chen H. Bilateral smallradial forearm flaps for the reconstruction of buccal mucosa aftersurgical release of submucosal fibrosis: a new, reliable approach.Plast Reconstr Surg 2000;6:1679-83.

18. Andreoni B, Marini A, Gavinelli M, Biffi R, Tiberio G, FarinaML, et al. Emergency management of caustic ingestion in adults.Surgery Today 1995;25:119-24.

Reprint requests:

Fiona Ryan, BDS MFDS RCSE (Eng)

Eastman Dental Institute

Flat 20

136 Queenstown Road

London SW8 3RR

England

[email protected]