a inorganic agrd + OgeC aa 216 ‘The category of corrosive substances is broad in nature. It includes acids such as hy - ic. and and: including droxide. ate, and potassium se, and a larger variety of miscellaneous products found around the home and workplace (e.g., creosote, electric dishwasher detergents, hydrogen fluoride, drain cleaners, toilet bow! cleaners). Their chemical and physical properties vary widely, although expected outcomes after a toxic ex- posure are similar, All corrosives produce ex- tensive tissue damage. but the site at which damage occurs and the specific form of dam- age depends on the type of corrosive involved, Table 10.1 lists common acidic and alkaline corrosive products, ‘Most households contain-a wide variety of corrosive substances that invite curious chil- dren to explore, or adults to us¢ inappropri: ately. The toxic potential of many of these substances is obvious to adults. and generally, they avoid them. All of these substances are extremely irritating 0 mucous membranes, ‘Thus. massive intentional ingestions are rare TABLE 10.1 ‘Acid Hydrochloric acid Melal cleaners Muriatic acio ‘Swimming poo! cloaners Toilet bow! cleaners Suituric acid Battery acid Toilet bow! and drain cleanars Alkali ‘Sodium or potassium hydroxide Ciinitest tablets Detergents Drano erystals Drain pipe and toilet bow! cleaners ‘Ammonia (NH.OH) solutions (hair products, jewelry cleaners, household cleaners) Electic dishwashing granules Potassium permanganate ‘Sodium carbonate (nonphosphate} detergents Sodium hypochlorite (bleach) goede ollchne covaine Tn salphuric avid 1 ovalicaatd , aoubdit oui) CoRROSIVES _X¢id), electric dishwasher poe and cit yachla/ic aoxs, Witvie apr Even small quantities (in the range of | mt, of liquid or a single granule of erystalling solid) can produce severe irritation of burning toa child within a short period of time. Chit. dren have been known to suffer serious injury from corrosive ingestions that required many years of reconsuructive surgery to comect, These injuries have occurred, for example, when they drank the remaining few drops of 2 liquid corrosive from an apparently empty container that had been carelessly discarded in a wastebasket (17,46). Some corrosive substances are not gener- ally recognized as being dangerous. Special precautions are, therefore, seldom taken to keep them away from an inquisitive child's reach, or to make sure that adults use them properly. Tas-scented bowl cleaners are in this cate- -y. Tissue damage from corrosives is listed among the more common type of poisoning emergencies that occur around the home. alkali: oracids-(S4). The major reason for this high incidence among children is that 00 many of these toxic substances are stored in old. unmarked beverage containers (63) Among adults, poisonings with corrosives are often related to suicide attempts (10). ‘Traditionally the te notes an acidic: substance. capable of inflicting tissue - injury. Caiistie) describes an alkaline sub- stance having similar properties. The Federal Hazardous Substance Act of 1967 specifi cally defines as corrosive any substance thet in contact with living tissue, will cause de struction by chemical action (42). This def nition does not differentiate acids from alka Throughout this chapter and book, the tem corrosive is used to encompass both extremes of pH, except where specifically indicated. Some pt moons . such as lemon ie Ss bled, shing, Pheer, 2» pe we aodCORROSIVES and carbonated beverages, can have a strongly acidic pH, but not be corrosive. Acidic com- pounds include 2 wide variety of tex. hydrochloricimuriat ) and organic (e.g... Oxalic, tartaric, ) acids. Even though all acids can imilar tissue damage, they differ ia intensity of damage. Not all acids are common ctises of poisoning. Nitti and phosphoric acids, for examples, are less commonly en- countered. Also, not all acids are suicieatly corrosive to be of major toxicologie concer, Acetic and tanaris acids exemplify these Mechanism of Toxici Corrosive damage is caused by direct chem- ical action on the involved tissue. Acids dena, Bre ‘tissue proteins. The resulting lesion (2uses cell death that is represented 25 coagu- lative necrosis. Consequently. both structural Sad enzymatic proteins are denatured but cel- morphology is not grossly interrupted. In ition. a tough. leathery scab (eschar) forms. which delays futher corrosive damace 2nd helps reduce systemic absorption. Thus, mage. especially with small quantities of cid, is often limited to local sites of injury tthe skin or gastrointestinal tract. Characteristics of Poisoning “After an acid ingestion, intense comosive 2 to the oral mucosa and esophagus oh ves is 2 function at nue mere iela ptoaen eons Qu ttle resents re asst stunt Gamage may vary depending on these eos une ea a ay recipitated blood may be found 2n the stomach, and is described as having . Damaged gast slands are usually not regenerated, but are re. placed by a thin epithelial layer. Gastric moti. ity is disrupted also (50), Ingested acid normally passes through the sophagus quickly and causes litle damage to this area. Studies have shown that esophageal damage occurs in as few as 6% to 20% of all acid ingestions (10.24). This is not to imply ‘hat significant damage could not result if acid were left in contact with esophageal tissue, For example, 30 seconds contact with 9% sul. furie acid solution causes coagulative necrosis in vitro (2), The extent of esophageal damage isa function of the volume of acid ingested. its strength. and length of contact. This is why emetics are contraindicated in acid i because they increase the contact likely to cause gastric necrosis and perforation ‘than weakerones, such as hydrochloric. How- ever. chronic gastric problems have been re. Ported more frequently after hydrochloric acid ingestion, rather than sulfuric acid, This may be duc to the severity of damage that occurs from sulfuric acid ingestion. Poisoning vic. tims are more likely to die shorly after inges- tion of the latter, ‘The premorbid condition of the stomach is a fairly good predictor of the site of gastric injury. In patients with a! before acid ingestion, toxic For those victims with a SS well as a wide variety of other toxi involvement (50). Table 10.3 lists major clinical manifesta- tions that have been reported for acid and ‘ytt eee 28 CORROSIVES TABLE 10.3. 9 Route of exposure Signs and symploms ingestion Severe buming pin in mouth, Inroat, ‘and abdomen vomiting, possibly blood-tinged Diarthea bloody. mucoid Stains around mouth Dysphagia Drooting ‘nat ion Pumonary edema Frothy spuum Moist rales : Hypotension Homoptysie Oyspnea Siaiing of skin Buming pain Conjunetvis Comeat destruction Pain, lacimation Pnotephobia Inhalation Dermat alkali poisonings, according to the route ‘of exposure. An eacellent review of the pathogenesis of acid toxicity is provided by Penner (50). Management of Poisoning Poisoning by acid, whether localized or temic, is a medical emergency and treatment must be initiated at once. Unfortunately. though reports of acid ingestion and resultant toxicity continue to appear in the literature, there is an insufficient number of controlled clinical studies that identify the best therapeu- management. The rules of treatment that follow are based on clinical experience, and do not always receive universal acceptance, Skin or Eye Contact Contamination of the skin or eye with acid must be given immediate attention. The area i 0 A 15-10 20- min wash is usually necessary to completely neuiralize and remove all residual traces of contaminant Contact lenses. if present, should be removed 10 avoid pro. Tonged contact of acid with ocular tissues, ‘Avmild-soap solution may be used 10 wash i fer washing, no cream, ointment, or dressing of gay kind should be applied to the affeced siea, These may cause further tissue injury 0 . an already damaged area, and make it difficult for emergency personnel to remove them without inflicting additional ieritation, trauma, and intense pain. Ingested Acid Management of a corrosive acid ingestion is outlined in a decision flow chan, Fig. 101 The immediate concern for acid solutions that th co . Antacids may be given as demul- cent, Under no circumstance should carbon ated beverages or sodium bicarbonate bs used because carbon dioxide gas is released. which quickly distends the stomach wall. Distenton imposes a greater chance for perforation of already weakened tissues and may hasten the time for gastcie emptying. If the ingested cid was concentrated (mineral or organic) itis ut” likely that the patient will be able to s¥ allow. and dilution becomes a mute point recut- ‘spontaneous ive it emesis is common enough with comes gestion. If emesis is prolonged, anveme® may be necessary to control vomiting. and fluid « may s replacement to correct circulatory shoe be necessary, ; otCORROSIVES Corrosive (Caustic, Acid) Ingestion 1 Sosatie ingest IMMEDIATELY: Dilute REVIEW HISTORY: Clanty ingredients ol pro Onterming i exposure OETERNINE PATIENT SYMPTOMS: Any broauet concentration sulfici od exposure potentially toxic oF ©F patients symptom | fet to produce corrosive effect ‘Unknown mute coanicostésoI0 THERAPY + Ingested maltrial rigate exposed suraces a5 el lnltation, dysphagia, excess eroding cious burns. uct. Determira cancentration. product foo cute 1008 corasive cr exposure cieany nootone and ESTABLISH AIRWAY CONTROL AND IVICP SUPPORTIVE RYE FOR SUP MEASURES AS NECESSARY. EXAMINE. ESOPHARYNX ——- Fousmuerons brede! denis ramey eae! | REFEa FOR escPHAGOScOPY | excnacononycamot be tsopragorcoy ean te | Petomed wit 2 nous Berlomed ton 3 Rows i i IMATE ConficasrEAoID zucaney—peesronm SSorwscoscorr peTFoau 1 sOPY —— ESOPHAGOSCOPY : on notuns HD ENOGEEOPY | i Yond our of the stomach as completely as Possible to reduce the risk of heat formation when the lavage fluid is added. Then. cold Water or milk can-be used’as the lavage fluid, followed by antacid washes. The tube should be repositioned frequently to assure that all aces of acid have been removed. : Surgical resection. of damaged. tissue is Sometimes advised. It is not always possible (0 easily identify the damaged area and after fesection, leaking may occur at anastomoses. When tissue has been damaged beyond repair, itis usually removed surgically (17). rt - We Antibiotics should be used only if infec- tion occurs. The value of corticosteroids after acid ingestion is questionable because Stricture is less common than alkal In facts injury may continue to develop over 90 min ot longer (52). The patent must be Closely monitored during this period and Ue "ROVIDE SUPPORTIVE CARE AND FOLLOW UP AS INOICKTE: ciation.) ment continued, even in the absence of per- ceptible or worsening symptoms. “onmoveny of ita: Frequently, while managing a victim of acid ingestion, the corrosive agent is treated by di- lution but damage due to exothermic heat pro- duction is ignored. This results in the follow- ing dilemma: To dilute (neutralize) o¢ not to lute—that is the question! Considerable heat is released when strong acids conie in contact with water or antacids. For example, 53. mL of sulfuric acid, 91.6% by weight, mixed with 34 mL of water results in an al- most instantaneous solution temperature of (50). When i The resulting diluted solution, how- ver, is still strongly acidic and highly corro- sive (40.220 CORROSIVES Moreover, heat is released when acids react ith antacids, The heat of neutralization of | mole of sulfuric acid agnesium hydrox- ide suspension (80 mg/mL) is about 40 kcal. X (0 mL of antacid would be required to neutzalize the acid, resulting in a final mixture temperature of about 62°C (50). Hydrogen fluoride SpiieTENETED induces damage that differs from other corro- sives, and it is described separately. Hydro- fluoric acid is a widely used industrial com- pound that exists as an extremely corrosive, colorless volatile liquid. Its commercial uses include glass a fer chip etching, and cleaning metal. and production of various syn- thetic chemicals. Some rust remover’ agents contain hydrofluoric Industrial smoke often contains high levels of HF be- cause it is evolved from buming coal. The exposure limit for HF is 3 ppm. Sodium fluoride is a soluble salt that is used as a rodenticide. insecticide. and anthelmintic for swine. As expected. fluoride salts are more commonly encountered around the home than HF, and it is this group of products that is responsible for most acute fivoride poison- ings (47), Mechanism of Fluoride Toxicity Hydrogen fluoride causes deep corrosive le- sions on tissues. It has 2 high affinity for water and rapidly hydrolyzes to hydrofluoric ac, All fluorides are protoplasmic poisons. Fluo- rides bind many cations. most notably cal- cium. The binding of calcium results in the arrest of many cellular enzymatic procesies ‘and decreases the coagulation process. Al- though many believe that the cardiovascular collapse associated with fluoride toxicity.is ‘due to the precipitous ‘others support a theory involv. ing fluoride-induced potassium efflux from cardiac cells (43). The neurologic effects of fluoride toxicity are related also to the calcium-binding effect of fluorides. Toxic symptoms from sodium fluoride may appear after ingestion of as little as 200 mg. The lethal dose may be closer to 4 g (EI). 1 preceded by intense gastrointesti nal symptoms (Table 10.4). hypotension. and convulsions. If death does not occur immedi- ately, jaundice and oliguria may onset later. Chronic exposure has: produced skeletal fiuo- sosis (i... osteosclerosis. periosteal apposition of bone. and calcification of ligaments and Joints) (5). Management of Toxicity Fluorides are rapidly absorbed afterlinhala-” Quick treatment is necessary if the fluoride acute fluoride poisoning a sorbed is dependent principally on the solubi ity ofthe fluoride, and the duration of expo. ‘sure. Sodium fluoride, which is very soluble, is readily absorbed 75% 10 90% (43). : Knowledge of the relative solubility of vari- ous fluoride salts is beneficial in understand- ing one of the mechanisms for treating fluo. ride toxicity. a 43). As a result, abso ption is limited, pybrotlaaric a2, expawre vet mm ne intoxicated patient is to survive, Fluoride is TABLE 10.4, Characteristics of luore OO Leeaton Signs and eynpions Gastrointestinal Abdominal pain, nausea. vomiting, diarthea, salvation Neurologic Parosthesia, hyperactive ellexes. ‘lonic-tonic convulsions, positive Chvostek’s sign. ‘muscular pain and weakness teed Hypocalcemia, hyposiveeria Cardiovascular! Hypotension, respiratory respicatory stimulation followed BY epression € |CORROSIVES best inactivated by convertin, ble form, e. HF bums of g it (0 an insolu- + calcium fluoride. Treatment of the skin consists, first of all, of decontaminati ‘alcium fluoride. a rela- Ronabsorbable complex. and temic toxicity, thus. reduce syst n of plasma calcium or to Aggressive fluid replace. cessary to i teract losses from bums, g. and diarthea and to counterac: hypocatcemic-induced vasodilation. Whitford don (0°) demonstrated in rats thar admit i 'm bicarbonate, to induce meta- is, reduces fluoride toxicity replace it (60,62), ment is ne Boric Acid, Atone time boric acid (HBO. m 1) Was recom: ‘nded for more than 40 aw i medical uses. [t is ‘ater and is formed ‘into clumps, org Put where insects congregate, He, “8+. 35 sodium tetraborate) are widely will probably not decline. Ingestions of bor ric acid solution are re. Ported in individual Is who have acci Nn of baby (14,15,63, ic. Its greatest danger Hage MS where it concentrates. such ac the The fatal dose in adults is estimated, 12 be 15 t0 20 g. and in infants 5 io 6 g. but been fatal (63.68), a8 litle as one gram has After exposure, the thar iimmgaaon Me Palms. soles, and buttocks, The immediate cause of death is usually CNS de. Pression. If the patient sucviv. soning event, complicati fay necrosis, cerebral may appear, whe nee BORGER Tate 6ESO%6 OF thee who ingest a toxic d 7 . ingestion, gastric ev; fons. such as hepatic ‘dema, or renal failure, Skin: erythematous ("boiled labst desquamation, excoriation Lethargy, weakness CNS* depres Cardiovasc Jaundice Renal tailure “CNS. central nervous systems222 lod is or | hemodialysis (3.69). esas, one of the oldest disinfectants/deodorizers, is still used alone, and as an ingredient in many commercial products. Phenol is a significant cause of poisoning. Intoxication can occur after absorption ‘through intact skin Most poi- sonings are accidental. Phenol has a suongly characteristic odor and its presence can be readily detected on the breath. s (22). It is a cellular depressant and causes a variety of signs and symptoms (Table 10.6). ‘Death immediately after poisoning usually occurs from respira- tory depression. Survival beyond a day or two is often met with renal damage that eventually leads to death. Although esophageal stricture is rare, it is a long-term complication that may develop. The adult lethal dose is estimated at 10 to 30 g (22). Immediate emesis or lavage after phenol ingestion is important to consider. but are con- traindicated in esophageal injury. Ege whites, milk, or gelatin solution, which serve BF Pro - gen P (carbolic acid) poisoning ‘Nausea, vomiting, bloody diarrhea, abd cramping ‘Sweating (protuse) Cyanosis CNS stimulation, hyperactivity, convulsi US siewtaton, hyperactvy ons, followed ‘Stupor Hypoension Increased respirations tollowed by ss oe y depressed Pulmonary edema, pneumonia Esophageal stricture Homoiysis, methemogiabinemi Jaundice = Rona failure Cardiovascular collapst Ce F collapse, shock CORROSIVES tein sources to interact with phenol remaining in the stomach, may be given. Activated char- ‘coal, followed by a cathartic, may be preferred to ipecac-induced emesis or lavage in decon- tamination of the GI tract and preventing sys- temic absorption of phenol a |BpHof 11-5 orhigher. The label of an alkaline product is sometimes misleading when trying to determine the degree of alkalinity. A re- ported pH value of a product that is intended to be diluted before use may refer either to the concentrated or diluted form. The user may be misinformed if the label is only casually read. Careful reading of labels is always necessary. ‘One way to report the degree of alkalinity of a product is to list potency as a percent of Some household alkaline products contain this information. and 2 con- centration of sodium hydroxide greater than 1% can cause tissue dumage (49). The degree solutions. concentration is more critical than volume. In the United States, the greatest number vin? of injuries from corrosive substances involves ochygnasis — pyrenietign gh comen and ingestion of alkali, rather than acids. The rea- “& LE 10.6. CharScieristes of pheno! S018 probably related to the wider availabil- of alkaline household products. Also. the ‘oxic potential of many alkali products is not universally recognized, Although the term “acid’* is a common household term, “al- kali" or "base" is less common. As a results alkaline substances, such as dishwasher deter- gents and nonphosphate detergents, are stored carelessly in areas where children have €25Y access to them. marily to the esophagus th pasttic involvement reported in about — §. Seventy-five percent of all caus: tic injury tothe esophagus im children undet 5 years results from sodium hydroxide. Eigh'y" rable 10.2)»CORROSIVES a © ao 10: CTT Solid Fic. the severity of eso, 16d Gearee burns. The causative agent was known 1 three percent of these victims are under 3 Years, and 62% are males (6). Gastric acid is not suticiently strong or present in sufficient quantity to neutralize even small quantities of strong alkali, The physical form of an alkaline substance ‘may determine the site and severity of caustic damage, ‘Fig. 10.2). To illustrate, solid crystal- Jine forms are Not easily swallowed, nor are clbey readily spit out unless taken with lots of ‘fluid. They adhere to the glossopharyngeal. | and proximal esophageal mucosa to fatise deep, irregular painful bums (28). Be- “SSause of this adherence proximally, less dam- © is apt to occur distally. Liquid alkaline estances, on the other hand, pass freely Hough the esophagus and are considered to More hazardous (22). Tissue damage will re diffuse to the esophagus, as well as ne stomach (10.34.44. 52). Suicidal adults ingest alkaline products along with liq So that they can ingest larger quantities. ‘sophageal and gastric damage. there- Ge ypttstic bums cause much discomfort (ee Table 10.3). 4 lack of dysphagia does RO(necessarily mean that esophageal injury is ia Type of Caustic Agent 10.2 Relation of phageal injury tothe type of caustic agent ingested. Solid bars represent first-degree burns, hatched a A 7 7 'ars second-degree bums, and stippled bars third in 55 of 60 children with esophageal injuries. (From Unknown absent. and early management must still be initiated. Examining the mouth often confirms that an alkali substance was ingested. Some. times a probable diagnosis can only be made from the child's obvious distress, along with discovery of an overtumed or partially emp- tied alkaline-product container, Mechanism of Toxicity li is saponifica uh‘alkaliits saponif damage resulting a is enhances its pene- tration into tissues (58). Consequently, sys- temic complications are common, Esophageal damage after alkali injury oc- curs in stages (61). Initially. in the acute phase. which manifests within 3 to 5 days. there may be intramucosal or transmural dam- the periesophageal tissues and the mediastinum. Inflammation, ‘ee =i } ——. i i ‘edermx,’and congestion occur throughout the entire esophageal wall. In severe cases. the esophagus may perforate. The second stage occurs over the next 5 (0 12 days and is characterized by liquefactive necrosis resulting in intense inflammation and edema. This is the point at which the esopha- geal wall is most susceptible to ulceration, bleeding, and perforation. To illustrate the po- tential for damage, 2 10-sec exposure of rabbit esophagus to 7N (22.5%) sodium hydroxide produces necrosis in all layers of the tissue (31). This phase is associated with deposition of fresh grariulation tissue, which is eventually replaced by collagen fibers. ‘Afier the acute stage, healing and scarring begin. After 3 to 4: weeks, contraction and stricture are seen. Esophageal strictures are the most frequently observed complications of alkali ingestion. The usual incidence of stric- tures with granular ‘or solid lye ingestion is 10% to 25% compared to approximately 100% for liquid lye (6.28). ‘Management of Poisoning Skin and Eye Contamination ‘Skin-and. eye contamination should. be ‘flushed immediately and thoroughly with wa: least-15 10 20-min, Some treatment regimens suggest that severe alkali buns should be irrigated for at least 8 to 24 hr (38). All contaminated clothing and jewelry, and contact lenses if present, should be removed. ‘As with acids, no medication should be placed ‘on the lesion. Strang soap should not be used during or after the rinsing process, Ingestion of Alkali Ingestion of even a single granule of solid alkaline material or a milliliter or more of a liquid alkali warrants emergency consultation by qualified medical personnel. The extent of damage cannot be estimated from presenting symptoms. If a victim displays burns around the mouth and lips, then moderate-to-severe i ee 24 CORROSIVES toxicity may be suspected. nd the that ph por occurred. Refiex swallowing of iritatin fubstances is so quick that the substance ‘mouth only for a short period. ‘As with acids. the treatment regimen for alkali ingestion is not standardized, and there are controversial points of view. Many precau- ‘ons must be Kept in mind, For example, Emesis reexposes 1¢ esophagus to the corrosive. Moreover, there is a possibility of aspiration of contents to cause severe edema, inflammation, ulcer- ation of the glottis, and aspiration pneumo- present in the itis. ut is occasion ally performed only for large volu (50), Also, there is no great advantage t0 usi activated charcoal since it adsorbs caustics poorly. and interferes with the endoscopy pro- cedure used to determine extent of injury (29). ‘As a means of terminating exposure. dilu- tion or neutralization after alkali in minimize damage to the mouth. esophagus. and stomach. Those who disagree with this approach con- tend that damage is instantaneous. and the re- sulting exothermic reaction increases the risk of further damage and vomiting (29.50). Also. itis difficult to persuade a small child to drink TABLE 10.7, Composition of Drano crystals and Clinitest tablets Orano ery Sodium hydroxide 542% Sodium nitrate 30.45% tele shavings: 4.40% Inert substances Cinitest tablets eee Sodium hydroxide 5 : fe 2325 m9 Sodium carbonate 20.0m9 eae 20.0 mg Circ acig eee eee sea > vonaymino aj Baad wept™ 0t py deers utth >, pbestbyalizorty™ ie aatweCORROSIVES 100 80 80 70 60 so 40 30 20 10 cr 130m Ono Gry Degrees Centigrade 30 60 FIG. 10.2. The n (From ret. $5.) anything after ingestion of a corrosive because of the pain and tendemess experienced, Rumack and Burtingion (33) examined the neutralizationidilution question. In a series of in vitro experiments, a weighed quantity of crystal Drano or a Clinitest tablet (Table 10.7) was ex- Posed to water, milk, lemon juice. of vinegar. The resulting temperature was determined and Plotted as shown in Figs. 10.3 and 10.4, Itcan be seen from these figures that the choice of diluent makes a difference in the amount of heat formed and its rate of forma- ion. Milk appears to be the diluent of choice 100 ntest? Tabet Fa Te ena 90 Ovgrees Centigrade 225 I Drano 1nd 1 See af Exch Owvent 90 Time~Seconds 120 ‘eat of reaction that occurs when various diluents are added to Crystal Orano, for Clinitest tablets, Heat production was slower when milk was added to Drano. It is difficult to stare with certainty that milk should be used to dilute Drano erystals since the temperature at the end of 2 min is similar as with the other diluents. Diluted solutions of vinegar or lemon juice (neutralizing avents) Produce a significant increase in temperature, as compared to milk, and are not indicated in the management of ingested alkali. lf swallowing is possible, antacids and dairy Products, such as ice cream and milk, are per- missible. As long as the individual can swal- FIG. 10.4. The heat of reaction that oc- curs when various diluents are added to Ciinitest tablets. (From ref. 55.) 120 &low. all medications and clear liquids can be given orally and the diet increased progres- sively as tolerated. Lesions may develop for 24 hr or more after ingestion. Patients must be observed closely’ for several days after ingestion. Endoscopic exami- nation has proved to be useful in assessing esoph- ageal damage after alkali ingestion (71). ‘When surgery is indicated it must be per- formed quickly. Early indications for surgery include mediastinal drainage after acute perfo- ration, tracheostomy for laryngeal edema and respiratory distress, or a gastrostomy for feed ing in acute severe injuries or extensive chronic strictures (6). Occasionally the esophagus will require surgical reconstruction. Steroids and Antibiotics The rationale for use of glucocorticoids is to reduce fibrosis and esophageal rupture after 220 Cumnusty cd alkali ingestion. It is based on animal studies ids within the first ¢ alkali damage has been to decrease collagen formation, fibro. plasia, and subsequent formation of scar tissue and stricture (20,64). Steroids are probably agus, and are questionable in neating third degree burns (8.23,25,61.65). On the other hand, steroids increase the possibility of infection, Antibiotics may be administered to reduce further complications from microbial invasion (45). Therapy with both agents must be initiated quickly to be effective. Some stud- ies have shown steroids to be ineffective in decreasing development of esophageal stric- ture after ingested alkali in children, and de- velopment of stricture is related to the severity of the initial corrosive injury (1). possible ingestion IMMEDIATELY: Ditute ested material. rigate exposed surtace. DETERMINE NATURE OF PRODUCT seus aon Caton Oateroent Ronionic detergent sater or Bleaching = Ammonia 1crd OF argent Quatemary Ammonium Compounds ‘Agent? awraria SWGOOM aa, (Hypochlorite) Product (Caustic, Comosive) DETERMINE AMOUNT inoesreD DETERMINE PROOUGT CONCENTRATION |. Nentove ———_potatay amaunt toxle amount household industrial strengt® Wun eaves gm) imal sige IoUCE emesis OBSERVE FOR SYMPTOMS f co rTEATAS POSSIBLE CORROSNE, we IG. 10.5. Emergency management outlin |ROSIVE MANAGEME! Flow chart illustrat ting the steps involved in 255655, sion ol the Soap and Detergent Ascociatony? 7 © NUseHOIS product. (Reproduced wi permis:CONROSIVES Hrnnionge iy Ny ’ enslng the sive af the HAN VEE A PevTeaE A He ais i even lly WhleHiOW ANE esnp lage Lue, Fur vets SHIEH, heigicnage May He Fequiredd aver many years Hie 1009 presents a Haw chant shat has Wa16% HOPHHTNE AEEHNINOS anil juncture in WAIABEHIEOE AF caRHANIVE jabennInys, Thin Way be ella when eH Hla alge Vie” AHN EA WW iy ehagner SRECTIG MAGMA COMROSTVES abn Batieles The tiie af sriall, Har disk shaped hasan) Hateries hi inereaked ay he uve ar canierts FaIEIAIINY. ane AEE electronic gaduetey has. WEEE WE HeeEnE yeuy The ynenence af NiWeNFian AT thee haneries hay increased pro (unttanately (4M), One earinate pots the nuns Ver 91040 490 tnyestions aanually in the United States (36). A suinmary af LE haery Nieatiane aver an Heamauth perind revealed the Ineation af the haneries hetire Ingestir ABT, Lanes ae discanibend; 14%), ave prod: Woks wand AMG, Hn the: manifueiver's packaye. Hearing ait baneries were nash commonly bwallawed (44.4%), wad LA buleries were in Bestel hy childven after they femaved them on ein avn hearing aids (87) gamated nsisting of an ama FG. 10.0, Gries wuntion al a miareunie naide button away cat cor ‘ ay . al une Onl Hauler enw arate, ghily compacted ete Ao Aalto at aura, atl» plat. QrOnTIN ETT ) Wri wlan Kap untae Nolarrally valle CORDA Webi a7 These haneries are constructed of a cathode a0 iW) anole esp) Separated by an elentiods. soakedt fale (Fig. 10.6), Most ofven disk hat- Heres aie passed Uuough the Gl tact without Newent (8,97), However, hatteries have been Knowle to become lodged within the esophagus aid teak ina the GL tract, resulting in severe Corrosive loxicily and, sometimes, death, isk batteries may contain oxide salts of Mercury, silver manganese, zinc, of cadmium: or luhiuin hydroxide. They also contain con- enurated polassium or sodium hydroxide as major ingredient In vitro studies have demonstrated that when the biteries come in contact with a Moist environment they quickly begin to re- ‘ise their coments. In une study, batteries were Immersed in normal saline in a 10 to 151 (volvo) ratia (68). The initial pH vas 1.0. Ihubbles were soon nated to emanate teom Whe hatteries, nid a black-brown precipicate formed, The solutions quickly became alka- Hine and achieved a tinal pit beeen >10 Wo > 12 by 25 he, Even used or discarded (uncharged) batteries produced a pH af 8 4, accompanied by a brown-black precipitate. 7,64). Activated cliatcal is not indicated because of the small but real risk of airway absteuction (36). Ie is ‘also uniformly unsuccessful as is ipecac- induced emesis (37), Catharties ae advocated {o hasten removal of batteries that will reach lectrolyte- waphite cathade, an él te all amained ina steel can coated with crnaily with gold and nickel. &the stomach or beyond, and H.-antagonists and antacids are advocated to help reduce gas- trointestinal bleeding. Benefit from these agents remains unproven. Metoclopramide may be given to hasten removal of batteries that demonstrate a persistent gastric position. The vast majority of battery ingestions are be- nign and do not require endoscopic or surgical intervention. ; Cop Cite Soaps and detergents constitute the largest class of household products found in greatest ‘quantity around the household. P Very few symptoms. other than upset storsach, will be experienced. lo The ‘most prominent symptoms produced by inges~ tion are usually nausea and vomiting. althouh diarthea can appear and may become severe. “Although the same general statement about emetic action of soap is true, stion of Strong detergents may cause a variety of reac- tions. depending on the specific product. De- tergents contain wide variety of inorganic and organic ingredients, among which are sur- factants and wetting agents. Surfactants may bbe anionic, cationic. of nonionic. fuce local irritation, whereas cationic deter- tenis may incite severe ieitation and possibly fects. are added to detergents 10 improve cleaning-détion of the product. usvally by in- setivating calcium and other minerals. Com- mercially used builders may include carbon- es, silicates, aluminosilicates, and sulfates. ‘The use of phosphates as a builder was popu- lar in previous years. Phosphates have been sed in recent years because of the largely replace concern about their effect on the environment. it may produce ‘oral and gastrointestinal burns (35)- ‘Other ingredients including whitening agents, fabric softeners, suds-contallins agents, and enzymes are frequently added. These are usually of no toxicologic concern. Granular soaps and detergents generally have a low order of toxicity. The exception is automatic dishwashing machine detergents, which are highly alkaline and produce como sive action (30). ater though gastric irritation may cause a gre Addition of erally incidence of nausea and vorniti “antidandruff agents” to shampoos increases the products’ toxicity. Id involve im ( ‘Spontaneous emesis should be expected; induct 2 Garren iighly al TABLE 10.8. Emetic action of household cleaning products in dogs eS for emesis Products Heavy-duty granular laundry detergent Lightduty liquid detergent General purpose liquid household cleaner ‘Bleach, quid (sodium hypochlorite) Tollet soap. ‘Mean emetic dose ‘Mean time (oa) 002-0.05 1-4 03-15 15-45 04-1.0 05-10 028 1-2. 50 0-60 30-50 Sootgeces—& CORROSIVES Liquid hard-surface Cleaners Pine oil or petscleum distillates quantity of such substances contai Products is generally of Ij their chance for being aspir is teal. Consequently, viet of these Products should Possible and not be made often contain though the ined in these. le toxic concem, ated during emesis ims who ingest one be kept as quiet as to vomit. (Refer to Ammonia, oven cleaners. and drain clean: Sous highly alkaline and extremely cone. sive. Ammonia solution (houschold. smn nia), per se. ranges fro: m 5% to 10% ammonia, an industrial strength solution 50% is also available. Ammonia wide variety of products, tion is seen on all cells. solutions must be treat ‘caustic substance. Inhalation of ammonia gas produces irrita- 'on of the upper respiratory tract, often caus- nS cough, dyspnea, and pulmonary edema. ‘Ontact with skin or eyes produces severe Pain and corrosive damage. Ingestion of am. Mronia solution resembles that of a typical al- taline corrosive. Treatment is the same as for Other alkaline ‘corrosive substances. A distinction must be made between ammo- nia. per se. and products advertised as having ammonia. These latter products contain small ‘Uantities of the substance and are usually of little toxic concem. 3% Most bleach products are solutions of '0 6% sodium hypochlorite (NaOCI in water. greater than is used ina and its corrosive ac- Ingestion of stronger ted the same as any ti it 229 which makes Bleach ingestion pro. imitation and comesion of mun Sous membranes with pain and infammatic ion, = Amount of bleac Spontaneously ere toxicity is often studies examined stion of chlorine bleach Bo esophageal strictures or perfo- stion includes et of cemulcents, such ag Neutralization with acidic Sc-induced emesis are con- Hypochlorous a when sediu with hydroch sacs ns, hen absorbed in small quantities, Fay itis betiered by the blood. However, iy is extre {© mucous membranes is and the GI tract Bleach should not be mixed with stro 2 Scidic of alkaline cleaning agents in an ec, Wented area, although this is apparently com: ‘mon practice in some houscholds (see the eave Study at the end of this chapter). When bleacy, Teacts with either acid or alkali. as shown in Fig. 107, either chlorine or ciloramine gee may be released. Both can cause lacrimation and irritation to the mucous membranes and Fespiratory passages if inhaled in sufficient Concentrations. In high concentrations, both Could cause asphyxiation. Some bleaches, especially the powdered Ones, contain other oxidizing agents, such as eroxides or perborates. When present, inges- tion of these types of bleaches must be treated more vigorously. ‘The toxicity potential for iodine may be overstated and overemphasized. fare (13) Its doubt thatthe quantity eo ained in 0.5 t0 1 ounce, which is the normal quantity found in most homes, would infict | | ij |; (OC!) ‘Strong ana = NH,CI’ = Strong a wagyrenene: f we el terleramne) serious injury. Mast fears of iodine or reasons for its bad image probably resulted from use in previous years of the 7% tincture, which is no longer used except in veterinary practice. odine is direct protein precipitant that is es, In the inces- line, it is converted to the less toxic iodide, and rapidly deactivated by food in the Gl tact. . Furthermore, it causes 9 strong vomiting re- flex, which removes much of the poison. All of these factors help minimize toxicity. Major effects after ingestion of iodine (2%) involve the GI tract, with nausea, vomiting, diarthea, and gastroenteritis being paramount. is. and other parent. Ingestion can quickly recognized by the appearance of brown stains in the mouth or on the lips. oF by brown-colored vomitus. Jodine ingestion should be treated to reduce A starch solution (1% to 10%) will absorb iodine vialasagen ih le se we Then. a 1% t0 5% solution of sodium thiosul- fate can be instilled to conven remaining io- dine to iodide. ic id be administered as quickly as possible to reduce the chance of esophageal fibrosis, a complica- tion that may occur later. which causes pulmonary edema (13) Quaternary Ammonium Compounds L Quaternary ammonium compounds (QACs) are cationic surfactants used in a wide variety of products, such as disinfectants, bacteri- cides, deodorants, and sanitizers. QACS are all potentially toxic. Toxicity varies with the specific compound, the concentration of prod- Cc CORKOSINES or strong aval nao i of chlorine or chi. sqeemine 025, uct. dose ingested, and the rate of adminisiza. tion. All QACs produce similar symptoms through a similar mechanism. Concentrations above one-percent produce superficial necrosis of mucous membranes, Causing Gl tract erosion, ulceration, and hern- omhaze. Edema of the glotis and brain has been reported. as well as damage to the heart, liver, and kidney. ‘All QACs cause disinfection only to chemi- cally clean areas. In the presence of any trace of soap, they are inactivated. Thus, soap is 8 Suitable means for preventing damage from QAC poisoning, from either skin contamina~ tion or oral ingestion. Ingestion of a clesning agent greater than 5% to 10% of QACs should be ueated as 2 corrosive alkaline ii iticn. SUMMARY There is a wide varieny of acids and alkali that have the potential to cause significant cor rosive damage. Although acids and alkali dif- fer in their pathophysiologic effects. precau- ions against exposures are similar. Table 109 lists some common household products that are rated based upon their relative toxicit Case Studies CASE STUDY: CORROSIVE ALKALI TABLET INGESTION History ‘A.38-year-old diabetic woman sought med ical atention after ingesting 75 Clinitest > lets (see Table 10.7) approximately one week previously. She was nauseated immediately after ingestion and vomited everything she © or drank. Still, she did not seek immediate medical attention. In the emergency room she