Emergency management and sequelae of acid ingestion

CONCEPTS, COMPONENTS, AND CONFIGURATIONS

Emergency Management and Sequelae of Acid Ingestion Larry A. Scher, MD Kimball L Maull, MD Richmond, Virginia

Because it causes immediate pain when taken into the mouth, strong mineral acid is less often swallowed than corrosive alkali, but psychotic, inebriated or determined individuals may consume lethal amounts. Burns of the oropharynx and glottis may lead to asphyxial death. Acid has only superficial effects upon the esophagus but, upon reaching the stomach, flows along the lesser curvature, induces pylorospasm, and pools in the distal antrum. Pyloric stricture is the most common late complication among survivors. Due to the rapidity with which acid acts, local and systemic therapy must be expeditious. Neutralization and demulcification are recommended but no time should be lost if weak alkali is not readily available. Lavage has limited applicability and induced emesis is strictly contraindicated. Aggressive intravenous fluid therapy, antibiotics, and opiates for pain are needed in most instances. Immediate gastrectomy and steroids are controversial but operative intervention is eventually required following most significant ingestions. Scher LA, Maull KI: Emergency management and sequelae of acid ingestion. JACEP 7:206-208, May 1978. acid ingestion, emergency care; poisoning, acid.

INTRODUCTION Of the over one million poisonings of all types that occur within the United States annually, 1 the ingestion of corrosives, though small in number, accounts for significant morbidity and mortality. 1 Corrosives, while ingested accidentally by children and alcoholics, may be consumed in large amounts by psychotics or those intent upon suicide. The management of such injuries has been difficult to categorize due to inherent problems in quantitation, vagaries in the postprandial state of the patients, and variations in the time from ingestion to treatment. 1 Further confusion results from reporting alkali and acid ingestion collectively as ~corrosive injuries. ''2-4 Since the differences far exceed the similarities, ~ in the following report the distinguishing features and emergency management of acid ingestion are emphasized. Alkali ingestion is cited only for clarification. ACID INGESTION Toilet bowl cleaners, disinfectants, automobile battery acids, soldering fluxes, and other commercially available household substances contain the potentially lethal hydrochloric, sulfuric, nitric, or phosphoric acids (Table 1). The severity of damage from their ingestion depends upon a number of factors, of which the most important are the concentration of the chemical and the duration of exposure. 3 Based upon the concentration of these acids as they are usually produced, sulfuric acid is the most corrosive and hydrochloric the least corrosive. ~ Hydrochloric acid and nitric acid have the added hazard of volatility and From the Departmentof Surgery (Trauma Division), Medical College of Virginia, Richmond, Virginia. Presented at the Fifth Annual ACEP/EDNA Scientific Assembly in San Francisco, November, 1977. Address for reprints: Kimball I. Maull, MD, Box 893 MCV Station, Richmond, Virginia 23298. 7:5 (May) 1978

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Table 1

Table 2

COMMONLY AVAILABLE HOUSEHOULD MINERAL ACIDS

DISTINGUISHING FREATURES OF ACID AND ALKALI INGESTION

Source

Feature Acid

Toilet bowl cleaners

Sulfuric Hydrochloric Phosphoric

Soldering fluxes

Hydrochloric

Antirust compounds

Hyd rofl uric Oxalic

Bleach, disinfectants

Oxalic

Battery fluid

Sulfuric

Slate cleaner

Hydrochloric

Acid

Emergency treatment

Antacids, demulcents

Weak acids, steroids

Pathologic changes

Coagulative necrosis

Liquifying necrosis

Site of greatest damage

Distal stomach

Mid-esophagus

Most common complication

Gastric outlet obstruction

Esophageal strictu re

Risk of malignancy

Yes - - gastric

Yes - - esophageal

and n u t r i t i o n M repletion is usually indicated. Emergency Management

c h e m i c a l p n e u m o n i t i s m a y complic a t e m o r b i d i t y f r o m i n g e s t i o n of these agents. 6 A l t h o u g h only a few drops of acid in the t r a c h e a m a y be f a t a l , t h e l e t h a l dose of i n g e s t e d m i n e r a l acid is a p p r o x i m a t e l y one ounce, depending upon the agent. 7 Clinical Features I m m e d i a t e p a i n upon i n g e s t i o n m a k e s t h e c o n s u m p t i o n of l a r g e q u a n t i t i e s of acid less common t h a n w i t h a l k a l i poisoning. So g r e a t is the p a i n , in fact, t h a t r e f l e x g l o t t i c spasm m a y result in the r e g u r g i t a tion of t h e i n t r a p h a r y n g e a l bolus, producing serious intra-oral, lingual, and facial b u r n s w i t h relative s p a r i n g of the upper g a s t r o i n t e s t i n a l tract. 1 This often occurs in children but an intent, e m o t i o n a l l y d i s t u r b e d person may swallow a significant volume, thereby producing the c h a r a c t e r i s t i c clinical picture. U n l i k e a l k a l i ingestion, acid ingestion p r i m a r i l y affects the stomach and does so in a very predictable fashion (Table 2). s Because of the relative resistance of the squamous lining and the brief exposure to the swallowed bolus, the esophagus is seriously involved in about 20% of acid ingestions, s Upon r e a c h i n g the stomach, however, the destructive chemical follows the " M a g e n s t r a s s e " from gastroesophageal j u n c t i o n along the lesser c u r v a t u r e to the pylorus (Figure 1). Pylorospasm is u s u a l l y i m m e d i a t e and results in pooling of acid in the prepyloric a n t r u m where the m a j o r i t y of the damage results, s When the stomach is empty, d a m a g e is more diffuse and more severe, s p a r i n g only the gastric fundus. 1 The clinical course following acid 44/207

Alkali

Fig. 1. Pathway ("Magenstrasse") for rapid transit taken by fluids from the esophagus to the pylorus without mixing with gastric contents.

ingestion m a y be f u l m i n a n t or prolonged, s D e a t h m a y result from circ u l a t o r y collapse, l a r y n g e a l e d e m a with a s p h y x i a or perforation of the stomach or esophagus w i t h peritonitis, mediastinitis, or both. s More commonly, the p a t i e n t presents w i t h severe epigastric pain and extreme thirst. Shock is common. There m a y be burns evident in the oropharynx, accompanied by local discomfort. The pat i e n t m a y vomit ~coffee grounds" or grossly bloody fluid w i t h s h r e d s of gastric mucosa. Speech m a y be affected because of pain and swallowing m a y be so u n c o m f o r t a b l e t h a t t h e p a t i e n t drools. If the p a t i e n t survives the acute episode, occasionally a n a s y m p t o m a t i c period m a y follow. More commonly, however, a progressive decline supervenes, s Anorexia, w e i g h t loss, epigastric fullness with b l o a t i n g and eructation, and vomiting all reflect progressive gastric outlet obstruction. Electrolyte i m b a l a n c e m a y complicate the picture and a period of r e h y d r a t i o n JACEP

T h e p r e s e n c e or a b s e n c e of o r o p h a r y n g e a l lesions is not a reliable indicator of the e x t e n t of internal damage, and prompt vigorous t h e r a p y should be a d m i n i s t e r e d to all p a t i e n t s following acid i n g e s t i o n 2 Provided a secure a i r w a y is established, t h e i m m e d i a t e goal is neut r a l i z a t i o n and dilution of the acid. A d m i n i s t e r a w e a k base such as milk of m a g n e s i a , lime water, or alumin u m hydroxide gel. Avoid carbonates or b i c a r b o n a t e s since, upon contact with an acid medium, carbon dioxide is r e l e a s e d a n d g a s t r i c d i s t e n t i o n m a y result. Soap solution is a good s u b s t i t u t e i f o t h e r d o s e s a r e not available. Follow n e u t r a l i z a t i o n with a d e m u l c e n t such as olive oil, egg white, or m i n e r a l oil. The use of a n a s o g a s t r i c tube is g e n e r a l l y c o n t r a i n d i c a t e d unless the p a t i e n t is seen i m m e d i a t e l y followi n g i n g e s t i o n , w h e r e u p o n a small, well lubricated, soft r u b b e r tube can probably be passed safely. This man e u v e r has the added a d v a n t a g e of direct i n s t i l l a t i o n of antacids a n d the s i m u l t a n e o u s m o n i t o r i n g of intragastric pH. E m e s i s is a risk, however, and m u s t be avoided because of the d a n g e r of aspiration. E a r l y a t t e n t i o n s h o u l d be directed to r a p i d volume e x p a n s i o n and pain control. Opiates are u s u a l l y required. The p a t i e n t should be started on p r o p h y l a c t i c a n t i b i o t i c s a n d observed closely, p r e f e r a b l y in a n intensive care unit, for signs of perfor a t i o n or peritonitis. In this regard, the use of steroids r e m a i n s c o n t r o v e r s i a l . In 1950 Spain 1° reported t h a t steroids inhibited fibroplasia a n d e x e r t e d an acute 7:5 (May) 1978

total gastrectomy and esophageal rep l a c e m e n t ( F i g u r e 3). s S h o r t of gastric or esophageal necrosis, this end stage gastroesophageal preparat i o n r e p r e s e n t s the m a j o r u n m e t challenge in acid ingestion and bespeaks the importance of the emergency physician in its m a n a g e m e n t .

REFERENCES

Fig. 2. Upper gastrointestinal series three weeks after acid ingestion demonstrates marked narrowing of distal antrttm.

a n t i - i n f l a m m a t o r y effect if given in the first 48 hours postinjury. Other authors2, 9 implicate steroid therapy in obscuration of developing signs of peritonitis in p a t i e n t s with acid ingestion. If t h e r e is c o n c o m i t a n t chemical pneumonitis, their use may be justified, b u t the ability to conduct reliable serial e x a m i n a t i o n s is invaluable and, for this reason, we do not favor routine steroid a d m i n i s t r a t i o n . Early experience with f u l m i n a n t illness following acid ingestion, leading to gastric necrosis, sepsis and death, prompted some a u t h o r s l~ to recommend early exploration and almost total gastrectomy for acid ingestion. Others 5 feel early operation should not be done except on specific indications of m a j o r bleeding, peritonitis or perforation. Esophagoscopy, however, should be performed within the first 24 hours down to, but not beyond, the p r o x i m a l a r e a of i n v o l v m e n t . E n d o s c o p i c e x a m ination is performed to confiri~ the presence of u p p e r g a s t r o i n t e s t i n a l injury, not to assess the e x t e n t or depth of injury. The latter is best followed by clinical e x a m i n a t i o n , plain radiographs, a n d c o n t r a s t s t u d i e s using w a t e r - s o l u b l e a g e n t s d u r i n g the initial period.

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Fig. 3. Upper gastrointestinal series six weeks after acid ingestion demonstrates extensive involvement o f distal esophagus and entire stomach.

Sequelae The most serious complication of acid i n g e s t i o n is n e c r o s i s of t h e stomach and/or esophagus leading to perforation, septicemia and death. 11 This may occur w i t h i n hours of ingestion, b u t more commonly develops 72 hours to two weeks following the insult, s If the p a t i e n t survives the initial period of risk, the most common l o n g - t e r m c o m p l i c a t i o n is p y l o r i c obstruction (Figure 2). s Gastric resection is required in most of these patients and is preferred to gastroenterostomy because of the u n c e r t a i n fate of the acid burned-stomach, s In 1949, O'Donnell et a112 reported a gastric carcinoma following gastroenterostomy for a nitric acid b u r n of the stomach. In 1972, E a t o n and T e n n e k o o n is reported two p a t i e n t s with squamous cell carcinoma in a stomach damaged by previous ingestion of m i n e r a l acid. Although these are isolated reports, it would appear t h a t the acid-burned stomach, much like the a l k a l i - b u r n e d e s o p h a g u s , may be at increased risk for neoplastic degeneration. Further data is needed to s u b s t a n t i a t e this possibility. In approximately 20% of acid ingestions, combined gastric and e s o p h a g e a l i n j u r y occur r e q u i r i n g

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1. Citron BP, Pincus IJ, Geokas MC, et al: Chemical trauma of the esophagus and stomach. Surg Clin North Am 48:13031311, 1968. 2. Nicosia JR, Thornton JP, Folk FA: Surgical management of corrosive gastric injuries. Ann Surg 180"139-143, 1974. 3. Allen RE, Thoshinsky MJ, Stallone RJ, et al: Corrosive injuries of the stomach. Arch Surg 100:409-413, 1970. 4. David LL, Raffensperger J, Novak GM: Necrosis of the stomach secondary to ingestion of corrosive agents. Chest 62:48-51, 1972. 5. Steigmann F, Dolehide, RA: Corrosive (acid) gastritis, Management of early and late cases. N Engl J Med 254:981-986, 1956. 6. Gray HK, Holmes CL: Pyloric stenosis caused by ingestion of corrosive substances: report of a case. Surg Clin North Am 28:1041-1056, 1948. 7. Polson CJ, Tattersall RN, Clinical Toxicology. Philadelphia, J B Lippincott, 1959. 8. Thornton JP: Surgical management of corrosive gastric injuries. J Natl Med Assoc 66"53-55, 1974. 9. Kirsh MM, Ritter F: Caustic ingestion and subsequent damage to the oropharyngeal and digestive passages. Ann Thorac Surg 21:74-82, 1976. 10. Spain D, Molomert W, Haber A: The effect of cortisone on the formation of granulation tissue in mice. Am J Pathol 26:710-711, 1950. 11. Gago O, Ritter FN, Martel W, et al: Aggressive surgical treatment for caustic injury of the esophagus and stomach. Ann Thorac Surg 13:243-250, 1972. 12. O'Donnell CH, Abbott, WE, Hirshfeld JW: Surgical treatment of corrosive gastritis. Am J Surg 78:251-255, 1949. 13. Eaton H, Tennekoon GE: Squamous carcinoma of the stomach following corrosive acid burns. Br J Surg 59:382-386, 1972.

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