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A wide variety of biologically harmful products, ranging from arsenic, found in ant killers, to sodium hydroxide and other caustics found in drain cleaners, is available in every home and workplace. Children are at highest risk for accidental ingestion of these products, with more than 5000 cases reported annually. (1) Severe damage to the upper gastrointestinal tract may occur within seconds. The extreme morbidity and occasional mortality that ensue are sufficient reasons to place a premium on prevention. Hazardous products should be kept out of the reach of children. Public education and the use of child-resistant containers have been of some benefit. (2) The practice of transferring poisons or caustic substances from their original containers to drink containers may result in a catastrophe, such as in the case of nine youths who mistook liquid lye for wine. (3)
Next to accidental intake, the ingestion of caustic agents with suicidal intent constitutes the most common mode of injury. (4) Additionally, the mentally retarded may ingest a variety of injurious materials, and caustic ingestion may occur as an unrecognized form of child abuse. (5) Ingested caustic substances can generally be classified as acid or alkali. The distinction is clinically important, because the two mechanisms of tissue damage are quite different.
Liquid or granular lye (sodium hydroxide or potassium hydroxide) is widely available in household toilet bowl cleaners, drain cleaners, oven cleaners, and myriad other household products. (6) Concentrated (25%-36%) liquid lye products were removed from the U.S. market in the mid-1970s because of the devastating injuries produced by accidental ingestion. Currently available lye products (e.g., drain cleaners) have a concentration of less than 10%. (7) However, damage to the esophagus occurs with exposure to concentrations well below this level. (8) Farm and industrial caustics of higher alkali concentration are available without poison-prevention safeguards. (9)
Clinitest tablets containing copper sulfate, sodium hydroxide, citric acid, and sodium carbonate are occasionally ingested accidentally or with suicidal intent. (10) If they get stuck in the esophagus, the presence of fluid initiates a vigorous chemical reaction, with the production of thermal damage that is additive to the caustic injury.
Small disc batteries of various sizes are tempting objects for children to swallow. If they lodge in the esophagus, severe injury occurs as the result of the leakage of potassium or sodium hydroxide. (11)
Acids account for approximately 15% of caustic ingestions. (6) (12) (13) Common sources include toilet bowel cleaners, swimming pool additives, antirust compounds, and soldering fluxes. (14) Household agents (e.g., Vanish, Sani-Flush, Lysol, Mister Plumr) often contain sulfuric, hydrochloric, or phosphoric acid. The esophagus has some resistance to acid injury, and esophageal burns occur in only 6% to 20% of acid ingestions. (15) Usually, acids cause more severe damage to the stomach than to the esophagus. (16)
Products containing ammonia are occasionally ingested but usually do not result in severe esophageal damage, perhaps because the severe odor limits the amount ingested. (13) Bleaching agents containing sodium hypochlorite have a higher pH than other acids and are not as damaging to the esophagus. (13) (17)
Caustic injury to the gastrointestinal tract is categorized in a manner similar to that for skin burns. (12) (18) First-degree burns are superficial, leading to mucosal hyperemia and edema; the mucosa may slough, but there is no scar formation (Fig. 58-1) (Figure Not Available) . Endoscopically, erythema is seen. A second-degree burn extends through the submucosa into the muscular layers and is associated with exudate, mucosal loss, and deep ulcerations. Characteristic endoscopic findings at this stage include focal necrosis and ulceration. Over a period of weeks to months, lumenal stenosis may occur. (12) A third-degree burn is transmural, with erosion into the mediastinum, pleural cavity, or peritoneal cavity, fistula formation, and possibly death. On endoscopy, multiple ulcerations are seen, as well as frank necrosis.
The actual physical form of the caustic agent plays an important role in determining the extent and location of mucosal damage. Crystalline caustics attach to oral mucosa, are more difficult to swallow, and may be spit out, leading to oropharyngeal burns but often without much esophageal damage. On occasion, during suicide attempts, patients ingest crystalline lye capsules. This may spare the pharynx and esophagus from injury, but severe gastric injury occurs. (19) Conversely, after a liquid caustic enters the posterior pharynx, the patient invariably swallows, resulting in burns in the esophagus. (13) (20)
Upper gastrointestinal disease may compound this problem by delaying transit, leading to further damage. Regurgitation may allow a to-and-fro movement across the esophagogastric junction that repeatedly brings the caustic into contact with the esophagus. (14) (21)
Alkalis lead to liquefaction necrosis. (22) The extent of mucosal damage is dependent on the concentration and the duration of mucosal contact. (23) Weak concentrations of alkali damage the mucosa and submucosa. Concentrations of 22.5% sodium hydroxide may cause severe inflammation and saponification of all esophageal layers. (23) (24) (25) Thrombosis of blood vessels further aggravates the situation. Microscopically, edema, cell necrosis, and infiltration with polymorphonuclear leukocytes are present and are followed by bacterial colonization. As little as 1 mL of a 30% solution (Liquid Plumr) of sodium hydroxide destroys a cat s esophagus. (26) Information such as this led to changes in the composition of such agents, and
Figure 58-1 (Figure Not Available) Esophageal injury after caustic
ingestion.
(A) The patient presented with retrosternal
pain and was found to have
mild-to-moderate esophageal damage with erythema.
(B) Focal ulceration proximal to the esophagogastric
junction indicates
more severe injury. This figure is depicted in the accompanying labeled
illustration.
(C) The mucosa was extensively burned by caustic
ingestion and is
edematous. The lumen is narrowed.
(From Silverstein FE, Tytgat GNJ. Atlas of gastrointestinal endoscopy.
Philadelphia: WB Saunders, 1987.)
Acids produce coagulative necrosis. The more concentrated the acid, the more severe the injury. (13) A mucosal coagulum that may help limit the penetration of the acid into the esophageal wall develops immediately. (6) (28) In patients with delayed esophageal emptying, more esophageal damage occurs. Usually, however, the stomach bears the brunt of injury in cases of concentrated acid ingestion. (13) If the stomach is empty, damage occurs along dependent areas, the greater curvature, and the antrum, with a tendency to spare the fundus. (29)
The ingestion of a caustic substance by adult patients is usually a suicide attempt and only rarely an accident. Children ingesting caustics usually do so accidentally, and the parent usually knows which agent was involved. (30) If there is a question as to what was ingested, the material should be brought in for inspection.
The extent or the severity of the burn cannot reliably be assessed by history. (6) (31) (32) (33) Symptoms may include burning of the lips, tongue, or pharynx, dysphagia, odynophagia, drooling, vomiting, and dyspnea (Table 58-1) . Hematemesis and abdominal pain may be indicative of gastric injury. Fifty percent of patients with at least two of three key symptoms (i.e., drooling, vomiting, and stridor) have serious esophageal injury, as compared with no esophageal injury in those with only one of these symptoms. Symptoms of third-degree burns are those of shock, mediastinitis, and peritonitis. Late or chronic manifestations of caustic ingestion include dysphagia secondary to esophageal stricture and vomiting resulting from antral scarring and gastric outlet obstruction. (19) (34)
The presence of oropharyngeal burns does not help in identifying patients with esophageal damage. (6) (31) (33) (34) Oral ulcers with white membranes and edema may be prominent. These lesions are quite painful and may bleed. (35) Excessive salivation is frequently present. (36) Hoarseness, wheezing, and stridor are suspicious for airway involvement and deserve careful evaluation. (37) In severe cases, the patient may not be able to swallow oral secretions and tends to sit forward drooling over a
| Burning of the lips, tongue, or pharnyx |
| Odynophagia |
| Dysphagia |
| Drooling |
| Vormiting |
| Dyspnea or stridor |
| Hematemesis |
| Abdominal pain |
Unless the patient is unconscious when first seen, the diagnosis may be established by history. A parent or friend may actually bring the caustic container. The patient, family, or friends should be questioned regarding any previous history of esophageal or gastric problems potentially confounding management.
If the airway is intact and vital signs are stable, evaluation of the extent of injury can be undertaken. Chest radiographs and abdominal flat and upright views should be evaluated for signs of pneumonitis, pleural effusion, or possibly free air in the mediastinal or peritoneal cavity. In the case of battery ingestion, the chest films are extremely important in confirming and localizing the problem. (39) Radiographic findings differentiate a battery from a coin, the more common esophageal foreign body, by a double-density appearance on frontal projection.
Poor correlation of symptoms and results of physical examination with the degree of mucosal damage make early endoscopy important in the evaluation of these patients. (3) (4) (13) (16) (27) (31) (32) (34) (36) (38) (40) With the use of smaller, flexible endoscopes, patients can be examined carefully with intravenous conscious sedation. Endotracheal intubation is warranted if respiratory distress is present. Endoscopic examination should be gentle to protect against iatrogenic perforation (17) (27) (41) (42) but has generally been safe. (31) (35) If viability of the tissue is a concern, the endoscopic examination should be terminated and not proceed beyond this point. If perforation has occurred, intraoperative endoscopy may be of benefit to define the extent of lumenal damage.
If one sees no esophageal or gastric damage in spite of a history of caustic ingestion or the presence of oropharyngeal burns, systemic antibiotics and corticosteroids can be avoided. (13) First-degree burns usually are indicated by scattered erythema or mucosal hemorrhage. Exudate and blisters are suggestive of more extensive injury, and ulcers with circumferential necrosis and black coagulum, indicative of severe injury, are harbingers of stricture formation. (13) (38) (43) (44)
Barium studies of the upper gastrointestinal tract are not warranted in the acute setting of caustic ingestion. Furthermore, barium precludes adequate visualization during endoscopy. If done, esophagrams typically show atony, dilatation, ulceration, and sloughing of mucosa. (45) The presence of intramural air or contrast material within the wall of the esophagus is indicative of extensive injury. (46) On follow-up examinations, multiple strictures are often present. The radiologic abnormalities are similar regardless of whether the caustic ingested was alkali or acid. Antral or pyloric channel ulcers or gastric outlet obstruction may be seen after ingestion of a strong acid. (19) (47) (48)
Computed tomography (CT) of the chest and abdomen may play a role in assessing the extent of damage or determining whether an abscess has developed.
The clinical outcome for patients who have ingested caustics is directly related to the severity of the damage. Patients who suffer only first-degree burns usually do well. Those who develop second-degree burns, particularly with circumferential involvement of the esophagus, have a much poorer outcome and a greater risk of stricture formation. (6) (13) (20) (22) (31) (34) (38) Third-degree burns with erosion into the mediastinum or peritoneal cavity usually require surgical intervention and are associated with significant morbidity and mortality. (3) (13) (19) (20) (31) (34) (38)
Acute airway obstruction can occur as a consequence of aspiration of the caustic material. Infectious complications and tracheoesophageal fistula can be extremely problematic. (49) In the case of a third-degree burn, adjacent organs may be involved. Aortic rupture, usually occurring within the first 2 weeks, has been reported. (50) Disseminated intravascular coagulation has also been reported in association with acid ingestion, leading to a fatal outcome. (51)
Predicting the risk of esophageal stricture formation in patients after caustic ingestion is difficult. Dysphagia that occurs immediately after a caustic injury results from esophageal spasm and acute edema. (27) Esophageal stenosis may occur as early as 2 weeks after a caustic burn. (52) Full-thickness circumferential burns predictably predispose to stricture development. (6) (34) Strictures may be insidious, and careful follow-up is important. (27)
After lye ingestion, the risk of squamous cell carcinoma of the esophagus increases approximately 1000-fold beyond that of the general population (Fig. 58-2) . (6) (34) (53) (54) (55) Of 502 patients with esophageal cancer, 36 (7.2%) gave a prior history of lye ingestion. (54) The mean latent time between lye ingestion and esophageal cancer was 41 years. (53) These patients tend to be younger that those who otherwise develop esophageal cancer, lending further support to the association. (53) The majority of lye-associated esophageal scar carcinomas are found in the area of the tracheal bifurcation. (53) (56) Periodic surveillance endoscopy may be warranted.
Gastric outlet obstruction, most commonly antral stenosis, usually occurs 2 to 6 weeks after the ingestion and may be confused with gastric carcinoma. (57) (58) (59) (60) Squamous metaplasia and gastric carcinoma have also been reported after acid damage to the stomach, although it is not clear that an increased risk of gastric cancer exists. (15) (61)
Immediately after a caustic ingestion, questions of neutralization invariably arise. Dilution with water or milk has been suggested. (10) (20) (62) Mild acids or alkalis should not be used to
Figure 58-2 Multiple esophageal strictures
and the development of squamous cell carcinoma 40 years after the ingestion
of
lye.
After the patient arrives in the emergency room, the status of the airway should be evaluated and stabilized. (63) Induced emesis is contraindicated, because vomiting has the potential of reexposing the esophagus to the damaging agent and may cause tears or perforations in the damaged esophagus. (20) Intravenous fluids are administered as necessary, and oral intake is prohibited. These patients should be followed closely for symptoms and signs of mediastinitis or peritonitis. If clinical or radiographic findings suggest perforation, surgical intervention is indicated. (3) Early endoscopy aids not only in acute management but also in long-term planning.
The use of antibiotics in the management of patients with caustic burns remains unsettled. Many authors suggest broad-spectrum antibiotics in this setting, aware that gram-positive organisms are often involved. (4) (17) (23) (27) (28) (37) (44) The use of antibiotics seems reasonable and appropriate in patients with second- and third-degree burns. If corticosteroids are used, antibiotics should be used concomitantly because of the increased risk of infection. (6) (31)
The use of corticosteroids remains largely empiric. Studies are controversial regarding the efficacy of steroids in decreasing stricture formation and fibrosis. (6) (12) (13) (14) (16) (17) (19) (22) (23) (25) (27) (28) (29) (31) (40) (42) (64) (65) (66) Increasing evidence indicates no benefit from the use of corticosteroids in preventing stricture formation or the need for esophageal resection. (67) Anderson and coworkers prospectively examined 60 children with caustic ingestion over an 18-year period and found no differences in complication rate and clinical outcome between the control and steroid-treated groups. The complications were related to the extent and severity of the injury. (67)
Despite these findings, opinions on the use of steroids in caustic injury vary. There may be a subset of patients yet to be defined who may benefit from corticosteroid therapy. If corticosteroids are used, they should be reserved for those patients with circumferential esophageal burns with increased likelihood of stricture development. With a deep burn, stricture may be unavoidable regardless of management. (27) (34) Many physicians recommend prednisone (60 mg in adults; 1-2 mg/kg in children) or its equivalent. (12) (14) (40) The duration of therapy recommended is variable, but 3 weeks seems to be the minimum for extensive burns. (13) (20) (27) There is a valid concern that corticosteroids may mask or even potentiate the development of mediastinitis or peritonitis. (4) (26) (28) (38) (44) (63)
Experimental animal studies suggest that inhibitors of collagen formation, including penicillamine, beta-aminopropionitrile, and N-acetylcysteine, might be useful, but no human data are available. (68) (69) (70) Sucralfate has been found to be of benefit in an uncontrolled report. (71)
Esophageal bougienage should be avoided during the acute phase of injury because instrumentation may increase the risk of perforation. (42) Early dilatation has been supported in an uncontrolled trial. (40) However, we and others recommend delaying dilatation for 2 to 4 weeks (4) (38) (42) and then proceeding very gently. Mild esophageal scarring usually responds to dilatation, but patients with very tight, long strictures or multiple strictures are thought to be at increased risk from instrumental perforation during dilatation and usually require surgery. (27) (34) (38) (42)
Studies in cats have demonstrated that, after lye burns of the esophagus, intralumenal stenting with silicone rubber catheters can prevent stricture formation. (52) However, other experimental data indicate that the presence of a tube in the esophagus is detrimental. (23) Data are insufficient to allow a judgment regarding the usefulness of this modality. (22) (66)
Clearly, the patient with perforation or impending perforation requires surgery. Patients with multiple, very tight strictures may require surgery as well. (34) (38) (42) Colonic interposition has
| Aspirin | Nonsteroidal antiinflammatory |
| Chloral hydrate | drugs |
| Clindamycin | Quinine |
| Cromolyn sodium | Potassium chloride |
| Emepronium | Quinidine |
| Ferrous sulfate | Tetracycline |
|
|
Vitamin C |
Most disc batteries pass through the gastrointestinal tract without causing damage. If a battery lodges in the esophagus, immediate removal is indicated. (2) (73) Endoscopic techniques are preferred to directly assess the burn area and to prevent perforation during the extraction. (2) (6) (20) (39)
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