What is the meaning of caustic ingestion?

Introduction/Background

Caustic ingestion may result in significant injury to the entire gastrointestinal tract, but most significantly the upper tract, including the oropharyngeal cavity, larynx, esophagus, and stomach.

The majority [68 %] of cases worldwide involve children as a result of unintentional, accidental ingestion of caustic substances. The remainder of cases reported are adults with psychiatric disturbances, some after suicide attempts, or alcoholics [1, 2].

As expected, the resultant severity of injury in caustic ingestion is determined by the type of ingested substance the amount and the time of tissue exposure.

Due to the substantial morbidity and mortality associated with these injuries, the medical community demanded legislative action. Through persistent efforts, the Federal Caustic Act of 1927 was enacted, requiring appropriate labeling of caustic substances, such as lye. Subsequently, the Poison Prevention Packaging Act of 1970 directed the US Consumer Product Safety Commission to require childproof containers and improved labeling of caustics and other potentially harmful household products. These legislative acts caused dramatic decline in the occurrence of this type of injury in developed countries. However, in developing countries the incidence is still much higher [3].

While the injury pattern frequently seen in children is usually relatively minor due to smaller amounts ingested, in adults much larger quantities of the caustic substance frequently result in severe injury [3–5].

Injury caused by alkali or acid results in a different injury pattern. For example, alkali causes almost no irritation to the oral cavity, which usually results in larger ingested volumes entering the GI tract. Furthermore, because Alkali materials are thicker, they lead to longer exposure durations in the esophagus, causing progressive injury via liquefactive necrosis.

This process may take as long as two weeks to manifest itself, and is heralded by progressive thinning of the esophagus lining. The stomach and duodenum, on the other hand, are less prone to such injury, due to the neutralizing effect of gastric acids and avoidance of pyloric spasm. Accordingly, maintenance of gastric emptying results in limited exposure of the gastric mucosa to alkali.

In contrast to alkali, acids induce a burning sensation with subsequent pain immediately after contact with oral mucosa; accordingly, the volumes traditionally ingested tend to be small. In addition, since acids lack viscosity, their transit time through the esophagus is rapid.

Subsequently, the duration of exposure to the gastric mucosa is extended due to acid induced pyloric spasm, resulting in acid exposure for protracted periods of time leading to coagulative necrosis. Endogenous gastric secretion is not considered to influence this process [1, 6–8].

Acid ingestion may still cause substantial damage to the esophagus, including perforation [9].

The extent of injury that results from caustic ingestion is estimated by the depth of the resultant caustic burn. First degree burns tend to involve only the mucosa, with localized redness and edema noted at endoscopy. Second degree burns involve the mucosa and sub- mucosa with blister formation evident, while third degree burns are characterized by a transmural process that affects the entire lining with findings of extensive ulceration and necrosis appearing as gangrene [10, 11].

Of note, the clinical findings in caustic ingestion can be highly variable, and often do not correlate with the injury grade noted at endoscopy [12, 13].

Patients with minimal ingestion may be asymptomatic but others may experience oropharyngeal, retrosternal or epigastric pain. Findings of shortness of breath, hoarseness and stridor suggest laryngeal trauma and demand laryngoscopic evaluation. Dysphagia, odynophagia and excessive salivation are suggestive of esophageal damage, abdominal pain; vomiting and hematemesis may suggest gastric damage. Continued pain, peritonitis, tachycardia, persistent leukocytosis, acidosis and pleural effusion should raise the suspicion of perforation [Fig. 1] [14–20].

Fig. 1

a: Resected stomach due to perforation [arrow] after caustic material ingestion. Note diffuse thrombosis of gastro-epiploic veins. b Stomach opened longitudinally. Note necrosis of gastric mucosa

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Ten percent of patients sustaining CMI will experience immediate complication [21, 22]. The most common serious immediate complications after caustic material ingestion therefore include: perforation, bleeding, but late findings include fistula formation [tracheobronchial, gastro colic or even entero-aortic]. Reported mortality approaches 10–20 %. Among those sustaining caustic injury in a suicide attempt, mortality may approach 75 % [6]. The delayed complications include stricture formation [Fig. 2] leading to malnutrition and long term risk of developing malignant transformation.

Fig. 2

Barium swallow four month after caustic ingestion injury. Note the long stricture of distal esophagus and gastric cardia. This patient was treated with colonic interposition

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Although there are few published prospective studies on the management of CMI, the current review will attempt to collate all current reports and expert opinions. This work was done as a preliminary study for a consensuses conference on the topic held in Milan, Italy in March 2015.

Method

An e-mail questionnaire was forwarded to all members of the WSES, World Society of Emergency Surgery, consisting of extensive questions pertaining to the diagnosis and treatment of caustic injuries. The question related to various aspects of diagnosis, initial management, surgical and medical treatments as well as questions on individual survey member and institutional experience with caustic ingestion injuries.

As a result of this questionnaire, a detailed literature search was performed in an effort to compare expert opinion with current available literature.

Literature search was designed in four levels and included:

1. 1.

   Epidemiology, toxicology and pathophysiology of caustic injury.

2. 2.

   Initial management and emergency interventions.

3. 3.

   Evaluation of caustic injury – endoscopy, Computerized tomography.

4. 4.

   Surgical management in the acute and late phaseof caustic injury.

5. 5.

   Early and late complications.

Results

Survey results

General information

Completed survey questionnaires were obtained from the following locations world-wide: Europe 9, Asia 9, South America 4, 3 in North America, 3, and Middle East, 3.

Nineteen of the hospitals that participated in the survey reported treating 1–5 cases annually, while three facilities reported over 15 cases per year. Table 1 shows general background information about the respondents and their associated medical facilities.

Table 1 General information about the work environment of the respondents to the survey

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Initial assessment and diagnostics

The preliminary treatment and imaging tests practiced by the survey participants is depicted in Table 2.

Table 2 Means of initial assessment and diagnostics of CMI, according to the survey respondents

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All survey participants initiated management via oro-tracheal or naso-tracheal intubation when patients were noted to present with obvious signs of dyspnea, stridor or laryngeal edema occurred.

Of those patients who were intubated, 14 % will require ventilator support for over one week. Seventy two percent of respondents placed a nasogastric tube on initial evaluation. Twenty percent of respondents indicated that they would insert a nasogastric tube regardless of initial findings while interestingly, 6 % reported that they would avoid placement of an NG tube in these patients.

Of those placing an NG tube, 67 % suggested the importance of doing so under endoscopic guidance, 45 % reported removing the NG tube after 3 days, while the remainder [55 %] left the tube in place for over a week.

Half of survey participants were reluctant to perform esophagography, while 29 % performed the examination on all patients; 21 % performed the study only on intubated patients.

Eighty three percent performed initial esophagogastroscopy on all patients whereas the other performed the exam only according to clinical presentation or when evidence of oropharyngeal involvement was evident.

Nighty percent of survey participants performed routine chest X-ray regardless of the patient’s underlying respiratory condition. The remaining performed a CXR based upon clinical indications. Twenty nine percent of respondents routinely ordered CT scan on all patients, but the remaining group performed this test only when signs of peritoneal irritation or suspected perforation were noted.

Treatment

The treatment provided by survey participants is presented in Tables 3 4 and 5.

Table 3 The use of medical treatment for CMI, according to survey respondents

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Table 4 The use of surgical intervention for CMI, according to survey respondents

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Table 5 Treatment of strictures

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Twenty five percent of respondents administered steroids to all patients, while 29 % admistered those to patients noted to have associated second degree burns. Forty six percent of the respondents stated that they did not admister steroids in any case. Thirty four percent of respondents administered antibiotics to all patients, while 34 % suggested such a need for those patients suffering second degree burns and 32 % administered antibiotics to patients requiring surgical intervention.

All participants proceeded to urgent surgical intervention when there were signs of peritonitis, free air, or esophageal perforation a small group [3 %] said they would suggest surgical intervention in the face of extensive third degree injury. Of those proceeding to surgical intervention, 52 % performed a traditional laparotomy, while 48 % consider a laparoscopic approach. The decision to perform restorative surgery was generally based upon patient stability: 31 % of respondents attempted restorative procedures at the initial operation, while the remaining majority deferred such extensive procedures until later time frames.

Twenty four percent of respondents performed initial endoscopic treatment of short or long stricture, deferring surgical intervention for treatment failures. The majority of respondents [76 %], attempted endoscopic management of short strictures, but felt that longer strictures would require surgical intervention.

Discussion

The diagnosis and treatment of caustic ingestion injuries has received only a modicum of attention in the literature. Furthermore, our review has identified only three randomized control trials addressing the effectiveness of steroid treatment [23–25]. Accordingly, the current relevant literature consists primarily of retrospective research and case studies.

The paucity of experience with this entity at any one center is evident from the finding that 80 % of our survey respondents treat fewer than 10 cases per year. Based on these findings, we believe that patients should be enrolled in well designed, prospective data bases; furthermore, in order to establish evidence based guidelines, a current management algorithm should be constructed based upon available knowledge.

Diagnosis and initial treatment

The initial approach to management should involve careful assessment of the extent of injury. Hence, it is important to document the type of ingested material, quantity ingested, and an attempt to estimate the exposure duration in the various organs.

A careful assessment of symptoms is paramount. Complaints of dyspnea, dysphagia, excessive salivation, hematemesis or hoarseness suggest severe injury [27]. Although laboratory tests do not always correlate with severe injury, leukocytosis >20,000 wbc/ml, elevated CRP and pH  90 % but with sensitivity of only 30–40 %. On the basis of these facts, these authors concluded that early endoscopy may not be replaced by CT [36].

Early endoscopy [within 12–24 h following ingestion] permits careful assessment of anatomic derangements, serving as a valuable aide in decision making in order to guide the need for further interventions. Delayed endoscopy [>48 h] should be avoided due to increased risk of perforation as the resultant of tissue edema and inflammation. The grade of injury based upon careful endoscopic assessment and physical examination appears to be closely correlated with the degree of urgency for surgical intervention, the development of subsequent complications and eventual mortality [11, 37–40]. In a series by Zarger SA et al., the authors noted that all patients who succumbed to their injury had grade III burns. Furthermore, those with grade IIb and III who survived developed late complications. Lastly, with the finding of an IIa or lesser grade burn portended a complication free clinical course [11]. While III degree burns generally suggest the need for urgent surgical intervention, it should be noted that, gastrectomy or esophagectomy based on endoscopy findings alone may lead to 10–15 % unnecessary surgical procedures [33, 34, 43]. Despite these findings and the correlation of the burn depth to outcome it is interesting to note that