Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Caustic Ingestion Today I will be discussing caustic ingestion. I will begin with a brief outline. We’ll start with the case presentation, followed by some history, epidemiology, pathophysiology, evaluation, management, complications, and finally the summary. MV is a six-year-old girl who reported swallowing a foreign body. The patient vomited several times, but no foreign object was expelled. Two hours later, at an outside hospital, PA and lateral films revealed an esophageal foreign body in the proximal esophagus consistent with a disc battery. The patient was then transferred to Texas Children’s Hospital for further care. On arrival, she complained of persistent burning in her throat without any respiratory distress. Incidentally, the family recalled that earlier in the day they had changed the disc batteries in their daughter’s toy cell phone. Past medical history was unremarkable. On exam, her oral cavity was clear. There was no neck crepitus. Breath sounds were equal bilaterally. She was taken immediately to the OR, which was approximately four hours after the original ingestion. Esophagoscopy was performed and a 3 volt disc battery measuring 2cm in diameter by 0.2cm in thickness was removed from the proximal esophagus. This is a picture of that. You can see the disc battery, and you can also see sloughing of the mucosa and discoloration. There was also what appeared to be some muscular involvement anteriorly there. Bronchoscopy was also performed. It showed no abnormality in the trachea. A nasogastric tube was placed. The patient was extubated and was transferred to the ICU for evaluation and observation. A chest x-ray was normal. The patient was placed on ampicillin and Zantac. On postop day #2, a gastrograffin swallow was performed and showed no extravasation. The patient was then transferred to the PCU to step-down unit. On the postop day #4, she was transferred to the floor, and clear fluids were begun. She was advanced to a soft diet and was then discharged home on postop day #6 with an NG tube in place and on Zantac. On the postop day #10, the patient returned to Texas Children’s for a repeat esophagoscopy and this showed two discrete anterior ulcerations that were healing. It was not felt that she was a high risk for stricture and so the NG tube was removed. She was discharged home on Zantac for one month. This is the intraoperative photo from the second esophagoscopy showing the two ulcerations anteriorly along the wall. In the late 19 th century and early 20 th century, commercial products containing strong lyes and acids became available to the general public. Pictured here is Chevalier Jackson whose work revolutionized bronchoesophagology. In 1927, he successfully lobbied for the Federal Caustic Act, and this required clear labeling of caustic substances that had been made available. Prior to that time, there really was no warning labeling or any other labeling on these items. In 1971, more legislation was passed. The Federal Hazardous Substances Act and Poison Prevention Act was passed. It banned excessively hazardous products and mandated that the concentrations be reduced to 10%. Previously, there had been no regulation of this. It also mandated child-resistant containers, and you can see right here some of the lids that are the child-resistant types. The act also mandated conspicuous warning labels for the cleaning agents containing strong bases and acids. Approximately 5,000-15,000 cases of caustic congestion occur in the US every year. About 50%-80% occur in the pediatric population. There is a 2:1 male to female ratio, and there is a bimodal distribution. Basically, in the early years, it is predominantly accidental ingestions. In that later group, it is predominantly intentional ingestions. Here you see a picture of one of Dr. Jackson’s early patients before the 1927 Federal Caustic Act was introduced. This shows a child in a very emaciated state, unable to eat and drink. Most ingestions occur at home and in the kitchen. Interestingly, high family stress is the most contributing factor. Marital conflicts, deaths in the family, mental illness, and physical illness are also common at the time of ingestion. Interestingly, as one would not expect, an unsafe home is not a primary factor. There was a change from solid to liquid lye products in the 1960s, and this lead to a change in both the type and the anatomical location of injuries. Prior to that time, solid products had been dispensed, and these solid products containing lye, in general, were difficulty to swallow. They would adhere to the mucosa, and oftentimes you would find oral injuries, oropharyngeal injuries, and more localized injuries. After the liquid products were introduced, which were made worse by being almost tasteless, they were easily swallowed, and with a single swallow or two, a large amount of mucosa from the mouth all the way down to the duodenum can be damaged. Here we have a classification of injury. A grade I burn is nonulcerative esophagitis. There is mild erythema. There is no sloughing, and there is edema of the mucosa. A grade II lesion shows a white exudate. There is also erythema in the area. An underlying ulceration may be apparent, and that may extend into the muscle layers. In a grade III lesion, the mucosa appears very dusky, very black, and transmural tissue is involved. There can be deep ulcerations that extend into the periesophageal space or perforations, and sometimes the lumen may be completely obliterated. The most common agents responsible for caustic ingestion fall into three categories. There is the alkali category, which technically is caustic agents with pH > 7; acids, otherwise known as corrosives, have a pH < 7; and, of course, there are also bleaches, which have a pH of approximately 7. The common agents that are ingested are generally the common agents that are used for cleaning in the area. In the US, they are liquid products such as Liquid Drano. In India, for example, the common products that are ingested are acid agents because more acids are used in the cleaning solutions there. This is an example of some common cleaning solutions containing strong acids and bases. In the household, you have alkali agents containing sodium hydroxide, potassium hydroxide, calcium hydroxide, in things like Liquid Drano. The common acids that are ingested are sulfuric acid and hydrochloric acid. Bleaches include chloride bleaches, and peroxide bleaches. Mildew removers that are used in bathrooms often contain bleaches. The most common ingestions in the United States, about 60% to 80% of the time, are alkali ingestions. This includes lye, as I previously mentioned, as well as ammonia. With this kind of ingestion you end up with, histologically, a liquefaction necrosis. This also causes denaturing of proteins, saponification of fat, and blood vessel thrombosis. The important thing is that there is very early disintegration of the tissues. This allows for very deep penetration and further damage into the muscle layer and beyond at times. About 30% of children ingesting alkali agents end up with esophageal burns, 80% having high grade II and III that do go on oftentimes to develop strictures. Burns tend to be at anatomically narrowing areas. at the cricopharyngeus, the arch of the aorta, etc. The stomach, interestingly, is spared in 80% of the ingestions. Severity of the injury is determined by the amounts of the agent ingested, and the type of the ingestion. If there is food in the stomach, there tends to be less of a caustic injury because of absorption. The GI transit time is also very important, as well as the presence of reflux. If there is significant reflux, the agent can reflux and cause additional damage in the area that had previously been damaged. This early disintegration of mucosa from alkali agents actually can occur over a three-day period after the ingestion, and about days 7-21 the esophagus wall is weakest. Superficial mucosal burns may tend to heal pretty well without sequelae. Burns that disrupt the submucosal and muscular layers often are complicated by severe mucosal loss. After this, an inflammatory reaction is set up. The body begins to try to heal this area, and fibroblasts move in, laying down collagen matrix. This matrix is pretty haphazard and begins to contract in about three weeks. This irregular collagen matrix allows for adhesive bands to form, and some pseudodiverticula can form between these bands. This process continues until finally there is pretty dense scar in the mucosa and in any of the muscular layers that had been previously damaged by the agents. In general, usually a completely circumferential lesion involving the entire wall leads to significant strictures in a clinical setting. We’ll talk a bit about disc battery ingestion. Up at the top on the left you can see an example of a disc battery. In the center picture, there is a PA view, which shows a round object could be mistaken as a coin. However, on the lateral view, as you can see, there is a slight irregularity of the contour, and this is the tip-off that it might be something other than a coin. These kinds of disc batteries are very common in hearing aids, calculators, other toys and devices; and, in fact, about 33% of the time with ingestions of batteries, the batteries are from the child’s own hearing aid. These products contain sodium hydroxide, potassium hydroxide, and mercury oxides. After the first hour, there is significant mucosal damage. Between two and four hours, there can be erosion to the muscular layer. Six hours and above, oftentimes you end up with perforation, sepsis, mediastinitis, and even death. This is a picture of a typical battery: the metal top, the anode and the cathode, and, in the center, electrolyte soaked separator. Then there is a plastic grommet or seal. When the battery is submerged in a saline solution, a current develops across that seal, and that leads to the leakage of the caustic contents. In general, a 7.9mm x 11.6mm diameter battery tends to pass pretty well through the GI tract. If it is 15mm or larger, it often gets lodged in the esophagus or in the stomach. A history of battery ingestion requires a very prompt evaluation, radiographic evaluation, and, if battery is seen, emergent removal. Serial radiographs can be used if the battery passes into the stomach. In general, if it remains in the stomach for about two days, it needs to be removed endoscopically. On all batteries there should be a serial number, and poison control hotlines can be used in an event of an ingestion. Identification from the actual battery or from a duplicate brought in by the parents is very helpful. The poison control centers have extensive databases that allow them to identify exactly what is in that battery, and they can make specific recommendations for treatment for each case. Hence, it is also very important to know that the ID often allows for identification of mercuric oxide-containing batteries, which is significant as there can be mercury poisoning related to those ingestions. Acid Ingestions are responsible for about 15% of caustic ingestions. Coagulative necrosis forms a coagulum and actually protects some of the underlying tissue, so the burns tend to be less significant. Esophageal burns will only occur about 6%-20% in those ingestions. The natural acidic pH in the stomach unfortunately often increases the injury and you there is a higher incidence of gastric complications. For several reasons, the antrum is most vulnerable. First, there is dependent pooling of the agent in that area, so there can be erosions and perforations. Also, the actual acidic pH of the agent that was ingested can cause pyloric spasm, preventing gastric emptying, which further exacerbates the problem. The unpleasant taste of the acids can also cause choking, sputtering, and vomiting of this agent before it is swallowed, often resulting in a chemical epiglottitis, and the airway is a big concern in these cases. Bleaches, fortunately, have essentially a neutral pH, and they are classified as only esophageal irritants. Many series have shown that there is really no significant injury related to these ingestions and therefore, an extensive workup is not necessary. However, it is important to keep in mind that acute laryngeal edema can occur with these ingestions, so close observation is required. As far as hair relaxers, this is fairly new in the literature. Many physicians in urban settings are reporting many more ingestions of hair relaxing agents. In fact, current numbers are about 30%-40% of all alkaline ingestions. Hair relaxer basically is an alkaline cream. Its pH is about 11-12. It functions by denaturingthestructural protein in the hair, making curly hair straight. Unfortunately, the FDA does not mandate that it is packaged in child safe containers. Even worse, these products tend to smell really good, and are usually packed in very attractive packages with lots of bright colors, which is very alluring to children. There was a meta-analysis done by Aronow et al, which found that actually only one case out of 213 had a very significant injury greater than grade I esophageal injury, and there was really no adverse outcome. Other literature confirms that there is really not a significant risk of injury with these agents. Therefore, these children can be managed with observation overnight, making sure that they have adequate p.o. intake in the morning, and can then be released. However, endoscopy is indicated if the symptoms do not resolve. We’ll now discuss clinical presentation. Unfortunately, when children ingest these substances, they are usually not being supervised by the parents, so oftentimes the history is inaccurate, and you do not know how much was ingested, or what was ingested. Sometimes the agent is in an unmarked container. It is very useful, however, to remind families that if they are able to bring in the container or even a remnant of the agent in the container, that is very helpful. Again, you can call poison control centers, and their databases will be able to help you in management. Often, when children present after caustic ingestion, they have some burns in the mouth, the oral cavity, and sometimes you see these gray pseudomembranes and eschars. It is very important to remember that there is no reliable relationship between the signs, symptoms, and physical exam. Therefore, this should never stop you from an endoscopic evaluation if your suspicion is high that there actually was ingestion. Dysphagia, odynophagia, and recurrent emesis are also other symptoms that often present with caustic ingestions. Hoarseness or stridor could be indicative that there might be some airway compromise, and substernal, back, and abdominal pain can indicate severe injuries. However, you can still have these severe injuries without any signs at all. In fact, 8%-20% of patients with significant esophageal or gastric injury had no obvious signs or symptoms at all. Unfortunately, lab values are not helpful. There was one study done by Rigoet al which found that only increasing age, ingestion of a very strong acid, white count greater than 20,000, and presence of deep gastric ulcers or significant gastric necrosis was a predictor of death. All the other lab values are really not worthwhile and do not tell us very much. As far as radiologic evaluation , a lateral neck film sometimes is helpful if you are concerned about airway compromise. This is a picture of a 23-month-old boy that ingested some Drano. There is pretty significant supraglottitis, and this child actually got an emergent tracheotomy shortly after this was taken. Chest x-rays and KUBs are also helpful in the diagnosis of an acute perforation. Barium esophagram has very little value acutely. It has extremely high false negative rates, and it is also not very good for picking up grade I and grade II lesions. Oftentimes it actually delays endoscopy, which is a definitive procedure. It is, however, indicated after 48 hours, because at that time endoscopy is no longer safe due to the increased risk of perforation and the weakness of the esophageal wall. If it is obtained before, however, as is pictured here on the right, a very dilated atonic esophagus is indicative of very severe full thickness injury, and the barium esophagram is actually very useful for long-term follow-up with the patients. The timing of endoscopy remains controversial. The general consensus is that if it is less than 24 hours, the full demarcation of the injury has not yet occurred, the the total injury may be underestimated. If it is greater than 48 hours, there is an increased risk of perforation. So, it is generally accepted that endoscopy should occur between 24 and 48 hours, and it is also fairly well accepted that when advancing a rigid scope, if a completely circumferential lesion is encountered, it is advisable to stop at that time to decrease the risk of perforation. Because of this, several authors in the country are moving towards flexible scopes, which sometimes can be threaded through that area more easily to examine the whole esophagus and the rest of the stomach. This is example of a grade II esophageal injury. You can see the sloughing off of the mucosa, with some damage to underlying tissues. This is another example. This is a patient who swallowed Drano and you can see the severe caustic injury. This is an endotracheal tube on the left, which is just posterior to a very damaged epiglottis, and the postcricoid space is on the other side. As far as initial treatment, first, of course, is always appropriate airway management. It has been suggested that diluting agents such as milk or water can be given to the patient. Milk is a neutral buffer. However, you have to be very careful with this. You do not want give too much because that can induce vomiting, further increasing the injury. Similarly, charcoal and emetics should not be used because they increase vomiting. Blind passage of a nasogastric tube is contraindicated, and perforations can occur in that manner. Neutralizing agents have been used in the past, vinegar for lye ingestion and sodium bicarbonates for acid ingestion. This is contraindicated because during the neutralization process, there is a very exothermic reaction, and this heat in the area can cause even further damage. Also lye acts extremely rapidly, and any neutralizing agent probably would not even help. Steroids are given to reduce stricture formation. They should be started about 24-48 hours for the full benefit of the anti-fibroblastic effect. Some studies suggest that strictures are actually even easier to deal with when they develop while the patient is on steroids. Dose is controversial, generally one to two mg/kg/day is recommended. In a grade-I injury, no steroids are recommended because in these cases there is really no stricture formation. In the grade II injuries, steroids are beneficial. It has been shown in many studies that stricture formation is decreased, and also that there is no increase in the infection or GI complications such as hemorrhage or death. In the grade III injury, steroids should not be used and are contraindicated because these cases usually go on to surgery, and the steroids can actually hamper those efforts as well as slow healing. Prophylactic antibiotic use has been controversial. Many authors recommended this, and some histologic studies show that there is translocation of the bacteria to the mucosal injury site. However, studies have failed to show that there is a decrease in stricture rate or infection rate. Obviously, antibiotics should be started if there is any sign of infection at all. As far as antireflux medications, damage secondary to reflux has been shown in animal studies. It has not been proven in human studies. Sucralfate therapy has promise in decreasing the damage of esophageal injury. However, it has to be crushed up and given as a slurry of the tablet form, so that makes it somewhat difficult. Since there is very little risk to this therapy, many authors recommend antireflux therapy even though there are no proven human studies. Further studies in this area are needed. Lathyrogens are agents that reduce collagen cross linking. Examples are N-acetylcysteine and penicillamine. They have been shown to reduce formation of collagen in the laboratory setting, although this has not been proven in humans. Penicillamine is the least toxic, and may have a role in the future. Many authors recommend esophageal stenting to reduce stricture formation. The most commonly used stent is a nasogastric tube. Silastic stents, other types of stents, and metal stents have been used in the past and are not as common any longer. The stents should be placed endoscopically to help make sure that you decrease the risk of perforation. Theoretically, the stent should remain in place to allow for re-epithelization to occur, and that is about two to three weeks, but this depends on the clinical setting. If there is really not a danger of stricture formation, they can be removed earlier. As far as the esophageal dilation, the technique is used to avoid stricture formation. The frequency is not really established. You can start bouginage in about two to three weeks after the initial injury. Long-term effectiveness is doubted by many, and with repeated dilations, there is an increased risk of perforation. Emergent esophagogastrectomy is a very controversial topic. Perforation of the esophagus, of course, requires this immediately. There is also a controversy depending on what center you are in as to the timing of the procedure. Some centers advocate surgery for all grade III and all grade II injuries. In the grade III injuries, this early surgery is necessary, and cannot be avoided, but in the grade II injuries, oftentimes the strictures do not even occur, so one should be very careful before performing surgery. As far as complications, several can occur with ingestion. These include nasopharyngeal stenosis, hypopharyngeal stenosis, and laryngeal stenosis, as well as fixation of the tongue and esophageal strictures. Here, on the right, is a picture of a fairly mature spiral esophageal stricture about mid esophagus, a couple of months after ingestion. About 10%-20% of caustic injuries develop strictures. Patients with long-term strictures have high morbidity, require many hospitalizations, numerous dilations, and experience nutritional shortfalls. Mortality actually approached about 40% in the early 1900s. Even today with our modern medical techniques and diagnostic procedures, mortality is estimated at between 0% and 20%. Here is an example, on your right, of various bougies and dilating instruments. Prograde dilation is generally begun under general anesthesia. If you have a very cooperative patient, usually only adults, sometimes additional dilations can occur in the office. This basically continues until you have a pretty good caliber and the patient’s symptoms have improved. It can be performed as needed in the future, and usually a barium esophagram is used to follow these patients. Retrograde dilation has also been used commonly in the past. Basically this has a continuous string in the esophageal lumen. It exits the nose and then exits the gastrostomy tube. You tie a Tucker dilator to the bottom of that and use it to pull it through. These dilations can occur daily in patients while they are awake. As far as the esophageal stricture, when repeated dilations fail and the strictures are so severe that you cannot really do dilation, surgical reconstruction is necessary. This consideration is beyond the scope of this talk, but basically there is a gastric pull up. You can use colon and jejunum as interpositions to reroute contents and local resection can be used with an end-to-end anastomosis or sometimes a colonic patch, in the case where there is a very defined area of stricture. As far as esophageal cancer, there is a 1000 fold increased risk of esophageal cancer 25 years after a caustic injury. Therefore, a very high suspicion has to be maintained for these patients, especially when they present years after the caustic ingestion with new symptoms of dysphagia or other symptoms. The age, interestingly, is about 40 years, which is significantly younger than the average esophageal cancer age. Also, prognosis is better than with the average esophageal cancer and it is thought that this is because the carcinoma develops within a very fixed scar and somehow limits distant metastasis. And for a patient update, the patient had a barium swallow that showed no signs of stricture formation. She is currently doing well, tolerating diet, and has had no other problems. Interestingly, the case was reported and is under investigation by the US Consumer Product and Safety Commission for two reasons: one, the toy had no protective mechanism to keep children from getting at the batteries; and two, there is also a concern as to why this size of a battery with this much voltage in disc form should be required in a toy such as this. Summary: Endoscopy is the gold standard for diagnosis. It is usually done 24-48 hours after the injury. It is very important to remember that there is no reliable relationship among signs, symptoms or physical exam. Alkali agents cause liquefaction necrosis, which allows deeper penetration and injury. Acids cause coagulative necrosis, a coagulum forms and protects some of the underlying tissue and sometimes helps to limit that injury. Bleach is only an esophageal irritant. It is unlikely that there will be significant injury related to bleach ingestion, so this can be treated conservatively. Hair relaxer ingestion can be managed with observation overnight and observation of adequate p.o. intake. Complications such as esophageal stricture remain a very significant source of morbidity following caustic ingestion. Case Presentation: MV is a 6 year-old girl who reported swallowing a foreign body at approximately 7:00 pm. The patient vomited several times but no foreign object was expelled. Her parents took her to an OSH in the Woodlands. At approximately 9:00 pm, PA and lateral films revealed an esophageal foreign body in the proximal esophagus consistent with a disc battery. The parents recalled that earlier in the day they had replaced the two disc batteries of their daughter’s toy cell phone. Reportedly, the child had placed the old batteries along with some coins in her pocket. The patient was then transferred to TCH for further care. She arrived at approximately 11:00 pm. She complained of persistent burning in her throat. She was not in any respiratory distress. Past medical history was unremarkable. Her oral cavity was clear. There was no neck crepitus. Breath sounds were equal bilaterally. She was taken immediately to the OR. Esophagoscopy was performed, and a 3.0 volt disc battery measuring 2cm in diameter and 0.2 cm thick was removed from the proximal esophagus. There was significant caustic injury at the site with discoloration and sloughing of the mucosa. The full depth of injury could not be determined. Bronchoscopy was performed and showed no abnormality in the trachea. An NGT was placed. The patient was extubated and was transferred to the ICU for observation. A CXR was normal. The patient was placed on Ampicillin and Zantac. On POD # 2 a gastrograffin swallow was performed and showed no extravasation. The patient was then transferred to the PCU. On POD #4 she was transferred to the floor and clears were begun. She was advanced to soft diet and was discharged home on POD # 6 with an NGT in place and on Zantac. 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