Caustic Ingestions

Caustic chemicals produce tissue injury by altering the ionized state and structure of molecules and disrupting covalent bonds. In aqueous solutions, the hydrogen ion (H+) produces the principal toxic effects for the majority of acids, whereas the hydroxide ion (OH-) produces such effects for alkaline substances.

Alkaline ingestions

Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small-vessel thrombosis and heat production occurs.

Severe injury occurs rapidly after alkaline ingestion, within minutes of contact. The most severely injured tissues are those that first contact the alkali, which is the squamous epithelial cells of the oropharynx, hypopharynx, and esophagus. The esophagus is the most commonly involved organ, with the stomach much less frequently involved after alkaline ingestions. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction. Over time, if the injury was severe enough, granulation tissue starts to replace necrotic tissue.

Over the subsequent 2-4 weeks, any scar tissue formed initially remodels and may thicken and contract enough to form strictures. The likelihood of stricture formation primarily depends upon burn depth. Superficial burns result in strictures in fewer than 1% of cases, whereas full-thickness burns result in strictures in nearly 100% of cases. The most severe burns also may be associated with esophageal perforation.

Acid ingestions

Acid ingestions cause tissue injury by coagulation necrosis, which causes desiccation or denaturation of superficial tissue proteins, often resulting in the formation of an eschar or coagulum. This eschar may protect the underlying tissue from further damage. Unlike alkali ingestions, the stomach is the most commonly involved organ following an acid ingestion. This may due to some natural protection of the esophageal squamous epithelium. Small bowel exposure also occurs in about 20% of cases. Emesis may be induced by pyloric and antral spasm.

The eschar sloughs in 3-4 days and granulation tissue fills the defect. Perforation may occur at this time. A gastric outlet obstruction may develop as the scar tissue contracts over a 2- to 4-week period. Acute complications include gastric and intestinal perforation and upper gastrointestinal hemorrhage.

Endoscopic view of the esophagus after ingestion of an acid is shown in the images below.

Caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive thrombosis of the esophageal submucosal vessels giving the appearance similar to chicken wire. Courtesy of Ferdinando L Mirarchi, DO, Fred P Harchelroad, Jr, MD, Sangeeta Gulati, MD, and George J Brodmerkel, Jr, MD.

Caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the appearance of the thrombosed esophageal submucosal vessels giving the appearance of chicken wire. Courtesy of Ferdinando L Mirarchi, DO, Fred P Harchelroad, Jr, MD, Sangeeta Gulati, MD, and George J Brodmerkel, Jr, MD.

Caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive burn and thrombosis of the submucosal esophageal vessels, which gives the appearance of chicken wire. Courtesy of Ferdinando L Mirarchi, DO, Fred P Harchelroad, Jr, MD, Sangeeta Gulati, MD, and George J Brodmerkel, Jr, MD.

Significant exposures may also result in gastrointestinal absorption of the acidic substances leading to significant metabolic acidosis, hemolysis, acute kidney injury, and death.

Common acid-containing sources include the following:

• Toilet bowl–cleaning products
• Automotive battery liquid
• Rust-removal products
• Metal-cleaning products
• Cement-cleaning products
• Drain-cleaning products
• Soldering flux containing zinc chloride

Common alkaline-containing sources include the following:

• Drain-cleaning products
• Ammonia-containing products
• Oven-cleaning products
• Swimming pool–cleaning products
• Automatic dishwasher detergent
• Hair relaxers
• Clinitest tablets
• Bleaches
• Cement

Cleaning substances, many of which contain potentially caustic agents, account for over 200,000 exposures per year reported to US poison control centers and represent the second most frequent category of exposure.[2, 3]

Approximately 80% of caustic ingestions occur in children younger than 5 years. Liquid ingestions can be quite serious. Critical solid ingestions are rare, because children generally do not swallow the burning particles that adhere to their oropharynx, but disk batteries and detergent pods are exposures that deserve particular attention in pediatric patients.[4, 5]

Most intentional ingestions occur in adults. Adult exposures have greater morbidity than childhood exposures because of the often higher volume of the exposure and the presence of possible co-ingestants. Occupational exposures often are more severe than other exposures because industrial products are more concentrated than those found in the home.[6]

As with all potential toxicants, the prognosis is a function of substance potency and exposure duration. Characteristics that increase the potential toxicity of these substances are the pH, the volume, and concentration of the agent; its ability to penetrate tissues; and its titratable reserve. The titratable reserve is a term that reflects the amount tissue required to neutralize a given amount of agent. Some substances are deadly even with small exposures, such as hydrofluoric acid. Some substances are relatively tolerable despite larger exposures, such as household vinegar.

Adults with psychiatric comorbidities have poorer prognosis. A retrospective study of 839 adults treated for caustic ingestion injuries treated at a single hospital reported that those with confirmed psychiatric diagnoses had a predicted 5-year survival of < 50%.[7]

Caustic agents should be stored in their original child-resistant containers. Many accidental childhood ingestions occur as a result of caustic substances being placed in easily accessed containers, such as milk cartons or soda bottles.

The reduced concentration of household products compared with their industrial strength counterparts has also been helpful in mitigating the severity of childhood exposures to agents such as household cleaners.

For patient education information, see First Aid for Poisoning in Children and Child Safety Proofing. as well as Battery Ingestion.

The physician should try to identify the specific agent ingested, as well as the concentration, pH, and amount of substance ingested. The time, nature of exposure, duration of contact, and any immediate on-scene treatment that was provided are important in determining management of toxicity.

The presence or absence of the following symptoms should be determined, since the presence of any of them suggests the possibility of significant internal injury (although their absence does not preclude significant injury):

• Dyspnea
• Dysphagia
• Oral pain and odynophagia
• Chest pain
• Abdominal pain
• Nausea and vomiting

Rapidly obtaining reliable information on the particular agent involved is vital. This is particularly true of uncommon caustic agents, some of which have important toxic concerns beyond those of a simple caustic ingestion.

A good example of this is the potential for abrupt, life-threatening hypocalcemia following ingestion of hydrogen fluoride, even in a relatively dilute form such as that found in some rust removers. Case reports of patients surviving such suicidal ingestions underline the value of being able to anticipate and aggressively manage the systemic hypocalcemia, which is unique to hydrogen fluoride, with intravenous calcium. Other examples of caustic agents with unique toxicities include phenol, zinc chloride, and mercuric chloride, all of which can cause significant systemic toxicity and which may require specifically directed management.

Material Safety Data Sheets (MSDS), online databases, and consultations with the local poison center are all ways for clinicians to rapidly familiarize themselves with unfamiliar caustic agents.

As with the history, physical examination findings may be deceptively unremarkable after a significant caustic ingestion, despite the presence of significant tissue necrosis.

Signs of impending airway obstruction may include the following:

• Stridor
• Hoarseness
• Dysphonia or aphonia
• Respiratory distress, tachypnea, hyperpnea
• Cough

Other signs of injury may include the following:

• Tachycardia
• Oropharyngeal burns – These are important when identified; however, significant esophageal involvement may occur in the absence of oropharyngeal lesions
• Drooling
• Subcutaneous air
• Acute peritonitis – Abdominal guarding, rebound tenderness, and diminished bowel sounds
• Hematemesis

Indications of severe injury include the following:

• Altered mental status
• Peritoneal signs
• Evidence of viscous perforation
• Stridor
• Hypotension
• Shock

Immediate, general complications of caustic and corrosive exposures may include airway edema or obstruction, which may occur immediately or up to 48 hours following an alkaline exposure. Gastroesophageal perforation and upper gastrointestinal hemorrhage may occur acutely in caustic exposure. Secondary complications include the following:

• Mediastinitis
• Pericarditis
• Pleuritis
• Tracheoesophageal fistula formation
• Esophageal-aortic fistula formation
• Peritonitis

Disk batteries deserve special attention because they can adhere to the esophageal or gastric mucoa, leading to perforation due to prolonged contact with extruded substances and residual electric discharge. See Disk Battery Ingestion for a detailed discussion.

Delayed perforation may occur as many as 4 days after an acid exposure. Delayed upper GI bleeding may occur in acid burns 3-4 days after exposure as the eschar sloughs. Deep circumferential or deep focal burns may result in strictures in more than 70% of patients; these strictures typically develop 2-4 weeks postingestion. Gastric outlet obstruction may develop 3-4 weeks after an acid exposure.

Some agents have the ability to cause systemic toxicity that affects the prognosis in addition to their caustic properties. These include the following:

• Phenol
• Zinc chloride
• Mercuric chloride
• Hydrogen fluoride
• Oxalic acid
• Detergent pods

In pediatric patients, detergent pods have been observed to sometimes cause altered mental status and lactic acidosis, hypothesized to be due to their ingredients of propylene glycol and or alcohol ethoxylates.

Cardiac arrest from sudden hypocalcemia may occur in patients who have ingested hydrogen fluoride–containing substances. Patients have been successfully resuscitated with aggressive use of intravenous calcium chloride.

Long-term risks include squamous cell carcinoma, which occurs in 1-4% of all significant exposures and may occur as late as 40 years after exposure.

The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents. In adults, 10% of caustic ingestions result in death.[8]

Approximately 10% of caustic ingestions result in severe injury requiring treatment. Approximately 1-2% of caustic ingestions result in stricture formation.[8]

Laboratory studies may include the following:

• pH testing of product: A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage,[9] but a pH outside of this range does not preclude significant injury.

• pH testing of saliva: Unexpected high or low values may confirm ingestion in questionable cases; however, a neutral pH cannot rule out a caustic ingestion.

• Complete blood count (CBC) and electrolyte, blood urea nitrogen (BUN), creatinine, and arterial blood gas (ABG) levels may all be helpful as baseline values and as indications of systemic toxicity.

• Liver function tests and a disseminated intravascular coagulation (DIC) panel may also be helpful to establish baselines or, if abnormal, confirm severe injury following acid ingestions.

• Urinalysis and urine output may help guide fluid replacement.

• Blood type and crossmatch are indicated for any potential surgical candidates or those with the potential for gastrointestinal bleeding.

• Obtain aspirin and acetaminophen levels as well as an electrocardiogram (ECG) in any patient whose intent may have been suicidal.

• In cases of hydrofluoric acid (HF) ingestion, precipitous falls in calcium level may lead to sudden cardiac arrest. Although ionized calcium levels are likely to have too long a turnaround to be clinically useful, cardiac monitoring and serial ECGs may help anticipate this event

Obtain an upright chest radiograph in all cases of caustic ingestion. Findings may include pneumomediastinum or other findings suggestive of mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign body). However, the absence of such findings does not preclude perforation or other significant injury.

Abdominal radiographic findings may include pneumoperitoneum, ascites, or an ingested button battery (metallic foreign body). If contrast studies are obtained, water-soluble contrast agents are recommended because they are less irritating to the tissues in cases of perforation.

Computed tomography (CT) scans will often be able to delineate small amounts of extraluminal air, not seen on plain radiographs.

Chirica et al cite CT as superior to traditional endoscopy for helping to decide whether patients require emergency resection or observation.[1]  Similarly, Bruzzi et al reported that emergency CT outperforms endoscopy in predicting esophageal stricture formation after caustic ingestion.[10]

On the other hand, Lurie et al evaluated the role of chest and abdominal CT in assessing the severity of acute corrosive ingestion and concluded that CT should not be the only basis for surgical decisions during the initial phase of acute corrosive ingestions. They noted that CT can underestimate the severity of corrosive ingestion as compared with endoscopy. In their retrospective study of 23 patients, endoscopy findings were graded as 0, 1, 2a, 2b, 3a, and 3b (Zargar criteria); and CT findings were graded as 0, 1, 2, and 3. Endoscopy grading was found to be higher than CT grading in 14 patients (66%).[11]

Airway protection is critical following caustic ingestion if there is any indication of airway compromise. This can develop rapidly and be complicated by multiple factors. See Emergency Department Care. Cardiac monitoring is indicated for any patient with a caustic ingestion.

Endoscopy is generally indicated for the following patients:

• Small children who are not tolerating liquids or with complaints of pain
• Patients with a disk battery ingestion identified in the esophagus or stomach
• Symptomatic older children and adults
• Patients with abnormal mental status
• Patients with intentional ingestions
• Patients in whom injury is suspected for other reasons (eg, ingestion of large volumes or concentrated products)

However, because of the risk of increased injury, esophagoscopy should not be performed in patients with evidence of esophageal or gastrointestinal perforation, significant airway edema, or necrosis and in those who are hemodynamically unstable. Endoscopy is typically avoided when more than 24 hours have elapsed after the ingestion due to decreased wound strength and an increased risk of iatrogenic perforation. 

Obtaining meaningful information from endoscopy after treatment with activated charcoal is very difficult. Routine use of activated charcoal is not recommended in caustic ingestions.

Endoscopic ultrasonography has been shown to more accurately show the depth of lesions than endoscopy alone.[12] Further studies will be necessary to determine the utility of this procedure in aiding in diagnosis and treatment.

Endoscopy findings are commonly graded as described in the table below.[13]

Classification of caustic mucosal damage ^[14]   (Open Table in a new window)

In patients with caustic ingestion, airway monitoring and control is the first priority. When airway compromise is present, a definitive airway must be established. In patients with a stable airway and no clinical or radiological sign of perforation, medical therapy should be initiated.[15, 16, 17, 18]

Arrangements should be made for urgent esophagogastroduodenoscopy (EGD) to grade the degree of injury and establish long-term prognosis, In asymptomatic patients, however, EGD may be withheld in favor of observation. Pediatric patients who remain asymptomatic for 2 - 4 hours after an exploratory ingestion and who are tolerating a normal diet may be discharged with appropriate follow-up and return precautions. Surgical consultation is indicated for suspected perforation. Because of the risk of late complications—most commonly, esophageal stricture formation—arrangements for follow-up need to be made.[15, 16, 17]

Adult patients with an unintentional exposure may be discharged after a 2- to 4-hour observation period if the clinician has no unique concerns regarding the ingested substance (eg, large volume, high concentration, agent with potential for systemic toxicity) and the patient meets all the following criteria:

• Asymptomatic
• Clear sensorium
• Able to ingest oral fluids without difficulty
• Demonstrates easy speech
• Reliable
• Familiar with delayed symptoms and able to return if any occur

Post-discharge arrangements may include the following:

• Psychiatric evaluation for all patients with intentional ingestion
• Follow-up esophagram 3-4 weeks postingestion

Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested. Obtain MSDS sheets when possible for workplace exposures. The product container or labels may be available. Avoid exposure to health care workers.

Do not induce emesis or attempt to neutralize the substance by using a weak acid or base. This induces an exothermic reaction, which can compound the chemical injury with a thermal injury. It may also induce emesis, re-exposing tissue to the caustic agent.

Small amounts of a diluent may be beneficial if administered as soon as possible after a solid or granular alkaline ingestion, to remove any particles that are adhering to the oral or esophageal mucosa. Water or milk may be administered in small amounts. It is very unlikely to be of any benefit after more than 30 minutes. This practice is controversial: Some of the literature available on this topic discourages the use of diluents because of the concern of inducing emesis resulting in re-exposure of tissue to caustic agent.

Diluents should not be used with any acid ingestion or liquid alkaline ingestion, as it could provoke vomiting. The resulting re-exposure of the oral or esophageal mucosa to the offending substance could worsen the injury or lead to perforation.

In the treatment area, patients suspected of ingesting a caustic substance should be triaged to a high priority for prompt evaluation and treatment. This includes prompt evaluation of airway and vital signs as well as immediate cardiac monitoring and intravenous access. Intravenous fluids and blood products may be required in the event of significant bleeding, vomiting, or third spacing.

Airway control

Because of the risk of rapidly developing airway edema, the patient’s airway and mental status should be immediately assessed and continually monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available. Gentle orotracheal intubation or fiberoptic-assisted intubation is preferred. Blind nasotracheal intubation should be avoided due to the increased risk of soft-tissue perforation.

If possible, it is best to avoid inducing paralysis for intubation because of the risk of anatomical distortion from bleeding and necrosis. If a difficult airway is anticipated, IV ketamine can be used to provide enough sedation to obtain a direct look at the airway.

Cricothyrotomy or percutaneous needle cricothyrotomy may be necessary in the presence of extreme tissue friability or significant edema.

Gastric emptying and decontamination

Do not administer emetics because of potential re-exposure of the vulnerable mucosa to the caustic agent. This may result in further injury or perforation.

Gastric lavage by traditional methods using large-bore orogastric Ewald tubes is contraindicated in both acidic and alkaline ingestions because of risk of esophageal perforation and tracheal aspiration of stomach contents.

In large-volume liquid acid ingestions, nasogastric tube (NGT) suction may be beneficial if performed promptly after ingestion. Pyloric sphincter spasm may prolong contact time of the agent to the gastric mucosa for up to 90 minutes. NGT suction may prevent small intestine exposure. Esophageal perforation is rare. NGT suction may be of particular value following ingestion of zinc chloride, mercuric chloride, or hydrogen fluoride, unless signs of perforation are present. Of note, intubation with sedation is likely necessary for patients to tolerate this procedure and allow clinicians to perform it without instigating secondary esophageal injury (from vomiting) and or aspiration. This should be done after consulting with a regional poison control center.

Activated charcoal is relatively contraindicated in caustic ingestions because of poor adsorption and endoscopic interference.

Dilution

Dilution may be beneficial for ingestion of solid or granular alkaline material if performed within 30 minutes after ingestion using small volumes of water. Because of the risk of emesis, carefully consider the risks versus benefits of dilution.

Do not dilute acids with water; this would result in excessive heat production.

Neutralization

Do not administer a weak acid in alkaline ingestions or a weak alkaline agent in acid ingestions. This may cause an exothermic reaction, with damage from the resulting heat. In addition, the risk of emesis makes this a hazardous intervention.

Hospitalization

Admit, for observation and possible endoscopy, all small children, symptomatic patients, those with altered mental status, and those whose ingestions are worrisome for other reasons, such as large volumes, high concentrations, or unique issues such as those posed by hydrogen fluoride or phenol. Admit all symptomatic patients to the ICU to closely monitor their airway status and to watch for signs of perforation.

Ensure that all patients take nothing per mouth (NPO) until the extent of injury has been determined. Establish an intravenous line to administer fluids and medications.

Administer parenteral analgesics as needed for pain. Monitor for signs of sedation and respiratory depression.

Rollin et al have proposed an algorithm for surgical management of caustic ingestion injuries in adult patients.[8]

If an ICU bed is not available or if endoscopy is not available when indicated, transfer is advised.

Airway management can be a multifaceted problem and may be best approached with the availability of a wide array of visualization techniques, and, if time allows, a team of experts. However, the rapid development of airway edema may prompt the need for rapid airway management with the best immediately available visualization approach.

Obtain a surgical consultation when any of the following are expected or observed:

• Perforation
• Mediastinitis
• Peritonitis

Obtain an endoscopic consultation for the following patients:

• Small children
• Symptomatic older children and adults
• Patients with altered mental status
• Patients with intentional ingestions
• Cases with a potential for significant injury (eg, ingestion or large volumes or concentrated products)

Consultation with the local poison control center may be helpful, particularly if unfamiliar or unique agents are involved. These may include industrial strength detergents, button batteries, zinc chloride, mercuric chloride, hydrogen fluoride, phenol, and Clinitest tablets.

Once a patient is stabilized, obtain a psychiatric consultation for any patients with a history of an intentional ingestion.

Corticosteroids remains a controversial treatment to attempt to decrease morbidity from caustic and corrosive injuries. Early use was driven by decreased stricture formation in animal models, but this benefit was not demonstrated in subsequent patient cohorts.[19, 20]  A more recent study that focused on high risk injuries only found a benefit from a short 3-day course (in contrast to longer duration treatment in earlier studies) of methylpredisonolone in pediatric patients with grade 2B esophageal injuries.[21] At this time, recommendations on the use, dose, and duration of corticosteroids remains contentious even among experts in the field.

Esophageal stricture can develop as early as 3 weeks after caustic ingestion, but typically occurs 8 weeks or longer afterwards. Strictures can be treated with esophageal dilatation, using bougies (usually Savary) or balloon catheters. Savary bougies are considered more reliable for treatment of consolidated and fibrotic strictures or long, tortuous ones, and bougie dilatation may pose lower risk of perforation, compared with rates as high as 30% reported with balloon dilatation of caustic strictures.[17]

However, in a study by Uygun et al, fluoroscopically guided esophageal balloon dilatation (EBD) was found to be a safe procedure, with a low rate of complications; and it had a 100% success rate. In their review of of 369 EBD sessions in 38 children (aged 14 months to 14 years, median 3.5 years) with caustic esophageal strictures, six (1.6%) esophageal perforations occurred in five patients (13.2%).[22]

Ugyun et al recommend that in children, dilatation should be performed gently with balloons of gradually increasing appropriate diameters over consecutive sessions. In addition, the study findings showed that EBD treatment was significantly faster and shorter in patients who began EBD earlier (mean, 15 days) after caustic ingestion than in those who began it later (mean, 34 days).[22]

When esophageal dilatation is not possible or fails to provide an adequate esophageal caliber in the long-term, esophageal replacement by retrosternal stomach or, preferably, right colonic interposition should be considered. Arguments can be made for either bypass or resection of the native esophagus.[17]

In the home, caustic substances should be kept in their original labeled containers to avoid accidental ingestion. They should be stored out of reach of toddler-aged children.

In the workplace, policies and procedures need to be developed and disseminated, so that employee exposures can be treated quickly and effectively.

Patients who have experienced caustic injury are at increased risk for esophageal cancer (both adenocarcinoma and squamous cell carcinoma), typically developing 1 to 3 decades after ingestion. Consequently, long-term endoscopic screening is recommended for these patients.[17]

Guidelines on pediatric gastrointestinal endoscopy from the European Society of Gastrointestinal Endoscopy (ESGE) and European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) include the following suggestions and recommendations for management of corrosive ingestion in pediatric patients[23] :

• Suggestion: Every child who has ingested a corrosive substance should have a thorough follow-up, with endoscopy dictated only by symptoms; depending on the symptoms, endoscopy should be performed within 24 hours. (Strong recommendation, high quality evidence.)
• Recommendation: Every child with a suspected caustic ingestion and symptoms or signs (eg, oral lesions, vomiting, drooling, dysphagia, hematemesis, dyspnea, abdominal pain) should undergo esophagogastroduodenoscopy (EGD) to identify all consequent digestive tract lesions. (Strong recommendation, high quality evidence.)
• Suggestion: In cases of suspected corrosive ingestion where the child is asymptomatic (no drooling of saliva/other symptoms, no mouth lesions) and adequate follow-up is assured, EGD may be withheld. (Weak recommendation, moderate quality evidence.)
• Recommendation: In patients with grade IIb esophagitis after corrosive ingestion, high doses of intravenous dexamethasone (1 g/1.73 m ² per day) should be administered for a short period (3 days), to prevent the development of esophageal stricture. No evidence of benefit exists for the use of corticosteroids in other grades of esophagitis (I, IIa, III). (Strong recommendation, moderate quality evidence.)

Supportive care, rather than specific antidotes, is the mainstay of management following caustic ingestions. Medications useful for this purpose include antibiotics, proton pump inhibitors, and analgesics. A systematic review and meta-analysis by Katibe et al concluded that the available evidence does not support the use of corticosteroids for the prevention of esophageal strictures following caustic ingestion, but noted that the overall quality of the evidence is limited.[24]

A significant exception to this would be the aggressive administration of intravenous calcium for dysrhythmias precipitated by hypocalcemia from hydrogen fluoride ingestion. Such therapy is best performed with the guidance of the toxicologist at the local poison center.

Class Summary

These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

Class Summary

These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.

Ampicillin and sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.

Class Summary

Proton pump inhibitors reduce exposure of injured esophagus to gastric acid, which may result in decreased stricture formation.

Pantoprazole (Protonix)

Indicated for short-term treatment of GERD associated with erosive esophagitis. Also effective in treating gastric ulcers, including those caused by Helicobacter pylori.

Class Summary

Narcotic analgesics should be used to reduce the pain associated with these ingestions.

Morphine

DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Various IV doses are used; commonly titrated until desired effect obtained.