Caustic Ingestions

Etiology

The etiology of caustic ingestion is either accidental ingestion (often the case in children) or intentional (such as suicidal acts in the adult). Children often ingest household substances such as bleach or ammonia. Most caustic exposures involved oral ingestion (76 percent) and occur in the home (93 percent of cases). The majority of these ingestions were unintentional (greater than 80 percent). Ingestions usually involve either an acid or an alkali. Each of these categories is unique in its pathophysiology and treatment approach.[2][3]

Epidemiology

The majority of caustic ingestions occur in pediatrics, with 2.16 million toxic exposures reported in the United States, and half of these occurring in the pediatric population. Most commonly, these ingestions are from household products and accidental in the pediatric population. In the adult population, the vast majority are intentional. "Lye" (alkaline substances such as sodium or potassium hydroxides normally contained in household cleaning products) substances make up the majority of caustic ingestions.[3]

Pathophysiology

The pathophysiology depends on the type of substance involved: either an alkali or an acid. Alkalis are substances that have a pH above 7.0, and the threshold is usually above 11.5 to cause direct injury to tissue through liquefaction necrosis. Liquefaction necrosis involves the dissolution of the tissue comparatively quickly to coagulation necrosis. As the cells are lysed, digestive enzymes are released and begin to dissolve the architecture of the surrounding stroma. Alkalis cause an early breakdown of the mucosa exposed and allow for deeper penetration and injury. As with all exposures, the contact time and strength of the alkali determine the extent of the injury. However, even weak concentrations of alkali substances can cause severe damage to tissue if left in contact long enough.

Acids are more apt to cause injury if the pH is less than 2 through coagulation necrosis. Coagulative necrosis is the default mode of necrosis for most of the body when tissue is hypoxic or ischemic. It is theorized that injury tends to be less severe in acidic ingestions due to the intact stroma of the tissue performing as a barrier to further injury. The mucosa of the esophagus has a mild alkali surface, and this may help to neutralize acidic substances, further preventing injury.[4][5]

History and Physical

The history of a patient with suspected caustic ingestion must include five basic parameters in determining the appropriate treatment. Some articles on this subject have done the helpful work of organizing them into a helpful mnemonic known as the "5 W's" which will be summarized here. This aspect encompasses the rapid assessment of relevant history.

• Who: Patient demographics are key in this section. Determine the patient's age and weight, along with any accompanying family, friends, or witnesses
• What: Characteristics of medications and poisons ingested
• When: Time and date of ingestion
• Where: Route of poisoning in addition to geographic location to determine any environmental factors that may be confounding
• Why: The clinician must determine intentionality as this may greatly affect discharge disposition when the patient has been stabilized

Patients with caustic ingestions may present with oral and tongue edema, drooling, and vomiting. Some patients may have upper airway edema and present with voice changes, stridor, and respiratory distress. Hematemesis may be present if there has been erosion into a vessel. If the esophagus or stomach are perforated, mediastinitis and peritonitis, respectively, can occur.[6] The physical exam includes a customary primary and secondary assessment, consistent with emergency department practice. 

Evaluation

The primary assessment involves ABC's: airway, breathing, and circulation. Particular attention in the full assessment must be paid to the adequacy of ventilation, mental status function, and cardiac functioning. Unstable patients should be monitored continuously on telemetry and assessment of vitals occurring every fifteen minutes until stable.[5]

Lab studies obtained may include a complete blood count, a metabolic profile that includes electrolytes, and an arterial or venous blood gas. Plain radiographs of the chest and abdomen may identify free air or pneumomediastinum.

In caustic ingestion, the grade of the injury should be determined, which will guide the next steps of management after initial resuscitation has been performed. Endoscopy has traditionally been used as a method of evaluating gastrointestinal injury. Contrast-enhanced computed tomography (CECT) has been proposed as an alternative to endoscopy for the evaluation of lesions.[6]

Treatment / Management

The airway should be secured in patients with signs of impending respiratory failure including drooling and voice changes. One study showed that 50% of adults with caustic ingestions required intubation.[6] Acquiring intravenous access is necessary. Determining the ingested substance will guide management.

In terms of caustic injury, current recommendations are to dilute with water, although this has limited benefit due to the damage being determined within the first few minutes of the injury. Activated charcoal and induction of emesis should not be used in these patients.[6]

Patients with suspected evidence of mediastinitis, peritonitis, or hemodynamic instability will require emergency surgery for evaluation of the extent of the injury. If there is scant evidence of these, CECT may be performed of the neck, thorax, and abdomen to determine grades of injury.

• Grade I: Normal-appearing organs
• Grade II: Mucosa is enhanced due to edema, with soft tissue inflammatory change
• Grade III: The absence of postcontrast wall enhancement

Grade I generally indicates no endoscopy and early discharge. Grade II generally indicates non-operative treatment and endoscopy if CECT is non-diagnostic. Intravenous corticosteroids may be indicated for some Grade II burns, however, this is somewhat controversial.[6] Grade III indicates emergency surgery.

The goal of emergency surgery is to remove all necrotic tissue with laparotomy being the standard approach. What is resected is determined by the extent of injured surfaces with a spectrum ranging from resection of specific spots to major procedures such as pancreaticoduodenectomy.[5]

Differential Diagnosis

Differential diagnoses should include but not be limited to other forms of trauma, including physical trauma (including car accidents or purposeful abuse), congenital abnormalities, and direct heat-base burns. These must be worked up depending on clinical suspicion. Often the history will be sufficient along with presenting symptoms of toxidromes, but concurrent injury or suspicious findings must be included in the clinician's initial differential.[5]

Prognosis

Prognosis depends most heavily on the extent of the initial injury with mild-moderate ingestions having the most favorable prognoses and severe ingestions requiring emergency surgery having the most complications. Grade III injury or above, involves emergency surgery immediately and follow-up care. Patients tend to do worse if they require surgery, and complications are high such as mediastinitis and perforation.[2][7][8]

An extremely important topic that the surgical team should discuss with the patient before radical resection or esophageal reconstruction is the quality of life after such surgical procedures. In one study, there were significant drops in quality of life scores compared to normal populations. This should not dictate whether surgery is performed or not, but discussing with and priming the patient for potential problems is paramount.[9]

Complications

The most common early-term sequelae are those of mediastinitis or hemodynamic instability related to bleeding. These require emergency surgery to salvage and repair the damage present in the thorax or abdomen. The most common late-term sequelae of caustic ingestion are stricture at any part of the gastrointestinal tract affected by the ingestion, with the most common being esophageal stricture. Often the treatment for this comes down to esophageal dilatation, but if this is unresponsive or not feasible, then the treatment becomes surgical resection with bypass or replacement. The choice to use bowel for bypass or to use gastric tissue to bypass depends on the severity of the stricture.

Prevention of stricture is a controversial topic. In patients with a superficial injury, early oral feedings are thought to prevent stricture. Nasogastric placement can be helpful but is thought to contribute to more stricture development overall. Stents have been tried in the past with limited success (less than 50%) and high rates of migration (up to 25%). No pharmacologic agents have been noted to have success in preventing the development of strictures in the gastrointestinal tract.[7][8]