Caustic ingestion in children

CAUSTIC INGESTION IN CHILDREN

I.       INTRODUCTION

•      Caustics and corrosives cause tissue injury by a chemical reaction. The vast majority of

caustic chemicals are acidic or alkaline substances that damage tissue by accepting a proton (alkaline substance) or donating a proton (acidic substance) in an aqueous solution.

•      Caustic ingestions occur most commonly in children,  especially those less than 6 years of age. In this age group ingestions are primarily accidental.

II.     EPIDEMIOLOGY

•      Reported to US poison control centers ingestions of caustic substances accounted for more

than  200,000  exposures  per  year.  Approximately 80%  of  caustic  ingestions  occur  in children younger than 5 years.

•      Mortality/Morbidity:  The  alkali  drain  cleaners  and  acidic  toilet  bowl  cleaners  are responsible for the most fatalities from corrosive agents:

-     Approximately 10% of caustic ingestions result in severe injury requiring treatment.

-     Between 1% and 2% of caustic ingestions results in stricture formation.

•      In Cambodia, lye or lye solution “Toeuk Kbong” has been used traditionally in the purpose of making some Cambodian cakes and implicated in traditional treatment of silk product in Khmer culture. Accidental ingestion of corrosive substance is almost alkali-based solution, which caused esophageal stricture being the common motif of hospitalization in pediatrics. Incidence of hospitalized caustic-esophageal stricture was 31 cases (40%) compared with a total numbers of caustic ingestion with 77 cases during 3 year period from July 2008 to May 2011 in Jayavarman VII children hospital Siem Reap-Angkor.

III.   ETIOLOGY

•      Common alkaline-containing sources

-     Drain cleaning products

-     Ammonia-containing products

-     Oven cleaning products

-     Swimming pool cleaning products

-     Automatic dishwasher detergent

-     Hair relaxers

-     Cement

•      Common acid-containing sources

-     Toilet bowl cleaning products

-     Automotive battery liquid

-     Rust removal products

-     Metal cleaning products

-     Cement cleaning products

-     Drain cleaning products

-     Soldering flux containing zinc chloride

IV.   PATHOPHYSIOLOGY

Caustic chemicals produce tissue injury by altering the ionized state and structure of

molecules and disrupting covalent bonds.

•      Alkaline ingestions

-     Severe injury occurs rapidly after alkaline ingestion, within minutes of contact. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction.

-     The ingestion of a strong alkali results in liquefaction necrosis, which is associated with deep penetration of the lining of the bowel and may result in perforation.

-     Injury most typically involves the esophagus, but gastric injury may also occur.

-     Over the next 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.

-     Absorption of caustic alkali may result in thrombosis of blood vessels, which further impedes the blood flow to already damaged tissue.

-     Alkalis are usually odorless and tasteless. This may result in consumption of a large volume of a caustic in cases of accidental ingestion.

-     Alkalis with a pH between 9 and 11, including  many  household   detergents, rarely  cause serious injury following ingestion.

-      Ingestion of even small quantities of an alkali with a pH above 11 may cause severe burns.

•      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.

V.     COMPLICATOIN AND PRONOSIS

•      Airway edema or obstruction may occur immediately or up to 48 hours following an

alkaline exposure.

•      Gastroesophageal perforation may occur acutely.

-     Secondary complications include mediastinitis, pericarditis, pleuritis, tracheoesophageal fistula formation, esophageal-aortic fistula formation, and peritonitis.

-     Delayed perforation may occur as many as 4 days after an acid exposure.

-     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.

-    Upper gastrointestinal hemorrhage may occur acutely in caustic exposures.

-     Delayed upper GI bleeding may occur in acid burns 3-4 days after exposure as the eschar sloughs.

-     Though many button batteries may pass through the GI tract without causing damage, they can result in perforation at any time during their course through the gastrointestinal system, particularly if they are damaged.

•      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

VI.    CLINICAL MANIFESTATION

•      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 are important in determining management of toxicity.

•      The  presence  or  absence  of  the  following  symptoms  should  be  determined  since  the presence of any of these symptoms suggests the possibility of significant internal injury. However, their absence does not preclude significant injury.

•      The most common symptoms following a caustic ingestion are :

-    Stridor, Hoarseness, dysphonia or aphonia

-    Cough,

-    respiratory distress, tachypnea, hyperpnea, dyspnea dysphagia,

-    Drooling,

-    feeding refusal,

-    retrosternal pain,

-    abdominal pain nausea and vomiting Hematemesis

•      Although minor symptoms do not rule out the presence of relevant injury, an increased number of symptoms correlate with a greater likelihood of significant injury.

•      Severe  symptoms  and  complications  reported  following  a  caustic  ingestion  include hemolysis, disseminated  intravascular coagulation, renal failure, liver failure, perforated viscus, peritonitis, mediastinitis, and death.

VII.  INVESTIGATION

1-   Laboratory Studies

•  pH testing of product

-     A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage.

-     A pH outside of this range does not preclude significant injury.

•  Complete blood count (CBC), electrolyte levels, BUN levels, creatinine level, and ABG

levels may all be helpful as baseline values and as indications of systemic toxicity.

•  Liver  function  tests  and  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.

•  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.

2-   Imaging Studies

•  Chest radiography: 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 findings does not preclude perforation or other significant injury.

•  Abdominal radiography: 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.

•  CT (chest and abdomen) will often be able to delineate small amounts of extraluminal air, not seen on plain radiographs

•  Endoscopy is generally indicated for the following patients:

-     Small children

-     Symptomatic older children and adults

-     Patients with abnormal mental status

-     Those 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.

•      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.[6] Further studies will be necessary to determine the utility of this procedure in aiding in diagnosis and treatment.

VIII. DIFFERENTIAL DIAGNOSIS

•      Gastroenteritis

•      Gastrointestinal Bleeding

•      Perforated Peptic Ulcer

•      Toxicity, Iron

•      Plant Poisoning, Oxalates

•      Croup or HYPERLINK "http://emedicine.medscape.com/article/800866- overview"Laryngotracheobronchitis

IX.   MANAGEMENT

1.   Prehospital Care

·    Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested.

·    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.

2.   Medication

·    Supportive care, rather than specific antidotes, is the mainstay of management following caustic ingestions:

-     Give IV fluid.

-     Nasogastric tube inserted with endoscopic examination for nutritional support and prevention infection.

-     The most significant therapeutic option in the acute post-injury phase (48–72 hours after ingestion), was a surgical gastrostomy, performed in children

unable to swallow liquids or saliva, to achieve adequate nutritional support.

-     When patients arrived at the hospital after a delay of 72 hours to 3 weeks after ingestion, endoscopy was not carried out due to the high risk of perforation. A

gastrostomy was performed in the presence of severe dysphagia or after an unsuccessful dilatation attempt in children admitted late at more than 3 weeks after the injury, with swallowing problems.

-     The first dilatation was always carried out at least 3 weeks after ingestion.

·    Steroids

May be used in an attempt to decrease stricture formation: Solucortef: 20mg/kg/d, bid (10

days, then prednisone 1mg/kg/d bid for 3 weeks).

·    Antibiotics: May be used in severe cases to prevent secondary infection. These agents should be administered if evidence of perforation exists.

-     Cephalosporin: Ceftriaxone 100mg/kg/d, one time per day for 10 days or

-      Ampicillin:  100mg/kg/d, one time per day for 10 days.

·    Proton Pump Inhibitor and H2 blocker

Proton pump inhibitors reduce exposure of injured esophagus to gastric acid, which may

result in decreased stricture formation. It is indicated for short-term treatment of GERD associated with erosive esophagitis. Also effective in treating gastric ulcers, including those caused by H pylori.

-     Omeprazole: 1mg/kg/day for 10 days

-     Tagamet: 20mg/kg/day bid for 10 days

·    Morphine : 0.1-0.2 mg/kg/dose IV/IM/SC 3 to 4 times per day

-     Analgesic Narcotic analgesics should be used to reduce the pain associated

with these ingestions.

·    Discharged patients should be able to ingest oral fluids without difficulty, demonstrate easy speech, be reliable, and be familiar with and able to return should any delayed symptoms occur.

·    Obtain a psychiatric evaluation for all patients with intentional ingestion.

·    Arrange for a follow-up esophagram 3-4 weeks postingestion.

X.     PATIENT EDUCATION AND PREVENTION

•      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.

•      Workplace policies and procedures need to be developed and disseminated, so that employee exposures can be treated quickly and effectively.

REFERENCES

1.   Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol. Dec 2007;45(8):815-917. [Medline].

2.   Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057.  [Medline]. [Full Text].

3.   Kay M, Wyllie R. Caustic ingestions in children. Curr Opin Pediatr. Jun 18 2009;[Medline].

4.   Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 26th Annual Report. Clin Toxicol (Phila). Dec 2009;47(10):911-1084.  [Medline].

5.   Riffat F, Cheng A. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus. 2009;22(1):89-94. [Medline].

6.   Kamijo Y, Kondo I, Watanabe M, Kan'o T, Ide A, Soma K. Gastric stenosis in severe corrosive gastritis: prognostic evaluation by endoscopic ultrasonography. Clin Toxicol.

2007;45(3):284-6. [Medline].