Corrosive ingestion

The history provided is concerning as it is consistent with the ingestion of a dangerous corrosive agent. For instance, solid preparations of sodium hydroxide (in combination with other agents) are commonly sold as drain cleaning products.

As with any risk assessment it is important to go to great lengths to determine the nature of the ingested substance. This may necessitate searching the home for drain cleaning products if the child’s father is unsure what the crystals were. If the product is known but you are still unsure of the contents then liaise with your regional Poison Information Centre. PIC staff  can rapidly obtain the relevant information by searching their databases and, if necessary, by accessing information from the product’s manufacturer. If the substance cannot be identified, then assume the most likely ‘worst case scenario’, track the patients clinical progress and keep an open mind.

Remember the key components of a risk assessment:

• agent(s) – (including pH for corrosive agents)
• dose(s) – (including concentration and volume for corrosive agents)
• time(s) of ingestion
• patient factors – (e.g. comorbidities)
• clinical progress – (What is the patient like now? Does the story fit?)

Try to determine if the pellets were ingested or spat out. If the pellets were spat out corrosive injury may be limited to the mouth and lips. Determining what signs and symptoms the child has now will help refine the risk assessment.

However, two key tips to remember when assessing patient’s with corrosive injuries are:

• The absence of lip or oral burns does not exclude significant gastrosophageal burns.
• Signs and symptoms correlate poorly with the extent of gastrointestinal injury

Most corrosive agents cause direct chemical injury. Some (see Q4) may also cause severe systemic toxicity.

The extent of direct chemical injury depends on:

• pH
• concentration
• volume ingested

Acidic agents cause protein denaturation resulting in coagulative necrosis. Alkaline agents are more dangerous as they cause liquefactive necrosis resulting in deep and progressive mucosal burns. Other corrosive agents may have reducing, oxidizing, denaturing or defatting actions.

Commonly available corrosive agents include:

• Sodium hydroxide — detergents, drain and oven cleaners, button batteries
• Sodium hypochlorite — bleaches and household cleaners (unintentional ingestion in children is generally benign, dilute solutions less than 150 mL do not cause significant corrosive injury)
• Ammonia — metal and jewelery cleaners, anti-rust products
• Hydrochloric acid — metal cleaners
• Sulfuric acid — drain cleaners, car batteries
• Button batteries — injury results from leakage of alkali, local electrical current discharge and direct pressure necrosis

Examples of corrosive agents that can cause severe systemic toxicity include:

• glyphosate (toxicity may be due to the herbicide’s polyoxyethyleneamine surfactant) — metabolic acidosis, shock, multi-organ dysfunction
• hydrofluoric acid — hypocalcemia
• mercuric chloride (inorganic mercury salts) — renal failure, shock
• oxalic acid — hypocalcemia, renal failure
• paraquat — pulmonary fibrosis, multi-organ dysfunction and shock
• phenol — coma, seizures, hepatotoxicity, renal failure
• phosphorus — hepatotoxicity, renal failure
• picric acid — renal failure
• potassium permangante — methemoglobinemia, multi-organ failure
• silver nitrate — methemoglobinemia
• tannic acid — hepatotoxicity

Remember (at the risk of excessive repetition…):

• The absence of lip or oral burns does not exclude significant gastrosophageal burns
• Signs and symptoms correlate poorly with the extent of gastrointestinal injury

Corrosive ingestion may result in immediate symptoms of injury to the gastrointestinal tract:

• mouth and throat pain
• drooling
• odynophagia
• vomiting
• abdominal pain

Upper airway injury is the most important immediate life-threat. Laryngeal injury and edema presents with:

• progressive stridor
• hoarseness
• respiratory distress

The  endoscopic findings of corrosive injuries are graded as follows:

• Grade 0 — normal
• Grade I — mucosal edema and hyperemia
• Grade IIA — superficial ulcers, bleeding and exudates
• Grade IIB — deep focal or circumferential ulcers
• Grade IIIA — focal necrosis
• Grade IIIB — extensive necrosis

Complications include:

• Perforation
  • Esophageal perforation and mediastinitis (chest pain, dyspnea, fever, subcutaneous edema)
  • perforation of the stomach or small intestine resulting in peritonitis
  • septic shock and multiple organ dysfunction syndrome (MODS)
• Esophageal strictures — occurs in 30% of patients with Grade IIB or II injury on endoscopy
• Esophageal carcinoma — may occur over 40 years after a Grade II or III corrosive injury

This boy’s father did the right thing:

Rinse the mouth with water as an immediate first aid measure.

Important things NOT to do include:

• do not induce vomiting
• do not administer oral fluids
• do not administer activated charcoal
• do not attempt pH neutralisiation
• do not perform gastric lavage or insert an nasogastric tube (until endoscopy is performed)

Use the Resus-RSI-DEAD approach.

Resuscitation:

Manage the patient in an area equipped for resuscitation with appropriately skilled staff.

Assess for life-threats – is there evidence of airway compromise? (see Q5)

• airway compromise from oedema may progress rapidly
• prepare to intubate early at the first signs of compromise, otherwise the edema may progress and a surgical airway become the only available option.
• Call for expert help (e.g. the most senior anesthetist available, with ENT back-up) and consider intubating while the patient is spontaneous breathing (e.g. gas induction in the operating theatre or an awake fiber-optic intubation in a cooperative patient).

Risk assessment (see Q1) — assess for evidence of corrosive injury (see Q5):

• symptoms and signs of gastrointestinal injury
• remember to check for corrosive injuries to other parts of the body such as the skin and eyes.

Supportive care and monitoring (including adequate analgesia)

• keep the patient NBM if symptomatic, pending endoscopic assessment.
• Do not insert a nasogastric tube until cleared of gastrointestinal injury (e.g. endoscopy)

Investigations, decontamination, enhanced elimination and antidotes:

• Perform a chest x-ray and abdominal x-ray for evidence of perforation if the child has suggestive symptoms or signs
• No further decontamination is needed
• Enhanced elimination is not useful
• No antidotes are available

Disposition is determined by the risk assessment and the child’s clinical progress.

The possibilities are:

• The child is asymptomatic at 4 hours post-ingestion, so a trial of oral fluids is performed. If this is tolerated well the child can be discharged (avoid discharging a child at night). Some experts advocate endoscopy following corrosive ingestion even in the asymptomatic patient.
• The child is symptomatic (e.g. throat pain, drooling, pain on attempting to swallow his own saliva, or has vomiting or abdominal pain). The child is kept NBM and admitted for observation and an endoscopy within 24 hours.
• The child has airway compromise. Take measures to secure the airway and arrange ICU admission.
• The child has evidence of gastrointestinal perforation, sepsis or hemodynamic instability. Arrange for an urgent surgical assessment and ICU admission.

No — unless there is evidence of gastrointestinal perforation, which may result in mediastinitis or peritonitis and subsequent severe sepsis.

The use of corticosteroids for the treatment of gastrointestinal corrosive injuries from alkaline agents is controversial. However there is no evidence that corticosteroids are effective in preventing esophageal stricture formation. Furthermore, there are concerns that corticosteroids may actually increase mortality in Grade III injuries, increase the risk of infection or conceal the symptoms and signs of perforation.

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