Caustic Ingestion Injuries

Caustic Ingestion Injuries . The ingestion of caustic substances is a medical emergency that can cause a wide spectrum of potentially serious injuries in the short and long term. Domestic products in their liquid form, and among them bleach (sodium hypochlorite), are the most frequently ingested agents. Ingestion of an acid is associated with more serious injuries.


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  • 1 Definition
    • 1 Etymology of the word
  • 2 Classification of injuries
    • 1 Clinical manifestations
    • 2 Pathophysiology
    • 3 Clinical criteria
    • 4 Diagnosis
    • 5 Injuries caused
    • 6 Preventive measures
  • 3 Reference
  • 4 See also
  • 5 sources


Damage to the esophagus and stomach from caustic ingestion is associated with high morbidity and mortality. In most cases the ingestion is accidental, practically universal in children, with a more even proportion in adults between accidental ingestion, predominantly, and for suicide purposes. In cases of voluntary ingestion, this is usually with higher volumes and with more corrosive agents, which conditions the appearance of more serious injuries.

word etymology

It is known as an injury (word derived from the Latin laesĭo) to a blow, wound, damage, harm or detriment. The concept is usually linked to physical deterioration caused by a blow, an injury or an illness . Substances that damage tissues on contact are known as caustic (adjective from the Latin causticus, “substance that burns” and destroys animal tissue ) or corrosive (adjective from the Latin corrosivus, “that corrodes” or has the virtue of corroding). [1]

Classification of injuries

Injuries caused by caustic substances are classified, from a pathological point of view, in a similar way to skin burns. Generally, alkalis induce liquefactive necrosis and acids coagulative necrosis. In general, there is a good relationship between the degree of depth of the lesion, the endoscopic findings and the prognosis. The most commonly ingested caustic substances are alkalis, such as sodium hydroxide, potassium hydroxide , sodium and potassium carbonate, ammonium hydroxide and potassium permanganate, generally used for kitchen cleaning.

Classification of injuries caused by caustic substances

These substances can be in the form of liquid, crystals or tablets. Less frequently, the ingestion is of acids for industrial use such as hydrochloric and sulfuric acid, which are not generally available to the public. However, these acid cleaning products are readily available in some countries. Also, various acidic substances are used by some communities to prepare special foods.

Clinical manifestations

The immediate clinical symptomatology is highly variable; from patients with few symptoms, which are the majority, to very severe cases with multiple local and systemic manifestations. There is not always a good association between symptoms and the extent of digestive injuries (up to 10% of patients with severe esophageal injuries are asymptomatic).

Caustic contact with the oropharynx, particularly with acids, produces oral burning, hypersalivation, and drooling, with edema, whitish exudates, and painful, friable ulcers on physical examination. Esophageal involvement induces dysphagia, odynophagia, heartburn, and chest pain. Epigastric pain, nausea, vomiting and hematemesis, with little clinical and analytical repercussion except in the case of aortoesophageal fistula, indicate gastric or duodenal involvement.

If there is respiratory involvement, by contact, aspiration or inhalation, stridor, hoarseness, cough and dyspnea may appear . Perforation usually occurs in the first 2 weeks and should be suspected if the patient’s clinical condition deteriorates with signs of mediastinitis or peritonitis. Other serious complications include respiratory distress, disseminated intravascular coagulation, aspiration pneumonia, septic shock, and the development of aortoesophageal or tracheoesophageal fistulas.

In general, the reappearance of dysphagia indicates stenosis —associated or not with an esophageal motor disorder— with a frequency that ranges between 5 and 73% of cases, due to the heterogeneity of the studies. Gastric or duodenal stenosis is expressed by a clinical picture of “retention stomach” with nausea, retention vomiting, progressive early satiety and weight loss, which appears after 3-6 weeks although it may take several years to manifest.

The risk of developing squamous cell carcinoma of the esophagus is increased 1,000-3,000 times compared to the normal population, with a latency period greater than 40 years. Mortality due to ingestion of caustics has decreased in recent years and ranges between 3 and 5%.


Damage to the esophagus caused by caustic depends fundamentally on three factors: a) the amount and concentration of caustic ingested; b) the type of caustic ingested c) the contact time of the caustic with the esophagus. Injuries caused by voluntary ingestion are usually more serious than accidental ingestion, since the latter is usually of smaller amounts.

Clinical criteria

The aggression of the ingested caustic is not limited to the esophagus either, being able to find gastric, duodenal injuries and, depending on the agent ingested, also systemic injuries. Alkalis in contact with the wall of the digestive tract produce necrosis due to liquefaction, which can cause lesions in all the layers of the esophagus, which can cause perforation of the organ.

In most cases the intake is practically in children

These alterations begin within a few seconds of contact of the alkali with the digestive tract. Between 2 and 3 days thrombosis of blood vessels, cell necrosis, microbial infiltration and saponification of fats are added. Between 4 and 7 days, the detachment of the mucous layer can be observed. These alterations configure the acute phase. Subsequently, a subacute or latent phase is established in which granulation tissue forms. This phase can be extended until the third week. The characteristics of the action of the alkali favor the penetration of the damage and prevent the effectiveness of the neutralization, conditioning the transmural injury of the caustic with its devastating consequences.

Around the third week, a process of fibrosis begins to be observed that can cause an esophageal stenosis, although this can also appear in the longer-term evolution. Before 1967 these products were in the form of crystals or solid particles. This conditioned caustic adhesion to the oropharyngeal and esophageal mucosa, producing lesions at that level and a burning sensation on the lips and tongue that prompted the patient to expel the product. The lesions produced by this form of presentation predominated in the oropharynx, affecting the esophagus to a lesser extent and rarely the stomach. Later, the cleaning product industry introduced concentrated liquid forms, which created a bigger problem.

These often colorless and odorless substances facilitate accidental ingestion. On the other hand, its higher viscosity determines a longer contact time with the esophageal mucosa, producing more serious injuries. The intake of acidic liquids, on the other hand, produces a coagulation necrosis that can in some way damage the digestive tract deeper. In addition, acid intake produces severe burning pain in the oropharynx that helps limit intake, especially if it is accidental.

Likewise, as it is a liquid product and passes quickly to the stomach , it causes less intense lesions in the esophagus, for which the protective effect of the squamous epithelium has also been invoked. In any case, some authors have described important lesions in the esophagus with perforation and/or formation of esophageal stenosis. When digestive tract damage is associated with organ perforation, the result is mediastinitis or peritonitis, which can lead to sepsis with multi-organ failure and death.


In the anamnesis it is important to highlight the type and amount of caustic ingested. The symptoms reported after the ingestion of caustics are mainly retrosternal and oropharyngeal pain, but abdominal pain, vomiting , dysphagia and stridor can also be observed. Digestive bleeding or symptoms related to perforation of the viscera may also occur, which can occur at any time during the course of the first 2 weeks . The presence of abdominal pain with rigidity and guarding suggests perforation. If it is in the esophagus, it will be associated with chest pain with irradiation to the back. Perforation with passage of caustic outside the viscera can affect neighboring organs, such as the pancreas and spleen.

Injuries to the esophagus from caustic ingestion

However, it is important to note that the symptoms are not clearly related to the severity of the digestive tract injury. Likewise, the presence or absence of oropharyngeal injuries does not predict esophageal injuries. This may be linked to the type of substance and its physical form. The association of stridor and dysphonia suggests involvement of the larynx and epiglottis, or caustic aspiration. A thorough clinical examination of the oropharynx, abnormal breath sounds, and abdominal palpation should be performed.

injuries caused

There are several endoscopic classifications of acute injuries, but the most widespread is the modified Zargar classification. It is important for the endoscopist to carefully describe these signs, detailing their topography and extent. Since these signs are important in the evolution of the patient and therefore will define its management. When the grades are 1 or 2a, the lesions are mild and the patient can be discharged, enabling the oral route of feeding. If more advanced grades such as 2b or 3 are observed, more careful management is required in special units, since these are the ones that can be complicated by perforation or later by stenosis .

Contrasted radiological studies currently have no greater indication in the acute phase, since they do not provide more data. The barium contrast study can be useful when the presence of gastroduodenal strictures is suspected and later in the evaluation of esophageal strictures.

Preventive measures

Above all, it is necessary to develop preventive measures to make the population aware of the danger of caustic substances. Treatment is based primarily on clinical experience and data from animal models, as there are few controlled studies on the management of caustic injuries.


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