Alkali poisoning

When sodium, potassium or calcium hydroxides enter the GI tract, alkali poisoning occurs. The peculiarity of such poisoning is that alkalis, without systemic toxicity, destroy the tissues of the digestive tract.

Epidemiology

According to WHO, alkali poisoning is quite rare in developed countries, and 68% of cases worldwide are due to alkali poisoning in children as a result of unintentional ingestion of caustic substances in the GI tract. Since children ingest small amounts of the chemically corrosive substance, the damage may be relatively minor.

As for adults, due to the larger volume of ingested alkali, poisoning is more serious, and the damage affects not only the mucosa and submucosal layer of the esophageal wall, but also its muscular and adventitial membranes. [1]

Causes of the alkali poisoning

The main cause of poisoning by caustic alkalis, including caustic soda (caustic soda or lye) and caustic potassium (potassium alkali) solutions, hydrated and quicklime (calcium hydroxide and oxide) is ingestion. And while in children such poisoning usually occurs quite accidentally, in adults it can be deliberate: in the presence of mental illness or suicide attempts.

Poisoning by household acids and alkalis, i.e. Their oral ingestion into the GI tract is the most common etiologic factor chemical burns of the esophagus and stomach. All caustic alkalis, which include strong bases with a hydrogen index (pH) of more than 10-12, even in minimal amounts are capable of causing severe damage to the oropharynx, larynx, and entire digestive tract. [2]

Alkalis penetrate deeper into tissues than acids and damage the esophagus the most. [3]

Risk factors

Specialists note such risk factors for severe damage to the GI tract in alkali poisoning as:

• concentration of the alkali solution (e.g., even a 1% aqueous solution of caustic soda has a pH˃13);
• the amount of alkaline ingested. While ingestion of small amounts of alkali may cause burns to the oropharynx and esophagus, in cases of deliberate ingestion of large amounts, both the stomach and small intestine are affected;
• duration of contact with GI tissues (the longer it is, the greater the alteration of any tissue);
• presence/absence of food in the stomach at the time of poisoning.

Pathogenesis

The mechanism of tissue damage in alkali poisoning is due to the electrostatic effect of alkaline hydroxide ions (hydroxyl group OH-) on monomers of globular proteins (albumin) of cell cytoplasm and blood plasma.

In fact, the pathogenesis lies in irreversible processes of alkaline hydrolysis of proteins - with absorption of intercellular fluid, as well as their denaturation (destruction) - due to disruption of hydrogen bonds in protein polypeptide chains, leading to their unfolding and changes in spatial configuration. As a consequence, albumin loses its original structure and functions, turning into loose hydrophilic albuminates. [4]

In addition, there may be additional tissue damage, since the contact of alkalis with hydrochloric acid of gastric juice and acidic mucins of the esophageal mucosa is an exothermic reaction, in which a significant amount of heat energy is released at once. [5]

The result of alkaline pH induced destruction of tissue proteins is the so-called collisional (liquefying or melting) tissue necrosis, which has a progressive character. [6]

Symptoms of the alkali poisoning

How many hours before lye poisoning manifests itself? As experts note, both the clinical picture of poisoning and the time of manifestation of its symptoms can vary greatly. Everything depends on the concentration of the chemical agent and the duration of its effect on tissues. Thus, after contact with 3-4% alkaline solution, the destruction of tissue proteins can develop over a long period of time, and at a concentration of alkaline solution of 25% and above, the reaction occurs immediately, causing deep damage to the esophagus and tissue disintegration in just a few seconds.

A minimal amount of caustic ingested into the digestive tract may be asymptomatic, and damage to the esophagus is possible without chemical burns to the oral cavity.

Typical first signs of poisoning manifest as pain in the mouth and pharynx with the formation of burn ulcers on the mucous membrane, shortness of breath and noisy breathing (stridor), increased salivation and hematogenous-toxic vomiting (without nausea!).

Clinical symptoms of oral alkali poisoning correspond to the stage of alkali damage and in the initial (acute) phase include: pain in the pharynx and its swelling; difficulty in swallowing (dysphagia); pain in the epigastric and epigastric regions, as well as burn toxemia resulting from tissue necrosis (with high temperature, rapid breathing and heartbeat against the background of decreased BP); shock.

A few days after alkali penetration into the GI tract, decomposition and rejection of dead tissue (with possible bacterial infection) continues. Then granulation tissue appears at the site of esophageal injury, ulcers are covered with fibrin. In uncomplicated cases, the esophagus begins to recover after two to three weeks, but healing of burn ulcers with scar formation occurs much later.

Poisoning by alkali vapors, i.e. Their inhalation exposure by inhalation, can cause irritation of the mucous membranes of the nose and sneezing; pain in the nasopharynx, throat and chest; hoarseness; difficulty breathing; coughing. And poisoning with caustic soda vapor (sodium hydroxide) leads to pronounced chemical burns of the respiratory tract with severe swelling and spasm of the larynx, upper airway obstruction, asphyxia and accumulation of fluid in the lungs.

Complications and consequences

Alkali poisoning can have complications and consequences such as:

• development of acute esophagitis;
• laryngeal stenosis;
• Disruption of the integrity of the wall (perforation) of the esophagus with the development of mediastinitis (inflammation of the mediastinum);
• with fistulas;
• narrowing (stricture) of the esophagus due to scar tissue formation;
• pyloric patency disorder;
• lack of hydrochloric acid in gastric juice (hypochlorhydria) and diffuse reduction in gastric volume (in cases of severe stomach damage);
• Intestinal perforation with gastrointestinal bleeding;
• peritonitis.

The distant consequences include metaplasia of the gastric mucosa and (in 0.8-4% of cases) the development of carcinoma (10-20 years after surviving esophageal alkali burn).

When alkaline vapors are inhaled, the effects may be expressed as chronic hoarseness; narrowing of the tracheal or bronchial lumen with development of reactive airway dysfunction syndrome, and in case of bronchial spasms - irritant bronchoobstructive syndrome. [7]

Diagnostics of the alkali poisoning

First of all, the exact chemical affiliation of the poisoning agent to alkali is established: the patient's vomit has an alkaline pH. Another important step is to assess the extent of the damage in order to prescribe adequate treatment.

Only instrumental diagnostics can objectively assess the extent of damage:

• Upper gastrointestinal endoscopy - esophagoscopy;
• Esophageal x-ray;
• Ultrasound and CT scans of the gastrointestinal tract.

Laboratory studies include a comprehensive assessment of liver and kidney function, blood tests (general, for acidosis, anemia, electrolytes, etc.). [8]

Differential diagnosis

Differential diagnosis is made with poisoning by acids and other aggressive chemicals. Read more in the publication - Chemical burns of the esophagus - Diagnosis

Treatment of the alkali poisoning

Conservative treatment of the consequences of caustic alkali poisoning begins with taking urgent measures.

What is the first emergency treatment? First of all, it is to call an ambulance. Secondly, immediately after accidental ingestion of any alkali, one should drink a glass of milk (although its effectiveness as an alkali neutralizer has not been proven), take the protein of two or three raw eggs or a mucilaginous decoction of oatmeal.

With regard to neutralization of alkali in the esophagus and stomach with water acidified with vinegar or citric acid, there is no consensus of experts because of the exothermic reaction (discussed in the Pathogenesis section). Also, activated charcoal is not accepted: it is better to use Atoxyl suspension or Enterosgel.

It should be borne in mind that gastric lavage in alkali poisoning by ingestion of large amounts of water with subsequent initiation of vomiting is contraindicated, as there is a risk of repeated exposure to the aggressive substance contained in the vomit masses and additional esophageal alteration (which is associated with the same exothermic reaction). In medical facilities - within the first two hours after ingestion of alkali nasogastric intubation and aspiration of gastric contents (since gastric lavage with a probe involves its insertion into the esophagus, which is fraught with its mechanical perforation).

What should I do if I inhale lye vapor? Get out into fresh air and breathe slowly. If breathing is accompanied by wheezing, pain behind the sternum is felt and severe coughing and shortness of breath begins - do not hesitate to call an ambulance. And while she goes to use an aerosol with adrenaline. A drop in BP, heart rate interruptions, seizures, loss of consciousness are indicators of the need for urgent delivery to the intensive care unit, where hemodynamic stabilization and respiratory function will be ensured.

Also read - Chemical burn with quicklime: what to do?

What medications are used in the treatment of alkali poisoning? Analgesics are used to relieve pain; antibacterial drugs are needed if the esophagus is perforated and infection has set in. To reduce damage to the esophagus, drugs that slow down the synthesis of hydrochloric acid in the stomach - proton pump inhibitors (Omeprazole, etc.) are administered; corticosteroids are prescribed to prevent narrowing of the esophagus, as well as in alkali vapor poisoning (although their efficacy has not been clinically confirmed). [9]

How doctors fight with general intoxication and shock - to maintain the functions of life-supporting organs, how and at what stage of lesion of the esophagus is carried out its bougering, in what cases surgical treatment of post-burn esophageal stenosis, is covered in detail in the article - Chemical burns of the esophagus - Treatment. [10]

Prevention

Poisoning by sodium, potassium or calcium hydroxides can be avoided by handling caustic substances with care and storing them where they will not only be inaccessible to children but also to adults with mental disabilities.

Forecast

In poisoning causing burns of the mucosa and submucosal layer of the esophagus, its function is restored over time. The formation of scar tissue and strictures in deeper injuries requires longer treatment, often with surgical intervention.

The deeper the esophagus is traumatized, the worse the prognosis due to the increased likelihood of systemic complications. [11]

In cases of severe poisoning and extensive burns with esophageal perforation, the mortality rate is up to 20%.