What Are the Symptoms of Ammonia Poisoning?

Ammonia is one of the common pollutants in buildings. It mainly comes from high-alkali concrete expansion agent and urea-containing concrete antifreeze. These materials gradually release the reduced ammonia gas from the wall as the temperature and humidity of the environment change, polluting the indoor environment. Ammonia has irritating and corrosive effects on the skin and mucous membranes. High concentrations can cause serious consequences, such as chemical laryngitis, chemical pneumonia, etc. Inhalation of very high concentrations can cause reflex respiratory arrest and cardiac arrest. However, the amount of ammonia emitted from general decoration materials is relatively small, which mainly causes irritation. Wet areas in the south also corrode furniture and buildings.

Ammonia poisoning

Ammonia is a colorless, strongly irritating gas. Soluble in water to form ammonia water, can be used as fertilizer. Ammonia can be liquefied at normal temperature to form liquid nitrogen, which is convenient for transportation. Ammonia is an important chemical raw material with a wide range of uses. It is often used in petroleum smelting, fertilizer manufacturing, synthetic fibers, and tanning. Pharmaceutical, plastic, dye and other manufacturing industries. In the production, transportation, storage, and use of ammonia, if the pipelines, valves, storage tanks are damaged, leakage of ammonia gas can cause poisoning. Ammonia has irritating and corrosive effects on the skin and mucous membranes. High concentrations can cause serious consequences, such as chemical laryngitis, chemical pneumonia, etc. Inhalation of very high concentrations can cause reflex respiratory arrest and cardiac arrest.

Introduction to ammonia poisoning

Ammonia is one of the common pollutants in buildings. It mainly comes from high-alkali concrete expansion agent and urea-containing concrete antifreeze. These materials gradually release the reduced ammonia gas from the wall as the temperature and humidity of the environment change, polluting the indoor environment. Ammonia has irritating and corrosive effects on the skin and mucous membranes. High concentrations can cause serious consequences, such as chemical laryngitis, chemical pneumonia, etc. Inhalation of very high concentrations can cause reflex respiratory arrest and cardiac arrest. However, the amount of ammonia emitted from general decoration materials is relatively small, which mainly causes irritation. Wet areas in the south also corrode furniture and buildings.

Mechanism of ammonia poisoning

Ammonia meets water in human tissues to produce ammonia water, which can dissolve tissue proteins and play a role in saponification with fat. Ammonia can destroy the activities of various enzymes in the body and affect tissue metabolism. Ammonia has a strong stimulating effect on the central nervous system.
1. Ammonia is strongly irritating. Inhaling high concentrations of ammonia can excite the central nervous system and cause convulsions, convulsions, lethargy and coma. Inhalation of extremely high concentrations of ammonia can cause cardiac arrest and respiratory arrest reflexively.
2. Ammonia-based alkaline substances, ammonia water has a strong corrosive effect. Alkaline burns are more serious than acidic burns, because alkaline materials have strong penetrability, and ammonia water burns on the skin are deep, susceptible to infection, and difficult to heal, similar to 2nd degree burns.
3 Ammonia is inhaled into the airways to meet with water to form ammonia water. Ammonia can penetrate into the submucosa, interstitial lungs, and capillaries through the mucosa, alveolar epithelium, and cause:
(1) Vocal cord spasm, edema of the throat, and tissue necrosis. Necrosis can cause suffocation. Damaged mucosa is susceptible to secondary infection.
(2) Trachea and bronchial mucosal damage, edema, bleeding, spasm, etc. Affect the ventilation function of the bronchi.
(3) Alveolar epithelial cells, pulmonary interstitial, and pulmonary capillary endothelial cells are damaged, permeability is enhanced, and pulmonary interstitial edema. Ammonia stimulates sympathetic nerve excitement, causes common lymphatic spasm, obstructs lymphatic reflux, and increases pulmonary capillary pressure. Ammonia destroys alveolar surfactants. These effects eventually lead to pulmonary edema.
(4) Mucosal edema, increased secretion of inflammation, pulmonary edema, decreased alveolar surfactants, and narrowing of the trachea and bronchial lumen severely affect the ventilation and ventilation functions of the lungs, causing systemic hypoxia.

Clinical manifestations of ammonia poisoning

When exposed to ammonia, it will smell a strong irritating odor, tears, and tingling in the eyes. Excessive ammonia splashing into the eyes can damage the cornea and cause corneal ulcers. In severe cases, it can cause corneal perforation, cloudy crystals, and iris inflammation, which can lead to blindness.
Inhalation of ammonia can cause throat, sore throat, and hoarseness. High inhaled ammonia concentration can cause throat spasms, vocal cord edema, and suffocation.
Ammonia entering the trachea and bronchi can cause cough, expectoration, and blood in the sputum. In severe cases, hemoptysis and pulmonary edema, dyspnea, white or bloody foamy sputum, and large, medium vesicles in both lungs.
Inhalation of high concentrations of ammonia can cause convulsions, convulsions, drowsiness, and coma. Individual patients inhale extremely concentrated ammonia and may experience respiratory arrest.
Patients with secondary pulmonary infections had high fever, hemoptysis, yellow sputum, difficulty breathing, and cyanosis. Damage to the digestive tract can cause abdominal pain, vomiting, etc., and later appear jaundice and liver function damage (toxic hepatitis).

Diagnosis of ammonia poisoning

1. History of exposure to ammonia.
2. Breath and skin smell of ammonia.
3 Clinical manifestations of skin, mucous membrane, and respiratory tract injuries.

Diagnostic criteria for ammonia poisoning

Ammonia poisoning

There were only transient eye and upper respiratory tract irritation symptoms and no significant positive signs in the lungs.

Mild poisoning

Mild poisoning can be diagnosed according to the following indicators:
1. Tears, sore throat, hoarseness, cough, expectoration with mild dizziness, headache, fatigue, etc .; conjunctiva, congestion of the pharynx, edema, dry rales in the lungs.
2. Chest X-ray signs, enhanced lung texture or blurred edges, consistent with bronchitis or peribronchitis.
3 Blood gas analysis: When breathing air, the arterial blood oxygen partial pressure is lower than the expected value of 1.33-2.66kPa (10-20mmHg).

Ammonia poisoning moderate poisoning

1. Hoarseness, cough, sometimes with bloodshot sputum, chest tightness, difficulty breathing, often dizziness, headache, nausea, vomiting, fatigue, etc .; mild cyanosis, dry and wet rales in the lungs.
2. Chest X-ray signs: enhanced lung texture, blurred edges or reticular shadows, or reduced lung field transparency, or scattered or patchy shadows with blurred edges, consistent with the manifestations of pneumonia or interstitial pneumonia.
3 Blood gas analysis can maintain arterial blood oxygen partial pressure greater than 8kPa (60mmHg) when inhaling low concentration of oxygen (less than 50% oxygen).

Severe poisoning

Severe poisoning can be diagnosed if you have 1.2.3 or 4 of the following.
1. Severe cough, a lot of pink foamy sputum, shortness of breath, chest tightness, palpitations, etc., and often irritability, nausea, vomiting, or coma; respiratory distress, obvious cyanosis, and both lungs covered with wet and dry rales.
2. Chest X-ray signs: patchy, cloud-like shadows with lighter edges and blurred edges in the two lung fields can be merged into large or butterfly-shaped shadows, which is consistent with severe pneumonia or edema.
3 Blood gas analysis, the arterial blood oxygen partial pressure is still lower than 8kPa (60mmHg) under the condition of inhaling high concentration of oxygen (greater than 50%).
4 The degree of respiratory damage is consistent with moderate poisoning, and asphyxia caused by severe laryngeal edema or bronchial mucosal necrosis; or severe pneumothorax or mediastinal emphysema; or more obvious heart, liver, or kidney organ damage.

Routine treatment of ammonia poisoning

1. Quickly leave the poisoning scene and breathe fresh air or oxygen. Respiratory stimulants may be used when breathing is shallow or slow. Cardiopulmonary resuscitation should be performed immediately for those who have stopped breathing or heartbeat. It should not be easily abandoned. Laryngeal spasm and vocal cord edema should be intubated or tracheotomy quickly.
2. Remove clothing and thoroughly wash ammonia-exposed skin with water or 1% to 3% boric acid water. Rinse the eyes with 1% to 3% boric acid water, and then order antibiotics and cortisone eye drops.
3 Intravenous 10% glucose solution, calcium gluconate, adrenocortical hormones, antibiotics, to prevent infection and edema of the throat.
4 Nebulized inhaled flumesol, antibiotic solution.
5. Patients with coma use a 250% 20% mannitol intravenous injection, once every 6 to 8 hours, to reduce intracranial pressure.

Hyperbaric oxygen therapy for ammonia poisoning

1. Principles of treatment Whether patients with ammonia poisoning can be treated with hyperbaric oxygen has been debated. Some people worry that during the pressurization process, respiratory secretions or exudates may be pressed into the bronchus and alveoli, blocking the airway and exacerbating the infection. Therefore, it is considered that ammonia poisoning should not be treated with hyperbaric oxygen. The author believes that when the patient is in the dangerous stage of severe hypoxia, pulmonary edema, cerebral edema, and shock, if the hypoxia is not corrected in time, the control of pulmonary edema, cerebral edema, and shock will soon endanger life. At this time, only hypobaric oxygen therapy can quickly correct hypoxia, control pulmonary edema and brain edema, break the vicious circle, create conditions for the body to recover and strive for sufficient time. Hyperbaric oxygen treatment principle:
(1) Quickly correct tissue hypoxia: bronchial and alveolar damage caused by ammonia poisoning, pulmonary edema, which impairs the ventilation and ventilation function of the lung, and the partial pressure of arterial oxygen (PaO2) can be lower than 8.0kPa (60mmHg). In severe cases, it is as low as 4kPa (30mmHg), which causes severe hypoxia. In this case, using a nasal tube to inhale oxygen at normal pressure, the partial pressure of arterial blood oxygen will not be higher than 8.0 9.3kPa (60 70mmHg), and the partial pressure of arterial blood oxygen is very easy to breathe pure oxygen in high pressure environment. Increase to 13.3 26.6kPa (100 200mmHg). This can quickly correct the tissue's hypoxia. Improve tissue aerobic oxidation, increase energy supply, and correct tissue acidosis.
(2) The volume of air bubbles in the airway shrinks or breaks under high pressure, and the foam in the airway decreases, keeping the airway open.
(3) Hyperbaric oxygen can reduce intracranial pressure and prevent cerebral edema.
(4) High air pressure can prevent pulmonary edema.
(5) Hyperbaric oxygen can control shock.
(6) Hyperbaric oxygen can quickly improve hypoxia in various organs and accelerate the repair of various organs, such as heart, liver, kidney, and brain.
2. Treatment methods and precautions due to the general danger and critical condition of ammonia poisoning, severe damage to the respiratory tract mucosa, deep wounds, secretions and exudates may block the respiratory tract. therefore:
(1) The treatment pressure should not be too high, and 0.2MPa is appropriate. The pressure increase time is appropriately extended to 40 to 50 minutes to prevent the pressure from changing drastically and the respiratory tract being blocked by falling objects. The decompression time should also be extended by 40-50 minutes accordingly. The voltage stabilization time is unchanged, and the oxygen absorption time cannot be extended at will.
(2) When performing hyperbaric oxygen treatment, medical staff should accompany the cabin to monitor, tracheal intubation and tracheotomy items should be prepared; sputum suction device and large empty needle should be prepared. Routine treatment should not be interrupted in the cabin.
(3) After the first hyperbaric oxygen treatment, if the hypoxia correction is not satisfactory, and pulmonary edema and brain edema are not controlled, another hyperbaric oxygen treatment can be performed after the portal hour.

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