Poisoning mechanism: Chlorine gas reacts with mucous membranes and respiratory tract water to form hydrogen chloride and new ecological oxygen after inhalation. Hydrogen chloride can cause mucositic edema, congestion and necrosis of the upper respiratory tract; New ecological oxygen has a strong oxidizing effect on tissues and can form ozone with cytoplasmic toxicity. Excessive chlorine concentration or prolonged contact time can often lead to deep respiratory tract lesions, damage to bronchioles and alveoli, bronchiolitis, pneumonia and toxic pulmonary edema. Due to the stimulation effect, local smooth muscle spasm aggravates ventilation disorders and aggravates hypoxia; High concentration of chlorine can also stimulate the vagus nerve and cause reflex heartbeat arrest.
Clinical manifestations
Acute poisoning is mainly a manifestation of respiratory damage.
a. Onset and disease change are generally rapid.
b. Pharyngitis, bronchitis, pneumonia, or pulmonary edema may occur, manifested as sore throat, choking cough, small amount of sputum, shortness of breath, chest tightness or pink foamy sputum, dyspnea, etc., and there may be no obvious positive signs or dry and wet rales in the lungs. Sometimes accompanied by nausea, vomiting and other symptoms.
c. Severe patients may still have acute respiratory distress syndrome, with progressive respiratory tachynea and distress, tachycardia, and refractory hypoxemia, which is ineffective with general oxygen therapy.
d. A small number of patients have asthma-like attacks, wheezing, and wheezing sounds in the lungs.
At very high concentrations, it can cause glottic spasm or edema, bronchospasm, or reflex respiratory center depression and cause rapid asphyxiation.
f. Complications mainly include secondary infection of the lungs, myocardial damage, pneumothorax, mediastinal emphysema, etc.
g. X-ray examination: there may be no abnormalities, or there may be enhanced lung texture on both sides, blurred shadows of punctate or flaky borders, or cloud-like and butterfly wing shadows.
h. Blood gas analysis: The partial pressure of arterial oxygen is significantly reduced in patients with severe disease.
i. Electrocardiogram: After poisoning, due to hypoxia, pulmonary hypertension and autonomic nerve dysfunction, etc., it can lead to myocardial damage and arrhythmia.
Eye damage: Chlorine can cause acute conjunctivitis, and high concentrations of chlorine or liquid chlorine can cause eye burns.
Skin Damage: Liquid chlorine or high concentrations of chlorine can cause acute dermatitis or burns at exposed skin sites.
Treatment
The person who inhales the gas immediately leaves the scene and goes to a fresh place to keep quiet and warm. Rinse thoroughly with clean water immediately when eyes or skin come into contact with liquid chlorine.
Those with symptoms after inhalation should be observed for at least 12 hours and treated symptomatically. those with a large inhalation volume should be bed rested, oxygenated, and given aerosol inhalation such as asthma refreshing aerosol, ventolin or 5% sodium bicarbonate plus dexamethasone.
Reasonable oxygen therapy is required for acute poisoning; early, moderate, and short-term adrenal glucocorticoids; maintain airway patency; For the prevention and treatment of pulmonary edema and secondary infections, see < Treatment > of toxic pulmonary edema caused by acute irritant gases;
Other symptomatic treatment.
Eye and skin burns are treated as acid burns, see < Treatment of Chemical Eye Burns> and < Treatment of Chemical Skin Burns>.
Standard
Workshop air hygiene standard: China MAC 1 mg/m^3; ACGIH TLV-STEL 2.9 mg/m3 (1 ppm) in the United States; TLV-TWA 1.5 mg/m3 (0.5 ppm)
China's National Standard for Diagnosis of Occupational Diseases: Diagnostic Standards and Treatment Principles of Occupational Acute Chlorine Poisoning GB4866-1996.
Hazardous Regulation: GB2.3 Class 23002 (Liquefied). Original Iron Gauge: Dramatic Toxic Gas Body, 31001. UN NO.1017。 IMDG CODE 2028 page, class 2. Secondary Hazard 6.1.