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ToxicityNH3 presents a contact toxic substance directly reacting with the tissues affected with it. Gas, in contact with the tissues, is dissolved in them forming ammonium hydroxide — a corrosive alkaline solution. In contact with the skin I—II degree burns are formed, with bulbar conjunctiva — ulcerations, with mucous membranes of respiratory tract — lesions of different degree develop from hyperemia and edema to necrosis, and contact with alveolar and capillary membranes produces an acute pulmonary edema. When ammonia concentration is equal to 50 ppm its smell is felt, 700 ppm — produce an erosion of the eyes, and in 5000 ppm — an instant death comes. In pathoanatomical studies ulceronecrotic alterations are found in:he pharynx, larynx, trachea and bronchi on the background of hyperemia Ј nd edema of mucous membranes. Symptoms depending on NH3 concentration: In mild degrees — symptoms of affection of the eyes, respiratory tract, skin and mucous membranes, larynx and pharynx. Acute conjunctivitis — pain, blepharospasm, lacrimation. Respiratory signs: dry cough, heartburn behind the breast bone and dyspnea. A few hours later an acute toxic pulmonary edema develops. Several days later an acute chemicakpulmonary lesion develops accompanied by pains behind the breast bone, in the thorax, dyspnea, cough, sometimes, with bloody sputum, elevation of body temperature, asthenia. On X-ray examination it is manifested with increased lung pattern and "snow flakes". In 2-3 weeks these symptoms disappear. In contact of liquid ammonia with the skin an erythema, rarely with vesicles, develops. When it gets into the organism it exerts its irriatting effect on the esophagus and stomach (pain in the epigastrium, vomiting). In medium gravity: Pain in the mouth, throat, difficult breathing, fear of death, bloody discharges from the nose, aphonia. Ocular signs — blepharospasm, corneal opacity, vesicles on the cornea. Then cyanosis of the skin of face, hands, mucous membranes, edema and vesicles that increase, merge and open, serohemorrhagic content is discharged from them; moist rales are in the lungs. In 2-3 days a condition may, somewhat, improve, but a cough with sputum intensifies and traces of necrotic tissues are seen in it. On X-ray there are areas of atelectasis and indurations disappearing in a few days. A grave form. If the death did not come at once from acute asphyxia, hereinafter 3 clinical phases develop: initial, improvement and aggravation. For the first phase, signs of acute toxic pulmonary edema and cardiovascular insufficiency are typical. Pulmonary edema bears a hemorrhagic character, takes a grave course and may be the cause of death. In the second phase, AP normalizes, clinical manifestations of pulmonary edema diminish, but on X-ray the interstitial edema of pulmonary tissue is defined. The third is the phase of aggravation conditioned by addition of infection. After a period of false improvement — signs of ARF, dyspnea, cyanosis, rales, elevation of body temperature, weakness and decrease of appetite are noted. On pulmonary X-ray examination — consolidation of shadows or localized atelectases are observed. Treatment: a withdrawal of victims from a gased zone, a wash-out of affected areas with large amounts of water (better with Na borate, acetic or citric acid), antibiotics, aerosoles and sputum diluting agents, hormones. In laryngospasm — tracheostomy, in pulmonary edema — a change over to APV under PPEE, analgetics and other symptomatic therapy. Дата добавления: 2015-02-05 | Просмотры: 669 | Нарушение авторских прав |