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Poisoning with OPCOrganophosphorus compounds (OPC) are referred to anticholinesterase agents. Cholinesterase ensures a hydrolysis of acetylcholine down to choline and acetic acid. Inhibition of cholinesterase leads to stopping or sharp decrease of enzymatic hydrolysis of acetylcholine that is accumulated in tissues and in toxic amounts predetermines a whole variety of clinical picture of poisonings. Inhibition of cholinesterase activity does not come at once and achieves its peak in 10-60 min, more rarely — to 2hrs., and in exceptional cases — in 12-21 hrs. As far as cholinesterase is the mediator of parasympathetic nervous system, poisoning is manifested with signs of stimulation of vagus nerve: increase of sweating, miosis with a loss of pupillary reflex, spasm of accommodation interfering with vision, bradycardia, intensification of intestinal peristalsis, sometimes, vagal cardiac arrest, increased secretion of intestinal glands leading to vomiting, diarrheas, hypersalivation and expectorations from respiratory tract that causes bronchospasm and respiratory failure. At first, convulsions of skeletal and mimic musculature appear, sometimes, a sharp elevation of muscular tone with opisthotonus and sardonic smile. Motor anxiety is replaced by paralysis with a complete loss of muscular tone and disappearance of peripheral reflexes. Breathing becomes diaphragmatic and then stops at all. It is associated with the effect of OPC upon neuromuscular synapses resemling the action of myorelaxants of depolarizing type. The inhibition of cholinesterase activity of the brain leads to the disorder of higher nervous activity. A deep coma with inhibition of reflexes and retrograde amnesia come to replace a short period of excitation. A leading syndrome of poisonings with OPC are respiratory disorders caused by secretion of bronchial glands, filling a bronchial tree with abundant liquid mucus that is manifested by cyanosis, hurried grunting breathing with moist rales in the lungs. A great amount of liquid is being aspirated from the trachea, a clinical picture resembles pulmonary edema. Another cause of respiratory disorder is paralysis of cross-striated musculature including a respiratory one. Disorders of cardiovascular system are closely connected with respiratory disorder. Tachycardia and elevated AP in poisonings of medium degree and in the initial period of severe degree are explained by excitation of ganglia 2nd adrenals as a result of which norepinephrine secretion is reinforced and he tone of all sympathetic nerves is elevated. Hereafter, bradycardia advances down to 10 beats per min and AP decrease. By laboratory data — a decrease of cholinesterase acitivity down to zero is determined that continues up to 5-7 days. All this varied symptomatology may be brought to three stages of poisoning with OPC (E.A. Luzhnikov, 1978): I — psychomotor excitation, miosis, feeling of tightness in the chest, II — predominate individual or generalized muscular fibrillations, tonoclonic spasms, choreic hyperkinesia, rigidity of the chest, respiratory disorder because of growing bronchorrhea. Comatose state; III — depression of respiratory center up to a complete respiratory arrest. A maintenance of life is possible only by means of controlled respiration. Further, paralyses of respiratory muscles and muscles of extremities appear, drop of AP, cardiac rhythm disorders (bradycardia, ventricular fibrillation, myocardial conduction disorders) are noted. Treatment of OPC poisonings along with urgent detoxication (repeated gastric lavages, salt laxative, abundant washing of skin and mucous membranes) and therapy according to syndromes assume comprehensive ways of influence on toxins and mechanism oftheir action (Table 29). However, in practice the antidote therapy comes down to the use of atropine in complex with cholinesterase activators. For one hour since the moment of starting the treatment and to a disappearance of all symptoms of muscarine-like effect of OPC, the "intensive atropinization" is carried out up to the appearance of signs of overdosage (dryness of mucous membranes and skin, dilatation of pupils, moderate tachycardia). In subsequent 3-4 days this state is maintained by repeated atropine administration in lesser doses. Table 29 Main ways of influence on intoxication with OPC
For one hour since the moment of starting the treatment the dose of atropine at the I stage of poisoning (excitation) makes up 2-3 mg, at the II stage (stage of convulsions) — 20-25 mg, at the III stage (paralyses) — 30-50 mg. A daily dose of atropine at these stages of poisoning makes up 4-6, 30-50 and 100-150 mg, respectively. At the same time with the "intensive atropinization" cholinesterase reactivators are applied — dipiroxime, isonitrazin and dietixime. A maximum of their action is due to the first 6-8 hours after OPCs penetration into the organism, they are introduced only in the first 24 hours. Administration of cholinesterase reactivators later, when OPCs are absent in blood, is not expedient and dangerous. Dipiroxime is introduced i/m by 150 mg. At the I stage of poisoning its total dose is 150-450 mg. At the II and III stages it is administered every 1-3 hrs bringing a total dose to 1.2-2 g. Starting from the II stage, dipiroxime administration is supplemented with intramuscular or intravenous introduction of isonitrazin (by 3 ml 40% solution), in case of need, repeatedly in 30-40 min not exceeding the total dose of 3-4 g. Dietixime, its single dose makes up 250 mg, is administered in the total dose to 5-6 g. Дата добавления: 2015-02-05 | Просмотры: 800 | Нарушение авторских прав |