АкушерствоАнатомияАнестезиологияВакцинопрофилактикаВалеологияВетеринарияГигиенаЗаболеванияИммунологияКардиологияНеврологияНефрологияОнкологияОториноларингологияОфтальмологияПаразитологияПедиатрияПервая помощьПсихиатрияПульмонологияРеанимацияРевматологияСтоматологияТерапияТоксикологияТравматологияУрологияФармакологияФармацевтикаФизиотерапияФтизиатрияХирургияЭндокринологияЭпидемиология

Poisoning with ethylene glycol

Usually, poisoning with ethylene glycol (antifreeze) is associated with its intake to achieve intoxication. Its minimal toxic dose for a man is 30-50 ml and lethal — 100 ml and higher.

Mechanism of action:

As the majority of spirits ethylene glycol exerts a narcotic effect. At the initial stage of cerebral effects symptoms of intoxication are, primarily, due to the effect of ethylene glycol upon CNS.

Being a vascular and protoplasmic poison, ethylene glycol causes edema, swelling and necrosis of vessels. The result of this effect is an oxygen deprivation of the brain.

The latter is further aggravated by a decrease of oxygen transport function of hemoglobin. Oxygen deprivation leads to a shift of AAB to the side of acidosis and metabolic processes are also disturbed.

Psychopathologic and neurologic pictures are due not only to an oxygen deprivation, but to individual hemorrhages by the type of hemorrhagic encephalitis as well. At the early stage of intoxication patients die from an acute cardiovascular insufficiency or pulmonary edema. If a poisoned man came out from the stage of cerebral effects, a further symptomatology is i:he result of action of ethylene glycol oxidation products — oxalic acid and its salt — calcium oxalate, acetaldehyde. 25% of ethylene glycol is removed from the organism in the form of oxalic acid and the remaining quantity is, evidently, oxidized down to C0₂ and water.

An affection of the kidneys is due not only to precipitation of crystals of calcium oxalate in the tubules and toxic effect of oxalic acid, but the effect of ethylene glycol itself as well.

Clinical picture. Three stages of poisoning are distinguished: initial symptoms, cerebral effects and renal. These stages are not always distinctly differentiated and not in every victim we may observe all three stages. The intoxication has an undulating course and not always a sequence is maintained in the process of poisoning development.

1. Stage of initial symptoms: a sensation of intoxication that rapidly passes off and asymptomatic period (latent) comes on and lasts from 2 to 24 hours. Then euphoria, ataxia, headache, dizziness, sometimes, nausea, vomiting, pains in the loins and abdomen develop. Such condition lasts 4-12 hours. In mild cases a further development of intoxication does not come and in subsequent 24 hours only flaccidity, nausea and headache are maintained. This form results in recovery.

2. Stage of cerebral effects. In a graver intoxication euphoria is soon replaced by depression, inhibition, a condition similar to a narcotic one that is the precursor of coma.

In preserved consciousness victims complain of headache, pain in the loins and abdomen, disorder of taste sensations, numbness in fingers, chill, disagreeable sensations in the chest; atactic gait, dilated pupils with weak reaction to light. Vomiting taking, quite often, uncontrollable character and, sometimes, fibrillar muscular twitchings are noted.

Of the symptoms of CNS injury are different degree of stupor, from mild to grave comatose condition.

Psychopathologic manifestations of intoxication come down to a memory disorder, weak orientation or complete disorientation, mental confusion or unconscious state, psychomotor excitement that precedes a coma.

Neuropathologic symptomatology reflects a severity of intoxication. Coordination disorders, dysarthria, flaccid facial expression, sometimes, diplopia are typical for the initial stage. But when stupor is growing on, tendon reflexes are reinforced and meningeal symptoms appear.

On the part of blood: hematocrit, hemoglobin and the number of erythrocytes are high, neutrophilic leukocytosis in complete absence of eosinophils and decrease of lymphocytes.

An oxygen deprivation rapidly develops. Already in the first 24 hours metabolic disorders are revealed: increased blood residual nitrogen, acidosis, acetonemia, chlorides, sugar and blood urea are elevated.

Urination, in the first 24 hours in cases of medium severity, is normal or increased, in graver cases an oliguria may come. In the urine — protein, lixiviated erythrocytes and what is the most characteristic — crystals of calcium oxalate are found.

Often, comatose condition results in death, 60% die on the first day, 15-20% of intoxicated — on the second day. In a number of cases the intoxication may stop in the narcotic state. Not turning into coma a narcotic state is replaced by stupor after which euphoria follows. Such a course is giving hope and if ARF does not develop, the process of recovery advances. Defective memory is being kept rather long.

3. Stage of renal symptoms. Usually, after recovery from a stupor in poisoned persons their condition is improved for a short period (from a few hours to 2-3 days), later a toxic nephrosonephritis develops. Sometimes, affection of the kidneys and liver develops without a stage of initial and cerebral symptoms.

At this stage — dizziness, headaches, unquenchable thirst, pains in the loins and abdomen, painful urination are noted. Oliguria — down to anuria. The urine acquires a colour of meat waste.

Face and mucous membranes are hyperemic with cyanotic tint. A body temperature is elevated, bilateral Pasternatsky's symptom is positive, enlarged painful liver.

Bradycardia is typical, heart sounds are quiet and pulmonary edema is possible.

In blood: neutrophilic leukocytosis, accelerated ESR, hyperglycemia, hyperchloremia are observed.

Hereafter, uremia develops and patients die with manifestations of uremic coma.

Pathoanatomically, a characteristic picture of hydrochemical degeneration of tubular epithelium with precipitation of crystals of calcium oxalate in the lumen is noted.

Treatment: Urgently cause vomiting, a gastric lavage (10 1) with water through a tube is compulsory, it may be done with 2% sodium bicarbonate.

Antidote — ethyl alcohol that is a competing substance and it inhibits ethylene glycol oxidation. It is introduced through a tube at the end of gastric lavage, as well as intravenously as 5-10% solution 1 ml/kg of patient's body weight.

Ethylene glycol and its metabolytes, in the first 24 hours, being yet in the blood are removed by means of hemodialysis. Therefore, in view of difficulties with diagnosis, a procedure of hemodialysis is justifiable even in suspicion of ethylene glycol poisoning. Otherwise, inactivity in confirming the diagnosis may cost the patient's life in the future. Plasmapheresis and hemosorption are less effective.

Plasma alkalinization is carried out to fight against growing acidosis under the control of urine reaction (appearance of persistent alkaline reaction) and BE of blood.

Abundant alkaline drinking is recommended.

Magnesium sulfate 25% — 5.0 ml is introduced to form a soluble magnesium oxalate in the urine. In order to bind an oxalic acid CaCl₂ solution 80-100 ml/ day is administered in the first 24 hours.

A water load is carried on with crystalloids with forced diuresis.

With the aim of decreasing a catabolism, concentrated 10-40% glucose with insulin, anabolic hormones, significant doses of ascorbic acid and vitamins of B group are prescribed.

An oxygenotherapy is being carried out. In respiratory disorder — APV by indications and situation therapy are fulfilled.

Дата добавления: 2015-02-05 | Просмотры: 643 | Нарушение авторских прав