Toxic encephalopathy is a combination of neurological disorders caused by exposure to toxins, poisons or industrial chemicals. Clinical manifestations are diverse, depend on the etiological factor, may include atactic and convulsive syndrome, hallucinations, speech, vision, hearing and cognitive disorders, lesions of cranial nerves, specific skin manifestations. The diagnosis uses anamnesis data, the results of a general examination, laboratory and instrumental tests. Treatment includes antidote, detoxification, pathogenetic and symptomatic therapy.
ICD 10
G92 Toxic encephalopathy
General information
Toxic encephalopathy (TE) is the most severe clinical form of intoxication. The structure of morbidity among the population is dominated by TE, provoked by the abuse of alcoholic beverages (15-18% of the total) and narcotic drugs (8-13%). The third place is occupied by poisoning with heavy metals (manganese, lead, mercury – about 5-7%), occurring in production conditions and in workers of mining organizations. Most often, pathology is observed in people of working age – from 25 to 55 years. Among men, the incidence rate is slightly higher than among women.
Causes
All toxic encephalopathies occur against the background of poisoning of the body with a substance toxic to the central nervous system. The cause may be either a single contact or reception (acute TE), or prolonged toxin saturation (chronic TE). The most common causes of this group of pathologies include:
- Alcohol abuse, drugs. It includes chronic consumption of large doses of alcohol, followed by vitamin B1 deficiency. Narcotic substances – heroin, cocaine, amphetamine, etc. also have a toxic effect on the central nervous system.
- Work in hazardous industries. The cause of encephalopathy can be prolonged contact with substances such as methanol, ethylene glycol, lead, manganese, mercury, organophosphates, carbon monoxide when working at a factory or in a mine. It is possible to simultaneously receive a large dose of the chemical in man-made disasters, erroneous eating.
- Uncontrolled medication intake. Excessively high doses or a combination of a large number of pharmacotherapeutic agents can have a detrimental effect on the central nervous system. The development of TE can be caused by benzodiazepine derivatives, barbiturates, antidepressants, cholinolytics and nonsteroidal anti–inflammatory drugs (primarily salicylates).
- Pathology of the liver and kidneys. The liver and kidneys are the organs responsible for the disposal of toxic metabolic products. With severe renal or hepatic insufficiency, the negative impact of exogenous poisons increases, natural metabolites toxic to the central nervous system accumulate – ammonia, organic acids.
Pathogenesis
The mechanisms of development of various forms of toxic encephalopathies have not been thoroughly studied. There is also no clear relationship between clinical manifestations and morphological changes in the nervous system. It is generally believed that the basis of TE is both the direct effect of a toxic substance and a violation of the blood supply to the brain due to damage to cerebral vessels. This, in turn, leads to degenerative-dystrophic changes in the tissues and swelling of the meninges.
Hemodynamic and cerebrospinal fluid disorders occur, which further aggravates the toxic and hypoxic effects on the central nervous system. As a result, disseminated areas of necrosis of the cortex and subcortical structures, fragmentation of myelin sheaths are formed. Taking into account a specific substance, certain features associated with the increased susceptibility of certain structures of the nervous system and the ability of compounds to heat up in various organs can be revealed.
Tetraethyl lead and mercury can be deposited in parenchymal organs and the nervous system. With saturnism, damage to neurons in the central nervous system, segmental demyelination, followed by axonal damage to peripheral nerves, is observed. Mercury has a toxic effect on the neurons of the occipital lobe cortex and granular cells of the cerebellum, the pathology is accompanied by axonal degeneration and demyelination of peripheral nerves. Carbon monoxide causes acute hypoxia of the brain by interacting with hemoglobin and creating a stable compound – carboxyhemoglobin.
OPC cause a violation of the function of acetylcholinesterase, an enzyme of one of the main mediators of the central nervous system – acetylcholine, which leads to overexcitation of M- and N-cholinergic receptors. Hydrogen sulfide has a negative effect by binding active amino acids, blocking copper-containing enzymes, disrupting the metabolism of serotonin, tryptophan, nicotinic acid and vitamin B6. When poisoning with salicylates and ethylene glycol, the emerging metabolic acidosis plays a leading role.
Symptoms
Clinical manifestations directly depend on the toxin that caused the disease. With an overdose of salicylates, general malaise, nausea with vomiting, ringing or tinnitus, speech disorders, sound and visual hallucinations occur at first. Sometimes there is a convulsive syndrome, cognitive disorders, a comatose state. Carbon monoxide poisoning is accompanied by general cerebral symptoms, memory impairment, hallucinations, ataxia, hypertonicity of skeletal muscles, choreic hyperkinesis and depression of consciousness.
TE in cases of hydrogen sulfide poisoning is characterized by intense persistent headache, dizziness, small-scale tremor, intoxication, slowing down of active movements and other manifestations of akinetic-rigid syndrome. With mercury encephalopathy, the first signs are vegetative vascular disorders and neurasthenia syndrome, combined with severe gastrointestinal disorders. Gradually, large-scale tremor, “mercury erethism”, cerebellar ataxia, dysarthria and dementia are formed.
Lead TE is characterized by severe diffuse headache, general weakness, malaise, memory impairment, static tremor, severe visual impairment, central paresis and paralysis. In some cases, the lesion of motor and mixed cranial nerves, epileptic seizures is determined. A typical manifestation is a purple-gray border that occurs along the dentition (Bruton’s symptom). When poisoning with ethylene glycol, horizontal nystagmus and a general condition simulating alcohol intoxication are noted. With severe poisoning, a convulsive syndrome, a soporotic state or coma occurs.
TE caused by OPC is accompanied by ataxia, severe cephalgia and dizziness, myoclonus of individual muscles and disorders of the autonomic nervous system. With severe poisoning, hallucinations, delirium are observed. Manganese TE is manifested by muscular hypotension, general lethargy and drowsiness, emotional lability, walking disorders, forced smile or forced laughter, tremor of the tongue and lips. In severe cases, “manganese madness” is formed.
Acute alcoholic encephalopathy is characterized by pronounced cerebral symptoms, ophthalmoplegia, strabismus, nystagmus, loss of tendon and periosteal reflexes, hyperkinesis, cerebellar movement coordination disorder, vegetative vascular dysfunction and mental disorders. In the chronic form of alcoholic TE, vegetative and neuroendocrine disorders occur, insomnia or anxious dreams, tremor, dementia.
Diagnostics
In the process of diagnosis, the neurologist is guided by anamnestic information, complaints of the patient, the results of physical, laboratory and instrumental methods of research. Taking into account the form of toxic encephalopathy, various diagnostic techniques can play a decisive role in making a final diagnosis. The general program of examination of a patient with suspected TE consists of the following items:
- Collection of complaints and anamnesis. It often allows you to identify a toxic substance that provoked a violation of the patient’s condition. The probable etiology may be indicated by lesions of other organs and systems established during the conversation. Attention is focused on the nature of speech – the presence of dysarthria, incoherence of what was said.
- External inspection. A physical examination evaluates the pulse, blood pressure, the condition of the skin and visible mucous membranes, the volume of active and passive movements in order to search for paresis, paralysis and spontaneous muscle twitching, the tone of the periosteal and tendon reflexes. The functions of cranial nerves, visual and hearing acuity are examined for rapidly developing blindness and deafness, nystagmus and other symptoms.
- General clinical laboratory tests. In the blood test, anemic syndrome, leukopenia, neutrophilic leukocytosis, pancytopenia, basophilic granularity of erythrocytes and increased ESR can be determined. Fresh erythrocytes, oxalates, hyaline cylinders, proteinuria, hematoporphyrin and heavy metal residues can be detected in blood test. In the biochemical analysis of blood, changes in the water-electrolyte and acid-base balance are noted, signs of a violation of porphyrin metabolism.
- Electroencephalography. EEG is used in the presence of convulsive syndrome, deep disturbance of consciousness. Slow waves of high amplitude, suppression of the alpha rhythm, general suppression of bioelectric activity or manifestations of convulsive foci may be present on the electroencephalogram.
- Additional diagnostic methods. Taking into account the clinical situation and the need for differential diagnosis with other pathologies, electromyography, spinal puncture, computer or magnetic resonance imaging of the brain, toxicological examination of hair and nails are additionally prescribed.
Treatment
The purpose of toxic encephalopathy treatment is to remove chemical substances from the body, minimize brain damage, and correct neurological deficits. Depending on the severity of the patient’s general condition, therapy is carried out in the department of clinical neurology or the intensive care unit and includes the following measures:
- Evacuation of the toxin from the body. In acute intoxication, provoked by ingestion of the chemical through the gastrointestinal tract, gastric lavage is performed with distilled water or specific reagents, after which enterosorbents are used.
- Detoxification therapy. It is aimed at binding or removing the toxin circulating in the blood. It is represented by intravenous infusion of plasma substitutes and specific antidotes, chelation therapy, hemodialysis.
- Symptomatic and pathogenetic therapy. It may consist of mask oxygen inhalation, artificial lung ventilation, prescription of antiepileptic and diuretic drugs, tranquilizers, nonsteroidal anti-inflammatory drugs, corticosteroids.
Prognosis and prevention
The outcome of toxic encephalopathy depends on the degree of damage to the central nervous system and the properties of the substance. Severe intoxication with heavy metals, OPC and ethylene glycol often leads to death. Clinical manifestations of poisoning with organic solvents can regress independently after a few days or weeks after the termination of contact. Prevention of TE is based on compliance with safety regulations, the use of personal protective equipment when working with toxic substances in everyday life and in conditions of harmful industries, strict compliance with the doctor’s recommendations during drug therapy, rejection of bad habits.