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Iskandarov A. I.,
Forensic Expertise Bureau of the Republic of Uzbekistan
Nadjmitdinov S. B., Tashkent Pediatric Medical Institute E-mail: [email protected]
CLINICAL AND MORPHOLOGICAL CRITERIA OF FORENSIC ASSESSMENT OF ACUTE POISONING WITH ETHYL ALCOHOL AND ITS SURROGATES
Abstract: In the course of the study, it was found that in cases of acute poisoning with ethyl alcohol and its surrogates, characteristic clinical signs of poisoning are observed, which depend primarily on the concentration (dose) of the poison taken and its physicochemical composition. Pathomorphological signs of poisoning with alcohol substitutes cause dystrophic changes in all internal organs, with predominant liver and kidney damage. Keywords: poisoning with alcohol and its surrogates, clinic, forensic medical examination.
According to statistical information of the World Health patterns of alcohol and its surrogate poisonings are still disputable.
The objective of the study is design of clinical and morphological criteria of the assessment of acute poisonings with ethyl alcohol and its surrogates in hot climate.
Material for the study were conclusions of forensic expertises on acute poisonings with ethyl alcohol and its surrogates for 2010-2017 and results of proper examinations of corpses (82) of people who died due to alcohol poisoning and 76 cases of poisoning with alcohol and its surrogates in alive people receiving therapy in the republican Scientific Center of Emergency Medical Aid (RSCEMA). We performed analysis of all clinical and laboratory research methods used in cases of poisoning with ethanol and its surrogates in RSCEMA, while in lethal cases we used common morphologic methods.
Results of the study. Poisoning with alcohol develops step-by-step. Clinical symptoms depend on the dose. It is considered to be acute poisoning when state of a person, who consumed a great dose of alcohol, suddenly worsens with appearance of disorders of consciousness, loss of ability to walk, ability to perceive environment, development of stupor and coma. On the basis of clinical symptoms observed in patients treated at RSCEMA and data of forensic conclusions we worked out a table of acute poisonings with ethanol in our conditions.
Symptoms of alcohol coma are not specific and do not represent a variant of narcotic coma. It is characterized by obstruction aspiration disorders (tongue falling back, hyper-salivation, bronchorrhea, aspiration with vomiting masses), stridor, tachypnoe, acrocyanosis, swelling of cervical veins, possible big bubbly crackling in lungs, widening of pupils (Tab. 1).
In autopsies of corpses of people who died due to alcohol poisoning we did not find any specific alterations. Often we observed cyanosis and edema of face, swelling of eye-lids. Blood was liquid. In 93% there were tard spots on heart and
Organization, every year about 4% of population of the world dies because of alcoholism and diseases of inner organs caused by alcohol, now it is approximately 2.5 million people [8]. However, these are average data in the whole world, while in some countries the rate of alcohol mortality can reach very high level. The highest numbers were registered in Russia and some countries of Eastern Europe [9].
The basic reasons of lethal poisonings with alcohol are: consuming much alcohol, especially on empty stomach, chronic alcoholism, specific style of life, alcoholism in the family [1].
Ethanol easily penetrates through tissue membranes, it is fast absorbed in stomach (20%) and small intestine (80%). In 1.5 hour average its concentration in blood reaches maximal level. Ethanol acts like a selective depressant ofCNS in small doses, and as a common depressant in big ones; it has psychotropic (narcotic) effect accompanied by suppression of excitement processes in CNS by means ofneurons' metabolism application, dysfunction of mediator systems, inhibition of oxygen utilization [2; 5].
Significant role in the pathogenesis of poisoning is played by metabolic toxicosis and oscidosis (accumulation of ethanol biotransformation products). The basic endogenic product is poisonous acetaldehyde, formed in all variants of oxidative degradation of ethyl alcohol. If dehydrogenesis aldehyde is not duly transformed to acetate, expressed intoxication develops. Acetaldehyde causes disorder of adrenaline and other catecholamines circulation in brain and in periphery, it damages cardiac-vascular system, liver, and kidneys [3; 4; 6].
Clinical and morphological symptoms of poisoning with alcohol surrogates differ from those of ethyl alcohol [7]. Lethal outcome in case of poisoning with alcohol surrogates often occurs in case of presence of low concentrations of ethyl alcohol in blood or even its absence.
At the moment clinical manifestations of acute poisonings with ethyl alcohol are well studied, though morphologic
Medical science
lung surface. We noted plethora and edema of meanings, brain, and lungs. In 87% cases bladder was overfilled by urine. During autopsy cavities always had alcohol smell. Surrogates of
Poisoning with methyl alcohol in our study was observed in 6 cases. Methyl alcohol is easily absorbed in blood. First it has light narcotic effect, then there is suppression of oxidation processes in tissues and development of oxygen starvation. Lethal dose in the cases occurred due to doses from 40 to 100 ml of the drunken poison.
According to clinical symptoms we differentiated the following doses:
1. narcotic, displayed by poisoning symptoms;
2. toxic, damage of kidneys and heart;
3. damage of CNS displayed, first of all, by loss of vision.
In case of increased dose of methyl alcohol polyorganic alterations are formed quite quickly, leading to death at a moment. These alterations involve central nerve system, gastrointestinal tract, parenchymal organs, and organs of immunogenesis. With dose of 3ml of 50% of methanol solution disorders of blood circulation and dystrophic alterations were non-significant and differently expressed. In case of increase of the dose there was sudden increase of pathologic morphological alterations in cen-
ethyl alcohol are its substitutes. They include all other alcohols (methyl, butyl, prothyl, etc), and ethylene glycol, dichlorethal of substances which are often used for intoxication.
tral neural system and lungs. We noted trophic effect of methanol on the central neural system. Less expressed alterations were observed in parenchymal organs and immunogenesis organs. All that indicated selective effect of that poison.
Poisoning with ethylene glycol in our study was observed in 2 cases. In these cases ethylene glycol was used for suicide. In human organism it is destroyed to very toxic products of glycolic and oxalic acid. As a result of that CNS is damaged, there is notable excitement, convulsions, loss of consciousness, disorders of respiratory and cardiac activities. Acute renal failure develops due to the formation of non-soluble salts of oxalic acid, which cause occlusion of renal channels. Autopsy in these cases showed cyanosis of skin, wide dark-purple spots, plethora, brain edema, liver enlargement, and toxic lesion of kidneys.
In autopsies we also observed alterations corresponding to clinical forms of poisoning. In case of death due to cerebral coma in both cases we noted sudden hyperemia of brain substance and its meanings, multiple small hemorrhages in
Table 1.- Dynamics of clinical symptoms of acute poisonings with ethanol dependent on the concentration (dose) of ethyl alcohol in blood
Alcohol concentration in blood (%o, mass/volume) Alcohol effect stage Clinical manifestations
0.01-0.05 Sobriety There is no clear effect. For a usual observer the behavior is normal. Slight alterations are identified using special tests.
0.03-0.12 Euphoria Slight euphoria, communicative, talkative. Increased self-confidentiality, weakening of inhibition reactions. Deterioration of attention, reasonableness, self-control, loss of capability for fine operations, manipulations.
0.09-0.25 Excitement Emotional instability, weakening of inhibition reactions. Loss of reasonableness. Deterioration of memory and comprehension. Weakening of sensory response; increase of response time. Slight disorder of coordination of motions.
0.18-0.30 Confused consciousness Disorientation, confused consciousness, dizziness. Increased emotionality (fear, anger, sadness, etc). Sensory dysfunction (diplopia, and so on), color perception, motion forms, size. Rise of pain sensation threshold. Disorder of balance, quite expressed disorder of coordination, swinging walk, inarticulate speech.
0.27-0.40 Stupor Apathy, general slackness, close to paralysis. Noticeable weakening of responses to any stimuli. Loss of coordination, inability to walk or stay. Vomiting, incontinence of urine and feces. Turbid consciousness, deep sleeping and stupor.
0.35-0.45 Coma Complete loss of consciousness; anesthesia. Suppression or absence of reflexes. Drop of body temperature. Urine and feces incontinence. Disorder of blood circulation and breathing.
0.50 and more Death Possible lethal outcome. Death due to paralysis of respiratory muscles.
inner organs under serous and in mucous membranes. One victim who died on the 7th day after poisoning had prevailing alterations in kidneys and liver. In liver there was plethora, edema, fatty dystrophy, and necrosis foci. Kidneys are enlarged, have multiple large focal hemorrhages and grey-yellow areas of necrosis, mostly in the cortex (toxic hemorrhagic necronephrosis). Histological study of the lumen of channels showed crystals of oxalates with characteristic structure.
The most severe damages were registered in case of poisonings with dichlorethan (6 cases). Dichlorethans are widely used as solvents for chemical cleaning of clothes, sticking of various surfaces and so on; it effects on almost all organs, and first of all, cardiovascular system, liver, and kidneys.
Clinical symptoms in all cases corresponded to acute poisoning: latent start with further development of toxic damage of brain substance (encephalopathy), headache, nausea, vomiting, dizziness, swinging walk, acute cardiovascular failure, damage of liver and kidneys. In 4 cases death occurred because of cerebral coma, and in 2 cases due to hepatic-renal failure.
Internal examination of corpse in all cases showed multiple hemorrhages in inner organs, damage of liver, kidneys, hemorrhages, and necrosis of gastric mucous membrane, specific smell of rotten dried mushrooms coming from cavities and organs.
Conclusion: Thus, in cases of acute poisoning with ethyl alcohol and its surrogates we could observe characteristic clinical symptoms of poisoning, dependent, first of all, on the concentration (dose) of taken poison and its physical-chemical composition.
Pathologic morphological symptoms of poisoning with alcohol surrogates are expressed dystrophic alterations in all inner organs with prevailing damages in liver and kidneys. We revealed the following symptoms: erosive gastritis, hyper coagulation, dystrophic alterations in liver and pancreas, and necrotic nephrosis.
Forensic histological examinations showed that macroscopic appearance of these poisonings had no specific symptoms. In relation to that, forensic diagnostics should be based on the data of clinical symptoms and forensic chemical blood and urine analysis of the victim.
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