TRAFFIC FATALITIES AND ALCOHOLIC LIVER DISEASE IN FINLAND - A COMPARATIVE STUDY OF THE YEARS 1982-1985 AND 1989-1990

M. Perola*, J. Pikkarainen^, and A. Penttilä*^Department of Forensic Medicine, University of Helsinki 2National Public Health Institute, Helsinki, Finland

Introduction

The presence of alcoholic liver disease is an indicator of an excessive consumption of alcohol or alcoholism. However, there are only a few studies where liver morphology has been applied for this purpose in traffic fatalities (1- 3). Liver disease is often the only finding at autopsy suggesting excessive consumption of alcohol. Therefore, we wanted to clarify the correlation between liver disease and traffic casualties - a positive finding would give important knowledge for the background of traffic accidents.

There has been a steady rise in the consumption of alcohol in Finland in the 1980s (4). The proportion of alcohol-associated drivers has also significantly increased in fatal road traffic accidents according to the Traffic Safety Committee of Insurance Companies of Finland (5). The purpose of this investigation was also to study whether the effect of these changes could be seen in the liver morphology of casualties in fatal road traffic accidents.

Material and Methods

According to the Finnish law, a casualty in an accident of any type has to be examined by the local police which practically always requests the provincial or university forensic pathologist to perform an autopsy. Therefore, the autopsy rate of traffic casualties is virtually 100 %. In the province of Uusimaa (total population 1.2 million) all forensic autopsies are performed at the Forensic Department of Helsinki University. The material investigated comprised all motor-vehicle drivers that died in road traffic accidents in Helsinki or in the surrounding province of Uusimaa during 1989-90. In the material were included also 5 Finnish drivers who died in foreign countries but were autopsied in Helsinki. The total number of cases was 117 (107 males, 10 females, age range 15-78 years, average 37,3 years). We compared the results with an earlier similar study (3) which comprised 96 unselected motor-vehicle drivers that died in traffic accidents in the same area during a 4-year period (1982-1985). The autopsy was performed in most cases within 4 days after death. The bodies were preserved at + 4° C between death and autopsy. The cases with a liver badly crushed, burned or taken for transplantation were excluded from the material (12 cases).

The total number of livers screened histologically was 105. Specimens of liver (3-4 mm thick) were cut from the anterior left lobe, fixed in a 3,5 % aqueous buffered solution of formaldehyde for 3-4 days, embedded in paraffin and 5 mm sections were stained by the Herovic method. Specimens were examined by

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light microscopy for the presence of fatty infiltration, fibrosis and inflammation by two of us (M .P./A.P.). The fatty change of liver was divided quantifically into 4 classes (3): None: no fat vacuoles or a few isolated ones; Slight: isolated vacuoles all over the specimen and/or limited accumulations of fat vacuoles, fatty change in less than 20 % of liver cells; Moderate: fat vacuoles in 20-60 % of liver cells; Severe: fat vacuoles in more than 60 % of liver cells. No diabetic was found amongst the group examined. To evaluate the effect of obesity for liver steatosis, the body mass index (BMI, kg/m2) was determined in each case. In addition to steatosis, the presence of increased fibrosis periportally, parenchymally or perivenularily was noted, as were cirrhosis, bridging fibrosis and (periportal or other) inflammation. The criteria for alcoholic hepatitis morphologically were hepatocellular damage associated with neutrophil infiltration and increased fibrosis (6).

Blood, vitreous humour and urine were applied for alcohol determination with at least two head-space GC determinations in each case. Screening of drugs was made in 96 out of the histologically examined 105 cases. Samples for drug determination included blood (quantitative measurement) and urine, stomach contents and liver (qualitative measurement).

The chi2 test was used in the statistical analysis.

Results

Pathological liver morphology was found in 50 cases (48 %) with slight (12 cases), moderate (19 cases) or severe (10 cases) steatosis, periportal fibrosis (18 cases), moderate periportal inflammation (10 cases), alcoholic hepatitis (7 cases) and cirrhosis (2 cases). The comparison of the two materials (1982- 85/1989-90) can be seen in Table 1.

Table 1. Pathological changes in liver of motor vehicle drivers in traffic casualties. A comparison between the materials of the years 1982-85 and 1989-90

Type of change 1982-85* 1989-90**

Fatty degeneration No or minimal 54 % 61 %Slight 28 % 11 %Moderate 12 % 18 %Severe 6 % 10 %

Periportal fibrosis 32 % 17 %Periportal inflammation 4 % 10 %Alcoholic hepatitis 7 % 7 %Cirrhosis 0 2 %

n = 96; **: n = 105

The difference in the degree of steatosis between the two materials was almost significant (p< 0.05) with a higher proportion of cases with moderate or severe change in 1989-90. No significant change was found in other parameters.

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Eleven victims in the present material had BMI greater than 30 kg/m2, of which three had no fatty change, three had slight, two moderate and three heavy steatosis, so they showed no inclination for any degree of steatosis.

Blood alcohol was found to be positive ( > 0,35 o/oo) in 25 of 105 cases. The BAC values varied between 0,67 o/oo and 2,90 o/oo (average 1,75 o/oo). No clear correlation was seen between the BAC and the degree of liver damage. However, more than half of the BAC positive cases had fatty degeneration of the liver present at autopsy, of which six had slight, six moderate and one heavy steatosis. There were only three BAC positive cases with no pathological changes of the liver present at the autopsy. In 17 cases the screening for drugs was positive (Table 2). The possible hepatotoxity of some drugs found seemed to have no effect on this material.

Table 2. Drugs found in toxicological screening of blood.

Case no. Drug Degree of liver steatosis

6 chinidin moderate7 diazepam none10 propyphenazone none14 amiloride moderate19 chinidin slight24 amiodarone none33 carbamazepine none47 carbamazepine slight51 diazepam none56 hydroxychloroquine moderate58 phenazone none60 phenazone heavy70 diazepam none77 phenazone heavy82 chloroquine heavy88 desmethyldiazepam none

Discussion

The annual statistics by Finnish insurance companies in 1989 and 1990, respectively, show that 28 % and 34 % of killed motor vehicle drivers in fatal road traffic accidents in Finland were under the influence of alcohol (5). Alcoholism is common among DWI offenders as are traffic accidents (7). It is, however, difficult to determine the actual significance of alcoholism or chronic heavy usage of alcohol as a risk factor in traffic fatalities. An alcohol-related death doesn't necessarily involve any chronic heavy user of alcohol or a heavy user might have an accident without clear evidence of any acute alcohol usage. It is obvious that there is much overlapping between these two examples. Our method, which applies (alcoholic) liver disease as an evidence of heavy usage of alcohol, gives a direct way to estimate the association of alcoholism and traffic fatalities. After exclusion of non-specific pathological changes of liver, (periportal inflammation or periportal fibrosis occurring without other changes,

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total of 6 cases) our results still show that pathological changes of liver occur in nearly half (n = 44, 42 %) of motor vehicle drivers in fatal traffic accidents. On the other hand, other studies indicate that alcohol is the most important source of liver disease in the Finnish forensic autopsy material (8). Therefore, it seems that the role of alcohol in traffic fatalities is still greater than that assumed on the basis of the material of the Finnish traffic accident research committees (5).

The comparison made with the earlier study (3) suggests that the prevalence of moderate and heavy steatosis among traffic casualties has increased since the 1982-85 period. Primarily this brings us to the conclusion that heavy use of alcohol and alcoholism among motor vehicle drivers who died in traffic accidents has increased. The increase of other general reasons for steatosis (diabetes, obesity) is hardly probable. Whether the increase is due to the general increase of alcohol consumption in Finland or more unspesific change in the population of traffic casualties remains unsolved.

The results of these two forensic autopsy series suggest that alcoholism and heavy usage of alcohol themselves are risk factors in the epidemiology of fatal road traffic accidents and should be considered as such when planning traffic accident prevention programs.

References:

1. Waller JA, King EM, Nielson G, Türkei HW. Alcohol and other factors in California highway fatalities. J Forensic Sei 1969, 14, 429-444.2. Hilden M, Christoffersen P, Juhl E, Dalgaard JB. Liver histology in a "normal" population - examinations of 503 consecutive fatal traffic casualties. Scand J Gastroenterol 1977, 12, 593-597.3. Penttilä A., Karhunen PJ., Dunbar JA., Pikkarainen J. Alcoholic liver disease in fatally injured motor vehicle drivers in Finland. Proceedings of the l l 1*1 World Congress of the International Association for Accident and Traffic Medicine. Dubrovnik 1988, 197-204.4. Savolainen VT, Karhunen PJ, Penttilä A. Delayed increases in liver cirrhosis mortality and frequency of alcoholic liver cirrhosis following an increment and redistribution of alcohol consumption in Finland: evidence from mortality statistics and autopsy survey covering 8,533 cases in 1968-1988. Ale Clin Exp Res (in press).5 The Traffic Safety Committee of Insurance Companies of Finland. Road accident investigation teams. Report on case investigations in Finland. 1991, Helsinki.6. International group. Alcoholic liver disease: morphological manifestations. Lancet 1981 ii, 707-711.7. Dunbar JA, Ogston SA, Ritchie A, Devgun MS, Hagart J, Martin TB. Are problem drinkers dangerous drivers ? An investigation of arrest for drinking, serum g- glutamyltransferase activities, blood alcohol concentrations, and road traffic accidents: the Tayside safe driving project. BMJ 1985, 290, 827-830.8. Savolainen VT, Liesto K, Männikkö A, Penttilä A, Karhunen PJ. Moderate alcohol consumption and alcoholic liver disease - evidence of a threshold level of effects of ethanol. Submitted for purification.

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