A nineteen-year-old female high school senior has been involved in a serious single-driver automobile accident. She is brought into a surgical trauma unit suffering from massive internal bleeding. Attempts to stabilize her prior to surgery are unsuccessful. She suffers from severe hypotension (low blood pressure) and shock and expires. Blood alcohol testing demonstrates that she was legally intoxicated. This is considered to be a likely cause of her accident. The county medical examiner requests an autopsy.
Findings Pertinent to This Case
The decedent was noted to be moderately obese. The cause of internal bleeding was discovered to be multiple sites of injury to major vessels relating to the crush injury of her thorax (chest). The autopsy was otherwise remarkable for the finding of hepatomegaly (hypertrophy of the liver). The liver weighed 2,200 grams (normal about 1,400 grams in a young female) and was noted to be pale and fatty appearing. Histologic investigation of the liver disclosed macrovesicular steatosis, the presence of excess lipid within hepatocytes (cells of liver parenchyma) as large vesicles. Liver cells contained large clear vesicles that displaced the position of the nucleus on routine hematoxylin-eosin (H&E) stained material (tissue processing removes lipid). Frozen tissue sections processed to maintain lipid showed positive staining of the vesicles with a stain for lipids (FIGURE 2-12). No other abnormality of the liver was noted. The decedent’s parents were interviewed and stated that their daughter drank large amounts of beer and other alcoholic beverages. This usually occurred as binge drinking during weekends. They estimated that it was common for their daughter to consume five to six cans of beer per day on an average weekend. Neither parent felt this amount to be excessive and denied their daughter was an alcoholic.
FIGURE 2.12
Discussion
Steatosis or fatty liver disease (FLD) can occur in the obese as a result of a number of metabolic diseases of the liver or with the ingestion of potentially toxic agents such as some drugs or notably alcohol (ethanol). FLD results when the liver’s ability to export fat is lower than the intake of exogenous and/or the production of endogenous lipids. Both decreased export and increased synthesis may occur in alcoholic FLD (AFLD). AFLD is almost always found in heavy drinkers, but even modest consumption of alcohol may result in the condition. Prolonged consumption of modest amounts of alcohol (about 50 grams per day, equivalent to about four twelve-ounce cans of beer) will result in AFLD in more than 40 percent of individuals. There is great individual variation in susceptibility to AFLD (and the more serious consequences of alcohol consumption). Females, the obese, and binge drinkers show much increased risk. Although AFLD is usually asymptomatic and is reversible with abstinence, continued alcohol consumption is likely to lead to serious and irreversible liver disease (cirrhosis see presentation on the liver).
Etiology and Pathogenesis
The etiologic agent is the toxic agent ethanol. Consumption of excess ethanol leads to derangement of liver metabolism and the deposition of lipid within the cells of the liver (alcoholic steatosis or AFLD). With continued consumption, this may progress to alcoholic hepatitis (inflammation of the liver) and alcoholic cirrhosis (scarring of the liver), resulting in hepatic failure and other systemic diseases.
Questions
1. Why are hepatocytes (liver parenchymal cells) particularly susceptible to deposition of lipid within the cells?
2. Why are frozen sections necessary to demonstrate steatosis in the liver?
3. What would have happened to the liver had the individual survived her accident and stopped drinking? What if she continued drinking?