Clinical History:

This 44-year-old woman was found down on the ground and was unarousable. She was transported to the hospital where it was noted that her pupils were of unequal size. There was a 5 cm laceration on the back of the scalp. Periorbital ecchymoses were present. The liver was palpated 10 cm below the costal margin. Blood pressure was 140/70, temperature 35.5, pulse 90, and respirations 25. Blood ethanol on admission was 0.17 gm%. A CT scan revealed bilateral subdural hemorrhages. She was evaluated by neurosurgery and then taken to surgery where subdural blood clots were evacuated. The ethanol level in the clots removed at surgery was 0.35 gm%. Her condition did not improve markedly, and two weeks later she became comatose and died.

Image 2.1:

This gross photograph depects the liver. Describe the appearance.

The liver is big and has a yellowish color.

Image 2.2:

The microscopic appearance of the liver is shown here. There is fatty change.

Image 2.3:

The gross appearance of the skull at autopsy is shown here. Note the fractures of the orbital plate.

Image 2.4:

The inner surface of the dura is depicted in this image. This is a bilateral subdural hematoma.

Questions:

1. What is the etiology for her liver disease?

Chronic alcoholism. The alcohol leads to the accumulation of fat in hepatocytes.

2. What is the relationship of her liver disease with the trauma?

Patients with severe liver disease may have hepatic encephalopathy which contributes to their falling and injuring themselves. The liver disease also leads to coagulation problems, and these accentuate the hemorrhage associated with the trauma.

3. How is the CNS hemorrhage produced?

Trauma with tearing of the bridging veins below the dura.

4. How do you explain the difference in ethanol level measured on admission and in the subdural blood clots?

The alcohol in the blood in the dural clots was not metabolized at the same rate, having been sequestered, and represents the level at a previous time.

5. How do you explain the injury pattern that relates a posterior scalp laceration to the orbital plate fractures?

The mechanism is a "contrecoup" injury in which the fall backwards produced the scalp laceration, but the force was transmitted to the opposite side of the brain to produce the orbital plate fractures.