Secondary ischaemic brain damage after head injury.

When the brain is examined within a few days of injury it can be surprisingly difficult to establish what has been the cause of death, or to determine with certainty which lesions are primary and which are secondary, apart from clear-cut complications such as intracranial haematoma or infection. Recent reports of continuous measurements of intracranial pressure after head injury (Lundberg, Troupp, and Lorin, 1965; Troupp, 1965 and 1967) suggest that many patients who die after head injury develop very high intracranial pressure before death without necessarily having a focal expanding lesion. The effect of a generalized increase in intracranial pressure on the brain is ultimately to produce a reduced perfusion of blood and the brain will then suffer hypoxic damage. In the belief that this may be one of the mechanisms contributing to brain damage after head injuries (and other lesions causing raised pressure) we have explored various aspects of the relationships between intracranial pressure and cerebral blood flow. The oxygen supply to the brain depends, as in any other tissue, on the equation: available oxygen = haemoglobin x oxygen saturation x blood flow. A reduced oxygen content of the blood is not uncommon after head injury, which makes the brain much more critically dependent on blood flow. Blood loss from associated injuries, which occurs in a third of all cases of head injury admitted to hospital, commonly gives a low haemoglobin. Respiratory difficulties are also frequent after head injury, either due to the unconscious state or to associated chest injuries, and as a result of ventilatory insufficiency the oxygen saturation is then reduced. Blood flow in the brain has a characteristic peculiar to its situation within a rigid closed cavity, namely, its susceptibility to surrounding tissue pressure. Indeed the supply of blood to the brain depends on cerebral perfusion pressure, which is the difference between systemic arterial pressure and intracranial pressure. Cerebral perfusion may be altered not only by systemic hypotension but also by raised intracranial pressure. Whilst hypotension is uncommon in patients suffering from head injury alone, the