Emergency Medicine 1: Prehospital management of cerebral herniation

Cerebral herniaton is a process where brain tissue is moved, because of high pressure. The tissue is moved from its origin to another loaction inside the skull, or down through the foramen magnum to the spinal channel. Cerebral herniaton is caused by increased intracranial pressure (ICP) due to volume filling processes, such as intracranial bleeding. Because herniation/ high ICP compresses vital structures and disturbs the natural blood flow, it is a highly lethal process.

Cerebral herniation should be suspected in a head trauma patient with a low, or rapidly falling level of consciousness. Abnormal extension of the extremities, or no reaction at all can be seen when the patient is subjected to painful stimuli. Often one or both pupils are dilated and not responsive to light as the herniation process compresses one or both of the oculomotor nerves. Because cerebral herniation is caused by increased ICP, the cushing's triad with hypertension, bradycardia and irregular breathing is also often seen. It is important to notice that all of these signs are seen in the late stages of raising ICP, and that absence of these signs does not exclude serous brain injury.

Management of all serious traumatic brain injuries:

Secure ABCs to prevent secondary brain damage, which is damage to brain parenchyma due to hypoxia or hypotension.
Secure the vertebral column according to local protocol.
Consider elevating the head end of the gurney about 30 degrees, this provides the optimal position to prevent further rise in ICP, because of increased venous return without compromising arterial flow to much.
Quickly and safely transport the patient to the closest appropriated trauma facility with neurosurgery, consider using air transport. Alert the trauma team well in advance.
Closely monitor and document vital signs and level of consciousness.

Management of the herniating patient:

Mild hyperventilation of the patient. This lowers the partial pressure of CO₂ in the parents’ blood, which will constrict cerebral vessels. The vasoconstriction decreases the volume occupied by blood vessels within the skull and reduces filtration of plasma over the capillaries, both lowering the ICP. It is important to not ventilate the patient too aggressively, as this will wash out too much CO₂, constricting the cerebral vessels to levels leading to ischemia. To the adult patient, hyperventilation should be administered as 20 ventilations per minute, with normal tidal volumes. To avoid ischemia hyperventilation should be monitored with capnometry or capnography, and EtCO₂be kept at levels from 30-35 mmHg or about 4,0-4,5 kPa. To avoid cerebral ischemia hyperventilation should not be used as a profilactic treatment, but only used in patients with suspected ongoing herniation. The hyperventilation should be discontinued when if the signs of herniation resolve.
Consider administrating a hypertonic solution IV, such as hypertonic NaCl or Mannitol if the transport time is intermediate or long. This will remove fluid from the brain due to the higher osmolality of the blood after such infusion. It is widely in use in the intrahospital setting, but there is some controversy to its use in the prehospital setting.