Head Injury — MRCS Part B Applied surgical science and critical care

An 82-year-old who has fallen, with a GCS of 11, opening into the physiology of the cerebrospinal fluid, cerebral blood flow and intracranial pressure.

Glasgow Coma Scale

Eyes (4): spontaneous, to voice, to pain, none. Verbal (5): orientated, confused, inappropriate words, incomprehensible sounds, none. Motor (6): obeys, localises to pain, withdraws, abnormal flexion, extension, none. This patient opens his eyes to pain (2), is confused (4) and localises (5): GCS 11. The scale is scored on the best response and is recorded as its components, because “M5” carries more meaning than a total.

Presentation

Headache, vomiting, amnesia, a falling conscious level, seizures, focal weakness, a dilated pupil, and the signs of a basal skull fracture: periorbital bruising (raccoon eyes), bruising over the mastoid (Battle's sign), blood behind the eardrum, and clear fluid from the nose or ear that is positive for beta-2 transferrin.

Urgent CT within an hour (NICE)

GCS under 13 on arrival or under 15 two hours after the injury, a suspected open or depressed skull fracture, any sign of a basal skull fracture, a seizure after the injury, a focal deficit, or more than one episode of vomiting. Anticoagulation, a dangerous mechanism, or amnesia of more than 30 minutes before the injury bring a scan within eight hours.

Cerebrospinal fluid

Made by the choroid plexus of the lateral, third and fourth ventricles at about 500 ml a day, so the 150 ml present is replaced three or four times daily. It flows from the lateral ventricles through the foramina of Monro into the third ventricle, down the cerebral aqueduct into the fourth ventricle, and out through the midline foramen of Magendie and the two lateral foramina of Luschka into the subarachnoid space, over the hemispheres and down around the cord. It is reabsorbed through the arachnoid granulations into the superior sagittal sinus. It floats the brain, cushions it against the skull, carries nutrients and waste, and buffers changes in intracranial volume.

Blood-brain barrier

Tight junctions between the capillary endothelial cells, backed by astrocyte foot processes. Water, oxygen, carbon dioxide, lipid-soluble molecules (alcohol, anaesthetics, most drugs that act on the brain) cross freely; glucose and amino acids cross by transporters; proteins, most ions and water-soluble drugs do not. It breaks down around tumours, abscesses and infarcts, which is why they enhance with contrast.

Cerebral blood flow

The brain takes about 15% of the cardiac output, roughly 750 ml a minute, for 2% of the body's weight. Flow is autoregulated between a mean arterial pressure of about 50 and 150 mmHg by myogenic changes in arteriolar tone; it rises steeply with arterial carbon dioxide (the basis of hyperventilation to lower pressure briefly) and with hypoxia below 8 kPa, and it follows local metabolic demand. Autoregulation is lost in the injured brain, so flow then follows pressure directly.

Pressure

Cerebral perfusion pressure is mean arterial pressure minus intracranial pressure; the target after injury is above 60–70 mmHg. Normal intracranial pressure is under 15 mmHg. The Monro-Kellie doctrine states that the skull is a fixed box containing brain, blood and cerebrospinal fluid, so an increase in one, or a haematoma, must be matched by a fall in another; fluid and venous blood are displaced first, then pressure rises steeply once about 100 ml of compensation is exhausted. Cushing's reflex is the response to that rising pressure: hypertension to preserve perfusion, with reflex bradycardia and irregular breathing, and it signals impending coning.