information repository image repository discussion group interactive trauma professional resources about search directory related sites new content




Intracranial Pressure

As the cranial vault is essentially a closed, fixed bony box, its volume is constant. This volume is described by the Monro-Kellie doctrine, proposed in the early part of the 19th century:

v.intracranial (constant) = v.brain + v.CSF + v.blood + v.mass lesion

As all these components are fluids, and non-compressible, once the cranial vault is filled, it's pressure rises dramatically. This intracranial pressure (ICP) rise can the lead to interruption of cerebral blood flow by reducing the cerebral perfusion pressure. As an intracranial mass lesion or oedematous brain expands, some compensation is possible as cerebrospinal fluid (CSF) and blood move into the spinal canal and extracranial vasculature respectively. Beyond this point, further compensation is impossible and ICP rises dramatically (figure 1).

Patients who are on the cusp of the graph have exaggerated ICP responses to events such as tracheal intubation, coughing or fighting a ventilator.

Key Recommendations

Maintenance of CPP reduces mortality in severe head injury.


ICP monitoring is recommended in most comatose patients with severe head injury.


ICP should be treated when above 20mmHg, but maintenance of CPP is probably more important.


The normal ICP is 5 - 15 mmHg. There is no defined set point at which treatment for intracranial hypertension should be initiated, but levels above 20mmHg are usually treated. However it is probably more important to maintain an adequate cerebral perfusion pressure. In a hypotensive patient, even a small increase in ICP could be harmful. Alternatively, an elevated mean arterial pressure may protect against a raised ICP.

ICP measurement is necessary to accurately determine CPP. However ICP measurement per se has not been conclusively shown to alter outcome in head injury patients. This is due to a combination of factors, primarily that ICP monitoring is now so accepted for severe head injury, and forms the basis for modern brain injury management, so that it would be difficult to conduct a study with a control arm. Secondly, as mentioned previously, previous studies have concentrated on controlling ICP, whereas modern brain injury protocols focus on maintenance of CPP. Thirdly, failure of a therapy should not necessarily implicate the measurement tool that therapy is directed against.

There is a substantial body of evidence to support the use of ICP monitoring. Several studies have reported substantial lowering in mortality after ICP monitoring and control was introduced. Similarly studies have shown a lower mortality in those patients whose ICP could be controlled compared to those in which it could not. ICP monitoring is now a central part of critical care management for the severely brain injured patient.

Indications for ICP monitoring.

All patients with severe head injury (GCS<9) and those patients with moderate head injury (GCS 9-12) at increased risk (see below) or who cannot be followed with serial neurological examination (eg. anaesthetised for other procedure).

Indications for ICP monitoring Risk of raised ICP
Severe Head Injury (GCS 3-8)  
  • Abnormal CT scan
  • Normal CT Scan
    Age > 40 or BP < 90mmHg or abnormal motor posturing
  • Normal CT scan
    No risk factors
Moderate Head Injury (GCS 9-12)  
  • If anaesthetised/sedated
  • Abnormal CT scan
approx. 10-20% will deteriorate to severe head injury
Mild Head Injury (GCS 13-15)  
  • few indications for ICP measurement
Only around 3% will deteriorate 5:1 2000


Monro A. Observations on the structure and function of the nervous system. Edinburgh, Creech & Johnson 1823 p.5

Kellie G. An account of the appearances observed in the dissection of two of the three individuals presumed to have perished in the storm of the 3rd, and whose bodie were discovered in the vicinity of Leith on the morning of the 4th November 1821 with some reflections on the pathology of the brain. Trans Med Chir Sci, Edinburgh 1824;1:84-169

Lang EW, Chesnut RM. Intracranial pressure and cerebral perfusion pressure in severe head injury. New Horizons 3:400-409, 1995

Chesnut RM, Marshall LF, Klauber MR et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216-222, 1993

Eisenberg H, Frankowski R, Contant C et al. Comprehensive central nervous system trauma centers: High dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg 1988;69:15-23

Marmarou A, Anderson RL, Ward JD et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 75:S59-S66, 1991

Marshall LF, Gautille T, Klauber MR et al. The outcome of severe closed head injury. J Neurosurg 75:S28-S36, 1991

Gopinath SP, Contant CF, Robertson CS et al. Critical thresholds for physiologic parameters in patients with severe head injury. Congressof Neurological Surgeons Annual Meeting. Vancouver, 1993

Colohan AR, Alves WM, Gross CR, et al. Head injury mortality in two centers with different emergency medical services and intensive care. J Neurosurg 71:202-207, 1989

Ghajar JB, Hairiri RJ, Paterson RH. Improved outcome from traumatic coma using only ventricular CSF drainage for ICP control. Adv in Neurosurg 21:173-177, 1993

Narayan RK, Kishore PR, Becker DP et al. Intracranial pressure: to monitor or not to monitor? A review of our experience with acute head injury. J Neurosurg 56:650-659, 1982