For over twenty years aggressive hyperventilation of the patient suffering from traumatic brain injury (TBI) has been standard practice around the world.

The original concept behind the use of this technique was to reduce intracranial pressure. However, there have been no studies to show that the patient's neurological outcome is improved by this practice.

A recent report by the American College of Neurosurgeons (based on research of all applicable literature from the last 25 years) now casts severe doubt on the routine use of this technique in patients suffering from traumatic brain injury (TBI).

In their "Guidelines for the management of Severe Head Injury" 1, clear clinical evidence supports their call for a discontinuance of prophylactic hyperventilation as a treatment for TBI.

In 40% of patients suffering from TBI, brain swelling and an increase in intra- cranial pressure occurs 2. High intra- cranial pressure following traumatic brain injury is one of the main causes of death in these patients 3,4,5, and it has been assumed that hyperventilation is of benefit to all patients.

Intra-cranial pressure reduction is achieved through hyperventilation by constricting the vessels in the brain and reducing cerebral blood flow. Twenty years of research clearly shows that, in the first day following injury, the cerebral blood flow is less than half the norm 6,7,8,9,10,11,12,13,14, 15, and that aggressive hyperventilation potentially risks causing cerebral ischaemia.

It has also been found (in some patients), that aggressive hyperventilation can actually cause an increase in intracranial pressure16 .

So what is the answer for those who are at the frontline in the treatment of patients with TBI?

The recommendations of the American College of Neurosurgeons are quite clear and are backed by a significant amount of scientific evidence.

Prophylactic hyperventilation should be avoided during the first five days following severe TBI and should be especially avoided during the first 24 hours.

There is irrefutable scientific evidence to show that patients with TBI have low cerebral blood flow and it is strongly suggested that in the first hours after injury the cerebral blood flow approaches levels that are consistent with causing brain ischemia. Hyperventilation will further reduce cerebral blood flow values but will not consistently cause intracranial pressure levels to fall. It has also been shown, in a randomised clinical study, that outcomes for TBI patients are worse if they are aggressively hyperventilated17.

Limiting the use of hyperventilation following severe TBI to those patients where the deterioration in their neurological condition warrants this type of intervention, may be a safe option. Also, limiting the length of time that hyperventilation is employed should be considered.

When hyperventilation is considered a clinical necessity how do we decide when to hyperventilate? Monitoring the patient's intracranial pressure and cerebral blood flow are ways of identifying the point at which cerebral ischemia may occur, but this is impossible to undertake in the field.

Regardless of the type of injury, hyperventilation is never a substitute for good, consistent, ventilation on 100% oxygen.

The use of Automatic Transport Ventilators (ATVs) as opposed to bag- valve-mask devices provides these consistent ventilations. ATVs with the added feature of a manual ventilation button allows for controlled hyperventilation by the operator.

By using ATVs and controlling the Expiratory Time (which cannot be achieved consistently when using a bag- valve-mask device) allows for the best exchange of gases and removal of CO2 from the blood stream. By ensuring good gas exchange we are also assisting in the reduction of intracranial pressure by reducing the PaCO2 levels.

Based on this research, we all should reevaluate our protocols and consider whether hyperventilation or good ventilation should be our main aim in traumatic brain injured patients.

References.

1."Guidelines for the Management of Severe Head Injury": A joint initiative of:
The Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrauma and Critical Care. 1995, Brain Trauma Foundation

2. Miller JD, Becker DP, Ward JD et al: Significance of intracranial hypertension in severe head injury. J Neurosurg 47:503-510, 1977

3. Becker DP, Miller JD, Ward JD et al: The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg 47:491-502, 1977

4. Marshall LF, Smith RW, Shapiro HM: The outcome with aggressive treatment in severe head injuries. I. The significance of intracranial pressure monitoring. J. Neurosurg 50:20-25, 1979

5. NarayanRK, Kishore PRS, Becker DP, et al: Intracranial pressure: To monitor or not to monitor. J Neurosurg 56:650-659,1982

6. Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischaemia. J Neurosurg 75:685-693,1991

7. Bouma GJ, Muizelarr JP, Stringer WA, et al: Ultra early evaluation of regional cerebral blood flow in severely head injured patients using xenon enhanced computed tomography. J Neurosurg 77:360368, 1992

8.Cruz J: Low clinical ischaemia threshold for cerebral blood flow in severe acute brain trauma. Case report. J., Neurosurg 80:143-147, 1994

9. Fieschi C, Battistini N, Beduschi A, et al: Regional cerebral blood flow and intraventricular pressure in acute head injuries, J Neurol Neurosurg Psychiatry 37:1378-1388, 1974

10. Jaggi JL, Obrist WD, Gennareli TA, et al: Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. J Neurosurg 72:176-182, 1990

11. Marion DW, Darby J, Yonas H: Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 74:407-414, 1991

12. Muizelaar JP, Marmarou A, Desalles AA, et al: Cerebral blood flow and metabolism in severely head injured children. Part 1: Relationship with GCS score, outcome, ICP, and PVI. J Neurosurg 71:63-71, 1989

13. Robertson CS, Clifton GL, Grossman RG, et al: Alterations in cerebral availability of metabolic substrates after severe head injury. J Trauma 28:1523-1532, 1988

14. Salvant JB, Muizelaar JP,: Changes in cerebral blood flow and metabolism related to the presence of subdural hematoma. Neurosurgery 33:387-393, 1993

15. Schroder ML, Muizelaar JP, Kuta AJ: Documented reversal of global ischaemia immediately after removal of an acute subdural haematoma. Neurosurgery 80:324-327, 1994

16. Obrist WD, Langfitt TW, Jaggi JL, et al: Cerebral blood flow and metabolism in comatose patients with acute head injury. J Neurosurg 61: 241-253, 1984

17. Muizelaar JP, Marmarou A, Ward JD, et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomised clinical trial . J Neurosurg 75: 731-739, 1991