A middle aged man had a sudden collapse with no precipitating features. His GCS on presentation was 3, with unequal but reactive pupils and CT brain showed a large subarachnoid bleed with midline shift. Neurosurgical opinion was to observe for clinical improvement, after which an intervention might be indicated. He was sedated on ICU and his MAP maintained above 80mmHg with noradrenaline. Nimodipine was commenced and mannitol was administered. After 24 hours he had a sedation hold and he began to localise and open eyes spontaneously. He was transferred to the neurosurgical unit.
Should all patients with non-traumatic intracranial haemorrhage have intracranial pressure (ICP) monitoring established?
Non-traumatic forms of intracranial haemorrhages account for 10 – 30% of all stroke hospital admissions, leading to catastrophic disability, morbidity and a mortality of 30 – 50%. The risk of neurological deterioration is highest during the first 24 hours after ictus and such patients should be managed in a critical care setting (1).
The maintenance of adequate cerebral perfusion pressure (CPP) is crucial in ensuring a more favourable outcome. This is usually achieved by the manipulation of ICP and mean arterial pressure (MAP) through surgical and medical measures as –
CPP = MAP – ICP – CVP
There are several types of ICP monitoring systems (2):
extradural fibre-optic probe laid between the dura and skull via a burr hole
subarachnoid screw applied via a burr hole
ventricular drain placed during craniotomy
intracerebral transducer placed within brain tissue
When it is not possible to insert an ICP monitoring device, the ICP can be estimated from a transcranial Doppler examination.
Two prevailing strategies for the management of elevated ICP have evolved from the experience in traumatic brain injury (3) – the ‘Lund concept’ and the ‘Rosner concept’. The ‘Lund concept’ assumes a disruption of the blood brain barrier and recommends therapeutic measures which normalise all essential haemodynamic parameters. The ‘Rosner concept’ assumes an intact pressure autoregulating system within the brain and hence emphasises maintaining a high CPP to minimise reflex vasodilataion or ischaemia at the expense of increased cardiopulmonary stress.
Controlling ICP reduces the likelihood of secondary brain injury including brain herniation and other catastrophic structural damage. There is no fixed ICP point above which mortality clearly increases and hence there is no acceptable threshold above which treatment should be instigated. Studies (4) quote a figure between 15 and 25 mmHg; a level of 20 mmHg is now generally accepted.
The Brain Trauma Foundation (5) recommend that all salvageable patients with a) severe traumatic brain injury and an abnormal CT and b) patients with normal CT scans but with 2 or more of the following: age over 40, unilateral or bilateral motor posturing and systolic BP less than 90 mmHg be considered for ICP monitoring (table 1). This would not only allow for treatment to be directed but also detection of subsequent complications. In the case of non-traumatic haemorrhage, caution must be exercised when extrapolating evidence from traumatic brain injuries.
Despite all the theoretical advantages, there are no RCTs showing an outcome benefit for patients with ICP monitoring when compared with patients without ICP monitoring. Indeed a recent observational study suggested that a CPP/ICP orientated therapy will increase treatment intensity and ventilator days in traumatic brain injuries without an improvement in outcome (6).
More recently, there has been a movement away from ICP monitoring (7), to focus instead on CPP management on the basis that if we can perfuse the damaged brain adequately we should reduce secondary injury. The rationale of any CPP augmentation is to increase CBF in brain regions which have critically low blood flow. In 1990, Rosner (3) proposed that CPP should be maintained above 70 mmHg and showed a good outcome in 68% of cases studied (n=38). His assumption of an intact autoregulating system is optimistic at best. Elf K et al (8). on the other hand, found that CPP augmentation was detrimental. Hence, the effects of CPP augmentation are difficult to predict. Robertson et al (9). compared CPP control (aiming for a CPP greater than 70 mmHg) and primarily ICP control and found a 5-fold increase in ARDS in the CPP targeted group but no difference in outcomes between the two.
- Steiner LA and Andrews PJD. Monitoring the Injured Brain: ICP and CBF. BJA 2006; 97: 26-38.
- Rincon F and Mayer SA. Clinical review: Critical care management of spontaneous intracerebral haemorrhage. Critical Care 2008; 12: 237-252.
- Rosner M and Daughton S. Cerebral Perfusion Pressure Management in Head Injury. J Trauma 1990; 30: 933-940.
- Marmarou A et al. Impact of ICP Instability and Hypotension on Outcome in Patients with Severe Head Injury. J Neurosurgery 1991; 75: S59-S65.
- Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury. J Neurotrauma 2007; 24(S1): S1-S106.
- Cremer OL et al. Effect of Intracranial Pressure Monitoring and Targeted Intensive Care on Functional Outcome After Severe Head Injury. Crit Care Med 2005; 33: 2207-2213.
- Springborg et al. Trends in monitoring patients with aneurysmal subarachnoid haemorrhage. BJA 2005; 94: 259-270.
- Elf K et al. Cerebral Perfusion Pressure Between 50 and 60 mmHg May Be Beneficial in Head-Injured Patients: A Computerised Secondary Insult Monitoring Study. Neurosurgery 2005; 56: 962-971.
- Robertson C et al. Prevention of Secondary Ischaemic Insult After Severe Head Injury. Crit Care Med 1999; 27: 2086-2095.