The Vittamed 505 non-invasive autoregulation monitor
The Vittamed 505 offers the non-invasive technique of continuously and non-invasively monitoring thecerebrovascular autoregulation dynamic in real time. The monitor provides information about the blood volume dynamics in the smallest vessels responsible for cerebral blood flow autoregulation, the small arterial vessels and arterioles. In a healthy brain, small arteries in the brain expand and contract automatically to compensate for rises and falls in cerebral perfusion pressure which is equal to the difference between arterial blood pressure (ABP) and intracranial pressure (ICP).
Cerebral autoregulation can compensate to an extent to swelling of the brain from traumatic brain injury. However once the arteries are fully expanded, no further compensation can occur. The scientific studies (1,2) have found that impairment of cerebral autoregulation is associated with worse outcome in severe traumatic brain injuries (TBI) and the authors suggested that loss of autoregulation may be an early sign that ICP will rise. Another study (3) found that patients who lose cerebral autoregulation should be managed using special treatment protocol in order to improve outcomes.
Cerebral autoregulation monitor provides useful clinical information as an early prognostic marker for patients with traumatic brain injury, allowing more focused and more reliable treatment decisions in the cases of still intact or impaired cerebrovascular autoregulation. A recent consensus paper suggested that treatment targets should be adjusted based on the state of cerebral autoregulation (4).
The Vittamed 505 ultrasonic device consists of a portable monitoring unit and a disposable headframe, designed to be easily fitted to a patient’s head with minimal training. No accurate location of the transintracranial acoustic path is required on the head to generate a signal, and results can be obtained in a few minutes, generating a continuous monitoring trace.
The Technology
The Vittamed 505 monitor uses transintracranial ultrasound to assess the change in the time an ultrasound pulse takes to cross the brain as intracranial blood and CSF volume varies. It generates a pressure-reactivity index measure (PRx), which is the phase difference between intracranial pressure and arterial blood pressure waves. Normal or intact cerebrovascular autoregulation has a negative correlation and up to 160 degrees in phase difference between ABP and ICP slow waves, i.e. cerebral arterioles constrict with increasing cerebral perfusion pressure, while a positive correlation or almost zero phase shift between ABP and ICP slow waves shows non-reacting cerebral vessels and impaired autoregulation.
Vittamed Technologies has demonstrated that the Vittamed 505 monitor generates similar autoregulation readings to invasive ABP and ICP slow wave monitoring in patients with traumatic brain injury (5,6).
Vittamed Technologies already patented [ European Patent No 2 111 787 B1 ] fully non-invasive version of Vittamed 505 which does not need ABP reference signals. Reference signal for phase shift monitoring and automatic PRx calculation is obtained by sophisticated automatic analysis of non-invasively recorded intracranial blood volume slow, respiratory and pulse waves.
It was demonstrated, that non-invasive monitoring delivers similar autoregulation readings to invasive monitoring (5,6).
One hour session of Simultaneous invasive (iPRx) and non-invasive determination (nPRx) of cerebral autoregulationin TBI patient.
Non-invasive cerebrovascular autoregulation monitor Vittamed 505
Cerebrovascular autoregulation
In a healthy brain, small arteries in the brain expand and contract automatically to compensate for rises and falls in cerebral perfusion pressure and to keep cerebral blood flow stable. This is known as cerebral autoregulation. Cerebral autoregulation can compensate to an extent the swelling of the brain from traumatic brain injury. However once the arteries are fully expanded, no further compensation can occur. Indeed two studies (1,2) have found that impairment of cerebral autoregulation is associated with worse outcome in severe traumatic brain injury and the authors suggested that loss of autoregulation may be an early sign that ICP will rise. Another study found that patients who lose cerebral autoregulation should be managed using special and different treatment protocols than the TBI patients with still intact autoregulation. Autoregulation targeted therapy is the only way to improved TBI patients’ outcomes (3), leading to a recent consensus paper suggesting that treatment targets should be adjusted based on the state of cerebral autoregulation (4).
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1 Hiler et al, J Neurosurg. 2006 May;104(5):731-7
2 Balestreri et al, Acta Neurochir (Wien). 2004 Feb;146(2):131-41
3 Howells et al, J Neurosurg 2005 102: 311-317
4 Andrews et al: NICEM consensus: Intensive Care Med 2008: 43: 1362-1370
5 Ragauskas et al: Med Engineering & Physics: 2003: 25: 667-678
6 Ragauskas et al: Acta Neurochir : 2005: [Suppl] 95: 367-370