Thermal Perfusion Probe for Monitoring Regional Cerebral Blood Flow

Number: 0703

Policy

Aetna considers a thermal perfusion probe for monitoring regional cerebral blood flow experimental and investigational because there is insufficient evidence of the clinical value of these approaches in the management of individuals with acute neurological disorders (e.g., head injury, subarachnoid hemorrhage, or following neurosurgery) or for other indications. 

See also CPB 0663 - Cerebral Perfusion Studies.

Background

Cerebral blood flow (CBF) is essential for normal metabolism of the brain.  Ischemic brain injury occurs when CBF is insufficient to meet metabolic demand, which can occur in acute neurological disorders (e.g. head injury, subarachnoid hemorrhage, or following neurosurgery).

Various imaging techniques have been attempted to identify individuals at risk for secondary ischemic brain injury and manage response to therapies.  Some of these techniques are still evolving (e.g., stable-xenon-enhanced computed tomography (XeCT), perfusion computed tomography, perfusion magnetic resonance imaging, single photon emission computed tomography (SPECT) and positron emission tomography (PET)).  While these techniques can provide regional information about CBF, the data provided is a single snap shot in time.  Methods for the continuous measurement of CBF have been investigated and are now commercially available.  One such method is a thermal perfusion probe, which is placed intra-cerebrally via a burr hole in the vascular area of interest in the brain.  The probe is connected to a monitor that displays CBF data. 

The QFlow 500 probe (Hemedex, Inc, Cambridge, MA) is an example of a commercially available thermal perfusion probe that has received 510(k) marketing clearance from the Food and Drug Administration (FDA).  It is used along with the Bowman Perfusion Monitor, Model 500 (Hemedex, Inc, Cambridge, MA).  According to the manufactures website, one potential application of the device is for monitoring CBF in patients with traumatic brain injury to help identify secondary ischemic injury to the brain.  The manufacturer states that, by measuring continuous, real-time CBF, clinicians may identify cerebral edema and measure tissue blood flow response to therapies.  Another potential neurological application is monitoring CBF following neurosurgery (e.g., aneurysm and subarachnoid hemorrhage procedures).

Current literature on thermal perfusion probes has focused on their clinical feasibility and technical capabilities.  Jaeger et al (2005) measured regional cerebral blood flow (rCBF) using the QFlow in patients with severe subarachnoid hemorrhage (n = 5) and traumatic brain injury (n = 3) and compared these results to brain tissue oxygen measurements (P(ti)O(2)) using the Licox (GMS, Kiel-Mielkendorf, Germany) for an average of 9.6 days.  The data indicated a significantcorrelation between CBF and P(ti)O(2) (r = 0.36).  After 400 intervals of 30-min duration, the QFlow and the P(ti)O(2) measurements correlated 72 % of the time when P(ti)O(2) changes were greater than 5 mm Hg (r > 0.6).  In 19 % of the intervals a statistically significant correlation was observed (r < 0.6).  During the remaining 9 %, no correlation was found (r < 0.3).  The authors suggested that the level of P(ti)O(2) is predominately determined by rCBF, since changes in P(ti)O(2) were correlated in 90 % of episodes to simultaneous changes of CBF.  Phases of non-monitoring were mostly due to fever of the patient, when the system does not allow monitoring to avoid overheating of the cerebral tissue. 

Vajkoczy et al (2003) obtained rCBF using thermal-diffusion (TD) microprobes to prospectively diagnose symptomatic vasospasm in 14 patients with high-grade subarachnoid hemorrhage (SAH) who underwent early clip placement for anterior circulation aneurysms.  The TD microprobes were implanted into the white matter of vascular territories that were deemed at risk for developing symptomatic vasospasm.  Data on arterial blood pressure, intracranial pressure, cerebral perfusion pressure, rCBF, cerebrovascular resistance (CVR), and blood flow velocities were collected at the patient's bedside.  The diagnosis of symptomatic vasospasm was based on the manifestation of a delayed ischemic neurological deficit and/or a reduced territorial level of CBF as assessed using stable XeCT scanning in combination with vasospasm demonstrated by angiography.  Bedside monitoring of TD-rCBF and CVR allowed the detection of symptomatic vasospasm.  In the 10 patients with vasospasm, the TD-rCBF decreased from 21 +/- 4 to 9 +/- 1 ml/100 g/min), whereas in the 4 other patients the TD-rCBF value remained unchanged (mean TD-rCBF = 25 +/- 4 compared with 21 +/- 4 ml/100 g/min).  Based on a comparison of the results of TD-rCBF and Xe-enhanced CT studies, as well as the calculation of sensitivities, specificities, predictive values, and likelihood ratios, the investigators identified a TD-rCBF value of 15 ml/100 g/min as a reliable cutoff for the diagnosis of symptomatic vasospasm.  In addition, the investigators found that TD flowmetry was characterized by a more favorable diagnostic reliability than transcranial Doppler ultrasonography.  The authors concluded that TD flowmetry represents a promising method for the bedside monitoring of patients with SAH to detect symptomatic vasospasm.

Tasneem and colleague (2017) stated that neuro-critical care patients are at risk of developing secondary brain injury from inflammation, ischemia, and edema that follows the primary insult.  Recognizing clinical deterioration due to secondary injury is frequently challenging in comatose patients.  Multi-modality monitoring (MMM) encompasses various tools to monitor cerebral metabolism, perfusion, and oxygenation aimed at detecting these changes to help modify therapies before irreversible injury sets in.  These tools include intra-cranial pressure (ICP) monitors, transcranial Doppler (TCD), Hemedex (thermal diffusion probe used to measure regional CBF), micro-dialysis catheter (used to measure cerebral metabolism), Licox (probe used to measure regional brain tissue oxygen tension), and continuous electroencephalography.  Cerebral blood flow can be measured by inserting a thermal diffusion probe (TDP) directly into brain parenchyma.  The commercially available system includes the Hemedex monitoring system, which is not MRI compatible.  It allows regional CBF (rCBF) monitoring by assessing thermal convection due to tissue blood flow.  The probe tip is inserted into white matter of brain and its utility depends on proximity to the area of interest.  Thermal diffusion probe has been validated by Xenon perfusion CT and CBF level below 15 ml/100 g/min is identified as threshold for diagnosis of hypo-perfusion.  Per MMM consensus guidelines, TDP should be placed in vascular territory of ruptured aneurysm to monitor for vasospasm.  Quantification of rCBF with TDP is highly dependent on patient's core body temperature and is significantly altered in conditions of hyperthermia.  To-date, there are no published studies of improved outcome with treatment strategies directed solely by CBF monitoring, however it appears to be a promising tool to use in conjunction with other parameters.  Nevertheless, MMM is now a reality commonly used in advance neuro-critical care units throughout the world.  Although various studies have shown the physiologic feasibility of monitoring various neurologic parameters, there is still no published data from randomized trials to support that targeting any variable improves clinical outcome.  The authors concluded that although further research is needed to demonstrate the impact of MMM on improving clinical outcomes, their contribution to illuminate the black box of the brain in comatose patients is indisputable. 

Current literature on thermal perfusion probes has focused on their feasibility and technical capabilities.  Prospective clinical outcome studies are needed to determine their clinical value over other standard methods of identifying individuals at risk for secondary ischemic brain injury (e.g., head injury, subarachnoid hemorrhage, or following neurosurgery) and in monitoring response to therapies.

The above policy is based on the following references: