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.
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.
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.
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes not covered for indications listed in the CPB:
Other CPT codes related to the CPB:
61000 - 64999
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
320 - 326
Inflammatory diseases of the central nervous system
330.0 - 337.9
Hereditary degenerative diseases of the central nervous system
340 - 349.9
Other disorders of the central nervous system
430 - 438.9
800.00 - 804.99
Fracture of skull
850.00 - 854.19
Intracranial injury, excluding those with skull fracture
Special screening for neurological conditions
The above policy is based on the following references:
De Georgia MA, Deogaonkar A. Multimodal monitoring in the neurological intensive care unit. Neurologist. 2005;11(1):45-54.
Jaeger M, Soehle M, Schuhmann MU, et al. Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen. Acta Neurochir (Wien). 2005;147(1):51-56.
Vajkoczy P, Horn P, Thome C, et al. Regional cerebral blood flow monitoring in the diagnosis of delayed ischemia following aneurysmal subarachnoid hemorrhage. J Neurosurg. 2003;98(6):1227-1234.
Thome C, Vajkoczy P, Horn P, et al. Continuous monitoring of regional cerebral blood flow during temporary arterial occlusion in aneurysm surgery. J Neurosurg. 2001;95(3):402-411.
Steiner LA, Czosnyka M. Should we measure cerebral blood flow in head-injured patients? Br J Neurosurg. 2002;16(5):429-439.
Vajkoczy P, Roth H, Horn P, et al. Continuous monitoring of regional cerebral blood flow: experimental and clinical validation of a novel thermal diffusion microprobe. J Neurosurg. 2000;93(2):265-274.
Bouma GJ, Muizelaar JP. Evaluation of regional cerebral blood flow in acute head injury by stable xenon-enhanced computerized tomography. Acta Neurochir Suppl (Wien). 1993;59:34-40.
Jagoda AS, Cantrill SV, Wears RL, et al. Clinical policy: Neuroimaging and decision making in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2002;40:231-249.
Haberl RL, Villringer A, Dirnagl U. Applicability of laser-Doppler flowmetry for cerebral blood flow monitoring in neurological intensive care. Acta Neurochir Suppl (Wien). 1993;59:64-68.
Hemedex, Inc. Bowman Perfusion Monitor [website]. Cambridge, MA: Hemedex; 2002. Available at: http://www.hemedex.com/bpmonitor.html. Accessed March 9, 2005.
U.S. Food and Drug Administration (FDA), Center for Devices and Radiologic Health (CDRH). QFlow 500 Perfusion Monitoring System. 510(k) Summary of Safety and Effectiveness. 510(k) No. K013376. Rockville, MD: FDA; May 8, 2002. Available at: http://www.fda.gov/cdrh/pdf/k013376.pdf. Accessed October 26, 2006.
Barth M, Capelle H-H, Münch E, et al. Effects of the selective endothelin A (ETA) receptor antagonist clazosentan on cerebral perfusion and cerebral oxygenation following severe subarachnoid hemorrhage – preliminary results from a randomized clinical series. Acta Neurochir (Wien) 2007;149(9):911-918.
Rosenthal G, Sanchez-Mejia RO, et al. Incorporating a parenchymal thermal diffusion cerebral blood flow probe in bedside assessment of cerebral autoregulation and vasoreactivity in patients with severe traumatic brain injury. J Neurosurg. 2011;114(1):62-70.
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