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Letter to the Editor |
Hannover, Germany
Dear Editor:
I read with great interest the recent report of Näslund et al, "Decreased Pulsatile Blood Flow in the Patella in Patellofemoral Pain Syndrome (October 2007, pages 1668–1673), focusing on a potential underlying pathomechanism in patellofemoral pain syndrome (PFPS). They recruited a total of 22 patients suffering PFPS as a diagnosis of exclusion (with 34% of PFPS patients having diffuse increase uptake of technetium-99m bone scans), aged 20 to 50 years, and compared them to otherwise healthy visitors of a local health club who were age- and sex-matched to the PFPS patients. Interestingly, Näslund et al hypothesized that knee joint flexion changes patella perfusion in PFPS patients but not in controls. I would like to comment on some technical and pathophysiological issues in this letter.
Patella perfusion was determined using a photoplethysmography system with an 804-nm light-emitting diode for "deep tissue monitoring" of blood flow. They cite a published study on 20 healthy subjects focusing on the patella bone perfusion2; however, at least to me, it is not clear what the interobserver and intraobserver reliability of this interesting, novel noninvasive technique for measuring bone perfusion was. Furthermore, as a near-infrared system was used, I would appreciate it if the authors could comment on how they overcame the problem of reflexion and light absorption at the bone barrier using their near-infrared beam. It would help if they could comment on how deep in the patella they can determine the blood flow (ie, superficial, at the center of the patella, or toward the retropatellar margin) or if they measure a sum signal. To date, at least to the best of my knowledge, there is no further report on the use of photoplethysmography for bone perfusion studies.
Muscle blood flow can be determined using photoplethysmography as done by another research group, who stated that an abnormally elevated intramuscular pressure impairs muscle blood flow at rest after exercise.8 They found that venous obstruction reduces muscle blood flow following exercise. Recently, skin and muscle blood flow were determined with photoplethysmography,5 describing that 2-Hz transcutaneous electrical nerve stimulation (TENS) increases trapezius muscle but not skin blood flow.
Given the application and proper acquisition of bone perfusion using photoplethysmography as stated by Näslund et al, several potential applications could be focused on. Focal bone necrosis, for example, could be one potential field as well as scaphoid perfusion in patients suffering scaphoid fractures to elucidate the vitality of the fragments, especially in prolonged healing situations.
As stated by Näslund et al, several other perfusion techniques have been published. Recently, Hempfing et al1 published the patellar bone blood flow among 10 patients undergoing total knee arthroplasty by a standard medial parapatellar approach. The laser Doppler flowmetry probe was placed in the spongious part of the patella close to its center through a 3.5-mm-diameter drill hole. When the knee was flexed, the blood flow determined by laser Doppler flowmetry was reduced by 71%, significantly with a lost pulsatile signal pattern in 80%. Näslund et al found a median change of –26% from resting values for the pulsatile blood flow among patients suffering PFPS, which was significantly different from the patella-healthy subjects, who had no change of patella blood flow at all. Changes of musculoskeletal perfusion have been reported in Achilles tendinopathy as well, where dorsiflexion of the ankle leads to a disruption of pathological Achilles tendon blood flow assessed by power Doppler ultrasonography from Ohberg and Alfredson.4 Nicholls et al3 found the patella blood flow significantly reduced by both the medial and lateral approach for total knee arthroplasty using laser Doppler flowmetry with the PeriMed System.
Besides PFPS, knee osteoarthritis might therefore change patella bone blood flow in a way simultaneous to PFPS, although different technologies are used to assess patella bone blood flow in the available reports. Surgery such as resurfacing can reduce oxygen saturation of the bone tremendously.6 Interestingly, intraosseous hypertension and intraosseous venous congestion within the medullar canal of the condyle may lead to knee osteonecrosis.7
Therefore, besides arterial blood flow, the oxygenation as well as the venous outflow might affect the microcirculatory environment in the knee. Näslund et al stated in the discussion that "not only arterial but also venous blood flow is likely to have a pulsatile component," which is, in my view, of utmost importance. Because they reported a change in pulsatile blood flow during knee flexion in PFPS patients only, and given a venous pulsatile origin of the signal, a smaller plethysmographic signal might indicate less venous blood flow. Whether this leads to venous congestion due to reduced blood flow with associated increased venous blood pressure or to a higher venous clearance with decreased venous blood pressure is interesting to speculate on, and I would appreciate if the authors could comment on this issue in detail. Given a venous origin of the observed signal changes, the ischemic genesis of PFPS should be questioned, and a venous congestion genesis might at least contribute to PFPS, which has to be determined in future studies.
REFERENCES
Karolinska Institutet, Stockholm, Sweden
We appreciate the opportunity to respond to Dr Knobloch’s letter regarding our article "Decreased Pulsatile Blood Flow in the Patella in Patellofemoral Pain Syndrome." Dr Knobloch wants us to clarify some technical and physiological issues.
First, our novel, noninvasive photoplethysmographic technique cannot to be compared to near-infrared spectroscopy or to any other photospectrometric technique because we do not use a spectrometric algorithm. Instead, we are using a new paradigm: the migration of erythrocytes.4 Because bone tissue is transparent to near-infrared light, the pulsatile light that is reflected and analyzed is the light reflected from the blood within the bone tissue. The pulsatile component is derived from the blood flow because no change in volume is possible. For that reason, we see no problems with reflexion and light absorption at the bone barrier.
Dr Knobloch also wants to know how deep in the patellar bone we have recorded blood flow pulsations. As we discussed in our first methodological article,4 we chose the reported wavelength, together with the specific optical geometry of the probe, and studied the patellar bone because it would be obvious that the pulsatile signals could emerge from no other tissue than the bone tissue in the patella. For the moment, we regard the pulsatile signal as a signal consisting of a sum of photons scattered from different depths. We cannot isolate a measurement of the blood flow in the cortical bone at this time.
Determinations of skeletal blood flow are not easily made in humans.3 Blood flow in bone tissue has been measured both indirectly (bone scan, single photon emission computed tomography, microsphere method, position emission tomography) and directly (laser Doppler flowmetry). The latter technique requires surgical manipulation of the bone and may therefore produce artifacts attributable to local manipulation of the vessels. As per our previous article,4 we measured the decrease or increase in the pulsatile blood flow after different interventions. Right now, we are unable to measure absolute blood flow within bone tissue.
As little is known concerning blood flow regulations in bone tissue,2 it is difficult to conduct true reliability studies. How can one ascertain that the pulsatile blood flow has not changed since the last recording when we do not know what stimulus could have had an impact? For how long will the blood flow be changed after muscle activity, joint motion, or just standing still in an upright position? For the moment, few studies have quantified the repeatability or reproducibility of any type of photoplethysmographic measurement.1 This lack of studies concerning reliability is not an exceptional situation for our novel technique. Many of the photometric techniques available on the market and several indirect physiological measurements have the same problem. But we are planning to report repeated photoplethysmographic recordings from different situations: after rest and muscle activity, at different times of the day, and in both sexes. From these studies, we eventually will be able to discern if pulsatile blood flow in the patellar bone varies and, if so, how it varies. We also hope to be able to calculate interobserver and intraobserver reliability.
Dr Knobloch quite correctly points out that our method cannot differentiate between flow pulsations in arterial and venous compartments of the vasculature in the patella. This is inherent in the technique, as the wavelength used is common to arterialized and venous (desaturated) blood. Moreover, the following elements are in series: arterial inlet, rigid chamber with arterial and venous conduits, and venous outlet. Thus if we observe that pulsations of the internal flow velocity decrease, we cannot tell a priori whether a restriction is applied to the arterial inlet, the venous outlet, or both. Certainly a statement that pulsatile patellar perfusion is reduced can be made, but that is all so far. We agree that it would be of great interest to differ between arterial inlet and venous outlet restrictions. This is so because the overall hydrostatic pressure inside the patellar vascular bed will be reduced in the first case and increased in the second case. This will certainly be an area for future development.
Dr Knobloch points out that our novel photoplethysmographic technique offers several potential and exciting applications. We agree wholeheartedly. Bone necrosis, fracture healing, and osteoarthritis are areas that our group plans to study in the future.
REFERENCES
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