We propose that IOP varies because of the variability in capillaries contacted by the needle tip. Our work demonstrates that, even with a repeatable technique, a wide range of IOP values is obtained by putting a needle into bone [12]. The spread of those values and their correlation with the associated PP supports the concept that the IOP is a reflection of local perfusion conditions in a small blood pool at the needle tip. We suggest that a higher IOP and PP are present where there is contact with an artery and a lower IOP if only fat and small blood vessels or veins are contacted. The significant fall in IOP with arterial occlusion (IOPb – IOPa 24.8 mmHg to 7.7 mmHg p < 0.0001) and the lesser rise in IOPb to IOPv (24.8 mmHg to 29.1 mmHg, p < 0.0001) with venous occlusion indicates that the majority of the recorded IOPb is due to the arterial supply side rather than being a venous back pressure.
For decades IOP has been measured in order to understand osteonecrosis and other diseases [13, 14]. Yet no other solid organ has had pressure measured in this way. Previous authors have usually considered IOP to have a static or constant value which was said to increase in osteonecrosis, with steroids and with bone pain. Many investigators have found IOP to be variable, so making measurement of IOP difficult to interpret [4].
The loss in both IOP and the pulse pressure wave with proximal arterial occlusion also demonstrates that most of the IOP and all the pulse pressure wave is due to arterial side supply pressure. Any residual pressure after clamping the proximal artery represents the true venous back pressure at the needle tip. Similarly, the increased IOP and preservation of the PP with proximal venous occlusion probably represents the best possible supply pressure obtainable at capillary level at that needle tip.
Any single IOP measurement is therefore of limited value whereas by subtracting IOPv – IOPa it is possible to obtain, for the first time, a useful idea of the perfusion pressure range obtainable at a needle tip deep in cancellous bone. Although subtraction has been used with imaging such as in digital angiography [15], we can find no previous description of this concept in perfusion studies.
Pulse pressure was taken as the difference between the top and the bottom of the IOP trace and was proportional to the absolute IOP as in Fig. 1. The subtraction difference between venous occlusion (IOPv) and arterial occlusion (IOPa) or IOPv-IOPa indicates the range of pressure obtainable at that individual needle tip. PP is therefore a variable which is usually dependent on the basal or initial IOPb. IOPv-IOPa is more an indication of the perfusion range obtainable at that needle tip. We would expect that in ischaemic bone, irrespective of the basal IOPb, the IOPv-IOPa difference, which is a measure of perfusion would be less than in healthy bone.
We were interested in the effect of steroids on IOP in a model which had previously been developed to explore perfusion physiology and the effects of loading on IOP [16]. The present study confirmed that steroid treatment raised IOP, as most previous authors have found [17]. The corticosteroid dose used in our model was one which caused cachexia and weight loss much like that seen in man with heavy corticosteroid use causing a type of diabetic keto-acidosis. The photographs and angiograms showed an increase in bone vascularity. In this model a large dose of steroid appeared to cause the intraosseous space to shrink, rather than the fat cells swelling, as described in other models. Here the bone appears ‘emptier’ after steroid treatment and this allowed better filling of the microvascular tree and therefore a better supply pressure or IOPb at the needle tip. There was an associated significant increase in the steroid treated pulse pressure. Importantly, the perfusion or IOPv-IOPa in the treated subjects did not reduce, as might be expected in ischaemic bone, but remained similar to that in healthy bone. In our model the already satisfactory perfusion in normal control bone did not improve further by shrinking the intraosseous volume. We remain unable to offer an explanation as to how corticosteroids cause osteonecrosis in other models or in man.
If, irrespective of the initial IOPb, there is little difference in IOPv-IOPa, it would be reasonable to suppose that the perfusion achievable at the needle tip is poor. Conversely and irrespective of the initial IOP, if there is a large ‘subtraction’ value it would be reasonable to suppose that at the needle tip good perfusion is attainable. We suggest that this new physiological subtraction approach could also be used clinically in other situations, for example, in compartment syndromes. If a catheter or needle in the affected calf muscle shows little change in pressure with proximal thigh tourniquet applications at venous or arterial occlusion pressure, then there is a poor perfusion at the catheter tip. A wider perfusion pressure range would indicate that there is better perfusion at the needle tip and that surgical intervention is not urgently required.
There are several possible limitations in this work. The subjects were of different gender, weights and ages. The control and steroid treated groups were of different sizes. IOP was measured in the proximal tibia for ease of access while the femora were used for the micro angiograms as the upper tibial IOP needles might have damaged the proximal tibia and distorted the angiograms. Needle placement was by hand to within a few millimeters’ accuracy only. Anaesthesia in these subjects was brittle and experimental duration varied. We did not obtain histology. We were unable to record blood pressure. Corticosteroids are known to raise systemic blood pressure and that may have caused a rise in IOP. Had that been the only cause, we would not have expected the visible barium and micro angiogram changes. Other possibilities exist, for example, that the pressure changes reflect flow through porous lacunocanalicular channels. We suggest that the observed speed of pressure change and visible pulsatility on traces excludes the possibility of pressure changes being the result of flow in micro channels. The sensitivity of the recording system may affect the pulse volume to a degree. The fluid or saline column within the needle from the blood pool up to the pressure transducer inevitably had a certain viscosity or inertia which might reduce the range seen in pulse pressure records.
