Thanks so much for stopping by and for your explanation of the scan. It was music to my ears. As everyone here, I just want to make as informed a decision as possible.. I think it is absolutely something that could help me to do so.
Hopefully I am anatomically correct! I will check with Foresee to get more details.
Each "shot" of the fibroscan probe gives you a wave propagation pattern that ideally is smooth and reflects only one "clean' wave that propagates through the liver and is followed by rapid ultrasound pulses that identify zones of higher density that the elastic wave generates as it travels through the liver. This is one dimension of the two dimensional plot that is generated for each shot, the second one is time. Therefore the angle of this density pattern is ideally the propagation speed of the elastic wave. There is a direct formula between (the tangens of) that angle and the elastic module of the material, expressed in Kilopascal. That is a fixed formula, nothing to manipulate or judge. What is open for interpretation is whether the wave is clean and smooth enough or contains artefacts. The " algorithm" is not the relation between the liver stiffness and the fibrosis stage, but at this point in the process it is an imaging processing program that "looks " at the picture of the individual shot and determines A: Is there a clean wave or too many artifactual secondary scatterwaves? B; If the machine algorithm accepts the individual picture as worth evaluating, it then "measures" the above mentioned angle or slant and prints/overlays the results of its interpolation/calculation on top of the twodimensional picture. The human eye and brain can see if A: a picture was accepted that was too scattered/artefactual and or B: that the superimposed "slant line" was yes or not not placed correctly on the true elastic wave that can be seen. Ideally the operator can agree with the machines "acceptance decisions and placements" and then everything is according to "protocol". Now you have to trust me that a humans image processing capacity are still vastly superior to that of such a software and as such improper machine acceptances should be discarded. If you dont, your results will simply wobble much more around the true elasticity, which is all we are trying to measure. The placement in one of the "F" categories is simply done by overlaying the patients Kilopascal results on the frequency distribution of the trial results that link the two methods together. There is no computer algorith involved here and no more protocol. If the reference intervals should be slightly adjusted from time to time (like to the "American population") it does not mean that your fibroscan elasticity measurements have changed - maybe you are now just scratching the surface of the 95% intervall for stage 3 fibrosis.
When several pieces of information come together, like in your sons case, it is likely that he has cirrhosis that has led to one of its major complications :ie portal hyprtension. The term cirrhosis is broad and complex and the functional consequences of intense fibrosis are severalfold :
1. Restriction of portal blood flow, leading to higher than normal pressure in all of the portal vein connected blood vessels, with the tendency of the body to develop collateral ways to remove the blood from the portal system, therefore esophageal and gastric varices, in the spleen the extra venous pressure can lead to enlargement.
2. The synthetic capacity of the liver can be reduced due to a reduced mass of functional hepatocytes. (Albumin, clotting factors, prothrombin time etc). Also some factor stimulating platelet synthesis is produced in lesser quantity, so, together with enhanced splenic activity, platelet numbers move downwards.
3. In cirhosis/intense fibrosis the intimate exchange between the portal blood and the hepatocytes can be reduced so the processing and cleaning -detoxifying and metabolic functions of the liver deccrease, because the space of Disse is filled with fibers now precluding proper contact and diffusion of the portal blood to the processing hepatocytes. The processing of intestinal ammonia into nontoxic urea is one example of the livers detoxifying capacities that slowly fail, leading to accumulation in the systemic circulation with subclinical and manifest hepatic encephalopathy. Thats why your son is on lactulose, to counteract the ammonia production and more.
The clinician is in the difficult position to estimate the overall situation of the three components of declining liver structure/function from a limited set of parameters. Thus overall the term cirrhosis can mean many substages and subfunctioon declines that can only be estimated. Everything in the diagnostic armamentarium needs to be put together to come up wit the best possible estimation.
glad to see you had a chance to stop back :-) i had a question about a fibroscan i had in Aug in boston. wanted your opinion on the results and what stage you would have put me at. the reason i ask is the person that did the scan was very young and i had a feeling they had not done many before. i had a biopsy about 6 weeks later that had me stage 1 grade 1. here is the exact measurement from the fibroscan form:
median fibroscan measurement 8.8 kpa
IQR 1.1 kpa
number of attempts 11
number of measurements obtained 9
Elaine's (child24angel) 24-year old son, Nick has hemophelia and is a 3X non-responder with apparent cirrhosis. If you think your expertise could be helpful, it would be great if the two of you could get together in some capacity.
Forgot to ask, re your protocol. Since your're not using computer alogorithms to correlate scan results with biopsy stages -- how do you determine then if someone is a stage 2 as opposed to a stage 3? Is this something you can "see" like a pathologist sees under a microscope? If so, then this is a radically different approach from the scan protocol where I don't believe the operator "sees" anything, although I could be wrong on that.
But if you do actually see fibrotic tissue/bridging, etc -- then the type of "double" report I mentioned could be very useful, in spite of bringing operator bias/error back into the equation as we now have with needle biopsy.
As a personal example, I had the same biopsy slide set read by four different pathologists, all supposedly excellent, at four different hospitals, including the scan center's pathologist. I was staged at: 3, 2, 2.5 and 3. Pathologist bias therefore was a full stage. My scan put me somewhere between stage 2 and 3 and was taken three years after the biopsy mid treatment. A second scan put me closer to stage 2 and was taken I think four months after I stopped treating.