I think 1 in 4 plays is reasonable and low risk. You simply agree, before the game that he will play a very limited, set amount and no more. As far as sickle cell trait or even vs sickle cell diease, it is incorrect to say that 50% or even 100% of the cells will sickle. You can also have some fetal hemoglobin. With sickle cell trait:
http://sickle.bwh.harvard.edu/sickle_trait.html
In addition some disease associations have been noted with sickle cell trait which might not result from polymerization of hemoglobin S but from linkage to a different gene mutation. The association of hemoglobin S with cases of renal medullary carcinoma, early end stage renal failure in autosomal dominant polycystic kidney disease, and surrogate end points for pulmonary embolism are not necessarily the result of hemoglobin S polymerization. Complications from sickle cell trait are important because about three million people in the United States have this genotype, about 40 to 50 times the number with sickle cell disease.
People with uncomplicated sickle cell trait have a normal blood examination as assessed by conventional clinical methods, including normal red cell morphology, indices, reticulocyte counts, and red blood cell survival by chromium labeling. Conventional methods of detecting hemolysis are negative, such as measurements of serum haptoglobin, bilirubin, and LDH. Erythrocyte density distribution is normal, adherence to endothelium is not increased, altered membrane lipids and proteins are not detectable, cytoplasmic inside-out vesicles with high calcium content are absent, and permanently distorted erythrocytes are not observed.
When blood is drawn with anaerobic technique into a syringe with dilute buffered glutaraldehyde one obtains an accurate picture of circulating erythrocytes in vivo (the Sherman test). No sickled cells are observed at rest, but exercise to exhaustion at sea level regularly induces mild levels of reversible sickling in peripheral venous blood (less than 1%). Exposure to altitude hypoxia will progressively increase the extent of sickling observed with sickle cell trait from 2% at 4,050 ft. to 8.5% at 13,123 ft. Hypobaric chamber exposures used for military aviation training, involving hypoxic exposures simulating 10,000 to 25,000 ft from ninety to six minutes, did not cause hemolysis in subjects with uncomplicated sickle cell trait (3).
Determination that a clinical syndrome is due to sickle cell trait rather than a subtle form of sickle cell disease is difficult. Reversible sickling and unsickling of erythrocytes (reflecting the rapid formation and dissolution of deoxy-hemoglobin S polymers) takes place in seconds. Hence, the presence or absence of intravascular sickled erythrocytes in tissue specimens depends upon the degree of oxygenation of the sample just before fixation and only has clinical relevance if fixation occurred at oxygen tensions identical to those extant during generation of primary lesions. Agonal hypoxemia causes artifactual intravascular sickling. Conversely, blood samples smeared in room air and then fixed will show artifactual unsickling. One cannot determine the role of hemoglobin S in clinical events from the presence or absence of intravascular sickling in blood samples, biopsy specimens, or autopsy specimens unless these were rapidly fixed at physiologic oxygen tension.
You don't need to throw the baby out with the bathwater. For him to play 1 in 4 plays, he is in my opnion, not going to have significant physiologic stress levels. In my opinion he could dress and play 1 in 4 plays. It is consequitive plays that would induce significant stress. Rotating him in for one play is low risk in my opinion. You simply make hard and fast rules. You come up with a game plan that uses him only in certain situations or lives by a general rule that his playtime is limited so that he must not play in consequitive plays. sitting out 3 plays per every one he is used is a very conservative guidleine that should ensure a low risk scenario.
quoting Saaz:
Wow... This is my fist post. The 'post reply' button was never there before, does it just magically appear? Maybe I am blind and missed it until now.
Anyway, I am happy to be able to respond to this board, I have read it for several years now.
I am no hematologist, but I do happen to be an MD in another field of medicine and have at least been exposed to the concepts at play here. I would have SERIOUS reservation with allowing RC to play. We already know he has had an adverse outcome with the thin air. We know that the spleen and gallbladder that were removed played no part in causing the sickle crisis he suffered last time, but were merely affected by it to the point requiring surgical removal. We do not know exactly how to quantify the exertion required to precipitate another event with him. 1 play in 4? 2 plays per series? And if he gets in at all you know he will lobby to stay in, especially in a close game.
If he suffers another sickle crisis, his spleen will not be there to filter out the sickled cells, and I would think he would be at even more risk for pulmonary of bony infarcts.
Also, it is my understanding that having sickle trait only means that one of two genes are defective, but that all red blood cells will have approximately 50-50 good hemaglobin to bad hemaglobin. It is not that only 50% of the RBC have a chance to sickle, they all do.
Given that he has another unspecified condition that predisposes him to sickle crises, I am shocked that the team MDs are even considering him to be cleared to play. Forget the medical legal implications. Think about his family. I love the Steelers as much as any fan, but to allow him to play, in my opinion, is foolish.
