To my mind, there is no doubt that what Dilish has described is typical post mortem lividity, as has been excellently discussed by Bish sir,. The reference quoted by him gives a detailed discussion of the process. The time course, the location and the type of death, all fit in very nicely. What Arvind has mentioned is a part of the same process. Indeed, the oxygen continues to leave Haemoglobin even after death, as cells are not dead for quite sometime after bodily death, and as long as some oxygen is available, keep extracting it from hemoglobin, thereby desaturating it. Calling it paying the Oxygen debt may be slightly fanciful, as the term is mostly reserved for post exercise recovery, but in essence is not substantially different. The distinction probably is more semantic than real (as in the case of lividity Vs. cyanosis). There is one difference between cyanosis and lividity though : in cyanosis, the reduced haemoglobin remains almost exclusively intravascular, while in lividity, due to permeability changes in capillaries, red cells leak out in extravascular space. After some period of hypoxia, the RBC membrane cannot maintain its integrity and so hemolysis takes place with free hemoglobin escaping into tissue spaces. This hemoglobin sometimes reacts with gases being formed during early putrefactive process (eg. sulphur dioxide and methane) and may form darker colored sulphmethhemoglobin etc., which may impart characteristic dark coloration to skin, nail bed etc. Now comes the question of explosive G forces which will force blood in the extremities to the digits. This is a tricky situation, because it the limbs fly out with digits outwards, then the inertial reaction will tend to force blood out from the torn vessels at the proximal end, rather than digitwards. If, on the other hand, limbs tumble and rotate somehow (quite possible with wind drag and aerodynamic forces), then the blood may be pushed towards the digits with considerable force and will cause rupture of capillaties and escape of hemoglobin into extravascular space instantaneously. In this case, it does not have to wait for hypoxic capillary permeability changes to occur. Ultimately, the dark coloration which was noticed has to be due to either reduced Hb per se, or one of its oxidation (not oxygenation) products. I quite agree with Bish sir that this seems to be the most logical explanation. Just to be morbid, I would have loved to have hypothesized that this phenomenon was due to interaction of Hb or some other blood component with some exotic chemical compound released during explosion, but the the magnitude at which the torn limbs will be accelerated away from the centre of explosion precludes any meaningful interaction of blood in that limb with any product of the explosive compounds. A most ridiculous notion. Don't give it another thought. Sudhanshu