The snake could not have survived past the point where it developed a circulatory system in the egg if it had no blood pigment. Blood gets it's color from hemoglobin (the oxygen transport protein). Animals with mutations in all the subunits of hemoglobin abort early in gestation due to tissue hypoxia and death. Thus, although the animal appears to lack blood color, the fact that it is alive is incompatible.
More likely the culprit is one of a number of rare recessive forms of albinism which manifest with neurological and immune dysfunction. This is a result of the origin of melanocytes and the location of pigment synthesizing enzymes and transport molecules on the chromosomes.
Melanocytes are of neural origin and thus problems with melanocyte development can be paired with neural dysfunction. Frequently, albinos have difficulty with vision (pigment related) along with nystagmus (sweeping eye motions) which is caused by a related neural deficit.
Proteins which transport formed pigment share a significant amount in common with the granules used for storing and releasing hydrolytic enzymes (antibacterial, fungal, parasitic) and those necessary to engulf and destroy pathogens intracellularly. Thus mutations in these areas can cause massive immune system deficits in addition to albinism.
Thus it is likely that the animal in question died as a result neurological/immunological causes (e.g neural systems failure or an inability of the host to resist infection).
This is seen in the white animal deaths mentioned above and also in severe, rare forms of human albinism with death occurring in early postnatal life.