ALB and Sepsis: The major histopathologic finding in CIM is relatively selective loss of myosin, which can be identified as a lack of reactivity to myosin ATPase in non-necrotic fibers.[10,11] CIP appears to be a common complication of severe sepsis and is thought to represent a neurologic manifestation of the systemic inflammatory response syndrome.[12–14] There is some correlation with elevations in blood glucose and reductions in serum albumin.[15,16] Sepsis may be a common pathologic mechanism underlying the development of CINM.[17]