In a recent review Latronico et al. has described the pathophysiology of CIP and CIM as a complex, involving metabolic, inflammatory and bioenergetic alterations.[7] The severity of the polyneuropathy depends on the length of stay in the ICU, as also with increasing serum glucose and decreasing serum albumin concentrations.[1] Endoneural oedema promoted by hyperglycemia and hypoalbuminemia can induce hypoxia by an increase in intercapillary distance and other mechanisms.[1] Cytokines and inflammatory mediators also play an important role. Here, ALB is linked to hereditary sensory and autonomic neuropathy.