In patients new product with septic shock [8] or severe sepsis and coma [9] the prevalence may reach up to 100%. In the majority of patients with sepsis a combination of both CIP and CIM was described [10].Independent risk factors for CIPNM are, amongst others, severity of illness, duration of MOF with or without SIRS, duration of vasopressor and catecholamine support, hyperglycemia and duration of intensive care unit (ICU) stay [1].The clinical features of CIP and CIM are almost identical and include muscle weakness and atrophy primarily of the lower limbs and respiratory muscles, delayed weaning from the respirator not explained by pulmonary or cardiovascular findings, and prolongation of the mobilization phase [1]. Moreover, a number of complications, such as pneumonia, deep vein thrombosis and pulmonary embolism may be attributed – at least in part – to CIPNM [11].

On neurological examination, decreased or absent tendon reflexes, especially with CIP, muscular atrophies and symmetrical flaccid tetraparesis are present [1].The gold standards used to diagnose CIPNM are electrophysiological stimulation (EPS) and muscle biopsy. Characteristically, electromyography (EMG) and nerve conduction velocity (NCV) studies demonstrate the preservation of the speed of impulse in the presence of decreased compound muscle (CMAP) and sensory nerve (SNAP) action potential amplitudes [12]. These findings are highly consistent with a relatively pure axonal polyneuropathy. Furthermore, EMG discloses signs of denervation like fibrillation potentials and positive sharp waves in a widespread distribution.

For the definite diagnosis of CIM and to differentiate between CIP and CIM the histological assessment of a muscle biopsy is the preferable method [1].For CIPNM no specific pathogenic-based therapy is proven. For prevention, sepsis should be treated with maximum effort, including intensive insulin therapy (IIT) [13]. Muscle relaxants and corticosteroids should be administered at the lowest doses needed, whereas the potentially detrimental effect of the latter has been controversially discussed [14].However, there is weak evidence from a retrospective chart analysis of prospectively collected data, that early IgM-enriched IVIG application may prevent CIPNM [15].IVIG contains natural polyreactive antibodies derived from human plasma of healthy donors directed against endogenous and exogenous antibodies, immunomodulating peptides and various cytokines [16].

The pathophysiologic rationale for using IVIG to treat CIPNM is based on the Anacetrapib association of CIPNM with pro-inflammatory cytokines accompanied by increased E-selection expression [3,17]. This favors the accumulation of neurotoxic factors in the endoneurium and causes extravasation of activated leukocytes both resulting in neuron damage [18].