Critical illness polyneuropathy and myopathy are common neuromuscular complications secondary to sepsis

Abstract

We read the case report with great interest by Song et al. [1]. The reported case was diagnosed as acute motor axonal neuropathy, a variant of Guillain–Barre syndrome (GBS) based on the clinical symptoms and laboratory and electrophysiological results. Nevertheless, the case may be misdiagnosed, since there are the overlaped evidences of other diseases, which are the same with onset histories, physical examinations, the laboratory and electrophysiological results, etc. Although these evidences have been leveled at various aspects of GBS diagnosis, nowadays the pathological and immunological proofs, for instance, the muscle and nerve biopsy as well as humoral antibodies analysis have almost been supportively used in excluding these diseases with some identical characteristics from the neuromuscular spectrum for clinical diagnosis. There are two kinds of neuromuscular abnormalities in ICU. The first kind refers to the neuromuscular disease such as GBS in ICU. Another one, flaccid paralysis without preexisting neuromuscular disorders is acquired in ICU like critical illness polyneuropathy (CIP) and/or critical illness myopathy (CIM). GBS is often hard to be differentiated with CIP/CIM, especially an axonal damage form of GBS may be more difficult to distinguish from CIP due to the similar electromyography signs. Generally, CIP or CIM should be the foremost suspected disorder after sepsis, after all, the most likely cause of limb muscle weakness in ICU is CIP/CIM [2], because *70% of the patients with sepsis or systemic inflammatory response syndrome [3], and up to 100% of the patients with multiple organ failure (MOF) developed CIP and/or CIM [4]. CIP and CIM prolong weaning from mechanical ventilation and physical rehabilitation. Making an accurate diagnosis for GBS will be lying on the full analysis of clinical, laboratory and electrophysiological data, and the adequate experience from the clinician. Although detailed history, careful physical examinations, routine laboratory studies, and electrophysiological investigations might be very useful in the common patients, the muscle and nerve biopsy could give supportive discrimination between CIP/CIM and GBS, after the patients suffering from sepsis or MOF. Albuminocytological dissociation in the cerebrospinal fluid (CSF) is the highly specialized characteristic of GBS; however, the clinician still needs to consider that non-immunological factors can also increase the protein levels in CSF, i.e. fake albumino-dissociation phenomenon. As a matter of fact, not only hemorrhagic stroke rupturing into the fourth ventricle like this case can cause the protein levels to enhance in CSF, but also even the reduplicative lumbar punctures can also result in the ascending of the protein levels in CSF. So, it is necessary to prove the myosin depletion in the muscle fibers through a biopsy in CIM [5], X.-K. Wang J. Zhu Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China