Critical Illness Neuropathy

Question 1

CIP

Answer 1

Causes: MODS, Sepsis

Question 2

CIM

Answer 2

Causes: Pneumonia, Severe Asthma,

Liver Transplantation, Lung Transplantation, High Dose IV Corticosteroids, Non-depolrazing Neuromuscular blocking agents

Question 3

Risk

Answer 3

The risk of having CIP/CIM was almost five times greater in patients with MOF than in those without

Question 4

Clinical Features

Answer 4

The main clinical features of ICU-acquired neuromuscular disorders include difficulty in weaning patients from the ventilator, flaccid tetraparesis or tetraplegia, hyporeflexia and muscular atrophy.

Question 5

Frequency

Answer 5

CIP has a reported frequency of 32.6-100% depending on the criteria used for the diagnosis, the timing of diagnosis and the type of patients.

Question 6

Definition

Answer 6

CIP is a sensory-motor axonal polyneuropathy; and is usually suspected in ICU patients who, after a period of days or weeks, cannot be weaned from the ventilator despite the absence of pulmonary or cardiac causes of respiratory failure or because of various degrees of limb weakness.

Question 7

CIM

Answer 7

CIM is a syndrome with a continuum of myopathic findings, from myopathies with pure functional impairment and normal histology (acute quadriplegic myopathy) to myopathies with atrophy and necrosis.

Question 8

Diagnosis

Answer 8

Conventional neurophysiological methods that is, nerve conduction studies and needle EMG require the patient’s collaboration to distinguish CIM from CIP (including Biopsy). Finally, as mentioned above, it is not rare for CIM and CIP to coexist.

Question 9

Pathogenesis

Answer 9

Bioenergetic failure is thought to be a relevant pathophysiological mechanism explaining MOF and CIP.

Question 10

Axonopathy

Answer 10

In fact, nerve action potential generation and terminal axon structural integrity are critically dependent on axonal transport of proteins and other molecules. Axons are devoid of the machinery for biosynthetic processes; all axonal components are synthesized in the cell body, and then transported to their final destination within the axon. This transport requires considerable energy expenditure because material is moved rapidly. If the nerve cell does not receive adequate nourishment or the cell cannot use the energy, the axonal transport fails and distal axonopathy ensues.