39. ICU Neuropathy Flashcards
What are the causes of muscle weakness in critically ill patients?
- Pre-existing medical conditions
Guillain–Barre´ syndrome
Myasthenia gravis
CNS lesions, e.g. trauma, polio, MND - Drug related
Muscle relaxants
Aminoglycosides (may interfere with neuromuscular transmission)
Magnesium (in pre-eclampsia)
Steroids (typically proximal weakness/wasting)
Poisoning, e.g. botulinum toxin, organophosphates - Metabolic
Hypokalaemia
Hypophosphataemia - Myopathy (acquired)
Immobilization, disuse atrophy
Malnutrition
Necrotising myopathy
Critical illness myopathy (CIM) - Critical illness neuropathy
Tell me a bit more about critical illness neuropathy.
- This is an acquired neuropathy
commonly found in association with
severe sepsis and multiple organ failure,
increasing in frequency with prolonged
ICU stay and sepsis. - The problem affects more than half of adult patients
admitted to general ICUs for more than 1 week
and more than 70% of those with sepsis and multiorgan failure. - It has been recognized as a clinical entity since 1983 when described by
Bolton et al. - The cause remains unknown and there is no specific treatment.
- Clinically, there is a flaccid weakness
with absent/reduced tendon reflexes
and muscle wasting.
How can CIW present
Neuromuscular weakness typically presents when attempting to wean the
patient from the ventilator. Earlier diagnostic clues may be a relative lack of movement after regaining consciousness and/or the loss of deep tendon reflexes.
Other diagnoses should be considered, although most cases will be due to
critical illness polyneuromyopathy.
Spinal cord disease should be excluded,
West Nile virus infection, acute
disseminated encephalomyelitis, etc.
A neuromuscular transmission defect
(e.g. NMBs, unrecognized myasthenia gravis).
Porphyria and recurrent chronic inflammatory demyelinating
polyneuropathy.
Differentiating the most common causes of ICU-acquired generalized weakness
Differentiating the most common causes of ICU-acquired generalized
weakness (myopathy, neuropathy, or a combination of the two),
is useful because they have differing prognoses.
Electromyography is helpful in differentiating CIP from CIM.
An elevated serum creatine kinase may help to identify CIM.
Muscle biopsy can address the relative contribution of
myopathy to the picture because the neuropathy can be adequately
assessed electrophysiologically (nerve conduction studies).
CSF protein levels are normal (cf. Guillain–Barre´ ).
CIM
The prognosis for recovery from a CIM is more favourable, most patients
recovering fully within 1–3 months.
Patients with widespread muscle necrosis may recover incompletely
CIP
Patients with CIP recover slowly because the axons regenerate at 1 mm/day.
This takes many months and recovery is often incomplete Evidence of
polyneuropathy is apparent after 5 years in over 90% of CIP patients.