List the potential causes of profound weakness in the critically ill, and outline how you would determine which factors were contributory.

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College Answer

Profound weakness in the critically ill can be as a result of a number of different pathophysiologic mechanisms.     Residual  paralysis  should  be  considered  and  excluded  by  nerve  stimulator examination   (minimal   response   to   train   of   four;   post-tetanic  facilitation,   possibly  some improvement with reversal of blockade).  Residual sedation should also be considered, but once aroused, patient should be able to demonstrate more appropriate strength (and/or response to antidotes: e.g. naloxone, flumazenil).  Critical illness polyneuropathy presents after a week or so of critical illness, typically with limb weakness and atrophy, reduced deep tendon reflexes, loss of peripheral sensation to touch and pin prick, but relative preservation of cranial nerve function. Electrophysiological studies reveal motor and  sensory axonal neuropathy, and  biopsies reveal axonal degeneration and denervation atrophy of muscles.   An acute myopathy (especially in association with neuromuscular blockade and corticosteroids) may present with similar motor findings  but  with  no  sensory  abnormalities.  Creatine  kinase  should  be  elevated. Electrophysiological testing is consistent with a myopathy, and muscle biopsy reveals loss of thick filaments. Spinal cord lesions should be associated with a sensory level and hyperreflexia.  Cranial nerve abnormalities suggest brain-stem problems or Guillain-Barre syndrome.

Discussion

The topic of weakness comes up frequently in these exams.

A generic approach to the patient with generalised weakness in the ICU is discussed elsewhere.

In short:

  • Exclude sedation and paralysis
  • Gather a history to exclude an existing illness which might be contributing
  • Perform a physical examination looking for characteristic signs

The following tests and imaging studies could be useful:

  • Electrolyte levels
  • CK level
  • B12 level
  • Acetylcholine receptor antibodies (for myasthenia gravis)
  • CXR looking for malignancy (as support for a diagnosis of Eaton-Lambert syndrome)
  • Inflammatory markers
  • Lumbar puncture
  • Nerve conduction studies
  • Electromyography
  • MRI of the brainstem and spine
  • Muscle biopsy if no satisfactory explanation is found.

References

References

Oh's Intensive Care manual:

 

Chapter   51   (pp. 568)  Acute  cerebrovascular  complications by Bernard  Riley  and  Thearina  de  Beer

 

Chapter   57   (pp. 617)  Neuromuscular  diseases  in  intensive  care by George  Skowronski  and  Manoj  K  Saxena

 

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal of Medicine 366.24 (2012): 2294-2304.

 

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

 

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care unit." Critical care 8.6 (2004): 416.

 

Mareska, Michael, and Laurie Gutmann. "Lambert-Eaton myasthenic syndrome." Seminars in neurology. Vol. 24. No. 2. [New York]: Thieme-Stratton Inc.,[c1981-, 2004.

 

Reeves and Swenson have an excellent online textbook chapter (12) entitled "Evaluation of the Patient with Weakness"