Acute neuromuscular weakness in the intensive care unit


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Acute neuromuscular weakness in the intensive care unit

  1. 1. Acute neuromuscular weakness in the intensive care unit From: Crit Care Med 2006 Vol. 34, No. 11 By : Bobby Varkey Maramattom, MD, DM Date: 95-12-25 2006.01.09 ICU Journal Reading Chi-Mei Medical Center Department of Intensive Care Medicine
  2. 2. Introduction <ul><li>critically ill patients have a higher likelihood of acquiring neuromuscular weakness by multiple factors </li></ul><ul><li>weakness acquired in ICU due to critical illness myopathy (CIM) or polyneuropathy (CIP) is 2  -3  more common than primary neuromuscular disorders </li></ul>
  3. 3. <ul><li>Variety of mononeuropathies or plexopathies related to ischemia, pressure palsies, prolonged recumbency, compartment syndromes, hematomas, or other causes </li></ul><ul><li>this review will, however, focus on patients with generalized neuromuscular weakness in the ICU. </li></ul>
  4. 4. <ul><li>Difficult to properly exam. Weakness </li></ul><ul><li>Particular attention should be paid to use of neuromuscular blockers, steroids, antiretroviral agents, statins, and fibrates </li></ul><ul><li>Drugs , renal function, drug interaction </li></ul>
  6. 7. <ul><li>muscle wasting or swelling, muscle tenderness, fasciculations 肌束顫搐 (random single muscle fiber twitches visible in superficial muscles ) or myokymia 肌躍 (undulating rippling movement of muscle fibers beneath the skin that mimics a wriggling worm) , myotonia < delayed relaxation of muscle after voluntary contraction (action myotonia) or mechanical stimulation (percussion myotonia) > , presence of tendon reflexes, and skin lesions </li></ul>
  7. 8. <ul><li>Lambert-Eaton syndrome --- Facilitation of sluggish reflexes after repetitive tendon taps or brief isometric exercise </li></ul><ul><li>Important skin lesions such as the heliotrope rash of dermatomyositis, purpura, telangiectasias, digital ulcers, splinter hemorrhages, or the palmoplantar hyperkeratosis and raindrop lesions of arsenic poisoning </li></ul><ul><li>“ train of four” stimulation </li></ul>
  8. 13. <ul><li>MRI of brain and spine----encephalopathy, CNS involvement, hyperreflexia, spasticity, extensor plantar responses, sensory levels, or multifocal neurologic signs , and also polytrauma, coagulopathies, systemic malignancies, or infective causes of neuromuscular weakness such as West Nile virus or paralytic rabies ----- suspicion of UMN involvement </li></ul>
  9. 14. <ul><li>“ locked-in state”---fully conscious but anarthria, quadriplegic, and able to communicate only through eye blinks or vertical eye movements--- ventral pontine infarction, midbrain infarction, hematomas, central pontine myelinolysis, trauma, and central nervous system infections, GBS, amyotrophic lateral sclerosis, myasthenia gravis, critical illness polyneuropathy, or critical illness myopathy -> need very careful exam. </li></ul>
  10. 15. <ul><li>transverse myelitis or myelopathy -- most common noncompressive myelopathy causing quadriparesis, also infectious myelitis by viruses such as Coxsackie virus, herpes, or CMV or bacteria including Mycoplasma or Legionella , multiple sclerosis, Devic’s disease ( Neuromyelitis Optica ), collagen vascular diseases, or spinal cord infarction  may respond to high-dose IV methylprednisolone </li></ul>
  11. 16. Spinal cord infarction <ul><li>aortic dissection, acute aorto-iliac occlusion, and thoracoabdominal aortic surgeries </li></ul><ul><li>after cardiac arrest and global hypotension. ---- predilection for the lumbosacral cord to be involved -> potentially suffer a “double hit” with cortical watershed infarctions producing brachial paresis and spinal cord infarction resulting in paraplegia. </li></ul><ul><li>Unexplained hypotension or bradycardia in unconscious trauma should prompt evaluation of spinal cord injury with a whole-spine MRI if possible </li></ul>
  12. 17. . <ul><li>acute flaccid areflexic weakness that mimics GBS during stage of spinal shock </li></ul><ul><li>Myelopathy ---early bowel or bladder dysfunction, a sensory level, neck pain, or impalpable lower limb pulses </li></ul><ul><li>Infectious acute poliomyelitis---polio virus, West Nile virus (meningo-encephalitis with an acute flaccid paralysis , predominantly proximal, asymmetric weakness; axonal pathology ; IgM titer) </li></ul>
  13. 18. <ul><li>amyotrophic lateral sclerosis -- present with respiratory failure due to primary involvement of phrenic motor neurons , clear-cut on electrophysiological studies, and widespread denervation </li></ul>
  14. 19. Polyneuropathies <ul><li>30–60% of ICU patients </li></ul><ul><li>CIP occur as early as 2–5 days in sepsis or SIRS, but most often it takes 1 wk of MV </li></ul><ul><li>difficult to wean the patient from the ventilator and lung, chest wall, or cardiac causes of failure to wean have been excluded. </li></ul><ul><li>most common variety of polyneuropathy encountered in ICU is CIP followed by CIM </li></ul><ul><li>SIRS and MOF related </li></ul><ul><li>additional factors such as use of NM blocking agents, corticosteroids, cytotoxic drugs, and status asthmaticus </li></ul>
  15. 20. <ul><li>typical CIM/CIP patient has a flaccid quadriparesis and is often areflexic or hyporeflexic </li></ul><ul><li>Cranial nerves are often spared </li></ul><ul><li>Differentiation between CIP and CIM often rest on electrophysiology---sensory nerve action potentials amplitudes are normal in CIM and reduced or absent in CIP </li></ul>
  16. 21. <ul><li>CIM ---- number of terminologies such as acute quadriplegic myopathy, critical care myopathy, acute necrotizing myopathy of intensive care, thick filament myopathy, acute corticosteroid myopathy, acute myopathy in severe asthma, and acute pancuronium-associated myopathy </li></ul><ul><li>Histopathologically, four subtypes of CIM have been identified on muscle biopsy— the necrotizing ( POOREST) , cachectic, acute rhabdomyolysis, and the thick filament (myosin) loss type </li></ul>
  17. 22. <ul><li>Creatine kinase levels are elevated in about 50% of patients with CIM </li></ul><ul><li>The long-term outcome following CIP/CIM ultimately depends on the underlying illness </li></ul><ul><li>CIP have suprisingly good clinical outcome </li></ul>
  18. 23. GBS <ul><li>Ascending paralysis with respiratory and cranial nerve involvement and diffuse areflexia or hyporeflexia </li></ul><ul><li>weakness developing before admission, preceding upper respiratory or diarrhea, CNS involvement, albumino-cytological dissociation on CSF, and demyelinating features </li></ul><ul><li>features of demyelination on nerve conduction studies and show a good response to intravenous immunoglobulin (IgIV) or plasma exchange </li></ul><ul><li>regional variants or an axonal form of GBS, which-- poorer prognosis </li></ul>
  19. 25. Neuromuscular Junction Disorders. <ul><li>myasthenia gravis, Lambert-Eaton myasthenic syndrome, prolonged neuromuscular blockade, and antibiotic- induced myasthenia </li></ul><ul><li>Lambert-Eaton myasthenic syndrome -- High-rate repetitive nerve stimulation studies and assessment of antivoltage gated calcium channel antibodies , responds variably to 3,4-diaminopyridine or IgIV </li></ul>
  20. 26. <ul><li>NM blockade -- prolonged by metabolic acidosis and dyselectrolemia ( hypoK)--act synergistically with sepsis and SIRS in pathogenesis of CIP and CIM. </li></ul><ul><li>Botulism( Clostridium botulinum) -- involves autonomic functions to producing flaccid paralysis and areflexia --- internal and external ophthalmoplegia, dry mouth, and a paralytic ileus --- Repetitive nerve stimulation studies may show features of presynaptic blockade---- trivalent antitoxin is administered before the toxin binds to presynaptic nerve terminals </li></ul>
  21. 27. <ul><li>Tick paralysis --- mostly in North America and Australia--- mimics GBS with an ascending motor paralysis, preserved sensations, and areflexia but Complete ophthalmoplegia provides clue --removal of tick can result in rapid resolution of paralysis </li></ul><ul><li>Hypermagnesemia mimics Lambert-Eaton myasthenic syndrome with respiratory failure, generalized weakness, and diminished reflexes </li></ul>
  22. 28. <ul><li>inflammatory myopathies two types are encountered frequently in the ICU: </li></ul><ul><li>A. dermatomyositis -- more malignant course, heliotrope may spread into the neck and back in a “shawl” sign, hyperpigmented or “salt and pepper” as in dark-skinned people, Rashes over the knuckles (Gottron’s sign) or subcutaneous calcifications, </li></ul><ul><li>B. Polymyositis </li></ul><ul><li>----Corticosteroids, methotrexate or azathioprine ; IgIV is used as a second-line agent in dermatomyositis </li></ul>
  23. 29. <ul><li> </li></ul>
  24. 30. <ul><li>Potassium disturbances are the most common disturbances that produce weakness---Hypokalemic periodic paralysis due to familial periodic paralysis or thyrotoxic periodic paralysis presents with recurrent weakness– rarely cause respiratory failure----- severe hypophosphatemia can aggravate muscle weakness </li></ul>
  25. 31. CONCLUSIONS <ul><li>differential diagnosis of generalized weakness depends on situation in which patient is encountered. </li></ul><ul><li>Consideration of common causes of neuromuscular weakness and adequate electrophysiological work-up </li></ul><ul><li>Nerve-muscle biopsies -- subclassification of the underlying syndrome and in prognostication </li></ul><ul><li>supportive care and multidisciplinary approach </li></ul>
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