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Theoretical mechanisms of neuromuscular complications of the systemic inflammatory response syndrome

(1) Sepsis induces a release of cytokines that cause increased capillary permeability. This effect, and other microvascular mechanisms, induce a critical illness polyneuropathy, with distal axonal degeneration of nerve and denervation atrophy of muscle. (2) Neuromuscular (N-M) blocking agents in the presence of systemic inflammatory response syndrome traverse the hyperpermeable capillary membrane and have a direct toxic effect on nerve, or cause "functional denervation" to increase denervation of muscle. (3) Steroids gain access to muscle by this mechanism, and, in the presence of denervation due to 1 and 2, induce a thick filament myopathy and various degrees of necrosis. Combinations of 1, 2, and 3 may occur in the same patient. (Adapted with permission from: Bolton CF. Neuromuscular complications of sepsis. Intensive Care Med 1993b;19:S58-63.)

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  • Asthma
  • COPD exacerbation
  • Critical illness and injury
  • Gram-negative sepsis
  • Neuromuscular blockade
  • Organ transplantation
  • Sepsis
  • Septic encephalopathy
  • Septic shock
  • Steroid myopathy
  • Systematic inflammatory response syndrome