Critical Illness Polyneuropathy CIP

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Critical Illness Polyneuropathy (CIP)

• Current Opionion in Critical Care
• vol 8(4) August 2002, pp. 302-310
• Presented by Ri ???

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Critical Illness Polyneuropathy (CIP)

• Definition
• Epidemiology
• Onset
• Diagnosis
• Risk factor
• Therapy
• Prognosis and Outcome

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Definition

• An acute, predominantly motor axonal
  polyneuropathy occurring in critically ill
  patients.
• Flaccid tetraparesis, failure to wean
• Cranial nerves are spared
• - Movement discrepancy about pain
• Distal gt proximal with muscle atrophy
• DTR ? or absent (13100)
• - CIP cant be r/o with DTR presence

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Epidemiology
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Onset

• Few study have addressed
• Evidence of very early onset of CIP
• - 80 within 72hr (Dutch study)
• - 100 in 25 days (Finland study)

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Diagnosis

• Clinical presentation
• Laboratory parameters
• Electrophysiologic studies
• Nerve and muscle biopsy
• Additional technique
• Differential diagnosis

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Clinical Presentation

• Difficulty weaning from ventilator
• Distal weakness with DTR ?
• - encephalopathy
• - sedation
• - specificity of DTR test

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Laboratory Parameters

• Not diagnostic
• Creakine kinase levels
• - Normality do not rule out N-M disease
• - marginally raised or normal in CIP
• - other contributing factor
• (convulsions, ischemia..)

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Electrophysiologic Studies

• Nerve conduction studies and EMG
• - valuable and sensitive
• - pure axonal polyneuropathy
• - severity quantification

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Electrophysiologic Studies

• Nerve conduction studies
• - ? amplitude of compound motor AP
• - severe muscle atrophy?
• - ? amplitude of sensory nerve AP
• - tissue edema?
• - latency and velocity are unchanged
• - repetitive stimulation r/o N-M synapse dz
• - muscle biopsy r/o myopathy

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Electrophysiologic Studies

• Electromyographic studies
• - signs of denervation
• - spontaneous activity with fibrillations
• - positive sharp waves
• - diaphramatic denervation
• - diaphramatic needle EMG
• - phrenic nerve conduction study EMG

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Nerve and muscle biopsy

• Have not been performed as routine.
• No inflammatory changes were found
• Nerve biopsy
• - No demyelination was found
• - Discrepancy between histologic and
  electrophysiologic studies
• - Early impairment of axonal transport and
  transmembrane potential
• ? Normal histological study cannot r/o CIP

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Nerve and muscle biopsy

• Muscle biopsy
• - Atrophy of type II fibers denervation
• - Fiber necrosis in 30
• - Primary or secondary?
• - No clear relationship with neurophysiology
• - Low motor amplitudes with normal sensory
  neurography, and little spontaneous activity
• Critical Illness Myo- and (poly)Neuropathy
• - CRIMYNE

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Additional Technique

• Quantitative EMG
• Muscle fiber excitability by direct muscle
  stimulation
• - differentiate myopathy and neuropathy

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Differential diagnosis
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Differential diagnosis
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Risk factors

• Systemic inflammatory response syndrome /or
  sepsis
• Steroids
• Neuromuscular blocking agents
• Aminoglycoside antibiotics
• Total parenteral nutrition
• Vasopressor support (gt3d)
• Immune mechanisms (neurotoxic factor)
• Neurologic failure (GCSlt10)
• Renal replacement therapy
• Low albumin and elevated glucose levels

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Therapy

• Neither therapy nor prevention is available
• Possible prevention
• - treatment of underlying sepsis /SIRS
• - glycemic control with insulin (?4048)
• - minimize steroid and depolarizing NMBA
• Possible treatment
• - intensive psychological care and reassurance
• - intensive physiotherapy and supportive care
• - intensive rehabilitation program

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Prognosis and Outcome

• Short-term prognosis
• - high mortality rate with sepsis/ SIRS
• - take weeks to months to recover
• - prolonged ventilator support?
• - scoring system? APACHE III
• Long-term prognosis
• - 50 chance of complete recovery
• - depending on the initial severity

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Take Home Message

• CIP is an acute, predominantly motor axonal
  polyneuropathy occurring in critically ill
  patients.
• Onset in 3d as 3 Ds (Difficulty weaning and
  Distal weakness with DTR ?)
• Electrophysiologic studies are valuable and
  sensitive
• Neither therapy nor prevention is available
• Weeks to months are needed to recover (50)

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In our patient

• 66y/o male with CHF for 2 yrs r/o DCM
• Underlying DM
• Cardiogenic shock s/p IABP at 6/17
• VT/VF s/p CPR at 6/18
• Heart transplantation at 6/22
• EMB at 7/7, 7/14 revealed no rejection

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Post OP

• 6/22 heart transplantation
• 6/25 general weakness
• 6/28 neurologist consultation
• - intact cranial nerve function
• - generally low muscle power (12 score)
• - DTR?at upper extremities, absent at lower
• - muscle atrophy without fasciculation

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Post OP

• 7/12 Electrophysiological study
• - NCV
• Markedly ?amplitude of CMAP and sensory AP
  with relative preserved conduction velocity in
  all tested nerves
• - EMG
• No active denervation change
• 7/16 Extubation

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Risk factors

• Systemic inflammatory response syndrome /or
  sepsis
• Steroids (Solumedrol 120mg iv q8h at 6/22)
• Neuromuscular blocking agents
• Aminoglycoside antibiotics
• Total parenteral nutrition
• Vasopressor support (gt3d)
• Immune mechanisms (neurotoxic factor)
• Neurologic failure (GCSlt10)
• Renal replacement therapy
• ?alb (3.3, 3.2, 3.1) and ? glu (283, 391, 469)

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• Thanks for your attention