Cin Cim Class

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    CIN CIM

    Prevalence time course early lab

    diagnosis in severe sepsis

    Moderater:Dr RK Singh

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    Objectives

    Definition of CIN CIM.

    Prevalence & Manifestations.

    Diagnosis High Risk Cases

    Management

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    Critical Illness Neuropathy and Myopathy

    Critical illness Polyneuropathy ( CIP ) , first

    described by Bolton and coleagues in 1986.

    Most common acquired neuromuscular

    condition in adult ICU.

    Almost affects 50 % of patients with sepsis

    and MODS.

    Neurology Clin. 28 (2010)961-977

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    Spectrum of manifestation

    Critically ill patient.

    Symmetric weakness.

    Flaccidity.

    Different degree of muscle atrophy.

    Reduction or absence of DTR.

    Distal loss of sensation.

    Facial and opthalmic muscle are less affected.

    Different degree of encephalopathy.

    Symptoms may start after 3 days of illness.

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    NeuromuscularWeaknessRelated to

    Critical Illness

    Critically ill

    ICU settings

    Respiratorydysfunction,Ventilated

    FlaccidWeakness

    Incidence:

    Adults, 25% of ICU patients.

    Pediatrics, less common.

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    How common is critical illness

    polyneuropahy & myopathy

    Early development of critical illness mypathy

    and neuropathy in patients with severe sepsis.

    48 patients with severe sepsis in ICU.

    Abnormal nerve conduction study (NCS) in

    63 %.

    50 % of the ptients developed neuromusculardysfunction.

    Neurology, 2006 67:1421-5

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    Onset time of critical illness myopathy

    and/or neuropathy during ICU stay

    Multi-center study.

    92 ICU patients.

    Daily measurement

    of action potentialamplitude andnerve conductionvelocity

    30 % developedeither CIMP orCINP

    Critical Care 2007, 11:R11

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    What about children?

    How common is CIN CIM?

    All children admitted to PICU of Sick Children

    Hospital of Toronto over 1 year of age were

    evaluated 3 times /week.

    Muscle weakness, reduced DTR, inability to

    wean MV.

    Incidence :14/830 (1.7 %).

    3 children under 3 years(0.7 % ) and 11 above

    10 years of age (5.1 %)

    Neurology 2003 ;61:1779-1782

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    ICU Related Neuromuscular weakness

    Critical illnessMyopathy

    Critical illnessMyopathy

    Mixed Type ofboth

    ProlongedNMJ blockade

    Others

    Rhabdomyolysis Cachectic myopathy MyopathiesGBS

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    CRITICAL ILLNESS MYOPATHY

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    Type of Critical illness Myopathy

    Acute necrotizing myopathy

    Occur after sepsis and trauma

    Generalized muscle weakness

    High serum creatine kinase

    Myoglobinuria

    Myopathy associated with NMB or Corticosteroid

    Diffuse muscle weakness

    Muscle atrophy

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    Incidence

    ARDS

    3%

    OrganTransplant

    7%

    SevereSepsis

    33%

    MOF

    50 %

    Steroid

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    CRITICAL

    ILLNESSMYOPATHY

    Increasedseverity of

    disease

    SystemicInflammatoryResponse

    Steroid

    NMB

    Hyperglycemia

    IV

    Steroid

    NMB

    Strongest factor

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    Risk Factors

    Sepsis

    SIRS

    Hyperosmolarity

    TPN

    GCS

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    Muscle weakness in critically ill children

    Neurology 2003 ;61:1779-1782

    840 patients

    14 patients (ave. 12 y/o) developed weakness(1.7 %).

    Age distribution 3

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    ICU ,

    ventilated,

    paralysed

    IV steroid

    for

    several

    days

    CIM

    Increased CK (Around D4) ;50-80% might

    be without CIM

    Failure to wean not related to

    cardiopulmonary disease

    Flaccid proximal quadriparesis

    Normal sensation,DTR normal/decreased

    DIAGNOSTIC CRITERIA

    Muscle BX, Electron Microscope Loss ofmyosin

    Electrphysiological study, Nerve

    conduction study,EMG

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    Pathology

    Scattered atrophic fibers.

    Loss of ATPase activity.

    Loss of myosin thick filaments.

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    Normal

    Nerve Stimulation

    Direct

    muscle

    stimulation

    Neuropathy

    Nerve Stimulation

    Direct

    muscle

    stimulation

    Myopathy

    Nerve Stimulation

    Direct

    muscle

    stimulation

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    Prevention

    Management Supportive

    Rehabilitation

    Avoide the Occurance

    PrognosisRecovery withinweeks to months.

    Variabe residual

    weaknessICU stay ,Morbidity,Mortality.

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    CRITICAL ILLNESS POLYNEUROPATHY

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    Mechanism

    (not clear)

    Axonal Degeration

    70 %

    Intact nerves 30 %

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    High Sugar SIRS

    Low

    Albumin

    Sepsis

    Crtical Illness

    Neuropathy

    Major Factors

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    CIM CIP

    Incidence More common Less Common

    Motor system Proximal Distal

    Sensory function Preserved Affected

    DTR Usually Normal Usually Absent

    Facial M Cranial N Preserved Usually Preserved

    Prognosis Better, Weeks to months

    , Residual weakness

    Weeks to months

    ,Residual Weakness,May

    remain quadreplegic

    Management Supportive,Preventive,

    Insulin

    Supportive,Preventive,

    Insulin

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    ICU ,

    ventilated,

    paralysedCIP

    Sepsis,SIRS

    ,MOF

    DIAGNOSTIC CRITERIA

    Failure to wean not related to

    cardiopulmonary disease

    Flaccid Quadriparesis

    Abnormal sensation distally, Cranial N

    preserved,DTR Absent or Decreased

    Normal CK,Normal CSF proteins

    Electrophysiological study,NCS,EMG

    Muscle Bx (Treatable Condition)

    It is difficult to differenciate

    CIM & CIP clinically

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    Normal nerve

    Nerve Action Potential:

    Normal amplitude &

    conduction velocity

    Axonal Neuropathy:

    Nerve Action Potential:

    Reduced amplitude & Normalconduction velocity

    Demyelinating Neuropathy:

    Reduced conduction velocity ,

    normal amplitude

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    Loss of myelinated

    nerve fibers

    Dgenerating Myelin

    Custers of Schwann

    cells without nerve

    fibers

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    THANK YOU