CIN CIM Prevalence time course early lab diagnosis in severe sepsis

Moderater:Dr RK Singh

Objectives
Definition of CIN CIM. Prevalence & Manifestations. Diagnosis High Risk Cases Management

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

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.

Critically ill

Flaccid Weakness

Neuromuscular Weakness Related to Critical Illness

ICU settings

Incidence: Adults, 25% of ICU patients. Pediatrics, less common.

Respiratory dysfunction, Ventilated

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 neuromuscular dysfunction.

Neurology, 2006 67:1421-5

Onset time of critical illness myopathy and/or neuropathy during ICU stay
Multi-center study. 92 ICU patients. Daily measurement of action potential amplitude and nerve conduction velocity 30 % developed either CIMP or CINP
Critical Care 2007, 11:R11

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

ICU Related Neuromuscular weakness

Critical illness Myopathy

Critical illness Myopathy

Mixed Type of both

Prolonged NMJ blockade

Others

GBS

Rhabdomyolysis

Cachectic myopathy

Myopathies

CRITICAL ILLNESS MYOPATHY

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

Incidence

Organ Transplant

Severe Sepsis 33%

MOF 50 %

ARDS

7%
Steroid

3%

Increased severity of disease

Hyperglycemia

CRITICAL ILLNESS MYOPATHY

Systemic Inflammatory Response

Strongest factor

IV Steroid NMB

Steroid

NMB

Risk Factors
Sepsis SIRS Hyperosmolarity TPN GCS<10 ARDS Pancreatitis Burn Asthama Organ Transplant Renal or Hepatic Failure

Steroid NMB Aminoglycoside Hyperglycemia

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 <3 years(0.5 %). More than 10 years (5.1 %) Length of PICU stay (4 -11 days) 9/14 received corticosteroids. 9/14 received NMB. 57% were transplant patients. 4/14 died(29%).

DIAGNOSTIC CRITERIA

ICU , ventilated, paralysed

IV steroid for several days

Failure to wean not related to cardiopulmonary disease

CIM
Flaccid proximal quadriparesis

Normal sensation,DTR normal/decreased

Increased CK (Around D4) ;50-80% might be without CIM Electrphysiological study, Nerve conduction study,EMG Muscle BX, Electron Microscope Loss of myosin

Pathology
Scattered atrophic fibers. Loss of ATPase activity. Loss of myosin thick filaments.

Nerve Stimulation Direct muscle stimulation Direct muscle Nerve Stimulation stimulation

Nerve Stimulation

Direct muscle stimulation Normal

Neuropathy

Myopathy

Management
Prevention Supportive Rehabilitation Avoide the Occurance

Prognosis

Recovery within weeks to months.

Variabe residual weakness

ICU stay , Morbidity,Mortality.

CRITICAL ILLNESS POLYNEUROPATHY

Axonal Degeration 70 %

Mechanism (not clear)

Intact nerves 30 %

Sepsis

Major Factors

High Sugar

Crtical Illness Neuropathy

SIRS

Low Albumin

CIM Incidence
Motor system Sensory function DTR Facial M Cranial N Prognosis

CIP Less Common

Distal Affected Usually Absent Usually Preserved

More common
Proximal Preserved Usually Normal Preserved

Better, Weeks to months Weeks to months , Residual weakness ,Residual Weakness,May remain quadreplegic Supportive,Preventive, Insulin Supportive,Preventive, Insulin

Management

DIAGNOSTIC CRITERIA

Failure to wean not related to cardiopulmonary disease ICU , ventilated, paralysed

Sepsis,SIRS ,MOF

CIP

Flaccid Quadriparesis

Abnormal sensation distally, Cranial N preserved,DTR Absent or Decreased

Normal CK,Normal CSF proteins

It is difficult to differenciate CIM & CIP clinically

Electrophysiological study,NCS,EMG

Muscle Bx (Treatable Condition)

Normal nerve Nerve Action Potential: Normal amplitude & conduction velocity

Axonal Neuropathy: Demyelinating Neuropathy: Nerve Action Potential: Reduced conduction velocity , Reduced amplitude & Normal normal amplitude conduction velocity

Loss of myelinated nerve fibers

Dgenerating Myelin
Custers of Schwann cells without nerve fibers

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