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Guillain Barre Syndrome

Guillain Barre Syndrome ( GBS )  a group of





The most frequent cause of acute generalized
Since the virtual elimination of poliomyelitis, GBS
has become the leading cause of acute flacid
paralysis in western country and development

Peak in young adult and eldery  Allan.Epidemiology  Udaya 2000 : incidence GBS 1 – 3 / 100. USA and Australia.000 population in Europe.000. and 35 patients with respiratory failure.7 cases per 100. 1 patient in ICU . 1994 : incidence 1. mortality 1 – 5 %  RSHS 2000 : 24 patient 4 patient died with respiratory failure 2001 : 21 patients : 3 patient died.

Clinical features of Guillain Barre Syndrome  Motor dysfunction Symmetrical limb weakness : proximal. or global Neck muscle weakness Respiratory muscle weakness Cranial nerve palsies : III-VII. IX-XII Areflexia Wasting of limb muscles . distal.

touch and pain distally Ataxia . vibration. paraesthesiae Loss of joint position sense. Sensory dysfunction Pain Numbness.

 Autonomic dysfunction Sinus tachycardia and bradycardia Other cardiac arrhytmias ( both tachy and brady ) Hypertension and postural hypotension Wide fluctuations of pulse and blood pressure Hypersalivation Anhydrosis or excessive sweating Urinary sphincter disturbances Constipation Gastric dysmotility Abnormal vasomotor tone causing venous pooling and facial flushing .

Guillain Barre Syndrome and variants Weakness Is Predominant Acute inflammatory demyelinating Polyradiculoneuropathy ( AIDP ) Acute motor axonal neuropathy ( AMAN ) Acute motor sensory axonal neuropathy ( AMSAN ) .

Weakness Is Not Predominant Fisher syndrome Acute panautonomic neuropathy Pure sensory neuropathy .

constipation. Complete ophthalmoplegia in 3 % .5 %.Features of Acute Inflammatory Demyelinating Polyradiculoneuropathy ( AIDP ) CLINICAL Two-thirds of patients have antecedent infection or another provocative event Symptoms begin with paresthesias and pain (50%) followed by muscles weakness in the legs. The average time to onset of recovery is 4 weeks 80 % of patients recovery within 6 months 15 % have severe residual disability Mortality rate 3 % .5 % . about 10 % begin with arm weakness. partial in 15 % Autonomic manifestations include labile blood pressure. abdominal distension and bolating Disease progresses for days to 4 weeks. rarely weakness begins in the face. bladder dysfunction. cardiac arrhythmias.

especially related to compylobacter jejuni infection. ophthalmoparesis.10 % . Abrupt onset of weakness. with rapid progression to quadriplegia and often early respiratory insufficiency. Patients may have facial weakness.Features of Acute Motor Sensory Axonal Neuropathy (AMSAN) CLINICAL FEATURES Commonly preceded by diarrhea. and autonomic instability Patients have longer recovery periods with significant residual deficits than in AIDP Mortality rate 5 % .

especially Campylobacter jejuni Affects children and young adults in Northern China primarily. it occurs sporadically in North America Mortality rate  5 % CEREBROSPINAL FLUID CHANGES Protein is elevated in most cases after the first week Spinal fluid cell counts are normal . and elsewhere.Features of Acute Motor Axonal Neuropathy ( AMAN ) CLINICAL FEATURES The condition is often preceded by a history of diarrhea.

followed in 3 – 4 days by limb and gait ataxia Complete ophthalmoplegia evolves over several days Areflexia is typical Sensory loss is usually mild in the distal limbs A mild degree of muscle weakness may be present There is an excellent prognosis for full recovery .Features of Fisher Syndrome CLINICAL FEATURES Syndrome usually begins with diplopia.

as are motor nerve conduction studies .Features of Fisher Syndrome ( cont’d ) CEREBROSPINAL FLUID The protein is usually elevated after 7 – 10 days of illness No significant pleocytosis occurs ELECTRODIAGNOSTIC STUDIES Decreased amplitude of sensory nerve action potentials that return with time is common Sensory conduction velocities are normal.

dizziness. and postprandial bloating. decreased sweating. diarrhea. nausea. and distal sensory loss in one – fourth CEREBROSPINAL FLUID Elevated protein without pleocytosis occurs in the . vomiting. and impotence Muscle strech reflexes are lost in one third of patients. orthostatic hypotension.Features of Acute Panautonomic Neuropathy CLINICAL FEATURES Onset occurs over 1 – 2 weeks in most patients but may be subacute ( over 8 weeks ) Manifestations include : lightheadedness. constipation. voiding problems. Other findings include : heat intolerance. dry eyes. blurred vision.

little or no motor involvement.Features of Pure Sensory Neuropathy Clinical features :  Small number of cases GBS  Manifestation include : ataxia. sensory neuropathy.  Severe cases may have of the face and trunk. areflexi. have an common .

Antecedent Events for Guillain – Barre Syndrome INFECTIONS Viral Epstein – Barr virus Cytomegalovirus Human immunodeficiency virus Influenza viruses Coxsackie viruses Herpes simplex Hepatitis A and C viruses Others* * Isolated reports of various individual viruses or bacteria .

INFECTIONS Bacterial infections Campylobacter jejuni Mycoplasma pneumoniae Escherichia coli Other* Parasitic Malaria Toxoplasmosis * Isolated reports of various individual viruses or bacteria .

SISTEMIC ILLNESS Hodgkin’s disease Chronic lymphocytic leukemia Hyperthyroidism Collagen vascular diseases Sarcoidosis Renal disease .

g..swine flu ) Envenomization Drug ingestion .OTHER MEDICAL CONDITIONS Pregnancy Surgical procedures Bone marrow transplantation Immunizations ( e.

diaphoresis.Criteria for admitting GBS patients to ICU Vital capacity less than 12 ml / kg Deteriorating vital capacity less than 18 to 20 mL/kg. paradoxical breathing Poor cough. aspiration pneumonia Progressive weakness associated with difficulty swallowing Major dysautonomic features ( wide blood pressure and pulse fluctuations : arrhythmias. profound ileus with risk of visceral rupture ) Hypotension precipitated by plasma exchange. heart block. pulmonary edema. accumulating secretions. clinical signs of diaphragmatic fatigue including tachypnea. or plasma exchange planned in a ventilated or .

Autonomic dysfunction Dysautonomia Sinus tachycardia Labile heart rate Orthostatic hypotension Sustained hypertension Paroxysmal hypertension “ Vagal spells “ Other arrhythmias Abnormal drug responses Urinary retention Urinary incontinence Impotence ( males ) Constipation Ileus Fecal incontinence No. cases Percent 62 14 32 5 40 13 8 2 46 4 2 24 15 2 37 8 19 3 24 8 5 1 27 2 2 14 9 1 .

ICU Complication       Mortality 1 – 5 % Tracheostomy  pneumoni Urinary infection Phlebilitis Pulmonary emboli Depression .

Treatment  Supportive care remains unequivocally the most important component of treatment  Essentially all patient should be observed in hospital for at least 2 – 3 week  Patient with severe disease especially there with respiratory insufficien requiring intubation. And with autonomic instability need closed observation and manually in an Intensive Care Unit .

 * Prevent the multiple medical complication as result prolonged Immobility * Rehabilitation effort during the acute phases * Pain control * Psychological suport for patient and families .

Outcome and prognosis  Udaya : .cardiac arest 25 % .36 % improvement the first week .85 % improvement fourth week Death rate 13 % become 5 % in ICU Cause of death : .respiratory failure 75 % .

Poor Prognostic Features for Guillain Barre Syndrome Older age Rapid onset prior to presentation (  7 days ) Ventilator dependency Inexcitable or reduced amplitude motor evoked responses No treatment ( plasma exchange or intravenous immunoglobulin ) Preceding diarrheal illness .

Factor associated with poor outcome  Aetiology Previous gastrointestinal infection Cytomegalovirus  Clinical features Older age Shorter latency to nadir Longer time to clinical improvement Need for mechanical ventilation Greater disability and disease severity .

 Electrophysiology Absent or reduced CMAP ( mean distal CMAP amplitude  20 % of the lower limit normal ) Inexcitable nerves  Biochemical markers Anti-GM1 antibodies Neurone specific enolase and S-100b proteins in CSF .