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    Jurnal GBS

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    dzakiyah
    Guillain-Barré syndrome is an acute demyelinating polyneuropathy characterized by ascending motor weakness, sensory disturbances, and autonomic dysfunction following a respiratory or gastrointestinal infection. It has several subtypes including acute inflammatory demyelinating polyradiculoneuropathy and Miller Fisher syndrome. Diagnosis involves neurological exams, nerve conduction studies, lumbar puncture, and ruling out other conditions. Treatment focuses on supportive care, immunotherapy like intravenous immunoglobulin or plasma exchange, and rehabilitation. Prognosis depends on factors like severity and treatment, with most patients recovering but some experiencing persistent disability or mortality.

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    Jurnal GBS

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    dzakiyah
    16 views16 pages
    Guillain-Barré syndrome is an acute demyelinating polyneuropathy characterized by ascending motor weakness, sensory disturbances, and autonomic dysfunction following a respiratory or gastrointestinal infection. It has several subtypes including acute inflammatory demyelinating polyradiculoneuropathy and Miller Fisher syndrome. Diagnosis involves neurological exams, nerve conduction studies, lumbar puncture, and ruling out other conditions. Treatment focuses on supportive care, immunotherapy like intravenous immunoglobulin or plasma exchange, and rehabilitation. Prognosis depends on factors like severity and treatment, with most patients recovering but some experiencing persistent disability or mortality.

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    Guillain-Barré syndrome is an acute demyelinating polyneuropathy characterized by ascending motor weakness, sensory disturbances, and autonomic dysfunction following a respiratory or gastrointestinal infection. It has several subtypes including acute inflammatory demyelinating polyradiculoneuropathy and Miller Fisher syndrome. Diagnosis involves neurological exams, nerve conduction studies, lumbar puncture, and ruling out other conditions. Treatment focuses on supportive care, immunotherapy like intravenous immunoglobulin or plasma exchange, and rehabilitation. Prognosis depends on factors like severity and treatment, with most patients recovering but some experiencing persistent disability or mortality.

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    Download as pptx, pdf, or txt
    16 views16 pages

    Jurnal GBS

    Uploaded by

    dzakiyah
    Guillain-Barré syndrome is an acute demyelinating polyneuropathy characterized by ascending motor weakness, sensory disturbances, and autonomic dysfunction following a respiratory or gastrointestinal infection. It has several subtypes including acute inflammatory demyelinating polyradiculoneuropathy and Miller Fisher syndrome. Diagnosis involves neurological exams, nerve conduction studies, lumbar puncture, and ruling out other conditions. Treatment focuses on supportive care, immunotherapy like intravenous immunoglobulin or plasma exchange, and rehabilitation. Prognosis depends on factors like severity and treatment, with most patients recovering but some experiencing persistent disability or mortality.

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    of 16

    GUILLAIN-BARRE SYNDROME

    Dzakiyah Nurul Isra


    Nudya Ayu P.P.P.H
    Ikandi Praharsiwi
    INTRODUCTION
    Guillain-Barré syndrome (GBS) is an acute demyelinating polyneuropathy. Its
    features are ascending motor weakness, sensory and autonomic dysfunction frequently
    followed by prodromal illness (usually a respiratory or gastrointestinal infection).

    Many antecedent infections have been identified--, including Campylobacter


    jejuni, cytomegalovirus (CMV), Mycoplasma pneumonia, Epstein-Barr virus, and
    influenza virus. Immunization, and parturition have also been associated with GBS.

    GBS usually begins abruptly with distal, relatively symmetrical onset of


    paresthesias. Sensory disturbances are accompanied by or quickly followed by
    progressive limb weakness
    AIM

    Aim in this paper is present clinical features, subtype,


    diagnostic and treatment of GBS
    EPIDEMIOLOGY

    Ten studies reported on the incidence in children (0-15 years old), and
    found the annual incidence to be between 0.34 and 1.34/100,000.

    The overall incidence of GBS worldwide is 1.1–1.8 cases per 100,000 per
    year, with higher rates in males than females. There is a bimodal age incidence, with
    peaks occurring in young adults and the elderly
    CLINICAL FEATURES
    • Symptoms

    The clinical features of GBS are variable. Weakness and sensory


    disturbance are the most common presenting symptoms

    • Signs

    On clinical examination a flaccid areflexic paralysis is found. Muscle


    wasting usually occurs within two weeks of the onset of symptoms and can be
    severe.

    Autonomic dysfunction is common


    GBS SUBTYPES

    • Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

    • Acute motor axonal neuropathy (AMAN)

    • Acute motor and sensory axonal neuropathy (AMSAN)

    • Miller Fisher syndrome (MFS)


    INVESTIGATIONS
    • Serum biochemistry

    • Inflammatory markers

    • Anti-ganglioside antibodies

    • Infection screen

    • Radiological

    • Lumbar puncture

    • Nerve conduction studies

    • Respiratory function tests


    DIFFERENTIAL DIAGNOSIS
     Neurological

    • Myasthenia gravis

    • Eaton-Lambert (myasthenic) syndrome

    • Multiple sclerosis

    • Transverse myelitis

     Metabolic

    • Hypokalaemic periodic paralysis

    • Hypermagnesaemia

    • Hypophosphataemia

    • Acute intermittent porphyria


    DIFFERENTIAL DIAGNOSIS
     Infective

    • Post diphtheria neuropathy

    • Polio

    • Botulism

    • Tick paralysis

     Drugs / toxins

    • Heavy metal poisoning (e.g. lead)

    • Biological toxins (including snake and scorpion toxins)

    • Drugs (including stavudine, nitrofurantoin and aminoglycosides)


    MANAGEMENT

    Multi-disciplinary input is important in all aspects of the care of patients with


    GBS both in the acute phase and rehabilitation of patients. Therapies may be classified
    as being supportive or immunomodulatory

    • Airway and Respiratory

    Around 30% of patients with GBS require ventilatory support

    • Anaesthetic considerations

    Suxamethonium is absolutely contraindicated in patients with GBS


    MANAGEMENT
    • Cardiovascular

    Autonomic dysfunction occurs in around 70% of patients and may be life-


    threatening. Care should be taken when treating extremes of blood pressure with
    vasoactive drugs as patients may be particularly sensitive to their effects

    • Gastrointestinal

    Good nutrition is important particularly for those patients with bulbar weakness,
    and those who are sedated and mechanically ventilated. Patients with autonomic
    dysfunction may be susceptible to the development of a paralytic ileus. This may be
    treated with prokinetic agents such as metoclopramide or erythromycin.
    MANAGEMENT
    • Neurological

    Non-opioid analgesics (Paracetamol, NSAIDs) in combination with opioid


    analgesia should be instituted initially, but may provide inadequate pain relief.
    Adjunctive treatments such as anticonvulsants and tricyclic antidepressants may be
    effective

    • Venous thromboembolism prophylaxis

    Low molecular weight heparin in combination with either pneumatic


    compression devices or anti-embolism stockings, are recommended until patients are
    able to walk unaided
    MANAGEMENT
    • Psychological

    • Rehabilitation

    • Intravenous immunoglobulin

    Intravenous immunoglobulin (IVIg) is an effective treatment for GBS and has


    been demonstrated to be comparable to plasma exchange in accelerating recovery

    • Plasma exchange

    Plasma exchange has been successfully used in mild, moderate and severe
    cases of GBS with differing numbers of exchanges depending on severity
    MANAGEMENT
    • Corticosteroids

    Corticosteroids have been used historically, in order to suppress


    inflammation associated with Guillain- Barré syndrome. They are now no longer
    used. There is no evidence that they improve recovery or affect long-term
    prognosis
    PROGNOSIS

    • Most patients with GBS recover completely but this may take many months
    of intensive therapy

    • 15% of patients suffer persistent disability

    • The mortality from GBS ranges from 2–12%

    • Markers of poor prognosis include age > 40 years, rapid onset of symptoms,
    severe weakness, association with precedent diarrhoeal illness or
    campylobacter infection, evidence of axonal damage on electrophysiological
    studies and lack of treatment with either plasma exchange or IV
    THANK YOU

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