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Guillain-Barré Syndrome: What you need to know?

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1 Guillain-Barré Syndrome: What you need to know?
France Ellyson Kuwait, 2014

Post infectious disorder in which the body’s immune system attacks the myelin sheath that surrounds the axons of many peripheral nerves

3 PATHOPHYSIOLOGY An immune-mediated response triggers destruction of myelin sheath Demyelination process is accompanied by edema and inflammation peripheral nerves Demyelination of axons result in loss of conduction

4 PATHOPHYSIOLOGY The inflammation process may lead to various degrees axonal injury This signals poorer recovery

5 PATHOLOGY MMN Multifocal Motor Neuropathy

6 EPIDEMIOLOGY Rare disorder: Average yearly incidence of
1-3 cases / population Occurs world wide / Affects all races Affects ♂ and ♀ equally Persons of all ages are at risk (peak ages 50-74) Unknown etiology Upper respiratory tract infection, viral infection, Gi infection, ? vaccination

Characterized by motor weakness and areflexia Usually begins in legs and progresses to trunk and arms Resp. failure is due to mechanical failure and fatigue of intercostals and diaphragm 85% have cranial nerve involvement. Facial nerve (VII) most frequently affected along with CN IX, X, XI and XII. With sensory changes – paresthesia , tingling, pins and needles, heightened sensitivity to touch or numbness Facial cranial nerve: inability to smile, frown, whistle, drink with straw Cranial Nerve !X and X: Dysphagia and laryngeal paralysis and Vagus nerve deficit – autonomic dysfunction

About 25 % patients experience pain Pain is often worse at night and interferes with sleep Many patients experience autonomic dysfunction Decreased or absent deep tendon reflexes Vibration and proprioception are typically affected GBS does not affect consciousness, pupils or cognitive function

3 phases: Acute (Progressive) stage lasting 3 –4 weeks Plateau stage : symptoms remain unchanged for 2 – 4 weeks Recovery stage

10 DIAGNOSTIC CRITERIA Patient history CSF analysis
There are approximately 50 differential diagnosis CSF analysis Increase protein (Albumin-cytological dissociation) Normal cell count Electromyography (EMG) Shows segmental demyelination Conduction slowing or block (more apparent in the motor nerves than in sensory nerves)

11 MANAGEMENT OF GBS No known preventive treatments Therapies aim:
Lessen the severity of the illness Accelerate the recovery There are two components to care Supportive care Specific therapies

12 SUPPORTIVE CARE Respiratory failure Dysautonomia
Venous Thromboembolism Pain Dysautonomia (or autonomic dysfunction) is any disease or malfunction of the autonomic nervous system (ANS). The autonomic nervous system controls a number of functions in the body, such as heart rate, blood pressure, digestive tract peristalsis, and sweating, amongst others. Dysfunction of the ANS can involve any of these functions.

13 RESPIRATORY FAILURE Most serious and common complication
Occurs in approximately 40% of cases Secondary to weakness of respiratory muscles and diaphragm Vital capacity needs to be measured regularly Patients will be intubated electively when vital capacity falls below 20 ml/kg (ICU admission) Anxiety and insomnia are classic symptoms

14 DYSAUTONOMIA Occurs to some extent in most patients with GBS
More acute in those patients with respiratory problems and severe motor deficits Dysfunction in the sympathetic /parasympathetic systems: Hypertension Orthostatic hypotension Cardiac arrhythmia

5% PE in patients immobilized ≥ 2 weeks Accounts for 28% of the deaths due to GBS Preventative treatments: Anticoagulation, SCDs TED stockings Passive ROM /early mobilization

16 PAIN Commonly presents as lumbar pain.
Discomfort is secondary to acute pain in nerve roots Treat with analgesia Due to immobilization Passive range of motion Pins and needles or burning pain Anticonvulsant drugs / elavil / neurontin / Lyrica/ Cymbalta

17 SPECIFIC THERAPIES Immunoglobulin (IVIgG)
Plasma exchange (Plasmapheresis or PLEX)

IVIG is usually given on 5 sequential days for overall dose of 2 gms/kg of body weight Some patients need second course of treatment IVIG is derived from fractionated, purified human plasma collected from a large pool of multiple donors Mechanism of action is unclear

19 IVIG SIDE EFFECTS Most side effects are mild and transient
Most frequent: rashes, chills, fever, mild hypotension, nausea, malaise, headache, mild arthralgias and short term aseptic meningitis More serious and rare: fatal anaphylactic shock, stroke, renal impairment, hemolytic anemia and transmission of blood born pathogens

20 PLASMA EXCHANGE Removal of immunoglobulins and antibodies from the serum by removing the blood from the body, separating cells from the plasma, and replacing the cells in fresh frozen plasma, albumin, or saline Most common regime 5 – 10 days of treatments

Hypotension /dizziness Fluctuation in circulatory volumes Anemia / Hemorrhage Infection Hypocalcemia

22 REFERENCES Barker, E. (2002). Neuroscience Nursing. A Spectrum of Care (2nd ed.). St. Louis: Mosby. Hickey, J. V. (2003). The Clinical Practice of Neurological and Neurosurgical Nursing (5th ed.). Philadelphia: Lippincott Williams & Wilkins, Chapter 32 Info Neuro: Neuro-Patient Resource Centre: Kirmse,MSN,RN, CNS., J., (2009). The Nurse’s Role in the Administration of Intravenous Immunoglobulin Therapy. Home Healthcare Nurse. 27(2): February 2009. Ruts, L., van Koningsveld, R. & van Doorn, P.A. (2005). Distinguishing acute onset CIDP from Guillain-Barré syndrome with treatment related fluctuations. Neurology 2005 ;6:  Van Doorm,P.A. Ruts, L. &Jacobs, B. (2008). Clinical features, pathogenesis, and treatment of Guillian- Barré syndrome. Lancet Neurol 2008;7:

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