Guillain barre syndrome (Short Lecture by Dr Aslam)
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This document provides information about Guillain-Barr辿 syndrome (GBS). GBS is an acute onset of symmetrical muscle weakness and paralysis caused by damage to peripheral nerves. It is considered an autoimmune condition that can affect both motor and sensory nerves. Clinical symptoms include muscle weakness, absent reflexes, pain, and possible respiratory failure. Diagnosis involves neurological exams, cerebrospinal fluid analysis, and electrophysiological tests. Treatment focuses on plasma exchange, immunoglobulin therapy, and other supportive care. Most patients recover fully, but some have long-term weakness or neurological issues.
Guillain barre syndrome (Short Lecture by Dr Aslam)
- 1. S Y N D R O M E GUILLAIN BARRE A S L A M A B D U L V A H I D 膸 莨 - 2 1 3 1 4 6 1 8 8 S C H O O L O F M E D I C I N E S O U T H E A S T U N I V E R S I T Y
- 2. LEARNING OBJECTIVES ETIOLOGY & PATHOGENESIS CLINICAL SYMPTOMS & SIGNS DIAGNOSIS OF GBS DIFFERENTIAL DIAGNOSIS OF GBS MANAGEMENT & PROGNOSIS
- 3. W H A T I S G B S ? It is an acute or subacute onset of generally symmetrical and progressive lower motorneurons paralysis of limbs. A disease which rapidly damages peripheral nerves. May hinder movement, sensation or organ function depending on which nerves are involved Named after French neurologists Georges Gullain and Jean Alexandre Barre-1916
- 4. Often the cause of GBS is unknown Often follows GI infection with diarrhoea or respiratory infection The GI infection due C.jejuni often precedes to GBS It occurs in all parts of the world and in all seasons, affecting children and adults of allages and both sexes. Rare only 1 -2 cases per 100,000 people world-wide each year Most common cause of sudden onset flaccid paralysis E T I O L O G Y
- 5. C L I N I C A L M A N I F E S T A T O N 1.Muscle weakness and Flaccid paralysis - In 25% of patients this weakness affect the respiratory muscle causes respiratory inadequacy 2. Possible Respiaratory Failure 3. ANS Dysfunction - Urinary Retention - Flushing of the face - Cardiac arrythmia- - Orthostatic Hypotension 4. May or may not experience pain -Pain most commonly in Back, Shoulders and Thighs
- 6. 2 main subtypes 1. AIDP-ACUTE INFLAMATORY DEMYELINATING POLYNEUROPATHY 2. AMAN-ACUTE MOTOR AXONAL NEUROPATHY P A T H O P H Y S I O L O G Y
- 8. A M A N ACUTE MOTOR AXONAL NEUROPATHY
- 11. Symptoms are symmetrical progressive weakness of more than one limb Absent reflex/hyporeflexia High levels of proteins in CSF (>0.55g/L) < 10 WBC per mm 3 in CSF Neurophysiological studies Nerve Conduction Study(NCS)- decreased conduction velocities Electromyography(EMG)- decreased muscle recruitments D I A G N O S I S
- 12. Plasmapheresis (Plasma Exchange) Immunoglobulin (IV) Corticosteroids are not given Mechanical Ventilation IV antibiotics therapy Manual movement of limbs Anticoagulent therapy to prevent DVT Physical and Occupational therapy Pshychological therapy T R E A T M E N T
- 13. 2-5% OF GBS patients die o Respiratory paralysis o Cardiac arrest Most patients have a full recovery 30% of patients residual weakness after 3 years 3% of patient weakness and tingling after many years P R O G N O S I S
- 14. Peripheral neuropathy associated with GBS comes on with a sudden onset. Syndrome is autoimmune Demyelinating Ascending Symmetrical condition Affect both sensory & motor neuron Symptoms include parasthesis, absent of reflexes, pain, muscle weakness, may progress to possible respiratory paralysis S U M M A R Y
- 15. ANS dysfunction (Arrhythmia, Orthostatic hypotension) Medical emergency Findings that support positive diagnosis of GBS o Sensory & Motor symptoms o CSF high level of protein, low level of WBC Neurophysiological studies like NCS, EMG Treatment: Plasmapheresis, Immunoglobulin, Antibiotics & Anti-coagulant therapy S U M M A R Y