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Guillain-Barre Syndrome (GBS) (Clinical Presentation (Pain is common e.g.…
Guillain-Barre Syndrome (GBS)
An acute inflammatory demyelinating ascending polyneuropathy affecting the PERIPHERAL NERVOUS SYSTEM (SCHWANN CELLS TARGETED) following an upper respiratory tract infection or GI infection
Epidemiology
Peak ages 15-35 years and 50-75 years
The most common acute polyneuropathy
More common in MALES than females
Aetiology
Zoster
HIV
Mycoplasma
EBV
Cytomegalovirus (CMV)
In some cases no obvious infection can be found
Campylobacter jejuni
Risk Factors
Vaccinations have been implicated
Post-pregnancy - incidence decreases during pregnancy but increases in months after delivery
History of respiratory or GI infections 1-3 weeks prior to onset
Pathophysiology
It is thought that these infectious organisms share the same antigens as those on Schwann cells, leading to autoantibody mediated nerve cell damage formation via molecular mimicry
Nerve cell damage consists of damage to the Schwann cells and thus demyelination resulting in the reduction in peripheral nerve conduction resulting in an acute polyneuropathy
GBS is usually triggered by infection e.g. Campylobacter jejuni, EBV or cytomegalovirus (CMV)
Clinical Presentation
Pain is common e.g. in back and limb but sensory signs may be absent
Sensory signs include parenthesis - but there are very few sensory signs
In 20%, respiratory muscles and facial muscles are affected - respiratory involvement requires ITU admission
Reflexes are lost early in the illness
The PROXIMAL MUSCLES are more affected e.g. trunk, respiratory and cranial nerves (esp. CN7)
Autonomic feature such as sweating, raised pulse, BP changes, arrhythmias may be present
1-3 weeks post infection a SYMMETRICAL ASCENDING MUSCLE WEAKNESS starts - this may advance quickly, affecting all limbs at once and can lead to paralysis
There is a progressive phase of uptimes to 4 weeks, followed by recovery
Differential Diagnosis
Other causes of acute paralysis, e.g. hypokalaemia, stroke, brainstem compression, encephalitis, spinal cord compression, poliomyelitis, vasculitis, myasthenia gravis
Diagnosis
Lumbar puncture
CSF has raised protein but normal white cell count
Spirometry
To monitor FVC if there is respiratory involvement
Decreased FVC indicates the need to admit to ITU to maintain airways
Nerve conduction studies (NCS)
DIAGNOSTIC if matches with clinical examination
Show slowing of conduction, prolonged distal motor latency +/- conduction block
Treatment
Plasma exchange
Low molecular weight heparin e.g. SC ENXOPARIN and compression stocking to reduce risk of venous thrombosis
IV IMMUNOGLOBULIN for 5 days
Decreases duration and severity of paralysis
Contraindicated in patients with IgA deficiency - screen for deficiency
Prognosis is good with 85% making a complete/near-complete recovery, but 10% are unable to walk alone at 1yr, mortality is 10%
If FVC <80% then ventilate and admit to ITU - MONITOR FVC 4 HOURLY