GUILLAIN BARRE

SYNDROME

BY
DR.SAMI HUSSAIN
DR.ZAEEM UR REHMAN KHAN
DR.HAMMAD AJMAL
A post-infectious polyneuropathy involving
mainly motor but also sensory and
sometimes autonomic nerves.
The most common cause of acute flaccid
paralysis in infants
 CAUSES
Respiratory infections :
Viral: CMV, EBV, Varicella virus , Influenza virus
Bacterial: Mycoplasma pneumoniae, H influenza
Lyme disease, HiB
Gastrointestinal infections :
Campylobactor jejuni (bloody GE)
Helicobacter pylori
Vaccinations
rabies, influenza, conjugated meningococcal vaccine,esp
serogroup C. , OPV
Post surgery
Consumption of undercooked poultry, Unpasteurized milk,
Contaminated water
 TYPES OF GBS

1 AIDP : Acute Inflammatory Classic type (mixed)

Demyelinating
Polyradiculoneuropahty;
2 AMAN : Actue MotorAxonal Pure motor GBS
Neuropathy;
3 AMSAN : Acute Motor Sensory Pure sensory GBS
Axonal Neuropathy;
4 MFS : Miller Fischer Syndrome Miller-Fisher syndrome ( hypotonia,
ophthalmoplegia, ataxia)
5 Pure pan-dysautonomia

* Asbury AK. New concepts of Guillan-Barre syndrome. J Child Neurol 2000; 15:183–191.
 SIGNS & SYMPTOMS
1. Ascending weakness :
• bilateral symmetrical weakness
• usually start in LL, then UL
• Cranial nerves might be affected
2. Areflexia ( Hallmark)
3. Atonia ( hypotonia)
 SYMPTOMS (AUTONOMIC SYMPTOMS)

1 - BP: orthostatic hypotension, labile hypertension

2 - bradycardia, arrythmia
3 - atonic bladder
4 – constipation
5 - flashing and/or sweating
6 - alteration of temperature
 SERIOUS MANIFESTATIONS

1 Resp failure
Diaphragmatic weakness
Resp muscle weakness
Oropharyngeal weakness
2 Cardiac arrest
3 Aspiration pneumonia
 INVESTIGATIONS

• Routine labs should be normal.

• The best initial diagnostic step is
LP/CSF analysis.
• In GBS CSF classically shows
Albumino-cylotogic dissociation i.e
elevated proteins, but no cells.
• The most accurate test is
EMG/nerve conduction studies
Differential Diagnosis

•Vitamin B12 deficiency

•Spinal cord injuries(traumatic, vascular)
•Poliomyelitis
•Tick paralysis
•Spinal cord compression
•Conversion disorder
•West Nile Disease
 PROGNOSIS

Regressive : Good in 90% : Recovery, usually

beginning 2 to 4 weeks after progression stops
starting from the last muscles affected till
lower limb (descending pattern )
Chronic relapsing : < 5%
Mortality : due to complications, esp in infancy
 MANAGEMENT

1 General care
2 Specific treatment
3 Complication treatment
 General care
• Monitoring of vital signs
• Bowel care
• Bed sores
• Nutrition care
• Nursing care
• Repeated spirometries
• Bowel and bladder care
• Tube feeding
• DVT prophylaxis (due to immobility)
• Ventilatory support if required(If Vital Capacity
reduces below 15ml/kg it represents
diaphragmatic involvement, and necessitates
transfer to ICU and intubation)
 Specific treatment

The initial therapy is plasmapheresis or IVIG.

Steroids have no role in GBS treatment.

1. IVIg : 2 g/kg of body weight divided into five

consecutive daily doses of 400 mg/kg each.

Side effects
• chemical meningitis,
• acute tubular necrosis & renal failure
• thomboembolic events,
• rarely anaphylaxis.
2.Plasmapheresis :
50 ml plasma/Kg – 5 exchanges on
alternate days (10 day course)
Problems
• difficulty with placement and
maintenance of central lines
• hypotension during exchanges.
Complications treatment
1.Artificial respiration : Resp failure (20%
cases)
2.Pain killers : Muscle pain
(Narcotics should be avoided. Pain
is best managed with
carbamazepine or gabapentin.)
3.Immunosuppressives: Chronic
relapsing
THANK YOU