Patients with GBS need special care when coming to the surgery. They have a high risk of aspiration, airway compromise, autonomic instability, altered response to NMBs. It is the duty of the anesthesia providers to recognize those problems and minimize the complications.

1. Guillain Barre’ syndrome(GBS)
and Anesthesia consideration
Dr. Tenzin Yoezer
15/6/2019
KGUMSB

2. History
• 52 yr old female, previously well with history of chronic alcohol abuse
presented with bilateral lower limb weakness and pain for 3 days.
• Limb weakness was progressive and on 4th day onwards became bed
bound
• 1 week prior to limb weakness had self limiting loose stool
• While in P/ling hospital developed seizure(type of seizure not
mentioned)
• Referred to JDWNRH for further mx
• While in ER developed two episodes of seizure and didn’t gain
consciousness

3. History
• Was intubated and kept in AICU
• O/E – mild icteric
• Other examination were unremarkable except
• Limb examination:
• Both UL and LL power – grade 2
• Tone – flaccid
• Reflex – not mentioned
• Initial lab reports at P/ling:
• WBC- 18 LFT - normal
• Neu – 86% RFT - normal
• Hb – 12 USG - normal
• Plt – 324 CXR - NAD

4. • Managed as:
• Peripheral alcohol neuropathy
• Alcohol withdrawal seizure
• Sepsis
• Aspiration pneumonia
• GBS
• AB – Ceftriaxone, Gentamycin

5. • All the vitals stable throughout the illness
• CT brain: atrophy with mild ventricular dilatation
• ECG - sinus rhythm
• ESR – 40
• CSF studies – no cells, protein -137.8 mg/dL
• Neurophysiological studies – report not available

6. • On 14th day of illness IVIg was initiated after consulting
neurologist(HVO): for 5 days
• IVIg 400 mg
• IV drip 20 mL/hr x 1 hr
• 40 mL/hr x 1hr
• 60 mL/hr x 1 hr
• 80 mL/hr x 1 hr

7. • While in the ward developed 4th degree sacral bed sore.
• Brought in OT for W/D
• Face mask with TIVA:
• Inj Midazolam 2mg
• Inj Fentanyl 50 mcg
• Inj Propofol 100 + 20 mg

8. Final diagnosis
• Acute inflammatory demyelinating polyradiculopathy
• Complex partial seizure
• Grade IV seizure

9. Guillain Barre’ Syndrome

10. Introduction
• First described in 1859
• Acute inflammatory demyelinating peripheral polyneuropathy usually
secondary to immunologic response to viral or bacterial infection
(usually respiratory or GI )
• Ascending progressive muscle weakness, autonomic dysfunction and
areflexia
• It causes significant morbidity requiring long hospital stay and
significant period of rehabilitation
• Approximately 10-15% require long term residual disability assistance

11. Epidemiology
• Worldwide incidence is 1.1 – 1.8 cases per 100,000/year
• M> F
• Bimodal age incidence:
• peak in young adults and elderly
• > 50 yrs : incidence rises to 3.3 cases per 100,000/year
• Strong association(70%) with precedent respiratory and GI origin
infection
• There is weak association between GBS and vaccination

12. Clinical features
• Symptoms :
• Weakness and sensory disturbances in LL- pain, numbness,
parasthesia
• Progressive ascending motor weakness
• Respiratory mucles weakness and respiratory failure
• Facial nerve paralysis
• Bulbar weakness(involvement of CIX-CXII)- difficulty in
swallowing,chewing, slurring of speech, chokking on liquids
• Opthalmoplegia

13. Clinical features
• Signs:
• Flaccid areflexic paralysis
• Muscle wasting
• Autonomic dysfunction
• Arrhythmias
• Swing in BP
• Urinary retention
• Paralytic ileus
• Hyperhidrosis

14. GBS subtypes
• 1) Acute inflammatory demyelinating polyradiculoneuropathy(AIDP)
• 2) Acute motor axonal neuropathy(AMAN)
• 3) Acute motor and sensory axonal neuropathy(AMSAN)
• 4) Miller Fisher syndrome(MFS)
• 5) chronic inflammatory demyelinating polyradiculopathy(CIDP)

15. Acute inflammatory demyelinating
polyradiculoneuropathy(AIDP)
• Most common form – 85 – 90%
• Symmetrical ascending motor weakness with hypo- or areflexia
• Underlying pathological process is inflammation and destruction of
the myelin sheaths surrounding peripheral nerve axons by activated
macrophages
• Slowing and blockage of conduction
• Muscle weakness
• Severe cases develop secondary axonal damage

16. Acute motor axonal neuropathy(AMAN)
• More common in Japan and China
• Young people
• Summer months
• Association with Campylobacter jejuni
• C/F similar to AIDP but tendon reflexes may be preserved
• Electrophysiological test distinguish from other variants – selective
motor nerve and axonal involvement
• Binding of antibodies to ganglioside antigen on the axon
• Macrophages invasion, inflammation and axonal damage

17. Acute motor and sensory axonal neuropathy(AMSAN)
• Both motor and sensory fibers involved
• Severe
• Associated with prolonged or even partial recovery
• C/F are similar to AMAN but also involves sensory
symptoms
• Pathology – antibody mediated axonal damage

18. Miller Fisher syndrome
• Presents with ataxia, areflexia and ophthalmoplegia
• 25% may develop limb weakness
• Electrophysiological studies – sensory conduction failure
• Antiganglioside antibodies to GQ1b are found in 90% of pt and are
associated with opthalmoplegia
• Pathological – demyelination of nerve roots

19. chronic inflammatory demyelinating
polyradiculoneuropathy(CIDP)
• Chronic form of GBS
• C/F similar to AIDP
• Slow and progressive
• Or relapsing

20. Investigation
• Serum biochemistry :
• Raised ALT, GGT – 35%
• Raised creatinine
• In SIADH – deranged urea and electrolyte
• Inflammatory markers
• ESR – mostly raised
• CRP – sometimes raised

21. Investigation
• Antiganglioside and antibodies
• Anti-GM1 – positive in 25% ( worse outcome)
• Ant-GD1a – associated with AMAN subtype
• Ant-GQ1b – Miller-Fisher syndrome
• Infection screen:
• Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, herpes
simplex virus, Mycoplasma pneumoniae, HIV

22. Investigation
• Radiological
• CT – to exclude other causes of symptoms and evidence of raised ICP
• MRI – may show selective anterior spinal nerve root enhancement
with gadolinium
• Excludes cervical nerve impingement
• Lumbar puncture
• Protein – raised(may be normal in first 2 weeks)
• Cell count and glucose - normal

23. Investigations
• Nerve conduction studies
• Findings depend on subtype of GBS
• Majority show demyelinating pattern
• Some show axonal loss with little or no demyelination
• Respiratory function tests
• Reduced vital capacity, max inspiratory and expiratory pressure
• ABG – progressive respiratory failure

24. Differential diagnosis
• Neurological
• Myasthenia gravis
• Eaton-Lambert(myasthenic) syndrome
• Multiple sclerosis
• Transverse myelitis
• Metabolic
• Hypokalemic periodic paralysis
• Hypermagnesaemia
• Hypophosphatasemia
• Acute intermittent porphyria
• Infective
• Post diphtheria neuropathy
• Polio botulism
• Tick paralysis
• Drugs/toxins
• Heavy metal poisoning
• Biological toxins(snake and scorpion)
• Drugs(stavudine, NFT, aminoglycosides)
• Other
• Acute polymyositis
• Critical illness myopathy

25. Diagnostic criteria for GBS, from stoelting
• Features required for diagnosis
• Progressive b/l weakness in arms and legs
• Areflexia
• Features strogy supporting the
diagnosis
• Progression of symptoms over 2-4 wks
• Symmetry of symptoms
• Mild sensory symptoms and signs
• Cranial nerve involvement(esp b/l facial
nerve weakness)
• Decrease nerve conduction velocity
• ANS dysfunction
• No fever at onset
• Elevated conc of protien in CSF with cell
counts < 10/mm3
• Spontaneous recovery starting 2-4 wks
after progression halts
• Features making diagnosis likely
• Definite sensory level
• Marked persistent bowel and bladder
dysfunction
• > 50 white cells/mm3 in CSF

26. Management
• Multi-disciplinary inputs
• Therapies
• Supportive
• Immunomodulatory

27. Supportive care
• Airway and respiratory
• Around 30% require ventilatory support
• Deterioration of respiratory function may be rapid
• Vital capacity provides information of about respiratory sufficiency
• Max inspiratory and expiratory pressure provide information about
power of respective group of respiratory muscles
• Both test can be difficult to interpret in pts with bulbar
weakness(difficulty in forming a seal around the mouth)

28. Airway and respiratory
• ABG – evidence of respiratory failure
• Desaturation can be late sign
• Clinical indication for intubation and ventilation are:
• Vital capacity of <1L or <15 mL/kg
• Max inspiratory pressure of < 30 cmH20
• Max expiratory pressure of < 40 cm H20
• Bulbar involvement with inability to cough, swallow and protect the airway
• Evidence of respiratory failure on ABG and autonomic instability
• Tracheostomy should be considered if prolonged respiratory support
is needed

29. Cardiovascular
• Autonomic dysfunction in 70% - life threatening
• ECG, BP and fluid balance
• Most common arrhythmia – sinus tachycardia
• Other arrhythmias – atrial and ventricular tachycardia, prolonged QT interval,
AV block, asystole
• BP fluctuates- severe HTN and hypotension
• Orthostatic hypotension is common
• Care should be taken when treating extremes of BP with vasoactive agents as
pt may be particularly sensitive to their effects(upregulation of post synapting
response)
• Intubated patient with autonomic dysfunction may develop instability after
tracheal suction

30. Gastrointestinal
• Good nutrition is important particularly for those with bulbar
weakness, sedated and mechanically ventilated
• Dietician recommendation
• Pt with autonomic dysfunction – paralytic ileus
• (prokinetic agents – metoclopramide, erythromycin)

31. Neurological
• Neuropathic -50%
• NSAIDs in combination with opioids
• May add adjunctive such as anticonvulsants(Gabapentin
or carbemazepine), Tricyclic antidepressant

32. Venous thromboembolism prophylaxis
• High risk for DVT and PE
• LMWH in combination with pneumatic compression device or
anti-embolism stocking recommended until pt can walk

33. Psychological
• High incidence of depression
• Counselling and psychiatric help
• In UK – Guillain-Barre support group

34. Rehabilitation
• 40% pt needs
• Careful attention should be paid to limb positioning and posture as
limb weakness can lead to nerve compression and palsies, pressure
sore and contracture
• Extensive input from physiotherapists and occupational therapist is
essential to provide tailored strengthening exercise and support
• Patient may also suffer from persistent fatigue- responsive to exercise
programme

35. Immunomodulatory
• IV immunoglobulin (IVIg)-15 mlL/kg
• Its effect is comparable to plasma exchange
• Most effective if administered within 2 weeks of the onset of
symptoms
• Advantages over plasma exchange:
• Widely available
• Less labour intensive
• Less side effect
• Indication: muscle weakness and respiratory depression

36. • IVIg contains donor IgG antibodies – reduces severity of autoimmune
inflammation in GBS by blocking Fc receptors
• Prevents antibody mediated cell destruction
• Alters complement activation
• Contraindication to IVIg:
• Previous anaphylactic reaction to IVIg and IgA deficiency
• Side effects of IVIg: nausea, headache, dermatological
disorders(erythroderma), fluid overload, deranged LFT, venous
thromboembolus, ARF, anaphylaxis
• No evidence of repeated treatment beneficial

37. Plasma exchange
• Aim – to remove antibodies associated with underlying autoimmune
response
• Accelerates recovery
• Improvements have been demonstrated in regaining muscle strength,
ability to walk, reduce duration of ventilator
• More beneficial if commenced within week of the onset of symptoms
• But can be beneficial upto 30 days after onset of illness
• Indication – same as IVIg
• CI: coagulopathy, overwhelming sepsis, hemodynamic instability and shock
• Side effects: nausea, vomiting, diarrhea, fever, coagulopathy,
immunosuppression, hypoglycemia

38. Role of corticosteroids
• No evidence that they improve recovery or affect long term prognosis

39. Prognosis
• Most recover fully
• 15% may suffer persistent disability
• 10% are unable to walk unaided at 1 yr
• Recurrence in 2-5%
• Mortality – 2-12%
• Common death – venous thromboembolism, pneumonitis,
arrhythmias and complication related to dysautonomia

40. Marker of poor prognosis
• Age > 40
• Rapid onset of symptoms
• Severe weakness esp if mechanical ventilation is required or marked
upper limb weakness
• Associated with precedent diarrheal illness or campylo bacter
infection
• Evidence of axonal damage on electrophysiological studies
• Lack of treatment with either plasma exchange or IVIg

41. Anesthesia consideration

42. Anesthesia consideration
• Aspiration risk due to to bulbar dysfunction
• Perioperative respiratory insufficiency due to muscle weakness
(anticipate need for postoperative ventilation)
• Autonomic dysfunction with possible hemodynamic instability
& autonomic hyperreflexia type reactions:
• Arrhythmias, cardiac arrest
• Physical stimulation can precipitate hypertension & tachycardia
• Altered response to neuromuscular blocking drugs (NMBs):
• Succinylcholine contraindicated due to hyperkalemia risk
• NdMR (nondepolarizing muscle relaxant) sensitivity
• ↑ risk of venous thromboembolism

43. Anesthesia consideration
• Goals:
• Minimize aspiration risk-consider prophylaxis, RSI
• Maximize respiratory function – avoid NMBs or reduced dose of NdMR and
full reversal, secretions, pain mx)
• Maintain hemodynamic stability
• Conflicts:
• RSI vs avoid succinylcholine
• Hemodynamic stability
• Neurological deficits and regional techniques

44. Pregnancy consideration
• Uterine tone is maintained – can deliver vaginally
• IUGR and oligohyramniosis – LSCS
• Extent of disease guides for GA/RA- no prospective randomized trial
• Document pre-existing deficits
• If GA chosen: avoid sux, minimal or avoid NdMR
• RA – safely used even in the presence of autonomic
dysfunction(Brooks et al) with SA and EA (Alici et al)

45. Reference
• GUILLAIN-BARRÉ SYNDROME ANAESTHESIA TUTORIAL OF THE WEEK 238
29th August 2011 Dr Sonya Daniel ST3, Southampton General Hospital, UK
Dr Richard Green( anesthesia tutorial week)
• https://www.anesthesiaconsiderations.com/guillain-barre-syndrome-
considerations
• The choice of anesthesia for cesarean section in patients with Guillain
Barre Syndrome – The dilemma continues Suman Arora ,NeeruSahni,
Latha Y
• Stoelting anesthesia and co-existing disease 7th edition p321-322

46. Thank you