CASE 5: GBS

Question 1

What are A fibres?

Answer 1

Large
Myelinated
Fast

Question 2

What are B fibres?

Answer 2

Medium
Myelinated
Slower

Question 3

What are C fibres?

Answer 3

Small, unmyelinated, slow (pain fibres)

Question 4

What type of Peripheral neuropathy is GBS?

Answer 4

Polyneuropathy

Question 5

What is the cause of GBS

Answer 5

Autoimmune

Question 6

Most common form of GBS?

Answer 6

Acute inflammatory demyelinating polyradicularneuropathy

Question 7

Provide an example of a common virus causing GBS?

Answer 7

Gastroenteritis caused by camplyobacteria jejuni

Question 8

How is GBS diagnosed?

Answer 8

1: Clinical exam: Symmetrical flaccid weakness & areflexia
2: Lumbar puncture: increased protein, normal WBC.
3: Nerve conduction studies: decreased conduction velocities

Question 9

Clinical Presentation (Signs & Symptoms) of GBS

Answer 9

Motor
- Progressive, mostly symmetric muscle weakness (Affected distally to proximally)
- Absent or depressed deep tendon reflex
- Compromised respiratory muscles (mechanical ventilation) + facial muscles affected = dysphasgia & dysarthria

Other clinical features
- Sensory loss (glove & stocking paraesthesia)
- Autonomic dysfunction (cardiac arrhythmias, fluctuations in BP, lack of sweating,)

Note:
Types of Sensory loss
- Paraesthesia = pins/needles or tingling ie abnormal sensation often without an external stimulus

• Hyperesthesia = increased sensitivity eg light touch may feel painful
• Hypoesthesia = decreased sensitivity ie reduced sensation

Question 10

GBS assessment (HINT: 4 subcategories)

Answer 10

1: Resp Subjective
- Symptoms: SOB/cough/wheeze/sputum
- Recent illness or infection?

2: Resp objective
- Auscultation
- Respiration rate/effort
- 02 saturation
- Lateral basal expansion

3: Neurological exam
- MMT
- Sensation
- Reflexes
- Tone
- Coordination
- Proprioception
- Balance

4: Functional
- Gait
- Timed 5 x STS
- TUG

Question 11

Acute Medical Management of GBS

Answer 11

• Immunotherapy (immunoglobin)
• Plasmapheresis (plasma exchange)
• Monitor respiration status (intubation if needed)
• Autonomic stability eg manage BP
• Complication management eg VTE -
  (anticoagulator)

*VTE = Venous thromboembolism

Question 12

Physiotherapy Acute Management

Answer 12

Respiratory care (Spirometry & IMT) –> rationale: diaphragmatic & intercostal muscles are weak (risk of atelectasis)

Positioning/Passive ROM

Prevent complications - VTE (circulation exercises eg ankle pumps) + pressure sores = reposition every 2hrs + pressure relieving cushions

Question 13

Physiotherapy recovery Management

Answer 13

• Strengthening + gait retraining + functional mobility
• Sensory re-education
• CV fitness - start with low impact & monitor vitals throughout
• Education + pacing strategies (fatigue! Break up tasks. Important tasks when energy is highest, etc)

Question 14

Why would you anticipate high protein in a lumbar puncture for someone with GBS?

Answer 14

The inflammation/demyelination of peripheral nerves results in the blood-nerve barrier becoming more permeable which means that protein then leaks into the CSF (especially albumin)

Question 15

What are some key LMN signs from GBS?

Answer 15

• Fasciculations
• Hyporeflexia

Question 16

Prognosis?

Answer 16

Prognosis: recovery begins 2-4 weeks after progression halts.

Recovery may take weeks or months (6-18 months)

80-85% make a complete recovery within 4-6 months.

Question 17

Typical timeline for GBS following infection ie when do symptoms onset

Answer 17

1-3 weeks after a flu or vital infection. Symptoms then progress over days to 4 weeks. Recovery starts two to four weeks after progression halts.

Question 18

Strategies for preventing muscle contracture

Answer 18

Stretching
Active Exercises
Massaging

Question 19

What is one of the biggest leading causes of death in the GBS population?

Answer 19

VTE = venous thromboembolism

Question 20

What are the six stages of GBS progression

Answer 20

1: Viral infection
2: Tingling and numbness in scattered areas, particularly distally
3: Scattered weakness, decreased reflexes
4: On ventilator, complete paralysis
5: Gradual recovery, walking with assistance
6: Complete recovery

Question 21

Complications for GBS

Answer 21

Common Complications of Guillain-Barré Syndrome (GBS):

Pressure Injuries (Pressure Sores)
- Cause: Prolonged immobility and reduced sensation make skin more vulnerable to pressure damage.
- Risks: Common over bony prominences such as the sacrum, heels, and elbows.
- Management: Regular repositioning, skin inspection, use of pressure-relieving surfaces (e.g., air mattresses).

Venous Thromboembolism (VTE – DVT and Pulmonary Embolism)
- Cause: Immobility reduces the calf muscle pump action, increasing the risk of blood clots.
- Risks: Especially high in patients with flaccid paralysis.
- Management: Anticoagulant therapy, compression stockings, early mobilisation, passive range of motion exercises.

Joint Contractures
- Cause: Flaccid paralysis and immobility lead to soft tissue shortening around joints.
- Common Sites: Ankles (plantarflexion), knees, elbows, and fingers.
- Management: Daily passive range of motion, proper limb positioning, and splinting if needed.

Respiratory Complications
- Cause: Weakness of respiratory muscles leads to hypoventilation and poor secretion clearance.
- Examples: Respiratory failure, atelectasis, and pneumonia.
- Management: Respiratory physiotherapy, suctioning, assisted coughing techniques, mechanical ventilation when necessary.

Autonomic Dysfunction
- Cause: Involvement of autonomic nerves, which is common in GBS.
- Features: Fluctuations in blood pressure, cardiac arrhythmias, abnormal heart rates (bradycardia or tachycardia), sweating disturbances, and bowel/bladder dysfunction.
- Management: Careful monitoring in ICU, supportive management, medications as needed for cardiovascular stability.