common neurologic disease

1. UoG, GCMHS
Department of Anaesthesia
CRITICAL CARE MODULE
Common neurologic diseases in ICU
January, 2019
1

2. Outline:
 introduction
 Coma
 Status epilepticus
 Stroke
 Guillain-Barré Syndrome
2

3. Introduction
-Altered levels of consciousness and coma are among the most
common problems encountered in critically ill patients
-Consciousness is awareness of self and the environment
-The normal state of consciousness can range from being alert and
aware to a stage of sleep
-It is a result of complex interactions between reticular activating
substance within the brainstem, cortex and the sensory stimuli
3

4. -Abnormal levels of consciousness represent a wide spectrum of
conditions ranging from feeling lethargic to coma.
-Any alteration in the complex interactions of ascending reticular
activating system(RAS) and its numerous connections can lead
to abnormal levels of consciousness
4

5. 5
1. Coma
-Unarousable unresponsiveness or the absence of any
psychologically understandable response to external stimulus
or inner need which is caused by disease, injury, or poison
-The patient is unaware of self and environment and does not
respond to vigorous stimulation.

6. Spectrum of abnormal levels of consciousness
Persistent vegetative state (PVS)
-Patients are in a state of partial arousal and may briefly respond
to sound or visual stimuli
-They withdraw to noxious stimuli but are unable to interact or
respond voluntarily or purposefully when stimulated
It is a chronic condition, diagnosed after 30 days of persistent
altered consciousness
6

7. Spectrum of abnormal levels of consciousness--
Minimally conscious state (MCS)
-Patients in MCS display deliberate or cognitively mediated
behaviour. They may intermittently follow commands or have
understandable but inconsistent verbal output
Locked-in syndrome
-Patients have intact cognition but complete paralysis of voluntary
muscles in all parts of the body. Can communicate using blinking /
up-and-down eye movements
7

8. Spectrum of abnormal levels of consciousness--
Clouding of consciousness:
-A state of reduced wakefulness or awareness, characterized by
impaired attention and memory. Patient is easily distracted and
sometimes hyperexcitable, startled by stimuli.
 Acute confusional state:
-Impairment of consciousness in which stimuli are intermittently
misinterpreted. Patients are drowsy, disorientated in time and
occasionally place and person and have poor short-term memory
8

9. Spectrum of abnormal levels of consciousness--
Delirium:
-Acutely developing impairment of consciousness, attention,
disordered thinking- fear, disorientation, visual hallucinations,
delusions and misperceptions of sensory stimuli
- there can be some temporary improvements in between
-Commonly due to metabolic, toxic, or endocrine derangements.
-Very common in hospitalized patients
-Follows a fluctuating course and rarely lasts more than a week.
9

10. Spectrum of abnormal levels of consciousness--
Obtundation:
-Mental blunting with apathy and inactivity. Patient is drowsy with
reduced alertness, has a decreased interest in the environment and
responds slowly to stimulation
Stupor: Similar to deep sleep or unresponsiveness. Patient can be
aroused by episodes of repeated, vigorous stimuli. As stimulation
decreases, patient lapses back into a state of decreased
responsiveness. Even when aroused, communication is by
monosyllabic(saying very little) sounds and simple behaviour.
10

11. Differential diagnosis for Coma
Guillain-Barre syndrome
Locked-in syndrome
Botulism
Psychogenic unresponsiveness
11

12. Causes of coma
 Brain injury- trauma, cerebrovascular accident, meningo -
encephalitis, malaria, ictal (or post-ictal), space-occupying lesion
 Metabolic- hypoglycaemia or hyperglycaemia, severe electrolyte
disturbance (e.g. Na+), renal failure, liver failure
 Sepsis
 Drug-related or poisoning- opiates, benzodiazepines, carbon
monoxide poisoning, recreational drugs, alcohol
12

13. Causes---
 Haemodynamic- related to poor cerebral perfusion (cardiac
arrest, severe heart failure, arrhythmia, hypotension)
 Respiratory- low PaO2 and/or high PaCO2
 Endocrine- myxoedema, Addison’s disease
 Temperature disturbance- hyperpyrexia, hypothermia
13

14. Assessment
 ABC
 Once patient is stable, collateral history from family etc
 GCS:
o 3- lowest score; indicates deep coma or death
o <8- severe reduction in consciousness and the patient is
unlikely to be able to maintain their airway spontaneously,
thus should be intubated and ventilated
o 15- highest score; indicates normal conscious level
14

15. Assessment--
 AVPU scale
o Alert- meaning spontaneous eye opening, speaking and intact
motor functions- e.g, moving limbs.
o Voice- responds when spoken to -e.g, grunt or actual speech.
o Pain- responds to pain- e.g, sternal rub.
o Unresponsive- if no response to pain, i.e. no eye, voice or
motor movement.
15

16. Examination:
o Baseline observations- BP, PR, temperature (rectal ideally - if
hypothermic, consider myxoedema coma), capillary blood glucose
and oxygen saturation
o Response to external stimuli- usually none present
o Primary survey of skin and mucous membranes- any evidence of
hyperpigmentation, sepsis, myxoedema, intravenous drug
misuse, anaemia, jaundice, purpura, cherry-red discolouration
(suggesting carbon monoxide poisoning)
o Smell the patient's breath for evidence of ketones, solvents, and
alcohol
16

17. Examination--
o Assess responsiveness and GCS or simpler AVPU scale
o Respiratory, abdominal (any chance of intra-abdominal bleeding),
cardiovascular and neurological examination
o Remember, if the patient is paralysed and ventilated then
neurological examination will be limited
17

18. Examination--
-Particular aspects to focus on include:
Pupils- abnormal movements, size, response to light stimulus.
Fundoscopy to look for papilloedema
Corneal reflex
Gag reflex
Respiratory pattern
Response to painful stimuli
Plantars
Doll's head manoeuvre
Any evidence of head injury- e.g, bruising behind the ear, or
panda eyes
18

19. Useful focal indicators of pathology
Pupillary reactions and corneal reflexes
o Unilateral pupillary dilatation with lack of response to light-
uncal herniation of the temporal lobe over the tentorium
entrapping the third nerve
o Pupil fixed in the mid position with loss of light reflex- typical of
midbrain lesions
o Small pupils with response to light- lesions in the pons
o Fixed dilatation- suggests significant damage to the brainstem
19

20. Pupillary reactions and corneal reflexes--
o Horner's syndrome- occurs in lesions of the hypothalamus or
brainstem and in diseases affecting the wall of the carotid artery
o Small pupils reacting briskly to light- metabolic cause (e.g,
hepatic or renal failure)
o Corneal reflexes- these are normally intact until there is a very
deep coma. In drug intoxication, they may be absent in a patient
otherwise in a light coma. Otherwise, loss of corneal reflex is
indicative of a poor prognosis
20

21. • Horner's syndrome- a pattern of symptoms
occurring as a result of damage to nerves in
the cervical region of the spine manifested by:
– droping eyelids
– constricted pupils and
– absence of facial sweating.
21

22. Spontaneous eye movements
• Conjugate deviation of the eyes- possible focal hemispheric or
brainstem lesion
• Depression of the eyes- lesion in the midbrain at the level of the
tectum
• Skew deviation of the eye- lesion at the pontomedullary
junction.
22

23. Spontaneous eye movements--
• Uncoordinated eye movements- a small amount of eye
divergence is normal in unconsciousness but more significant
incoordination suggests damage to the oculomotor or abducent
nerves in the brainstem or pathways
• Normal roving eye movement- similar to those of sleep- often
occurs in light coma, and cannot be faked, so excludes the
possibility of psychogenic unresponsiveness (jerky eye
movement)
23

24. Reflex eye movements
 Oculocephalic response
-The patient's head is rotated from side to side and the position of
the eyes is observed. The eyes will move together in the opposite
direction to the head movement (normal oculocephalic
response, also called doll's eye movement)
-Where a brainstem lesion is present, this eye movement is
absent or asymmetric
24

25. Reflex eye movements--
 Oculovestibular testing (instil 20ml ice-cold water into the
external auditory meatus):
Psychogenic coma- nystagmus with quick movement away from
water (shows active pons and intact corticopontine connections)
Tonic, conjugate movement in the direction of the ear with water
-suggests a cause situated above the tentorium with intact pons
Disconjugate /no response- lesion within the brainstem.
25

26. Respiratory pattern (if not on a ventilator)
 Deep breathing: acidosis
 Regular shallow breathing: drug overdose
 Long-cycle, Cheyne-stokes respiration: damage at the
diencephalon
 Short-cycle, Cheyne-Stokes respiration: damage at the medulla
 Central neurogenic hyperventilation: lesions in the low midbrain
and upper pons
 Yawning, vomiting and hiccupping: brainstem lesions
26

27. Motor function
 Abnormalities on one side indicate the probability of a focal cause
(sometimes seen in hepatic encephalopathy) and hypoglycaemia
 Seizures- hemispheric damage
 Multifocal myoclonus- metabolic or anoxia causing diffuse
cortical irritation
27

28. Investigation
-Dictated by presenting history and examination findings
Urgent blood sugar testing (at the bedside)
Urea and electrolytes, sugar, calcium, liver function
FBC and clotting screen to exclude coagulopathy
Urgent blood gas analysis (including COHb if indicated)
Blood and urine poison/drug screen/alcohol level
28

29. Investigation--
Plasma creatine kinase and test urine for ‘positivity’ for blood if
rhabdomyolysis possible (immobility, recreational drugs,
hyperpyrexia)
Metabolic screen (thyroid function, cortisol)
Septic screen + malaria screen
Lumbar puncture (+ preceding CT scan if concerned about raised
ICP)
CT scan
Other neurological tests, e.g. EEG. MRI
29

30. Management
ABC- ensure adequate (protected) airway, breathing, circulation
Correct rapidly remediable causes promptly, e.g. hypoglycaemia,
status epilepticus, specific antidote (e.g. naloxone for opiate
toxicity)
If meningitis suspected, give antibiotics immediately (e.g.
ceftriaxone)
30

31. Management---
Prioritize investigations based on likely diagnosis; treat
accordingly
Institute measures to lower intracranial pressure if concerned
about coning
Urgent referral to neurosurgeon if CT demonstrates space-
occupying lesion (e.g. haematoma) or for brain decompression
(craniectomy)
31

32. Management---
Urgent consideration of thrombolysis if cerebral infarct or
embolus
Consider duration of coma when treating metabolic abnormality
Correction of Na+ and glucose may need to be more gradual
Unconscious patients involved in a traumatic event have an
unstable spine until specifically excluded, and should be managed
accordingly
32

33. Management---
Consider active warming (for hypothermia) or cooling (for
prolonged cardiac arrest or, possibly, head injury)
If rhabdomyolysis present, ensure adequate circulating volume,
urinary alkalinisation, and relief of any compartment syndrome
33

34. Management---
Long-term management
o DVT prophylaxis
o Nursing measures to prevent contractures and pressure sores
o Oral & eye care
o Bladder and bowel care
o Nutritional support
34

35. 2. Status epilepticus
WHO definition
-Persistent seizures over a period of time- originally described
over a 30 min period as this was when decompensation occurs
and neuronal damage begins, or lack of recovery between
seizure episodes
-Now clinically accepted as seizures persisting for longer than 5
minutes, allowing for more rapid diagnosis and treatment, with
subsequent reduction in neuronal damage
35

36. 36
Classifications of SE
Generalised convulsive status epilepticus (GCSE)- can be tonic-
clonic, tonic or clonic
Partial or focal SE
Non-convulsive status epileptics (NCSE)- can also encompass
absence SE

37. Epidemiology
o Incidence- between 10 and 60 cases per 100,000 person/years.
The incidence is higher in poorer populations. It recurs in about a
third of patients
o Risk factors include age under 5 years or elderly age, genetic
predisposition, intellectual disability and structural brain
pathology
o Potential precipitants include drug withdrawal, intercurrent
illness, metabolic disturbance (e.g. hypoglycemia),
cerebrovascular event and alcohol intoxication or withdrawal
37

38. Cause of SE
Neurological: trauma, intracerebral haemorrhage, infarction,
tumours, cerebral infection (meningitis, encephalitis)
Drugs: poor compliance with anti-epileptic medication in
known epileptics, toxicity including tri-cyclic antidepressants,
flumazenil, cocaine; withdrawal e.g. from alcohol
38

39. Cause of SE--
Electrolyte disorders- hyponatraemia, hypoglycaemia,
hypocalcaemia, hypomagnesaemia
Eclampsia
Hepatic encephalopathy, uraemia
Infection- pyrexia is common cause for seizures in paediatric
population (called febrile seizures)
Pseudoseizures
39

40. Systemic effects of SE
Organ
system
Effect
CVS Sympathetic overdrive, tachycardia, arrhythmias
Initial increase in blood pressure and peripheral vascular resistance,
followed by normalization and possible hypotension
Respiratory
system
Increased respiratory rate and tidal volume
Respiratory acidosis and when combined with metabolic acidosis leads
to low pH on arterial blood gases
Increased pulmonary vascular resistance and pulmonary oedema
illustrated in animal studies
CNS •Increased cerebral metabolic rate, hyperthermia, intracranial
hypertension, raised intracranial pressure and cerebral oedema
Metabolic early: lactic acidosis, hyperglycaemia; late - hypoglycaemia
Endocrine Increased circulating catecholamines
Renal Rhabdomyolysis
Temperatur
e
Increased core temperature
Other Trauma secondary to seizure: fractures, dental damage 40

41. Treatment of acute status epilepticus
-Priorities of treatment in SE:
Airway?
Terminate seizure activity as soon as possible
Maintain cardiorespiratory function
Prevent injury
Avoid secondary medical complications
41

42. 42
- The National Institute for Clinical Excellence has recommended
the following strategy divided into different stages:
 1st Stage (0–10 min) Early Status
o Secure airway and resuscitate
o Administer oxygen
o Assess cardiorespiratory function
o Establish intravenous access

43. 43
 2nd Stage (0–30 min)
o Institute regular monitoring
o Consider possibility of non-epileptic status
o Emergency anti-epileptic drug treatment (AED)
o Emergency investigations (next slide)
o Administer 50ml of 50% dextrose and/or intravenous
thiamine if there is history of alcohol abuse or poor nutrition
o Correct acidosis if severe with bicarbonate (not necessary in
most cases)

44. Emergency investigations
o Arterial blood gases
o Biochemistry- blood glucose, renal, liver function, calcium,
magnesium
o Haematology- full blood count, clotting profile
o AED levels
o Venous blood sample and urine sample for toxicology screen
o Chest X-ray- aspiration
o CT scan/ LP
44

45. 45
 3rd Stage (0–60 min) Established Status
o Establish aetiology
o Alert anaesthetist and ICU
o Identify and treat any medical complications
o Pressor therapy if required

46. 46
 4th Stage (30–90 min) Refractory Status
o Transfer to ICU
o Establish intensive care and EEG monitoring (next slide)
o Initiate intracranial pressure monitoring if there is persistent
high intracranial pressure
o Initiate long-term maintenance AED therapy

47. Monitoring
o Regular neurological observations
o Heart rate, ECG, blood pressure measurements
o Temperature
o Arterial blood gas
o FBC, clotting, biochemistry
o Drug levels
o EEG required for refractory status epilepticus
47

48. Terminating seizure activity
 Premonitory stage
-Diazepam10–20 mg PR, repeat once 15 min later or midazolam 10
mg buccal
 Early status
-Lorazepam 0.1 mg/kg IV bolus, repeated once after 10–20 min
-Usual AED medication
48

49. Terminating seizure activity---
 Established status
-One of the following:
• Phenytoin infusion 15–18 mg/kg at rate of 50 mg/min
• Fosphenytoin infusion 15–20 mg phenytoin equivalents (PE)/kg at
rate of 50–100 mg PE/ min
• Phenobarbitone bolus 10–15 mg/kg at rate of 100 mg/min
49

50. Terminating seizure activity---
 Refractory status
-General anaesthesia with one of the following:
• Propofol 1–2 g/kg bolus, then 2–10 mg/kg per hour
• Midazolam 0.1–0.2 mg/kg bolus, then 0.05– 0.5 mg/kg per hour
• Thiopentone 3–5 mg/kg bolus, then 3–5 mg/kg per hour (reduce
rate after 2–3 days as fat stores deplete)
• Consider tapering dose after 12–24 hours after last known
seizure
50

51. Complications of SE
System Complications
CNS -Cerebral hypoxia, Cerebral oedema, Cerebral haemorrhage, Cerebral
venous thrombosis
CVS -Myocardial infarction, Hyper/hypotension, Arrhythmias, Cardiac arrest,
Cardiogenic shock
Respiratory
system
-Apnoea, Respiratory failure, Pneumonia, Pulmonary oedema
Metabolic
system
•Hyponatraemia
•Hypoglycaemia
•Hyperkalaemia
•Metabolic acidosis
•Acute tubular necrosis
•Acute hepatic necrosis
•Acute pancreatitis
Miscellaneous Disseminated intravascular coagulopathy
Rhabdomyolysis
Fractures
51

52. Prognosis
-The prognosis of patients with status epilepticus is related to the
aetiology, age, duration of seizures and prompt initiation of
treatment
-Overall mortality is approximately 20–30% rising with age
52

53. 3. Stroke
A stroke means that the blood supply
to a part of the brain is suddenly cut
off
A common cause of stroke is a blood
clot that forms in a brain
blood vessel (artery)
Blood supply to the brain comes mainly
from four blood vessels (arteries)- the
right and left carotid arteries and the
right and left vertebrobasilar arteries
53

54. 54
The area of brain affected and the extent of the damage depend
on which blood vessel is affected.
If you lose the blood supply from a main carotid artery then a
large area of your brain is affected, which can cause severe
symptoms or death

55. Types of stroke
55

56. Who is affected by stroke?
-Each year around 120,000 people in the UK have a first stroke and
about 30,000 have a recurrent stroke
-The largest cause of disability in the UK and 3rd most common
cause of death after heart disease and cancer
-Most cases occur in people aged over 65. Each year about 1 in 100
people over the age of 75 will have a stroke
-But a stroke can occur at any age - even in babies
56

57. Causes
 Haemorrhagic, embolic or thrombotic
 ‘Secondary’ stroke may occur with meningitis, bacterial
endocarditis, subarachnoid haemorrhage, and vasculitis
 Dissection and cerebral venous thrombosis need to be
considered, as anticoagulation is indicated for both (unless a
large infarct is established as there is an increased risk of
bleeding)
57

58. Causes--
-Dissection should be suspected in younger patients, often
presenting with severe headache or neck pain + Horner’s
syndrome + seizures after trauma or neck manipulation
 Cerebral venous thrombosis may mimic stroke, tumour,
subarachnoid haemorrhage, or meningo-encephalitis, and may
present with headache, seizures, focal signs, or obtundation
58

59. What are the symptoms of a stroke?
-Functions of different parts of the body are controlled by
different parts of the brain
-Symptoms vary depending on the part of the brain is affected
and on the size of the damaged area
Weakness of an arm, leg, or both- total paralysis of one side of
the body to mild clumsiness of one hand
Weakness and twisting of one side of the face ( drool saliva)
59

60. What are the symptoms of a stroke?--
Problems with balance, co-ordination, vision, speech,
communication or swallowing
Dizziness
Numbness in a part of the body
Headache
Confusion
Loss of consciousness (occurs in severe cases)
60

61. Investigation
Brain scan (CT scan or MRI scan)- determine the type of stroke
(ischaemic or haemorrhagic)
Blood tests- blood sugar level and cholesterol level
Chest X-ray and ECG to check for heart or lung conditions which
may be a cause of stroke (for example, atrial fibrillation)
Ultrasound scan of the carotid blood vessels
61

62. Treatment of stroke
To protect the penumbra with close attention to oxygenation,
hydration, tight glycaemic control, and avoidance of pyrexia
Blood pressure control is needed for severe hypertension
(e.g.>200/120mmHg) and for hypotension
62

63. Treatment of stroke---
Aspirin is given early for thrombotic stroke.
-Early anticoagulation probably benefits intracranial stenosis,
stroke-in evolution, complete vessel occlusion with minimal
deficit, and in low-risk patients with a high probability of
recurrence (secondary prevention)
63

64. Treatment of stroke---
For thrombolysis, reperfusion extent depends on aetiology with
basilar> middle cerebral artery > internal carotid, and embolic >
thrombotic
-Studies with rt PA (0.9mg/kg) given within 3hr of stroke onset
(and tight BP control) show favourable outcomes. However,
there was a 6-fold increase in haemorrhage (to 5.9%), of whom
60% died. This was more common in the elderly and with more
severe stroke.
64

65. Treatment of stroke---
Some centres perform intra-arterial or ultrasound-enhanced
thrombolysis
Neurosurgical intervention + decompression may be considered
for cerebellar haematoma, cerebellar infarction, and the
‘malignant middle cerebral artery syndrome’ (for massive
infarction on the non-dominant side)
65

66. Rehabilitation
 Aimed to maximise activity and quality of life following a stroke
 Good-quality rehabilitation is vital following a stroke and can
make a big difference to your eventual outcome
 Different specialists involved- physiotherapists, occupational
therapists, speech therapists, dieticians, psychologists, specialist
nurses and doctors
66

67. 4. Guillain–Barré syndrome
-Guillain -Barre syndrome (GBS) is an immune mediated disorder
which is associated with demyelination of peripheral nervous
system and progressive muscle weakness
-The syndrome is an immunopathy with an acute, often fulminant
evolution of demyelinating inflammatory polyradiculopathy
67

68. 68
-The basic disease process in GBS is immunologic
-Antibodies directed against peripheral nerve tissue damage
peripheral myelin and Schwann cells
-Axonal damage is thought to be secondary, but primary axonal
involvement has also been reported

69. 69
-Consequently GBS has been subdivided into different clinical
variants:
 Acute inflammatory demyelinating polyradiculoneuropathy
(AIDP)
 Acute motor axonal neuropathy (AMAN) &
 Acute motor sensory axonal neuropathy (AMSAN)
 Acute sensory neuronopathy
 Acute pandysautonomia
-About 95% of cases of Guillain-Barré syndrome are AIDP

70. 70
Epidemiology
-The incidence of typical Guillain-Barré syndrome in Europe is 1.2-
1.9 per 100,000
-There is an increased incidence in males. Peak ages are 15-35
years and 50-75 years

71. Risk factors
 History of Campylobacter Jejuni gastroenteritis or respiratory
infection from 1-3 weeks prior to the onset of weakness
 Vaccinations: live and dead vaccines have been implicated
 Malignancies: e.g., lymphomas, especially Hodgkin's disease
 Postpartum period: incidence decreases during pregnancy but
increases in the months after delivery.
71

72. Presentation
History
 Weakness:
– In 60% of cases, onset occurs approximately three weeks after a viral
illness
– The condition usually presents with an ascending pattern of progressive
symmetrical weakness, starting in the lower extremities
– Reaches a maximum severity two weeks after initial onset of symptoms
and usually stops progressing after five weeks
– Facial weakness, dysphasia or dysarthria (inability of articulating words)
may develop
– In severe cases, muscle weakness may lead to respiratory failure
72

73. 73
 Pain: neuropathic pain may develop, particularly in the legs.
Back pain may be another feature
 Reflexes: reduced or absent
 Sensory symptoms: these can include paraesthesiae and
sensory loss, starting in the lower extremities
 Autonomic symptoms: reduced sweating, reduced heat
tolerance, paralytic illeus and urine retention.

74. 74
Examination
-The following features may be present:
 Hypotonia
 Demonstrable altered sensation or numbness
 Reduced or absent reflexes
 Facial weakness- may be asymmetrical
 Autonomic dysfunction- fluctuations of HR and arrhythmias,
labile BP and variable temperature
 Respiratory muscle paralysis

75. Differential diagnosis
-Other causes of acute paralysis include:
Brain: stroke, brainstem compression, encephalitis
Spinal cord: cord compression, poliomyelitis, transverse myelitis
Peripheral nerve: vasculitis, lead poisoning, porphyria
Neuromuscular junction: myasthenia gravis, botulism
Muscle: hypokalaemia, polymyositis
75

76. • Botulism- Food poisoning from ingesting
botulin; not infectious; affects the CNS; can be
fatal if not treated promptly
76

77. Investigations
-Diagnosis is usually made on clinical grounds. However, the
following may be helpful:
Electrolytes- SIADH
Lumbar puncture- most patients have elevated CSF protein
Antibody screen- antibodies to peripheral and central nerves
may be present
Spirometry- FVC is a major determinant of the need for
admission to ICU and then the need for intubation.
77

78. Investigations--
Nerve conduction studies
-The most useful confirmatory test and are abnormal in 85% of
patients, even early on in the disease
-They should be repeated after two weeks if they are initially
normal
-A decrease to less than 20% of predicted normal is associated
with a poorer prognosis
ECG
78

79. Management
 Supportive
 Immunological
 Supportive:
o Airway & respiratory
o Deep vein thrombosis (DVT) prophylaxis: compression
stockings, LMWH
o Pain relief: may be required for neuropathic pain
o Psychological
o Rehabilitation
79

80. Management--
Airway & respiratory
-Around 30% of patients with GBS require ventilatory support.
Deterioration in respiratory function may be rapid and frequent
assessments should be made in all patients
-Clinical markers suggestive of the need for ventilatory support
include bulbar weakness, inability to lift the head, upper limb
weakness and tachypnoea
80

81. Management--
Admission to ICU: intubation and assisted ventilation may be
required
-Clinical indications for intubation and ventilation include:
Vital capacity < 1L or < 15 ml/kg
Maximum inspiratory pressure < 30cmH2O
Maximum expiratory pressure < 40cmH2O
Bulbar involvement with inability to cough, swallow and
protect the airway
Evidence of respiratory failure on ABG and autonomic
instability
81

82. Management--
 Immunological therapy
Plasma exchange
More improvement with plasma exchange than supportive care alone,
without a significant increase in serious adverse events
Plasmapheresis at 50ml/kg/day, 5 times, over 1-2 weeks within 4 weeks of
onset increases speed of recovery and improves neurological outcome
Significant increase in the risk of relapse during the first 6-12 months
82

83. Management---
However, after one year, full recovery was significantly more likely and severe
residual weakness less likely with plasma exchange
Intravenous immunoglobulin (IVIg):
In severe disease, intravenous immunoglobulin started within two weeks
from the onset accelerates recovery as much as plasma exchange
Significantly much more likely to be completed than plasma exchange
Giving intravenous immunoglobulin after plasma exchange did not confer
significant extra benefit
83

84. Management---
IVIg at 400mgkg/day for 5 days is as effective as
plasmapheresis, and there is no additional benefit to
combining the two therapies.
Corticosteroids: combined with other treatments (alone
affect the long-term outcome, and may even delay recovery)
84

85. Complications
-Possible complications include:
Persistent paralysis
Respiratory failure requiring mechanical ventilation
Hypotension or hypertension
Thromboembolism, pneumonia, skin breakdown
Cardiac arrhythmia
Ileus
Aspiration pneumonia
Urinary retention
Psychiatric problems- e.g., depression, anxiety
85

86. Prognosis
-With modern intensive care support, the outcome is excellent for
most patients. However, about 3% of patients die.
Neurological problems persist in up to 20% of patients (half of are
severely disabled)
About 10% of patients die from respiratory failure, pulmonary
emboli or infection
Mortality- due to severe autonomic instability or from the
complications of prolonged intubation and paralysis
86

87. Prognosis--
Poor prognosis is associated with rapid progression of
symptoms, advanced age and prolonged ventilation
High age, preceding diarrhoea, and degree of muscle dysfunction
at hospital admission and at one week are independently
associated with being unable to walk at four weeks, three
months, and six months respectively.
87

88. Thank you!!!
88