Guillain-Barré syndrome

Neurology

Clinicals - History

Fact Explanation
Weakness of the legs and arms Guillain-Barré syndrome (GBS) is a autoimmune disease affecting the peripheral nervous system (AIDP - acute inflammatory demyelinating polyradiculoneuropathy). It usually follows an infection. That infection/antigens trigger the production of antibodies. The cross reactivity between neural antigens and those antiganglioside antibodies due to molecular mimicry causes neuronal damage. The primary target is Schwann cell surface causing widespread myelin damage. Macrophage activation creates a variable degree of secondary axonal damage. Pathologically both humoral and cellular immune mechanisms are involved.
When the peripheral nervous system is affected, It produces a symmetrical motor weakness which usually starts from the lower limbs and ascends upwards. (Ascending flaccid paralysis)

Proximal muscles will involve earlier than the more distal ones. Patient may complain of difficulty in rising up from sitting position or climbing stairs. The symptoms are bilateral and reach their peak by the second week.
Though the weakness usually affect the lower limbs, it progresses rapidly (usually over periods of hours to days) to affect trunk and bilateral upper limbs too. Therefore severity may range from mild weakness to complete tetraplegia. Patient may complain this as a generalized fatigue.
Acute inflammatory demyelinating polyradiculoneuropathy is the most common subtype of GBS.(90%) So, this symptom is the most common one among all others.
Descending weakness is a rare but occurs in some sub types such as Miller Fisher syndrome and pharyngeal-cervical-brachial sub type. defined by rapidly progressive oropharyngeal and cervicobrachial weakness associated with areflexia in the upper limbs. Serial nerve conduction studies suggest that PCB represents a localised subtype of Guillain-Barré syndrome characterised by axonal rather than demyelinating neuropathy. This variant is often associated with IgG anti GT1a.
Weakness of the legs and arms
Guillain-Barré syndrome (GBS) is a autoimmune disease affecting the peripheral nervous system (AIDP - acute inflammatory demyelinating polyradiculoneuropathy). It usually follows an infection. That infection/antigens trigger the production of antibodies. The cross reactivity between neural antigens and those antiganglioside antibodies due to molecular mimicry causes neuronal damage. The primary target is Schwann cell surface causing widespread myelin damage. Macrophage activation creates a variable degree of secondary axonal damage. Pathologically both humoral and cellular immune mechanisms are involved.
When the peripheral nervous system is affected, It produces a symmetrical motor weakness which usually starts from the lower limbs and ascends upwards. (Ascending flaccid paralysis)

Proximal muscles will involve earlier than the more distal ones. Patient may complain of difficulty in rising up from sitting position or climbing stairs. The symptoms are bilateral and reach their peak by the second week.
Though the weakness usually affect the lower limbs, it progresses rapidly (usually over periods of hours to days) to affect trunk and bilateral upper limbs too. Therefore severity may range from mild weakness to complete tetraplegia. Patient may complain this as a generalized fatigue.
Acute inflammatory demyelinating polyradiculoneuropathy is the most common subtype of GBS.(90%) So, this symptom is the most common one among all others.
Descending weakness is a rare but occurs in some sub types such as Miller Fisher syndrome and pharyngeal-cervical-brachial sub type. defined by rapidly progressive oropharyngeal and cervicobrachial weakness associated with areflexia in the upper limbs. Serial nerve conduction studies suggest that PCB represents a localised subtype of Guillain-Barré syndrome characterised by axonal rather than demyelinating neuropathy. This variant is often associated with IgG anti GT1a.
Numbness or tingling Sensory symptoms often precede the weakness. Most patients with AIDP complains of mild sensory involvement. But in acute motor sensory axonal neuropathy (AMSAN), another subtype of GBS, sensory axons are mainly involved, making sensory involvements such as numbness, tingling and sensory impairments predominant in toes and fingertips. These symptoms are generally benign, and tend to progress upward, although they usually do not extend beyond the wrists or ankles.

Acute motor sensory axonal neuropathy (AMSAN) is a sub type characterized by acute onset of distal weakness, loss of deep tendon reflexes and sensory symptoms. Mildly reduced nerve conduction velocities combined with a marked reduction of muscle action and sensory nerve action potentials are the nerve conduction test results. In severe forms, respiratory and bulbar symptoms will occur. Primary axonal degeneration takes place in this subtype too. But it has a poorer prognosis.
Numbness or tingling
Sensory symptoms often precede the weakness. Most patients with AIDP complains of mild sensory involvement. But in acute motor sensory axonal neuropathy (AMSAN), another subtype of GBS, sensory axons are mainly involved, making sensory involvements such as numbness, tingling and sensory impairments predominant in toes and fingertips. These symptoms are generally benign, and tend to progress upward, although they usually do not extend beyond the wrists or ankles.

Acute motor sensory axonal neuropathy (AMSAN) is a sub type characterized by acute onset of distal weakness, loss of deep tendon reflexes and sensory symptoms. Mildly reduced nerve conduction velocities combined with a marked reduction of muscle action and sensory nerve action potentials are the nerve conduction test results. In severe forms, respiratory and bulbar symptoms will occur. Primary axonal degeneration takes place in this subtype too. But it has a poorer prognosis.
Pain in affected lims Pain usually proceeds the weakness in some patients and raised with movements. It is severe, deep, aching or cramping in nature and involves the affected muscles or back. It gets worsen at night. The origin of the pain is either nociceptive or neuropathic. Pain in affected lims
Pain usually proceeds the weakness in some patients and raised with movements. It is severe, deep, aching or cramping in nature and involves the affected muscles or back. It gets worsen at night. The origin of the pain is either nociceptive or neuropathic.
Muscle pain Cramping muscle pain and local muscle tenderness are uncommon findings of GBS. They are thought to be caused by inflammation of surrounding nerves. Muscle pain
Cramping muscle pain and local muscle tenderness are uncommon findings of GBS. They are thought to be caused by inflammation of surrounding nerves.
Difficulty in swallowing The ascending disease progression eventually affects nuclei of cranial nerves IX, X, XI and XII or below (lower motor neuron lesion). Oropharyngeal dysphagia arises from abnormalities of muscles, nerves or structures of the oral cavity, pharynx, and upper esophageal sphincter which are supplied by the cranial nerves mentioned above. Difficulty in swallowing
The ascending disease progression eventually affects nuclei of cranial nerves IX, X, XI and XII or below (lower motor neuron lesion). Oropharyngeal dysphagia arises from abnormalities of muscles, nerves or structures of the oral cavity, pharynx, and upper esophageal sphincter which are supplied by the cranial nerves mentioned above.
Drooling of saliva This is due to difficulty in swallowing (Oropharyngeal dysphagia). Facial, oropharyngeal and oculomotor muscles are affected as well which may result in a drooling. This mimics Bell's palsy. Drooling of saliva
This is due to difficulty in swallowing (Oropharyngeal dysphagia). Facial, oropharyngeal and oculomotor muscles are affected as well which may result in a drooling. This mimics Bell's palsy.
Shortness of breath Shortness of breath or shortness of breath on exertion occurs late in the course. This suggests diaphragmatic and intercostal muscle weakness due to phrenic nerve and intercostal nerves involvement respectively.
Shortness of breath is also attributed to the bulbar weakness and Oropharyngeal dysphagia.

In acute motor axonal neuropathy, early and severe respiratory involvements are common. It is a subtype that cause motor symptoms only. There is no sensory involvement. Pathology is primary axonal degeneration. This subtype commonly affect children and young adults. Campylobacter jejuni serology is positive up to 75% of cases. anti-GM and anti GD1a antibodies are often positive.
Shortness of breath
Shortness of breath or shortness of breath on exertion occurs late in the course. This suggests diaphragmatic and intercostal muscle weakness due to phrenic nerve and intercostal nerves involvement respectively.
Shortness of breath is also attributed to the bulbar weakness and Oropharyngeal dysphagia.

In acute motor axonal neuropathy, early and severe respiratory involvements are common. It is a subtype that cause motor symptoms only. There is no sensory involvement. Pathology is primary axonal degeneration. This subtype commonly affect children and young adults. Campylobacter jejuni serology is positive up to 75% of cases. anti-GM and anti GD1a antibodies are often positive.
Double vision It is usually the result of impaired function of the extraocular muscles due to affected cranial nerves (III, IV, and VI) which innervate them.
This can be accompanied with ataxia, areflexia and bilateral ophthalmoplegia which are collectively called as Miller Fisher syndrome.
Miller Fisher syndrome is a rare sub type. Accounting for about 5% of GBS cases, it manifests as a descending paralysis. 96% of patients with Miller Fisher syndrome are positive for anti-GQ1b antibodies.
Double vision
It is usually the result of impaired function of the extraocular muscles due to affected cranial nerves (III, IV, and VI) which innervate them.
This can be accompanied with ataxia, areflexia and bilateral ophthalmoplegia which are collectively called as Miller Fisher syndrome.
Miller Fisher syndrome is a rare sub type. Accounting for about 5% of GBS cases, it manifests as a descending paralysis. 96% of patients with Miller Fisher syndrome are positive for anti-GQ1b antibodies.
Faintishness/ collapse Sympathetic and parasympathetic system dysfunction is a common finding in GBS. Wide fluctuations in blood pressure, orthostatic hypotension and cardiac arrhythmias can cause sudden collapse or faintishness.
Acute autonomic neuropathy is the rarest form of GBS in which the autonomic symptoms specially cardiovascular are predominant. The mechanism fo this sub type has not been clarified.Autoantibodies to nicotine ganglionic acetylcholine receptors likely have a pathogenic role. The recovery is slow and may be incomplete.
Faintishness/ collapse
Sympathetic and parasympathetic system dysfunction is a common finding in GBS. Wide fluctuations in blood pressure, orthostatic hypotension and cardiac arrhythmias can cause sudden collapse or faintishness.
Acute autonomic neuropathy is the rarest form of GBS in which the autonomic symptoms specially cardiovascular are predominant. The mechanism fo this sub type has not been clarified.Autoantibodies to nicotine ganglionic acetylcholine receptors likely have a pathogenic role. The recovery is slow and may be incomplete.
Urinary symptoms Urinary retention may occur in up to one third of
patients. Bladder dysfunction is particularly common
in GBS secondary to sacral parasympathetic nerve and pudendal motor nerve dysfunction. They are consisted of nocturnal or diurnal urinary frequency, sensation of urgency, urinary incontinence and enuresis and difficulty in voiding including hesitation and prolongation.
Urinary symptoms
Urinary retention may occur in up to one third of
patients. Bladder dysfunction is particularly common
in GBS secondary to sacral parasympathetic nerve and pudendal motor nerve dysfunction. They are consisted of nocturnal or diurnal urinary frequency, sensation of urgency, urinary incontinence and enuresis and difficulty in voiding including hesitation and prolongation.
Proceeding events Acute infectious illnesses are well-known antecedent events in two thirds of patients who have GBS. Respiratory tract infection or gastroenteritis are the commonest. So,the most common symptoms reported before the onset of GBS are fever, caugh, soar throat, abdominal pain or loose stools. Campylobacteriosis is the most common precipitant in GBS. Other antecedent infections include cytomegalovirus, HIV, Epstein-Barr virus, and varicellazoster virus.
Vaccinations, surgical procedures, and trauma are the other common triggering conditions. This particular illness or event usually occur 1-3 weeks prior to the onset of weakness.
Proceeding events
Acute infectious illnesses are well-known antecedent events in two thirds of patients who have GBS. Respiratory tract infection or gastroenteritis are the commonest. So,the most common symptoms reported before the onset of GBS are fever, caugh, soar throat, abdominal pain or loose stools. Campylobacteriosis is the most common precipitant in GBS. Other antecedent infections include cytomegalovirus, HIV, Epstein-Barr virus, and varicellazoster virus.
Vaccinations, surgical procedures, and trauma are the other common triggering conditions. This particular illness or event usually occur 1-3 weeks prior to the onset of weakness.

Clinicals - Examination

Fact Explanation
Signs of autonomic dysfunction Autonomic disturbance is seen in more than 50%. It usually manifests as tachycardia but more serious autonomic nervous system dysfunction may occur, including life-threatening arrhythmias, hypotension, hypertension, and gastrointestinal dysmotility. Signs of autonomic dysfunction
Autonomic disturbance is seen in more than 50%. It usually manifests as tachycardia but more serious autonomic nervous system dysfunction may occur, including life-threatening arrhythmias, hypotension, hypertension, and gastrointestinal dysmotility.
Facial weakness Sudden weakness or paralysis on face that causes it to droop. Ptosis and drooling are also accompanied. This is due to facial nerve paralysis along with oropharyngeal and oculomotor nerves. Facial weakness is usually unilateral and rarely bilateral. Facial weakness
Sudden weakness or paralysis on face that causes it to droop. Ptosis and drooling are also accompanied. This is due to facial nerve paralysis along with oropharyngeal and oculomotor nerves. Facial weakness is usually unilateral and rarely bilateral.
Opthalmoplegia Oculomotor nerve involvement in GBS causes weakness in eye movements due to extra occular muscle paresis. Bilateral ophthalmoplegia is common in miller fisher sub type of GBS. Opthalmoplegia
Oculomotor nerve involvement in GBS causes weakness in eye movements due to extra occular muscle paresis. Bilateral ophthalmoplegia is common in miller fisher sub type of GBS.
Dysarthria Slurring of speech can be observed due to bulbar palsy. Paralysis of oro pharyngeal musculature causes deficiency in articulation and slow rate of speech. Dysarthria
Slurring of speech can be observed due to bulbar palsy. Paralysis of oro pharyngeal musculature causes deficiency in articulation and slow rate of speech.
Slurring of speech Slurring of speech can be observed due to bulbar palsy. Paralysis of oro pharyngeal musculature causes deficiency in articulation and slow rate of speech. Slurring of speech
Slurring of speech can be observed due to bulbar palsy. Paralysis of oro pharyngeal musculature causes deficiency in articulation and slow rate of speech.
Poor respiratory effort When the ascending paralysis affects the phrenic and intercostal nerves, diaphragmatic and intercostal muscle weakness take place. This weakness along with bulbar weakness and oropharyngeal dysphagia results in poor respiratory effort. Poor respiratory effort
When the ascending paralysis affects the phrenic and intercostal nerves, diaphragmatic and intercostal muscle weakness take place. This weakness along with bulbar weakness and oropharyngeal dysphagia results in poor respiratory effort.
Single Breath count The patients is asked to count in normal speaking voice following a maximum effort of inspiration. Studies have suggested that SBC correlates with standard measures of pulmonary function. If the patient can count to "10" on one breath they likely have a forced vital capacity of about 1000 ml, if they can count to "25" then the vital capacity can be estimated at about 2000 ml. Single Breath count
The patients is asked to count in normal speaking voice following a maximum effort of inspiration. Studies have suggested that SBC correlates with standard measures of pulmonary function. If the patient can count to "10" on one breath they likely have a forced vital capacity of about 1000 ml, if they can count to "25" then the vital capacity can be estimated at about 2000 ml.
Limb weakness Weakness or reduced power of the distal limb muscles is the striking feature of GBS. This weakness initially affect the lower limb before rapidly progress to the trunk and upper limb within hours to days due to ascending acute inflammatory demyelinating polyradiculoneuropathy (AIDP). AIDP usually affects proximal muscles. Patient may show difficulty when he/she is asked to stand from a sitting position. Limb weakness
Weakness or reduced power of the distal limb muscles is the striking feature of GBS. This weakness initially affect the lower limb before rapidly progress to the trunk and upper limb within hours to days due to ascending acute inflammatory demyelinating polyradiculoneuropathy (AIDP). AIDP usually affects proximal muscles. Patient may show difficulty when he/she is asked to stand from a sitting position.
Areflexia Complete areflexia often occurs in affected limbs. Reflexes sometimes may be reduced. Areflexia peaks within 4 weeks.
Areflexia is manifested in an ascending pattern. First it affects lower limb deep tendon reflexes (Ankle and knee jerks) and then with the progression it may affect the upperlimb reflexes such as biceps and triceps jerks. It is common to several subtypes such as acute inflammatory demyelinating polyradiculoneuropathy and Miller fisher syndrome. Deep tendon reflexes may be preserved in acute motor axonal neuropathy.
Areflexia
Complete areflexia often occurs in affected limbs. Reflexes sometimes may be reduced. Areflexia peaks within 4 weeks.
Areflexia is manifested in an ascending pattern. First it affects lower limb deep tendon reflexes (Ankle and knee jerks) and then with the progression it may affect the upperlimb reflexes such as biceps and triceps jerks. It is common to several subtypes such as acute inflammatory demyelinating polyradiculoneuropathy and Miller fisher syndrome. Deep tendon reflexes may be preserved in acute motor axonal neuropathy.
Dysesthesia Mild sensory impairment, tingling or numbness are not uncommon in acute inflammatory demyelinating polyradiculoneuropathy. These signs usually do not go above wrist of ankle. These sensory symptoms are more predominant in acute motor sensory axonal neuropathy. Dysesthesia
Mild sensory impairment, tingling or numbness are not uncommon in acute inflammatory demyelinating polyradiculoneuropathy. These signs usually do not go above wrist of ankle. These sensory symptoms are more predominant in acute motor sensory axonal neuropathy.

Investigations - Diagnosis

Fact Explanation
Full blood count Has a less value in diagnosis. But it is used to exclude competing diagnoses and assess functional status and prognosis. Full blood count
Has a less value in diagnosis. But it is used to exclude competing diagnoses and assess functional status and prognosis.
Creatine phosphokinase (CPK) Creatine phosphokinase is done to exclude several differential diagnoses such as myopathies or systemic inflammatory conditions. Creatine phosphokinase (CPK)
Creatine phosphokinase is done to exclude several differential diagnoses such as myopathies or systemic inflammatory conditions.
Nerve conduction tests Nerve conduction studies helps to establish the diagnosis of GBS and to identify the GBS subtype. Nerve conduction signs of GBS can include nerve conduction slowing, prolongation of the distal latencies and prolongation or absence of the F-waves of the motor nerves. Sensory nerve conduction studies help to differentiate sub types. Nerve conduction tests
Nerve conduction studies helps to establish the diagnosis of GBS and to identify the GBS subtype. Nerve conduction signs of GBS can include nerve conduction slowing, prolongation of the distal latencies and prolongation or absence of the F-waves of the motor nerves. Sensory nerve conduction studies help to differentiate sub types.
Electromyography (EMG) EMG has a limited value. Reduction in motor unit recruitment and absence of denervation help to support the suggestion of a demyelination though they can not be used to differentiate GBS from wallerian degeneration. Electromyography (EMG)
EMG has a limited value. Reduction in motor unit recruitment and absence of denervation help to support the suggestion of a demyelination though they can not be used to differentiate GBS from wallerian degeneration.
Cerebrospinal fluid (CSF) analysis Elevated CSF protein (>400 mg/L) with normal cell count (albumino cytological dissociation) is characteristic for GBS. Mononuclear cell count may be either normal or less than 50 cells/mm. The CSF is normal in the first week of the illness but protein level rises significantly during the second week.
Around 10% will not have a protein elevation and this includes patients with the Miller-Fisher variant.
Cerebrospinal fluid (CSF) analysis
Elevated CSF protein (>400 mg/L) with normal cell count (albumino cytological dissociation) is characteristic for GBS. Mononuclear cell count may be either normal or less than 50 cells/mm. The CSF is normal in the first week of the illness but protein level rises significantly during the second week.
Around 10% will not have a protein elevation and this includes patients with the Miller-Fisher variant.
MRI scan This is not usually done. But contrast-enhanced spinal MR imaging can be used as a supplementary diagnostic modality in the diagnosis specially when the clinical and electrophysiologic findings are equivocal. Marked enhancement of nerve roots of
the conus medullaris and cauda equina have been reported may play a role in diagnosing GBS.
MRI scan
This is not usually done. But contrast-enhanced spinal MR imaging can be used as a supplementary diagnostic modality in the diagnosis specially when the clinical and electrophysiologic findings are equivocal. Marked enhancement of nerve roots of
the conus medullaris and cauda equina have been reported may play a role in diagnosing GBS.

Investigations - Management

Fact Explanation
Peak flow meter Peak flow meter measures peak expiratory flow rate (PEFR) which is used in assessing the respiratory function. It is readily available and reproducible. Peak expiratory flow (PEF) is the maximal flow achieved during the maximally forced expiration initiated at full inspiration, measured in liters per minute or in liters per second.
A fall in the peak expiratory flow rate to one quarter
the predicted value but record normal Paco2 values imply that it's safe to withhold assisted ventilation. So, serial measurement of PEFR in Guillain Barre syndrome to predict the involvement of respiratory muscle is clinically important to give warning of the hypoventilation and need for ventilator support.
Peak flow meter
Peak flow meter measures peak expiratory flow rate (PEFR) which is used in assessing the respiratory function. It is readily available and reproducible. Peak expiratory flow (PEF) is the maximal flow achieved during the maximally forced expiration initiated at full inspiration, measured in liters per minute or in liters per second.
A fall in the peak expiratory flow rate to one quarter
the predicted value but record normal Paco2 values imply that it's safe to withhold assisted ventilation. So, serial measurement of PEFR in Guillain Barre syndrome to predict the involvement of respiratory muscle is clinically important to give warning of the hypoventilation and need for ventilator support.
Spirometry FEV1/FVC ratio represents the proportion of a person's vital capacity that they are able to expire in the first second of expiration. That value is below normal/ reduces if respiratory function is getting compromised. Spirometry
FEV1/FVC ratio represents the proportion of a person's vital capacity that they are able to expire in the first second of expiration. That value is below normal/ reduces if respiratory function is getting compromised.

Management - Supportive

Fact Explanation
Deep vein thrombosis prophylaxis Deep vein thrombosis prophylaxis should be given to all patients due to increased risk. Subcutaneous anticoagulation with fractionated or unfractionated heparin and graduated compression stockings should be instituted until the patient is able to walk independently. Deep vein thrombosis prophylaxis
Deep vein thrombosis prophylaxis should be given to all patients due to increased risk. Subcutaneous anticoagulation with fractionated or unfractionated heparin and graduated compression stockings should be instituted until the patient is able to walk independently.
Analgesia As the origin of the pain is either nociceptive or neuropathic, it is difficult to control it with simple analgesics or nonsteroidal anti-inflammatory drugs. Sometimes even opioids may not provide adequate pain relief. Sometimes opioids may worsen some autonomic symptoms instead. Some studies shows that gabapentin and carbamazepine are beneficial for some patients with GBS. If this pain tends to continue as a chronic pain, Tricyclic antidepressants and tramadol may be added for the chronic/ long term management. Analgesia
As the origin of the pain is either nociceptive or neuropathic, it is difficult to control it with simple analgesics or nonsteroidal anti-inflammatory drugs. Sometimes even opioids may not provide adequate pain relief. Sometimes opioids may worsen some autonomic symptoms instead. Some studies shows that gabapentin and carbamazepine are beneficial for some patients with GBS. If this pain tends to continue as a chronic pain, Tricyclic antidepressants and tramadol may be added for the chronic/ long term management.
Respiratory assistance Patient should be closely monitored regarding the respiration. This includes maximal inspiratory pressures and vital capacities. If vital capacity is less than 20 mL/kg or maximal inspiratory pressure is worse than -30 cmH2O, he/ she must be electively intubated ideally in an intensive care setting.

The duration of ventilation may lengthy. If it exceeds 2 weeks, tracheostomy should be considered. Weaning should be guided by serial lung function monitoring and assessment of strength.
Respiratory assistance
Patient should be closely monitored regarding the respiration. This includes maximal inspiratory pressures and vital capacities. If vital capacity is less than 20 mL/kg or maximal inspiratory pressure is worse than -30 cmH2O, he/ she must be electively intubated ideally in an intensive care setting.

The duration of ventilation may lengthy. If it exceeds 2 weeks, tracheostomy should be considered. Weaning should be guided by serial lung function monitoring and assessment of strength.
Haemodynamic monitoring This should be started as early as possible. Pulse and blood pressure which tends to fluctuate should be monitored frequently or with a multi-monitor. This should be ideally continued until the patient is off ventilator support and have begun to recover. Prolonged hypotensive state should be managed with fluid bolus, whereas hypertension should be treated with short acting antihypertensives such as labetalol. Haemodynamic monitoring
This should be started as early as possible. Pulse and blood pressure which tends to fluctuate should be monitored frequently or with a multi-monitor. This should be ideally continued until the patient is off ventilator support and have begun to recover. Prolonged hypotensive state should be managed with fluid bolus, whereas hypertension should be treated with short acting antihypertensives such as labetalol.
Nutrition Nasogastric or gastric tube feeding should be considered early. High energy and high protein diet is helpful to prevent muscle wasting and to assist respiratory weaning. Continuous enteral feeding is better tolerated than bolus feeding. Nutrition
Nasogastric or gastric tube feeding should be considered early. High energy and high protein diet is helpful to prevent muscle wasting and to assist respiratory weaning. Continuous enteral feeding is better tolerated than bolus feeding.
Positioning Patient's position on bed should be changed time to time in order to prevent pressure sores with prolonged bedridden state. Positioning
Patient's position on bed should be changed time to time in order to prevent pressure sores with prolonged bedridden state.
Rehabilitation Following the acute state, patient should be managed in a multidisciplinary approach to focus on improving independence including training on activities of daily living. This includes physiotherapy, occupational therapy and speech therapy. Rehabilitation
Following the acute state, patient should be managed in a multidisciplinary approach to focus on improving independence including training on activities of daily living. This includes physiotherapy, occupational therapy and speech therapy.
Physical therapy Patient should be involved in daily range of movement exercises. This helps to prevent disuse atrophy and contractures. This should be followed by active muscle strengthening exercises. Physiotherapists assist to correct functional movements. physiotherapy is useful in regaining strength, endurance, and gait quality. Ankle-foot orthosis can be used for lasting foot drop. A wheelchair should be supplied as an early aid to improve activities of daily living. Physical therapy
Patient should be involved in daily range of movement exercises. This helps to prevent disuse atrophy and contractures. This should be followed by active muscle strengthening exercises. Physiotherapists assist to correct functional movements. physiotherapy is useful in regaining strength, endurance, and gait quality. Ankle-foot orthosis can be used for lasting foot drop. A wheelchair should be supplied as an early aid to improve activities of daily living.
Speech and language therapy Speech and language therapists help regain speaking and swallowing abilities, This is particularly useful in patients who were intubated. These patients are those who were suffering from severe oropharyngeal weakness in acute stage. Speech and language therapy
Speech and language therapists help regain speaking and swallowing abilities, This is particularly useful in patients who were intubated. These patients are those who were suffering from severe oropharyngeal weakness in acute stage.
Education and counselling of the patient and family Even on discharge patient may suffer several disabilities. Long term disability brings some psychological issues such as mild depression and mental fatigue.
Caregivers may anxious or worried about the special care they should give, inability to return to driving and work, financial constraints and issues regarding
marital stress.
So, both parties should be thoroughly educated regarding the disease, home care and prognosis. Counselling should be applied if needed.
Education and counselling of the patient and family
Even on discharge patient may suffer several disabilities. Long term disability brings some psychological issues such as mild depression and mental fatigue.
Caregivers may anxious or worried about the special care they should give, inability to return to driving and work, financial constraints and issues regarding
marital stress.
So, both parties should be thoroughly educated regarding the disease, home care and prognosis. Counselling should be applied if needed.

Management - Specific

Fact Explanation
Immunotherapy Immunotherapy comprises intravenous immunoglobulins or plasma exchange. Both have been shown to be equally efficacious. Immunotherapy
Immunotherapy comprises intravenous immunoglobulins or plasma exchange. Both have been shown to be equally efficacious.
Plasmapheresis Plasmapheresis removes circulating antigen -antibody complexes which initiate the disease progression. It has been proven to reduce the time for recovery, and the need and duration of ventilation. Plasmapheresis is more effective in severe disease when is used within the first week of symptom onset. Usually four plasmapheresis sessions are needed for severe disease. Two sessions will be sufficient for mild disease. Plasmapheresis
Plasmapheresis removes circulating antigen -antibody complexes which initiate the disease progression. It has been proven to reduce the time for recovery, and the need and duration of ventilation. Plasmapheresis is more effective in severe disease when is used within the first week of symptom onset. Usually four plasmapheresis sessions are needed for severe disease. Two sessions will be sufficient for mild disease.
Intravenous immunoglobulin (IV Ig) IV Ig is a blood product which contains the pooled, polyvalent, IgG antibodies extracted from the plasma of donors. In GBS,it is recommended to start IV Ig within 2 weeks of symptom onset. The usual dose is 0.4 g per kg per day for 5 days.
IG blocks Fc receptors on macrophages preventing antibody targeted attachment on Schwann cell membrane and myelin or on axolemma. The usage of it hastens recovery and reduces long-term morbidity. The complications of immunoglobulin therapy is low than plasmapheresis. IV Ig is contraindicated in IgA deficiency and renal failure.
Intravenous immunoglobulin (IV Ig)
IV Ig is a blood product which contains the pooled, polyvalent, IgG antibodies extracted from the plasma of donors. In GBS,it is recommended to start IV Ig within 2 weeks of symptom onset. The usual dose is 0.4 g per kg per day for 5 days.
IG blocks Fc receptors on macrophages preventing antibody targeted attachment on Schwann cell membrane and myelin or on axolemma. The usage of it hastens recovery and reduces long-term morbidity. The complications of immunoglobulin therapy is low than plasmapheresis. IV Ig is contraindicated in IgA deficiency and renal failure.
Corticosteroids Though oral steroids are recommended in some studies, some studies say they are not beneficial and may even be harmful. It may cause inhibition of the macrophage repair process. Intravenous corticosteroids also do not have any significant short- or long-term benefits. Corticosteroids
Though oral steroids are recommended in some studies, some studies say they are not beneficial and may even be harmful. It may cause inhibition of the macrophage repair process. Intravenous corticosteroids also do not have any significant short- or long-term benefits.
Treatment setting Diagnosed GBS patients should be admitted to a hospital for close monitoring. Patients with respiratory insufficiency or autonomic dysfunction with cardiovascular complications should be continuously monitored in an emergency care setting. If ventilatory support is required, patient should be sent to intensive care unit. Treatment setting
Diagnosed GBS patients should be admitted to a hospital for close monitoring. Patients with respiratory insufficiency or autonomic dysfunction with cardiovascular complications should be continuously monitored in an emergency care setting. If ventilatory support is required, patient should be sent to intensive care unit.

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