Guillian Baare Syndrome

8/14/2019 Guillian Baare Syndrome

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GUILLIAN BAARE

SYNDROME

Mr. JEO THOMAS

1ST M.sc NURSING

SCON







ANATOMY OF NEURON



ANATOMY



MYELIN SHEATH





DEFINITION

Guillain-Barre syndrome is a rareautoimmune disorder of theperipheral nervous system. GBS isa demyelinating disease, meaningthat segments of myelin arestripped from their insulatingposition around nerves, reducing

the propagation of electricalnerve impulses.This causes loss of reflexes, muscle weakness, andtemporary paralysis (loss of

muscle strength).



DEFINITION

Guillain-Barré syndrome is anautoimmune attack of theperipheral nerve myelin. Theresult is acute, rapid segmentaldemyelination of peripheralnerves and some cranial nerves,producing ascending weakness

with dyskinesia (inability toexecute voluntary movements),hyporeflexia, and paresthesias

(numbness).



INCIDENCE

vThe annual incidence of Guillain-Barréis 0.4-4.0 cases perpopulation of 100,000

vEighty-five percent of patientsrecover with minimal residualsymptoms.

vDeath occurs in 3% to 8% of cases,

resulting from respiratory failure,autonomic dysfunction, sepsis, orpulmonary emboli.

vIt is slightly more common in menthan women, and can affect



ETIOLOGY

•

Guillain-Barre syndrome is anautoimmune disorder (the body'simmune system attacks itself).

• Exactly what triggers Guillain-

Barre syndrome is unknown.

• It often follows a minor infection,usually a lung infection or

gastrointestinal infection.Usually, signs of the originalinfection have disappearedbefore the symptoms of Guillain-

Barre begin

http://www.nlm.nih.gov/medlineplus/ency/article/000816.htm




Common cause•

Campylobacter jejuni, abacterium that appears tocause the most commonly

reported infection precedingGBS, is widely prevalent inthe gastrointestinal tracts of many animals, notablycattle and poultry, swine,

sheep, and even in pets







CLASSIFICATIONvAcute inflammatory

demyelinatingpolyneuropathy (AIDP)

vAcute motor axonalneuropathy (AMAN)

vAcute motor sensory axonalneuropathy (AMSAN)

vMiller Fisher syndrome

(MFS)



Acute inflammatory demyelinatingpolyneuropathy (AIDP)

• It is the most common form of GBS,and the term is often usedsynonymously with GBS. It iscaused by an auto-immuneresponse directed againstSchwann cell membranes.

• Most common variant, 85% of cases

• Primarily Motor• Generally preceded by bacterail or

viral infection

• Symptoms generally resolve with



Acute Motor Axonal Neuropathy(AMAN)

• Motor only with early and severerespiratory involvement,primary axonal degeneration

• More prevalent amongst pediatricage groups

• Up to 75% positive for C. jejuni

serology• Characterized by a rapidly

progressive weakness, ensuing

respiratory failure, and good





Miller Fisher Variant

• Triad: opthalmoplegia, sensory ataxia,areflexia

• 5% of all cases

• Patients may also have mild limbweakness, ptosis, facial palsy, orbulbar palsy.

• The ataxia tends to be out of proportionto the degree of sensory loss.

• Recovery generally occurs within 1-3

months

th h i l



pathophysiologyPrecipitating factors:c.jejuni,epsteinbarr

virus

Cellular and humoral immune

mechanisms activates.infectious agents are thought to induce

antibody production against specific

gangliosides and glycolipids, such asGM1 and GD1b, distributed throughoutthe myelin in the peripheral nervoussystem.



The virulence of organism is thought tobe based on the presence of specificantigens in its capsule that are

shared with nerves.

Immune responses directed against thecapsular components produceantibodies that cross-react withmyelin to cause demyelination.

Results in defects in the propagation of electrical nerve impulses, with eventualconduction block and flaccid paralysis. Insome patients with severe disease, asecondary consequence of the severe

inflammation is axonal disruption and loss.





DAMAGED MYELIN



CLINICAL MANIFESTATIONAscending weakness usually

beginning in lower extremities andspreading rapidly to upperextremities and trunk and evenface.

Paresthesia: tingling sensation mayoccur at early stage of disease.

Three phases : Initial phase

Plateau phase

Recovery phase



Weakness

– The classic clinical picture of weakness

is ascending and symmetrical innature. The lower limbs are usuallyinvolved before the upper limbs.Proximal muscles may be involvedearlier than the more distal ones.

Trunk, bulbar, and respiratory musclescan be affected as well.

– Weakness develops acutely andprogresses over days to weeks.

Severity may range from mildweakness to complete tetraplegia withventilatory failure. Peak deficits arereached by 4 weeks after the initialdevelopment of symptoms.The

progression of symptoms beyond that



Sensory changes

–Most patients complain of paresthesias, numbness, orsimilar sensory changes.Sensory symptoms oftenprecede the weakness. Theyare frequently ascending innature and are morepronounced in a distaldistribution.

–

Sensory symptoms are usually



Cranial nerve involvement

– Cranial nerve involvement isobserved in 45-75% of patientswith GBS. Common complaintsmay include the following:

• Facial droop

• Diplopias

• Dysarthria

• Dysphagia

– Facial and oropharyngeal weaknessusually appears after the trunk and limbs are affected.

PAIN



PAIN – Most patients complain of back and leg

pain, often described as aching or

throbbing in nature. The mechanismof pain is thought to be inflamednerve roots. Dysesthesias frequentlyare described as burning, tingling, orshock like sensations and are often

more prevalent in the lowerextremities than in the upperextremities. Other pain syndromes inGBS include the following:

• Myalgic complaints, with cramping andlocal muscle tenderness

• Visceral pain• Pain associated with conditions of

immobility (eg, pressure nerve palsies,decubitus ulcers)

– The intensity of pain on admission

correlates poorly with neurologic



Autonomic changes

– Autonomic nervous systeminvolvement with dysfunction in thesympathetic and parasympatheticsystems can be observed in patientswith GBS.

– Autonomic changes can include thefollowing:

• Tachycardia

• Bradycardia

• Facial flushing

• Paroxysmal hypertension

• Orthostatic hypotension

• Anhidrosis and/or diaphoresis



• Urinary retention and paralytic ileusalso can be observed.

• Dysautonomia is more frequent in

patients with severe weakness andrespiratory failure.

• Autonomic changes rarely persist in

a patient with GBS



Respiratory involvement

40% of patients have respiratory or

oropharyngeal weakness. Typical complaints include the

following:• Dyspnea on exertion

• Shortness of breath

• Difficulty swallowing

• Slurred speech

• Ventilatory failure with requiredrespiratory support is observed inup to one third of patients at some

time during the course of their

v Typical symptoms include:



Typical symptoms include:v Loss of reflexes in the arms and legs

v Muscle weakness or loss of muscle function (paralysis)v In mild cases, there may be no weakness or paralysis

v May begin in the arms and legs at the same time

v May get worse over 24 to 72 hours

v May occur in the nerves of the head only

v May start in the arms and move downward

v May start in the feet and legs and move up to the arms and head

v Numbness,decreased sensation

v Sensation changes

v

Tenderness or muscle pain (may be a cramp-like pain)v Uncoordinated movement

v Additional symptoms may include:

v Blurred vision

v Clumsiness and falling

v Difficulty moving face muscles

v Muscle contractionsv Palpitations (sensation of feeling heartbeat)

v Emergency symptoms (seek immediate medical help):

v Breathing temporarily stops

v Can't take a deep breath

v Difficulty breathing v Difficulty swallowing

COMPLICATION













COMPLICATIONvRespiratory weakness/failure (20-30%

will need intubation at some point

during admission)vAutonomic dysfunction in up to 65%

including: arrythmias, hypotension orhypertension, fluctuating BP, , urinary

retention.vPain in up to 85%: typically back

pain,and musculoskeletal, the straightleg raise test will be positive

vPapilledema (secondary to high CSFprotein)

vDVT

vSIADH (26%)

vAcute Renal Injury (secondary to IVIG TX)

DIAGNOSTIC MANAGEMENT



DIAGNOSTIC MANAGEMENT• HISTORY COLLECTION

• PHYSICAL EXAMINATION• Serum lab tests

• Lumbar Puncture

• Electromyogram (EMG orElectromyography)

• Nerve Conduction Study

(Electroneurograph)• Echocardiogram (ECHO) or

Electrocardiogram (ECG)

•



Medical management

•

Plasmapheresis (PlasmaExchange)

• Intravenous Immunoglobulin(IVIg)

• Medications:Muscle and joint pain can betreated with over-the-counter

analgesics such as aspirin. If necessary, stronger painmedication (e.g., acetaminophenwith hydrocodone) may be

prescribed. Muscle spasms can be





NURSING DIAGNOSES

• Ineffective breathing pattern and

impaired gas exchange related• to rapidly progressive weakness and

impending respiratory• failure•

• Impaired physical mobility related toparalysis• • Imbalanced nutrition, less than body

requirements, related• to inability to swallow• • Impaired verbal communication

related to cranial nerve• dysfunction• • Fear and anxiety related to loss of

control and paralysis



THANK YOU

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Guillian Baare Syndrome

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