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GUILLAIN-BARRE SYNDROMESYNDROME

Imran Khan Salarzai

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OBJECTIVES at the end of this presentation the student will be able to:

Define GBS.Identify the prevelance of GBS.Discus the causes of GBS.Describe the pathophysiology of GBS.Identify S/S of GBS.Explain the diagnosis of GBS.Discus medical management of GBS.Formulate Nursing diagnosis and intervention

of GBS.

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GUILLAIN-BARRE SYNDROME GUILLAIN-BARRE SYNDROME (GBS) is

an acute inflammatory process that involves degeneration of the myelin sheath of peripheral nerves characterized by varying degrees of motor weakness and paralysis.

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PREVALENCE 1.9 per 100, 000 persons are affected 85% have complete recovery within 6-

12 months. 7-15% experience permanent damage

including persistent weakness, sensory loss.

Mortality rates vary but < 5%. Occurs at all ages, peak in young

adulthood (15-35yrs) and elderly person (50-70yrs).

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CAUSES: Idiopathic.

post infections. RT and GIT infection.

campylobacter jejuni . (20 to 30%) EBV and CMV. (13%) mycoplasma pneumonia.

Recent immunization. MMR vaccine.

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PATHOPHYSIOLOGY GBS is a post infectious, immune-mediated

disease. Cellular and humoral immune mechanisms probably play a role in its development. Most patients report an infectious illness in the weeks prior to the onset of GBS. Many of the identified infectious agents are thought to induce production of antibodies that cross-react with specific gangliosides and glycolipids, such as GM1 and GD1b, that are distributed throughout the myelin in the peripheral nervous system.

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CONT…. The pathophysiologic mechanism of

GBS can be typified by Campylobacter jejuni infections. The virulence of C jejuni is thought to be based on the presence of specific antigens in its capsule that are shared with nerves.

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CONT… Immune responses directed against

lipopolysaccharide antigens in the capsule of C jejuni result in antibodies that cross-react with ganglioside GM1 in myelin, resulting in immunologic damage to the peripheral nervous system. This process has been termed molecular mimicry.

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CONT… Pathologic findings in GBS include

lymphocytic infiltration of spinal roots and peripheral nerves (cranial nerves may be involved as well), followed by macrophage-mediated, multifocal stripping of myelin. This phenomenon results in defects in the propagation of electrical nerve impulses, with eventual absence or profound delay in conduction, causing flaccid paralysis. Recovery is typically associated with remyelination.

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SIGN & SYMPTOMSMotor Manifestations:

Ascending symmetric muscle weakness flaccid paralysis without muscle atrophy

Decreased or absent deep tendon reflexes (DTRs) Respiratory compromise (dyspnea, diminished breath

sounds, decreased tidal volume and vital capacity) and respiratory failure

Loss of bowel and bladder control (less common) Sensory Manifestation:

Paresthesias & Pain (cramping) Numbness generally begin in the toes and fingertips.

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CONT….• Cranial Nerve Manifestations:

– Facial weakness– Dysphagia– Diplopia– Difficulty speaking

• Autonomic Manifestations – Labile blood pressure– Cardiac dysrhythmias– Tachycardia.

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DIAGNOSIS Hx:

Loss of reflexes such as the knee jerk reaction can be an early clue to a clinician.

Lumber puncture. Elevated protein level in CSF

Nerve conduction ( slow) Electromyography (EMG)

Altered Respiratory function

MRI

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MANAGEMENT IV Immunoglobulin (IVIG)

Act by reducing the amount of anti-myelin antibodies through the binding of the defective antibodies by healthy antibodies contained in the IVIG solution, and in suppressing the immune response.

Plasmapheresis

Symptomatic managementPrevent complications

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NURSING DIAGNOSIS • Inability to sustained spontaneous ventilation

related to progression of disease process.• Risk for aspiration related to dysphagia.• Pain related to paraesthesias.• Impaired verbal communication related to

intubation or paralysis of muscles of speech.• Self-care deficit related to inability to use

muscles to accomplish ADL.

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NURSING INTERVENTIONS Assess pain. Administer analgesics (NSAIDS to opioids). Cardiac monitoring (tachycardia). Elevate bed to 30o at night to reduce

orthostatic hypotension. Treat severe hypertension with short

acting antihypertensive drugs. encourage patient and his or her family. Establish sleep routine, administer

sedatives and hypnotics if needed.

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CONT….

Use devices to reduce risk of skin break down.Assess frequently for wounds and skin break down.Assess gag, cough and swallow reflex to prevent choking and monitor pharyngeal function.Patent airway.Oxygen administration.Suctioning, adjusting the endotracheal or nasotracheal airways. Chest physiotherapy.

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