Guillain-Barré Syndrome Miss Fatima Hirzallah

Guillain-Barré syndrome is an autoimmune attack on the peripheral nerve myelin. The result is acute, rapid segmental demyelination of peripheral nerves and some cranial nerves, producing ascending weakness with dyskinesia (inability to execute voluntary movements), hyporeflexia, and paresthesias (numbness). An antecedent event (most often a viral infection) precipitates clinical presentation.

Etiology 1-Etiology unknown 2- but it involve an immune mediated response involving cell mediated immunity and development of IgG. 3- patient with viral infection for at least 3 week ( e.g. infuenza, hepatitis A,B, or C, and HIV). 4- bacterial infection( mucplasma pneumonia), or some vaccines( rabies,tetanus, infuenza) 5- other predisposing factor( surgery, lymphoma, trauma)

The annual worldwide incidence of Guillain-Barré syndrome is 0.6 to 1.4 cases per 100,000, and it is more frequent in males between 16 and 25 years of age and between 45 and 60 years of age Results of studies on recovery rates differ, but most indicate that 60% to 75% of patients recover completely. Residual deficits of varying degree occur in 20% to 25% of patients

Pathophysiology Myelin is a complex substance that covers nerves, providing insulation and speeding the conduction of impulses from the cell body to the dendrites. Guillain-Barré syndrome is the result of a cell- mediated immune attack on peripheral nerve myelin proteins that causes inflammatory demyelination.

Clinical Manifestations Guillain-Barré syndrome typically begins with muscle weakness and diminished reflexes of the lower extremities. Hyporeflexia and weakness may progress to tetraplegia. Demyelination of the nerves that innervate the diaphragm and intercostal muscles results in neuromuscular respiratory failure. Sensory symptoms include paresthesias of the hands and feet and pain related to the demyelination of sensory fibers.

The antecedent event usually occurs 2 weeks before symptoms begin. Weakness usually begins in the legs and progresses upward. Maximum weakness, the plateau, varies in length but usually includes neuromuscular respiratory failure.

Assessment and Diagnosis 1- signs and symptoms include- motor weakness, paresthesia and sensory deficit, and cranial nerve dysfunction. 2-A history of a viral illness in the previous few weeks suggests the diagnosis. 3-- there is ascending weakness which lead to respiratory arrest. 4-CSF protein level will be elevated. 5-nerve conduction studies. Evoked potential studies demonstrate a progressive loss of nerve conduction velocity.

Medical Managment Plasmapheresis and immunoglobulin (IVIg )are used to affect directly the peripheral nerve myelin antibody level Respiratory therapy or mechanical ventilation may be necessary to support pulmonary function and adequate oxygenation. Some clinicians recommend elective intubation before the onset of extreme respiratory muscle fatigue..

Nursing Mangement 1. Maintaining surveillance for complication. 2. initiating rehablilitation. 3. facilitating nutritional support. 4. providing comfort and emotional support. 5. patient education.

Nursing Diagnoses Ineffective breathing pattern and impaired gas exchange related to rapidly progressive weakness and impending respiratory failure Impaired bed and physical mobility related to paralysis 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

THANKS