Guillain-barré syndrome

36 Guillain-barré syndrome




Overview/pathophysiology


Guillain-Barré syndrome (GBS) is a rapidly progressing polyneuritis of unknown cause. An inflammatory process enables lymphocytes to enter perivascular spaces and destroy the myelin sheath covering peripheral or cranial nerves. Posterior (sensory) and anterior (motor) nerve roots can be affected because of this segmental demyelinization, and individuals may experience both sensory and motor losses. There is relative sparing of the axon. Respiratory insufficiency may occur in as many as half of affected individuals. Life-threatening respiratory muscle weakness can develop as rapidly as 24-72 hr after onset of initial symptoms. In about 25% of cases, motor weakness progresses to total paralysis.


Peak severity of symptoms usually occurs within 1-3 wk after onset of symptoms. A plateau stage follows that usually lasts 1-2 wk. The recovery stage starts with a return of function as remyelinization occurs, but it may take months to years for a full recovery. Fifteen percent of patients have full neurologic recovery, and another 65% have mild deficits that do not interfere with activities of daily living (ADLs). Eighty percent to 90% of patients either recover completely or have only minor residual weakness or abnormal sensations, such as numbness or tingling. Of GBS patients, 5%-10% may have permanent severe disability. Deficits are the result of axonal nerve degeneration.


GBS may follow a recent viral illness, such as upper respiratory infection (URI) or gastroenteritis, rabies or influenza vaccination, lupus erythematosus, or Hodgkin’s disease or other malignant process. Although the exact cause of GBS is unknown, it is believed to be an autoimmune response to a viral infection. Campylobacter jejuni enteritis has been identified as a trigger for GBS in more than 26% of cases. Cytomegalovirus also has been implicated.



Health care setting


The patient is likely to be in acute care (intensive care unit [ICU]) when the neurologic deficit is progressing and in an acute rehabilitation setting during the recovery phase.



Assessment


Progressive weakness and areflexia are the most common indicators. Typically, numbness and weakness begin in the legs and ascend symmetrically upward, progressing to the arms and facial nerves. Ascending GBS is most common, but descending GBS, in which cranial nerves are affected first and weakness progresses downward with rapid respiratory involvement, also can occur. Variants of GBS include primarily a motor component, and another called Miller Fisher syndrome is characterized by abnormal muscle coordination, paralysis of eye muscles, and absence of tendon reflexes. Peak severity usually occurs within 10-14 days of onset. GBS does not affect level of consciousness (LOC), cognitive function, or pupillary function.




Anterior (motor) nerve root involvement:


Weakness or flaccid paralysis that can progress to tetraplegia. Respiratory muscle involvement can be life threatening. There is loss of reflexes, muscle tension, and tone, but muscle atrophy usually does not occur.



Autonomic nervous system involvement:


Sinus tachycardia, bradycardia, hypertension, hypotension, cardiac dysrhythmias, facial flushing, diaphoresis, inability to perspire, loss of sphincter control, urinary retention, adynamic ileus, syndrome of inappropriate antidiuretic hormone secretion, and increased pulmonary secretions may occur. Autonomic nervous system (ANS) involvement may occur unexpectedly and can be life threatening, but usually it does not persist for longer than 2 wk.



Cranial nerve involvement:


Inability to chew, swallow, speak, or close the eyes.



Posterior (sensory) nerve root involvement:


Presence of paresthesias, such as numbness and tingling, which usually are minor compared with the degree of motor loss. Ascending sensory loss often precedes motor loss. Muscle cramping, tenderness, or pain may occur.



Physical assessment:


Symmetric motor weakness, impaired position and vibration sense, hypoactive or absent deep tendon reflexes, hypotonia in affected muscles, and decreased ventilatory capacity.



Diagnostic tests


Diagnostic tests are performed to rule out other diseases, such as acute poliomyelitis. Diagnosis of GBS is based on clinical presentation, history of recent viral illness, and cerebrospinal fluid (CSF) findings.




Lumbar puncture and CSF analysis:


About 7 days after initial symptoms, elevated protein (especially IgG) without an increase in white blood cell (WBC) count may be present. Although CSF pressure usually is normal, in severe disease it may be elevated.



Electromyography and nerve conduction studies:


Reveal slowed nerve conduction velocities soon after paralysis appears because of demyelinization. Denervation potentials appear later.



Serum complete blood count (CBC):


Will show presence of leukocytosis early in illness, possibly as a result of the inflammatory process associated with demyelinization.



Evoked potentials (auditory, visual, brain stem):


May be used to distinguish GBS from other neuropathologic conditions.





Nursing diagnosis:


Ineffective breathing pattern

related to neuromuscular weakness or paralysis of the facial, throat, and respiratory muscles (severity of symptoms peaks around wk 1-3)


Desired Outcome: Deterioration in patient’s breathing pattern (e.g., Pao2 less than 80 mm Hg, vital capacity less than 800-1000 mL [or less than 10-12 mL/kg], tidal volume less than 75% of predicted value, or O2 saturation 92% or less via oximetry) is detected and reported promptly, resulting in immediate and effective medical treatment.











































ASSESSMENT/INTERVENTIONS RATIONALES
Assess patient’s respiratory rate, rhythm, and depth. Observe for changes in mental status, LOC, and orientation. Auscultate for diminished breath sounds. Accessory muscle use, nasal flaring, dyspnea, shallow respirations, diminished breath sounds, and apnea are signs of respiratory deterioration, which necessitates prompt notification of the health provider for rapid intervention.
Observe for changes in mental status, LOC, and orientation. These changes may signal reduced oxygenation to the brain as a result of ineffective breathing pattern.
Assess for ascending loss of sensation by touching patient lightly with a pin or fingers at frequent intervals (hourly or more frequently initially). Assess from the level of the iliac crest upward toward the shoulders. Measure the highest level at which decreased sensation occurs. Decreased sensation often precedes motor weakness; therefore, if it ascends to the level of the T8 dermatome, anticipate that intercostal muscles (used with respirations) soon will be impaired.
Assess patient for the presence of arm drift and inability to shrug the shoulders. Alert health care provider to significant findings. Shoulder weakness is present if patient cannot shrug shoulders. Arm drift is present if one arm pronates or drifts down or out from its original position. Arm drift is detected in the following way: have patient hold both arms out in front of the body, level with the shoulders and with palms up; instruct patient to close eyes while holding this position. These findings need to be reported promptly because they are known to precede respiratory dysfunction.
Assess patient’s ability to take fluids orally. Assess patient q8h and before oral intake for cough reflexes, gag reflexes, and difficulty swallowing.
As prescribed, keep patients with impaired reflexes and swallowing nothing by mouth (NPO).
These assessments detect changes or difficulties that may indicate ascending paralysis.

Impaired swallowing and cough and gag reflexes likely will necessitate parenteral feedings to prevent aspiration until reflexes return to normal.
Assess patient for breathlessness while speaking. To assess for breathlessness, ask patient to take a deep breath and slowly count as high as possible on one breath. Alert health care provider to significant findings. A reduced ability to count to a higher number before breathlessness occurs may signal grossly reduced ventilatory function.
Monitor effectiveness of breathing by checking serial vital capacity results on pulmonary function tests. If vital capacity is less than 800-1000 mL or is rapidly trending downward or if patient exhibits signs of hypoxia such as tachycardia, increasing restlessness, mental dullness, cyanosis, decreased pulse oximetry readings, or difficulty handling secretions, these findings must be reported immediately to health care provider to prevent further deterioration in status. Vital capacity initially is measured q2-4h and then more frequently if deterioration is present.
Assess arterial blood gas levels and pulse oximetry. These assessments detect hypoxia or hypercapnia (PaCO2 more than 45 mm Hg), a signal of hypoventilation. PaO2 less than 80 mm Hg or O2 saturation 92% or less usually signals need for supplemental oxygen.
Raise head of bed. This position promotes optimal chest excursion by taking pressure of abdominal organs off the lungs, which may increase oxygenation.
Encourage coughing and deep breathing to the best of patient’s ability. These actions mobilize and enable expectoration of secretions to optimize breathing pattern. This position also will reduce aspiration risk.
Prepare patient emotionally for life-saving procedures or for the eventual transfer to ICU or transition care unit for closer monitoring. The patient may require tracheostomy, endotracheal intubation, or mechanical ventilation to support respiratory function.
For other interventions, see Risk for Aspiration in “Older Adult Care,” p. 90.  
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Guillain-barré syndrome

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