Guillain-Barré syndrome
Guillain-Barré syndrome: Excerpt from Professional Guide to Diseases (Eighth Edition)
Guillain-Barré syndrome is an acute, rapidly progressive, and potentially fatal form of polyneuritis that causes muscle weakness and mild distal sensory loss. Recovery is spontaneous and complete in about 95% of patients, although mild motor or reflex deficits in the feet and legs may persist. The prognosis is best when symptoms clear between 15 and 20 days after onset.
Causes and incidence
Precisely what causes Guillain-Barré syndrome is unknown, but it may be a cell-mediated immunologic attack on peripheral nerves in response to a virus. The major pathologic effect is segmental demyelination of the peripheral nerves. Because this syndrome causes inflammation and degenerative changes in both the posterior (sensory) and anterior (motor) nerve roots, signs of sensory and motor losses occur simultaneously.
This syndrome (also called infectious polyneuritis, Landry-Guillain-Barré syndrome, and acute idiopathic polyneuritis) can occur at any age but is most common between ages 30 and 50; it affects both sexes equally. In the United States, it has an incidence of 0.6 to 2.4 cases per 100,000 people.
Signs and symptoms
About 50% of patients with Guillain-Barré syndrome have a history of minor febrile illness (10 to 14 days before onset), usually an upper respiratory tract infection or, less commonly, gastroenteritis. When infection precedes onset of Guillain-Barré syndrome, signs of infection subside before neurologic features appear. Other possible precipitating factors include surgery, rabies or swine influenza vaccination, viral illness, Hodgkin’s or other malignant disease, and lupus erythematosus.
Symmetrical muscle weakness, the major neurologic sign, usually appears in the legs first (ascending type) and then extends to the arms and facial nerves in 24 to 72 hours. Sometimes, muscle weakness develops in the arms first (descending type) or in the arms and legs simultaneously. (See Testing for thoracic sensation.) In milder forms of this disease, muscle weakness may affect only the cranial nerves or may not occur at all.
Another common neurologic sign is paresthesia, which sometimes precedes muscle weakness but tends to vanish quickly. However, some patients with this disorder never develop this symptom. Other clinical features may include facial diplegia (possibly with ophthalmoplegia), dysphagia or dysarthria and, less commonly, weakness of the muscles supplied by cranial nerve XI. Muscle weakness develops so quickly that muscle atrophy doesn’t occur, but hypotonia and areflexia do. Stiffness and pain in the form of a severe “charley horse” commonly occur.
The clinical course of Guillain-Barré syndrome is divided into three phases. The initial phase begins when the first definitive symptom appears and ends 1 to 3 weeks later, when no further deterioration manifests. The plateau phase lasts several days to 2 weeks and is followed by the recovery phase, which is believed to coincide with remyelination and axonal process regrowth. The recovery phase extends over a period of 4 to 6 months; patients with severe disease may take up to 2 years to recover, and recovery may not be complete.
Significant complications of Guillain-Barré syndrome include mechanical ventilatory failure, aspiration, pneumonia, sepsis, joint contractures, and deep vein thrombosis. Unexplained autonomic nervous system involvement may cause sinus tachycardia or bradycardia, hypertension, postural hypotension, or loss of bladder and bowel sphincter control.
Diagnosis
A history of preceding febrile illness (usually a respiratory tract infection) and typical clinical features suggest Guillain-Barré syndrome.
Several days after onset of signs and symptoms, cerebrospinal fluid (CSF) protein levels begin to rise, peaking in 4 to 6 weeks, probably as a result of widespread inflammatory disease of the nerve roots. CSF white blood cell count remains normal, but in severe disease CSF pressure may rise above normal. Probably because of predisposing infection, CBC shows leukocytosis and a shift to immature forms early in the illness, but blood studies soon return to normal. Electromyography may show repeated firing of the same motor unit instead of widespread sectional stimulation. Nerve conduction velocities are slowed soon after paralysis develops and show demyelination. Diagnosis must rule out similar diseases such as acute poliomyelitis.
Treatment
Treatment is primarily supportive, including such measures as endotracheal (ET) intubation or tracheotomy if the patient has difficulty clearing secretions. Preventing complications is another goal of treatment.
Plasmapheresis is useful in decreasing severity of symptoms, thereby facilitating a more rapid recovery. I.V. immune globulin is equally effective in reducing the severity and duration of symptoms.
Special considerations
Monitoring the patient for escalation of symptoms is of special concern.
❑Watch for ascending sensory loss, which precedes motor loss. Also, monitor vital signs and level of consciousness.
❑Assess and treat respiratory dysfunction. If respiratory muscles are weak, take serial vital capacity recordings. Use a respirometer with a mouthpiece or a facemask for bedside testing.
❑Obtain arterial blood gas measurements. Because neuromuscular disease results in primary hypoventilation with hypoxemia and hypercapnia, watch for respiratory failure. Be alert for signs of rising partial pressure of carbon dioxide (such as confusion and tachypnea).
❑Auscultate breath sounds, turn and position the patient, and encourage coughing and deep breathing. Begin respiratory support at the first sign of dyspnea or with decreasing partial pressure of arterial oxygen.
❑If respiratory failure becomes imminent, establish an emergency airway with an ET tube.
❑Give meticulous skin care to prevent skin breakdown and contractures. Establish a strict turning schedule; inspect the skin (especially sacrum, heels, and ankles) for breakdown, and reposition the patient every 2 hours. After each position change, stimulate circulation by carefully massaging pressure points. Also, use foam, gel, or alternating pressure pads at points of contact.
❑Perform passive range-of-motion exercises within the patient’s pain limits. When the patient’s condition stabilizes, change to gentle stretching and active assistance exercises.
❑To prevent aspiration, test the gag reflex, and elevate the head of the bed before giving the patient anything to eat. If the gag reflex is absent, give nasogastric feedings until this reflex returns. If the patient has severe paralysis and is expected to have a long recovery period, a gastrostomy tube may be necessary to provide adequate nourishment.
❑As the patient regains strength and can tolerate a vertical position, be alert for postural hypotension. Monitor blood pressure and pulse during tilting periods and, if necessary, apply toe-to-groin elastic bandages to prevent postural hypotension.
❑Inspect the patient’s legs regularly for signs of thrombophlebitis (localized pain, tenderness, erythema, edema, and positive Homans’sign), a common complication of Guillain-Barré syndrome. To prevent thrombophlebitis, apply antiembolism stockings and give prophylactic anticoagulants, as ordered.
❑If the patient has facial paralysis, give eye and mouth care every 4 hours.
❑Watch for urine retention. Measure and record intake and output every 8 hours, and offer the bedpan every 3 to 4 hours. Encourage adequate fluid intake of 2 qt [2 L] per day, unless contraindicated. If urine retention develops, begin intermittent catheterization as ordered. Because the abdominal muscles are weak, the patient may need manual pressure on the bladder (Credé’s method) before he can urinate.
❑To prevent or relieve constipation, offer the patient plenty of water, prune juice, and a high-bulk diet. If necessary, give daily or alternate-day suppositories (glycerin or bisacodyl) or enemas, as ordered.
❑Before discharge, prepare a home care plan. Teach the patient how to transfer from bed to wheelchair, from wheelchair to toilet or tub, and how to walk short distances with a walker or a cane. Teach the family how to help him eat, compensating for facial weakness, and how to help him avoid skin breakdown. Stress the need for a regular bowel and bladder routine. Refer the patient for physical therapy as needed.
❑Refer the patient’s family to the Guillain-Barré Syndrome Foundation International.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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