Chapter 46: Problems Of The Peripheral Nervous System Flashcards
Stages of acute GBS
Acute or initial period last 1 to 4 weeks and begins with the onset of symptoms and ends when no further deterioration occurs.
The plateau period lasts for several days up to two weeks.
The recovery phase can last from 4 to 6 months but possibly up to two years. This is when remyelination and regeneration occur. Some may never completely recover.
Pathophysiology of Guillain-barre syndrome
Uncommon, In men slightly more than women, and European Americans. Immune mediated pathological process where demyelination of the Myelin sheath of the peripheral nerves, progressive motor weakness and sensory abnormalities occur. Usually begin in the legs and spreads to the arms. Some patients may require mechanical ventilation because of the week or paralyzed respiratory muscles. Most patients report an acute illness before it develops such as gastroenteritis, Trauma, surgery, immunization, upper respiratory tract infection, cytomegalovirus or Epstein-Barr virus.
GBS assessment
Obtain a complete history and describe the symptoms in chronological order. Typically does not affect the level of consciousness, cerebral function, pupillary constriction or dilation. The cranial nerve most often involved include VII. Assess the facial nerve and the ability to smile, frown, whistle, drink from a straw, dysphasia. Other nerves involved maybe nine, 10, 11, and 12. Monitor blood pressure closely hypertensive and hypotensive episodes, bradycardia, heart block, Asystole (from CN X autonomic dysfunction).
Manifestations of GBS
A sending muscle weakness to flaccid paralysis without atrophy. Decreased or absent deep tendon reflexes, respiratory compromise or failure, loss of bowel and bladder control, ataxia, paresthesias, pain and cramping, facial weakness, dysphagia, diplopia, difficulty Speaking, labile blood-pressure, cardiac dysrhythmias, tachycardia
Descending GBS
Initially experiences weakness of the face or bulbar muscles of the jaw, the sternocleidomastoid muscle, muscles of the tongue pharynx and larynx. Weakness progresses downward to involve the limbs. Respiratory function is quickly affected. Often includes ophthalmoplegia paralysis of the eye muscles causing diplopia. If papillary response to light is affected, functional blindness may result. Numbness is more common in the hands than in the feet. Deep tendon reflexes are decreased or absent
Plasmapheresis
For non-ambulatory adult patients need to seek treatment within four weeks. Ambulatory patients need to seek treatment within two weeks. Do not use corticosteroids unless necessary. It removes the circulating antibodies thought to be responsible for the disease.
Plasma is separated from the whole blood and blood cells are returned. The patient maybe transfused with a colloidal substance such as albumin. Usually receives 3 to 4 treatments 1 to 2 days apart.
Weigh the patient before and after the procedure, using proper shut care. Check for patency, assess bruits every 2 to 4 hours, keep an double bulldog clamps at the bedside, observe the puncture site for bleeding or a ecchymosis. Observed for complications. Atropine used during the procedure for bradycardia.
Result complications of plasmapheresis
Trauma or infection at the site. Hypokalemia with hypertension, tachycardia, dizziness, and diaphoresis. Administer fluids for it. Hypokalemia and hypocalcemia. Monitoring electrolytes and replace.
Priority care for GBS
Maintain adequate respiratory function. Monitor closely for signs of respiratory distress. Assess respiratory rate, rhythm, and the depth every 1 to 2 hours. Check vital capacity every 2 to 4 hours and auscultate the lungs every four hours. Monitor cough and swallowing. Cognitive change can indicate hypoxia.
Elevate bed at least 45°, suction but pay attention for vagal nerve stimulation. Monitor sucretions and use chest physiotherapy. Breathing exercises and incentive spirometer. Obtain ABG values and use pulse oximetry.
Decrease in vital capacity to 15 to 20 mL per kilogram and inability to clear secretions indicate need for intubation. Keep equipment at bedside
Managing GBS
Place on a cardiac monitor and watch for dysrhythmias. Improve mobility and prevent complications of immobility. Assist with ambulation and transfers. Monitor nutrition and use a feeding tube if needed, malnutrition places the patient at risk for pressure ulcers. Use a prophylactic anticoagulant to prevent deep vein thrombosis. Manage pain which is usually worse at night. Promote communication and use an alternate way like blinking or a board if needed. Provide emotional support.
Myasthenia gravis
Chronic disease characterized by fatigue and weakness primarily in muscles innervated by the cranial nerves as well as in skeletal and respiratory muscles. This is an autoimmune disease that can be from mild to severe and may have remissions and exacerbations. PGA is 20 to 30 and women are affected more. It is caused by an auto antibody attack on the acetylcholine receptors. As a result nerve impulses are not transmitted to skeletal muscle and the muscles cannot contract.
There is a relationship between it and hyperplasia of the thymus gland. It is also strongly associated with hyperthyroidism
Manifestations of myasthenia gravis
Progressive muscle weakness proximal but usually improves with rest poor posture ocular palsies ptosis weak or incomplete eye closure diplopia respiratory compromise loss of bowel and bladder control fatigue sensory manifestations include muscle achy, paresthesias, decreased smell and taste.
Assessments of myasthenia gravis
It is usually slow it can be rapid from infection, emotional upset, pregnancy, or anesthesia. A temporary increase in weakness can be after vaccination, menstruation, and exposures to extremes in temperature. Weakness usually affects the proximal muscle.
Assess areas of weakness including dysphasia and difficulty with the respiratory. Ask about difficulty holding up the head, brushing teeth, combing hair, or shaving. Ask about the history of thymus gland tumor. PERRLA is usually normal. Most patients have weakness in the muscles for facial expression, chewing, and speech. Ask about weight loss. Notice a weakness in the voice. Severe cases can include problems with respiratory function, control of the bowel and bladder. Muscle atrophy is rare. Reflexes are usually not affected. Pain is not usually a concern.
Testing for myasthenia gravis
Thyroid function is tested for thyrotoxicosis. Test for acytelcholine receptor antibodies. X-rays and CT scan is done to detect a thymoma on the thymus gland. Pharmacologic test with cholinesterase inhibitors such as tensilon test. Can use prostigmin also
EMG.
Tensilon testing
Edrophonium chloride (tensilon) increases ACh availability. 2 mg is injected IV. If this is tolerated an additional 8 mg is injected after 30 seconds. Within 30 to 60 seconds of the first dose, most myasthenic patients show marked improvement in muscle tone that lasts for two to five minutes. It may be false positive If patient tries too hard or negative if the patient is too weak.
It can be used to determine whether increasing weakness in a previously diagnosed patient is due to a cholinergic crisis which is too much cholinesterase drugs or a myasthenic crisis which is to little cholinesterase inhibitor drugs. In a cholinergic crisis muscle tone does not improve after giving Tensilon. Weakness may increase and fasciculations/facial twitching may occur.
It poses a danger of ventricular fibrillation and cardiac arrest which are rare. Have atropine sulfate the antidote available in case these complications occur.
Management of myasthenia gravis
Presentation is muscle weakness that increases when the patient is fatigued and limits his or her mobility. Management includes treatments that affect the symptoms of myasthenia gravis without influencing the course of disease such as anticholinesterase or cholinergic drugs. Therapeutic efforts to induce remission such as immunosuppressive drugs corticosteroid, plasmapheresis and thymectomy. Not all patients have respiratory compromise but it is a nursing priority.
Assess muscle strength before and after activity. Try to avoid fatigue. Plan around energy levels. Provide assistance when the patient is weak. Maintain body alignment, perform active or passive range of motion exercises every 2 to 4 hours, Reposition every two hours.
Give anticholinesterase and immunosuppressive drugs on time to maintain therapeutic levels and improve muscle strength. Document the response to the medication. Plasmapheresis may help.
