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Read the Article: Moore, A.S. & Shepard, L.H. (2014). Myasthenia gravis vs. guillain-barré syndrome what's the difference? Nursing Made Incredibly Easy! 12 (4). 21-30. Initial Discussion Post: Select one (1) of the following Nursing Diagnoses: Impaired Spontaneous Ventilation Impaired Swallowing Care Giver Role Strain Address the following: 1. Is the nursing diagnoses that you selected appropriate for the patient with a diagnosis of myasthenia gravis, Guillain-Barre syndrome or both? Explain your answer. 2. Provide an outcome for the nursing diagnosis that you selected making sure that is specific to the needs of the patient with myasthenia gravis or Guillain-Barre syndrome. 3. Identify two (2) interventions that will help your patient with myasthenia gravis or Guillain-Barre syndrome reach the outcome for the nursing diagnosis. Base your initial post on your readings and research of this topic. www(dot)NursingMadeIncrediblyEasy(dot)com July/August 2014 Nursing made Incredibly Easy! 21 20 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com Myasthenia gravis vs. Guillain-Barr é syndrome What's the difference? Managing the care of patients with a neuro- logic disorder can be complicated. Provid- ing nursing care for these patients becomes even more complex when the signs and symptoms of two completely different con- ditions are closely related. Prime examples of this are myasthenia gravis (MG) and Guillain-Barré syndrome (GBS). This article will help you differentiate between these two conditions so that you can be better prepared to plan, manage, and implement appropriate nursing interven- tions when providing care for patients with MG or GBS (see Comparing MG and GBS and Comparing assessments and interventions for MG and GBS ). MG: Not so fast MG is an acquired autoimmune disease. The autoantibody attack, which takes place on the acetylcholine (ACh) receptors of the myoneural junction, impairs transmissions of nerve impulses, causing weakness of the voluntary skeletal muscles (see MG: How it happens ). The disease's course varies from remissions, when no activity occurs, to pe- riods of flare-ups known as exacerbations. The disease isn't considered hereditary, although genetic abnormalities have been linked to it. Possible contributing factors to Henrick5000/ i Stock Recognizing the differences between these two neurologic disorders can help you better manage the care of your patients. By Ann S. Moore, MSN, RN, and Leslee H. Shepard, EdD, MSN, RN, CMSRN Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 22 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com MG include an overgrowth of the thymus gland, as well as hyperthyroidism, which may lead the primary care provider to pre- scribe diagnostic imaging such as a chest X-ray or computed tomography. Because the antibodies (immune proteins) that are believed to target the Ach receptors are produced in the thymus gland, the pri- mary care provider may opt to remove it (thymectomy). MG can develop at any age and is seen in both men and women. In women, MG occurs more often in those younger than age 40, but in men it's more likely to occur later in life. MG is a chronic condition with- out any known cure, but with proper man- agement, patients can achieve a good quality of life. A concern for women who are pregnant is that the infant may be born with MG Comparing MG and GBS MG (descending type) GBS (ascending type) Trigger - Unknown - Often follows viral infections, such as herpes simplex, AIDS, or mononucleosis - After surgery - Severe illness Incidence - Twenty per 100,000 individuals affected - Onset most common in women in their 20s and 30s; men in their 50s and 60s - Men more commonly affected - Unrelated to ethnicity - One or two per 100,000 individuals affected - Incidence increases with advancing age - Men and women equally affected - Unrelated to ethnicity Diagnostic testing - Edrophonium test - No specific test - Diagnosis is based on medical history and presenting signs and symptoms of increasing muscle weakness and decreased breathing Basic pathophysiology - Target: Neuromuscular junction - Autoimmune attack on the ACh receptors that block nerve impulses to the skeletal muscles - Target: Myelin sheath surrounding axons of peripheral nerves - Cell-mediated autoimmune reaction directed at peripheral nerves, interrupting nerve signals Course of progression - Chronic - Signs and symptoms begin proximally and progress downward - Progressive condition - Acute (early hours after trigger) - Rapidly progressive weakness begins in the lower extremities and progresses upward - Spontaneous recovery occurs in 4 months up to 2 years Source: Adapted from Tucker KL. Myasthenia gravis and Guillain-Barré syndrome. Presentation at the American Association of Neuroscience Nursing Triad Chapter Quarterly Continuing Education Session, 2010. Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. www(dot)NursingMadeIncrediblyEasy(dot)com July/August 2014 Nursing made Incredibly Easy! 23 (known as neonatal MG), which is caused by the mother's abnormal antibodies enter- ing the neonate's bloodstream. When this occurs, the infant presents with muscle weakness of the upper extremities and facial muscles, which puts him or her at risk for aspirating while feeding. The abnormal anti- bodies are typically cleared within 2 months, relieving the infant from symptoms. Recognizing signs and symptoms Although the onset of MG is typically slow, certain conditions, such as infection or preg- nancy, can lead to a rapid onset. The initial assessment finding for MG is generalized weakness that gets worse with activity and progresses over time. The weakness is associ- ated with the specific muscles involved, which usually include the facial and laryn- geal muscles, all extremities, and intercostal muscles. Often, you'll find that early involvement affects the levator palpebrae, which are the muscles of the eyes and the eyelids. Specific signs and symptoms include pto- sis (drooping eyelids) and diplopia (dou- ble vision). The patient will appear to have little to no facial expression and, because the 50 laryngeal muscles are involved, he or she will have dysphagia (difficulty swallowing) and dysphonia (impairment of the voice). These patients won't com- plain of associated pain, but they may report muscle achiness. Diagnostic tests can help When the medical diagnosis of MG is being confirmed, you can anticipate that the primary care provider will order an edrophonium test, which includes I.V. Comparing assessments and interventions for MG and GBS MG GBS Assessment findings (signs and symptoms) - Weakness of the arms and legs that improves with rest - Oculomotor disturbances - Difficulty chewing, swallowing, speaking - Reflexes intact - Tingling in the legs - Weakness is widespread, including the respiratory muscles, and isn't improved with rest - Almost total paralysis - Difficulty swallowing - Difficulty breathing - Respiratory failure - Reflexes often absent Interventions - Plasmapheresis - IVIG - Thymectomy (removal of the thymus gland) Precautions - Aspiration precautions - Falls precautions Medications - Anticholinesterase drugs: pyridostigmine bromide, neostigmine, and ambenonium chloride - Immunosuppressant drugs: prednisone, azathioprine, cyclosporine, mycophenolate mofetil, and cyclophosphamide - Plasmapheresis - IVIG - Mechanical ventilation Precautions - Aspiration precautions - Falls precautions Medications - Alpha-adrenergic blocking agents - Low-molecular-weight heparin: enoxaparin - NSAIDs - Acetaminophen Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 24 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com administration of an acetylcholinesterase inhibitor, such as edrophonium chloride or neostigmine. The test is considered positive if the patient has an immediate improvement in muscle strength that lasts for about 5 minutes. Although this test is the most common, other diagnostic procedures include the ice pack test, which is used to differenti- ate MG from other neurologic conditions. The patient who presents with ptosis and/or diplopia is deemed positive if there's a raise of 2 mm of the palpebral fissure (eyelid) following the removal of the ice pack. When applying the ice pack, take precautions to avoid burning the eyelid. This can be done by covering the ice pack with a towel to prevent direct application on the eye and allowing the ice pack to remain on the eye for no more than 2 minutes. Other tests include electromyography (EMG) or repetitive electrical nerve stimula- tion, which may show progressively increasing muscle weakness. With single- fiber EMG, increased jittering in facial mus- cles is a positive result for MG. If ptosis is suspected, blood testing can be performed to detect the antibodies associated with MG. Blood testing has a reasonable sensi- tivity of 80% to 96%; however, in MG limit- ed to eye muscles (ocular myasthenia), the sensitivity falls to 50% (negative in up to 50% who have MG). Treatments on tap One treatment you can anticipate being ordered for your patient is an exchange of Recognizing adverse reactions of pyridostigmine bromide Mild Moderate Severe Central nervous system - Headache - Watery eyes ____________________ - Slurred speech - Confusion - Seizures - Worsening MG symptoms Respiratory - Increased bronchial secretions - Cough - Respiratory insufficiency - Difficulty breathing Cardiovascular ____________________ ____________________ - Swelling of face, lips, tongue, or throat Gastrointestinal - Queasiness - Flatulence - Loose stools - Nausea - Vomiting - Diarrhea - Abdominal cramping ____________________ Skeletal muscles - Muscle weakness - Muscle twitching - Extreme muscle weakness Genitourinary - Increased urination ____________________ ____________________ Integumentary - Increased sweating - Itching - Pale skin - Mild rash - Hives Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 26 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com MG: How it happens M oto r n e rv e impul ses t r a v e l to m oto r n e rv e te rmin a l. A cet yl c h o lin e (A C h) i s r e l ease d. A C h diffu ses ac r oss s yn a p se . A C h r ece p to r s i tes in m oto r e nd pl ates d e p o l a ri ze mu sc l e fib e r. De p o l a ri zat i o n s pr ea d s, ca u s in g mu sc l e co n t r act i o n. No rmal n e ur o mu sc ular t ran s mi ss i o n Axon ACh ACh release site Normal ACh receptors Motor end plate of muscle Nerve impulses plasma known as plasma- pheresis. This procedure has been known to work quickly by reducing the level of self-attacking antibodies; however, the duration of the effect is short lived. When manag- ing this treatment, keep in mind that the basic proce- dures for administering blood and blood products apply. Specific guidelines will be provided by your indi- vidual facility. To ensure the best out- comes for your patient, recognize that other variables may lead to poor out- comes, such as if the patient is immobile or paralyzed. Complications include cardiac arrhythmias, transient hyperten- sion, orthostatic hypotension, and urinary retention. Surgical management is another option that may be offered to your patient. In an effort to achieve either partial or complete remission of MG, the surgical removal of the thymus gland, known as a thymecto- my, may be performed. When caring for these patients, expect to provide usual pre-, intra-, and post-op care. The focus in the postoperative stage should be the respira- tory system. Your patient may not see improvement for months, but most patients eventually see benefits. Using medications safely The most common initial medication you can anticipate being prescribed for your patient is pyridostigmine bromide. This anticholinesterase inhibitor works by slowing the breakdown of acetylcholine. When administering this drug, under- stand that the dosage will vary for each patient but, in all cases, the dosage will be gradually increased to achieve optimal effectiveness. You should also be aware of potential adverse reactions (see Recog- nizing adverse reactions of pyridostigmine bromide ). Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. www(dot)NursingMadeIncrediblyEasy(dot)com July/August 2014 Nursing made Incredibly Easy! 27 What to look for ■ Extreme muscle weak- ness ■ Fatigue ■ Ptosis (drooping of the upper eyelid) ■ Diplopia ■ Difficulty chewing and swallowing ■ Sleepy, masklike expres- sion ■ Drooping jaw ■ Bobbing head ■ Arm or hand muscle weakness Motor nerve impulse Vesicle containing ACh Neuromuscular junction Blocked ACh receptors M oto r n e rv e impul ses t r a v e l to m oto r n e rv e te rmin a l. A C h i s r e l ease d. A C h diffu ses ac r oss s yn a p se . A C h r ece p to r s i tes, w ea k e n e d o r d est r o y e d by attac h e d a n t ib o di es, bl oc k A C h r ece p t i o n. Ne ur o mu sc ular t ran s mi ss i o n in MG De p o l a ri zat i o n a nd mu sc l e co n t r act i o n d o n' t occ ur. N e ur o mu sc ul a r t r a n s mi ss i o n i s bl oc k e d. Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 28 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com Other pharmacologic interventions include corticosteroids, immunosuppressant drugs, and cyclosporines. Nursing considerations Because MG is a chronic disease, patients may be cared for in the home, at an acute care hospital, or, depending on severity, in a long-term-care facility. In the event of a sudden exacerbation of MG signs and symptoms, known as myasthenic crisis, your top priority will be managing respiratory distress. Myasthenic crisis is an emergent complication that's often precipitated by infection. The patient in crisis will display sudden respiratory distress, difficulty swallowing, extreme muscle weakness, and the sudden onset of other typical signs and symptoms of MG. In some cases, mechanical ventilation may be required. When a crisis occurs, you should expect to manage several interventions concurrently, including: - providing ventilator support - performing ongoing pulmonary assessment - monitoring lab results - ensuring strict intake and output - managing tube feedings, if applicable - increasing the frequency of oxygen - measuring oxygen saturation levels - reconciling the list of medications - consulting with the primary care provider about the need to discontinue or change any medications that can cause respiratory depression, such as sedatives. The patient with MG is at high risk for injury because the disease causes weakness. Take precautions to prevent falls by lower- ing the bed and ensuring that the bed wheels are locked, making frequent rounds according to your facility's policy, and offering toileting and nourishment regular- ly. Measures that can prevent aspiration and respiratory distress include elevating the head of the bed, feeding the patient slowly, and having suction available at the bedside. Follow your facility's guidelines to ensure that your patient remains safe. Teaching self-care When teaching your patients how to self- manage MG, always assess their willingness and readiness to learn to ensure that they get the most out of the education. Individu- alize the education to include information on the prescribed medication and the im- portance of adherence to the medication regimen. Teach patients to recognize the signs of exacerbations, detect early signs of com- plications, and make lifestyle changes to help alleviate symptoms. These changes include getting plenty of rest; conserving energy to minimize weakness; and avoid- ing precursor events that can trigger clini- cal manifestations, such as exposure to infection. Finally, teach them the impor- tance of keeping regularly scheduled fol- low-up appointments. GBS: Steering a rapid course GBS is characterized by muscle weakness, leading to acute onset of motor paralysis. Because it can progress rapidly, resulting in neuromuscular respiratory failure, the onset of GBS should be considered and treated as a medical emergency. Occasion- ally, a lumbar puncture (also called a spi- nal tap) may be performed. If high levels of protein are detected and there's no infec- tion, this is an indication that your patient may have GBS. Like MG, GBS is an autoimmune disor- der in which the body's immune system mistakenly attacks part of the nervous system. As a result, the immune system begins to destroy the myelin sheath that surrounds the axons and peripheral nerves and/or attacks the axons them- selves. This acute inflammatory disorder of the peripheral nervous system causes the brain to receive fewer sensory signals, affecting the patient's ability to feel texture, heat, and pain. MG is chronic; GBS is acute. Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. www(dot)NursingMadeIncrediblyEasy(dot)com July/August 2014 Nursing made Incredibly Easy! 29 Sometimes fi guring out what's wrong with you can be confusing! Although GBS is one of the more com- mon peripheral nervous system disorders, the syndrome itself is uncommon. The primary cause of GBS isn't known, but several conditions have been associated with it. Your patient assessment may reveal a recent episode of an acute illness or infec- tion that may be linked to the patient's gas- trointestinal or respiratory tract. The patient may report recent immunizations, surgery, or some type of trauma within the previous 2 or 3 weeks before the onset of GBS. Diagnosis depends on signs and symptoms No specific test is used to diagnosis GBS. A patient is diagnosed with the condition based on medical history and presenting signs and symptoms. GBS starts as muscle weakness that typi- cally begins in the legs and spreads to the arms and upper body. This ascending paral- ysis can progress very quickly. A decline in respiratory function is the primary symptom that must be managed. The patient may also present with any combination of the following signs and symptoms: - the sensation of “pins and needles” in the fingers and/or toes - severe lower back pain - difficulty controlling the bowel and bladder - problems with facial movement that affect speaking, chewing, and swallowing - variable changes in vital signs, such as bradycardia, tachycardia, or high or low BP. Focus on treatments These treatments may speed recovery and reduce the severity of the condition. - Plasmapheresis is used to remove the circulating antibodies thought to be re- sponsible for GBS. In this procedure, plasma is selectively separated from whole blood. The blood cells are returned to the patient without the plasma. The body usually manufactures more plasma or the patient is transfused with colloidal substitute, such as albumin, to make up what was removed. Treatments should be started within several days to 30 days after the onset of signs and symptoms. Check your facility's policies, procedures, and guidelines on how to safely perform plasmapheresis. Keep in mind that patients usually receive three to four treatments, which are usually 1 to 2 days apart. If no improvement is seen, the pri- mary care provider may opt for a second course of treatment. - I.V. immunoglobulin (IVIG) is another treatment that may be prescribed for the pa- tient with GBS. IG contains healthy antibod- ies from blood donors. Using IVIG can block the damaging antibodies that may contribute to GBS. As with plasmapheresis, policies, procedures, and guidelines on how to administer IVIG will be provided by your facility. In most cases, IVIG will be used in combination with plasmapheresis; however, you may find that one or the other has been prescribed. - Respiratory therapy will be required for patients with GBS. Therapy includes in- centive spirometry, chest physiotherapy, and close monitoring for deterioration that may lead to respiratory failure. In the event that the patient loses the ability to breathe spontaneously, mechanical ventilation is required for support of pulmonary function until the patient's re- spiratory muscles regain spontaneous respirations. Medications to the rescue The patient's signs and symptoms deter- mine what medications are prescribed. Tachycardia and elevated BP are managed with short-acting medications, such as alpha-adrenergic blocking agents. Due to patients' impaired mobility, low-molecular- weight heparin, such as enoxaparin, and low-dose aspirin may be prescribed, along Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 30 Nursing made Incredibly Easy! July/August 2014 www(dot)NursingMadeIncrediblyEasy(dot)com with other nonpharmacologic deep venous thrombosis prophylaxis, such as elastic compression stockings or sequential com- pression boots. Pain medications are usually prescribed in the form of nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen. Nursing considerations The primary nursing management of a patient with GBS should be centered on problems with the airway related to re- spiratory muscle weakness or paralysis, decreased cough reflex, and immobiliza- tion. Due to the progressive muscle weakness, you should plan interventions that focus on preventing complications related to immobility, such as ensuring skin integrity. Measures to prevent altera- tions in skin integrity include turning the patient every 2 hours; ensuring adequate hydration; keeping the skin clean and dry; performing skin assessments to inspect for breakdown; and placing pad- ding to protect bony prominences, such as elbows and heels, to reduce the risk of pressure ulcers. When patients develop difficulty with swallowing or speaking during hospital- ization, consider instituting advance directives. This should be done before the progression of the disease when the patient is unable to make his or her wishes known. In addition, collaborate with the primary care provider to obtain a speech and physical therapy consult. The evalua- tive services will help with decisions regarding skilled nursing facility place- ment or rehabilitative services. Adequate nutrition can be made possible with main- tenance fluids and total parenteral nutri- tion, which is required for patients on mechanical ventilation. Teaching self-care The recovery phase for patients with GBS can be long, ranging from 4 months to 2 years. Patient teaching associated with self- care at home should be focused on inter- ventions that improve muscle strength. You should emphasize range-of-motion exercises and other activities that promote extremity strength. Your patients may have poor en- durance at first, so help him or her under- stand energy-conserving techniques. Recognizing the differences In the course of your career, you may be as- signed to manage the care of patients with various neurologic disorders. During the initial stages, many neurologic conditions have similar signs and symptoms, making them difficult to differentiate. However, after the patient has been diagnosed, it becomes clear which course of action is needed to help restore health. MG and GBS are two conditions with similar broad- spectrum signs and symptoms, such as weakness. Upon closer inspection, the differences will be revealed, letting you plan optimum nursing care. ■ Learn more about it Hinkle JL, Cheever KH. Brunner & Suddarth's Textbook of Medical-Surgical Nursing. 13th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2013. Ignatavicius DD, Workman ML. Medical-Surgical Nursing: Patient-Centered Collaborative Care. 7th ed. St. Louis, MO: Elsevier; 2012. Pellico LH. Focus on Adult Health: Medical-Surgical Nursing . Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2012. Porth CM. Essential of Pathophysiology: Concepts of Altered Health States. 3rd ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2010. Tucker KL. Myasthenia gravis and Guillain-Barré syn- drome. Presentation at the American Association of Neuroscience Nursing Triad Chapter Quarterly Continuing Education Session, 2010. At Winston Salem State University in Winston Salem, N.C., Ann S. Moore is an Instructor of Nursing and Leslee H. Shepard is an Associate Professor of Nursing. The authors have disclosed that they have no financial relationships related to this article. DOI-10.1097/01.NME.0000450275.16317.ea on the web GBS/CIDP Foundation International: http://www(dot)gbs-cidp(dot)org Myasthenia Gravis Foundation of America: http://www(dot)myasthenia(dot)org Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited