Acute Care II Comprehensive Case Study



Acute Care II Comprehensive Case StudyLaura LangenhopWright State UniversityAcute Care II Comprehensive Case StudyPatient informationM.H. is a 35 year-old Caucasian Female SourcePatient and patient’s husband, reliable resourcesChief ComplaintAcute Respiratory FailureHistory and PhysicalM.H. is a 35 year-old female seen on hospital day two. The patient presented with increased shortness of breath. The shortness of breath started two weeks ago. The patient had a cough accompanied with the shortness of breath. Sputum color was yellow. The patient states she went to her primary care physician who placed her on oral Levaquin for pneumonia. The patient has taken the Levaquin as prescribed with no relief. The patient also was having difficulty chewing and swallowing her food for the last couple of days. Subsequently, the patient has noticed increased fatigue and a weight loss of five pounds in the last week. Upon arrival to the emergency department, the patient continued to have increased respiratory failure and was intubated. The patient was changed from oral Levaquin to intravenous Vancomycin and intravenous Zosyn for broad-spectrum coverage for both aspiration pneumonia and community-acquired pneumonia. The patient had a bronchoscopy completed revealing right lower lobe mucus plugging. Cultures were obtained. The patient was placed on 40 mg of intravenous Methylprednisolone every eight hours for wheezing as well as Albuterol-Atrovent inhalers ordered every four hours by the pulmonologist. Initial assessment of the patient revealed ptosis and lid-lag. The patient’s husband stated that recently the patient had been experiencing blurry vision. Medical HistoryIron deficiency anemia Gastro-esophageal reflux diseaseSurgical HistoryWisdom teeth removal in 2011Family HistoryMother, Alive. Congestive heart failure, diabetes type 2, coronary artery disease, hypothyroidismFather, Alive. Hypothyroidism, coronary artery disease, rheumatoid arthritisSocial HistorySocial drinker. Two to three glasses of wine per weekDenies smokingDenies recreational drug useImmunizationsInfluenza vaccine two weeks prior to admission 10/15/2014AllergiesNo known drug allergiesHome Medications300 mg of iron sulfate twice dailyCurrent Medications0.9% Sodium Chloride @ 100 mL/hr300 mg Iron sulfate twice daily per NG tube100 mg of Ascorbic acid twice daily with Iron sulfate per NG tube3.375 g intravenous Zosyn every 6 hours1000 mg intravenous Vancomycin every 12 hours Ipratropium-Albuterol (Duoneb) 0.5 mg-3mg/3mL every four hours inhalation 1.25 mg for wheezing.5,000 units of subcutaneous heparin every eight hours40 mg Pantoprazole intravenous daily 40 mg IV Methylprednisolone Q8 hoursReview of Symptoms (Following extubation three days later)General: The patient reports fatigue, malaise. Denies fever. Denies chills, night sweats, or sleep disturbancesNeurological: Denies dizziness, syncope, or headache. Patient denies confusion, speech problems, or memory loss.HEENT: Patient reports diplopia that started over the last month that comes and goes throughout the day. Patient is currently with diplopia. Patient denies headache. Denies sore throat, cough, hearing loss, problems with speech, or nasal drainage.Neck: Denies lymphadenopathy or tenderness of the neckRespiratory: Denies dyspnea, hemoptysis, wheezing, or orthopnea. Patient denies any sputum productionCV:Denies chest pain or palpitations. Patient denies syncope or tachycardia. Denies lower extremity edema.Abdomen:Without complaints of nausea, vomiting, or diarrhea. Denies having a difficult time eating, chewing, drinking, or swallowing. Denies unintentional weight loss. GU:Patient denies change in urinary frequency, urgency, or dysuria. M/S: Denies joint pain, join swelling, or muscle pain. The patient denies problems with fine motor skills. The patient states she is weak currently and have felt weak the last few of days. Skin:Denies ecchymosis, lesions, or trauma to the skin Psychosocial:No history of depression, anxiety. Physical ExaminationVital Signs: Temperature 98.7 degrees FarenheitBlood Pressure 122/67RR 16HR 100 bpmSpO2 100% on 5 L nasal cannulaGeneral:This is a 35 year-old Caucasian female resting in bed in NADNeurological:Patient is able to follow commands. Intact cranial nerves II-VII.HEENT:The patient’s skull is normocephalic and a-traumatic. There are no masses or lesions palpated. Sclera are white. Conjunctiva are pink. PERRL @ 4 mm. Ptosis assessed bilaterally. The patient is without nystagmus, hemorrhages, or exudates. Tympanic membranes are pearly grey bilaterally without erythema. Nasal mucosa is pink and moist and septum is midline. Oral mucosa is pink, moist, and without erythema. Nasogastric tube assessed in right nare. Neck:The patient’s trachea is midline. The patient is without lymphadenopathy. The neck is supple. Negative for JVD. CV:Patient with a normal heart rate and regular rhythm. The patient has an S1 and S2. No murmurs, gallops, or clicks auscultated. Brisk carotid upstrokes without bruits. The PMI is located at the fifth intercostal space one centimeter lateral to the mid-sternal line. Respiratory:Patient with equal air entry. Lung expansion is equal. Breathing pattern regular and easy. Lung fields are clear to auscultation with a diminished right lower lobe. Patient without retractions, wheezing, or rhonchi. Negative for tactile fremitus. Abdomen: The abdomen is soft and non-distended. Bowel sounds active throughout all quadrants. The patient is negative for mass upon lite, moderate, and deep palpation. Negative for hepatomegaly or splenomegaly on physical examination. G/U: Foley catheter in place draining clear/yellow urine. No vaginal discharge. M/S: The patient moves all extremities weakly. There are 2+ reflexes that are symmetric. Extremities:Peripheral pulses 2+ and normal. No pedal edema present. No clubbing or cyanosis. The patient’s capillary refill is less than three seconds. Skin:Skin is warm and dry. Normal coloration for ethnicity. Nails without cyanosis.Laboratory FindingsTable 1: Complete White Blood Cell count and Renal PanelComplete Blood Cell Count(CBC)ResultsNormal ValuesRenal PanelResultsNormal ValuesWBC6.73.8-10.8 K cells/mLSodium140 mmol/L135-146 mmol/LRBC4.533.8-5.1 M cells/mLPotassium4.3 mmol/L3.5-5.3 mmol/LHemoglobin1611.7-15.5g/dLChloride101 mmol/L98-110 mmol/LHematocrit47.835-40%CO225 mmol/L21-23 mmol/LMCV7880-100 fLBUN10 mg/dL7-25 mg/dLMCH3027-33pg/cellCreatinine0.6 mg/dL0.5-1.2 mg/dLMCHC3532-36 g/dLGlucose98 mg/dL65-99 mg/dLRDW11.511-15%Calcium9.2 mg/dL8.6-10.2 mg/dLPlatelet239140-400 K/uLPhosphorous3.5 mg/dL2.5-4.5 mg/dLMPV11.67.5-11.5 fLMagnesium2.1 mg/dL1.5-2.5 mg/dLAnion Gap11 mEq/L8-16 mEg/LAlbumin4.2 g/dL3.6-5.1 g/dLTable 1 normal diagnostic values adapted from (Gomella, 2007) Clinician’s pocket reference 11th edition. Garden Grove, CA: McGraw HillTable 2. Arterial Blood gas and Other Laboratory TestingArtrial Blood GasResultsNormal ValuespH7.377.35-7.45BNP98<100pCO24135-45Lactic Acid1.60.5-2.2PO28880-100 mmHgAST18 U/L0-35 U/LHCO32322-26 mmol/LALT26 U/L0-35 U/LCO2 Content2423-27 mmol/LTroponin 10.04 ng/mL0-0.1 ng/mLBase Excess0-2 to 2CK230 mU/L25-145 mU/LCarboxyhemoglobin0.1UnknownT32.8 nmol/L1.5–2.9 nmol/LMethoglobin0.1%0-1.5%Free T41.2 ng/dL0.8–1.7 ng/dLReduced Hemoglobin2%0-5%TSH0.67 mcIU/mL0.35–3.0 mcIU/mL [mIU/L]% Hemoglobin97%95-98%Acetylcholine Receptor Binding61.28<0.02IgG596 mg/dL700-1500 mg/dLAcetylcholine Receptor Antibodies88<0.02MusK antibodies55.6<10Uric Acid3.8 mg/dL1.4–5.8 mg/dLVitamin D-25-Hydroxy42 ng/dL20–50 ng/mLTable 2. Normal diagnostic values adapted from (Nicoll, Lu, Pignone, & McPhee, 2012) Pocket Guide to Diagnostic Tests 6th edition. New York, NY: McGraw Hill. Diagnostic FindingsOn admission, a chest radiograph and head computed tomography (CT) scan were completed. The chest radiograph revealed a right lower lobe infiltrate with bilateral haziness. The CT scan of the head was negative for mass, tumor, intracranial bleed, or ischemia. The patient received intravenous antibiotics and clinically improved. A bronchoscopy was completed while patient was intubated. Right lower lobe mucous plugging was assessed. Cultures were sent by the pulmonologist to the lab for diagnostics and cytology. After passing her spontaneous breathing trial, the patient was extubated and placed on 5 liters of nasal cannula to maintain a SpO2 of greater than 92%. The patient continued to complain of diplopia. Ptosis was assessed on examination. The patients reported problems with swallowing prior to admission. Subsequently, antibody screening for myasthenia gravis was completed and an electromyogram was ordered. A swallow evaluation by a speech therapist was also ordered. The patient passed her swallow evaluation. Antibody screenings revealed acetylcholine and mUsk antibodies were present in the blood. An electromyogram (EMG) was also ordered. Decreased amplitude and action potential were evaluated on the EMG. Intravenous steroids were continued and 30 mg of Mestinon was ordered four times a day by the neurologist. Differential DiagnosisMyasthenia gravis is the first differential diagnosis for this patient. Myasthenia gravis is an autoimmune disorder affecting the nicotinic acetylcholine receptors. Muscle-specific kinase (MuSK) and Lipoprotein-related protein 4 (LRP4) have been recently found as targets (Aknin & Panse, 2014). On the surface of muscles cells, acetylcholine receptors are found (Aknin & Panse, 2014). Typically, impulses travel down a nerve path to the acetylcholine receptors in order for a muscle to contract. In patients with myasthenia gravis, the density of the acetylcholine receptor is reduced resulting in decrease endplate conduction (Aknin & Panse, 2014). The decreased conduction and impulses cause fatigue and continued muscle weakness (Drachman, 2012). Myasthenia gravis is more prevalent in women than in men. In the early course of myasthenia gravis, the ocular nerves and muscles are more involved (Drachman, 2012). Initial complaints of diplopia and ptosis are common. Patients may have difficulty in swallowing. Dysphagia can come from weakness of the palate, tongue, or pharynx (Kellerman, 2015). Nasal and oral aspiration of liquids or food can occur as a result of difficulty swallowing. Bulbar weakness is prevalent in MuSK antibody–positive myasthenia gravis. If weakness is restricted to the extra-ocular muscles for three years or greater, patients are most likely experiencing ocular myasthenia gravis (Drachman, 2012).This specific patient had complaints of shortness of breath and was febrile as an outpatient. After assessment of the patient, her healthcare provider prescribed Levaquin, a fluoroquinolone, for community acquired pneumonia. The patient continued to decline since the Levaquin can weaken neuromuscular transmission, thus helping to cause a myasthenia crisis (Drachman, 2012). Since the patient’s respiratory status improved with the removal of the Levaquin and with the initiation of steroids, one can consider the possibility of a myasthenia gravis diagnosis. The patient also had ptosis and diplopia, common symptoms in patients with myasthenia gravis. Laboratory work and an electromyogram will be beneficial in making the diagnosis (Drachman, 2012). Aspiration pneumonia is another differential diagnosis for this patient. Per the patient and her husband’s reports, the patient had been experiencing difficulty in swallowing and chewing food over the past couple of weeks. Aspiration pneumonia occurs when food travels down the trachea instead of being swallowed to the gastrointestinal tract (Ferri, 2015). Bacteria arise from aspirated material causing pneumonia (Ferri, 2015). Streptococcus pneumoniae, staphylococcus aureus, haemophilus influenza, and pseudomonas aeruginosa are common pathogens associated with aspiration pneumonia. A chest radiograph of the patient reveals a right lower lobe infiltrate that is consistent with aspiration pneumonia since most aspiration particles travel via the right main-stem bronchus (Ferri, 2015). The patient likely has aspiration pneumonia, but the reason behind the inability to swallow appropriately remains in question. Given the patient’s age and other confounding symptoms, the nurse practitioner should consider a neurologic etiology. Lambert-Eaton Syndrome is a type of myasthenia that is commonly seen in patients with oat cell carcinoma (Ropper, Samuels, & Klein, 2014). In patients with Lambert-Eaton Syndrome, muscles of the shoulder, trunk, pelvis, and lower extremities become weak. Patients will have difficulty rising from a chair, walking, or climbing (Ropper, Samuels, & Klein, 2014). The patient in this case has fatigue of her lower extremities, making this a possible diagnosis. However, the patient does have ptosis, dysphagia, and diplopia making Lambert-Eaton Syndrome a possible, but not probable, diagnosis. The other factor is the patient does not have a history of oat cell carcinoma and the CT scan of her chest did not reveal any nodule implying a cancer etiology. Lambert-Eaton Syndrome is a differential diagnosis for this patient. However, given the signs, symptoms, and history of this patient, the diagnosis is improbable (Ropper, Samuels, & Klein, 2014). Guillan Barre Syndrome is another possible diagnosis. Guillan Barre Syndrome (GBS) is a disease state preceded by an illness and on occasion can follow an administration of the influenza vaccine (Hauser & Amato, 2012). GBS is a rapid motor paralysis that can be with or without sensory disturbance (Hauser & Amato, 2012). Paralysis is typically described as ascending paralysis. Most patients have pain in their heads, necks, and backs on admission to the hospital with 30% of patients requiring mechanical ventilation for respiratory failure. Patients with GBS have loss of control of their autonomic nervous systems and may have huge fluctuations in blood pressure, heart rate, and may even acquire arrhythmias (Hauser & Amato, 2012). GBS is commonly an acute inflammatory demyelinating polyneuropathy. Cellular and humoral immunity are damaged in patients with GBS. Paralysis and hemodynamic instability are caused by infection and vaccinations. In this specific case study, the patient is at risk for Guillan Barre given the recent infection and vaccination (Hauser & Amato, 2012). However, the patient is not experiencing paralysis and the muscle weakness is not ascending in nature, making this diagnosis unlikely. Diagnostic Tests and RationaleComputed Tomography (CT) Scan of the Chest A computed tomography scan of the chest is a diagnostic test completed in patients with likely myasthenia gravis due to risk of a thymoma. Most patients with myasthenia gravis have an abnormal thymus gland (Daroff, Fenichel, Jankovic, & Mazziotti, 2012). In patients with myasthenia gravis, 10% have a thymoma and 70% have lymphoid follicular hyperplasia (Daroff et al., 2012). All the immune mediators related to myasthenia gravis are housed in the thymus. When a thymus is enlarged and shows risk of causing increased symptoms, a thymectomy is done. A CT scan is the first choice, however, in diagnosing a patient with a thymoma or enlarged thymus gland. Specificity of a CT of the chest is as high as 95% in diagnosis (Pirronti et al., 2002). It is also important to note that patients who are positive for AChR antibodies are likely to have developed a thymoma (Kellerman, 2015).Chest radiographA chest radiograph is one of the first tests completed in the hospital setting. This patient had a history of shortness of breath resulting in acute respiratory failure. Since pneumonia was suspected, a chest radiograph can rule in the diagnosis (Vincent et al., 2013). In patients within the intensive care unit setting, a chest radiograph has 92% sensitivity and 91% specificity for diagnosing pneumonia (Vincent et al., 2013). Key features of a chest radiograph for pneumonia are infiltrates seen on the film. A patient may concurrently have fevers, decreased appetite, and chills. Electromyogram (EMG)An electromyogram (EMG) is another test helpful in diagnosing myasthenia gravis. An electromyogram (EMG) is ordered to record the electrical activity of the muscle. The EMG can detect neuromuscular disorders by detecting how active the muscles are in the patient (Aminoff, 2012). Fatigability of the patient’s muscles is also detected. Electrical activity of muscles at rest and during activity are recorded and used to make a diagnosis of a neuromuscular disorder. In muscles that are at rest, electrical activity is minimal. A patient with an autoimmune or inflammatory process can have abnormal spontaneous activity (Aminoff, 2012). The information received from the EMG aids in the diagnosis of myasthenia gravis. Acetylcholine receptor antibody testing (AChR)Acetylcholine receptor antibody testing (AChR) is a blood test that detects antibodies against one’s acetylcholine receptors. In patients with generalized symptoms, only 85% will have antibodies in their testing (Goldman et al., 2012). Only half of patients with ocular involvement with their myasthenia gravis will show antibodies. In patients where AChR do not show in their laboratory work and continue to have symptoms highly specific myasthenia gravis, muscle-specific kinase (MuSK) antibody levels should be drawn (Goldman et al., 2012). Tensilon TestThe tensilon test may be completed in order to diagnosis myasthenia gravis. The tensilon test uses Edrophonium or Neostigmine, short-acting cholinesterase inhibitors. When administered intravenously, the medication prolongs effects of acetylcholine and improves myasthenia weakness (Goldman et al., 2012). Typically, 2 mg of Edrophonium is given intravenously followed by 6 mg if no adverse reactions occur (Goldman et al., 2012). The complication of this test is that it has to be completed under close medical observation since the Edrophonium can cause bradycardia and subsequent syncope. Atropine should be readily available when completing this test (Goldman et al., 2012). The tensilon test is a great method in distinguishing between myasthenia gravis and a cholinergic crisis. The tensilon test in myasthenia gravis will improve muscle weakness and in a cholinergic crisis, the muscle weakness will worsen muscle weakness (Kellerman, 2015). Prioritized PlanIn this patient with myasthenia gravis, treatment includes symptom control, immunosuppression, and a possible thymectomy (Kellerman, 2015). The initial treatment choice is symptom control. Acetylcholinesterase inhibitors lengthen action potential at the post-synaptic cleft (Kellerman, 2015). Mestinon and Prostigmin are common acetylcholinesterase inhibitors (Kellerman, 2015). Mestinon can be effective in controlling mild symptoms. Mestinon is ordered between 30 mg and 90 mg every three to four times a day (Drachman, 2012). Adverse effects include abdominal cramps, nausea, vomiting, and diarrhea. An overdose of acetylcholinesterase inhibitors may lead to severe hypotension and bradycardia. Patients with symptoms beyond bulbar and ocular symptoms will benefit more from immunosuppression (Kellerman, 2015). Long-term use of Mestinon exists, but must be given at night since there is variable absorption of the medication when given during the day (Drachman, 2012). In the state of Ohio, the advanced practice registered nurse can prescribe acetylcholinesterase inhibitors (The Ohio Board of Nursing, 2014). Prednisone is the steroid of choice for long-term myasthenia gravis symptoms. While in the intensive care unit, the patient will be on methylprednisolone for rapid effects (Marino, 2014). Prednisone has a fast onset of action compared to other immunosuppressive agents used. Initiating patients on high doses of steroids to achieve a quick clinical response is sometimes preferred (Kellerman, 2012). Other immunosuppressive treatments can be used with steroids. Initiating multiple immunosuppression medications should be completed in an inpatient situation. Prednisone can exacerbate symptoms in the short term and those symptoms can increase with higher doses (Kellerman, 2015). To prevent exacerbation of symptoms, lower doses, such as 15–20 mg, are initiated and then titrated depending on the patient’s response. The disadvantage is that it takes longer to achieve significant symptomatic improvement (Kellerman, 2012). In the state of Ohio, the advanced practice registered nurse can prescribe prednisone (The Ohio Board of Nursing, 2014). A thymoma is an accumulation or growth of abnormal epithelial cells (Aknin & Panse, 2014). As stated above, patients with myasthenia gravis may have a thymoma, causing worsening symptoms. A thymectomy should be considered for patients less than 60 years of age and have no contraindications to surgery (Aminoff & Kerchner, 2014). In a patient where myasthenia gravis is a recent onset, as with the patient in the case study, pharmacological treatment is given first and reassessment of the thymoma on an outpatient setting is completed to decide if surgery is an option or if remission has occurred (Aminoff & Kerchner, 2014). Plasmapharesis and intravenous immunoglobulin (IVIG) are also considered in the treatment of acute exacerbations on myasthenia gravis (Aminoff & Kerchner, 2014). If immediate improvement is required due to the severity of weakness, IVIG should be administered or plasmapheresis should be undertaken (Kellerman, 2015). The patient’s IGG level was low on admission, requiring an IGG dose of 0.66 mL/kg. Plasmapharesis should be an option when the patient is unable to progress with care despite medications and IVIG. Plasmapharesis clears pathological antibodies from the patient’s system (Marino, 2014). Plasmapahresis acts more rapidly the IVIG. In this case, the patient received IVIG first and improved with different antibiotics, Mestinon, and steroid therapy. However in other cases, plasmapharesis may be an option (Marino, 2014). In the state of Ohio, the acute care nurse practitioner can only prescribe immunoglobulin’s if it is within their standard care agreement (The Ohio Board of Nursing, 2014). The patient was also started on intravenous Zosyn and Vancomycin for broad-spectrum antibiotic coverage. A bronchoscopy was completed revealing mucous-plugging in the right lower-lobe. Cultures were obtained. Once cultures results come back, de-escalation of antibiotics can be done. The patient will remain on deep vein thrombosis (DVT) prophylaxis with 5,000 units of Heparin administered subcutaneously every eight hours. The patient was initiated on peptic ulcer prophylaxis with intravenous Pantoprazole 40 mg daily. In the state of Ohio, the ACNP with a CTP may prescribe Heparin and Pantoprazole (Ohio Board of Nursing). Follow-Up The patient in this case study has myasthenia gravis. Most likely, the symptomology started prior to the pneumonia diagnosis. The fluoroquinolone prescribed exacerbated the illness. The patient was given Mestinon and Methylprednisolone in the acute management of the illness with clinical improvement. It is important for the acute care nurse practitioner to follow daily with complete blood cell counts and renal profiles for the intensive care unit patient. On the outpatient setting, the acute care nurse practitioner should follow CBC trends since the patient will eventually change to oral prednisone. Also, following symptomology and AChR antibody levels will lead the acute care nurse practitioner in deciding if the patient’s dosage of medications should be adjusted or if the medication should be changed (Aminoff & Kerchner, 2014). Patients with myasthenia gravis may have difficulty with swallowing. The patient in this case study stated she was having difficulty swallowing. Because of risk for aspiration, a swallow evaluation by a speech therapist should be completed in order to develop a nutrition plan (Kellerman, 2015). In a patient with continued aspiration and no recovery of swallowing function, a percutaneous endoscopic gastrostomy tube can be considered. In this case, the patient passed her swallow evaluation. However, the patient should have continued observation of her swallowing capabilities (Drachman, 2012). Azathioprine, Mycophenalate, and Cyclosporine can also be used in myasthenia gravis patients for immunosuppression. Typically, Azathioprine, Mycophenalate, and Cyclosporine are used for long-term therapy (Drachman, 2012). For the intermediate term, glucocorticoids and cyclosporine generally produce symptom improvement within a one to three month period. The benefits of azathioprine and mycophenolate mofetil usually begin after many months. These medications have advantages for the long-term treatment of a patient’s myasthenia gravis (Drachman, 2012). Azatioprine is used as a steroid-sparing agent. Azatioprine can take up to six months to show effects. Adverse effects that may lead to discontinuation of the medication include fever, abdominal pain, nausea, and vomiting (Kellerman, 2015). Patients typically start at a dosage of 50 mg per day and titrate by 50 mg per week to reach a goal of two to three mg/kg/day (Kellerman, 2015). Mycophenolate is used more commonly than azathioprine because of its fewer side effects. Mycophenolate also begins to work within three month of initiation. Cyclosporine is used when patients fail therapy with Mycophenolate and Aztioprine. Doses should be titrated based on trough levels between 50 and 150 mg/dL (Kellerman, 2015). Depending on the patient’s response to Mestinon, other immunosuppression may be started. It is important to educate patients regarding infection, illness, pregnancy, stress, and warm weather as they may cause myasthenia symptom exacerbation (Nan, 2014). Patients should be urged to take periods of rest during the day in order to regain strength. Patients should also be educated on signs and symptoms of an acute respiratory illness and be urged to contact healthcare providers in order to prevent a crisis from occurring (Nan, 2014). Health Promotion There are certain medications that can exacerbate myasthenia gravis and cause a myasthenia crisis. Though the providers treating patients with myasthenia gravis are aware of these medications, the patient should also be aware in order to avoid worsening symptoms. Fluoroquinolones, aminoglycosides, and macrolides should be avoided in patients with myasthenia gravis (Drachman, 2012). Non-depolarizing agents, local anesthestics such as Procaine, botulinum, quinine, allopurinol, metoprolol, propranolol, and atenolol are also medications that should be avoided. The medications listed have properties in their drug profiles that can exacerbate myasthenia gravis and worsen symptoms (Drachman, 2012).In patients that are intubated, the acute care nurse practitioner will order ventilator-associated pneumonia (VAP) prevention including elevating the head of the bed 30 degrees and ordering the patient to receive mouth care every four hours (Isakow & Kollef, 2012). The nurse practitioner will do spontaneous breathing trials in order to evaluate the patient’s ability to be extubated. The patient will be placed on peptic ulcer prophylaxis. Subcutaneous Heparin and sequential compression devices are ordered to promote deep vein thrombosis prophylaxis (Isakow & Kollef, 2012). The acute care nurse practitioner will wean the ventilator setting as the patient tolerates (Isakow & Kollef, 2012). Spontaneous breathing trials and the rapid shallow breathing index are pertinent in patients with myasthenia gravis (Souter & Manno, 2013). Minute volume recovery time can be used to predict extubation success (Souter & Manno, 2013). Patients with neuromuscular disease tend to have more of an issue with airway patency and can suffer from stridor post-extubation. The patient was ordered intravenous Methylprednisolone for such events. Once extubated, the patient will work with physical and occupational therapy to prevent deconditioning (Isakow & Kollef, 2012). Nutrition is pertinent in a patient in the intensive care unit. A nasogastric tube was placed while the patient was intubated in order to deliver trophic feeds. The target in terms of feeds for this patient is to receive low dose feeding with 500 kcal per day (Dellinger et al., 2012). The low dose feeding will help with gut motility. The feeds will then be advanced as tolerated (Dellinger et al., 2012). Following extubation, a swallow evaluation was completed since the patient has had trouble swallowing in recent months. Continued observation of the patient’s ability to swallow is important for respiratory and infection purposes (Isakow & Kollef, 2012). The patient has been vaccinated already with the influenza vaccine. The patient should also consider having the pneumonia vaccine administered to her. Patients with myasthenia gravis will experience an exacerbation of symptoms with infections. As recorded in this case study, pneumonia was the infection that initiated the symptoms. The pneumonia vaccine should be given to this patient on an outpatient basis in order to prevent infection in the future (Kollef & Isakow, 2012). ReferencesAknin, S. B., & Panse, R. L. (2014). Myasthenia gravis: A comprehensive review of immune dysregulation and etiological mechanisms. Journal of Autoimmunity, 90, 90-100. , M. J. (2012). Electrodiagnostic Studies of Nervous System Disorders: EEG, Evoked Potentials, and EMG. In D. L. Longo, D. L. Kasper, J. L. Jameson, A. S. Fauci, S. L. Hauser, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). Retrieved from , M. J., & Kerchner, G. A. (2014). Nervous system disorders. In M. A. Papadakis, & S. J. McPhee (Eds.), Current medical diagnosis & treatment. New York, NY: McGraw Hill.Daroff, R. B., Fenichel, D. M., Jankovic, J., & Mazziotti, J. C. (2012). Disorders of neuromuscular transmission. In Bradley’s neurology in clinical practice (6th ed.). Retrieved from , D. B. (2012). Myasthenia Gravis and Other Diseases of the Neuromuscular Junction. In D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, J. L. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). Retrieved from , F. F. (2015). Aspiration pneumonia. In Ferri’s clinical advisor. Retrieved from , L., Schafer, A. I., Arend, W. P., Armitage, J. O., Clemmons, D. R., Drazen, J. M., ... Scheld, W. M. (2012). Disorders of neuromuscular transmission. In Goldman’s Cecil Medicine (24th ed.). Retrieved from , L. G., & Haist, S. A. (2007). Clinicians pocket reference (11th ed.). Retrieved from , S. L., & Amato, A. A. (2012). Guillain-Barré Syndrome and Other Immune-Mediated Neuropathies. In D. L. Longo, D. L. Kasper, J. L. Jameson, A. S. Fauci, S. L. Hauser, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw Hill.Kellerman, R. D. (2015). The Nervous System. In E. T. Bope, & R. D. Kellerman (Eds.), Conn’s current therapy 2015. Retrieved from , M., & Isakow, W. (2012). The Washington manual of critical care (2nd ed.). New York, NY: Lippincott Williams & Wilkins.Marino, P. L. (2014). The ICU book (4th ed.). New York, NY: Wolters Kluwer.Nan, N. (2014). First Consult. Retrieved from , D., Lu, C. M., Pignone, M., & McPhee, S. J. (2012). . In Pocket Guide to Diagnostic Tests (6th ed.). Retrieved from , T., Rinaldi, P., Batocchi, A. P., Evoli, A., Schino, C., & Marano, P. (2002). Thymic lesions and myasthenia gravis. Diagnosis based on mediastinal imaging and pathological findings. Acta Radiologica, 43(4), 380-384. Retrieved from , A. H., Samuels, M. A., & Klein, J. P. (2014). Adams and Victor’s principles of neurology (10th ed.). Retrieved from , M. J., & Manno, E. M. (2013). Ventilatory Management and Extubation Criteria of the Neurological/Neurosurgical Patient. The Neurohospitalist, 3(1), 39-45. Ohio Board of Nursing. (2014). Formulary with index for CTP prescribers. Retrieved from , L., Mark, C., Mendoza, M., Saket, R., Gardner, M., Turk, B., & Escobar, G. (2013). Automated identification of pneumonia in chest radiograph reports in critically ill patients. 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