Acute Care II Comprehensive Case Study - Weeblylauralangenhop.weebly.com/uploads/1/3/4/1/13414304/acute... · Web viewAcute Care II Comprehensive Case Study Laura Langenhop Wright

Running head: langenhop_COMPREHENSIVE CASE STUDY 1

Acute Care II Comprehensive Case Study

Laura Langenhop

Wright State University

langenhop_COMPREHENSIVE CASE STUDY 2

Acute Care II Comprehensive Case Study

Patient information

M.H. is a 35 year-old Caucasian Female

Source

Patient and patient’s husband, reliable resources

Chief Complaint

Acute Respiratory Failure

History and Physical

M.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 History

Iron deficiency anemia

Gastro-esophageal reflux disease

Surgical History

Wisdom teeth removal in 2011

Family History

Mother, Alive. Congestive heart failure, diabetes type 2, coronary artery disease,

hypothyroidism

Father, Alive. Hypothyroidism, coronary artery disease, rheumatoid arthritis

Social History

Social drinker. Two to three glasses of wine per week

Denies smoking

Denies recreational drug use

Immunizations

Influenza vaccine two weeks prior to admission 10/15/2014

Allergies

No known drug allergies

Home Medications

300 mg of iron sulfate twice daily

Current Medications

0.9% Sodium Chloride @ 100 mL/hr


300 mg Iron sulfate twice daily per NG tube

100 mg of Ascorbic acid twice daily with Iron sulfate per NG tube

3.375 g intravenous Zosyn every 6 hours

1000 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 hours

40 mg Pantoprazole intravenous daily

40 mg IV Methylprednisolone Q8 hours

Review of Symptoms (Following extubation three days later)

General: The patient reports fatigue, malaise. Denies fever. Denies chills, night sweats, or

sleep disturbances

Neurological: 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 neck

Respiratory: Denies dyspnea, hemoptysis, wheezing, or orthopnea. Patient denies any sputum

production

CV: 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 Examination

Vital Signs:

Temperature 98.7 degrees Farenheit

Blood Pressure 122/67

RR 16

HR 100 bpm

SpO2 100% on 5 L nasal cannula

General: This is a 35 year-old Caucasian female resting in bed in NAD

Neurological: 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 Findings

Table 1: Complete White Blood Cell count and Renal Panel

Complete Blood Cell

Count(CBC)

Results Normal Values

Renal Panel Results Normal Values


WBC 6.7 3.8-10.8 K cells/mL

Sodium 140 mmol/L 135-146 mmol/L

RBC 4.53 3.8-5.1 M cells/mL

Potassium 4.3 mmol/L 3.5-5.3 mmol/L

Hemoglobin 16 11.7-15.5g/dL

Chloride 101 mmol/L 98-110 mmol/L

Hematocrit 47.8 35-40% CO2 25 mmol/L 21-23 mmol/L

MCV 78 80-100 fL BUN 10 mg/dL 7-25 mg/dL

MCH 30 27-33pg/cell

Creatinine 0.6 mg/dL 0.5-1.2 mg/dL

MCHC 35 32-36 g/dL Glucose 98 mg/dL 65-99 mg/dL

RDW 11.5 11-15% Calcium 9.2 mg/dL 8.6-10.2 mg/dL

Platelet 239 140-400 K/uL Phosphorous 3.5 mg/dL 2.5-4.5 mg/dL

MPV 11.6 7.5-11.5 fL Magnesium 2.1 mg/dL 1.5-2.5 mg/dL

Anion Gap 11 mEq/L 8-16 mEg/L

Albumin 4.2 g/dL 3.6-5.1 g/dL

Table 1 normal diagnostic values adapted from (Gomella, 2007) Clinician’s pocket reference 11th

edition. Garden Grove, CA: McGraw Hill

Table 2. Arterial Blood gas and Other Laboratory Testing

Artrial Blood Gas Results Normal Values

pH 7.37 7.35-7.45 BNP 98 <100pCO2 41 35-45 Lactic Acid 1.6 0.5-2.2PO2 88 80-100

mmHgAST 18 U/L 0-35 U/L

HCO3 23 22-26 mmol/L

ALT 26 U/L 0-35 U/L

CO2 Content 24 23-27 mmol/L

Troponin 1 0.04 ng/mL 0-0.1 ng/mL

Base Excess 0 -2 to 2 CK 230 mU/L 25-145 mU/L

Carboxyhemoglobin 0.1 Unknown T3 2.8 nmol/L 1.5–2.9 nmol/L

Methoglobin 0.1% 0-1.5% Free T4 1.2 ng/dL 0.8–1.7


ng/dLReduced

Hemoglobin2% 0-5% TSH 0.67

mcIU/mL0.35–3.0 mcIU/mL [mIU/L]

% Hemoglobin 97% 95-98% Acetylcholine Receptor Binding

61.28 <0.02

IgG 596 mg/dL 700-1500 mg/dL

Acetylcholine Receptor

Antibodies

88 <0.02

MusK antibodies

55.6 <10

Uric Acid 3.8 mg/dL 1.4–5.8 mg/dL

Vitamin D-25-Hydroxy

42 ng/dL 20–50 ng/mL

Table 2. Normal diagnostic values adapted from (Nicoll, Lu, Pignone, & McPhee, 2012) Pocket

Guide to Diagnostic Tests 6th edition. New York, NY: McGraw Hill.

Diagnostic Findings

On 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 Diagnosis

Myasthenia 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 Rationale

Computed 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 radiograph

A 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 Test

The 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 Plan

In 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).

http://accessmedicine.mhmedical.com.ezproxy.libraries.wright.edu:2048/drugs.aspx?globalId=6363


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).


References

Aknin, S. B., & Panse, R. L. (2014). Myasthenia gravis: A comprehensive review of immune

dysregulation and etiological mechanisms. Journal of Autoimmunity, 90, 90-100.

http://dx.doi.org/10.1016/j.jaut.2013.12.011

Aminoff, 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.).

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Aminoff, 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

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