Case Study
James Morasco
College of Southern Nevada – Nursing 211 Clinical
Professor Judith Alewel, MSN, RN
October 15, 2012

Introduction
AV is a 57 year old male whom presented to the Emergency Department of Valley Hospital Medical Center in Las Vegas, NV on September 7, 2012 with the classic signs and symptoms of a left-sided middle cerebral artery (MCA) infarct and was admitted to the medical intensive care unit (MICU). These signs included left sided facial drooping, non-reactive left pupil, right sided weakness in the upper and lower extremities, and the inability to speak. Along with the signs and symptoms of the stroke, a 12-lead EKG revealed that he also has atrial fibrillation. The initial computerized tomography (CT) scan of his brain revealed nothing, but a subsequent MRA (magnetic resonance angiogram) concluded that he did, in fact, have an occluded branch of the left MCA that eventually converted to become hemorrhagic and he was admitted to the MICU. The MRA also found a persistent left trigeminal artery, which is insignificant to his presenting disease process. Along with all of this, a two dimensional echocardiogram revealed some significant hearts problems that will be discussed later. I cared for this patient during the clinical shift on September 18, 2012.
History and Physical The only history and physical that was available in this patient’s chart was some narrative comments from his daughter notated by the physician, and this is most likely due to the fact that the patient could not verbalize anything on his own. According to his daughter (who lives with the patient), AV has had atrial fibrillation for “a long time,” and has managed it with digoxin. He also has a history of hypertension that he manages with metoprolol, he has type II diabetes mellitus that he controls with his diet, and he has no surgical history whatsoever. Upon admission, the physical findings were very typical of a left MCA infarct. His presenting vital signs were as follows: Blood pressure 145/95, heart rate 106 beats per minute, respiration rate 20 breaths per minute, oral temperature 36.8⁰ Celsius, oxygen saturation 97% on two liters of oxygen via nasal cannula. His left pupil was 2mm larger than his right, and did not react to light. His right pupil was 4mm, and did react to light. Neither of his two eyes accommodated when tested, and there was left-sided hemiparesis in his face. His gag reflex was absent when tested as well. Right-sided hemiparesis in his upper extremity was present, but his lower right extremity was just weakened as he was able to move his leg. He was able to dorsiflex and plantar flex both of his feet with grades of +1 on the right and +3 on the left. The left side of his upper body had good strength of +3, and right grip strength of 0. His heart sounds were abnormal, as an S3 sound and murmur were auscultated, but there were no carotid bruits heard. The cause of this was later found to be severe mitral and moderate tricuspid valve regurgitation. His lung sounds were clear in all fields bilaterally. His bowel sounds were present and normoactive and he didn’t report any pain or tenderness when palpated. The rest of his skin was clean, dry, intact, and no lesions or bruising was noted.
Systems Review – Assessment When I entered the patient’s room, I introduced myself and asked the patient if I could do a physical assessment on him, and he shook his head yes. I asked if he could speak English, and he again shook his head yes. While speaking Spanish, I asked if he could speak Spanish, and he again shook his head yes. I then asked if he would mind if I turned the light on, and he shook his head no. I took his vital signs, which were as follows: Blood pressure 120/81, heart rate 92 beats per minute, respiration rate 18 breaths per minute, oral temperature 36.5⁰ Celsius, oxygen saturation 98% on two liters of oxygen via nasal cannula.
AV appears his documented age and is alert. When I asked him if he knows where he is, he mumbled something, but it wasn’t very clear or rational, so expressive aphasia is noted and assessing orientation cannot be done at this time. He doesn’t appear to be in distress, his body parts appear equal and proportionate bilaterally, and he appears to be lying in bed comfortably with the head of his bed elevated approximately 50 degrees. AV’s mood is pleasant, and appears clean but not groomed. When asked about pain, he shakes his head no. I asked him to use his hands to rate his pain on a zero-to-ten scale, and explained the scale to him. He held up a zero. I asked him if that means everywhere, and he shook his head yes. I pointed to the window, the television, and the curtain and asked him to remember these items. Three minutes later I asked him to point to the items from earlier, and he pointed out all three in the same order I did.
His skin is warm, dry, intact, and the color is appropriate for his race and nationality. He has a twenty gauge peripheral IV in his right forearm that was inserted on September 16, 2012. The IV site does not have any redness, swelling, edema, or signs of infiltration or extravasation. When asked about pain at the IV site, the patient shakes his head no.
AV denies having a headache and experiencing any dizziness. His facial expression is asymmetrical, as the left side of his face is drooped a small amount. The scleras of both eyes are white, and his pupils are both equal and round bilaterally. The right pupil is quickly reactive to light, but the left pupil is sluggish but equal in its response to light. Neither of his eyes accommodates, but they can both slowly track the six cardinal positions. When holding an alcohol swab underneath his nose, AV backed away, indicating that he could smell it. He has aphagia, his uvula is midline with no redness or swelling in his throat, and his mucous membranes are moist. His gag reflex is not intact, and he cannot swallow. His neck has full range of motion with good strength against resistance, has no jugular vein distention on either side, and has no lumps or bumps. AV also denies pain and tenderness on his neck. His carotid pulses are equal, irregular rhythm, and thready with no bruits present upon auscultation.
His chest doesn’t have any abnormal pulsations, heaving or lifts when his heart beats and he denies any numbness, tingling, or pain in his extremities. AV has even brachial, radial, and pedal pulses bilaterally rated at a +1 and mildly thready. The cause of his thready pulse is most likely due to the atrial fibrillation that is evident on the telemetry monitor he is wearing. His apical heart beat was auscultated as irregular, nominal strength, and a murmur is noted at the third intercostal space at the left sternal border. Capillary refill is less than two seconds, and there is no peripheral edema noted.
When asked if he has had a cough, AV shakes his head no, and responds the same way when I ask if there is any pain when he breathes. His breathing isn’t labored, and his chest expands symmetrically with each breath. His anteroposterior to transverse ratio is two-to-one, and his lung sounds a clear in all fields bilaterally.
AV’s abdomen has a PEG tube located in the upper left quadrant of his abdomen receiving Jevity 1.2 at a rate of sixty five milliliters an hour continuously. It was placed there surgically on September 9, 2012 and he reports that there is no pain at the insertion site. The site’s dressing is clean, dry, intact, and there is no drainage noted. The patient uses a urinal to void into, and the urinal at the bedside has clear, light yellow urine in it. He is also continent of his bowels, and he uses a bedpan to defecate. He denies constipation, and bowel sounds are normoactive in all quadrants.
The range of motion of AV’s upper extremities differs from left to right. The left side has full range of motion, while the right side is slightly limited in speed and strength. Left sided grip strength is +3. The right sided grip strength is +1 at first, and slowly gets stronger to +2. Push and pull strength is rated the same way with the upper extremities with the left getting a +3, and the right getting a very slow +2-3. His lower extremities are different, however. They are equally strong in pushing, pulling, plantar, and dorsiflexion at +3 all around, and he can move his toes freely bilaterally.
Systems Review – Labs and Diagnostics The laboratory values for AV were quite unremarkable when he arrived at the hospital. He only had a few lab values that were elevated, and the rest were in the normal range. For instance, mean corpuscular volume (MCV) was slightly elevated at 101.4fL, and the normal range is 80.0-100.0fL. This elevation is most likely due to vitamin B12 or folic acid deficiency (Pagana & Pagana, 2009, p. 460). Because the MCV is slightly elevated, the mean corpuscular hemoglobin (MCH) will be elevated as well because the size of the red blood cells has increased, so both numbers will go up together (Pagana & Pagana, 2009, p. 460-461). The MCH was 33.9pg, and the normal range is 27.0-33.0pg. AV’s mean platelet volume (MPV) was also elevated at 13.7fL, with a normal range of 7.5-11.5fL. This elevation is most likely due to his valvular heart disease of mitral and tricuspid valve regurgitation (Pagana & Pagana, 2009, p. 420). His blood glucose was 134mg/dL, which is above the normal range of 65-99mg/dL. This is due to the fact that AV has diet-controlled type II diabetes mellitus. His total bilirubin was also slightly increased at 1.3mg/dL, and the normal range is 0.2-1.2mg/dL. This is caused by an increase in breakdown of red blood cells in his system, most likely due to atrial fibrillation and the cerebrovascular accident (CVA) (Pagana & Pagana, 2009, p. 130). Other than these, the rest of his lab values were within normal limits at admission.
The day that I cared for AV, his lab values had mostly stabilized. One value that was out of range was WBC at 12.0k/uL, with a normal range of 3.8-10.8k/uL. This could be due to an infectious process or stress, so we will monitor his temperature to see if it rises and intervene further if necessary (Pagana & Pagana, 2009, p. 549). His MCH remained slightly elevated at 33.8pg, but MCV and MPV had returned to within the normal range. His blood glucose also remained high at 276mg/dL. I questioned the order for Jevity for the blood sugar elevation, but I was told by the nurse that the physician was not concerned about his elevated blood glucose and did not want to order any insulin, other medication, or Glucerna.
One lab value that was normal before and is now low is creatinine. The level on the clinical date was 0.60mg/dL, and the normal range is 0.79-1.33mg/dL. This is most likely caused by the decreased muscle mass from being in the hospital bed for so long and suffering some muscle atrophy (Pagana & Pagana, 2009, p. 206). In addition to these, the last lab value that was out of the normal range was the serum osmolality. His level was at 306mOsm/kg, and the normal range is 275-300 mOsm/kg. This is most likely due to the hyperglycemia (Pagana & Pagana, 2009, p. 392). The first diagnostic study performed on AV was a CT scan of his brain without contrast. This was performed within an hour of his arrival to the emergency department, and the scan revealed no evidence of any acute intracranial process. The next study was an ultrasound of his carotid arteries, which resulted in no significant stenose being visualized. Approximately twenty-one hours after his arrival, a MRA was performed and revealed a branch of the left MCA was occluded, along with a persistent trigeminal artery. Immediately after the MRA, an MRI was performed. This revealed a large left MCA distribution infarction. Later that night, another CT scan of the head was performed. This revealed an evolving left MCA infarct with new foci of hyperattenuation in the region of the infarct and a small amount of hemorrhage could not be excluded, along with a 4mm midline shift to the right. Approximately twelve hours later, another CT scan was performed. This revealed a stable left frontal MCA distribution infarct with increasing edema, mass effect, and right midline shift increase from 4mm to 8mm. Four days later, another CT scan was performed. This revealed hemorrhagic conversion of the infarct with the midline shift increasing from 8mm to 11mm, along with mild hydrocephaly. The next day, about twenty four hours after the last scan, another CT scan was performed. This scan was interesting, because it revealed that the midline shift had decreased to 8mm from 11mm, and the hemorrhage had decreased in size from 2.7 x 1.8 x 1cm to 2.5 x 1.6 x 0.9 cm. Two days later, a chest x-ray was performed and revealed no acute radiographic abnormalities.
Finally, on September 17, 2012, a two-dimensional echocardiogram was performed. This revealed many interesting things. The left ventricular internal chamber dimension was normal at 52mm, the left atrium was dilated at 46mm, the aortic root was mildly dilated at 40mm, the left ventricular wall thicknesses were hypertrophied at 12mm, left ventricular function was normal with fractional shortening of 31% and an ejection fraction of 58%, three aortic leaflets were structurally normal, mitral leaflets demonstrated mild sclerosis, normal tricuspid leaflets, no intracavitary thrombus or mass, and no pericardial effusion. The color-flow Doppler revealed normal transaortic flow patterns with no stenosis or regurgitation, a severe jet of mitral valve regurgitation filling the enlarged left atrium with a grade or 3 to 4 out of 4, and moderate tricuspid regurgitation rated a 2 to 3 out of 4 with elevated right ventricular systolic pressure of 45mmHg. The regurgitation found is due to the patient’s chronic atrial fibrillation (Gaasch, 2012). A follow-up CT scan of the head was to be performed sometime on September 18, 2012 during clinical, but it wasn’t performed during clinical hours.
Systems Review – Medications AV is not on very many medications when compared to many other patients admitted to the IMC unit. The first medication listed is Symmetrel (amantadine), which is an antiviral. This works by preventing penetration of the influenza A virus into the host cell (Vallerand & Sanoski, 2012, p. 126). 100mg of this medication is being given for influenza prophylaxis twice daily though his PEG tube. Before giving this medication you should assess the patient’s vital signs, with an emphasis on respirations and temperature. The most common side effects are dizziness, insomnia, and hypotension. This medication appears to be working because AV doesn’t have any signs or symptoms of influenza. The next medication is Lanoxin (digoxin), which is an inotrope. This helps improve the contractility of the heart, and thus increases cardiac output and increases tissue perfusion (Vallerand & Sanoski, 2012, p. 431). 125mcg is being given once daily intravenously for atrial fibrillation. Before giving this medication you should assess vital signs, the IV site, and the EKG monitor. The most common side effects are fatigue, nausea, and bradycardia. This medication is effective because the patient’s heart rate decreased from 92 to 80 beats per minute. Another medication AV is currently taking is Lopressor (metoprolol), which is a beta blocker. This dilates myocardial blood vessels and slows the heart rate (Vallerand & Sanoski, 2012, p. 853). 50mg is being given twice daily for hypertension through AV’s PEG tube. Before giving this medication you should assess blood pressure, pulse, and the EKG monitor. The most common side effects are fatigue, weakness, and hypotension. This medication was effective because AV’s blood pressure never got above normal parameters. The next medication is Carafate (sucralfate), which is an antiulcer agent. 1,000mg is being given twice daily for ulcer prophylaxis through his PEG tube. This works by binding to damaged tissue and protecting it from enzymes and acids to promote healing (Vallerand & Sanoski, 2012, p. 1166). Before giving this medication you should assess vital signs, bowel sounds, and abdominal pain. The most common side effects are constipation, drowsiness, and dizziness. This medication is effective because AV has no signs or symptoms of ulcers. The last scheduled medication is Zestril (lisinopril), which is an ACE inhibitor. 10mg is being given once daily for hypertension through AV’s PEG tube. This acts by preventing angiotensin I from converting to angiotensin II in the renin-angiotensin-aldosterone system. This prevents vasoconstriction and blood pressure elevations, and also increased renal perfusion preventing diabetic renal complications (Vallerand & Sanoski, 2012, p. 160). Before giving this medication you should assess blood pressure, pulse, and the EKG monitor. The most common side effects are dizziness, dry cough, and hypotension. This medication was effective because his blood pressure never got above normal limits. The first medication taken as needed is Duramorph (morphine), which is an opioid analgesic. 2mg is to be given as needed for pain every three hours for pain through the IV line. Before giving this medication you should assess the patient’s pain level, blood pressure, pulse, and respiratory status. The most common side effects are drowsiness, dizziness, and nausea. This medication was not given, but the desired therapeutic effect would be a decrease in the pain level reported by the patient. The last medication ordered for AV is Zofran (ondasetron), which is an antiemetic. 4mg is to be given as needed for nausea every four hours for nausea through the IV line. This medication works by blocking the action of serotonin on the 5-HT3 receptor, which causes nausea (Vallerand & Sanoski, 2012, p. 948). Before giving this medication you should assess bowel sounds, abdominal pain, and abdominal distention. The most common side effects are headache, constipation, and diarrhea. This medication was not given to AV during clinical hours, but the desired therapeutic effect is to decrease the level of nausea experienced by the patient.
Systems Review – Pathophysiology of Condition One The first and most critical condition is a left middle cerebral artery (MCA) infarct with hemorrhagic conversion. In AV’s case is was an embolic stroke that caused the infarct and subsequent hemorrhage, and this type of stroke is the most common type to occur in the middle cerebral artery, and is responsible for the rapid development of neurological deficits (Ignatavicius & Workman, 2010, p. 1031). With this patient, his chronic hypertension is the most likely cause of the hemorrhagic conversion; this is because the arterial vessel wall was vulnerable to ischemia and was weakened when the oxygen supply was blocked, and a sudden rise in blood pressure ruptured the vessel, causing bleeding to occur directly within the brain tissue (Ignatavicius & Workman, 2010, p. 1031). One source could have possibly been his carotid arteries if they were stenosed, but they were both found to be normal upon completion of an ultrasound study (Ignatavicius & Workman, 2010, p. 1031). The source of the embolus that occluded the left MCA was most likely from his heart, as he has chronic atrial fibrillation and this can cause emboli to develop within the atrium, only to be expelled later and travel through the circulatory system and cause a stroke (Ignatavicius & Workman, 2010, p. 670 & 745). In addition, persons with both hypertension and type 2 diabetes mellitus have a fourfold increase in stroke incidence and an eightfold increase in stroke mortality, and this patient happens to have both (Huether, 2008, p. 382). Also, males are affected by MCA stroke three to one, and Mexican Americans’ risk is almost twice the number for whites (Slater, 2011).
When an injury to the left frontal lobe occurs, it can have many effects on an individual depending on where specifically it occurs. In AV’s case, he developed dysphasia, dysphagia, and contralateral motor loss mostly in the upper extremity. Evidence points to a superior division infarct because of his symptoms of significant involvement of the upper extremity and partial sparing of the leg and foot (Slater, 2011).
Systems Review – Pathophysiology of Condition Two The second condition of AV’s that is being covered is atrial fibrillation. Atrial fibrillation is the result of multiple rapid impulses from many different places depolarizing the atria in a completely disorganized manner, and the atria essentially quivers (Ignatavicius & Workman, 2010, p. 745). This results in a loss of atrial kick, no atrial contractions, no clearly defined P wave on an EKG, and an irregular ventricular response that is often rapid (Ignatavicius & Workman, 2010, p. 745). Because of this, the ventricles also have reduced filling which results in decreased cardiac output and decreased tissue perfusion throughout the entire body (Ignatavicius & Workman, 2010, p. 745). This also makes the ventricles have to work much harder, thus the thickening of the left ventricular wall noted in the echocardiogram. The atrial fibrillation also allows blood to pool within the atria and potentially leads to thrombus formation, which increases the risk of stroke and pulmonary embolism (Ignatavicius & Workman, 2010, p. 1031). In the case of AV, this is exactly what led to his stroke, with a little help from his chronic hypertension to rupture the ischemic vessel (Ignatavicius & Workman, 2010, p. 1031).
Care Plan – Diagnosis One
The first, and priority nursing diagnosis for AV is as follows:
Decreased cardiac output R/T altered heart rhythm aeb arrhythmias, tachycardia, murmurs
The goal for this patient was to demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within normal parameters throughout the clinical shift. One of the interventions performed was to place AV into a semi-Fowler’s position with the legs down, thus decreasing the workload of breathing and decrease preload and overall workload of the heart (Ackley, 2010, p. 199). Another intervention performed was to apply sequential compression devices as ordered. This promotes venous return and prevents deep vein thrombosis (Ackley, 2010, p. 199). The third intervention performed was to assess blood pressure, pulse, and overall condition before administering medications to the patient. This is done before administering any medication to ensure patient safety (Ackley, 2010, p. 199). The final intervention for this diagnosis is to closely monitor fluid intake because weak ventricles may not be able to handle an increase in fluid volume (Ackley, 2010, p. 199). By the end of the clinical shift, the goal was met as AV remained stable and showed no signs of fluid volume excess.
Care Plan – Diagnosis Two
The second nursing diagnosis for AV is as follows: Impaired bed mobility R/T deconditioning aeb slowed movements, neuromuscular impairments, decreased muscle strength
The goal for this patient was to demonstrate optimal independence in positioning, exercising, and performing functional activities in bed during the clinical shift. One of the interventions performed was to periodically sit him up as tolerated and dangle his legs. This reduces the workload of the heart, improves circulation and lung ventilation, and stimulates reflexes and awareness of surroundings (Ackley, 2010, p. 543). Another intervention performed was to assess the patient’s risk for falls, establish fall prevention strategies, and implement them. This will decrease the patient’s risk for falls, which in turn maintains his progress (Ackley, 2010, p. 544). The third intervention performed was to keep his call light, urinal, and bedside table all within reach. This makes him not have to reach out to grab something, thus further reducing his fall risk (Ackley, 2010, p. 545). The last intervention for this diagnosis was to emphasize the practice of all exercises taught to him by the physical therapist. This helps rebuild lost muscle and tone what is already there (Ackley, 2010, p. 545). The goal was met throughout the shift by the patient positioning himself well in bed and showing a strong desire to exercise and get stronger.
Care Plan – Diagnosis Three
The third nursing diagnosis for AV is as follows:
Risk for Aspiration – Risk Factors: Depressed gag reflex, tube feedings, gastrointestinal tubes, impaired swallowing
The goal for this diagnosis was to maintain a patent airway, and digest gastric feedings without aspiration. The first intervention performed was to maintain the elevation of the head of the bed above 30 degrees, as this helps prevent aspiration with gastric feedings (Ackley, 2010, p. 152). The next intervention performed was to assess the lung sounds before and after tube feedings. This is because auscultation of lung sounds has been shown to be specific in identifying patients at risk for aspiration (Ackley, 2010, p. 152). The third intervention performed was to have a suction machine available at the bedside. This is because a patient with aspiration needs immediate suctioning and may require further lifesaving interventions such as intubation (Ackley, 2010, p. 152). The final intervention performed was to auscultate bowel sounds frequently, and note if they are decreased, absent, or hyperactive. These findings are important in diagnosing many disorders that can lead to aspiration (Ackley, 2010, p. 152). The goal for this diagnosis was met by AV by not aspirating or showing any signs of aspiration.
Care Plan – Diagnosis Four
The final nursing diagnosis for AV is as follows:
Impaired verbal communication R/T alteration of central nervous system aeb difficulty expressing thoughts verbally, inappropriate verbalizations, difficulty forming words
The goal for this diagnosis was for the patient to demonstrate understanding and communicate even if not able to speak throughout the clinical shift. The first intervention performed was to identify the language spoken, which facilitates more efficient communication (Ackley, 2010, p. 233). The next intervention performed was to use therapeutic communication techniques. This was done because effective communication facilitates positive relations between the patient and the nurse (Ackley, 2010, p. 233). Another intervention performed was using therapeutic touch as appropriate to convey caring to the patient (Ackley, 2010, p. 233). The final intervention for this diagnosis was to be persistent in deciphering what the patient was saying and not pretend to understand when the message is unclear. This was done because when the patient is truly understood, they tend to experience greater satisfaction with nursing care (Ackley, 2010, p. 233).
Conclusion
The typical course of treatment for these conditions varies depending on a few different factors, and one of them is the presence of hemorrhage. This alone will change the course of treatment completely because if no hemorrhage is present, then antithrombolytics like tPA would be used to break up the clot and restore perfusion to the brain (Slater, 2011). The early decision to not use them in AV’s case was a smart one, as the hemorrhage did not show up on CT scan for a few days after the stroke happened. Using tPA would have proven to be catastrophic by enabling the hemorrhage to be much worse than what had naturally occurred. The recovery of this patient was remarkable to me because of the very quick reversal of symptoms. When I cared for him, he was in the hospital for eleven days at that point, and he was incredibly stable with most of his strength back. The one order from the physician I had questioned both during the clinical shift and until finishing my research on the pathophysiology, was the lack of insulin or diet modifications for the patient’s type II diabetes mellitus. During my research I found that the American Stroke Association guidelines for blood glucose are pretty liberal, and they don’t recommend intervention until the blood glucose reaches a level above 300mg/dL (Slater, 2011). This concerned me during the clinical shift and in the days following, but I now realize the physician had nothing to really worry about as AV’s blood glucose never got above 260mg/dL.
This was an incredibly interesting case for me to study, and I learned many things that will help me in my future career as a registered nurse.

References
Pagana, K.D. & Pagana, T.J. (2009). Mosby's Manual of Diagnostic and Laboratory Tests (4th edition). St. Louis, MO: Mosby.
Gaasch, William H., M.D. (2012, July 20). Patient Information: Mitral Regurgitation (Beyond the Basics). Retrieved from http://www.uptodate.com/contents/mitral-regurgitation- beyond-the-basics#H8
Huether, Sue E. (2008). Understanding Pathophysiology (4th edition). St. Louis, MO: Mosby
Ignatavicius, D. D. & Workman, M.L. (2010). Medical-Surgical Nursing: Patient-Centered Collaborative Care (6th edition). St. Louis, MO: Elsevier Inc.
Slater, Daniel I., M.D. (2011, December 19). Overview of Middle Cerebral Artery Stroke. Retrieved from http://emedicine.medscape.com/article/323120-overview#showall
Ackley, Betty J. (2010) Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care (9th edition). St. Louis, MO: Mosby.
Vallerand, A.H. & Sanoski C.A. (2012). Davis’s Drug Guide for Nurses (13th edition). Philadelphia, PA: F.A. Davis Company