Running head: DUNBAR CASE STUDIES Dunbar: Case Study One and Two Whitney L. Dunbar Wright State University Nursing 7201 May 2, 2013 Dr. Kristine Scordo 1 DUNBAR CASE STUDIES 2 Dunbar: Case Study One and Two Case Study One 1. What is the most likely diagnoses for this patient and what are the criteria for this diagnosis? What is your rationale? The most likely diagnosis for this patient is right-sided heart failure secondary to pulmonary hypertension (PH). The etiology of secondary PH for this patient is related to the consumption of the anorectic medications, fenfluramine and phentermine. PH exists once pulmonary artery pressures escalate to a level that is unsuitable for usual cardiac output. PH initiates structural deformities mostly in the smaller pulmonary vessels, involving intimal hyperplasia, medial hypertrophy, adventitial excess, originating thrombosis, different amounts of inflammation, and plexiform arteriopathy. These alterations may result in additional restriction of the arterial bed. The limitation of the flow within the pulmonary arterial circulation produces enhanced pulmonary vascular resistance (PVR) and eventually right-sided heart failure. The hemodynamic classification of PH consists of a mean pulmonary artery pressure of more than 25 mmHg, a pulmonary capillary wedge pressure, left atrial pressure, or left ventricular enddiastolic pressure less than or equivalent to 15 mmHg, and a PVR more than three Wood units (American Heart Association (AHA), 2009). Right-sided heart failure starts developing when the rising of systolic pressure in the right ventricle reacts to the increase in PVR in order to maintain an adequate cardiac output. Right ventricle failure happens in PH when the right ventricle myocardium develops ischemia as an outcome of extreme demands and insufficient right ventricle coronary blood movement (Longo et al., 2012). Tricuspid and pulmonary valve insufficiency and cor pulmonale are found in severe cases of PH in addition to right ventricle failure (Papadakis, McPhee, & Rabow, 2013). DUNBAR CASE STUDIES 3 There are various pathogenic pathways that have been linked to the evolution of PH, comprising of pathways at the molecular and genetic levels and in the smooth muscle, endothelial cells, and adventitia (AHA, 2009). Secondary PH can occur with various ailments, involving systemic sclerosis, hepatic cirrhosis and portal hypertension, human immunodeficiency virus, chronic thromboembolic disease, and the consumption of anorectic medications (Papadakis et al., 2013). The criterion for PH includes a history from the patient, physical symptoms the patient exhibits, and diagnostic tests. Obtaining a history from the patient aids in narrowing down the differential diagnoses. The patient presents with a complaint of dyspnea for seven months that started with dyspnea while exercising on her stationary bike and has progressed to dyspnea with minimal exertion. Patients with PH typically present with dyspnea on exertion initially and eventually dyspnea at rest with advanced stages of PH. Dyspnea occurs from a decreased amount of oxygen in the blood either from not enough oxygen existing or due to insufficient gas exchange. Also, the patient presents with a complaint of fatigue for seven months and two syncope episodes in the past month. Fatigue and syncope are outcomes from decreased cardiac output that are associated to elevated pulmonary artery pressure or bradycardia. The patient complains of occasional substernal chest pressure with excessive exertion. Patients with PH can present with dull, retrosternal chest pain like angina pectoris (Papadakis et al., 2013). The patient states she has abdominal fullness and this can be related to right ventricular dysfunction due to PH (AHA, 2009). There are various physical findings this patient exhibits for PH. First, the patient appears to be anxious, in mild distress, and has slightly labored respirations. This can be caused by the lack of oxygen existing in the blood. Second, the patient exhibits central cyanosis with cyanosis DUNBAR CASE STUDIES 4 of the lips. Central cyanosis is associated with hypoxemia, pulmonary-to-systemic shunt, intrapulmonary shunt, and abnormal ventilation perfusion. Third, the patient has jugular venous distention and trace edema of the ankles. Patients with moderate to severe PH may exhibit these signs due to right ventricular dysfunction, tricuspid insufficiency, or both. Fourth, the patient has a positive hepatojugular reflux (HJR). Patients with PH can have a positive HJR due to high central venous pressure. Fifth, the patient has a prominent S2 at the second intercostal space at the left sternal border and a grade III/VI holosystolic murmur at the left sternal border amplified with inspiration. These two physical findings of patients with PH are a result of tricuspid insufficiency. Sixth, the patient has a right ventricular S4 and a left parasternal heave. Patients with PH may exhibit a right ventricular S4 and a left parasternal heave due to the existence of high right ventricular pressure and hypertrophy. Seventh, the patient has a slightly distended abdomen and patients with PH can display a distended abdomen due to right ventricular dysfunction. Eighth, the patient has an elevated jugular vein pressure (JVP) at nine centimeters. Ninth, the patient exhibits prominent A-waves in the jugular venous pulse due to an increase in right atrial contraction from PH. The increase in JVP and the A waves in the jugular venous pulse are related to an excess of right ventricular pressure amongst failure that is linked with a condensed, less compliant right ventricle (AHA, 2009). The third criteria for PH includes diagnostic tests. The patient had an electrocardiogram (ECG) and a chest x-ray performed. The patients’ ECG displays right axis deviation and right atrial enlargement. The ECG of patients with PH typically shows right axis deviation, right atrial enlargement, and right ventricular hypertrophy. Right ventricular hypertrophy can display on the ECG with elevated R-waves, specifically, a R/S ratio greater than one in lead V1. Other criteria of right ventricular hypertrophy include a deep S-wave in leads V5 or V6 that is greater than DUNBAR CASE STUDIES 5 seven millimeters and has a R-wave less than five millimeters. Usually, there is ST segment depression and a negative T-wave in the right precordial leads (Ellis, 2012). This patient exhibits these changes in their ECG. The patients’ chest x-ray presents cardiomegaly with enlargement of the pulmonary trunk. The chest x-ray of patients with PH usually appears to have dilated central pulmonary arteries and an enlarged pulmonary outflow tract. In advanced stages of PH, right ventricular and atrial expansion may be observed. Further diagnostic testing should be implemented for confirmation of PH (Papadakis et al., 2013). 2. What diagnostic test should be performed? Explain your rationale? When a history, a physical exam, a risk factor assessment, a chest x-ray, and an ECG are obtained and there is suspicion for PH, an echocardiogram should then be performed. A Doppler echocardiogram is noninvasive and can offer an approximation of the right ventricle systolic pressure, right atrium and ventricle evaluation, left heart disease, valvular heart disease, congenital heart disease, and recognize any potential cardiac causes of PH. If the right ventricle systolic pressure is more than 40 mmHg it usually deserves additional evaluation in the patient with unexplained dyspnea (AHA, 2009). In a systemic review and meta-analysis of 29 studies, for diagnosing PH, the sensitivity and specificity for echocardiography was 83% and 72% (Janda, Shahidi, Gin, & Swiston, 2011). There are many other pivotal tests that can be implemented in order to diagnose a patient with PH. After an echocardiogram is performed, a ventilation-perfusion (VQ) lung scintigraphy or a computed tomography pulmonary angiogram (CTPA) is executed in order to rule out chronic thromboembolic PH in a patient with unexplained dyspnea and suspected PH (AHA, 2009). A retrospective study consisting of 227 patients from a hospital setting were tested for chronic thromboembolic PH using a VQ scintigraphy or a CTPA. The study supported that the DUNBAR CASE STUDIES 6 VQ scintigraphy had a sensitivity of 96% to 97.4% and a specificity of 90% to 95% compared to CTPA sensitivity of 51% and a specificity of 99% (Tunariu et al., 2007). If the results of the VQ scan are normal or low probability then specific tests should be performed in order to rule out other possible causes of dyspnea. Pulmonary function tests may be implemented to obtain the patients’ ventilatory function and gas exchange. Overnight oximetry can contribute to the assessment of a sleep disorder. Human immunodeficiency virus screening is checked for the human immunodeficiency virus infection. Antinuclear antibody serology is drawn for the assessment of scleroderma, systemic lupus erythematosus, and rheumatoid arthritis. A liver function test is drawn to assess for portopulmonary hypertension. A cardiopulmonary exercise test should be performed to establish a baseline and prognosis (AHA, 2009). If a patient is believed to have PH after a noninvasive assessment, the patient should have a right heart catheterization (RHC) completed prior to starting treatment. A RHC is the test performed to confirm diagnosis of PH and to describe the hemodynamic profile in better detail and accuracy. The RHC assesses oxygen saturations within the vessels and heart, right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary arterial wedge pressure, cardiac output and index, PVR, systemic blood pressure, heart rate, and reaction to acute vasodilator. However, this patient would not be a candidate for the acute vasodilator test due to the treatment being long-term calcium channel blockers. Calcium channel blockers should not be initiated to a patient with right-sided heart failure due to the negative inotropic effect (AHA, 2009). The sensitivity and specificity for RHC are 93% and 95% for identifying PH (Roldan, 2012). 3. What is the appropriate therapy for this patient? Include all types of therapy and rationale for your choices. DUNBAR CASE STUDIES 7 Patients diagnosed with any form of PH can be initiated on a few different medications. First, fenfluramine and phentermine will be discontinued due to the adverse effects and the probable cause of the patients PH. Second, the patient may continue her oral contraceptive medication but she should use dual birth control methods because pregnancy is contraindicated for patients with PH. Third, patients with PH may be placed of oxygen therapy to maintain oxygen saturation greater than 92%. A six-minute walk test can be executed for this patient due to her dyspnea on minimal exertion and will help determine if the patient needs to be placed on oxygen therapy. Any patient with PH should be educated to let their healthcare provider know when they are traveling to a high altitude destination or traveling by airplane due to potential hypoxia pulmonary vasoconstriction. Fourth, this patient may be started on warfarin anticoagulation due to the patient taking oral contraceptives and having right-sided heart failure. These are two risk factors for developing a venous thromboembolism. It would be recommended to start this patient on warfarin 5 mg by mouth (PO) daily to a goal INR of 1.5 to 2.5. After initiating warfarin the patient should return in four days to recheck her INR and adjust warfarin dosage according to results. Once the INR is at therapeutic level, an INR can be checked monthly. A prothrombin time and hematocrit should be monitored with the INR. Fifth, diuretics are used to manage fluid overload from right-sided heart failure. This patient would be started on furosemide 40 mg PO twice a day. It is suggested to start furosemide for patients with heart failure and edema between 20 to 80 mg/dose once or twice daily. Doses can increase in additions of 20 to 40 mg/dose at interims of six to eight hours and can be titrated up to 600 mg/day. The patients weight, intake and output, relief of symptoms, blood pressure, and hearing should be closely monitored. Serum electrolytes and renal function should be carefully monitored for hypokalemia and altered kidney function. Sixth, some patients with idiopathic PH DUNBAR CASE STUDIES 8 (IPH) are prescribed digoxin when they have right-sided heart failure, a low cardiac output, and atrial arrhythmias. Digoxin increases cardiac output and slows down the ventricular rate. This medication would not be prescribed for this patient at this time since she has secondary PH due to taking anorectic agents. Before prescribing digoxin the healthcare provider should reevaluate if there is any improvement of PH once the anorectic medications are discontinued. Also, there is limited research on digoxin and its benefits on PH (AHA, 2009; Lexi-Comp, Inc., 2013). Seventh, the patient should receive her vaccinations when they are due because having PH can place her at a higher risk for becoming critical, for example, if she were to acquire influenza or pneumonia. A nurse with a certificate to prescribe (CTP) in Ohio may prescribe warfarin per institutional protocol or it is physician initiated or physician consulted. A nurse in Ohio with a CTP may prescribe oxygen, furosemide, digoxin, and vaccinations (Ohio Board of Nursing, 2013). Acute vasodilator testing can be performed during the patients’ RHC and can help guide the proper PH treatment for the patient. If the result is positive then the patient will be placed on an oral calcium channel blocker. Since this patient has right-sided heart failure, it would not be recommended to implement the acute vasodilator test, therefore, would not be placed on an oral calcium channel blocker. Consequently, this patient would be placed on another medication to improve her PH (AHA, 2009). Since the acute vasodilator test would not be performed on this patient, the health care provider needs to determine if this patient is low risk or high risk based on their clinical assessment. There are three different classes of drugs that may be used for patients with PH in addition to the previous stated medications. There is the prostacyclin class that consists of epoprostenol, treprostinil, and iloprost. Patients with PH lack prostacyclin synthase that results DUNBAR CASE STUDIES 9 in insufficient productions of prostacycline I2, a vasodilator with antiproliferative effects. Therefore, prostacyclins have become a basis of PH therapy. Also, the endothelian receptor antagonist (ERAs) class includes bosentan, sitaxsentan, and ambrisentan. These medications block endothelin-1, a vasoconstrictor and a smooth muscle mitogen that can add to the progression of PH. In addition, the phosphodiesterase inhibitors (PDE-5) class entails sildenafil and tadalafil. These medications assist to extend or augment the effects of vasodilating cyclic nucleotides, cyclic adenosine monophosphate and cyclic guanosine monophosphate. When the patient is considered low-risk then an oral ERA or a PDE-5 would be the suggested first line of treatment. If oral treatment were not suitable, a prostacyclin would be considered. An intravenous (IV) prostacyclin is the advocated first line of treatment for a patient that is considered high risk that is established from clinical assessment (AHA, 2009). This patient would be considered high risk due to her presenting signs and symptoms of right-sided heart failure, dyspnea with minimal exertion, and fatigue at rest. The recommended medication for patients with severe PH is to initiate IV epoprostenol. Studies have reported improvements in functional class, exercise intolerance, hemodynamics, and survival of IPH with IV epoprostenol. For example, a randomized trial of 81 functional class III and IV IPH patients exhibited substantial progression in the crucial six-minute walk test. The patients treated with epoprostenol had a 32-meter increase in length compared to a 15-meter reduction with only conventional therapy. Subordinate results consisted of hemodynamics and quality of life improvements with epoprostenol. Even though this patient does not have IPH, observational studies have reported positive outcomes of IV epoprostenol with several forms of secondary PH and it is the only medication that has exhibited the ability to extend survival. Epoprostenol needs to be administered through a continuous IV infusion. Educating the patient on sterile technique DUNBAR CASE STUDIES 10 for preparation of epoprostenol, managing the ambulatory infusion pump, and proper care of the central venous catheter are vital for the patient with PH to learn because an infection or an infusion interruption can be life-threatening. Typically, it is initiated in the hospital at a dose of 2ng/kg/min. The dose may be changed according to the patients’ symptoms of PH and the side effects of epoprostenol. Therefore, this patient would be started at 2ng/81.8kg/min. It is thought that the ideal dose may be found between 25 and 40 ng/kg/min for adult patients. Elevated cardiac output failure may result from a chronic overdose and the long-term consequences could be detrimental or unknown. The healthcare provider should educate the patient on the use of epoprostenol and the common side effects that consist of headache, jaw pain, flushing, nausea, diarrhea, skin rash, and musculoskeletal pain. The patient should be educated on what signs and symptoms need to be reported to their healthcare provider immediately (AHA, 2009). A nurse with a CTP can prescribe Epoprostenol when it is physician initiated or the nurse with a CTP is within a specialty clinic (Ohio Board of Nursing, 2012). The healthcare provider should review all medications, necessary laboratory values, if the patient has insurance coverage, and answer all questions and concerns the patient may have before prescribing a medication. A follow-up appointment should be scheduled with follow-up laboratory blood work. There are a few different treatment options for patients with PH who are not effectively responding to their primary monotherapy. First, patients can be started on a combination therapy that consists of a prostacyclin with an ERA or a PDE-5. The goal of combination therapy is to augment efficiency while reducing toxicity. Second, patients who are not responding to monotherapy could have an atrial septostomy performed. This procedure constructs a right to left inter-atrial shunt that leads to a reduction in right heart filling pressures, advances right heart function, and enhances left heart filling. Even though the formed shunt declines systematic DUNBAR CASE STUDIES 11 arterial oxygen saturation, it is projected that the enhanced cardiac output should have the outcome of a general increase of systemic oxygen supply. Third, a lung transplant is another option if monotherapy is not effective for a severe PH patient. It can be challenging to figure out the appropriate timing for lung transplantation. Lung transplants are reserved for patients who are in end-stage pulmonary disease and continue to have progression of PH despite optimal medical management (AHA, 2009). A multidisciplinary management approach for patients with PH is ideal for their treatment because it can increase the length of their life. The treatment should be individualized. Therefore, there should be many referrals and consults for this patient with severe PH. There should be a referral to cardiac rehabilitation because they can provide assistance in improving her health and well being with her cardiac complications (AHA, 2009). Additional referrals and consults for this patient include a cardiologist, a pulmonologist, a dietician, a social worker, and a pharmacist. Also, the healthcare provider should recommend a smoking cessation class for this patient due to her history of smoking and offer psychiatry if she feels overwhelmed or depressed about her diagnosis. Case Study Two 1. What is your differential diagnosis? Explain. There are many differential diagnoses for this patient that will be discussed. First, acute kidney injury (AKI) secondary to contrast induced nephropathy can be a diagnosis for this patient. AKI is described as an increase in serum creatinine by equal or greater than 0.3 mg/dL within 48 hours, an increase in serum creatinine equal or greater than 1.5 times the patients’ baseline within the previous seven days, or urine output less than 0.5 ml/kg a hour for six hours. This patients’ serum creatinine has increased to 2.9 mg/dL from 1.6 mg/dL (1.8 times baseline DUNBAR CASE STUDIES 12 within seven days) and currently only has 200 mL of urine over 24 hours (about 8 cc an hour). Therefore, this patient meets the definition of AKI. Contrast induced nephropathy is described as an increase in serum creatinine of equal or greater than 0.5 mg/dL or a 25% rise from the patient’s serum creatinine baseline after 48 hours from a radiological procedure. This patients’ serum creatinine increased by 1.3 mg/d and over 25% from his baseline within 48 hours after receiving contrast media from the coronary angiography procedure (Kidney Disease Improving Global Outcomes (KDIGO), 2012). Second, AKI secondary to hypovolemia due to dehydration may be a diagnosis for this patient. Typically, intravenous isotonic sodium chloride is given to patients who are at a high risk for contrast-induced nephropathy prior to their procedure in order to prevent intrarenal hemodynamic alterations and direct tubule-toxic effects. This patient is at high risk due to his type two diabetes and coronary artery disease. The patient did not receive any intravenous fluids besides intravenous nitroglycerin prior to the coronary angiography and this patient may not have been drinking fluids prior to admission. Hypovolemia is a cause of prerenal failure due to decreased renal perfusion from reduced intravascular volume. When a patient is undergoing a procedure where they will be receiving contrast media, hypovolemia enhances the toxic effect and can lead to AKI. An indication of prerenal failure is a blood urea nitrogen (BUN) to creatinine ratio of more than 20:1. This patients’ BUN to creatinine ratio is 23.8:1 and indicates prerenal failure (KDIGO, 2012). Third, AKI related to acute tubular necrosis is another potential diagnosis for this patient. Acute tubular necrosis can occur when there is prolonged ischemia to the kidney and causes necrosis of the proximal tubules of the outer medulla and the proximal convoluted tubules. The prolonged ischemia is followed by reperfusion. Acute tubular necrosis is expressed by a severe DUNBAR CASE STUDIES 13 increase in plasma BUN and serum creatinine. This elevation can occur from hours to weeks. This patient potentially could have had ischemia prior, during, or after the coronary angiography from hypovolemia. The contrast media from the coronary angiography is another cause of nephrotoxic acute tubular necrosis (KDIGO, 2012). Fourth, AKI related to acute interstitial nephritis is another possible diagnosis. It entails interstitial inflammation with edema and potential tubular cell damage. Drugs cause the majority of cases of acute interstitial nephritis, but it can be caused by an infection, an immunologic disorder, or an idiopathic condition. Manifestations of acute interstitial nephritis include fever, rash, arthralgia, and peripheral blood eosinophilia. This patient is afebrile and does not have a rash or arthralgia, but it may be to soon for these signs and symptoms to appear. Acute interstitial nephritis should be something to consider if this patient were to develop these signs and symptoms later (Papadakis et al., 2013). Fifth, AKI secondary to atheroembolic renal disease (AERD) is another possible diagnosis for this patient. AERD happens when small elements built up of hardened cholesterol and fat spread to the small blood vessels of the kidneys. It can then cause a reduction of blood flow to the tissues and produce swelling and tissue damage that can harm the kidneys. Also, it can harm the skin, eyes, muscles and bones. It can occur one week after receiving contrast media. Manifestations include blindness, blue toes, hypertension, decrease in sensation, decrease or no urine output, drowsiness, swelling in the legs, weight loss, nausea, and dry itchy skin (Brenner, 2007). 2. What is your next step to diagnose the problem? Explain. Of what value is a urinalysis and urinary electrolytes? DUNBAR CASE STUDIES 14 The next step to establishing the possible diagnosis of AKI secondary to contrast induced nephropathy involves the combination of medication review, new laboratory tests, and the laboratory tests that have already been implemented to help narrow down the differential diagnoses. The healthcare provider should review what medications the patient has taken in the last 24 to 48 hours that could possibly cause injury to the kidneys. The patient received contrast media and angiotensin-converting-enzyme inhibitor in the last 24 to 48 hours that could cause injury to the kidneys. The laboratory tests that should be ordered are a fractional excretion of sodium (FeNa), erythrocyte sedimentation rate, urine osmolality, urine specific gravity, urine sediment, urinalysis, and urine electrolytes. A renal function panel was already drawn and is another test that allows the healthcare provider to assess kidney function. Also, laboratory tests can help determine the severity of the renal disease. A treatment plan can be determined with the proper diagnostic assessment (Longo et al., 2012). A renal ultrasound could be ordered to rule out AERD if still questioning diagnosis after urine electrolytes, urine analysis, physical assessment of patient, and a history review of patient (Brenner, 2007). A urine analysis (UA) can have great value in helping diagnose a kidney disease. It can offer information comparable to a renal biopsy that is cost-effective and non-invasive. The collected urine should be assessed within an hour in order to prevent destruction of formed elements. A UA includes a urine dipstick analysis and a microscopic evaluation if the urine dipstick has positive results. The urine dipstick includes measuring urinary pH, protein, hemoglobin, glucose, ketones, bilirubin, nitrates, and leukocyte esterase. Microscopy examines for crystals, cells, casts, and infecting organisms. For example, if the results displayed pigmented granular casts and renal tubular epithelial cells alone or in casts, the healthcare provider would think the patient has acute tubular necrosis. Another example, interstitial DUNBAR CASE STUDIES 15 nephritis usually exhibits white blood cells, white blood cell casts, red blood cells, and a small amount of protein on the urine dipstick and microscopic examination. In further detail, when there is more than 150mg of protein being excreted in urine in a 24-hour period, it signifies an underlying kidney malfunction in an adult. The source is usually glomerular when proteinuria is more than 1 gram a day to less than 2 grams a day. There are several causes along the nephron segment that result in less than 1 gram a day of proteinuria (Papadakis et al., 2013). The measurement of urinary electrolyte concentrations has a vital part in the diagnosis and treatment plan for different kidney diseases. Typically, sodium, potassium, chloride, and calcium are the electrolytes that are measured for this test. The normal level for urine sodium is 40 to 220 mEq/L a day but it depends on the patient’s salt and water intake. Urine sodium can be used as an approximation of the patient’s volume status. Salt-wasting nephropathy and diuretics are causes for a high urine sodium level. A low urine sodium level can result from chronic kidney disease, glomerulonephritis, hepatorenal syndrome, kidney injury, or nephrotic syndrome. The normal results for urine potassium is 25 to 125 mEq/L a day but can vary due to dietary intake of potassium. An increase in urine potassium may signify acute tubular necrosis, hypomagnesemia, diabetic acidosis, renal tubular acidosis, and use of non-potassium-sparing diuretics. A decreased urine potassium level can be caused from adrenal gland insufficiency, hypoaldosteronism, and medications that include beta-blockers, potassium-sparing diuretics or nonsteroidal anti-inflammatory drugs. The normal urine chloride level is between 110 to 125 mEq a day and depends on the patient’s salt and fluid intake. An increase in urine chloride can result from adrenocortical insufficiency, inflammation of the kidney, and production of large amounts of urine. A low chloride urine level can be caused by Cushing syndrome, salt retention, and fluid loss. The normal calcium urine level is between 100 to 300 milligrams a day but can DUNBAR CASE STUDIES 16 vary with diet. A high urine calcium level can be caused from chronic kidney disease, leaking of urine from the kidneys, and loop diuretics. When there are low calcium urine levels, thiazide diuretics may be the source (Goldman & Schafer, 2012). 3. What are the indications for dialysis in AKI (acute kidney injury)? Be specific. There are many indications for dialysis when patients have AKI. First, refractory potassium is an indication for dialysis in AKI. If the potassium level becomes more than 6.5 mmol/L it can cause cardiac conduction abnormalities. Therapeutic measures that stimulate the intracellular shift of potassium are implemented to decrease the potassium level and when they are drained, the potassium level can rise. Therefore, the excess of potassium can only be eradicated with dialysis. Second, metabolic acidosis with a pH less than 7.2 can indicate dialysis when sodium bicarbonate is no longer effective. Severe metabolic acidosis can injure cardiac function and intensify hyperkalemia. Salicylates, ethylene glycol, methanol, and metformin are examples of poisons, drug overdoses, and toxic compounds that can lead to metabolic acidosis and AKI. Third, dialysis may be started when a patient displays no signs of renal function recovery with a serum creatinine greater than 12 mg/dL or a BUN level more than 100 mg/dL. Fourth, progressive uremia is another indication for dialysis with AKI because it can cause bleeding diathesis, encephalopathy, nausea, vomiting, dehydration, seizures, and pericarditis. Fifth, pulmonary edema from fluid overload that is resistant to diuretic therapy is another indication for dialysis with AKI and typically seen in patients with heart failure (Gutierrez & Morn, 2010; KDIGO, 2012). 4. Write a set of admitting orders for the patient. Be specific. Admission orders. Admit to Critical Care Medicine, Coronary Intensive Care Unit DUNBAR CASE STUDIES 17 Diagnosis. AKI secondary to contrast induced nephropathy. Secondary diagnosis: Angina, Hypertension, Type II diabetes mellitus, Diabetic retinopathy, Coronary artery disease Condition. Serious Allergies. No known drug allergies Vital signs. Continuous ECG monitoring; Blood pressure, heart rate, respiratory rate, oxygen saturation every hour; Temperature every four hours. Call physician if systolic blood pressure less than 90 or greater than 160, diastolic blood pressure less than 50 or greater than 100, mean arterial pressure less than 60, heart rate less than 50 or greater than 120, respiratory rate less than eight or greater than 30, temperature less than 97.5°F or more than 101.0°F, any other sudden changes in vital signs, or urinary output is less than 30 ml for two hours Activity. Up as tolerated Nursing. Record admission height and weight; Record daily weights; Accurate intake and output measured and documented every hour; Insert a foley catheter for accurate intake and output; Encourage incentive spirometer; Encourage cough and deep breathing; Measure blood glucose with glucometer before meals and at bedtime; Get a 12 lead ECG stat; If patient develops chest pain obtain a stat ECG and notify physician Diet. 1500- calorie diabetic/renal/2g sodium diet; Encourage fluids; 0.8 to 1.0 g/kg per day of protein intake (KDIGO, 2012) Intravenous orders. Insert two peripheral IVs; #1. 500 ml 0.9 Normal saline at 999 ml/hr; #2. 1000 ml 0.9 Normal saline at 100ml/hr Medication orders. Continuous IV nitroglycerin at 5 mcg/min, raise by 5 mcg/min every three to five minutes to 20 mcg/min, and if there is no response at 20 mcg/min, then titrate up by 10 to 20 mcg/minute every three to five minutes with a maximum of 400 mcg/min (Lexi- DUNBAR CASE STUDIES 18 Comp, Inc., 2013); Sliding scale regular human insulin subcutaneous injections before meals and at bedtime with target plasma glucose of 70 to 150 mg/dL; If plasma glucose is less than 70 then initiate hypoglycemia protocol; 70 to 150 receives no insulin; 151 to 200 receives two units; 201to 250 receives four units; 251 to 300 receives six units; 301 to 350 receives eight units; 351 to 400 receives 10 units; greater than 400 call physician; Hold ACE inhibitor; ASA 81 mg by mouth daily; Metoprolol 25 mg by mouth twice a day (Hold if heart rate less than 60 or systolic blood pressure less than 100) Laboratory orders. Renal function panel every eight hours; Complete blood cell count daily; Urinalysis daily; MRSA by PCR once; Erythrocyte sedimentation rate once Special orders. Respiratory therapy to maintain oxygen saturation greater than 92% with lowest amount of required oxygen; Consult nephrology and cardiology; Nursing pneumococcal and influenza vaccine screen and administration per local protocol; Physical and occupational therapy Thank you, Whitney Dunbar, ACNP-Student 5. Complete the following chart with the values present in prerenal and acute renal failure. Be certain to reference the chart. Table 1 Laboratory Values Present in Prerenal and Acute Renal Failure Laboratory Test Prerenal Acute Renal Failure FeNa < 1% >2% BUN to creatinine ratio > 20:1 < 20:1 Urine specific gravity >1.020 1.010 to 1.020 DUNBAR CASE STUDIES 19 Urine osmolality, mOsm per kg >500 250-350 Urine sodium concentration, <20 >20 Bland, Hyaline Casts Granular Casts mEq per L (mmol per L) Urine sediment Note. Normal laboratory values (Gutierrez & Morn, 2010; Papadakis et al., 2013). DUNBAR CASE STUDIES 20 References American Heart Association. (2009). ACCF/AHA 2009 expert consensus document on pulmonary hypertension: A report of the american college of cardiology foundation task force on expert consensus documents and the american heart association: Developed in collaboration with the american college of chest physicians, american thoracic society, inc., and the pulmonary hypertension association. Circulation, 119, 2250-2294. doi: 10.1161/CIRCULATIONAHA.109.192230 Brenner, B. (2007). Brenner and rector’s the kidney (8th ed.). Philadelphia, PA: Saunders Elsevier. Ellis, K. (2012). EKG plain and simple (3rd ed.). Upper Saddle River, NJ: Prentice Hall Health. Goldman, L., & Schafer, A. (2012). Goldman’s cecil medicine (24 ed.). Philadelphia, PA: Saunders Elsevier. Gutierrez, C., & Morn, C. (2010). Common renal conditions. FP Essentials, 375, 1-44. Retrieved May 2, 2013, from http://www.aafp.org/fpe/2010/0800/375.pdf. Janda, S., Shahidi, N., Gin, K., & Swiston, J. (2011). Diagnostic accuracy of echocardiography for pulmonary hypertension: A systematic review and meta-analysis. Heart, 8, 612-622. doi: 10.1136/hrt.2010.212084 Kidney Disease Improving Global Outcomes. (2012). KDIGO clinical practice guidelines for acute kidney injury. Kidney International Supplements, 2, 1-137. Retrieved May 20, 2013, from http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pd f Lexi-Comp, Inc. (2013). Lexi-DrugsTM. Lexi-Comp, Inc. Accessed May 16, 2013. DUNBAR CASE STUDIES 21 Longo, D., Fauci, A., Kasper, D., Hauser, S., Jameson, L., & Loscalzo, J. (2012). Principles of internal medicine (18th ed.). New York, NY: McGraw Hill Education. Ohio Board of Nursing (2012). The formularly developed by the committee on prescriptive governance. Retrieved May 29, 2013, from http://www.nursing.ohio.gov/PFS/AdvPractice/Formulary_11-19-12.pdf Ohio Board of Nursing (2013). The formularly developed by the committee on prescriptive governance. Retrieved May 29, 2013, from http://www.nursing.ohio.gov/PDFS/AdvPractice/4-30-13_Formulary.pdf Papadakis, M., McPhee, S., & Rabow, M. (2013). Current medical diagnosis and treatment (52nd ed.). New York, NY: McGraw Hill Medical. Roldan, C. (2012). The ultimate echo guide (2nd ed.). Philadelphia, PA: Lippincott Wiliams Wilkins. Tunariu, N., Gibbs, S., Win, Z., Gin-Sing, W., Graham, A., Gishen, P., & Al-Nahhas, A. (2007). Ventilation-perfusion scintigraphy is more sensitive than multidetector ctpa in detecting chronic thromboembolic pulmonary disease as a treatable cause of pulmonary hypertension. Journal of Nuclear Medicine, 48, 680-684. doi: 10.2967/jnumed.106.039438