Advance Kidney Injury Care Plan

Care Plan Paperwork (Part I) Directions: Complete all areas from the information provided in the case study and your own research. Pathophysiology: Acute Renal Failure How does the disease affect the body? The kidneys are not getting enough blood flow due to low blood pressure. This causes the kidneys to be overwhelmed and start to cause a build-up of water, sodium and waste products in the body and a decrease of urine output. How is it diagnosed? Diagnosis is made on labs (BUN, Na, and GFR) and also on renal ultrasonography, CT and MRI imaging. What are the current treatments and prognosis? Dialysis is the best treatment for ARF Intrarenal injury caused by ischemia has a higher mortality rate What are your Priority Assessments based on Patho (include body systems and specific things you would assess)? I would do neuro checks every 4 hours, do strict I&Os to calculate urine output, do an EKG for the hyperkalemia and hemodynamic changes Source for pathophysiology information: Your Patients Signs and Symptoms Expected from Patho:  Temporal wasting is a sign of catabolism  Hypotension causing the hypoperfusion to the kidneys  Tachycardia is a compensation for the hypotension  Tachypnea is a compensation for the hypotension Unexpected findings:  Fever due to the E.coli Your Patients Lab values- Include all labs (with normal ranges next to them) and explain trends/reason for abnormal labs. Sodium 148 H (135-145) Potassium 6 H (3.5-5) Chloride 105 (96-106) Carbon Dioxide 12 L (22-28) BUN 134 H (5-20) Creatinine 8.7 H (0.84-1.21) UOP in 24 hours 50 mL L (720 mL +) pH 7.2 L (7.35-7.45) PaCO2 33 L (35-45) PaO2 83 (75-100) Creatine phosphokinase 88 (10-120) Troponin 0.1 (0-0.4) Urine sodium 45 H (20) Source for lab interpretation: Expected from Patho:  UOP – oliguria is expected because the kidneys are not getting enough blood flow so the kidneys release aldosterone to retain water  Urine sodium >40 mEq is consistent with intrarenal injury  BUN:Cr ratio is 15:1 which is consistent with intrarenal injury  Hyperkalemia is indicative of the oliguric phase in acute renal failure  Hypernatremia is expected because aldosterone is retaining sodium  Metabolic acidosis is expected because of the formation of oxygen free radicals due to reperfusion Unexpected findings: Your Patient’s Diagnostic tests Expected from Patho:  EKG   o Sinus tachycardia o Left ventricular hypertrophy o No ischemic changes Chest X-ray o Prominent pulmonary arteries with diffuse alveolar infiltrates consistent with pulmonary edema Renal ultrasound o No hydronephrosis o Kidneys are 9 cm bilaterally and echogenic Unexpected findings: Patient Data Pt Initials: LH Age: 72 Gender: M DOB: 3/16 Admission date: Wt: Admitting diagnosis: hypernatremia and unresponsiveness Current Medical Dx: acute renal failure Surgical procedures: none Pertinent PMH/PSH: HTN, DM Type 2, Chronic Kidney Disease Stage 3, mild dementia, benign prostatic hypertrophy Most Recent V/S, BP 80/40 Pulse: 130 RR: 28 Temp: 101.3F 02Sat: 90 Pain: responsive to painful stimuli Acceptable Pain level Bed Rest none Current treatments (IV, catheters, tubes, drains. O2, etc.)  Left forearm IV, Intubated Orders: CRRT V/S frequency: Continuous Consults: Renal, Pulmonary Other Activity: Isolation: Medication Administration Allergies NKDA Weight 91 Kg ***Use the ATI Medication Template instead of your usual medication grid What are normal VS for age? BP ___131____ /___85___ Pulse __58__ RR ___19___Temp__98.2__ 02Sat__92___ Assessment Time: General appearance Your Initial Assessment 0800 Unconscious Head & neck Temporal wasting Integument No tenting or rashes on skin Dry mucous membranes IV Status (rate, type) 18 G left Forearm Respiratory Clear bilateral breath sounds Cardiovascular Sinus tachycardia without rubs gallops or murmurs Neurological Unconscious, responsive to painful stimuli Pain assessment Responsive to painful stimuli (Pain Scale & Score) Gastrointestinal (nutrition) Genitourinary Soft abdomen but grimacing on deep palpation Normal active bowel sounds in all 4 quadrants Low urine output White blood cells and red blood cells and muddy casts Musculoskeletal Temporal wasting Growth & Development WNL Psychosocial Lives by himself, daughter checks in on him frequently Other Medication Administration Allergies: NKDA Weight Kg No PRNs that haven’t been given in last 48 hours. 1. Medication name 1. Frequency Safe Dose Range Safe? 1. Drug Category 1. Contraindications 2. Dose & Route 2. Times given (Show calculations) (Y/N) 2. Purpose YOUR patient is 2. Adverse Reactions taking 3. Administration Concerns Lisinopril Q day 40 mg PO = max dose Y ACE Inhibitors 1. Aliskiren, Valsartan PO 5 mg Hypertension 2. Dizziness, hypotension, cough 3. Take with or without food Atorvastatin QHS For patients taking Y HMG CoA reductase 1. Cyclosporine, gemfibrozil, PO 20 mg atorvastatin for maintenance, inhibitors pazopanib, red yeast rice, it is suggested not to go over tipranavir 80 mg a day For Hyperlipidemia 2. Insomnia, UTI, nausea, dyspepsia 1. D/C if pt develops myopathy or renal failure Amlodipine Q day 10 mg is the highest dose Y Calcium Channel Blocker 1. Dantrolene PO 10 mg recommended for tablets Hypertension 2. Edema, pulmonary edema 3. Don’t admin to pts with hypertrophic cardiomyopathy PO 5 mg Type 2 diabetes Tamsulosin PO 0.4 mg Q day after same meal each day 0.8 mg = max dose Y Alpha 1 blockers BPH Aspirin PO 81 mg Q Day Daily limit is 4,000 mg. 81mg a day is safe Y Analgesic / cardiovascular agent Stroke Prevention Dopamine 5 mcg/kg/min IV IV infusion 5 mcg x 91 kg = 455 mcg / min Max dose = 50 mcg x 91 kg = 4,550 mcg / min Y Inotropic agent Increase renal blood flow 2. Abdominal pain, diarrhea, hypoglycemia 3. Hypoglycemia patient education 1. Isoniazid, nicardipine, Prazosin 2. HA, orthostatic hypotension, rhinitis 3. Do not crush chew or open capsules 1. other NSAIDS 2. N/V, stomach pain, heartburn 3. drink full glass of water after taking tablets 1. Selegiline, tranylcypromine 2. Ventricular arrhythmia, A Fib, dyspnea, gangrene 3. Drug is stable for 24 hours after dilution Care Plan (Part II) Nursing Diagnosis 1 Nursing Diagnosis 2 Decreased Cardiac Output r/t elevated potassium levels interfering with conduction system Excess fluid volume r/t decreased urine output and sodium retention Nursing Diagnosis 3 Nursing Diagnosis 4 Impaired urinary elimination r/t need for dialysis Impaired mucous membrane r/t irritation from nitrogenous waste products Nursing Diagnosis #1 Respiratory Cardiac GI/GU Clear bilateral lung sounds Intubated Sinus tachycardia Bowel sounds in all 4 quadrants Pain with deep palpation Decreased UOP with muddy casts Musculoskeletal NURSING DIAGNOSIS #1 Temporal wasting Decreased Cardiac Output r/t elevated potassium levels interfering with conduction system Integument Psychological Puritis Dry mucous membranes Anxiety r/t intubation Neuro Unconscious Responsive to painful stimuli Other Hx of CKD, HTN, and dementia Expected Outcomes Outcome 1. Patient will demonstrate adequate cardiac output as evidenced by blood pressure, pulse rate and rhythm within normal parameters and adequate urinary output before discharge. Interventions Interventions with rationales for each Outcome. Minimum of 6 interventions per outcome. (What did you do? What did you plan to do?) 1. recognize primary characteristics of decrease CO like fatigue, dyspnea, edema orthopnea, increased CVP. Recognize secondary characteristics of decrease CO like weight gain, hepatomegaly, JVD, palpitations, lung crackles, oliguria, coughing and skin color changes 2. Monitor and report presence od degree of symptoms including dyspnea at rest, JVD, S3 gallops. These are symptoms that are consistent with heart failure and decreased CO 3. monitor orthostatic blood pressure and daily weights Evaluation Outcome is in progress. Patient has been given inotropic agents to help with cardiac output and is being put on CRRT to get rid of waste in the blood. 4.Place patient in semi fowlers or high fowlers position with legs down to decrease the work of breathing and decrease venous return and preload 5.Closley monitor fluid intake including IVF and maintain fluid restriction if ordered because in patients with decreased cardiac output, poorly functioning ventricles may not tolerate increased fluid. 6.Look at lab data including ABGs, BUN, CBC and electrolytes. Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. Outcome 2. ********************************************************************* 1. Note results of echocardiogram because dopamine can cause palpitations and other heart concerns Patient will remain free of side effects from dopamine used 2.Only give patient small amounts of coffee or caffeine to avoid cardiac dysthymias Outcome is being met. Patient currently is showing no side effects from the use of dopamine and is showing an cardiac output cardiac output. 3.Offer Zofran after meals if patient becomes nauseas. 4. Monitor for orthostatic hypotension and daily weights 5.titrate dopamine within defined parameters to maintain contractility 6.Administer oxygen as needed to increase availability to the myocardium to relive symptoms related to hypoxemia Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. Nursing Diagnosis #2 Respiratory Cardiac GI/GU Clear bilateral lung sounds Intubated Sinus tachycardia Bowel sounds in all 4 quadrants Pain with deep palpation Decreased UOP with muddy casts Musculoskeletal NURSING DIAGNOSIS #2 Temporal wasting Excess fluid volume r/t decreased urine output and sodium retention Integument Psychological Puritis Dry mucous membranes Anxiety r/t intubation Expected Outcomes Neuro Unconscious Responsive to painful stimuli Other Hx of CKD Interventions Interventions with rationales for each Outcome. Minimum of 6 interventions per outcome. (What did you do? What did you plan to do?) Outcome 1. 1. Monitor strict input and output. Notice trends reflecting decreasing urine output in relation to fluid intake. Patient will maintain urine output of 45 mL / hour (0.5 mL x 91 kg) or more with normal urine osmolality and specific gravity before discharge 2. Monitor serum and urine osmolality, serum sodium, BUN/creatine ratio and hematocrit for abnormalities. 3. Provide a restricted sodium diet to allow the kidneys to excrete excess fluid. 4.Administer appropriate diuretics and check blood pressure before administration. After administration note blood pressure and urine outputs. Evaluation Outcome has not been met yet. Patient has only had a urine output of 2 mL an hour for the past 24 hours. Patient has an indwelling foley for measuring urine output and is about to start his first round of 5.Insert an indwelling catheter and measure urine output hourly. Notify physician if less than 45 mL / hour for 6 or more hours. This is defined as oliguria 6.Perform CRRT because patient is hemodynamically unstable, and the excessive fluid must be removed. Outcome 2. Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. 1. Monitor vital signs and note decreasing blood pressure, tachycardia and tachypnea. Monitor for S3 heart sounds. Patient will maintain normal central venous pressure, pulmonary 2.Monitor patient’s behavior for restlessness, anxiety, or confusion. Use safety precautions if symptoms capillary wedge are present. If there is excess fluid it compromises cardiac output causes cerebral tissue hypoxia. pressure, cardiac output and vital signs before discharge. 3.Maintain rates of all IV infusion carefully utilizing an IV pump to prevent inadvertent exacerbation of excess fluids 4.Consult with physician if signs and symptoms of excess fluid volume persist or worsen 5.Monitor central venous pressure, mean arterial pressure, pulmonary capillary wedge pressure and cardiac output index. Note and report trends indication increasing or decreasing pressures over time. Alteration in any of these parameters may indicate the patient ins going into show. 6.Monitor daily weights by using the same scale and time each day. Changes in body weight indicates change in body fluid volume Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. Outcome is in progress. Patient’s vital signs are being controlled and cardiac output is being improved with use of dopamine. Nursing Diagnosis #3 Respiratory Cardiac GI/GU Clear bilateral lung sounds Intubated Sinus tachycardia Bowel sounds in all 4 quadrants Pain with deep palpation Decreased UOP with muddy casts Musculoskeletal NURSING DIAGNOSIS #1 Temporal wasting Risk for ineffective renal perfusion Integument Psychological Puritis Dry mucous membranes Anxiety r/t intubation Expected Outcomes Outcome 1. Patient will maintain normal blood urea nitrogen and serum creatinine levels before discharge Neuro Unconscious Responsive to painful stimuli Other Hx of CKD, HTN and DM type 2 Interventions Interventions with rationales for each Outcome. Minimum of 6 interventions per outcome. (What did you do? What did you plan to do?) 1. Monitor for changes in mental status and headaches. Changes in mental status from impaired renal function can range from difficulty in concentration, confusion, seizures and coma as the result of uremic toxins 2. Collect a 24-hour urine specimen for examination as ordered. Place on ice to preserve the quality of the urine. This gives a better assessment of kidney function. 3. Monitor laboratory data as ordered. Lab data includes BUN, serum creatinine, and GFR. Report abnormalities. Monitoring labs helps with direct therapy. Evaluation Outcome is in progress. Patient is being monitored closely. Labs are trending higher than normal but are expected to get WNL after CRRT. 4.Measure intake and output on a regular basis. Calculate intake against the output to monitor fluid retention 5.Weigh the patient daily 6.Monitor for edema Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. Outcome 2. Patient will maintain serum electrolytes within normal limits before discharge ********************************************************************* 1. Place patient on a telemetry monitor and look for dysrhythmias due to possible increase serum potassium ad phosphorus or low hemoglobin due to poor kidney function. 2. Monitor for changes in mental status and headaches. Changes in mental status from impaired renal function can range from difficulty in concentration, confusion, seizures and coma as the result of electrolyte imbalances 3. Monitor laboratory data as ordered. Lab data includes serum and urine electrolytes. Report abnormalities. Monitoring labs helps with direct therapy. 4.Complete a pain assessment, Assess and document the onset, intensity, character, location, duration, aggravating factors and reliving factors. Notify physician of any increase in pain or discomfort or if comfort measures are not effective. Generalized pain and muscle spams can be caused by electrolyte imbalances due to renal failures 5.Assess for signs of dehydration. Dehydration causes decreased renal perfusion and leads to renal failure 6.Monitor vital signs carefully Especially note new onset of hypertension from onset of kidney dysfunction or decreased mean arterial pressure. Chronic hypertension can lead to atherosclerosis, the Outcome is in progress. Patient is being monitored closely. Serum electrolytes are getting better but are not all WNL yet. most common cause of renal arty stenosis. Hypotension may lead to poor renal perfusion and acute renal failure Student:___________________________________________ Date:_________________ Article summary and application to patient (APA format including references) There have been many studies done on the relationship between acute kidney injury (AKI) and diabetes mellitus type two (DM). Although it is not directly understood how the pathophysiology of DM affects the kidney function, there is a lot of data that proves that having DM in your medical history decreases your risk of survival after acquiring AKI (Patschan & Müller, 2016). Many patients in these studies were also found to have chronic kidney disease (CKD) on top of DM and AKI. These diseases tend to share the same risk factors including hypertension, obesity and older age (Patschan & Müller, 2016). With the knowledge of having a higher risk of morbidity and mortality with DM and AKI, studies have shown that the target glucose level needs to be between 110-149 while patients are in the ICU recovering from AKI (Patschan & Müller, 2016). Blood glucose higher or lower can significantly injure the kidney more and increase risk of death. Studies have also shown that the use of insulin drips for patients in the ICU with DM and AKI decreased their chance of survival compared to the use of conventional insulin therapy (Patschan & Müller, 2016). My patient is a 72-year-old male with past medical history of DM type two, CKD stage three and hypertension. He developed AKI and was sent to the hospital for stabilization. After analysis of the relationship between DM and AKI, my patient had a very high risk of developing AKI and an even higher risk of morbidity and mortality from AKI. It is not known if the high levels of blood glucose or intrarenal atherosclerosis contributes greatest towards AKI, but my patient does have each of these issues and therefore is at a higher risk of morbidity and mortality from AKI. The insulin therapy used in the ICU for my patient was Glipizide, a conventional insulin therapy. By avoiding an insulin drip, my patient has a better chance of survival in regard to diabetic neuropathy damage to the kidney. Based on his past medical history, age, vital signs, and labs, my patients chances of survival are lower. References (include all process paper references) Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook (10th ed.). Maryland Heights, MO: Mosby Elsevier. Fitzsimmons, B., & Bohan, E. (2009). Critical care nursing: A holistic approach (pp. 891-898) (1010182177 777755919 P. G. Morton & 1010182178 777755919 D. K. Fontaine, Authors). Philadelphia, PA: Wolters Kluwer Health. Patschan, D., & Müller, G. A. (2016). Acute kidney injury in diabetes mellitus. International journal of nephrology, 2016. Student:___________________________________________ Date:_________________