Aki.docx

UNIVERSITY OF CEBU – BANILAD COLLEGE OF NURSING

RESOURCE UNIT IN ACUTE KIDNEY INJURY (AKI)

Submitted by: DIZON, MARISOL S. DOLINO, JACOB ERM JERICHO A. DUAVIS, MYRA LOU M. ENRIQUEZ, LESLIE ANN E. ESCABAS, KHIMBERLY T. GOLIS, DREXIE MARY E. IGNACIO, JERHAMIE ANGEL A. LAŇOJAN, CHRISTINE JIZZA R.

Submitted to: ANGELIQUE MARIE VILLAESTER, RN, MAN Clinical Instructor

VSMMC – TRAUMA February 04 – 07, 2019

General Objective: After 1 hour of discussion, the BSN 4A students will be able to understand and gain knowledge about Acute Kidney Injury (AKI). Specific Objectives 1. Define Acute Kidney Injury (AKI).

Time Allotment Acute kidney injury (AKI)—or acute renal failure (ARF), as it was previously termed—is 1 hour defined as an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or by azotemia (a rise in blood urea nitrogen [BUN] concentration). However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (eg, cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion, while a rise in the BUN level can also occur without renal injury, resulting instead from such sources as gastrointestinal (GI) or mucosal bleeding, steroid use, or protein loading. Therefore, a careful inventory must be taken before concluding that a kidney injury is present. Categories of AKI AKI may be classified into 3 general categories, as follows:  Prerenal - As an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons  Intrinsic - In response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage  Postrenal - From obstruction to the passage of urine While this classification is useful in establishing a differential diagnosis, many pathophysiologic features are shared among the different categories. Acute Kidney Injury Network classification system The Acute Kidney Injury Network (AKIN) has developed specific criteria for the diagnosis of AKI. The AKIN defines AKI as abrupt (within 48 hours) reduction of kidney function, manifested by any 1 of the following :  An absolute increase in serum creatinine of 0.3 mg/dL or greater (≥26.4 µmol/L)  A percentage increase in serum creatinine of 50% or greater (1.5-fold from baseline)  A reduction in urine output, defined as less than 0.5 mL/kg/h for more than 6 hours Signs and symptoms Skin

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Skin examination may reveal the following in patients with AKI:  Livedo reticularis, digital ischemia, butterfly rash  Palpable purpura: systemic vasculitis  Maculopapular rash: Allergic interstitial nephritis  Track marks (ie, intravenous drug abuse): Endocarditis Eyes Eye examination may reveal the following:  Keratitis, iritis, uveitis, dry conjunctivae: Autoimmune vasculitis  Jaundice: Liver diseases  Band keratopathy (ie, hypercalcemia): Multiple myeloma  Signs of diabetes mellitus  Signs of hypertension  Atheroemboli: Retinopathy (ie, Hollenhorst plaque in cholesterol microembolism) Ears Examination of the patient’s ears may reveal the following signs:  Hearing loss: Alport disease and aminoglycoside toxicity  Mucosal or cartilaginous ulcerations: granulomatosis with polyangiitis (Wegener granulomatosis) Cardiovascular system Cardiovascular examination may reveal the following:  Irregular rhythms (ie, atrial fibrillation): Thromboemboli  Murmurs: Endocarditis  Pericardial friction rub: Uremic pericarditis  Increased jugulovenous distention, rales, S3: Heart failure Abdomen The following signs of AKI may be discovered during an abdominal examination:  Pulsatile mass or bruit: Atheroemboli  Abdominal or costovertebral angle tenderness: Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis  Pelvic, rectal masses; prostatic hypertrophy; distended bladder: Urinary obstruction  Limb ischemia, edema: Rhabdomyolysis Pulmonary system Pulmonary examination may reveal the following:

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Rales: pulmonary edema, infectious pulmonary process Hemoptysis: ANCA vasculitis, anti–glomerular basement membrane (anti-GBM, Goodpasture) syndrome

2. Explain the Acute Kidney Injury (AKI) pathophysiolog y.

The kidney normally receives 20% to 25% of cardiac output or approximately 1200 mL/min of blood flow. This flow is normally protected by autoregulation mechanisms, keeping flow and pressure constant and maintaining oxygen delivery, which is necessary for the wide variety of highly metabolic renal functions, underscoring the kidney's vulnerability to ischemic and toxic injury.The 3 major determinants of renal blood flow are cardiac output, renal perfusion pressure, and glomerular hemodynamic factors. Cardiac output is affected by volume status, inotropy, and sodium/water retention. Renal perfusion pressure is influenced by mean arterial pressure, renal artery integrity, and renal venous outflow. Afferent and efferent arterial vasoconstriction and

vasodilatation of the glomerulus ultimately determine glomerular filtration pressure and GFR. Glomerular autoregulation by this means is functional only when systolic arterial pressure is 80 to 170 mm Hg. Renal blood flow and urine formation are also regulated by the renin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone from the hypothalamus. Renal endothelial-derived prostaglandins (eg, PGE2) modulate the renal/glomerular vasoconstriction caused by increased sympathetic tone and vasoactive drugs. Loss of these prostaglandins by administration of aspirin, nonsteroidal anti-inflammatory drugs, and other prostaglandin inhibitors can result in severe intrarenal vasoconstriction, decreased GFR, and onset or worsening of AKI. 3. Identify Diagnostic Considerations different disease Several laboratory tests, including the following, are useful for assessing the etiology of management. acute kidney injury (AKI) and can aid in proper management of the disease:  Complete blood count (CBC)  Serum biochemistries  Urine analysis with microscopy  Urine electrolytes In some cases, renal imaging is useful, especially if renal failure is secondary to obstruction. The American College of Radiology recommends ultrasonography, preferably with Doppler methods, as the most appropriate imaging method in AKI Although acute kidney injury (AKI) is a potentially reversible condition, it can occur in patients with chronic renal failure. Every effort should be made to identify reversibility, even if improvement in renal function is marginal. The best way to identify reversibility is by tracking the rate of deterioration of renal function. If there is an acceleration of the rate at which the patient’s renal function is worsening, the cause should be sought and treated. Differentials to consider in AKI include the following:  Abdominal aneurysm  Alcohol toxicity  Alcoholic ketoacidosis  Chronic renal failure  Dehydration  Diabetic ketoacidosis

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Gastrointestinal (GI) bleeding Heart failure Metabolic acidosis Obstructive uropathy Protein overloading Renal calculi Sickle cell anemia Steroid use Urinary obstruction Urinary tract infection Urine output in differential diagnosis Changes in urine output generally correlate poorly with changes in the glomerular filtration rate (GFR). Approximately 50-60% of all causes of AKI are nonoliguric. However, the identification of anuria, oliguria, and nonoliguria may be useful in the differential diagnosis of AKI, as follows:  Anuria (< 100 mL/day) - Urinary tract obstruction, renal artery obstruction, rapidly progressive glomerulonephritis, bilateral diffuse renal cortical necrosis  Oliguria (100-400 mL/day) - Prerenal failure, hepatorenal syndrome  Nonoliguria (>400 mL/day) - Acute interstitial nephritis, acute glomerulonephritis, partial obstructive nephropathy, nephrotoxic and ischemic ATN, radiocontrastinduced AKI, and rhabdomyolysis Differential Diagnoses  Acute Tubular Necrosis  Azotemia  Chronic Kidney Disease  Emergent Management of Acute Glomerulonephritis  Hemolytic Uremic Syndrome in Emergency Medicine  Henoch-Schonlein Purpura  Hyperkalemia  Hypermagnesemia  Hypernatremia  Hypertensive Emergencies

Approach Considerations Measures to correct underlying causes of acute kidney injury (AKI) should begin at the earliest indication of renal dysfunction. Serum creatinine does not rise to abnormal levels until a large proportion of the renal mass is damaged, because the relationship between the glomerular filtration rate (GFR) and the serum creatinine level is not linear, especially early in disease. Indeed, the rise of serum creatinine may not be evident before 50% of the GFR is lost. It cannot be overstated that the current treatment for AKI is mainly supportive in nature; no therapeutic modalities to date have shown efficacy in treating the condition. Therapeutic agents (eg, dopamine, nesiritide, fenoldopam, mannitol) are not indicated in the management of AKI and may be harmful for the patient. Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment and may include the following measures:  Correction of fluid overload with furosemide  Correction of severe acidosis with bicarbonate administration, which can be important as a bridge to dialysis  Correction of hyperkalemia  Correction of hematologic abnormalities (eg, anemia, uremic platelet dysfunction) with measures such as transfusions and administration of desmopressin or estrogens Volume overload Furosemide can be used to correct volume overload when patients are still responsive; this often requires high intravenous (IV) doses. Furosemide plays no role in converting an oliguric AKI to a nonoliguric AKI or in increasing urine output when a patient is not hypervolemic. However, response to furosemide can be taken as a good prognostic sign. Hyperkalemia Hyperkalemia in patients with AKI can be life-threatening. Approaches to lowering serum potassium include the following:  Decreasing the intake of potassium in diet or tube feeds  Exchanging potassium across the gut lumen using potassium-binding resins  Promoting intracellular shifts in potassium with insulin, dextrose solutions, and beta agonists  Instituting dialysis

Nephrotoxic agents In AKI, the kidneys are especially vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, nonsteroidal anti-inflammatory drugs [NSAIDs]) should be avoided or used with extreme caution. Similarly, all medications cleared by renal excretion should be avoided, or their doses should be adjusted appropriately. A 2013 study indicated that triple therapy using nonsteroidal anti-inflammatory drugs (NSAIDs) with 2 antihypertensive medications—a diuretic along with an angiotensinconverting enzyme (ACE) inhibitor or an angiotensin-receptor blocker (ARB)— significantly increases the risk of hospitalization for AKI, particularly in the first 30 days of treatment with these drugs. Consultation Nephrology consultation should be sought early in the course of AKI. A nephrologist can help to optimize management and avoid the preventable complications of AKI. Dialysis Dialysis, especially hemodialysis, may delay the recovery of patients with AKI. Most authorities prefer using biocompatible membrane dialyzers for hemodialysis. Indications for dialysis (ie, renal replacement therapy) in patients with AKI are as follows:  Volume expansion that cannot be managed with diuretics  Hyperkalemia refractory to medical therapy  Correction of severe acid-base disturbances that are refractory to medical therapy  Severe azotemia (BUN >80-100)  Uremia Timing and intensity Great controversy exists regarding the timing of dialysis. Older studies suggested decreased mortality with early, versus late, initiation of dialysis, but timing of dialysis initiation has not been assessed in large, randomized, controlled trials. Approaches vary widely at present. The Acute Renal Failure Trial Network (ATN) Study found that increasing the intensity of dialysis (either intermittent or continuous) did not improve clinical outcomes (morbidity/mortality). The best evidence suggests that patients with dialysis-dependent AKI should receive at least 3 hemodialysis treatments per week with a delivered Kt/V

value of 1.2, or continuous hemodialysis (continuous venovenous hemodialysis or hemofiltration) of 20 mg/kg/h (prescribed). CRRT There seems to be no difference in outcome between the use of intermittent hemodialysis and continuous renal replacement therapy (CRRT), but this question is currently under investigation. CRRT may have a role in patients who are hemodynamically unstable and who have had prolonged renal failure after a stroke or liver failure. Such patients may not tolerate the rapid shift of fluid and electrolytes caused during conventional hemodialysis. Peritoneal dialysis Peritoneal dialysis is not frequently used in patients with AKI. Nevertheless, it can technically be used in acute cases and probably is tolerated better hemodynamically than is conventional hemodialysis. NURSING INTERVENTIONS: 1. Know the risk factors and diagnostic criteria for AKI. 2. Teach patient about risk factors for AKI including nephrotoxic medications, and emphasize that they should report any change in urination, urine appearance, and urine output after starting any new medication. 3. Caution patients using NSAIDs to be mindful of potential adverse effects, such as hypersensitivity and hemodynamically mediated acute kidney injury and to drink plenty of water when taking these medications. 4. Evaluate the patient's serum creatinine level before administering any potentially nephrotoxic drugs. 5. Clean all equipments used between patients, practice scrupulous hand hygiene, and instruct patients on infection prevention, because sepsis is a common risk factor for acute kidney injury. 6. Prioritize IV fluid administration for patients in the initial stages of an acute kidney injury. Perform strict input and output measurement. 7. Asses heart and lung sounds for adventitious breath sounds or extra heart sounds. 8. Assess dependent and periorbital edema. 9. Monitor mentation and changes in level of consciousness. 10. Monitor diagnostic studies Radiology: Chest x-ray, ultrasound or CT of kidneys, Lab: urine, blood. 11. Administer medications as ordered by the physician.

4. Discuss health teachings related to the disease.

12. Nutrition management and education. Restrict intake of sodium and potassium. 13. Fluid replacement therapy. 14. Monitor daily weight of patient. 15. Monitor for hypervolemia in oliguric phase and hypovolemia in diuretic phase. 16. Monitor potassium levels and ECG. 17. Monitor GCS, as waste product accumulation can affect mental status. 18. Ensure adequate protein intake. 19. Monitor closely for signs of infection as this is a common cause of death with AKI. 20. Encourage patient to do respiratory exercises, may be with the help of an incentive spirometer. Lifestyle and home remedies Choose lower potassium foods. Your dietitian may recommend that you choose lower potassium foods. High-potassium foods include bananas, oranges, potatoes, spinach and tomatoes. Examples of low-potassium foods include apples, cauliflower, peppers, grapes and strawberries. Avoid products with added salt. Lower the amount of sodium you eat each day by avoiding products with added salt, including many convenience foods, such as frozen dinners, canned soups and fast foods. Other foods with added salt include salty snack foods, canned vegetables, and processed meats and cheeses. Limit phosphorus. Phosphorus is a mineral found in foods, such as whole-grain bread, oatmeal, bran cereals, dark-colored colas, nuts and peanut butter. Too much phosphorus in your blood can weaken your bones and cause skin itchiness. Your dietitian can give you specific recommendations on phosphorus and how to limit it in your particular situation. Discharge Instructions for Acute Kidney Injury Drink less fluid, if instructed by the doctor. Keep a record of everything you eat and drink. Measure the amount of urine and stool you have each day. Weigh yourself every day, at the same time of day, and in the same kind of clothes. Keep a daily record of your daily weights. Take your temperature every day. Keep a record of the results. Learn to take your own blood pressure. Keep a record of your results. Ask your doctor when you should seek emergency medical attention. He or she will tell you which blood pressure reading is dangerous. Avoid contact with people who have infections (colds, bronchitis, or skin conditions). Practice good personal hygiene. This is especially important if you

have a catheter in place when you leave the hospital. Doing so helps keep you safe from infection. Take your medications exactly as directed. You may require frequent blood and urine tests to monitor your kidney function. References:  AACN Advanced Critical Care October/December 2010, Volume :21 Number 4 , page 350 – 356  https://www.mayoclinic.org/diseases-conditions/kidney-failure/diagnosis-treatment/drc-20369053  American Journal of Nursing, Volume 113, 2013  https://www.mountnittany.org/articles/healthsheets/1577  Macedo E, Mehta RL. When should renal replacement therapy be initiated for acute kidney injury?. Semin Dial. 2011 Mar-Apr. 24(2):132-7  Palevsky PM, Zhang JH, O'Connor TZ, Chertow GM, Crowley ST, Choudhury D, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008 Jul 3. 359(1):7-20.  Acute Kidney Injury. Author: Biruh T Workeneh, MD, PhD, FASN; Chief Editor: Vecihi Batuman, MD, FASN