Module 8 Inflammation II - Unit 3: Acute Kidney Injury (AKI) PDF

Critical Care Nursing Program Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Introduction In the previous unit on shock, we explored sepsis. The inf...

Critical Care Nursing Program Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Introduction In the previous unit on shock, we explored sepsis. The inflammation which is associated with sepsis is a very common cause of acute kidney injury (AKI) in intensive care patients. Inflammation as previously discussed causes a massive vasodilation which, if not treated immediately, impairs renal perfusion. Recall from pumping and perfusion that when patients have decreased cardiac output, the SNS and RASS are activated. These compensatory mechanisms are activated to increase fluid and perfuse vital organs. Chances are many of your patients will have hemodynamic instability or underlying kidney disease which will increase their risks of developing AKI during their ICU admission. This unit begins with an examination of the anatomy of the kidney, and continues with an exploration of the physiology of urine formation in terms of the following influencing factors: the functions of the nephron, renal blood flow, glomerular filtration, and hormonal influences. Types of acute kidney injury, assessment findings, diagnostics and treatments will be explored to assist the critical care nurse to optimize kidney function. Learning Outcomes On completion of this unit the learner will be able to: 1. Differentiate between autoregulation and the other factors which influence kidney hemodynamics. 2. Define acute kidney injury and failure, using RIFLE criteria. 3. Identify the etiologies for the three categories of acute kidney injury: prerenal, postrenal, and intrarenal. 4. Discuss the assessment findings and the diagnostic evaluation methods used in the diagnosis of acute kidney injury and failure. 5. Discuss the therapeutic strategies used with acute kidney injury and failure. Required Reading Please refer to your reading list for Inflammation II Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 1 of 9  Critical Care Nursing Program Renal Anatomy and Physiology Understanding normal kidney physiology and anatomy is essential for understanding altered states. Below is a couple of highlights: The nephron is the functional unit of the kidney. Each kidney consists of approximately one million nephrons. A nephron is comprised of two major components: the renal tubule and the glomerulus, its vascular structure. The upper portion of a nephron, located in the cortex of the kidney, is made up of two components: (a) the beginning of the renal tubule known as the glomerular or Bowman’s capsule and (b) a tangled cluster of blood capillaries called the glomerulus. Bowman’s capsule, together with the glomerulus, is called a renal corpuscle. The Bowman’s capsule is the cup-shaped mouth of the nephron. Water and solutes are filtered from the blood in the glomerulus through a special membrane called the glomerular-capsular membrane. The visceral layer of Bowman’s capsule and the endothelium of the glomerulus form this membrane. There is one afferent arteriole and one efferent arteriole forming the glomerulus of each renal corpuscle. Substances from the blood must pass through the three layers that comprise the glomerular-capsular membrane. The most important layer in diagnosing renal disease is the basement membrane which acts as the dialyzing membrane. After water and solutes pass through the glomerular-capsular membrane, the resulting product in the capsular space is called the filtrate. The filtrate proceeds to pass through four sections of the renal tubule (proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct) before it empties as urine into the minor calyces of the kidney. Urine is normally protein and RBC free as they are unable to pass through the glomerular-capsular membrane. Normal glomerular filtration rate (GFR) is 125 ml/minute and produces 180 litres of urine in 24 hours. However, we normally only excrete 1.5-2 litres daily. We need to excrete a minimum of 300-400 ml of urine a day in order to rid our bodies of waste products. Generally, we want patients to make 30cc urine/hr. There is a limit to auto regulatory mechanisms. Below a mean arterial pressure of 80 mmHg or above a mean arterial pressure of 180 mmHg, glomerular filtration rate is proportional to perfusion pressure. For example, when blood pressure drops for a few minutes, autoregulation maintains renal blood flow and thus glomerular pressure. However, when blood flow and glomerular pressure are greatly reduced, the powerful vasoconstriction mechanisms take over. When the degree of efferent arteriole vasoconstriction is high, the plasma remains in the glomerulus for a long time. Extra amounts of fluid are filtered and reabsorbed leaving a high concentration of plasma protein in the glomerulus. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 2 of 9  Critical Care Nursing Program This high concentration of plasma protein increases the plasma colloid osmotic pressure. The high colloid osmotic pressure causes the glomerular filtration rate to drop. As well, when cardiac output and blood pressure continue to fall, strong sympathetic stimulation causes arteriole vasoconstriction and autoregulation fails. Renal clearance is a good indicator of glomerular filtration rate. Creatinine clearance can be used to approximate GFR as creatinine is freely filtered and not reabsorbed in the kidney. In the clinical area, serum creatinine is most commonly used as an indicator of the GFR. Canadian measurements for BUN and creatinine are different from the US counterparts which are listed in your required readings. We will be using the Canadian measurements: Creatinine: 50-110 umol/L and BUN: 2.8-7.1 mmol/L. Blood Urea Nitrogen (BUN) 1. The normal BUN is 2.8-7.1 mmol/L. Urea is the end product of the metabolism of dietary protein and muscle tissue. 2. Two factors determine urea excretion: the concentration of serum urea and the glomerular filtration rate (GFR). The concentration of serum urea can increase with excessive protein intake or by catabolism related to starvation, infection, surgery, G.I. bleed, or drugs such as corticosteroids. When the GFR is slowed as it is with dehydration or hypovolemia (preload), the BUN will increase. 3. Since many factors may increase the BUN even though kidney functioning has not been altered, the BUN should be used in conjunction with creatinine levels as an indicator of renal function. Creatinine Serum creatinine, as discussed above, can be used as a useful indicator of glomerular filtration rate. The normal range for serum creatinine is 50 - 110 umol/l. 1. Creatinine is the end product of muscle metabolism and is relatively independent of dietary intake and fluid balance. 2. Serum creatinine is a better indicator of renal function than the BUN. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 3 of 9  Critical Care Nursing Program Renal Functions Acronyms are always helpful for us to remember important points. “A wet bed” is an acronym that can be used to remember the functions of the kidney. A -- Acid/Base Balance W -- Water Balance E -- Electrolyte Balance T -- Toxins, elimination B -- Blood Pressure E -- Erythropoetin D -- Vit D production Acute Kidney Injury Kidney function occurs along a continuum between normal function and death. Normal Risk Injury Failure Loss Death Acute Kidney Injury Acute kidney injury (AKI), as illustrated above, denotes injury, failure or loss of kidney function. It is the most common renal problem afflicting patients who are critically ill, is characterized by the following: 1. Sudden onset. 2. Acute deterioration. 3. Azotemia (presence of nitrogenous bodies, e.g., urea, uric acid, and creatinine in the blood). 4. Uremia (symptom produced by the retention of nitrogenous substances in the blood). 5. With or without oliguria. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 4 of 9  Critical Care Nursing Program 6. High mortality rate (35-86%). 7. Prognosis is good with early recognition and management. With early treatment 50-60% of patients have a good prognosis; however, 40-50% may go on to develop chronic renal failure. Acute kidney injury has three categories associated with the area of insult to the kidney: pre-renal (before), intrarenal (within) and postrenal (after). In pumping and perfusion, we discussed pre-renal acute kidney injury (AKI). Prerenal AKI can evolve into intrarenal AKI. When a decreased renal perfusion persists for a prolonged time period, ischemia may result and the pre-renal AKI condition can deteriorate into intrarenal AKI. Intrarenal AKI results from damage to the parenchyma of the kidneys from such etiologies as: infection, prolonged periods of ischemia (decreased blood flow to the kidneys), nephrotoxic agents, and immunologic and vascular disease processes. Medications such as NSAIDS and ACE inhibitors can contribute to renal decline. Damage to the kidneys affects their ability to properly filter the bodies wastes, produce urine and regulate acid-base, electrolyte and water balances. It is this damage to the cells of the kidneys that differentiates pre-renal AKI from intrarenal AKI. Renal parenchymal damage was formerly referred to as acute tubular necrosis (ATN). The trend is to use the new terminology intrarenal AKI. In intrarenal AKI, cellular debris from damage to cells accumulates in the renal tubules and obstructs flow of filtrate through the nephron. Pressures rise, filtration ceases and urine formation stops. The damaged cells continue to swell, obstruct, and become more damaged. In the nephron, the basement membrane of the glomerulus could be damaged and the kidney would not be able to conserve proteins. Proteins and other large molecules (glucose) would then be spilled into the urine. The kidneys may not be able to conserve sodium and water. Pre-renal and post-renal AKIs do not initially produce damage to the parenchyma of the kidneys. Therefore, the kidneys are able to normally conserve/excrete sodium and water. This is important especially in pre-renal AKI if the problem is secondary to fluid loss (preload). The conservation of sodium leads to water retention and an increase in fluid volume and therefore increase in blood pressure. Remember that if cardiac output is decreased then blood flow to the kidneys will be decreased and urine output will also decrease. Transfusion reactions and muscle damage can also have a toxic effect on the kidneys causing intrarenal AKI. Transfusion reactions cause hemoglobinuria, and muscle damage causes myoglobinuria. Hemoglobin and myoglobin (myoglobin is similar in function to hemoglobin and carries oxygen to the muscle fibres) break down into hematin that is excreted in the urine. When the levels of globulins become high from transfusion reactions or muscle damage, they can cause renal tubular damage. Please refer to your reading list for Inflammation II Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 5 of 9  Critical Care Nursing Program There are specific points about some of the diagnostic tests that must be emphasized before the discussion proceeds. These include: 1. Creatinine (Cr) clearance, serum blood urea nitrogen (BUN), and serum creatinine are most commonly used as indicators of renal function. Creatinine is a good indicator of renal function. As it is a by-product of muscle metabolism the rate of production is not influenced as much by diet or fluid balance as is the BUN. The BUN will increase earlier than creatinine. 2. Urine osmolality and specific gravity can be used to evaluate the ability of the kidneys to concentrate or dilute urine. Urine osmolality should vary with the osmolality of the serum. Thus, when the serum becomes hyperosmolar, urine osmolality should also increase because the kidneys should attempt to reabsorb water to return the serum to normal. Specific gravity measures the concentration of urine. Be aware that falsely high readings can occur when glucose or radiographic contrast media are present. 3. Urinalysis mirrors the structural integrity of the kidney. Casts and crystals indicate an inflammatory process. Monitor the patient’s urine colour, concentration, clarity and odour. Urine is normally clear and contains no detectable protein, glucose, or ketones. Hematuria always indicates pathology except when associated with menstruation. A few white cells are a common finding. Myoglobinuria and hemoglobinuria cause the urine to appear reddish-brown in colour and to test positive for occult blood. 4. Radiologic examinations are useful in helping to assess the structure and functioning of the kidneys. A renal biopsy is an invasive procedure and is usually only indicated when a diagnosis cannot be made based on other methods. Treatment for Intra-renal AKI Oliguric Phase The management of intrarenal AKI should begin with prevention. The following goals guide therapeutic management once it is decided that the patient has intrarenal AKI: 1. Correction of the cause. 2. Promotion of regeneration of functional kidney capacity. 3. Correction of fluid imbalances. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 6 of 9  Critical Care Nursing Program 4. Prevention of hyperkalemia and other life-threatening electrolyte imbalances. 5. Treatment of azotemia acidosis. 6. Prevention of further nephrotoxicity. 7. Improvement of nutritional status. A prealbumin may be ordered to asses a patient’s level of protein calorie malnutrition. Protein deficiencies can occur with inadequate availability of dietary protein, decreased ability to digest protein, increased protein loss, and with increased protein requirements. Patients with AKI are at high risk for protein deficiency and therefore need to have an appropriate nutritional assessment. 8. Avoidance and treatment of infection. 9. Prevention of anemia. The following table reflects the electrolyte imbalances that may be seen in intrarenal AKI: SERUM LABORATORY VALUE POSSIBLE EFFECT IN INTRARENAL AKI Na+ (sodium) Decreased Cl- (chloride) Increased K+ (potassium) Increased CO2 (serum bicarbonate or total Decreased CO2) BUN (blood urea nitrogen) Increased Cr (creatinine) Increased Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 7 of 9  Critical Care Nursing Program Ca++ (calcium) Decreased Mg (magnesium) Increased PO4 (phosphorus) Increased Albumin Decreased Hgb (hemoglobin) Decreased Hct (hematocrit) Decreased Signs and Symptoms - Diuretic Phase With the onset of the diuretic phase, the kidneys begin to produce greater than 400 ml of urine in 24 hours. However, the onset of diuresis does not coincide with a drop in BUN and creatinine levels. Patients in this phase are still at risk for various fluid and electrolyte imbalances. Dialysis Therapy Dialysis is the treatment modality in which removes excess toxins from your blood as well as excess fluid when kidney failure occurs (Canadian Kidney Foundation, 2021). There are three types of dialysis used: hemodialysis, continuous renal replacement therapy and peritoneal dialysis. Continuous renal replacement therapy (CRRT) is most commonly used in ICU’s. This is an advanced therapy that is beyond the scope of this course. As you become more experienced, you will learn how to effectively manage a patient receiving CRRT. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 8 of 9  Critical Care Nursing Program Treatment for Postrenal AKI The goal of therapy for post-renal AKI is to remove the obstruction and eliminate the life-threatening cause. When there is an acute cessation of urine output, postrenal AKI should be considered. This may be as simple as a blocked catheter. If it is a more serious kidney stone, this type of acute kidney injury can be reversed rapidly by surgical intervention. Antibiotics may be required to treat septicemia or pyelonephritis. As well, dialysis may be required to remove fluid and wastes until the obstruction can be removed. Once the obstruction is corrected, a diuretic phase occurs. During this time the patient must be closely monitored for fluid and electrolyte imbalances. The patient in the diuretic phase must be closely monitored for fluid and electrolyte imbalances. As well, the patient must be supported while regeneration of renal tissue occurs. Conclusion The knowledge and skills presented in this unit have prepared you to care for patients at risk or with a form of acute kidney injury, acute kidney failure, acute on chronic failure, or end stage kidney disease. Many critical care patients will experience acute kidney injury as a complication of their admission diagnosis. It is therefore important for critical care nurses to recognize those at risk and respond to optimize kidney function. Even if you are not currently working in a critical care environment, you can utilize this knowledge to plan care for patients in any acute or chronic care situation. Module #8: Inflammation II Unit #3: Acute Kidney Injury and Failure Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 9 of 9