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T2: AKI
Chapter 47: Acute Kidney Injury
| Question | Answer |
|---|---|
| Acute Kidney Injury (AKI) | Sudden, caused by acute tubular necrosis, diagnosed by acute reduction in urine output & or elevation in serum creatinine, is potentially reversible, primary cause of death is due to infection. |
| Chronic kidney disease (CKD) | Gradual, (over many year), caused by diabetic nephropathy, diagnosed by GFR <60 mL/min for >3 mo & or kidney damage >3 mo, progressive & irreversible, primary cause of death is cardiovascular disease. |
| Is characterized by a rapid loss of kidney function, accompanied by a rise in serum creatinine level & or a reduction in urine output. | Acute Kidney Injury |
| Accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood can occur if AKI is severe. | azotemia |
| AKI can develop over hours or days with progressive elevations of ____, ____, & _____, with or w/o a reduction in urine output. | BUN, creatinine, potassium |
| What are some prerenal issues that can cause AKI? | Causes are factors external to the kidneys that reduce renal blood flow such as severe dehydration, HF, or decreased CO. |
| This is caused by a decrease in circulating blood volume (e.g. severe dehydration, HF, decreased CO). | oliguria |
| What is the difference b/t prerenal oliguria and intrarenal oliguria? | In prerenal oliguria there is no damage to the kidney tissue (parenchyma). |
| What occurs with a decrease in circulating blood? | Autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and ADH attempt to preserve blood flow to essential organs. |
| Prerenal azotemia results in what? | Reduction in the excretion of sodium (<20 mEq/L), increased salt and water retention, and decreased urine output. |
| Prerenal conditions can lead to what if renal ischemia is prolonged. | intrarenal disease |
| What happens to the kidneys if decreased perfusion persists for an extended period of time? | The kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage). |
| What are some intrarenal causes of AKI? | Causes include conditions that cause direct damage to kidney tissue such as prolonged ischemia, nephrotoxins, Hgb released from hemolyzed RBCs, and myoglobin released from necrotic muscle cells. |
| How can nephrotoxins cause obstruction of intrarenal structures? | By crystallization or by causing damage to the epithelial cells of the tubules. |
| Hgb and myoglobin can block the tubules and cause what? | renal vasoconstriction |
| What diseases of the kidney can also cause AKI? | acute glomerulonephritis and systemic lupus erythematosus (SLE) |
| What is the most common cause of intrarenal AKI? | acute tubular necrosis (ATN) |
| ATN is primarily the result of what? | ischemia, nephrotoxins, or sepsis |
| These are responsible for 90% of cases of intrarenal AKI? | ischemic and nephrotoxic ATN |
| Severe kidney ischemia causes what? | A disruption in the basement membrane and patchy destruction of the tubular epithelium. |
| These cause necrosis of tubular epithelial cells, which slough off and plug the tubules. | nephrotoxic agents |
| How is ATN potentially reversible? | If the basement membrane is not destroyed and the tubular epithelium regenerates. |
| Involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes into the renal pelvis impairing kidney function. | postrenal causes of AKI |
| What are some postrenal causes of AKI? | benign prostatic hyperplasia, prostate cancer, calculi, trauma, extrarenal tumors |
| Bilateral ureteral obstruction leads to what? | hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage that results in a progressive decline in kidney function |
| If bilateral obstruction is relieved with 48 hours of onset this can occur, but if it is not relieved after 12 weeks then this is unlikely. | complete recovery |
| What are the clinical manifestations of AKI? | RIFLE - Risk is the first stage of AKI, Injury is the second stage which increases in severity to the final or third stage, Failure is final stage, Loss, End-stage kidney disease; loss and end-stage are the 2 outcome variables. |
| What are the phases of AKI? | oliguric, diuretic, and recovery |
| When a patient does not recover from AKI, then what can develop? | chronic kidney disease (CKD) |
| A reduction in urine output to less than 400 mL/day. | oliguria |
| When does oliguria usually occur after an injury to the kidneys? | within 1-7 days of the injury |
| When will oliguria occur if the cause is from ischemia? | within 24 hours |
| How long does the oliguric phase last? | On average about 10-14 days but can last months in some cases. The longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function. |
| A urinalysis may show casts, RBCs, and WBCs. The casts are formed from these, which detach or slough into the tubules. | mucoprotein impressions of the necrotic renal tubular epithelial cells |
| This has the potential to exacerbate all forms of AKI. | hypovolemia (volume depletion) |
| When urinary output decreases what occurs? | fluid retention |
| What can be seen with reduced urine output (anuria and oliguria)? | The neck veins may become distended with a bounding pulse. Edema and hypertension may develop. |
| Fluid overload can eventually lead to what? | HF, PE, and pericardial and pleural effusions |
| What is ammonia used for in the kidneys? | needed for hydrogen ion excretion |
| In kidney failure, the kidneys are not able to do what? | Synthesize ammonia or excrete acid products of metabolism. |
| What occurs in metabolic acidosis? | The serum bicarbonate level decreases because bicarbonate is depleted in buffering hydrogen ions. |
| With the development of severe acidosis, what can the patient develop? | Kussmaul respirations |
| What are Kussmaul respirations? | rapid, deep respirations |
| Why would a patient have Kussmaul respirations with severe metabolic acidosis? | To compensate by increasing the exhalation of carbon dioxide. |
| What happens to sodium when the tubules are damaged? | The tubules can't conserve sodium so the urinary excretion of sodium may increase, resulting in normal or below normal leveles of serum sodium. |
| Excessive intake of sodium should be avoided b/c it can lead to what? | volume expansion, hypertension, and HF |
| Uncontrolled hyponatremia or water excess can lead to what? | cerebral edema |
| The kidneys normally excrete 80-90% of the body's what? | potassium |
| What happens to potassium in AKI and why? | The serum potassium level increases b/c the kidney's normal ability to excrete potassium is impaired. |
| What are the symptoms of hyperkalemia in AKI? | Patients usually have no symptoms (asymptomatic). |
| Acute and/or rapid development of hyperkalemia may result in clinical signs that are apparent on ECG. What would these look like? | Peaked T waves, widening of the QRS complex, and ST segment depression. |
| Hospital acquired AKI often occurs in patient who have what? | multiorgan failure |
| What hematologic disorder is often present with AKI? | Leukocytosis |
| What is the most common cause of death in AKI? | infection |
| What are the most common sites of infection in AKI? | urinary and respiratory systems |
| This is an end product of endogenous muscle metabolism. | creatinine |
| This is an end product of protein metabolism. | urea |
| The kidneys are the primary excretory organs for? | urea and creatinine |
| What do the BUN and serum creatinine levels look like in kidney failure? | elevated |
| What are some of the neurologic changes that can occur due to waste products accumulating in the brain and other nervous tissue? | mild - fatigue and difficulty concentrating; severe - seizuer, stupor, and coma |
| During this phase of AKI, daily urine output usually is approx. 1-3 L buy may reach 5L or more. | diuretic phase |
| What causes the high urine volume during the diuretic phase of AKI? | Caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. |
| What happens to the kidneys during the diuretic phase of AKI? | The kidneys have recovered their ability to excrete wastes but not to concentrate urine. |
| Because of the large losses of fluid and electrolytes, the patient must be monitored for what? | hyponamtremia, hypokalemia, and dehydration |
| How long does the diuretic phase of AKI last? | 1-3 weeks |
| What occurs near the end of the diuretic phase? | The patient's acid-base, electrolyte, and waste product (BUN, creatinine) values begin to normalize. |
| When does the recovery phase of AKI begin? | When the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease. |
| How long does it take for major improvements to occur during the recovery phase of AKI? | In the first 1-2 weeks of this phase but kidney function may take up to 12 mths to stabilize. The outcome is influenced by the patient's overall health, the severity of the kidney failure, & the number & type of complications. |
| The urine specific gravity in oliguria of intrarenal AKI will be fixed at? | 1.010 |
| In intrarenal AKI why is the urine specific gravity fixed at 1.010? | This value reflects tubular damage with loss of concentrating ability by the kidneys. |
| Is the serum creatinine level normal, elevated, or decreased in intrarenal AKI? | elevated |
| Is the urinary secretion of sodium increased, decreased, or normal in intrarenal AKI? | increased |
| T/F: Is oliguria relieved after fluid replacement in intrarenal AKI? | False. Prerenal oliguria related to hypovolemis will usually respond to fluid replacement. |
| What are the diagnostic studies that are done for AKI? | A thorough history (prerenal causes w/a hx of dehydration, blood loss, or severe heart disease), inc. in serum creatinine, urinalysis, kidney ultrasonography, renal scan, CT scan, renal biopsy |
| An increase in serum creatinine may not be evident until what happens? | There is a loss of more than 50% kidney function. |
| What is the first test done to diagnose AKI and why? | Kidney ultrasonography b/c it provides imaging w/o exposure to potentially nephrotoxic contrast agents. |
| What can be seen with AKI using a CT scan? | Lesions and masses, as well as obstructions and vascular anomalies. |
| What is the best method for confirming intrarenal causes of AKI? | renal biopsy |
| What diagnostic studies are contraindicated for AKI? | Magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) |
| Why are MRIs and MRAs contraindicated in AKI? | The contrast medium (gadolinium) is nephrotoxic. |
| What are the primary goals of care for AKI? | Eliminate the cause. Manage signs and symptoms. Prevent complications. |
| What are some important nursing interventions with AKI? | Ensure adequate intravascular volume & CO by forcing fluids, loop diuretics (e.g. furosemide), osmotic diuretics (e.g. mannitol). Closely monitor fluid intake during oliguric phase. |
| What is the general rule for calculating the fluid restriction during the oliguric phase of AKI? | Add all losses for the previous 24 hours (e.g. urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g. respiration, diaphoresis). |
| What is one of the most serious complications in AKI and why? | Hyperkalemia b/c it can cause life-threatening cardiac dysrhythmias. |
| What are the various therapies used to treat elevated potassium levels? | Both insulin and sodium bicarb are temporary measures for tx of hyperkalemia by promoting a shift of K into the cells, but K will eventually be released. Only sodium polystyrene sulfonate (Kayexelate) & dialysis actually remove K from the body. |
| Why is calcium gluconate used in hyperkalemia? | It raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium. (Basically protects the heart from dysrhythmias, does nothing to the K.) |
| Why should kayexelate never be given to a patient with a paralytic ileus? | Bowel necrosis can occur. |
| What are some indications for renal replacement therapy (RRT)? | 1. volume overload resulting in compromised cardian &/or pulmonary status 2. elevated K level 3. met. acidosis (bicarb <15) 4. BUN >120 5. significant change in mental status and 6. pericarditis, pericardial effusion, or cardiac tamponade. |
| What are the different options of RRT? | peritoneal dialysis (PD), intermittent hemodialysis (HD), continuous renal replacement therapy (CRRT) |
| This RRT occurs at intervals of 4 hrs either daily, every other day, or three to four times per week and is the method of choice when rapid changes are required in a short period of time. | intermittent hemodialysis |
| This RRT has been used effectively and involves cannulation of an artery and a vein. | continuous renal replacement therapy |
| What is the primary challenge of nutritional management in AKI? | To provide adequate calories to prevent catabolism despite the restrictions necessary to prevent electrolyte disorders, fluid disorders, and azotemia. |
| What would the diet for an AKI patient look like? | High in carbs/fats and low in protein to prevent ketosis from endogenous fat breakdown & gluconeogenesis from muscle protein breakdown. Sodium is restricted to prevent edema, HTN, & HF. |
| What can be given as a nutritional supplement to provide a good source of nonprotein calories? | fat emulsion IV infusions |
| If a patient can't maintain adequate oral intake what is used? | Enteral nutrition is the preferred route for nutritional support. |
| When the GI tract isn't functional what is used to provide adequate nutrition? | parenteral nutrition |
| A patient with parenteral nutrition may need daily what? | HD or CRRT to remove the excess fluid |
| What should the nurse assess when caring for a patient with AKI? | Measure vital signs. Measure fluid intake & output. Examine urine (color, spec. gravity, glucose, protein, blood & sed.). Assess general appearance (skin color, edema, JVD, bruises). Observe dialysis access site (inflammation/exudate). |
| What else should the nurse assess in AKI patients? | Evaluate the patient's mental status & LOC. Examine the oral mucosa for dryness & inflammation. Auscultate the heart for the presence of an S3 gallop, murmurs, or a pericardial friction rub. Assess ECGs for dysrhythmias. Review labs & diagnostic tests. |
| What factors increase the risk for developing AKI? | Presence of preexisting CKD, older age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, & obstetric complications. |
| Careful monitoring of I&Os, fluid balance, & electrolyte balance is essential. What should be assessed & recorded? | Extrarenal losses of fluid from vomiting, diarrhea, hemorrhage, & increased insensible losses. |
| Prompt replacement of significant fluid losses will help prevent what? | Ischemic tubular damage associated with trauma, burns, and extensive surgery. |
| Intake & output records and the patient's weight are valuable indicators of what? | fluid volume status |
| Aggressive diuretic therapy for the patient with fluid overload resulting form any cause can lead to what? | A reduction in renal blood flow. |
| These drugs should be used sparingly in a patient at high risk. When used they should be given in the smallest effective dose for the shortest possible periods. | nephrotoxic drugs |
| These drugs can also decrease perfusion pressure and cause hyperkalemia. | ACE inhibitors |
| Because infection is the leading cause of death in AKI, this is critical? | meticulous aseptic technique |
| What are some acute interventions a nurse would implement with AKI patients? | Accurate I&Os, daily weights, assess for s/s of hyper/hypovolemia, meticulous aseptic technique, careful administration of nephrotoxic drugs, skin care measures, & mouth care. |
| Why is mouth care so important in AKI patients? | For preventing stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates the mucous membranes. |
| What discharge teaching would the nurse provide to a patient recovering from AKI? | Regulate protein & potassium intake. Follow-up care & regular evaluation of kidney function are necessary. Teach the pt s/s of recurrent kidney disease. Emphasize measure to prevent the recurrence of AKI. Make appropriate referrals for counseling. |
Created by:
eblanc1
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