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Chapter 47: Acute Kidney Injury

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