Week 13: Chp 62: Acute Kidney Injury Flashcards
What is Acute kidney Injury?
condition characterized by an acute, rapid loss of renal function
- a rapid and progressive azotemia, an accumulation of nitrogenous waste products such as urea, nitrogen, and creatinine and progressive increases in potassium
- oliguria may be present
- uremia may be present
- is reversible if addressed in a responsive and timely manner
Modifiable risk factors
sepsis, administration of contrast media, and exposure to nephrotoxins
Oliguria
a reduction of urine output to 400 mL/day
- may be present in acute kidney injury
- may be at risk for CKF (chronic kidney failure) if circulating fluid volume is not returned to normal
Uremia
renal function decline that involves multiple body systems
3 Major categories of Acute Kidney Injury (AKI)
- Prerenal causes
- Intrarenal causes
- Postrenal causes
Prerenal Causes
most common cause of AKI
- result of external factors (those that are not related to the anatomical structures of the urinary system) that reduce renal blood flow and lead to decreased glomerular perfusion and filtration
- prerenal causes: hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, and vascular obstruction (these can affect circulation)
Decreased Renal Perfusion affects the clearance of what?
waste products
-known as Azotemia (inability to get rid of waste products)
Azotemia
happens when your kidneys can not get rid of enough nitrogenous waste
-affects clearance of waste products
What affects circulation?
hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, and vascular obstruction
>these are prerenal causes
What happens when the renal system senses the decrease in perfusion?
the renin-angiotensin-aldosterone system (RAAS) is stimulated
-the RAAS is a compensatory mechanism that conserves sodium and water in order to maintain blood pressure
-the result is low urine output with an increase in BUN and creatinine (ratio of 10:1) and an inability of the kidneys to conserve sodium
>if renal perfusion remains compromised and compensatory mechanisms fail, intrarenal damage to renal tissue may occur
Intrarenal causes
involve direct damage to the renal parenchymal tissues, resulting in impaired nephron functioning
Nephron
functional unit of the kidney
-any direct assault to the nephron significantly compromises the perfusion and filtration of waste products
Damage to Nephron occurs as a result from?
prolonged ischemia, exposure to nephrotoxins such as aminoglycoside antibiotics, contrast dye used in imaging studies, hemoglobin released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells
Complications of nephrotoxins
cause crystallization or damage to the epithelial cells of the tubules
Complications if hemoglobin and myoglobin
block the tubules and cause renal vasoconstriction
Causes of AKI (intrarenal)
-acute glomerulonephritis and acute tubular necrosis (ATN)
Intrarenal causes: Acute tubular necrosis
intrarenal condition caused by ischemia, nephrotoxins, or pigments and accounts for 90% of all intrarenal cases
-the ischemia of the basement membrane and tubular epithelium seen in ATN result in a decreased GFR
-is reversible if identified early and appropriate measures are taken
>nephrotoxic agents such as aminoglycoside antibiotics are the causative factor; removal of these aids in reversing the disease process
Postrenal Causes
involve the mechanical obstruction of the lower urinary tract (the ureters, bladder, and urethra)
-as the urine leaves the kidneys, flow is obstructed at some point at the ureters or below, causing reflux into the renal pelvis, impairing kidney function
>post renal causes include: BPH, prostate cancer, calculi, trauma, and tumors
>potential for intrarenal damage is reversible if obstruction is removed
Postrenal causes include?
BPH, prostate cancer, calculi, trauma, or tumors
Which is a prerenal cause of AKI?
A. acute glomerulonephritis and neoplasms
B. septic shock and nephrotoxic injury from medications
C. pyelonephritis and calculi formation
D. hypovolemia and myocardial infarction
D. hypovolemia and myocardial infarction
(prerenal = result of external factors that reduce renal blood flow and lead to decreased glomerular perfusion and filtration)
Four Phases of Acute Kidney Injury
- Initiating phase
- Oliguric phase
- Diuretic phase
- Recovery phase
Phases of AKI: Initiating phase
“onset”, is the beginning phase of the insult, continuing until signs and symptoms appear
-can last for hours to days
-triggering events arise from prerenal conditions; decrease in circulating volume, resulting in an equal decrease in tissue oxygenation
-compensatory mechanisms cause the release of angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone to preserve the blood flow to essential organs
-vasoconstriction occurs along with sodium and water retention
-decrease in urine output, high specific gravity of urine and a low urine sodium concentration is observed
>if prerenal cause is corrected, the condition is reversible
Phases of AKI: Oliguric phase
a urine output below 400 mL/day
-when urine output decreases because of renal tissue damage
-urine with a fixed specific gravity (between 1.007 and 1.010) and a high sodium concentration (>40 mEq/L[>40 mmol/L])
> a high sodium concentration with a fixed specific gravity indicates intrarenal damage that does not respond to the compensatory mechanism of RAAS
-increases in BUN/creatinine, electrolyte abnormalities, acidosis, and fluid overload as a result of decreased GFR
-phase may last up to 14 days or longer depending on initiation of treatment
-the loner the oliguric phase lasts, the poorer the prognosis
Phases of AKI: Diuretic phase
occurs when the cause of AKI has been corrected
- there is an osmotic diuresis resulting from high urea levels
- urine output increases from 1 to 3 L to 3 to 5 L a day
- patient may experience severe fluid loss as a result of increased urination, leading to dehydration and causing electrolyte imbalances
- phase can last from 1 to 3 weeks
- as this phase ends, acid-base, electrolytes, BUN, and creatinine levels begin to normalize
Phases of AKI: Recovery phase
begins as the kidney begins to return to its regular excretory function
- the basement membrane is restored, and the GFR increases up to 70 to 80% of normal
- fluid and electrolyte balance normalize
- phase can last from several months to 1 year
Clinical Manifestations of AKI
- signs of volume overload due to decreased urine output, such as edema, pulmonary edema and shortness of breath, heart failure and jugular vein distention, hypertension, and dysthymias; chest pain; or pressure
- electrolyte imbalances include increased potassium, phosphorus, BUN/creatinine; decreased calcium, sodium, and pH; and metabolic acidosis
- may suffer from anorexia, nausea, constipation, or diarrhea
- may become confused or lethargic
- suffer seizures or coma r/t severe fluid and electrolyte imbalances
When the patient is in the diuretic phase of AKI, the nurse must monitor which serum electrolyte imbalance? A. Hypokalemia and hyponatremia B. Hypokalemia and hypernatremia C. Hyperkalemia and hyponatremia D. Hyperkalemia and hypernatremia
C. hyperkalemia and hyponatremia
Manifestations of Kidney Disease
- urine volume decreases
- fluid overload
- increased potassium
- decreased sodium
- decreased calcium/increased phosphorus
- metabolic acidosis
- anemia
- increased BUN
- increased creatinine
Manifestations of Kidney Disease: Urine volume decreases
- initiating phase: urine output decreases because of decreases in circulating volume and the resulting compensatory mechanism of RAAS
- oliguric phase: decreased filtration through damaged renal tissues
Manifestations of kidney disease: Fluid overload
due to decreases in urine output
Manifestations of kidney disease: increased potassium
impaired excretion
Manifestations of kidney disease: decreased sodium
inability to conserve sodium
Manifestations of kidney disease: decreased calcium/ increased phosphorus
- decreased GI absorption of calcium due to the kidney’s inability to activate vitamin D
- decreased calcium stimulates the parathyroid gland to release parathyroid hormone, which stimulates the release of calcium and phosphorous from bone
- decreased phosphorus clearance
Manifestations of kidney disease: metabolic acidosis
- decreased acid excretion
- increased loss of bicarbonate
- increased production of nonvolatile acids such as lactic acid or phosphoric acid
Manifestations of kidney disease: anemia
impaired erythropoietin production
Manifestations of kidney disease: increased BUN
impaired clearance, dehydration, increased protein intake and breakdown
Manifestations of kidney disease: Increased creatinine
impaired clearance; best indicator of renal failure
Goal of managing AKI
are to eliminate the cause, prevent complications, and assist patient in recovery
Assessment of adequate hydration includes?
monitoring of blood pressure, heart rate, urine output, and clinical signs such as the quality of pulses, skin color, temperature, and respiratory status
-fluid intake and output must be carefully and closely monitored and documented
Medications for AKI
- diuretic therapy, such as loop diuretics such as furosemide (Lasix) or bumetanide (Bumex), and an osmotic dietetic (mannitol) to treat fluid overload
- nephrotoxic and contrast dyes should be avoided or used with extreme caution
Nutrition for AKI
-provide calories to prevent catabolism despite the restrictions required to prevent electrolyte and fluid disorders and azotemia
>if do not receive proper nutrition and calories, then catabolism of body protein will occur, which causes urea, phosphate, and potassium levels to increase
-adequate carbohydrate, protein, and fat
-sodium is restricted to prevent edema, hypertension, and congestive heart failure
-potassium is restricted to avoid complications of hyperkalemia
Indications for Dialysis
- severe volume overload resulting in heart failure or severe respiratory distress
- elevated potassium level with ECG changes
- severe metabolic acidosis
- altered mental status
- pericarditis, pericardial effusion, and cardiac tamponade
Complications of AKI
hyperkalemia
-risk of life-threatening cardiac arrhythmias
Why is hyperkalemia a safety alert?
decreases the threshold necessary to generate an action potential, which can result in life-threatening dysrhythmias such as ventricular fibrillation, ventricular tachycardia, or asystole
- initial indication is peaked T waves
- worsening is indicative of widening of the QRS complex, the loss of P wave, and presence of sine wave
Medical Management of hyperkalemia
-stabilize myocardial cell membrane with IV calcium gluconate or calcium chloride (calcium chloride can cause severe irritation and pain when given IV)
-enhance cellular uptake of potassium:
>IV glucose followed by IV regular insulin (insulin facilitates movement of potassium)
>Albuterol, a beta agonist, facilitates intracellular movement of potassium
>Bicarbonate stimulates exchange of hydrogen ions and potassium ions
-enhance body elimination of potassium:
>administration of PO or rectum, sodium polystyrene; monitor for water and sodium retention; never give to someone with paralytic ileus
-administer furosemide
-emergent hemodialysis (HD)
Clinical Manifestations of AKI are r/t?
decreased glomerular filtration, resultant fluid overload, and impaired clearance of electrolytes and waste products >urinary output decrease to less than 400 mL in24 hours (oliguria) >Laboratory abnormalities: -Serum BUN elevation -Serum creatinine elevation -Normal or below-normal levels of serum sodium -Calcium deficit -Phosphorous excess -Potassium elevation (cannot excrete it) -Anemia (cant produce RBCs/ erythropoietin) -Metabolic acidosis >Fluid volume overload e/b -neck vein distention -bounding pulse -edema -hypertension -heart failure, if uncorrected -pulmonary edema, if uncorrected -pericardial and pulmonary effusion >lethargy >stupor
Nursing Diagnoses
- excess fluid volume r/t renal failure and fluid retention
- fatigue r/t anemia, metabolic acidosis, and uremic toxins
- potential complications: dysrhythmias arising from electrolyte imbalances
- potential complications: metabolic acidosis r/t the inability to excrete H+, impaired HCO3, reabsorption, and decreased synthesis of ammonia
Nursing Assessments
- vital signs
- urine output
- Lab values
- oxygenation and breath sounds
- peripheral vascular system
Assessments: Vital Signs
hypotension and tachycardia may be present initially, reflecting a hypovolemic state causing the AKI
-later hypertension will be present because of fluid overload
Assessment: urine output
urine output is decreased initially because of decreased circulating volume
-later, it will be decreased because of impaired clearance
Assessment: Lab values
- Bun/creatinine: increased because of the reduced clearance
- Potassium: increased because of the reduced clearance
- Sodium: decreased because of the kidneys inability to conserve sodium
- Hemoglobin/ hematocrit: decreased because of the kidney’s decreased production of erythropoietin
- Calcium/phosphorus: calcium is decreased because of the kidneys inability to activate vitamin D; phosphorus is increased because of the release of PTH in response to low calcium, releasing both calcium and phosphorus from bone
- Arterial Blood Gases: metabolic acidosis due to inadequate clearance of acid, increased loss of bicarbonate (HCO3), and increased production of nonvolatile acids
Assessment: Oxygenation and breath sounds
breath sounds may reveal rales due to fluid overload and pulmonary edema decreasing oxygenation and SPO2
Assessment: Peripheral vascular system
signs of fluid overload include edema and jugular vein distention
Nursing Actions
- manage fluid balance
- administer diuretics as ordered
- administer potassium-lowering therapy as necessary
- psotioning, ambulation, cough, and deep-breathing exercises
- weigh the patient daily
- skin care
- monitor and document food intake
Actions: manage fluid balance
initially, cautious fluid administration may be necessary to ensure adequate circulating volume
-later, fluid restriction may be necessary to ease or prevent complications of fluid overload
Actions: administer diuretics as ordered
necessary to relieve fluid overload
Actions: administer potassium-lowering therapy as necessary
elevated potassium can cause lethal dysrhythmias
Actions: positioning, ambulation, cough, and deep-breathing
positioning or ambulation as the patient tolerates eases the work of breathing and prevents complications of immobility such as atelectasis and pneumonia
Actions: weigh daily
increased weight may reflect fluid overload
-weight is used to make the dialysis plan
Actions: Skin care
edema decreases tissue perfusion and increases the risk of decubitus
-keep the skin clean and dry, and change the patients position frequently
Action: monitor and document food intake
provides information regarding nutrition status, which is important for healing
-consult dietician; for such diets as reduced sodium and potassium
Teachings: knowledge of cause and treatment of AKI
- helps ease anxiety and maximize compliance of treatment
- fluid and dietary restrictions (decreased sodium, limited protein), urine output monitoring, avoiding nephrotoxic substances (NSAIDs, some antibiotics, radiological contrast dye, alcohol) and dialysis if necessary
Well-managed patient
complies with prescribed treatment regimen and returns to normal urine excretion with the elimination of waste products from the circulation through proper glomerular membrane perfusion and filtration
- complications of heart failure, prolonged hypertension, pulmonary edema, dysrhythmia, or renal failure are avoided
- patient has complete recovery
