Acute Kidney Injury (AKI)
an abnormal abrupt drop in urine output
morphological types of AKI
1. Prerenal2. intrarenal3. post renal
BUN
the waste product of protein break down
Creatinine
waste product of muscle metabolism, filtered out of the blood by the kidneys, and excreted in urine
Prerenal AKI
causes are factors that reduce systemic circulation, causing a reduction in renal bf(anything that affects CO and bf to kidneys can cause this)ie: severe dehydration/ HF and dysrhythmias (problem with the pump itself)/ decreased CO/ Hemorrhage
Prerenal AKI
occurs when a sudden reduction in blood flow to the kidney (renal hypoperfusion) causes a loss of kidney function
AKI Prerenal think
1. lower GRF filtration2. Aldosterone is purposefully having to keep water and NA
A decreased GRF rate can cause
Oliguria
With prerenal oliguria there is NO
damage to the kidney tissue (parenchyma) like in intrarenal
Oliguria
caused by a decrease in circulating blood volume (severe dehydration, HF, decreased CO) and is READILY REVERSIBLE with appropriate treatment
With AKI: prerenal
autoregulatory mechanisms attempt to preserve bf: when there is a decrease in circulating blood volume increases angiotensin II, aldosteron, NORE, and antidiuretic hormone to attempt to preserve bf to essential organs
Prerenal azotemia results in a
reduction in the excretion of sodium (less than 20 mEq/K), increased salt and water retention, adn decreases urine output
Prerenal conditions contribute to
causes included conditions that cause direct damage to the KIDNEY TISSUEMedications (abx)/ contrasts and/or dyes/ direct trauma to the kidneys
AKI: intrarenal causes include:
1. prolonged ischemia/ nephrotoxins2. Hemoglobin released from hemolyzed RBCs3. Myoglobin released from necrotic muscle cells
Nephrotoxins can cause
obstruction of intrarenal structrues by crystallization or by causing damage to the epithelial cells or the tubules
Hemoglobin and myoglobin can
block the tubules and cause renal vasoconstriction
Diseases of the kidney such as
ACUTE GLOMERULONEPHRITIS and SYSTEMIC LUPUS ERYTHEMATOSUS may cause AKI
Intrarenal: Acute tubular necrosis (ATN)
is the most common intrarenal cause of AKI and is primarily the result of ischemia, nephrotoxins or sepsis
ATN: severe ischemia
causes disruption in basement membrane and patchy destruction of the tubular epithelium
ATN: nephrotoxic agents
cause necrosis of tubular epithelial cells, which slough off an plug the tubules
Ischemic and nephrotoxic ATN are responsible for
90% of intrarenal AKI cases
ATN Is
potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates
WHat is the most common causes of AKI for hospitalized pts
ATN (think intrarenal): risks associated with the development of ATN while in the hospital include..major surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, prolonged HOTN, and nephrotoxic agents
AKI: Postrenal
causes include mechanical obstruction of outflow. As the flow of urine is obstructed, urine reflux into the renal pelvis, impairing the kidney function
Postrenal causes
1. BPH2. Prostate cancer3. Calculi4. trauma5. extrarenal tumors6. Bilateral ureteral obstruction
Bilateral ureteral obstruction
leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage, resulting in progressive decline in kidney function
If bilateral obstruction is relieved within 48hrs of onset
complete recovery is LIKELYPROLONGED OBSTRUCTION can lead to tubular atrophy and irreversible kidney fibrosis
Post renal causes of AKI account for
1. Urine changes2. Fluid volume3. Metabolic Acidosis4. Sodium balance5. Potassium excess6. Waste production accumulation7. Neurological disorders
Urinary changes (oliguria)
1. urinary output less than 400 mL/day2. Occurs within 1 to 7 days after injury3. lasts 10 to 14 days4. Urinalysis may show casts, RBCs, WBCS
With urinary changes if the cause is ischemic
oliguria can occur within 24 hours
Urinary changes are the most common
INITIAL MANIFESTATION of AKI (oliguria)
The oliguric phase lasts on average
10 to 14 days but can last months in some cases. the longer the oliguric phases lasts, THE POORER THE PROGNOSIS FOR complete recovery of kidney function
about 50% of pt will not be
oliguric, making the initial diagnosis more difficult. changes in urine output generally do not correspond to changes in GRF.
Changes in urine output are often helpful in
differentiating the etiology of AKIexample: Anuria (no urinary output) usually seen with urinary tract obstructionsOliguria is commonly seen with prerenal causesnonoliguric AKI is seen with acute interstitial nephritis and ATN
Urinalysis may shows casts, RBCs, and WBCs
the casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules
Fluid Volume (oliguric phase)
1. decreased urine output2. fluid retention3. Fluid overload can lead to HF, Pulm edema, and pericardial/ pleural effusions
With fluid volume
Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI, especially prerenal causes
When urinary output decreases
fluid retention occurs. The severity of the manifestations depends on the extent of fluid overload. IN the case of reduced urine output ( anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and HTN may develop
Fluid retention
1. neck veins distended2. bounding pulse3. Edema4. HTN
Metabolic acidosis (oliguric)
1. impaired kidney cannot excrete H+2. Serum bicarbonate production is decreased3. severe acidosis develops (kussmaul respirations)
In the Normal kidney
excess H+ are excreted to maintain a physiologic balance of the blood pH.the impaired kidney cannot excrete H+ or the acid products of metabolism
Serum bicarbonate production is
decreased because of defective reabsorption and regeneration of bicarbonate ions. Serum bicarbonate is depleted through buffering of acidic H+ ions and metabolic end products
Pt with severe acidosis may develop
Kussmaul respirations (rapid deep respiration) in an effort to compensate for increasing the exhalation of CO2
Sodium imbalance (Oliguria)
1. increased excretion of sodium2. HYPONATREMIA can lead to cerebral edema
With sodium imbalance
Damaged tubules cannot conserve sodium. The urinary excretion of sodium may increase, resulting in normal or below-normal levels of serum sodiumExcessive intake of sodium should be avoided because it can VOLUME EXPANSION,HTN, and HF
Potassium excess (oliguric)
1. impaired ability of kidneys to excrete potassium2. Increased risk with massive tissue trauma3. ECG changes
With Potassium excess
the kidneys normally excrete 80-90 percent of the body's potassiumIn AKI the serum potassium level increase because the kidneys normal ability to excerete potassium is impaired
Hyperkalemia risk is increased is
AKI is caused by massive tissue trauma because the damaged cells release additional potassium into the ECF. Bleeding and blood transfusion may cause cellular destruction, releasing more potassium into the ECF. Metabolic acidosis worsens hyperkalemia as H+ enter the cells and potassium is driven out of the cells into the extracellular fluid
Pt with Hyperkalemia are often
asymptomatic but some may still complain of weakness with severe hyperkalemia because cardiac muscle is intolerant of acute increases in K+, emergency treatment of hyperkalemia is needed
Acute and/or rapid development of hyperkalemia may result in
clinical signs that are apparent on ECG. These changes include peaked T waves, widening of the QRS complex, and ST segment depression.
Waste product accumulation (oliguric )
elevated BUN and serum creatinine levels
Waste product accumulation
the Kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). elevated BUN level can also be cause by: Dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury,or GI bleeding
What is the best serum indicator of AKI?
Creatinine because it is not significantly altered by other factors!
Neurologic disorders (oliguric)
1. Fatigue and difficulty concentrating2. Seizures, stupor, coma
Neurologic disorders
Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue. The manifestations can be as mild as fatiguer and difficulty concentrating and then escalate to seizures, stupor, and coma
Hematologic disorders
ospital-acquired AKI after occurs in pt who have multiorgan failure. Leukocytosis is often present with AKI. the most common cause of death in AKI is infection. The most common sites of infection are the urinary and respiratory systems
Uncontrolled hyponatremia or water excess can lead to
CEREBRAL EDEMA
AKI Clinical Manifestations: Diuretic Phase
1. Daily urine output 1 to 3 L2. May reach 5 L or more3. Monitor for hyponatremia, hypokalemia, and dehydration
In this phase (diuretic)
the kidneys have recovered their ability to excrete waste, but not to concentrate the urine
With large losses of fluid and electrolytes
it requires the pt to be monitored for hyponatremia, hypokalemia, and dehydration
The diuretic phase may last up to
1 to 3 weeks and near the end of this phase, the pts acid-base, electrolytes and waste products (BUN and creatinine) values stabilize
the recovery phases begins with the
1. GRF increasing (allowing the BUN and serum creatinine levels to decrease)2. major improvements occur in the first 1 to 2 weeks of this phase, but kidney function may take up to 12 months to stabilize
The outcome of AKI is influence by the pts
Overall health, severity of kidney failure, and the number type of complications
Some pt with AKI do not recover and progress to
end-stage renal disease.The older adult is less likely to have a complete recovery of kidney function. Pts who recover may achieve clinically normal kidney function, but remain in an early stage of CKD
AKI: Diagnostic studies
. thorough history2. Serum creatinine3. Urinalysis4. Kidney ultrasonography5. Renal scan6. CT scan7. Renal biopsy
Thorough history
is essential for diagnosing the etiology of AKI. Consider prerenal causes when there is a history of dehydration, or blood loss. Suspect intrarenal causes if the pt has been exposed to potentially nephrotoxic drugs or contrast media used in radiologic study. Postrenal causes are suggested by a history of changes in the urinary stream, stones, BPH, or bladder or prostate cancer.
Increase in serum creatinine
may not be evident until there is a loss of more than 50% of kidney function. The rate of increase in serum creatinine is also important as diagnostic indicator in determining the severity of injury
Urinalysis
is important diagnostic test. urine sediment containing abundant cells, cast, or proteins suggests intrarenal disorders. the urine osmolality, sodium content, and specific gravity help in differentiating the causes of AKI. Urine sediment may be normal in both prerenal and postrenal AKI. In intrarenal problems, hematuria, pyuria, and crystals may be seen
kidney ultrasonography
Is often the first test done, since it provides imaging without exposure to potentially nephrotoxic contrast agents. It is useful for evaluating for possible kidney disease and obstruction of the urinary collection system
Renal Scan
Can assess abnormalities in kidney bf, tubular function, and the collecting system
CT scan
Can identify lesions, masses, obstructions, and vascular anomalies
renal biopsy
is considered the best method for confirming intrarenal causes of AKI
AKI Diagnostic studies: contraindicated
1. MRI with gadolinium contrast medium2. Magnetic resonance angiography (MRA with gadolinium contrast mediumContrast-induced nephropathy (CIN) (use ultrasound instead)
Pt with diabetes receiving metformin
the drug should be held for 48 hr prior to and after the use of contrast media to decrease the risk of lactic acidosis.
AKI interprofessional care
1. Ensure adequate intravascular volume and CO2. Closely monitor fluid intake during oliguric phase3. Hyperkalemia4. Indications for renal replacement therpay (RRT)
Ensure adequate intravascular volume and cardiac output (this is the first step)
. force fluids2. Loop diuretics (furosemide...Lasix)3. Osmotic diuretics (mannitol)
IF AKI is already established
forcing fluids and diuretics will not be effective and my in fact be harmful
Closely monitor fluid intake during the
OLIGURIC PHASE OF AKIGeneral rule for calculating the fluid restriction is to add all the losses for the previous 24hrs plus 600ml
Hyperkalemia
1. Insulin and sodium bicarbonate2. Calcium carbonate3. Sodium polystyrene sulfonate (kayexalate)
Hyperkalemia is one of the most
of the mostserious complication in AKI because it can cause life-threatening cardiac dysrhythmias
Two therapies that are used to treat elevated K+ levels temporarily are
. insulin and sodium bicarbonate : they promote a shift of K+ into the cells, but K+ will eventually be released
Calcium gluconate
raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium
Only kayexalate and dialysis actually remove
K+ from the bodynever give kayexalate to a pt with paralytic ileus becuase bowel necrosis can occur
Indications for renal replacement therapy (RRT)
1. volume overload2. elevated serum K+ levels3. Metabolic acidosis4. Significant change in mental status5. Pericarditis, pericaridal effusion,or cardiac tamponade
Volume overload
results in compromsied cardiac and/or pulmonary status
AKI planning
PT with AKI will1. completely recover without any loss of kidney function2. Maintain normal fluid and electrolyte balance3. Have decreased anxiety4. Adhere to and understand need for careful follow-up care
AKI: Nursing implementation
Health promotion1. identify and monitor populations at high risk (ELDERLY)2. Control exposure to nephrotoxic drugs and industrial chemicals3.prevent prolonged episodes of HOTN and hypovolemia
Health promotion1. identify and monitor populations at high risk (ELDERLY)2. Control exposure to nephrotoxic drugs and industrial chemicals3.prevent prolonged episodes of HOTN and hypovolemia
the expected outcomes are that the pt with AKI will1. regain and maintain normal fluid and electrolye balance2. adhere to treament regimen3. experince no complications4. have complete recovery
Waste product accumulation
the Kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). elevated BUN level can also be cause by: Dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury,or GI bleeding
What is the best serum indicator of AKI?
Creatinine because it is not significantly altered by other factors!
Neurologic disorders (oliguric)
1. Fatigue and difficulty concentrating2. Seizures, stupor, coma
Neurologic disorders
Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue. The manifestations can be as mild as fatiguer and difficulty concentrating and then escalate to seizures, stupor, and coma
Waste product accumulation
the Kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). elevated BUN level can also be cause by: Dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury,or GI bleeding