AKI concept map - 10th ed PDF

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10th ed...

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Disease: Acute Kidney Disease -

Ranging from slight deterioration in kideny function to severe impairment Raid loss of kidney function Potentially reversible High mortality Usually affect people with other life-threatening conditions Can be caused by acute glomerulonephritis and systemic lupus erythematosus

Azotemia: accumulation of nitrogenous waste products (urea nitrogen, creatinine) in the blood

Etiology Prerenal: -

Reduce systemic circulation Reduction in blood flow Decreased glomerular perfusion and filtration Mechanisms that increase angiotensin II, aldosterone, norepinephrine, and ADH, attempt to preserve blood flow to essential organs Contribute to intrarenal AKI If decreased perfusion is prolonged, kidneys lose their ability to compensate nd damage to kidy parenchyma occurs(intrarenal damage)

Prerenal oliguria: -

no damage to kidneys Oliguria is caused by a decrease in circulating blood volume( severe hydration, HF, decreased cardiac output) Reversible with treatment

Prerenal azotemia: results from -

from reduction in excretion of sodium Increased sodium retention Decreased urine output

Intrarenal: Causes: 46-2 -

Direct damage to kideny tissue resulting in paired nephron function Prolonged ischemia Nephrotoxins( aminoglycosides, antibiotics, contrast media ) Hemoglobin released from hemolyzed RBC Myoglobin released from necrotic muscle cells

Nephrotoxins: -

Cause obstruction by crystallizing or by causing damage to epithelial cells of tubules

Hemoglobin and myoglobin: -

Can block tubules and cause renal vasoconstriction

Acute Tubular Necrosis: -

Most common intrarenal cause of AKI Primarily the result of ischemia, nephrotoxins, or sepsis Ischemic and nephrotoxic ATN is responsible for 90% of intrarenal AKI cases Severe kidney ischemia causes a disruption in the basement membrane abd patchy destruction of the tubular epithelium cell which slough off and plug the tubules Potentially reversible if basement membrane is not destroyed and tubular epithelium regenerates Risk factors: major surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, prolonged hypotension, nephrotoxins

Postrenal: -

Mechanical obstruction in the outflow of urine If urine is obstructed in refluxes back into the kidney, impairing function

Causes: -

BPH Prostate cancer Calculi Trauma Extrarenal tumors

Bilateral ureteral obstruction: -

leads to hydronephrosis, increase in hydrostatic pressure, and tubular blockage resulting in progressive decline in kidney function If relieved in 48hrs, complete recovery is possible Prolonged obstruction can lead to tubular atrophy and irreversible fibrosis

S/S: -

RIFLE: Risk, Injury, FAILURE, loss(table 46-3)

Oiguric phase: Urinary changes: -

Reduction in urine output to less then 400mL/day Usually occurs 1-7 days within kidney injury If ischemia is cause, oliguria can occur within 24 hrs When nephrotoxic drugs are involved, the onset may be delayed for as long as 1 week Can last about 10-14 days on average The longer the oliguric phase lasts, the poorer the prognosis Changes in urine output doe not correspond to changes in GFR About 50% of pt will not be oliguric making diagnosis hard Anuria: No urine output Usually seen with urinary tract obstruction Oliguria is commonly seen with prerenal causes nonoliguric AKI is seen with acute interstitial nephritis and ATN U/S may show casts RBC, and white blood cells Urine osmolality is more accurate than specific gravity: 300-1300mOsm/kg Kidney failure: specific gravity may be fixed around 1.010 and osmolarity around 300 Proteinuria id kidney failure is related to Glomerular membrane dysfunction

Fluid volume: -

Hypovolemia can exacerbate all forms of AKI Fluid replacement is often sufficient treatment especially for prerenal causes In reduced urine output, JVD, edema, and Hypertension may be present Can eventually lead to HF, pulmonary edema, and pericardial and pleural effusions

Metabolic acidosis: -

Impaired kidneys cannot excrete H+ ions or the acid products of metabolism Serum bicarbonate production is decreased due to defective reabsorption and regeneration of bicornate ions Serum bicarbonate is depleted through buffering Pt may develop rapid, deep respiration(Kussmaul respirations) to expel CO2 and compensate

Sodium balance: -

Damaged tubules cannot conserve sodium Normal or below normal levels

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Excessive intake of sodium should be avoided because it can lead to volume expansion, hypertension, HF Uncontrolled hypotnatremia or water excess can lead to cerebral edema

Potassium balance: -

Normally 90% of K+ is excreted Serum levels increase due to impaired ability to excrete it Hyperkalemia risk increased if AKI is caused by massive tissue trauma because damaged cells release K+ into the ECF Bleeding and blood transfusions cause cellular destruction releasing more K+ Metabolic acidosis worsens hyperkalemia Pts with hyperkalemia may be asymptomatic or might just feel weakness Clinical signs of severe hyperkalemia are seen on an ECG

ECG of hyperkalemia: -

Peaked T wave Widening of QRS complex Depressed ST segment

Hematologic disorders: -

Leukocytosis Common cause of death is infection Common infection sits are the urinary and respiratory systems

Waste accumulation: -

Elevated BUN and serum creatine levels Elevated BUN is also caused by dehydration, corticosteroids, catabolism resulting from infections, fever, severe injury, or GI bleeding Best serum indicator for AKI is creatinine because it is not significantly affected by other factors

Neuro disorders: -

Nitrogenous waste products can accumulate in the brain and nervous tissue Can cause fatigue, difficulty concentrating, seizure, stupor, and coma.

Diuretic phase: -

Daily urine output is usually around 1-3 L but may reach 5L or more Nephrons still not fully function

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High urine volume is caused by osmotic diuresis from high urea concentration in glomerular filtrate Kidneys have recovered the ability to excrete wastes but not to concentrate urine Hypololemia and hypotension can occur from massive fluid losses Pts who developed and oliguric phase will have greater diuresis as kidney function returns Large losses of fluid and electrolytes require monitoring for hyponatremia, hypokalemia, and dehydration May last 1-3 weeks Kidney function may take up to 12mos to return to normal Outcome of AKI depends on condition of pt

Recovery Phase: -

GFR increased allowing for BUN and creatinine to be filtered out Major improvements in 1-2 weeks

DX studies: -

Urine output and serum creatinine are known diagnostic indicators U/A Urine osmolarity Specific gravity Urine sediment Kidney ultrasound Renal scan CT scan Biopsy

MRI and MRA not recommended due to nephrotoxic ability of the contrast medium gadolinium and can cause contrast induced nephropathy(CIN) Pts with diabetes on metformin should have it held 48rhs before and after contrast media use to decrease risk of lactic acidosis If contrast medium must be given, pt must be properly hydrated and lowest dose possible

Interprofessional care: -

Make sure the is adequate intravascular volume and cardiac output to ensure perfusion to kidneys Diuretics may be given and usually include loop or osmotic diuretic Do not force fluids or diuretics if AKI is already established as this could be harmful General rule for calculating fluid restriction: losses of the previous 24hours 600ml for insensible loss

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If hyperkalemia is present treat elevated levels (table 46-5) Only sodium polystyrene sulfonate (Kayexlate) and dialysis actually remove potassium other drugs cause K+ to shift back into the cell Never give (kayexlate) to a pt. with paralytic ileus as this could lead to bowel necrosis

Renal replacement therapy indication: 1. 2. 3. 4. 5. 6.

Volume overload resulting on compromised cardiac or pulmonary status Elevated serum potassium level Metabolic acidosis BUN greater than 120mg/dL Significant change I mental status Pericarditis, pericardial effusion, or cardiac tamponade

Best guidelines is status of pt

Nutritional therapy: -

Provide adequate calories to prevent catabolism 30-35 kcal/kg and 0.8-1.0 g of protein/kg of desired body weight Primarily carbs and fat to prevent ketosis and endogenous fat breakdown and gluconeogenesis from muscle breakdown Sodium and potassium restricted as ordered Enteral if pt cannot tolerate oral intake Parenteral if GI system is not working

Nursing assessment: -

Fluid intake and output Daily monitoring of urine output Examine color, specific gravity, glucose, protein, blood, and sediment Assess pt general appearance Evaluate mental status Examine oral mucosa for dryness and inflammation Auscultate lungs of adventitious sounds Monitor the heart for S3, murmur, or pericardial friction Assess ECG for dysrhythmias, Review labs and dx tests

Nursing implementation: -

Risk factors: Taking nephrotoxic drugs Exposure to nephrotoxic chemicals

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Prolonged episodes of hypertension and hypovolemia

Hospital risk factors: -

Preexisting CKD Older age Massive trauma Major surgical procedure Extensive burns Cardiac failure Sepsis Obstetric complications

Nursing actions -

Carefully monitor pts weight, I&O, fluid and electrolyte balance, Assess extra renal loss: vomit, diarrhea, hemorrhage, and increased sensible loss Fluid replacement to prevent ischemic tubular damage Measure weight Diuretic therapy Monitor kidney function for pts taking nephrotoxic drugs; must be given at lowest dose for the shortest period possible Caution pt about OTC pain meds especially NSAIDS as they can worsen CKD ACE inhibitors ca decrease perfusion pressure and cause hyperkalemia If diet, diuretics, and sodium bicarbonate do not reduce K+ then ACE inhibitors have to be reduced or eliminated ACE inhibitors are also used to prevent proteinuria in and progression of kideny disease

Acute Care: -

Holistic approach Manage fluid and electrolytes Take daily weights Aseptic technique to prevent infection Protect from infections Monitor for signs of infection Temperature may not always be elevated to to blunted febrile response to an infection Record and monitor antibiotics given due to how it could be affected by the kideny disease Nephrotoxic drugs used judiciously Hygiene

Ambulatory care: -

Regular evaluation and follow-up Teach pt s/s of recurring kidney disease

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Emphasize measure to prevent the recurrence of AKI Make appropriate referrals for counseling Pt may transition to dialysis or transplantation if they do not recover

Older adults: -

GFR declines with age Impaired function of other systems can increase risk of AKI Dehydration is a predisposing factor Hypotension, diuretic therapy, obstructive disorders, aminoglycoside therapy, surgery, and contrast media can cause AKI Mortality rate similar as younger pts Pt over 65 less likely to recover from AKI...