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Acute Kidney Injury

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Acute Kidney Injury
Pre-Renal (decreased blood flow into kidneys)
- Hypovolaemia (absolute loss of intravascular volume)
- Diuresis, diarrhoea, dehydration, haemmorhage, severe burns
- Relative decrease in of intravascular volume (total body fluid stays the same)
- Distributive shock
- Anaphylaxis, neurological injury, septic shock
- Cardiogenic
- Congestive heart failure (venous pooling --> less blood sent to kidneys
- Cardiogenic shock (MI, heart failure, arrhythmias)
- Distributive shock
- Obstructive
- Renal artery stenosis (narrowing of renal artery)
- Renal artery thrombus
- Hypovolaemia (absolute loss of intravascular volume)
Intra-renal
- ATN (acute tubular necrosis) *** most common for hospitilised pts Tubular epithelial cells necrose, slough off, causing obstruction in tubular flow, leading to back- flow of filtrate, further increasing blood waste products (nitrogenous wastes). Casts seen in urine.
- Ischaemic - prolonged hypoperfusion (prolonged pre-renal failure)
- Neophrotoxic
- Nephrotoxic drugs
- Vancomycin (glycopeptide antibiotic) Aminoglycoside (gentamicin) Chemotherapeutic agents Contrast dye NSAIDs Sulfonamides (trimethoprim, bactrim) Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride
- Haemolytic blood transfusion reaction (Haemoglobin release from RBCs)
- Block tubules, causing renal vasoconstriction
- Blood transfused is destroyed by patients immune system
- Myoglobin release from necrotic muscle cells
- Nephrotoxic drugs
- Pts at risk: Major surgery, shock, sepsis, blood transfusion reaction, muslce injury from trauma, prolonged hypotension, nephrotoxic agents
- Sepsis
- Bacterial infections (acute pyelonephritis (viral or fungal cause))
- Interstitial nephritis due to an allergic / hypersensitive reaction
- Penicillin, NSAIDs
- Immune reaction that damages the cells in glomerulus
- ATN (acute tubular necrosis) *** most common for hospitilised pts Tubular epithelial cells necrose, slough off, causing obstruction in tubular flow, leading to back- flow of filtrate, further increasing blood waste products (nitrogenous wastes). Casts seen in urine.
Post-renal
- Obstruction (renal calculi)
- BPH enlarged prostate
- benign prostatic hyperplasia
- neuromuscular disorders
- spinal cord disease
- strictures
- prostate cancer
Decrease in GFR - normal = 100% kidney function
- How much blood is filtered via the glomeruli per minute
- Stage 1 90-100% function
- Stage 2 60-89% kidney function
- Stage 3 30-59% kidney function
- Stage 4 15-29% kidney function
- Stage 5 less than 15% kidney function
Azotemia (accumulation of nitrogenous containing wastes in blood)
- Urea & Creatinine
- Creatinine 45-85 micromol/L Urea 3.o-8.5mmol/L
- Urea & Creatinine
Decrease in urine output (oliguria less than 400mLs/day)
Activation of the RAAS
- Reabsorption of H20 and Salt
- Fluid retention --> HTN, bounding pulse, heart failure, pulmonary oedema, peripheral oedema, pleural effusions.
- Monitoring?
- Assessments?
- Fluid retention --> HTN, bounding pulse, heart failure, pulmonary oedema, peripheral oedema, pleural effusions.
- Reabsorption of H20 and Salt
hyperkalaemia
- Complications?
- Resonium, insulin
- Which blood test?
- 3.5-5.5mmol/L
- Complications?
Metabolic acidosis due to H+ accumulation in blood
Increased mortality
Medical management
- Dialysis
Nursing Diagnosis At risk of
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- Description
- Stage 2 Mind Map on Acute Kidney Injury, created by Tafe Teachers SB on 06/05/2020.
- Created by
- Tafe Teachers SB
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- Created by Tafe Teachers SB · Aug 22, 2018
- Copied by Tafe Teachers SB · Jun 5, 2020
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