Acute Kidney Injury Flashcards
Acute kidney injury
Abrupt loss of kidney function whereby the kidney cannot effectively remove waste products (urea) or regulate water or electrolyte balance
* Marked by increased serum creatinine or blood urea nitrogen concentration, oliguria
Pathophysiology
Pre-renal: reduced renal blood flow (hypovolemia, HF, sepsis)
Intrinsic: conditions that affect the kidney, usually glomerulus or tubule (glomerulonephritis & tubular necrosis from drugs, toxins, inflammation)
* These conditions release vasocontrictors, causing ischemia
Post-renal: obstruction of the urinary tract that increases tubular pressure and reduces filtration drive (reduced GFR) - (urinary calculi, benign prostatic enlargement, prostate/cervical cancer)
Consequence
* Reduced RBF leads to ischemia, which causes a cascade of free radicals and cytokines, that initiate coagulation and apoptosis
* Cell injury continues despite restored RBF
* Tubular damage causes gap junction disruption, leading to filtrate to leak back (reduced GFR & oliguria)
Phases of AKI
Oliguric: initial phase, lasts 10-14 days, UO < 400ml/day
* Signs of oedema may be present, the longer this phase, the worse the prognosis
Diuretic: lasts 1-3 weeks, varies from 1-3L/day
* High diuresis from high urea, but unable to concentrate urine (may develop hypovolemia) but starts to improve
Recovery: GFR increases which allows BUN & creatinine to stabilise and decline (may take up to 12 months)
Manifestations
NB: many mild/moderate AKI patients are asymptomatic
- Oliguria
- Oedema
- N&V
- Fatigue/drowsiness, muscle twitching, seizures
- SOB, dyspnoea, chest pain
- High BUN & creatinine
- Hyperkalemia, arrythmias, CA
Diagnostic investigations
- BUN, creatinine
- FBC (check for infection, anemia, blood loss)
- Urinalysis (indicators for aetiologies - brown/sediment for tubular necrosis, hematuria for intra-renal injury)
- Electrolyes
- US/CT (identify diseases or obstruction)
- Angiography (diagnose vascular disorders)
*
Management/Treatment
- Treat precipitating cause
- Maintain fluid balance based on weight, CVP, urine output, BP & avoiding fluid excess (e.g. pulmonary oedema)
- Address electrolyte imbalances (restrict sodium and phosphate, increase calcium, IV insulin or salbutamol to reduce K, reduce salt)
- In diuretic patients, these may be opposite & will need to be supplemented
- Enteral or parenteral nutrition - the metabolic impairment disregulaes macro and micronutrient balance, and patients often have critical illness that leads to protein breakdown and insulin resistance
- Dialysis or RRT
Nursing management
- Strict FB to monitor injury progression & guide fluid replacement (this includes daily weight)
- Monitor urine specific gravity
- Assess for oedema
- Monitor HR, BP, CPV, JVP, RR (pt may be hypertensive and tachy)
- Lung auscultation for oedema
- Cardiac monitoring
- Monitor electrolyte status & signs of hyperkalemia (muscle weakness, cramping)
- LOC
- Skin care, infection control, psychological support
Complications
- Fluid overload & pulmonary oedema
- Seizures (increased wastes)
- Hyperkalemia & arrhythmias & muscle weakness
- Chest pain from endocarditis
- Permanent kidney damage
- Death
Haemodialysis
- Blood is removed from the body into a dialyzer machine and passes through a semipermeable membrane containing fibres that filters wastes out
- 3-4x a week, 4-5 hours
- Can cause low BP, dizziness, fatigue, chest pain, cramping from removing too much fluid
- Better for worse kidney injury, for those wanting HCT to control kidney care, better for obese patients or those with abdominal scarring
Peritoneal dialysis
- Sterile glucose solution (dialysate) runs via a tube into the abdominal cavity, and the peritoneum acts as the semi permeable membrane which filters wastes by diffusion and osmotic drive
- When there is an equilibrium with the bodys fluids, it is drained and replaced with fresh dialysate
- More flexibility, cheaper, less risk of infection but requires more training
Hemofiltration
- Similar to haemodialysis, but instead of by diffusion, it occurs by applying a pressure gradiant, whereby water moves across a very permeable membrane rapidly and drags with it many large molecular weight substances that are not able to be filtered with haemodialysis (more effective)
- Extra water and salt are then replaced with a substitution fluid