Acute Kidney Injury Flashcards
(44 cards)
What tests are done to determine if there is a problem with the kidneys?
-Bloods
=Serum creatinine-reference range 60-110 micromole/L
=Calculates estimated glomerular filtration rate- reference range >60 mL/min
-Urine
=Urine output
=Urinalysis- blood and/or protein in urine
What is acute kidney injury?
-An abrupt decrease in kidney function
=Retention of waste products
=Impaired fluid balance
=Abnormal electrolyte balance (potassium)
-Staging system to stratify in studies (based in serum creatinine and urine output)
AKI is defined as any of the following:
- Increase in serum creatinine by > 26.5 μmols/L in 48 hours or,
- Increase in serum creatinine by > 1.5x baseline creatinine within last 7 days or
- Urine volume < 0.5ml/kg/hr for 6 hours
Describe diagnosis of AKI
- Diagnosis relies on assessment of renal function/ urine output
- Many patients will have pre-existing CKD
- Review of clinical events will normally identify cause
Describe Stage 1 AKI
Serum creatinine:
=1.5-1.9 times baseline/ >/26.5 micromoles/L increase
Urine Output:
=<0.5ml/kg/hour for 6-12 hours
Describe Stage 2 AKI
-SC:
=2.0-2.9 times baseline
-UO:
=<0.5ml/kg/hour for >/12 hours
Describe Stage 3 AKI
-SC: =3.0 times baseline/ increase in serum creatinine to >/353.6 micromoles/L / Initiation of renal replacement therapy -UO: =<0.3ml/kg/hour for >/24 hours OR =Anuria for >/12 hours
What are the causes of AKI?
-Pre-renal
=Reduced perfusion
=Blood supply problem
=Cardiac failure, sepsis, blood loss, dehydration, vascular occlusion
-Renal
=Within kidney
=Glomerulonephritis, small-vessel vasculitis, acute tubular necrosis, interstitial nephritis
-Post-renal
=Obstruction
=Stones, prostatic enlargement, prostatic cancer, retroperitoneal fibrosis, ureteral valve stenosis
Describe pre-renal causes of AKI
-Volume depletion/ Hypovolaemia
=Diarrhoea, bleeding, third space loss (ascites), diuresis, sepsis
-Hypotension
=Heart failure, sepsis, oedematous states, drugs, liver failure
-Renal ischaemia
=Hepatorenal syndrome, arterial occlusions, dissection of abdominal aorta, severe renovascular disease, renal artery stenosis
-Drugs
=NSAIDs, calcineurin inhibitors, ACE/ARBs
What mechanisms lead to AKI?
- Reduced glomerular perfusion
- Glomerular filtration rate is reduced
- Constriction of efferent arteriole
What mechanisms are activated in hypovolaemia?
-Sympathetic NS =Tachycardia, vasoconstriction -Renin-aldosterone axis =vasoconstriction =aldosterone stimulates salt and water retention -Neuroendocrine axis =increased antidiuretic hormone (ADH) =Reduced urine output
What is the hypovolaemia-initial fluid resuscitation?
-IV fluid challenge
=500mL 0.9% sodium chloride or plasmalyte over 15 minutes
=Reasonable to repeat if no response
=Do not give more than 2000mL as resuscitation fluid without senior input
What are the drugs that make AKI worse?
- ACE inhibitors and Angiotensin receptor blockers
- Blood pressure lowering drugs (beta blockers, amlodipine/ calcium channel blockers)
- Diuretics
- Non-steroidal anti-inflammatory drugs
- Radiocontrast agents
What is the initial treatment of AKI?
- IV fluids
- Stop nephrotoxins (withhold lisinopril and other blood pressure lowering treatments, NSAIDs)
- Physiological monitoring (pulse, bp, fluid input and output)
Why is hyperkalaemia life-threatening?
-Can lead to abnormalities in electrical conduction system of the heart (main intracellular cation)
=cardiac arrest
=asystole/ ventricular fibrillation
- Broad QRS complexes
- Tenting of T wave
- Loss of p wave
- Abnormal rhythms
- Sine wave
What is the most appropriate initial treatment for hyperkalaemia?
-Intravenous calcium chloride/ gluconate
=protects heart from hyperkalaemia effects
=stabilises myocardium for 20-30 minutes
What is the treatment for hyperkalaemia?
-IV calcium salts if ECG abnormal (lasts 30 mins)
-Insulin/ glucose and nebulized salbutamol
=Pushes potassium into cells, lasts 4-6 hours
-Treat underlying cause
=Need to get kidneys working to excrete potassium
What does acute tubular injury cause?
-Ischaemia (even less oxygen to hypoxic medulla so disrupts cellular energetics)
-Tubular injury and cell death
=Back leak of glomerular filtration
=Tubular obstruction by cellular casts (sloughed cells block)
=Inflammation (neutrophils and macrophages)
=REDUCED GLOMERULAR FILTRATION
Describe acute tubular injury
-Diagnosis of exclusion
=Is there is a treatable cause of renal failure?
-Follows many different causes of AKI (most common cause)
=Currently no preventative strategies
-Recovery is normal outcome with support but long-term consequences
What suggests a glomerular cause of AKI?
-Urinalysis of protein and blood (active urinary sediment)
-Creatinine raised
=Glomerular nephritis (inflammatory crescent= mass of inflammatory cells)
How is systemic vasculitis diagnosed?
-Dipstick urinalysis (protein and blood)
-Serum anti-neutrophil cytoplasmic antibodies (ANCA)
-Often present with coincident infection
-Tissue diagnosis
=Kidney most common
=Lung
=Nerve
What is the treatment for systemic vasculitis?
-Glucocorticoids
=Oral prednisolone
-Plasma exchange
=Significant renal disease and/or pulmonary haemorrhage
-Cyclophosphamide (kill lymphocytes)/ Rituximab (monoclonal antibodies aimed at B cells)
What are the common intrarenal causes of AKI in a ITU setting?
- Acute tubular injury (may follow severe hypotension)
- Rhabdomyolysis (crush injury/ long lie on floor after fall- myoglobin released from damaged muscles and taken up by tubular cells but cant be removed)
- Contrast nephropathy
- Interstitial nephritis (drugs- penicillin, NSAIDs)
- Systemic vasculitis
- Myeloma (tumour of plasma cells)
- Haemolytic uraemia syndrome (E Coli 0157 infection)
How can post-renal causes be diagnosed?
-Ultrasound renal tract (shows hydronephrotic kidney)/ bladder scan (estimate volume in bladder)
=renal pelvis seems larger and darker, causes kidney to be dilated
Describe hydronephrosis
- Renal pelvis seems larger and darker, causes kidney to be dilated (pressure of fluid)
- Pressure over time built up= persists so damage to kidney cortex
