Acute Kidney Injury Flashcards
Define Acute kidney injury (AKI)
- The syndrome arising from a rapidly falling GFR
- Characterised by retention of both nitrogenous ( e.g urea & creatinine) and non-nitrogenous waste products, as well as disordered electrolyte, acid-base and fluid homeostasis
When is AKI diagnosed
- When serum creatinine is greater than or equal to 26.5 micromoles/l in less than or equal to 48 hours
- or rises to greater than or equal to 1.5-fold from baseline in the preceding 7 days
- Urine is less than 0.5ml/kg/h for 6 hours
How is kidney failure classified?
Stage 1: Creatinine rise greater than or equal to 26.5micro moles per litre in 48h OR 1.5-1.9 times from baseline
Urine output is less than or equal to 0.5ml/kg/h for 6-12h
Stage 2: Creatinine rises 2-2.9 times from baseline
Urine output is less than 0.5ml/kg/h for greater than or equal to 12 hours
Stage 3: Creatinine rise is greater than or equal to 3 times from base line OR rise to greater than or equal to 353.6 micro moles per litre OR RRT irrespective of serum creatinine
Urine output is less than 0.3ml/kg/h for greater than or equal to 24h or anuria for greater than or equal to 12h
What are the proximal tubular cells very susceptible to?
Hypotension & hypoxia
What percentage of CO is renal blood flow?
25%
What are some of the causes of AKI?
- hypovolemia
- Cardiac failure
- drugs
- renal artery occlusion
- small vessel vasculitis
- Tumours
- Papillary necrosis
Which locations of the kidney could AKI occur?
- Pre-renal
- Renal artery
- Small vessel disease
- Glomerular disease
- Acute tubular necrosis
- Acute interstitial nephritis
- Intra-tubular obstruction
- Post-renal obstruction
What is anti-GBM disease?
-an antibody disease; a rare autoimmune disorder in which circulating antibodies are directed against an antigen normally present in the GBM and alveolar basement membrane
Where do pre-renal causes of AKI take place?
Renal arteries& aorta
Where do renal causes of AKI take place ?
Kidneys (cortex & medulla)
Where do post-renal causes of AKI take place?
Collecting ducts
How can we classify AKI causes?
- pre renal
- intrinsic (renal)
- post renal
What are some causes of pre renal AKI
- Volume depletion
- Decreased effective volume
- Altered intrarenal haemodynamics
1. )NSAIDs
2. ) ACEi-A2RB-induced
What are some causes of intrinsic AKI
- Acute tubular necrosis
- Acute glomerulonephritis
- Acute interstitial nephritis
- Vascular (small/large vessel)
What are some causes of post renal AKI
- Ureteric obstruction
- Bladder outflow obstruction
What are the functions of kidneys ?
- ) Excretion of electrolytes
- ) Clearance of waste products
- )Receptor sites for hormones
- ADH
- Aldosterone
- ANP
- PTH - ) Gluconeogenesis
- ) Regulation of acid-base state
- ) Control of water balance
- ) Production of hormones
- Renin
- Vitamin D
- Erythropoetin
- Prostaglandins
What are the effects of AKI?
- Fluid overload/pulmonary oedema
- Hyperkalaemia
- uraemia
- metabolic acidosis
What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of 5.5-6.5mmol/L ie early hyperkalaemia
- Peaked T waves
- Prolonged PR segment
What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of 6.5-8mmol/L
- loss of p wave
- prolonged QRS complex
- ST- segment elevation
- Ectopic beats and escape rhythms
What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of greater than 8 mmol/L
- Progressive widening of QRS complex
- Sine wave
- Ventricular fibrillation
- Asystole
- Axis deviations
- Bundle branch blocks
- Fascicular blocks
What are the typical ABGs for metabolic acidosis?
- pH<7.3
- pCO2=low
- Po2= normal/high
- HCO3=low
What are the typical symptoms of metabolic acidosis?
- Breathless/tachypnoeic
- Nausea
- Non-specifically unwell
- The patient will hyperventilate to try get rid of the co2 and to try normalise the pH
What is Uraemia
- Retention of metabolic waste products that are otherwise excreted by the kidneys( sulphate, urea, ammonia, creatinine, phosphate etc)
- Clinically, we measure urea and creatinine
What are the effects of uraemia?
- ) Pericarditis: the pericardial membrane around the heart (which is normally very smooth with very little fluid) will become inflammed
- ) Pleurisy: Pleural effusion could occur (in between the lung& pleural membrane)
- ) Encephalopathy: brain disease/damage/malfunction; metabolic waste products may cause damage to the BBB and so cause lethargy,violence,comatised& change in mood/personality
What are pericardial tamponades?
- Heart stops pumping/producing BP- This could be fatal
- Compression of the heart occurs due to build up of fluid in the pericardium
How can we manage AKI?
- ) Exclude a life threatening complication
- ) Identify the aetiology…
- Hypovolemic: give fluids
- Low BP: fluids/drugs
- If drug induced: stop drugs
- If sepsis induced: treat sepsis - ) Supportive treatment: nutrition, ulcer prophylaxis
- ) Avoidance of progression: avoid nephrotoxic drugs/hypovolemia/hypotension
When do we give Renal replacement therapy( RRT)
-When it is indicated that there’s a life threatening complication of AKI e.g:
-Life threatening pulmonary oedema
-Severe metabolic acidosis
-Severe hyperkalaemia, especially if ECG changes
AND the following are present
-Uraemic pericarditis
-Uraemic encephalopathy
Outline the principle of RRT
- Blood from patient goes through a blood pump and into a filter that removes water& electrolytes
- The blood then flows through an air detector that detects any changes in air composition’
- The blood is then returned back to the patient
- Uses the principles of OSMOSIS; similar to a dialysis machine
Which insertion sites do we use to obtain vascular access in RRT
We use dual lumen catheters the insertion sites are: -Internal jugular vein -Femoral vein -Subclavian vein
Define azotenia
high levels of nitrogen containing compounds in the blood
