Acute kidney injury Flashcards
What sort of functions does the kidney carry out?
- Sodium + water balance, natiuresis/ diuresis & antidiuresis. Commonly lost in early AKI
- Excretion of waste products
- Hormone Production ( Activation of VItamind D and Production of EPO)
- maintains acid base homeostasis
What kind of loss in function do you get with kidney injury?
- Sodium / fluid imbalance
(a) loss of ability to excrete a fluid load
(b) Loss of ability to conserve sodium + Water - Accumulation of solutes and waste products
- Accumulation of Acid
- Abnormalities in endocrine function
- Anaemia (EPO)
- Bone Dsiease (Activation of Vitamin D)
What is the diagnostic criteria of Acute Kidney Injury
There are three stages of acute kidney injury
The criteria is
- Increase in serum creatinine ( showing poor excretion of toxins)
- Decrease in urine output
How much does serum creatinine have to go up by to make a diagnosis of Acute Kidney Injury? How much does urine have to go down by? Mention stages:
For Stage 1
- Urine output 6 hrs
- Creatinine rise of 25 micromol/L or 150-200 %
For Stage 2
- Urine Output 12 hours
- Greater than 200-300% from baseline increase in creatinine
For Stage 3
- Urine output
The causes of Acute Kidney Injury
- Pre-renal: Sudden severe drop in blood pressure or interruption of blood flow to kidney
- Intra-renal: Direct damage to the kidneys by inflammation, toxins, drugs, infection of prolonged reduced blood supply.
- Post Renal: Sudden obstruction of due to enlarged prostate, kidney stones, bladder tumour or injury
What are some causes of Pre-renal AKI?
Disordered Auto-regulation: NSAIDs, ACEi/ARBs, Calcineurin Inhibitors (cyclosporine + tacrolimus), hypercalcaemia
Hypovolemia:
Absolute: blood loss
Effective: Low CO, Cirrhosis, Sepsis, Third Spacing
This is restored by prompt reperfusion. Prolonged excessive activation of RAAS as it is compensating can cause renal ischemia.
What are some Intra-Renal Causes of AKI? What is the most common cause? What are all the causes?
Most common cause of intrinsic AKI = Acute Tubular Necrosis.
Interstitial: Acute Interstitial Nephritis
- Drugs
- infection
Glomerular: Glomerular Nephritis (inflammation), sometimes thrombosis, it is uncommon
Vascular: Vasculitis, Malignant HTN, Thrombotic microangiopathy, cholesterol emboli, large vessel disease,
What is Acute Tubular Necrosis, and what is it caused by?
Intrinsic AKI is caused by ischemia and prolonged hypoperfusion (ATN), tubular injury can also be caused by drugs. Can cause Oliguria which is variable.
At a cellular level, it is an ischemic depletion of ATP, release of reactive oxygen species and apoptosis. The is cell desquamation, obstructive casts and back-leak of tubular fluid. Regenerates post, regeneration of tubular endothelial cells. Rapid reperfusion can cause reperfusion injury.
What are post renal causes of AKI?
Post Renal
- neurogenic
- Anatomic: Blockage in ureter, bladder or urethra
What sort of diagnosis does oliguria support?
Acute Kidney Injury
Some clues to check if its chronic kidney injury may be important:
- Pre-existing diabetes mellitus, Hypertension, Age, Vascular Disease
- Previous serum creatinine measurement
- Small echogenic kidneys on ultrasound
If you are thinking its obstructive, what kind of things will you be looking for in your renal history and examination?
Often present with anuria
Often bladder is palpable on examination
Renal Ultrasound will show hydronephrosis
Tell me an important clinical feature of your physical exam, when you suspect pre-renal AKI?
You do a volume status
- Look at JVP, Postural BP drop, urinary concentration indices, and fluid challenge
Are there any other intrinsic renal disease clues?
urinalysis: including microscopy (red cell casts, proteinuria)
Vascular disease: Renal asymmetry on ultrasound, loin with macro haematuria, complete anuria
What is treatment of AKI?
AKI therapy apart from rare cases, is generally no proven therapies to hasten to AKI
What are the risk factors for AKI?
Think about all the different categories, pre-renal, renal, and post renal.
- Background: Elderly, CKD, Cardiac Failure, Liver disease
- Diabetes, vascular disease, background nephrotoxic medications
- Acute insult: Sepsis and hypoperfusion, Toxicity, Obstruction, Parenchymal kidney disease
Prevent AKI?
Optimisation of ECV is most important, as volume depletion is the most common significant risk factor for Acute Kidney Injury. Thus there is controvery in using loop diuretics.
What is your protocol to prevent AKI?
Monitor the patient: Regular weight, Regular obs, fluid status, urine volume. Measure urea, creatinine and venous bicarb every day
Maintain circulation: euvolaemia, resuscitation, oxygenation. It is important to pay important attention to his as fluid overload, is associated with poorer outcomes
Minimise any kidney insults” Drugs, contrast, high risk interventions, hospital acquired infections. Discontinue any nephrotoxins such as NSAIDS, antihypertensives if low BP
Manage any acute illness: Sepsis, heart failure, liver failure
What is a quick way to recognise AKI in terms of baseline creatinine or hours of oliguria?
Creatine increase of 1.5 x from baseline, presumed to have occurred in last 7 days
Oliguria of atleast 6 hours
Increase in serum creatinine of greater than or equal to 26.5 micromol/L
What are broad Catagories for investment of AKI?
S - Sepsis/ Hypoperfusion
T - Toxicity ( Contrast/ Drugs)
O - Obstruction
P - Parencymal Disease ( Acute Glomerular Nephritis, Myeloma)
How is oliguria defined
Oliguria is less than 400ml of urine in 24 hours it is more common in pre-renal azotaemia, and obstruction.
How is anuria defined
Anuria is urine less than 100 ml in 24 hours
Complete obstruction, major vascular catastrophy or severe ATN ( most common)
What does non oliguria generally present?
More intra-renal causes, oliguric renal failure has a greater fatality
What are some acute metabolic complications? And how do we address them?
Volume Overload: Salt and water restriction, diuretics. Dialysis for refractor cases
Hypocalcaemia: calcium carbonate, or calcium gluconate
Hyperkalaemia: Restrict intake, IV glucose and insulin, kayexalate, calcium gluconate, acute dialysis
Metabolic acidosis: Sodium bicarb only if HCO3
Hypocalcaemia, what are the most common causes? What are the signs of symptoms? What are two classic signs starting with T?
Hypocalcemia is commonly caused by chronic renal disease, Hypoparathyroidism and Vitamin D deficiency
Symptoms:
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers,[clarification needed] diminished calcium lowers the threshold for depolarization.[1] The symptoms can be recalled by the mnemonic “CATS go numb”- Convulsions, Arrhythmias, Tetany and numbness/parasthesias in hands, feet, around mouth and lips.
Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).
Oral, perioral and acral paresthesias, tingling or ‘pins and needles’ sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.
Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.
Latent tetany
Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)
Chvostek’s sign (tapping of the inferior portion of the cheekbone will produce facial spasms)[2]
Tendon reflexes are hyperactive
Life-threatening complications
Laryngospasm
Cardiac arrhythmias
Effects on cardiac output
Negative chronotropic effect, or a decrease in heart rate.
Negative inotropic effect, or a decrease in contractility
ECG changes include the following:
Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)
