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Acute kidney injury Flashcards

1
Q

What sort of functions does the kidney carry out?

A
  1. Sodium + water balance, natiuresis/ diuresis & antidiuresis. Commonly lost in early AKI
  2. Excretion of waste products
  3. Hormone Production ( Activation of VItamind D and Production of EPO)
  4. maintains acid base homeostasis
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2
Q

What kind of loss in function do you get with kidney injury?

A
  1. Sodium / fluid imbalance
    (a) loss of ability to excrete a fluid load
    (b) Loss of ability to conserve sodium + Water
  2. Accumulation of solutes and waste products
  3. Accumulation of Acid
  4. Abnormalities in endocrine function
    - Anaemia (EPO)
    - Bone Dsiease (Activation of Vitamin D)
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3
Q

What is the diagnostic criteria of Acute Kidney Injury

A

There are three stages of acute kidney injury
The criteria is
- Increase in serum creatinine ( showing poor excretion of toxins)

  • Decrease in urine output
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4
Q

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:

A

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

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5
Q

The causes of Acute Kidney Injury

A
  1. Pre-renal: Sudden severe drop in blood pressure or interruption of blood flow to kidney
  2. Intra-renal: Direct damage to the kidneys by inflammation, toxins, drugs, infection of prolonged reduced blood supply.
  3. Post Renal: Sudden obstruction of due to enlarged prostate, kidney stones, bladder tumour or injury
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6
Q

What are some causes of Pre-renal AKI?

A

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.

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7
Q

What are some Intra-Renal Causes of AKI? What is the most common cause? What are all the causes?

A

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,

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8
Q

What is Acute Tubular Necrosis, and what is it caused by?

A

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.

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9
Q

What are post renal causes of AKI?

A

Post Renal

  • neurogenic
  • Anatomic: Blockage in ureter, bladder or urethra
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10
Q

What sort of diagnosis does oliguria support?

A

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
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11
Q

If you are thinking its obstructive, what kind of things will you be looking for in your renal history and examination?

A

Often present with anuria
Often bladder is palpable on examination
Renal Ultrasound will show hydronephrosis

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12
Q

Tell me an important clinical feature of your physical exam, when you suspect pre-renal AKI?

A

You do a volume status

- Look at JVP, Postural BP drop, urinary concentration indices, and fluid challenge

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13
Q

Are there any other intrinsic renal disease clues?

A

urinalysis: including microscopy (red cell casts, proteinuria)

Vascular disease: Renal asymmetry on ultrasound, loin with macro haematuria, complete anuria

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14
Q

What is treatment of AKI?

A

AKI therapy apart from rare cases, is generally no proven therapies to hasten to AKI

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15
Q

What are the risk factors for AKI?

A

Think about all the different categories, pre-renal, renal, and post renal.

  1. Background: Elderly, CKD, Cardiac Failure, Liver disease
  2. Diabetes, vascular disease, background nephrotoxic medications
  3. Acute insult: Sepsis and hypoperfusion, Toxicity, Obstruction, Parenchymal kidney disease
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16
Q

Prevent AKI?

A

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.

17
Q

What is your protocol to prevent AKI?

A

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

18
Q

What is a quick way to recognise AKI in terms of baseline creatinine or hours of oliguria?

A

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

19
Q

What are broad Catagories for investment of AKI?

A

S - Sepsis/ Hypoperfusion
T - Toxicity ( Contrast/ Drugs)
O - Obstruction
P - Parencymal Disease ( Acute Glomerular Nephritis, Myeloma)

20
Q

How is oliguria defined

A

Oliguria is less than 400ml of urine in 24 hours it is more common in pre-renal azotaemia, and obstruction.

21
Q

How is anuria defined

A

Anuria is urine less than 100 ml in 24 hours

Complete obstruction, major vascular catastrophy or severe ATN ( most common)

22
Q

What does non oliguria generally present?

A

More intra-renal causes, oliguric renal failure has a greater fatality

23
Q

What are some acute metabolic complications? And how do we address them?

A

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

24
Q

Hypocalcaemia, what are the most common causes? What are the signs of symptoms? What are two classic signs starting with T?

A

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.)

25
Q

Has a major vascular issue occurred?

A

Ask for history of vascular disease
loin pain and frank haematuria
Complete anuria?

In terms of investigation there might be some renal asymmetry on US

26
Q

Two things that dialysis does?

A

Solid removal and fluid removal

27
Q

What is is peritoneal dialysis: Semi-permeable membrane in the visceral capillary wall lining the peritoneal cavity

A

Solutes leave the blood by diffusion
Fluids move from the blood to dialysate by a mix of osmotic and hydrostatic pressures. Glucose is the osmoticaly active agent.

28
Q

What is hemodialysis

A

Blood circulates in high volume through dialyser and there is filtration by osmosis.

29
Q

If suspected to be intra-renal, what are features of urine microscopy? What about for ATN? What about for pre-renal?

A

Red cells, cast and proteinuria
For ATN: You get red blood cells, pigmented and casts
urinalysis is normal in pre-renal

30
Q

three broad categories of investigations you must conduct?

A

volume studies, urine studies, renal ultrasound

31
Q

What are the indications for dialysis?

A 
A - cidosis
E - Electrolyte disturbance
I - Intoxication
O - Oedema/ Overload
U- uraemia ( Pericarditis, itch, uraemic frost, confusion ( look for the flap))
32
Q

Think, what are some other things that could occur?

What could occur in regards to bone? What about like the blood? Think broad, what are consequences of RAAS activation?

A
  • Blood: Anaemia due to low EPO
  • Osteodystrophy, rickets due to poor vitamin D activation, hypocalcaemia also contributes
  • Excessive activation of RAAs causes extensive vasoconstriciton

renal (4 decks)

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