AKI

Question 1

How do pre-renal causes lead to an AKI?

Answer 1

renal hypo perfusion leading to ischaemic damage–>acute tubular necrosis

can be cardiogenic (low CO or myocardial ischamia), hypovolaemic (blood loss or dehydration), sepsis (due to vasodilation and 3rd space loss), drug induced e.g NSAIDs and ACEi

Question 2

How do intra-renal causes lead to an AKI?

Answer 2

resulting from abnormalities within the kidneys i.e. glomerular, interstitial or the vessels e.g. malignant HTN, acute glomerulonephritis, acute tubular necrosis or acute pyelonephritis, DIC, vasculitis

Question 3

How do post renal causes lead to an AKI?

Answer 3

resulting from an obstruction anywhere from the renal calyces to the outflow tract from the bladder
SNIPPIN: stone, neoplasm, inflammation (stricture), prostatic hypertrophy (BPH), posterior urethral valves, infection (TB, schisto), Neuro (post op, neuropathy)

Question 4

what are the urine output and creatinine levels in stage 1 AKI?

Answer 4

creatinine >26umol/l (>1.5xbaseline)

urine output<0.5ml/kg/hr for 6-12 hrs

Question 5

what are the urine output and creatinine levels in stage 2 AKI?

Answer 5

creatinine 2-2.9 Xbaseline

urine output<0.5ml/kg/hr for >12hrs

Question 6

what are the urine output and creatinine levels in stage 3 AKI?

Answer 6

creatinine >353umol/l

urine output<0.3ml/kg/hr for 24hrs or anuria for 12hrs.

Question 7

what is a diagnosis of an AKI based on?

Answer 7

creatinine and eGFR levels

Question 8

management of an AKI

Answer 8

treat cause
fluid balance management
be wary of acidosis, hyperkalaemia.
drug review, stop nephrotoxic drugs

Question 9

what investigations would you order if you suspected AKI?

Answer 9

urine dip- (haematuria and proteinuria may suggest intrinsic renal disease)
US within 2hrs- small shiny kidneys suggest CKD
Liver function tests- to rule out hepatorenal syndrome

Question 10

What is acute kidney injury?

Answer 10

acute deterioration in renal function over hrs-days.

Question 11

What are the 3 phases of AKI?

Answer 11

Oliguria (obstruction from dead cells and oedema)
Polyuria (tubules open but not functioning)
Recovery

Question 12

what are the 2 main complications of AKI that can lead to death?

Answer 12

pulmonary oedema and hyperkalaemia

Question 13

what is the key part of assessing someone with an AKI?

Answer 13

Assess their fluid status.

Question 14

What is the classification of AKI based on?

Answer 14

GFR
or
urine output

Question 15

what are the main aspects of AKI management?

Answer 15

identify underlying cause
resuscitate A-E and monitor fluid status
prevent and treat complications such a hyperkalaemia and pulmonary oedema

Question 16

describe the management of hyperkalaemia?

Answer 16

10ml 10% calcium gluconate
100ml 20% glucose and 10U of act rapid insulin
salbutamol nebuliser 5mg
consider dialysis
Ion exchange resins e.g. calcium resonium 15g PO or 30mg PR

Question 17

How would you manage pulmonary oedema?

Answer 17

Sit the patient up and give high flowO2
morphine 2.5mg (+/- 10mg IV metoclopramide)
furosemide 120-250mg IV over 1hr
GTN spray +/- isosorbide mononitrate IV
If no response consider CPAP, haemofiltration/dialysis

Question 18

why can AKI lead to bleeding?

Answer 18

increase urea impairs homeostasis

Question 19

what are the indications for acute dialysis?

Answer 19

persistent hyperkalaemia (>7mM)
refractory pulmonary oedema
symptomatic uraemia (encephalopathy, pericarditis)
severe metabolic acidosis (pH<7.2)
poisoning e.g. aspirin

Question 20

what are the risk factors for Contrast nephropathy?

Answer 20

high contrast load
high iodine content of contrast
hypovolaemia
myeloma
age
hyperuricaemia
diabetes especially if taking Metformin
hypercalcaemia
pre-existing CKD

Question 21

What is acute tubulointerstitial nephritis?

Answer 21

an immune mediated hypersensitivity reaction to a drug or infection leading to acute kidney injury

Question 22

what are the presentations of acute tubulointerstitial nephritis?

Answer 22

systemic manifestations of hypersensitivity e.g. fever, arthralgia, rash
AKI (oliguria)
uveitis

Question 23

What would you expect to find on urine dip in a patient with acute tubulointerstitial nephritis?

Answer 23

proteinuria, haematuria, sterile pyuria (raised WCC in the absence of bacteriuria)

Question 24

what type of hypersensitivity reaction is involved in actor tubulointerstitial nephritis?

Answer 24

type 1 immune mediated ypersensitivity with raised IgE levels

Question 25

what would you expect to happen to the IgE levels and the eosinophils in acute tubulointerstital nephritis?

Answer 25

raised IgE levels | raised eosinophils

Question 26

what is the treatment for acute interstitial nephritis?

Answer 26

stop causative agent eg drug | steroids can hasten renal function recovery

Question 27

how is acute tubulointerstilal nephritis different to acute tubular necrosis?

Answer 27

acute tubulointerstilal nephritis involves inflammation of the tubules where as acute tubular necrosis involves ischaemia or toxic necrosis to the tubular cells.

Question 28

when skeletal muscles break down what does it release?

Answer 28

K, PO, urate | myoglobin and CK

Question 29

what is rhabdomyolysis?

Answer 29

muscle damage (skeletal muscle breakdown) with release of myoglobin can cause severe AKI

Question 30

what are some common causes of rhabdomyolysis?

Answer 30

crush injuries e.g. trauma, compartment syndrome, immobilisation uncontrolled fitting drugs e.g. statins, vibrates overdose on barbiturates, alcohol, heroin and ecstasy

Question 31

what drugs can lead to rhabdomyolysis?

Answer 31

statins and fibrates

Question 32

how does rhabdomyolysis present?

Answer 32

muscle pain and swelling, red-brown urine | AKI occurs 10-12 hrs later

Question 33

what would you expect on a urine dipstick in rhabdomyolysis?

Answer 33

+ve Hb, -ve RBC

Question 34

describe the management of rhabdomyolysis

Answer 34

manage hyperkalaemia IV rehydration central venous pressure monitoring if oliguric (this would require a central line access) Can use IV NaHCO to alkalinise urine and stabilise less toxic form of myoglobin.