Case 13 - Acute Kidney Injury Flashcards

1
Q

How is an AKI staged?

A

Via KIDIGO guidelines (how raised creatinine is)

Stage 1 - creatinine 1.5-2 x baseline
Stage 2 - creatinine 2-3 x baseline
Stage 3 - >3 x baseline

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2
Q

Which class of drugs should be suspended in an AKI and why?

A

ACE inhibitors / Angiotensin receptor blockers
NSAIDS
Aminoglycosides e.g, Gentamicin

They cause nephrotoxicity

Also consider stopping metformin

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3
Q

What are the pre-renal causes of an AKI?

A

Anything that causes reduced renal perfusion:

  • Dehydration
  • Sepsis
  • Hypotension
  • Shock
  • Hepatorenal syndrome
  • Renal artery stenosis
  • Severe heart failure
  • Intra abdominal hypertension /compartment syndrome
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4
Q

What are the Intra-renal causes of an AKI?

A
Drugs: NSAIDS, ACEi / ARBs, Gentamicin 
Glomerulonephrisis/vasculitis 
Contrast
Acute tubular nephrosis (ATN)
Interstitial nephritis (inflammation of kidney)
Myeloma (Plasma cell cancer)
Rhabdomyolysis
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5
Q

What are the post-renal causes of an AKI?

A

Prostate enlargement
Renal stones
Pelvic cancer

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6
Q

What are recommend criteria for diagnosing an AKI?

A

Rise in creatinine >26umol/L in 48 hours
Rise in creatinine >1.5 x baseline (best figure in last 3/12)
Urine output <0.5mL/kg/hr for 6 consecutive hours

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7
Q

What are the risk factors for developing an AKI?

A
Age > 75 years
Chronic kidney disease 
Cardiac failure
Peripheral vascular disease 
Chronic liver disease 
Diabetes
Drugs
Sepsis
Poor fluid intake
History of urinary symptoms
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8
Q

What are the signs and symptoms for an AKI?

A

Note: there may be no signs

Main signs: fatigue, malaise, rash, joint pains, nausea, vomiting, chest pain, palpitations, SOB, fluid overload, abdominal pain, oliguria (urine output less than 0.5mL/kg/hr), hypo or hypertension

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9
Q

What is the most urgent management in an AKI?

A

Assess potassium status

U&Es
Urgent ABG/VBG to check K+
ECG to look for signs of hyperkalamia

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10
Q

What are the main goals of treatment in an AKI?

A

Treat any life threatening hyperkalaemia

Treat hypotension by giving fluids

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11
Q

What would be raised on blood tests if a patient was dehydrated?

A

Urea (significantly raised)
Creatinine
Albumin
Heamtocrit

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12
Q

What are the ECG changes in severe hyperkalamia

A

Small or indiscernible p waves - low and flat
Wide QRS complex (similar to LBBB)
Slurring of S-T segment
Peaked T waves (think lots of Pot, lots of Tea)

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13
Q

How do you treat acute hyperkalaemia in adults?

A

Stabilise cardiac membrane - 10mL 10% calcium gluconate IV via a big vein over 2 mins, repeat until ECG improves

Give intravenous insulin + dextrose (glucose) - insulin stimulates intracellular uptake of K+, lowering the serum K+ by 1-2mmol/L over 60 mins
Alternately nebulised salbutamol

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14
Q

What is the definition of an acute kidney injury?

A

A clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes

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15
Q

What specific things would you look for on an examination of someone with an AKI?

A
Do full systemic examination 
Look specifically for:
- Palpable bladder
- Palpable kidneys 
- Abdominal/pelvic masses
- Renal bruits (sign of renovascular disease)
- Rashes
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16
Q

What tests and investigations would you do in a suspected AKI?

A

Bloods: U&E, LBC, LFT, clotting, CK, ESR, CRP
ABG
Urine dipstick - look for blood and protein
Urine culture - look for urine infection
Renal tract USS - look for obstructed kidneys (hydronephrosis)
Chest X-Ray (if signs of fluid overload) - look for pulmonary oedema or pneumonia
Stool culture - look for pathogens causing diarrhoea

17
Q

Why do you have to check kidney function before offering contrast investigations?

A

Contrast can be nephrotoxic

18
Q

Why is a urine dipstick in investigating a possible AKI?

A

+ proteinuria indicates intrinsic renal disease

If urine dipstick negative then this can exclude intrinsic renal disease - can look for pre and post renal causes

19
Q

What should you consider if both blood and protein are positive on a urine dipstick?

A

Glomerulonephtitis

20
Q

When is dialysis indicated in an AKI?

A
Persistent Hyperkalemia (K+ >7mmol/L)
Severe Metabolic acidosis (pH <7.2 or base excess <10)
Refractory pulmonary oedema
Uraemia encephalopathy (confusion, myoclonic jerks, seizures, coma)
Uraemia pericarditis (pericardial rub)
21
Q

Why is creatinine used as a marker of glomerular filtration?

A

It is normally completely filtered by the kidneys and therefore will only rise in the blood when the kidney is damaged

22
Q

Why are the renal tubules particularly susceptible to ischaemic damage during dehydration?

A

There is very little blood flow to the renal tubules (particularly in the medulla) - this is in order for the countercurrent multiplication mechanism to work

When you are dehydrated, blood flow to the kidney is reduced, resulting in ischaemia

23
Q

How does the RAAS system help to maintain renal blood flow?

A

When little blood flow reaches the juxtaglomerular apparatus
Kidneys release renin
Renin converts angiotensiongen to angiotensin I
ACE converts angiotensiongen I to angiotensin II
Angiotensin II causes aldosterone secretion
Aldosterone causes more sodium is reabsorbed
This increases blood pressure to allow more perfusion to the kidney

24
Q

What is acute tubular necrosis?

A

A condition usually due to the combination of factors which cause renal ischaemia and toxicity

e.g, hypotension, dehydration, sepsis with associated nephrotoxic drugs

25
Q

What are the 3 phases of acute tubular nephrosis (ATN)?

A

Oligouric phase - kidneys produce less than 500mls per day, there is fluid overload and electrolyte inbalance, creatinine rises
Maintenance phase - patient is no longer oligouric and increased output helps maintain fluid and electrolytes, creatinine is stable
Polyuric recovery phase - kidneys produce large amounts of urine, so the patient becomes hypovolaemic and unwell, patient are susceptible to electrolyte loss (hypokalaemia). Creatinine falls

26
Q

What is the definition of sepsis?

A

Systemic inflammatory response syndrome due to infection

27
Q

What are the SIRS criteria?

A
Two or more of the following:
Temp <36, >38
Tachycardia = HR >90bpm
Respiratory rate >20 per min or PaCO2 <4.3kPa
WCC >12x10^9/L or <4x10^9/L
28
Q

What is severe sepsis?

A
Sepsis along with signs or organ hypo-perfusion:
Hypoxemia
Oliguria 
Lactic acidosis 
Acute alterations in mental state
29
Q

What is septic shock?

A

Sepsis with hypotension (systolic BP <90, or a decrease of 40 from bass line)

30
Q

What investigations should be done for suspected sepsis?

A

Venous blood gas including glucose and lactate
Blood culture
Full blood count
CRP
U&E - check for kidney damage
Clotting screen - check for dysregulation of coagulation system

31
Q

What is the immediate treatment for sepsis?

A

Broad spectrum antibiotic at max dose without delay

IV fluid bolus without delay

32
Q

Why is lactate increased in sepsis

A

Due to a result of anaerobic respiration because of poor oxygen perfusion to tissues

33
Q

What is the treatment in fluid resuscitation?

A

Identify cause of deficit and respond
Give a fluid bolus of 500mL of crystalloid (E.g NaCl 0.9% / Hartmanns solution) over 15 mins

Reassess the patient in 15mins using ABCDE and give another 500mL if still needs fluid resuscitation

You can repeat process until you have give 2000mL of fluid - if there is still need for fluid resuscitation seek expert help

34
Q

When would you give a patient routine maintenance fluids?

A

If the patient is haemodynamically stable, but is unable to meet their daily fluid requirements via oral/enteral route

35
Q

What are the daily maintenance fluid requirements?

A

25-30ml/kg/day of water
1mmol/kg/day K+, Na+ and Cl-
50-100g/day of glucose to limit starvation ketosis

36
Q

When would you consider prescribing less maintenance fluid than advised?

A

For patients who are obese - adjust IV fluid to ideal body weight
Patients who are old or frail
Patients who have renal or cardiac failure
Patients who are malnourished and at risk of refeeding syndrome