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Year 3 > Case Eight - Case One > Flashcards

Case Eight - Case One Flashcards

1
Q

what is AKI

A

sudden decline in renal function significant enough to produce uraemia, and also often oliguria

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2
Q

what is oliguria

A

a urine output of <400ml/day

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3
Q

what is a severe AKI defined as

A

a creatine level of >500umol/L

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4
Q

what is the incidence of AKI

A

The approximate incidence of AKI is 180 per 1 million; before the age of 50, this value is 17 per 1 million, but as high as 950 per 1 million in those over 80.§

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5
Q

what are the three main categories that causes of AKI be divided into

A

prerenal
intra-renal
post-renal

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6
Q

what is the most common cause of AKI in the hospital

A

sepsis

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7
Q

what what is the prerenal causes of AKI

A

impaired blood flow to the kidney

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8
Q

what may impaired blood flow to the kidney be a result of

A

hypovolaemia, decreased BP, decreased CO, or vascular disease

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9
Q

what are the clinical signs of prerenal causes of AKI

A

history of blood/fluid loss,
sepsis leading to vasodilation,
cardiac disease,
postural hypotension,
weak and rapid pulse with low JVP

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10
Q

what are the three intra-renal causes of AKI

A
  1. acute tubular necrosis (ATN)
  2. Nephrotoxicity
  3. renal parenchymal disease
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11
Q

what is ATN

A

by far the most common cause of AKI, where toxicity and or ischaemia results in decreased GFR

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12
Q

what is nephrotoxicity causes by

A

ahminoglycosides

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13
Q

what is renal parenchymal disease a result of

A

ATN

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14
Q

what are the investigations for AKI

A

urine dipstick

urine microscopy - red cell casts and red cells

Blood tests- U+E’s - particularly Cr and K+, FBC, free haemoglobin and myoglobin

Kidney function is monitored through urine output analysis and creatinine clearance monitoring – creatinine clearance monitoring is the ideal, i.e. it is a more precise indication of GFR than serum urea monitoring alone!

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15
Q

what is the official definition of AKI

A

Acute kidney injury is a sudden decline in renal function significant enough to produce uraemia, and also often oliguria – a urine output of <400ml/day, which is the minimum volume required to remove waste products from the blood.

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16
Q

what is the diagnosis criteria for AKI

A
  • there is a rise of serum creatine of >26.5 in <48 hours
    OR
  • there is a rise in serum creatine to >1.5x the baseline level which was previously known or assumed 7 days prior to the presentation
  • there is a signifiant reduction in urine output compared to baseline
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17
Q

what is uraemia

A

a situation where there is enough urea in the blood to cause clinical symptoms, which may include anorexia and lethargy, and later, possible decrease in mental capacity leading to coma

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18
Q

what is the term azotaemia sometimes used for

A

sometimes used to describe levels of urea above normal but. not high enough to cause clinical signs

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19
Q

what is the mortality of those with an isolated AKI

A

5-10%

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20
Q

in those with other organ failure that then go into AKI, what is the mortality

A

50-70%

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21
Q

what are the three questions that need to be asked before diagnosing acute renal failure

A
  1. is the renal failure acute?
  2. is there a urinary tract obstruction?
  3. is there something rare that might be causing the AKI?
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22
Q

when should chronic renal failure be suspected (three things)

A
  • there is co-existing diabetes
  • there is increased blood pressure, and other signs of chronic disease
  • small kidneys are apparent on ultrasound with increased echogenicity
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23
Q

what percentage of severe AKIs are due to obstruction

A

25% - most commonly causes by prostatic hypertrophy

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24
Q

what is the main test for obstruction

A

USS of the kidneys

renal USS will not detect obstruction but dilation of the calyces, and in 5% of cases, such dilation may not be detected, culminating in a false negative result

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25
Q

what are the three procedures that may be carried out in order to relieve an obstruction

A

catheritisation

percutaneous nephrostomy

surgery to allow impact of stents while consideration of how to treat the underlying cause is undertaken

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26
Q

what are the rare suspects that may cause an AKi

A

E.g. glomerulonephritis, vasculitis, or interstitial nephritis. Do a dipstick test on anyone with suspected AKI, and if there are any irregular findings, send off for urgent analysis. Often there will be haematuria and/or proteinuria.

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27
Q

what causes account for 80% of the cases

A

pre-renal failure and acute tubular necrosis

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28
Q

what antibiotics are contraindicated in sepsis with AKI

A

treatment with gentamicin or vancomycin as these are nephrotoxic agents

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29
Q

impaired blood flow to the kidney (pre-renal causes) may be a result of what

A
  • hypovolaemia
  • hypotension
  • decreased CO
  • vascular disease
  • combinations of any of the above
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30
Q

how is the kidney able to maintain sufficient perfusion despite alterations in these conditions

A

through auto regulation, however in extreme circumstances, it cannot thus GFR will fail

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31
Q

what is this known as

A

prerenal uraemia

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32
Q

what drugs impair auto regulation and therefore may predispose to prerenal uraemia

A

ACE inhibitors and NSAIDs

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33
Q

what are the urine specific gravity and urine osmolarity tests

A

measures of the concentration of solutes in urine. they are quick and easy to carry out, but are unreliable in the presence of glycosuria or other unrelated conditions that disturb urine concentration

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34
Q

what are the kidneys particularly susceptible to

A

ischaemic damage and cholestatic jaundice

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35
Q

what conditions perpetuate renal ischaemia

A

gram-negative septicaemia, pre-eclamsia

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36
Q

what is treatment of ATN based on

A

increasing renal perfusion, while treating the underlying condition

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37
Q

how do ACE inhibitors damage the kidneys

A

they can lead to dilation of the efferent arteriole, thus lowering glomerular pressure, resulting in a reduced GFR. in patients with renal disease, this exacerbates the condition

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38
Q

how do NSAIDs damage the kidney

A

reduce prostaglandin production. prostaglandins are vasodilators - thus inhibition of their production may lead to vasoconstriction of the afferent arteriole, thereby causing reduced renal and reduced GFR

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39
Q

what is the first organ to be jeopardised when systemic circulation iOS compromised

A

kidneys

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40
Q

what is the well defined sequence of events that culminates in ATN

A
  • rapid reduction in GFR followed by a rapid increase in serum creatine and urea
  • extended period, typically 1-2 weeks where there is continued poor kidney function while serum creatinine and urea continue to rise
  • finally, there is restoration of kidney function, where GFR rises, whilst serum creatine and urea fall
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41
Q

what is the combination of factors that exist in ATN

A
  1. intra-renal vasoconstriction
  2. tubular cell injury
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42
Q

what is intra-renal vasoconstriction due to

A

due to decreased vasodilation occurring in the presence of other factors, including endothelial damage e.g in trauma or in infection, where leukocyte activation and release of PGE2, EACh, and bradykinin occurs

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43
Q

what does ischaemia initiate and what does this lead to

A

ishcaemia initiates rapid utilisation of intracellular ATP stores, which, once depleted, will cause the cell to die by necrosis or apoptosis.

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44
Q

what will happen to adjacent cells

A

they all lose their adherent quality and desquamate

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45
Q

what does this lead to

A

RBCs are able to escape into the tubule, squishing together to form casts.

Casts can then block the renal tubule, forming a backup of tubular fluid

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46
Q

where is the necrosis the worst

A

in the loop of Henle - especially when it lies in a relatively poorly perfused medulla and the proximal tubule

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47
Q

what growth factors are released during cell injury to assist in the regeneration process

A

insulin-like growth factor, epidermal growth factor and hepatocyte growth factor

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48
Q

what are the three ways in which ischamia results in a reduction of GFR

A

glomerular contraction

back-leak of filtration

obstruction of the tubule

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49
Q

what does treatment of ATN essentially

A

involve keeping the patient alive until the condition rectifies itself

50
Q

within what time period will AKI appear after taking a nephrotoxic drug

A

will appear within 2 weeks of taking a nephrotoxic drug

51
Q

what are ahminoglycosides

A

class of antibiotics that are most commonly associated with nephrotoxicity

52
Q

what are examples of ahminoglycosides

A

gentamicin, vancomycin, kanamycin, streptomycin

53
Q

what’s renal parenchymal diseased a result of

A

acute tubular necrosis

54
Q

what is kidney function monitored via

A

urine output analysis and creatine clearance monitoring

55
Q

what are the signs of hypovolaemia

A

JVP
low BP
low urine output
poor tissue turgor
fast, weak pulse

56
Q

what are the signs of fluid overload

A

raised BP
peripheral oedema
lung crepitations
gallop rhythm head on heart sounds

57
Q

where will oedema always be particularly apparent in fluid overload

A

in the hips

58
Q

what does the presence of small kidneys suggest

A

CKD

59
Q

what should you also stop if creatinine is >150mmol/L

A

stop metformin also

60
Q

what values in Hyperkalaemia are particually dangerous and what may they lead to

A

values above 6mmol/L and may lead to arrhythmias, particularly ventricular fibrillation or cardiac arrest

61
Q

what will an ECG of VF show

A

tall tended T waves
small or absent P waves
wide QRS complex
asystole
sinus wave pattern

62
Q

if VF is present, what is the imperative treatment

A

calcium gluconate

insulin

considering haemodialysis

63
Q

what is calcium gluconate

A

cardio protective

give a 10ml dose of 10% of solution every 2 mins until the ECG improves

64
Q

why is insulin given in VF

A

stimulates the uptake of glucose within the cell - and as glucose is taken up it is taken up in co-transport by potassium. giving insulin will lower the serum K+

65
Q

when is haemodialysis considered

A

if the patient is anuric - producing no urine

66
Q

what should be given if pulmonary oedema is present

A

venodilator - morphine
oxygen
loop diuretics

67
Q

when should dialysis be considered

A

Pulmonary oedema
Persistent hyperkalaemia, i.e. K+ >7mmol/L
Severe metabolic acidosis, i.e. pH <7.2, or base excess <10
Uraemic encephalopathy
Uraemic pericarditis, aka “uraemic rub”

68
Q

what do you treat acidosis with

A

sodium bicarbonate, this intervention will also help to lower the level of free potassium

69
Q

what happens if sodium bicarbonate is administered too quickly

A

the patient may become hypocalcaemic, which often causes tetany

70
Q

what do patients treated with haemodialysis require

A

70g protein daily to prevent negative nitrogen balance

71
Q

once the patient has a normal fluid and electrolyte balance, what should fluid intake equal

A

fluid intake should equal urine output + vomit + fistula losses + 500ml extra allowance

72
Q

what confirms acute tubular necrosis on urinalysis

A

muddy brown casts on urinalysis. renal tubular epithelial cells may also be seen

73
Q

what do leucocytes on urinalysis suggest

A

infection

74
Q

what do protein and blood suggest

A

acute nephritis

75
Q

how is AKI prevented

A

Avoiding nephrotoxic medications where appropriate

Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)

Additional fluids before and after radiocontrast agents

76
Q

what are the complications of AKIs

A

fluid overload, heart failure and pulmonary oedema

Hyperkalaemia

metabolic acidosis

uraemia which can leads to encephalopathy and pericarditis

77
Q

what tool is used to screen for frailty

A

Rockwood Fraility Score

78
Q

What is immediate management plan for sepsis

A

take lactate, urine output and blood culture

give IV fluids, antibiotics and oxygen

79
Q

what is septic shock defined as

A

Septic shock is defined as ‘a subset of sepsis, which describes circulatory, cellular, and metabolic abnormalities which are associated with a greater risk of mortality than sepsis alone’. In hospital, we suspect septic shock when patients fail to respond to initial treatment – specifically, ‘sepsis with persistent hypotension despite fluid correction and inotropes and a serum lactate of greater than 2mmol/L’.

80
Q

what is the most appropriate IV fluid therapy for initial resuscitation in a patient with sepsis

A

initial fluid resuscitation with a crystalloid given as a bolus over less than 15 mins

81
Q

what are crystalloids

A

solutions containing small molecules in water (sodium chloride, glucose or Hartmann’s)

82
Q

what are colloids

A

solutions with large molecular weight substances (e.g albumin, gelatine)

83
Q

what does the choice and rate at which IV fluids are given depend on?

A

What is the aim of IV fluid therapy? (resuscitation, routine maintenance, replacement and redistribution)

What is the weight and size of the patient, and therefore what are the fluid requirements?

Are there ongoing losses?
Are there significant co-morbidities which may affect redistribution of fluids? (liver, renal and/or cardiac impairment etc)

84
Q

what is the most appropriate antimicrobial for treatment of a likely urinary source of infection as per the BNF treatment summary

A

ceftriaxone

85
Q

why is lactate raised in sepsis

A

raised as a result of tissue hypoxia in sepsis; as a result of widespread systemic inflammation, there is organ hypoperfusion and subsequently the cells turn to anaerobic metabolism, which produce lactate

86
Q

what lactate value is considered a high risk criteria for sepsis

A

> 4mmol/L

87
Q

what is mild hyperglycaemia in sepsis a result of

A

stress response from release of cortisol and cathecolamines by the body during sepsis

88
Q

when should you urgently treat Hyperkalaemia

A

when the serum potassium exceeds 6.5 and/or there are ECG changes

89
Q

what are the three priorities with regards to management of acute hyperkalamia

A
  1. protecting the cardiac membrane
  2. shifting potassium intracellularly
  3. stopping any contributing medications
90
Q

what does IV calcium gluconate do

A

acts by reducing membrane excitatory effects of K on cardiac tissue rapidly, therefore reducing the potential for cardiac arrhythmias such as ventricular fibrillation, but has minimal effect on lowering serum K concentrations

91
Q

what can you give to shift potassium intracellularly

A

give 10 units Insulin with 25g glucose (an example of a treatment regime for this would be 10 units Actrapid in 250mls of 10% dextrose at 50ml/hr for 5 hours (25g)

92
Q

what else is given alongside insulin and glucose in severe, life-threatening Hyperkalaemia and when should it be avoided

A

nebuliser salbutamol 10-20mg is also given alongside insulin and glucose

avoid salbutamol if tachyarrhythmia present

93
Q

what are some examples of potassium binders and what do these do

A

sodium zirconium cyclosilicate and patiromer

act by promoting potassium excretion for managing Hyperkalaemia in adults

94
Q

what are the three main functions of the kidney

A

filter and excrete nitrogenous waste products

maintain acid base balance, by controlling reabsorption and excretion of electrolytes

produce certain hormones

95
Q

what hormones does the kidney produce

A

erythropoietin, renin and calcitriol

96
Q

why is creatinine in particular a useful marker of glomerular filtration

A

because it is completely filtered in the glomerulus

97
Q

what is GFR proportional to

A

1/ creatinine

98
Q

where does the RAAS system happen

A

in the juxtaglomerular apparatusw

99
Q

how does it act to increase overall effective circulating volume

A

increasing reabsorption of sodium ions

vasoconstriction the efferent arterioles

100
Q

what does histology of ATN show

A

sloughing of the renal tubular epithelium causing dilation and obstruction of tubules and some mild leukocyte infiltration

101
Q

what are the 3 phases of ATN

A
  1. oligourio phase
  2. maintenance phase
  3. polyuric recovery phase
102
Q

what is the oligourio phase

A

the kidneys produce less than 500mls of urine per day

103
Q

the loss of the kidney’s homeostatic functions in AKI will mean that the kidneys are:

A
  1. unable to regulate acid-base balance, leading to Hyperkalaemia, fluid retention and metabolic acidosis
  2. unable to excrete metabolic waste products, leading to build up of urea and creatinine
104
Q

what does this eventually lead to

A

multi-organ failure

105
Q

why is clotting measured in a patient with sepsis

A

sepsis can be a cause of disseminated intravascular coagulation (DIC)

106
Q

what is DIC characterised by

A

a clinical syndrome characterised by dysregulated coagulation

107
Q

what happens in DIC

A

tissue factor is released into the bloodstream as a result of cytokine release, endotoxin release or endothelial damage, which activates the coagulation pathway

this widespread coagulation consumes clotting factors, which causes bleeding in a addition to microvascular thrombosis

108
Q

what is the management of DIC

A

involves treatment of the underlying cause, and support blood product transfusion in life threatening bleeding

109
Q

what is Stage 1 AKI

A

Creatinine:
1.5 – 1.9 times increase from baseline OR
> 26.5 µmol/l increase

Urine:
< 0.5ml/kg/h for 6 – 12 hours

110
Q

what is Stage 2 AKI

A

Creatinine:
2.0 – 2.9 times increase from baseline

Urine:
< 0.5 ml/kg/h for > 12 hours

111
Q

what is Stage 3 AKI

A

Creatinine:
3.0 times increase from baseline
OR
Increase in serum creatinine > 353.6 µmol/L
OR
In patients < 18 years, decrease in eGFR to < 35ml/min per 1.73m

Urine:
< 0.3ml/kg/h for > 24 hours OR

Anuria for 12 hours

112
Q

what are the risk factors for developing an AKI

A

Risk factors for AKI:
Age 65 years or over;
History of AKI;
CKD (eGFR < 60mL/min/1.73m2);
Symptoms or history of urological obstruction, or conditions which may lead to obstruction;
Chronic conditions such as heart failure, liver disease, diabetes mellitus;
Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer);
Sepsis;
Hypovolaemia;
Oliguria (urine output < 0.5 mL/kg/h);
Nephrotoxic drug use within the last week;
Exposure to iodinated contrast agents within the past week

113
Q

what should you always remember to do in all patients with an AKI

A

obtain a urine dipstick
monitor urine output
compare the current renal function to historical records if available

114
Q

why is urine dipstick important in AKI

A

> 3+ Proteinuria - indicates intrinsic renal disease

Send Urine PCR / MSU - if dipstick positive

If - ve - prob excludes intrinsic renal disease - Save time and money

If blood and protein +ve - consider glomerulonephritis
Dipstick positive for blood and no RBC - consider myoglobin

115
Q

what drugs should be stopped in patients with AKI

A

Aminoglycosides (gentamicin)

ACE-inhibitors (ramipril)

ARBs (losartan)

Metformin

NSAIDs

Aciclovir

116
Q

what drugs should be monitored carefully, adjusting dose or withholding deeding on eGFR

A

DOACs (apixaban)

Co-amoxiclav

Low molecular weight heparin (tinzaparin)

Sulphonylureas (gliclazide)

117
Q

what opioids are considered safe to use in those with renal impairment

A

Opioids that are considered safer to use in those with renal impairment include oxycodone, fentanyl and hydromorphone; however, these patients are at high risk of opiate toxicity and adverse effects, and will require close monitoring, dose titration and input from specialist teams such as the pain team, renal team or the palliative care team.

118
Q

what about furosemide

A

may actually improve renal function in patients who have AKI secondary to cardiorenal syndromes,

119
Q

what is AIN

A

acute interstitial nephritis

this is a clinical syndrome characterised by inflammatory infiltrates in the renal intersitioum in response to a drug, infection or autoimmune process

120
Q

An 80 year old gentleman with type 2 diabetes was started on ibuprofen for hip pain last week. His regular medications include amlodipine and atenolol for hypertension. Last year he was in hospital with pneumonia, and developed AKI during that admission. He has now presented to ED with a fall.

How many risk factors associated with AKI does he have?

A

5

121
Q

Which factor does not affect estimated GFR?

A

weight

122
Q
A

Year 3 (63 decks)

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