High Yield Handout: AKI

Question 1

Define AKI clinically

Answer 1

Serum creatinine > 0.3 within 48 hours or >50% within 7 days

or

urine output <0.5 mL/kg/hour for >6 hours

Question 2

CardioRenal Syndrome

Answer 2

condition where therapy to relieve congestive symptoms of HF is limited by decline in renal function bidirectional

Question 3

How do we calculate GFR

Answer 3

using creatinine a small frail, old person may have lower muscle mass therefore only experience a mild elevation of creatinine with renal insufficiency

Question 4

KDIGO stage 1

Answer 4

increase in serum creatinine >0.3 or 50-99%

or

urine output of <0.5 for 6-12 hours

Question 5

KDIGO stage 2

Answer 5

increase in serume creatinine of 100-199%

or

urine output of <0.5 for 12-24

Question 6

KDIGO stage 3

Answer 6

increase in serum creatinine >200%

increase in serum creatinine of >0.3 to >4.0

urine output of <0.3 for >24 hours or anuria >12 hours

initiation of renal replacement therapy

Question 7

What data is important in the AKI case we had

Answer 7

increase in BUN/Cr

BNP declining

improvement of chest x-ray

normal EF per echo

Question 8

AKI symptoms

Answer 8

oliguria

dyspnea

worsening edema

tachycardia

hypotension

JVD

liver distension/tenderness

distended abdomen

Question 9

anascara

Answer 9

Is severe generalized edema that extends from the lower extremity proximally. It can
cause ascites as well as subcutaneous edema; associated with heart failure, cirrhosis, severe
malnutrition and renal failure.

Question 10

Fluid wave

Answer 10

detects large volumes of free intrabdominal fluid. It has a specificity of 80-90%; a
positive finding rules in ascites. However, its sensitivity is ~50%, so a negative test does not
exclude ascites (i.e. it is volume dependent).

Question 11

PND

Answer 11

Describes episodes of sudden dyspnea and orthopnea that awaken patient from sleep prompting the patient to sit up and stand up. There may be associated wheezing and coughing. PND may be mimicked by nocturnal asthma attacks

Question 12

puddle sign

Answer 12

~40-~50% sensitivity especially with small amount of ascites.

The patient places the ulnar surface of their
hand along the abdominal vertical midline. The
operator places one hand on one flank and taps
gently on the opposite flank. A positive sign
when the operator feels a moderate to strong
fluid wave emanating into the contralateral
side.

Question 13

OSE for kidney

Answer 13

T10-T11

vagus nerve

Question 14

Upper Ureter

Answer 14

T10-T11

Vagus

Question 15

Lower Ureter

Answer 15

T12-L2

pelvic splanchnic nerve

Question 16

Bladder

Answer 16

T12-L2

pelvic splanchnic nerve

Question 17

Kidney Chapman points

Answer 17

Anterior: one inch lateral and one inch
superior to the umbilicus

Posterior: between the transverse process
of T12 and L1 (on the ipsilateral side)

Question 18

5 model approach: Biomechanical

Answer 18

SD of OA/AA
SD of T-spin (T10-T11)
SD of psoas

Question 19

5 model approach:

Respiratory/Circulatory

Answer 19

O2 via mask/nasal canula

Lymphatics

diaphragms

Thoracic Area (pec traction/doming the diaphragm/thoracic pump)

Abdominal Area (abdominal pump/sacral rocking/pelvic diaphragm)

Extremity (effleurage/petrissage/pedal pump)

Rib raising

Question 20

5 model approach:

Neurologic

Answer 20

see other cards regarding nerve levels

Question 21

5 model approach:

Metabolic/Energetic/Immune

Answer 21

Loop diuretics

Fluid restriction

Remove offending agents like NSAIDs, PPI

Adjust meds based on renal function

Monitor I/O’s, weights

Question 22

5 model approach:

Behavioural

Answer 22

Exercise

Diet – restrict fluids

Avoid offending agents

Better management of CHF (inciting cause)

Question 23

What are the possible mechanisms to account for AKI in conjunction with
AHF?

Answer 23

neurohumoral adaptations

reduced renal perfusion

increased renal venous pressure

associations with heart failure with preserved ejection fraction

Question 24

neurohumoral adaptations and reduced renal perfusion

Answer 24

in the setting of HF, hemodynamic
derangements trigger activation of the sympathetic nervous system and
RAAS and increases in the release of vasopressin (andidiuretic hormone)
and endothelin-1, which promote salt and water retention and systemic
vasoconstriction. These pathways lead to disproportionate reabsorption
of urea compared with that of creatinine. They also overwhelm the
vasodilatory and natriuretic effects of natriuretic peptides, nitric oxide,
prostaglandins, and bradykinin. The systemic vasoconstriction increases
cardiac afterload which reduces cardiac output, can further reduce renal
perfusion.

Question 25

increased renal venous pressure

Answer 25

Increases in intra-abdominal or central
venous pressure, which should increase renal venous pressure, reduces
GFR. In other words, there is an inverse relationship between central
venous pressure and GFR. However, the mechanism by which renal
venous pressure might lead to reduction in GFR is not well understood

Question 26

Associations with heart failure with preserved ejection fraction (HFpEF):

Answer 26

renal dysfunction can lead to metabolic derangements resulting in
systemic inflammation and microvascular dysfunction, which can cause
cardiomyocyte stiffening, hypertrophy and interstitial fibrosis. Exact
relationships are not well understood.

Question 27

how do we treat AKI

Answer 27

1. Remove offending agents: NSAIDS, PPI, etc.
2. Judicious use of loop diuretics (furosemide)
3. Adjust medication dosing based on renal function
4. Supportive care: oxygen
5. Monitor weight, I’s & O’s
6. Fluid restriction
7. Monitor electrolytes (Na+, K+ ,Ca+, Mg+, etc.)
8. Case management/manager
9. Dietary consult

Question 28

long term management for AKI

Answer 28

1. Discussion with patient regarding personal wishes regarding Dialysis
   (both short and long-term), as well as other end-of-life matters such as
   Living Will and DPAHC.
2. Avoid nephrotoxic drugs, including OTC preparations such as NSAIDs,
   PPI, etc.
3. Regular monitoring of electrolytes, patient weight, fluid status, etc.

Question 29

complications of long term AKI management

Answer 29

1. Progression to oligouria or anuria: Dialysis (Renal Replacement Therapy) may be ‘initiated
   emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist,’ per
   the KDIGO guidelines. RRT should be continued until renal function is recovered or because
   continued provision of renal support is no longer consistent with the overall goals of care for
   the patient.