HYHO Acute Kidney Injury Flashcards
Acute Kidney Injury is characterized by an increase in what (diagnostic criteria)?
increase in serum creatinine of > or = to 0.3 mg/dL within 48 hrs or within 7 days
OR
urine output of <0.5 mL/kg/hour for >6 hours
Cardiorenal syndrome is a condition in which:
therapy to relieve congestive symptoms of HF is limited by a decline in renal function (as seen bc of the low GFR)
there is a bidirectional intx bw heart and kidneys!
What data would show signs of AKI (this is based on the case?)?
increase in BUN/CR
Normal EF on Echo
declining BNP from admission levels
improvement of findings on chest xray
What would you expect to see on renal US in a pt with chronic kidney dz?
decreased size of kidneys and/or cortical thinning;
It is important to identify underlying dz such as cystic kidneys
You can also identify hydronephrosis easily by US
What does a lack of hydronephrosis mean on US?
it eliminates any obstructive causes of kidney injury
What urine sodium value is expected with HF?
<25 meq/L
Extra info on it: renal perfusion is reduced with associated activation of RAAS and SNS, both of which promote sodium retention; however urine sodium are higher with concurrent diuretic therapy
What do you expect to see in lab values when exposed to IV contrasts?
typical increase in serum creatinine (25-50%) within 48 hrs after administration
(why its impt to take hx)
Undrlying kidney dz may have significant:
proteinuria, active urine sediment (hematuria +/- pyuria or casts) or small kidneys
is prerenal or postrenal azotemia more common in HF?
prerenal azoetemia (BUN/Cr>20)
What causes prerenal AKI?
hypovolemia, decreased CO, decreased effective circulating volume (CHF, liver failure,), impaired renal autoregulation (NSAIDS, ACE-i/ARBs, cyclosporine)
What causes intrinsic AKI?
Acute GN
damage to the tubules and interstitium (ischemia, sepsis/infection, nephrotoxins)
vascular causes (vasculitis, malignant HTN, TTP-HUS)
What nephrotoxins can cause intrinsic AKI?
exogenous: iodinated contrast, aminoglycosides, cisplatin, amphotericin B, PPis, NSAIDs
endogenous: hemolysis, rhabdomylosis, myeloma, intratubular crystals
What causes postrenal AKI?
bladder outlet obstruction, bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidneY)
PE finding of blue toes may indicate:
possible choelsterol emboli
PE finding of appearance of drug rash may indicate:
Acute interstitial nephritis (AIN)
PE finding of signs of volume contraction (tachy, skin tenting, dry oral mucosa, etc.) may indicate:
dehydration
PE finding of signs of volume overload AND heart failure signs may indicate:
cardiorenal syndrome
PE finding of jaundice + ascites may indicate:
liver dz with portal HTN
Signs + syx of AKI include:
decreased urine output
worsening dyspnea @ rest, orthopnea and/or PND
worsening edema moving from dependent edema to anasarca and/or ascites
TACHY, S3
hypotension
JVD
liver distention and/or tenderness w/ palpation
-distended abdomen: fluid wave, and/or puddle sign to assess for ascites
Skin tenting is best evaluated by:
pinching skin of forehead; skin of dehydrated pt will remain elevated rather than springing back to it’s original position
Signs of respiratory distress include:
tachypnea, hypoxia, increased work of breathing (retractions and tripod position)
What is PND and what can mimic it?
dyspnea and orthopnea that awakens pts from sleep prompting pt to sit up /stand up
May be associated with wheezing and coughing;
may be mimicked by nocturnal asthma attacks
What is anasarca?
severe generalized edema, extends from LE proximally
What can anasarca cause and what is it associated with?
can cause ascites as well as subq edema
It is commonly associated with HF, cirrhosis, severe malnutrition, and renal failure
What does fluid wave detect? What does a positive finding rule in?
large volumes of free intrabdominal fluid
+ rules in ascites (highly specific- 80-90%)
But 50% sensitivity so it does NOT exclude ascites (volume dependent)
How do you perform a fluid wave test?
- pt places ulnar surface of their hand along abdominal vertebral midline
- operator places on ehand on one flank and taps gently on the other flank
+ sign = when operator feels moderate to strong fluid wave emanating into the contralateral side
What is a puddle sign? What is a + sign?
- Auscultatory percussion sign that requires the pt to support themselves on hands/knees for 5 mins
- Operator then listens with the diaphragm while flicking finger over localized flank area of abdomen starting at lowest point and moving over to opposite flank
sudden + sign = when sudden increase in intensity and clarity of sound, signaling that the steth has passed edge of peritoneal fluid
What is the sensitivity of a puddle sign?
Sensitivity: 40-50% (especially of small amt of ascites)–>positioning of pt makes it very difficult to evaluate
OSE Kidney sympathetics:
T10-11
OSE Kidneys parasympathetic:
Vagus nerve
OSE Upper ureter sympathetics:
T10-11
OSE Upper ureter parasympathetics:
vagus n.
OSE lower ureter sympathetics
T12-L2
OSE lower ureter parasympathetics
pelvic splanchnic n.
OSE bladder sympathetics:
T12-L2
OSE bladder parasympathetics:
pelvic splanchnic n.
OSE Anterior kidney chapmans point
one inch lateral and one inch superior to umbilicus
OSE Posterior kidney chapmans point
between the transverse process of T12 and L1 (on ipsilateral side)
5 model approach: biomechanical
SD of OA, AA
SD of thoracic spine @ viscerosomatic levels (T10-T11)
SD of psoas muscles
5 model approach: Resp/Circulatory
O2 via mask/nasal canula
Lymphatics:
- thoracic inlet MFR
- thoracic area: pectoral traction, doming diaphragm, thoracic pump
- abdominal area: abdominal pump, sacral rocking, pelvic diaphragm
- extremities: effleurage, petrissage, pedal pump
- rib raising
5 model approach: Neuro
review OSE (sympathetics/PS for kidney, ureters, and bladder), chapman points, rib raising tx
5 model approach: metabolic/energetic/immune
- loop diuretics
- fluid restriction
- remove offending agents like NSAIDs, PPI, -adjust meds based on renal fxn
- monitor I/O’s, weights
5 model approach: Behavioral
exercise, diet (restrict fluids), avoid offending agents, better management of CHF (inciting cause)
What are the possible mechanisms to account for AKI in conjuctino with AHF?
neurohumeral adaptations, reduced renal perfussion, increased renal venous pressure, associations with HFpEF
Describe neurohumeral adaptations:
low yield maybe?
hemodynamic derangements trigger activation of SNS and RAAS and increases in ADH + endothelin-1 release, which promote salt and water retention and systemic VC; this leads to disproportionate reabsorption of urea compared with that of creatinine
they also overwhelm vasodilatory and natriuretic effects of natriuretic peptides, NO, PGs, and bradykinin
systemic VC increases cardiac afterload which reduces CO, and can further reduce renal perfusion
Describe how increased renal venous pressure is involved with AKI in conjunction with AHF?
(low yield maybe?)
increases in intra-abdominal/central venous pressure, which should increase renal venous pressure, reduces GFR
(aka inverse relationship bw central venous pressure and GFR)
How is HFpEF associated w/ AKI?
low yield maybe?
renal dysfxn can lead to metabolic derangements resulting in systemic inflammation and microvascular dysfunction, which can cause cardiomyocyte stiffening , hypertrophy, and interstitial fibrosis
What is the first treatment you should do for AKI and cardiorenal syndrome?
- remove offending agents: NSAIDS, PPI
After removing offending agents(1), what should you do for AKI/ cardiorenal syndrome (steps 2-9)?
- judicious use of loop diuretics (furosemide)
- adjust medication dosing on renal fxn
- supporative care: oxygen
- Monitor weight, I’s + O’s
- Fluid restriction (oral and IV)
- Monitor electrolytes (Ca, Na, K, Mg, etc.)
- Case management/manager
- Dietary consult
What is the mainstay of treatment for AKI?
loop diuretics (furosemide)
Can normal urine output be maintained even in face of low GFR?
yes;
ability for diuretic use to improve output = good prognosis
Which diuretics should you avoid in AKI/HF?
avoid K+ sparing diuretics (spironolactone) as they will complicate K+ management
Why is it important to monitor electrolytes in an AKI/cardiorenal syndrome pt?
electrolyte abnormalities can lead to arrhythmias which will have deleterious affect for both cardiac and renal fxn (monitor electrolytes, Mg and phosphate, and BUN/Cr as well)
When should a case manager especially get involved in patient care?
should be involved early when there are new complications or signs of deterioration
Advanced directives, Code status, DPAHC, etc. become impt and must be addressed early in hospitalization
What Long-term management is important in an AKI/cardiorenal syndrome pt?
- discussion with pt regarding personal wishes regarding dialysis (ST and LT), as well as other end-of-life matters such as Living Will and DPAHC
- Avoid nephrotoxic drugs, including OTC preparations such as NSAIDs, PPI, etc.
- Regular monitoring of electrolytes, pt weight, fluid status, etc.
What are complications of AKI? What can be initiated for it?
progression to oliguria or anuria
Dialysis (renal replacement therapy RRT) may be initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist per KDIGO guidelines
How long should RRT be continued if life-threatening changes occur in AKI pts?
continued until renal fxn is recovered or bc continued provision of renal support is no longer consistent with the overall goals of care for the pt
Why is Durable healthcare power of attorney important in the care of the patient?
DPAHC authorize another person (or surrogate) to make decisions on the pts behalf
Why is Living Will (LW) important in the care of the patient?
It summarizes choices about future medical care; typically addresses resuscitation and life support, but may include other preferences about treatment (feeding tube, dialysis, intubation/ventilator support)
If a patient has elected some restriction (do not resuscitate/intubate) in their living will, the physician:
MUST document the order appropriately
The presence of the LW alone does not prevent resuscitation
What characterizes stage 1 of KDIGO criteria?
increase in serum creatinine > or equal to 0.3 mg/dL or 50-99%
OR
urine output of <0.5 ml/kg/hour for 6 - 12 hours
What characterizes stage 2 of KDIGO criteria?
increase in serum creatinine of 100-199%
OR
urine output of <0.5 ml/kg/hour for 12-14 hours
What characterizes stage 3 of KDIGO criteria?
increases in serum creatinine of > or = to 200%
OR
Increase in serum creatinine of > or = to 0.3 mg/dL to > or = to 4.0 mg/dL
OR
urine output of <0.3 mL/kg/hr for > or = to 24 hrs or anuria for > or = to 12 hrs
OR
initiation of renal replacement therapy
What are we gonna get on this exam?
an AAAAAAAAA
