AKI: Management and Prognosis of Oligoanuria versus Nonoligoanuria Flashcards

1
Q

what should you NOT do for AKI?

A
  1. aggressive fluid therapy to “flush the kidneys/toxins” or Induce diuresis

diuresis does NOT mean higher GFR

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2
Q

what SHOULD you do in terms of fluids for AKI?

A
  1. correct dehydration and then maintain hydration

-rehydration is essential: correct prerenal azotemia and assess renal impairment, restore renal blood flow, hypovolemia prolongs renal hypoxia and increases tubular cell death

-isotonic, balanced, alkalinizing fluids for replacement: LRS, normosol/plasma-lyte A
-avoid 0.9% saline (acidifying)

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3
Q

recall dehydration versus volume depletion

A

dehydration: loss of total body water, produced hypertonicity, implies intracellular volume contraction

volume depletion: deficit in extracellular fluid volume; implies blood volume contraction

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4
Q

describe AKI fluid therapy for hypovolemia versus dehydration

A

hypovolemia: must correct within 1-2 hours!!

dehydration: correct over 6-8 hours, then aim to maintain hydration (no more, no less), caution if concurrent heart disease (go slower, over 24 hours)

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5
Q

what are the 3 components to fluid therapy?

A
  1. maintenance: covers normal losses
    -normal: approx 40-60ml/kg/day
    -urine output in AKI may not be normal!
    –polyuric or oliguric, so reassess often!! (at least 2x per day)
  2. rehydration/replacement: assess hydration status and correct accordingly
  3. ongoing losses (vomiting, diarrhea)
    -monitor ongoing losses

fluid rate = maintenance + replacement + losses

reassess and adjust often!!!!!

can also use the Ins and Outs method
-but does not account for dehydration, so reserve this method for after patient is rehydrated!!
-useful for all AKI settings, including anuria/oliguria, relative oliguria, and polyuria
-assess every 4-6 hours and adjust fluid rate accordingly

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6
Q

describe assessment of dehydration status

A

<5%: not detectable on PE

5-6%: tacky mucous membranes

6-8%: decreased skin turgor, dry mucous membranes

8-10% retracted globes within orbits

10-12% persistent skin tent, dull corneas, evidence of hypovolemia

> 12% hypovolemic shock, death

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7
Q

describe oliguric AKI

A
  1. UOP <1ml/kg/hr
  2. oliguria can be:
    -prerenal: hypovolemia, hypotension
    –assess volume status
    –PE, body weight, PCV/TS, blood pressure

-postrenal: UT obstruction or rupture
–check the patency of the urinary catheter/collection system
-image abdomen to assess bladder size and rule out obstruction/rupture

renal: kidneys are truly incapable of producing enough urine!! severe decrease in GFR, may occur with AKI or late stage 4 CKD

  1. unique challenges with renal oliguria:
    -overhydration likely
    -severe hyperkalemia
    -worse prognosis
  2. AVOID USING AT LEAST ONE JUGULAR vein for venipuncutre or catheter replacement; spare if there’s any chance of hemodialysis!!
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8
Q

how do you manage oliguric AKI?

A
  1. optimize renal perfusion
    a. assess hydration status:
    -if dehydrated: correct
    -if apparently euhydrated: could assume 5% dehydrated and give volume over 2 hr
    -clearly overhydrated: NO MORE fluids, move to next steps

b. assess BP: hypotension may need to be addressed with vasopressors after volume is replaced

  1. differentiate from CKD if still in doubt
    a. end stage CKD (stop here with 3 choices:
    -very poor prognosis owner discussion about goals
    -consider transplant or hemodialysis
    -euthanasia

b. AKI (3 choices)
-conservative therapy: challenging and caution with fluid overload
-renal replacement therapy
-process to alternative means to induce diuresis

c. alternative means to induce diuresis:
-osmotic diuretic: mannitol: contraindicated if not euhydrated
–or 10% dextrose

-loop diuretic: furosemide (no use with aminoglycoside toxicity; furosemide increases)

  1. alternative means to produce diuresis
  2. established ologuanuric AKI
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9
Q

describe overhydration, fluid overload, and oligoanuria

A
  1. fluid overload can lead to oligoanuria: too much fluid = too much pressure = can’t function!!
  2. signs of overhydration:
    -chemosis
    -serous nasal discharge
    -increased skin turgor: look like a balloon
    -peripheral edema
    -ascites
    -pleural effusion
    -pulmonary edema (and edema everywhere)
  3. fluid overload at any point is associated with decreased survival in AKI!! so monitor fluid therapy!!
    -hydration status, body weight, urine prod, etc.
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10
Q

describe hyperkalemia with AKI

A
  1. renal excretion is a major mechanism of removing K+ from body
  2. hyperkalemia is common with postrenal or renal oligoanurai!!
    -possible life threatening
    -can cause cardiac arrhythmias and muscle weakness
  3. treatment:
    -dilute (fluids)
    -excrete (furosemide)
    -move K+ intracellularly: dextrose (+/- regular insulin), sodium bicarbonate, albuterol
    -stabilize cardiac membrane excitability: give calcium gluconate (IV SLOWLY) = NO CHANGE IN K+ just makes environment safer for the heart
    -remove (dialysis)
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11
Q

describe hypokalemia with AKI

A
  1. possible with polyuria, diuretic use, or GI losses
  2. clinical signs:
    -muscle weakness
    -PU/PD: impairs urinary concentrating ability

treatment:
-IV fluid KCl supplementation
-oral supplementation (K+ citrate or gluconate) if eating/feeding tube
-monitor closely: avoid hyperkalemia!

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12
Q

describe metabolic acidosis and AKI

A
  1. kidneys reabsorb and excrete acids
  2. acidosis may improve with rehydration
  3. if persistent/significant pH <7.2 of HCO3 <12 mEq/L: sodium bicarbonate for slow correction
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13
Q

describe hyperphosphatemia and AKI

A
  1. decrease in GFR causes increase in phosphate
  2. increased calcium phosphorous product (>60-70): dystrophic tissue

treatment:
1. correct prerenal azotemia
2. phosphate binders if eating/feeding tube
3. renal replacement therapies

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14
Q

describe calcium disorders with AKI

A
  1. ionized hypocalcemia:
    -acute drop in GFR causes abrupt increase in phosphate complexes with iCa
    -may cause tetany
    -treat: calcium gluconate
  2. ionized hypercalcemia:
    -metabolic acidosis increases iCa by displacing i from albumin- usually mild
    -if treatment necessary: fluid therapy, sodium bicarb, furosemide
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15
Q

describe GI complications of AKI

A
  1. can cause anorexia, nausea, vomiting, ileus, pancreatitis

treat with:
1. antiemetic/antinausea
2. motility modifiers
3. appetitie stimulants
4. antacids if ulceration
5. magic mouthwash if oral ulceration

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16
Q

describe AKI nutritional support

A

AKI is a highly catabolic condition!!

anorexic patients:
-consider enteral feeding
-include food water volume in your fluid calculations

17
Q

describe SAH in AKI

A
  1. common!!
    -progressive sodium/volume loading from IVF may contribute
    -TOD
  2. approach:
    -if due to fluid overload: reduce fluid rate or stop fluids
    -antihypertensive meds
18
Q

describe considerations for drug therapy with AKI

A
  1. drugs only if needed!!
  2. avoid potentially nephrotoxic
  3. adjust dosage and frequency of renally excreted drugs
19
Q

describe renal replacement therapies

A
  1. indications:
    -animals that fail medical management: intractable hyperkalemia, life-threatening volume overload, persistent signs of uremia
    -acute poisoning/drug overdose with a substance that dialysis can remove
  2. goals:
    -support animal and allow time to recover nephron function!
    -to correct water solute and acid-base abnormalities
    -to remoce toxins
20
Q

describe AKi prognosis

A

50-50

azotemia no matter

ethylene glycol is worse
ologoanuric is wrose

better prognosis of hemodynamic, postrenal disease, and infectious disease