AKI: Management and Prognosis of Oligoanuria versus Nonoligoanuria Flashcards
what should you NOT do for AKI?
- aggressive fluid therapy to “flush the kidneys/toxins” or Induce diuresis
diuresis does NOT mean higher GFR
what SHOULD you do in terms of fluids for AKI?
- 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)
recall dehydration versus volume depletion
dehydration: loss of total body water, produces hypertonicity, implies intracellular volume contraction
volume depletion: deficit in extracellular fluid volume; implies blood volume contraction
describe AKI fluid therapy for hypovolemia versus dehydration
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)
what are the 3 components to fluid therapy?
- 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) - rehydration/replacement: assess hydration status and correct accordingly
- 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
describe assessment of dehydration status
<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
describe oliguric AKI
- UOP <1ml/kg/hr
- 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
- unique challenges with renal oliguria:
-overhydration likely
-severe hyperkalemia
-worse prognosis - AVOID USING AT LEAST ONE JUGULAR vein for venipuncutre or catheter replacement; spare if there’s any chance of hemodialysis!!
how do you manage oliguric AKI?
- 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
- 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
- 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)
- established ologuanuric AKI
describe overhydration, fluid overload, and oligoanuria
- fluid overload can lead to oligoanuria: too much fluid = too much pressure = can’t function!!
- signs of overhydration:
-chemosis
-serous nasal discharge
-increased skin turgor: look like a balloon
-peripheral edema
-ascites
-pleural effusion
-pulmonary edema (and edema everywhere) - fluid overload at any point is associated with decreased survival in AKI!! so monitor fluid therapy!!
-hydration status, body weight, urine prod, etc.
describe hyperkalemia with AKI
- renal excretion is a major mechanism of removing K+ from body
- hyperkalemia is common with postrenal or renal oligoanurai!!
-possibly life threatening
-can cause cardiac arrhythmias and muscle weakness - 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)
describe hypokalemia with AKI
- possible with polyuria, diuretic use, or GI losses
- 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!
describe metabolic acidosis and AKI
- kidneys reabsorb and excrete acids
- acidosis may improve with rehydration
- if persistent/significant pH <7.2 of HCO3 <12 mEq/L: sodium bicarbonate for slow correction
describe hyperphosphatemia and AKI
- decrease in GFR causes increase in phosphate
- increased calcium phosphorous product (>60-70): dystrophic tissue
treatment:
1. correct prerenal azotemia
2. phosphate binders if eating/feeding tube
3. renal replacement therapies
describe calcium disorders with AKI
- ionized hypocalcemia:
-acute drop in GFR causes abrupt increase in phosphate complexes with iCa
-may cause tetany
-treat: calcium gluconate - ionized hypercalcemia:
-metabolic acidosis increases iCa by displacing i from albumin- usually mild
-if treatment necessary: fluid therapy, sodium bicarb, furosemide
describe GI complications of AKI
- 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
