Acute Kidney Injury pt 2 Flashcards
contrast studies for AKI
Retrograde contrast cystourethrogram
- assess bladder & urethral integrity
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Antegrade pyelogram
- assess for ureteral obstruction
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Intravenous pyelogram
- assess for ureteral obstruction
- discouraged: concerns for contrast-induced renal injury
Cytology of Renal Aspirates for AKI
US-guided fine needle aspirates (FNA)
- e.g. lymphoma / other infiltrative diseases
- possibly non-diagnostic, non-representative
- low risk of bleeding (possible)
Histopathology of Renal Biopsies for AKI
- what we can learn
- risk
Percutaneous US-guided or surgical (laparasocpic) biopsy
- confirm suspected cause (e.g. ethylene glycol intoxication, lymphoma)
- may disclose non-specific findings
- assess severity of fibrosis, potential for renal recovery
- risk of hemorrhage
Management of AKI
- broadly, what actions must we take? what issues should we be aware of?
Specific therapies
- address underlying cause
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Emergency stabilization
- Hyperkalemia
- Cardiac arrhythmias
- Oligoanuria
- Fluid overload
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Supportive therapies
- Uremic syndrome
- Profound polyuria
Intravenous Fluid Therapy for AKI
- goals
- Goal: correction + maintenance of hydration, acid-base, electrolyte status
> fluid resuscitation (hypovolemia) → rehydration (dehydrated), maintenance (not eating/drinking), ongoing losses (polyuria, vomiting, diarrhea)
> maintain neutral fluid balance, i.e. total fluid in = total fluid out
<><><><><><><> - Aim for NORMOhydration
- Avoid dehydration
- Avoid overhydration
<><><><> - Diuresis ≠ maximizing GFR + renal blood flow + ↑ urinary excretion
- High fluid rate = fluid overload + organ edema + ↑ renal parenchymal pressure → ↓ renal blood flow + GFR
Assessment of Urine Output (UOP) - methods
- what else should we take into account?
- Indwelling urinary catheter & closed collection system
- Free-catch, spontaneous voiding
- Metabolic cage
- Weighing bedding & litter boxes (1 g = 1 mL)
- Serial body weights (before & immediately after voiding)
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In conjunction with hydration status: - suspect oligoanuriaàrule out pre-renal (dehydration) component
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Before concluding anuric, intrinsic AKI: - rule out post-renal (urinary obstruction, urine leakage into 3rd spaces) components
Intravenous Fluid Therapy
- fluid rates
- what do we do when euhydrated?
- Correct dehydration over 12-24 hours, close monitoring of UOP
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Once euhydrated: - adjust IV fluid rate to match urine output (q2-4h) → maintain normohydration
- measure “total in(s) & out(s)” regularly
Oligoanuria – Euhydrated Patient
- what should we do?
Fluid challenge: 10-20 mL/kg over 15 mins
- <5% dehydration = subclinical
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Assess urinary response:
- manual bladder palpation, ultrasound measurements, quantification of UOP
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If no response:
- ↓↓ IV fluid rate to match UOP only ± stop IV fluids
- insensible losses (~20 mL/kg/day) often met by IV medications, catheter flushes, nutrition
- proceed with diuretic trial…
Oligoanuria – Overhydrated Patients
- what should we do?
STOP IV fluids → proceed with diuretic trial…
- smallest possible volume to administer required medication
AKI fluid diuresis to improve GFR - efficacy, outcomes
In AKI, attempts at fluid diuresis to improve GFR are often futile and frequently result in fluid overload, which is associated with a worse outcome & higher mortality rate
Oligoanuria – Diuretic Trial
- what do we do? how does it work?
Furosemide – loop diuretic
- may initiate urine production
- 2-4 mg/kg IV 🐩, 2 mg/kg IV 🐈, follow by 0.5-1 mg/kg/hr CRI if effective
- if fail to establish urine flow: repeat IV bolus in 30 mins
- discontinue once acceptable urine production has been re-established
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Mannitol – osmotic diuretic
- ↑ intravascular volume, renal blood flow, renal tubular flow (wash out obstructive casts/debris)
- 0.5-1.0 g/kg IV over 15-20 mins
- contraindication: volume overload, cardiovascular disease → pulmonary edema
IV Fluid Plan – Polyuria
UOP may be substantial (up to 10x maintenance rate)
- important to keep up with polyuria → prevent dehydration
Life-Threatening Hyperkalemia with AKI
- what happens
- when to treat?
- goals
- Cardiac arrhythmias, neuromuscular weakness, ↓ myotatic reflexes
- [K+] not always associated with expected ECG findings, treat when > 6.5 mmol/L
<><><> - Acidemia (metabolic acidosis): outward movement of K+, inward movement of H+
- Alkalemia: inward translocation of K+ in exchange for H+
<><><> - Goal: antagonize K+ effects on myocardial cells, redistribute & eliminate K+
Cardiac Arrhythmias with AKI - what do we see? what can we do?
Severe bradycardia, atrial standstill; wide complex tachycardia, ventricular tachycardia
- no anti-arrhythmics prior to ↓ K+; treat with lidocaine → ventricular fibrillation, asystole
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10% calcium gluconate 0.5-1 mL/kg IV over 2-5 mins with ECG monitoring
- transient: cardioprotective for ~20 mins
- watch for arrhythmias
Life-Threatening Hyperkalemia - how do we treat?
Insulin-dextrose protocol
- regular insulin 0.25-0.5 U/kg IV + 50% dextrose 2-4 mL/U insulin (diluted 1:1)
- administer 1⁄4 of dextrose solution → regular insulin → remainder of dextrose solution
- 2.5% dextrose CRI
- monitor q1h: hypoglycemia, persistent hyperkalemia (repeat low dose regular insulin)
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- 50% dextrose 1-2 mL/kg IV bolus (diluted 1:1)
- Transient: address underlying cause!
Unsuccessful Medical Management of AKI
- what should we do? how to avoid?
- what will we see? reasons?
Consider early referral for:
- renal replacement therapies (RRT)
- peritoneal dialysis (PD)
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Life support treatment, no direct effect on renal recovery
- potentially reversible renal function, dialysable toxins
- oligoanuria, severe fluid overload
- life-threatening electrolyte (K+) abnormalities
- advanced uremia & hyperbilirubinemia, refractory to medical management
General Supportive Therapies for AKI
- Avoid concurrent nephrotoxic drugs
- Antiemetics
> maropitant, ondansetron - Gastrointestinal protectants
> omeprazole, pantoprazole
> famitodine - Pain management
- Early nutritional support
> high quality protein restricted diet - Phosphate binder
> sucralfate
Close Monitoring for the AKI patient
- Urine output production
- Serial reassessment of hydration status → IV fluid adjustment
- Daily fluid balance: total in(s) vs. out(s)
- Serial body weight q4-12 hr (same weighing scale)
- Respiratory rate & effort
- Serial PCV/TS, electrolyte & acid-base monitoring (K+, Na+)
- Serial creatinine
urine output production - normal vs messed up amounts
- normal = 1-2 mL/kg/hr
- polyuria =»_space; 2 mL/kg/hr
- relative oliguria = < 1 mL/kg/hr
- oligoanuria = < 0.3-0.5 mL/kg/hr
Fluid Overload
- how will we know when we see it?
- what to do?
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Acute weight gain
> anorexic patients: 0.1-0.3 kg/1000 kcal/day - NEW gallop sound, murmur (cats)
- Tachypnea, dyspnea
- Peripheral edema (jiggly dorsum, hock swelling)
- Chemosis
- Serous nasal discharge
- Pleural effusion, peritoneal effusion, +/- pericardial effusion (cats)
- Organ edema (pulmonary, GI)
<><><> - Stop IV fluid, furosemide, ± enteral hydration
Weaning of IV Fluid Therapy
- when to do it?
- considerations
- Resolved or stable azotemia ± eating or drinking
- Challenge: taper IV fluid rate by 25-50% per day
- Monitor hydration status, UOP, serial creatinine levels, serial body weights
> determine if capable of maintaining own fluid balance - Consider: esophagostomy tube
> enteral nutrition + ↑ water intake
AKI prognosis
- survival, mortality, recovery
Depends on the underlying cause of AKI - leptospirosis: > 80% survival
- NSAID toxicity: can do well
- ethylene glycol & lily intoxications: grave prognosis once in renal failure
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Mortality rates for AKI are high = ~50-60%
- oligoanuric AKI carries worse prognosis than polyuric AKI
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Renal recovery can take weeks to months
- ~60% develops CKD vs. ~40% recovers to normal renal function
