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Magdy M Khalil, MD, EDIC Prof. Pulmonary& Critical Care Medicine
Challenges in RICU: Oliguria
Oliguria: causes
Pre-renal (Hypo-perfusion) Hypovolemia ↓COP Relative hypovolemia
(vasodilatation in response to inflammation)
Post-renal Obstruction of the bladder neck, neurogenic
bladder, or therapy with anticholinergic drugs Blood clots, calculi Urethritis with spasm
‘Intrinsic’ renal failure Pre-renal failure. Allergic interstitial nephritis Autoimmune pulmonary- Renal syndromes
Oliguria : UO≤ 0.5 mL/kg/hAnuria : UO< 50 mL /d
AKI: Definition
Non-oliguric AKI
AKI: Diagnosis
Comprehensive history, Observation chart, Clinical examination, and A review of recent
investigations and drug therapies
• R/O obstruction
• Consider pre-renal
• Think of renal
AKI: Clinical examination
Full bladder/patent catheter Neck veins Signs of hypovolemia:
tachycardia, dry mucous membranes, hypotension, low CVP, peripheral hypoperfusion (altered mentation and
cold clammy skin with delayed capillary return)
Heart
AKI: Investigations
AKI biomarkers S. creatinine NGAL (neutrophil gelatinase-associated lipocalin), IL-
18, KIM-1, Cystatin C, and L-FABP
BUN/creatinine (>20 ?pre-renal, <10-15?ATN) Urine: concentrated, SG>1.018, osmolality >350
mosm/l; urine Na <10 mmol/l and the FeNa<1%........ ?pre-renal
Ultrasound
AKI: Management
Ensure a non-obstructed outlet, Treat underlying illness, Maintain an adequate renal perfusion,
correction of fluid depletion reversal of hypotension
Avoid nephrotoxic agents, Adjust dose of renally excreted drugs, and Renal replacement therapy (RRT) should
an indication arise.
AKI Management: Fluid therapy
Type: crystalloids vs colloids (high MW hetastarch×)
Rate: 10–15 ml/kg (large bore cannula)
End points: MAP (65-90 mmHg), CVP (8-12 mmHg), pulse pressure variation, CO, ScvO2/SvO2, PAOP, UO, lactic acidosis, and skin perfusion. RI
Safety: hypervolaemia is avoided
Fluids should be given early & targeted
1) Type ,2) Rate, 3) End
points, 4) Safety
limits
AKI : Vasoactive and inotropic drugs
Vasopressors : norepinephrine phenylephrine low-dose vasopressin, terlipressin
Ino-constrictors: epinephrine dopamine
Inodilators: Dobutamine dopexamine
Livosimendan Chronotropy Intra-aortic balloon counterpulsation Natruritic peptides
The choice of drug should be driven by hemodynamic characteristics of the patient
Low-dose dopamine “renal dose” 1–3 mcg/kg/min produces preferential
dopaminergic (and β-adrenergic effects) over α-adrenergic actions (>5 mcg/kg/min) and thereby causes renal vasodilation and increases urinary output.
Improve UOP but confers no significant protection from renal dysfunction
Fenoldopam mesylate is a selective dopamine α-1 receptor agonist that can improve renal blood flow without increasing cardiac output
AKI: Diuretics
Diuretics have traditionally been used to ‘convert’ the oliguric state to non-oliguric…..? ATN.
The use of diuretics should be restricted to the treatment of volume overload and occasionally hyperkalaemia
Caution is advised as there is reasonable concern that excessive reliance on diuretics might delay initiation of RRT.
AKI: RRT
Clinical uraemia, Severe hyperkalaemia, Persistant acidosis, and Non-responsive volume/fluid overload
Early vs late!
AKI: Dose adjustments
Nephrotoxics : avoid Loading dose: OK Maintenance: ↑intervals/ Dialysable vs non
dialyasable Creatinine clearance ? Dilution effect of FT !
AKI: Contrast nephropathy
Prevention: Acetyl cysteine Bicarbonate Theophylline Hydration
Avoid if unnecessary !
• CVP, PCWP, CI
• Bl. chemistery
• Urine analysis
• Fluid resuscitation
• Vasopresors• Inotropes
Exclude volume overload
Diuretics
Exclude obstruction
• Diagnostic workup
• ? Diuretic• ?RRT
Pre-renal?
• U Catheter/flush
• US
Hypovolemia
HF
• Inotropy• Inodilation• Specific
therapies
Management of oliguria/anuria
Response
Adjust therapy
Renal?
Concurrent pathology
