Management of Oliguria

Diagnostic LAB Approaches

• Urine analysis
• Blood urea nitrogen (BUN) and serum
creatinine
• Serum sodium
• Serum potassium
• Acid-base balance
• Complete blood count (CBC)
 Imaging studies
• Renal ultrasonography
• Voiding cystourethrography - Indicated for
suspected bladder outlet obstruction
• Radionuclide renal scanning - May be useful in the
assessment of transplant rejection and obstruction
• Chest radiography - May be indicated if pulmonary
edema is suspected
• Echocardiography – May be useful in the presence
of congestive heart failure
 Methods to asses volume status in renal patient
Method Invasive or noninvasive Comments

Of limited value but serial examinations may detect

Physical exam Noninvasive
changes in organ perfusion

Requires use of standardized measures of vascular pedicle

Chest radiograph Noninvasive width and cardiothoracic ratio. Serial chest X-ray may be
helpful in determining effects of fluid therapy

Central venous pressure Invasive Poor correlation with fluid responsiveness

Pulmonary capillary wedge

Invasive Poor correlation with fluid responsiveness
pressure

Single measures of cardiac chamber volume hard to

Echocardiogram Noninvasive
assess. Serial measures may be helpful

Esophageal doppler Invasive Not useful for continuous measurements

Vena cava diameter Noninvasive Body habitus dependent

Bioimpedance Noninvasive Not able to assess intravascular volume

Urine analysis
• In prerenal failure, a few hyaline and fine, granular casts may be observed
with little protein, or red cells. Heme-positive urine in the absence of
erythrocytes suggests hemolysis or rhabdomyolysis.
• In intrinsic renal failure, hematuria and proteinuria are prominent. Red cell
casts are characteristically observed in acute glomerulonephritis.

BUN and Serum Creatinine

• In prerenal failure, elevation of BUN levels is marked and the BUN-to-
creatinine ratio is greater than 20. The hallmark of established acute kidney
injury is a daily increase in serum creatinine levels (0.5-1.5 mg/dL daily) and
BUN levels (10-20 mg/dL daily).

Although serum creatinine levels are the criterion standard for diagnosis of
acute kidney injury, they remain an unreliable indicator during acute changes in
kidney function for the following reasons:
• Serum creatinine levels can widely vary with age, gender, lean muscle mass,
muscle metabolism, and hydration status
• Serum creatinine levels may not change until about 50% of kidney function
has already been lost
• Elevations in BUN levels can also result from steroid therapy, parenteral
nutrition, GI bleeding, and catabolic states.
Serum Sodium
• Hyponatremia is a common finding that is usually dilutional,
secondary to fluid retention and administration of hypotonic
fluids.
• Occasionally, hypernatremia may complicate oliguric acute kidney
injury and is usually a result of excessive sodium administration
(improper fluid administration or overzealous sodium
bicarbonate therapy).

Serum Potassium
• Hyperkalemia is an important complication because of reduced
glomerular filtration, reduced tubular secretion.
• Hyperkalemia is most pronounced in patients with excessive
endogenous potassium production, which occurs in
rhabdomyolysis, hemolysis.
• Hyperkalemia represents a life-threatening emergency that must
be promptly and aggressively treated, primarily because of its
depolarizing effect on cardiac conduction pathways.
Acid-Base Balance
• The impaired renal excretion of nonvolatile acids and
decreased tubular reabsorption and regeneration of
bicarbonate results in metabolic acidosis with a high
anion gap.

Complete Blood Count

• Anemia is a result of dilution and decreased
erythropoiesis.
• Patients with oliguria that is secondary to SLE may
display neutropenia and thrombocytopenia.
• Eosinophilia is consistent with allergic interstitial
nephritis. Prolonged acute kidney injury can result in
functional platelet disorders.
Renal Ultrasonography
• Ultrasonography provides important information
regarding kidney size and echogenicity, renal blood flow,
collecting system, and bladder wall.
• A Doppler study is critical in the evaluation of vascular
obstruction.

Electrocardiography
• Electrocardiography is indicated if hyperkalemia is
suspected or has been detected by laboratory tests.

Renal Biopsy
• In general, kidney biopsy is not necessary in the initial
evaluation; however, if prerenal and postrenal causes have
been ruled out and an intrinsic renal disease is suspected.
 Treatment

AKI CKD

*Management of
*Diet
*Management of HTN
electrolytes and
acid-base balance *Fluid management
*Dialysis
*Management of -HD
*Dialyisis
Hyperkalemia -PD
-IHD
-SLED *Management of Urological *Renal
-CRRT obstruction transplantation
-Acute PD
Fluid Management
• The major goal of fluid management is to
restore and maintain normal intravascular
volume. Patients with oliguric acute kidney
injury may present with hypovolemia,
euvolemia, or volume overload, and an
estimation of fluid status is a prerequisite for
initial and ongoing therapy.
.
Diuretics,

Although diuretics seem to have no effect on the outcome of established AKI, they
appear to be useful in fluid homeostasis and are used extensively. They have also been
used to reduce the requirement for renal replacement therapy. The use of isotonic
sodium chloride solution in conjunction with diuretics is debatable.

Furosemide (Lasix)
• Furosemide increases the excretion of water by interfering with the chloride-binding
cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the
thick ascending loop of Henle and the distal renal tubule. It is a potent and rapid-
acting agent with peak action at 60 minutes and a 6- to 8-hour duration of action.
• In renal failure, higher doses must be used for greater diuretic effect. Doses as high
as 600 mg/day may be needed under monitored conditions.
• Frequently, IV doses are needed in AKI to maintain urine output. IV infusions are
often helpful in intensive care settings, in which larger doses are necessary. This
method promotes a sustained natriuresis with reduced ototoxicity compared with
conventional intermittent bolus dosing.
Management of Hyperkalemia
• In practice, the definitive therapy for significant hyperkalemia accompanying
oliguric acute kidney injury frequently includes dialysis. The other forms of
therapy outlined in this section serve primarily to tide over the crisis.
• Serum potassium levels of 5.5-6.5 mEq/L should be treated by eliminating all
sources of potassium from the diet or IV fluids and administration of a cation
exchange resin, such as sodium polystyrene sulfonate (Kayexalate). Kayexalate
requires several hours of contact with the colonic mucosa to be effective, and
the rectal route of administration is preferred. Complications of this therapy
include hypernatremia and constipation.
• Emergency treatment of hyperkalemia is indicated when serum potassium
exceeds 6.5mEq/L or if peaked T waves are present. In addition to Kayexalate,
patients should receive calcium gluconate (with continuous electrocardiographic
monitoring) to counteract the effects of hyperkalemia on the myocardium.
• Uptake of potassium by cells can be stimulated by infusion of glucose and insulin
or by beta-agonists (albuterol by nebulizer). The efficacy and convenience of
nebulized albuterol has been well described in hemodialysis patients with
hyperkalemia, but it can cause tachycardia.
Management of Urologic Obstruction
• Patients with oliguria secondary to obstruction
frequently require urologic care. The site of
obstruction determines the primary therapy.
• Relief of obstruction is often followed by
postobstructive diuresis. The resultant
polyuria, hypokalemia, and hyponatremia
should be managed with vigorous fluid
replacement guided by frequent
determinations of urinary flow rate, urinary
electrolytes, and serum electrolytes.
Management of Other Electrolytes and Acid-Base Balance
• The primary treatment for hyponatremia is free water restriction; however,
a serum sodium level of less than 120 mEq/L or accompanied central
nervous system (CNS) dysfunction may require 3% sodium chloride
infusion.
• Mild metabolic acidosis is treated with oral sodium bicarbonate or sodium
citrate. Severe acidosis (pH < 7.2), especially in the presence of
hyperkalemia, requires IV bicarbonate therapy

Management of Hypertension
• Mild hypertension usually responds to salt restriction and diuretics.
Moderate, asymptomatic hypertension is most commonly treated with oral
or sublingual calcium channel blockers or with IV hydralazine.
• For patients with hypertensive encephalopathy, treatment may require
continuous sodium nitroprusside infusion with monitoring of thiocyanate
levels. Because nitroprusside therapy requires careful drip calculations and
administration, other immediate alternatives include a nicardipine drip or
labetalol. Once the hypertensive crisis has been controlled, oral long-acting
agents can be initiated.