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Changes in urine output (UO) encompass a variety of complaints, the most common being a decrease in UO in a postoperative patient because of changes in intravascular volume. Also considered in this chapter are other causes of decreased UO, increased UO, and blood in the urine. Components of these evaluations also are covered in other chapters where indicated. The function of the kidney may be divided into two major categories: fluid management and solute management.
UO is considered one of the three major indicators of end-organ perfusion (remember from Chapter 12 : UO, mental status, and skin temperature). In postoperative patients, a decreased UO must be considered a decrease in intravascular volume until proved otherwise because of the frequency of this occurrence and because of the seriousness of underestimating fluid resuscitation in a sick patient.
Remember that the postoperative or gravely ill patient has undergone neuroendocrine changes that help retain fluid and that third spacing of intravascular fluid is to be expected.
How is the UO being measured?
Indwelling urinary catheters give the most reliable estimates of hourly output but are not always clinically appropriate. Routine intake and output (I/O) measurements without catheters can over- or underestimate UO volumes by a factor of close to 100%.
What are the current trends over the past 2 to 3 hours, and what is it over the past 24 hours?
Oliguria is defined as less than 400 mL/day (<20 mL/hour). Anuria is defined as less than 50 mL/day. Great variances in hourly output suggest collection errors or postrenal obstruction.
Have there been recent changes in laboratory studies including those for potassium, creatinine (Cr), blood urea nitrogen (BUN), and urinalysis (UA)?
Has the patient undergone a surgical procedure, and if so, how long ago was it performed?
Pay special attention to surgeries involving bladder, ureters, or kidneys, including renal transplants.
Also be mindful that ureters may be damaged in any pelvic or extraperitoneal surgery.
Are there any other symptoms, including abdominal pain, fever, or dysuria?
Are there any changes in vital signs?
If an indwelling urinary catheter (Foley) is present, it may be flushed gently with 20 to 30 mL normal saline (NS) to dislodge sediment or clots. Check with the chief resident or the attending physician before flushing a catheter in place after surgery on the bladder or urinary tract.
Take steps to evaluate the hydration status of the patient. Repeat taking the vital signs and order orthostatic blood pressure (BP) measurements.
If the patient is immediately postoperative, and fluid shifts out of the intravascular space are clinically apparent, a fluid bolus of 500 mL crystalloid is appropriate; note that the fluid status of a patient must be evaluated (see Chapter 12 ).
If the patient is stable and comfortable, 30 to 60 minutes is appropriate. If there is a significant change in vital signs or symptoms, the patient must be evaluated immediately.
What are the causes of decreased UO?
In the postoperative patient, intravascular fluid deficit is such a common cause of decreased UO that there is a tendency to believe that this is always the case. The fluid status should be quickly assessed, but do not forget to evaluate for other causes of oliguria. Decreased UO may be conveniently divided into three categories. Pre-renal causes of oliguria are often a result of poor kidney perfusion. Renal causes of oliguria include the major renal pathologies and result in poor kidney function (i.e., urine formation). Postrenal causes of oliguria often are a result of external forces that block the flow of urine anywhere along the tract from the kidney to the outside world. These are listed in Table 33.1 .
Prerenal | Renal | Postrenal |
---|---|---|
Volume Depletion | Glomerular Nephritides | Ureteral Obstruction (Must be Bilateral) |
Third spacing | Acute glomerulonephritis | Retroperitoneal mass |
Hemorrhage | Vasculitis | Sloughed papillae |
Gastrointestinal losses | Malignant hypertensive nephropathy | Strictures/valves |
Renal losses | Renal thrombosis | Stones, clots |
Poor Cardiac Output | Tubular Interstitial | Bladder N eck O bstruction |
---|---|---|
Congestive heart failure | Pyelonephritis | Prostatic hypertrophy |
Tamponade | Hypercalcemia | Tumor |
Myocardial infarction | Multiple myeloma | Sphincter spasm |
Pulmonary embolus | Acute interstitial nephritis | Strictures/valves |
Shock/Sepsis | Acute Tubular Necrosis | Urethral Obstruction |
Hepatorenal Syndrome | Postischemic Injury | Strictures/Valves |
Prolonged vasopressor use | Bladder Rupture | |
Nephrotoxic Agents | Blocked Catheter | |
Antibiotics | ||
Contrast dye | ||
Anesthetics | ||
Nonsteroidal antiinflammatory drugs | ||
Chemotherapeutic agents |
Vascular Problems | ||
---|---|---|
Emboli | ||
Renal vessel thrombosis |
Remember that renal and prolonged pre- and postrenal causes of oliguria can lead to azotemia.
Hypotension and shock
Acute renal failure
This may require dialysis for treatment
Hyperkalemia
Review trends in vital signs (VS) of the past 24 to 48 hours. What is the HR? Is the patient increasing tachycardic? Have there been any episodes of low BP?
Review the fluid balance.
What is the patient’s current weight versus admission (or clinic) weight?
Has UO changed? When did this change begin?
Has the patient required diuretics?
Physical obstruction may be associated with abdominal discomfort, agitation, and sensation of needing to urinate. A serious deterioration of clinical status including neurologic changes or metabolic derangements may indicate hypotension or acute renal failure.
Look for evidence of dehydration. Resting tachycardia or postural changes in pulse rate (a drop of 15 beats/minute) or BP (a drop in systolic BP [SBP] of 15 mm Hg or any decrease in diastolic BP [DBP]) indicate decreased intravascular volume. This is most likely because of under-resuscitation, but be mindful of early sepsis or cardiogenic shock.
Support cardiac output and perfusion.
A fluid bolus is indicated for patients who are intravascularly depleted.
Determine cause of decreased UO.
Once this is determined, the management is more clear.
Is there a condition that would predispose a patient to decreased UO? (See Elevator Thoughts.)
Review trends in UO and I/Os, and review changes in weight.
Review recent laboratory studies trends.
VS: | Tachycardia or postural BP changes (dehydration) | ||||||||||||||||||||||||||||||||||||||||||||||||
MS: | Decreased mental status (decreased perfusion) | ||||||||||||||||||||||||||||||||||||||||||||||||
HEENT: | Dry or sticky mucous membranes and flat neck veins (dehydration) | ||||||||||||||||||||||||||||||||||||||||||||||||
Full neck veins (tamponade) | |||||||||||||||||||||||||||||||||||||||||||||||||
Resp: | Rales and decreased aeration (fluid overload and congestive heart failure [CHF]) | ||||||||||||||||||||||||||||||||||||||||||||||||
Abd: | Pain and distention (obstruction of urinary tract and urinary tract infection [UTI]) | ||||||||||||||||||||||||||||||||||||||||||||||||
GU: | Dysuria (UTI) | ||||||||||||||||||||||||||||||||||||||||||||||||
Skin: | Decrease in warmth or turgor, and dry axilla (dehydration) | ||||||||||||||||||||||||||||||||||||||||||||||||
Itching (azotemia) | |||||||||||||||||||||||||||||||||||||||||||||||||
Rectal: | Enlarged prostate or mass | ||||||||||||||||||||||||||||||||||||||||||||||||
Tubes: | Blocked urinary catheter | ||||||||||||||||||||||||||||||||||||||||||||||||
Additional tests: |
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To differentiate renal causes from prerenal causes, calculate the fractional excretion of sodium (FENa) as follows:
U Urine
P Plasma
Cr Creatinine
V Urine volume
As the urine volume cancels out, a simplified formula is:
This is the ratio of Na + excreted over Na + filtered. A FENa less than 1% is indicative of pre-renal causes of renal failure. A FENa greater than 1% is indicative of renal causes of failure.
This is the most common etiology.
Confirm with physical examination and laboratory studies.
Fluid bolus with 500 mL crystalloid; may repeat if not effective.
If, after two fluid boluses, no effect is noted, reevaluate fluid status. Be cautious in elderly patients, those with CHF or atrial fibrillation (AF) as the excess volume cannot be easily tolerated and can further exacerbate any pump issues. Add invasive monitoring (central venous pressure [CVP], indwelling urinary catheter, and Swan-Ganz catheter), as necessary.
Monitor rehydration, as needed, with frequent vital sign checks, UO, and electrolyte evaluations.
Order daily weights and strict I/O measurements.
Rule out myocardial infarction (MI), as necessary.
If CHF, evaluate as directed in Chapter 28 ; evaluate oxygen status, and begin diuresis, as follows:
Furosemide (Lasix) 20 to 80 mg intravenously (IV) over 2 to 5 minutes. The dose may be doubled and administered every hour as needed to a total dose of 400 mg if no response is noted. Note that that furosemide lasts 6 hours so that initial responses to doses will need to be evaluated over the course of hours. Do not expect immediate results. Doses of greater than 100 mg should be given slowly (<4 mg/minute) to avoid ototoxicity. Also use caution when used in conjunction with aminoglycoside antibiotics.
Hydrochlorothiazide (a thiazide diuretic) 25 to 50 mg PO or metolazone (Zaroxolyn) 2.5–5 mg PO may be added once or twice a day to furosemide therapy (a loop diuretic) for more effective diuresis. We do not frequently use metolazone in practice.
If furosemide therapy is ineffective, consider use of chlorothiazide (Diuril; a thiazide diuretic) 250 mg IV every 6 hours, ethacrynic acid (Edecrin) 50 mg IV every hour for 2 doses or bumetanide (Bumex) 1 to 10 mg IV over 1 to 2 minutes.
Monitor diuresis, as needed, with frequent checks of vital signs and evaluations of electrolytes.
Supplemental potassium (K + ) may be necessary with massive or prolonged diuresis.
This is most likely if UO is absent or is fluctuating widely.
Place a urinary catheter if one is not already in place.
Note the postvoid residual. If the residual volume is greater than 400 mL and the discomfort is relieved, leave the catheter in place and reassess in 1 to 2 days. This will give the distended bladder muscles a chance to recover function. Additionally, prescribe tamsulosin (Flomax) 0.4 mg PO every day to help with relaxation of the smooth muscle and improve urine flow.
Always consider when inserting a urinary catheter in a patient with a cardiac murmur. Note that in the past, there was great concern over subacute bacterial endocarditis prophylaxis in a patient with a cardiac murmur undergoing a genitourinary (GU) procedure. Current guidelines do not recommend antibiotic prophylaxis for those undergoing a GU procedure (i.e., Foley catheter insertion).
If a urinary catheter is already in place, flush with 20 to 30 mL sterile NS.
This must be done with extreme caution in the setting of recent bladder or kidney surgery. If the catheter will not flush, replace with a new catheter.
Make sure the catheter is not clamped for some reason (as after an abdominal or pelvic computed tomography [CT]).
Look for nonbladder causes of postrenal oliguria such as stones or mass externally obstructing the urinary tract.
Order daily weights and strict I/O measurements.
Confirm with physical examination and laboratory studies.
Consult specialists, as necessary.
Order daily weights and strict I/O measurements.
Manage associated problems.
Hyperkalemia
Limit exogenous K+. Place on continuous cardiac monitoring. Treat severe hyperkalemia as outlined in Chapter 12 .
Calcium gluconate 5 to 10 mL of a 10% solution IV over 2 minutes.
This is symptomatic relief only to stabilize neuromuscular and cardiac effects of hyperkalemia and does not alter the concentration of potassium in the serum. Its effects last only 1 hour.
50% dextrose in water, 50 mL IV followed by regular insulin 5 to 10 U effects a shift of the extracellular potassium to intracellular. Its effects last 1 to 2 hours.
Sodium bicarbonate 1 ampule (44.6 mmol) IV also effects a shift of potassium from the extracellular to the intracellular space.
The glucose/insulin/bicarbonate therapies, as follows, may be combined in an IV bag.
1000 mL 10% dextrose in water + 3 ampules of sodium bicarbonate + 20 U regular insulin to run at 75 mL/hour until the desired K + level is reached.
Sodium polystyrene sulfonate (Kayexalate) 15 to 30 g (4 to 8 tsp) in 50 to 100 mL of 20% sorbitol PO every 3 to 4 hours or in 200 mL 20% sorbitol of 20% dextrose in water rectally (PR) by retention enema for 30 to 60 minutes every 4 hours.
This is chelation therapy and is the only treatment listed here that will actually remove potassium from the body. In the absence of functioning kidneys, the only other option is hemodialysis, which can remove up to 25 to 30 mEq/hour.
Metabolic acidosis
Evaluate with arterial blood gas and serum bicarbonate levels ([HCO3−]) and treat as necessary (see Chapter 12 ), as follows:
Mild: pH 7.30 to 7.35
Moderate: pH 7.20 to 7.29
Severe: pH <7.20
Mild and moderate acidosis generally requires no specific therapy short of reversal of the underlying cause. Severe acidosis that results in decreased mental status, hyperventilation, cardiac abnormalities, and hypotension is treated with sodium bicarbonate as determined by the following formula:
Bicarbonate required (in mmol) = (wt in kg) (0.4) (desired [HCO 3 − ]) – (measured [HCO 3 − ])
Replace bicarbonate slowly, over 24 hours (i.e., one-half to one-third of the deficit in the first 6 to 12 hours with the remaining deficit replaced in the remaining 12 to 18 hours). The usual desired [HCO3−] is generally 15 mE/L. Remember that the goal of bicarbonate therapy is not to normalize the pH but rather to reverse the physiologic effects of acidosis. This usually occurs when the pH is greater than 7.20. Remember also that severe acidosis is also associated with hyperkalemia, as intracellular K + is exchanged with extracellular hydrogen ions.
Fluid overload
Treat with diuretics as listed above. If the kidneys are not sufficiently excreting free water despite diuretic therapy, there are only two ways to decrease the total body water:
Decrease the input by restricting oral and IV intake of fluid to minimum
Fluid reduction by dialysis
Make sure the patient is oxygenating well. Treat symptoms of CHF as outlined in Chapter 28 .
Sit the patient up to allow maximum aeration of the lungs.
Morphine sulfate 2 to 4 mg IV every 5 to 10 minutes up to 10 to 12 mg will pool the blood in the splanchnic circulation and decrease pulmonary edema.
Hold morphine sulfate treatment if symptoms of decreased respiratory drive or hypotension are apparent.
Reverse the effects of morphine sulfate as necessary, with naloxone hydrochloride 0.2 to 2 mg IV, IM, or subcutaneously (SC) to a total of 10 mg. Note that the half-life of naloxone effect is shorter than that of most narcotics and that repeat doses may be necessary.
Nitroglycerin ointment 2.5 to 5.0 cm topically every 4 hours.
Nitroglycerin tablets 0.3 to 0.6 mcg sublingual (SL) every 5 minutes or nitroglycerin spray 1 puff every 15 minutes may be used if ointment is not available. Hold nitroglycerin for SBP of less than 90 mm Hg.
Adequate function of nitroglycerin is generally confirmed by a headache that usually responds to acetaminophen (Tylenol and others) 350 to 1000 mg PO every 4 hours as needed. Diuretic therapy as outlined earlier.
Uremia
This is manifested by elevated BUN with symptoms of decreased mental status, pericarditis, or seizures. It is treated with hemodialysis.
Stop any nephrotoxic medications (nonsteroidal antiinflammatory drugs and aminoglycosides), and adjust the doses of renally excreted medications.
Limit magnesium- and aluminum-containing medications.
Determine if the patient requires dialysis. The following are indications for dialysis:
Fluid overload unresponsive to diuretics and resulting in CHF or edema
Hyperkalemia, severe and symptomatic, with serum K + at 6 to 8 mmol/L
Metabolic acidosis, severe, acute, and symptomatic, pH of less than 7.2
Uremia, severe with symptoms of decreased mental status, pericarditis, or seizure, and BUN at greater than 35 mmol/L
A nephrologist should be consulted to confirm the need for dialysis and to arrange the therapy.
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