Oliguria

Description, Causes and Risk Factors: Oliguria is defined as passing a reduced urine volume. It is a clinical characteristic of AKI (acute kidney injury). Oliguria is defined as a urine output that is:
  • Less than 1 mL/kg/hour in infants.
  • Less than 0.5 mL/kg/hour in children.
  • Less than 400 mL/day in adults.
Oliguria affects people of all ages. It is more common in neonatal and older age groups because of comorbid conditions and is more common in early childhood because of the high incidence of illnesses that lead to dehydration. The pathological processes involved are either pre-renal, renal or post-renal. Pre-renal problems account for approximately 70% of outpatient cases of acute kidney injury (AKI) and up to 60% of hospital-based cases. Oliguria is rarely found in CKD (chronic kidney disease).
  • Pre-renal causes include may include dehydration, vascular collapse, low cardiac output.
  • Renal problems are associated with structural renal damage, e.g. acute tubular necrosis, primary glomerular diseases or vascular lesions.
  • Post-renal causes are any mechanical or functional obstruction to the flow of urine. The most common cause is a blocked catheter. This usually responds to release of the obstruction.
Oliguria can have many causes. Some are overt and apparent, such as septic shock, whereas others are concealed and subtle, such as myoglbuline release or drug toxicity. The main functional derangement in patients with acute oliguria is a sudden and severe decrease in the glomerular filtration rate (GFR), sufficent to result in increase in the plasma urea and creatinine concentratons, retention of salt and water, and the development of the acidosis and hyperkalemia. Urine output is a function of glomerular filtration and tubular secretion and reabsorption. Glomerular filtration is directly dependent on renal perfusion, which is a function of three determinants: Ciruclating blood volume, cardiac output, and renal perfusion pressure which depends on arterial pressure and renal vascular resistances. The intra-renal vasculature is capable of preserving glomerular filtration rate (GFR) in the face of varying systemic pressure through important neurohumoral autoregulating mechanisms that affect the affarent and efferent arterioles modulating the renal perfusion pressure. The renin-angiotensin aldosterone system is perhaps the most significant one. The relation between urine output and renal function is complex. Oliguria may indeed be more profound when tubular function is intact. When volume depletion and hypotension occur, vasopressin secretion is strongly stimulated and, as a consequence, the distal tubules and collecting ducts become fully permeable to water. Concentrating mechanisms in the inner medulla are also aided by low flow through the loop of Henle and thus, urine volume is minimized and urine concentration maximized. Conversley, when the tubules are injured, maximal concentrating ability is impaired and urine volume may even sometimes be normal. These phsyiologic effects from the basis of clinical rules to distinguish prerenal from renal oliguria. As described, a high urine osmolality coupled with a low urine Na in the face of oliguria and azotemia is strong evidnce of intact tubular function. However, this situtation should definately not be interpreted as benign or even as prerenal azotemia since intact tubular function may also be seen with various forms of disease such as glomerulonephritis. Sepsis, the most common condition associated wiith AKI in the ICU, may also alter renal function without any characterstics changes in urine indices. Oliguria indicates either an important reduction in GFR related to a decreased renal perfusion or a mechanical obstruction to urine flow. Reduction in GFR linked to decreased renal perfusion can be related to the following conditions:
  • Absolute decrease in blood volume due to trauma, hemorrhage, burns, diarrhea or sequestration of fluid as in pancreatitis or abdominal surgery.
  • Relative decrease in blood volume in which the primary disturbance is an alteration in the capacitance of the vasculature due to vasodilation. This is commonly encountered in sepsis, hepatic failure, nephrotic syndrome, and use of vasodilatory drugs including anesthetic agents.
  • Decreased cardiac output that can happen in many clinical situations.
  • Decreased renal perfusion pressure that may be due to structural causes such as thromboembolism, atherosclerosis, dissection, inflammation (vasculitis especially scleroderma) affecting either the intra or extrarenal circulation. Although renal arterial stenosis present as subacute or chronic renal dysfunctions, renal atheroembolic disease can present as AKI with acute oliguria. Renal atheroemboli usually affects older patients with a diffusive erosive atherosclerotic disease. It is most often seen after manipulation of the aorta or other large arteries during arteriography, angioplasty or surgery. This condition may also occur spontaneously after treatment with heparin, warfarin or thrombolytic agents. Drugs such as cyclosporin, tacrolimus and ACE inhibitors cause intrarenal vasoconstriction resulting in reduced renal plasma flow. Rarely, decreased renal perfusion may also occur as a result of an outflow problem such as renal vein thrombosis or abdominal compartment syndrome which is a symptomatic organ dysfunction that results from an increase in intra-abdominal pressure.
  • Abdominal compartment syndrome leads to AKI and acute oliguria mainly by directly increasing renal outflow presure, thus reducing renal perfusion. Other possible mechanisms decreasing renal perfusion pressure include directly parenchymal compression, is the primary mechanism of renal dysfunction. Genreally intra-abdominal pressure can lead to oliguria and prssure usually lead to anuria.
Symptoms: Generally, a key symptom of oliguria is a decreased amount of urine being produced and excreted. Additional symptoms vary depending on the type of oliguria present. Signs of physiologic oliguria include dehydration, pale mucous membrane, a weak pulse, a rapid or irregular pulse, and a history of fluid loss (through excessive vomiting or diarrhea, for example). Signs of pathologic oliguria typically include a history of progressive kidney disease with symptoms such as poor appetite and weight loss. Symptoms of oliguria may be observed during a physical examination, with revealing signs such as fluid infiltration into the tissues surrounding the urinary tract, and pain in the abdomen on palpation. Diagnosis: Findings will vary according to the cause. The patient may be very unwell - extremely breathless, pale, clammy and shut down peripherally with an unrecordable blood pressure.
  • There may be signs due to acute kidney injury (AKI), e.g. edema, anemia.
  • Signs of congestive heart failure, e.g. gallop rhythm and hepatomegaly.
  • Hypertension may be present.
  • Signs of the underlying disease, e.g. a butterfly rash on the face and joint swelling suggest systemic lupus erythematosus.
Your doctor may want to perform a number of tests to find the cause of the decrease urine production:
  • Urinalysis: Urine is analyzed in the laboratory to look for protein, white cells and red cells to identify a kidney or bladder infection, or kidney inflammation (glomerulonephritis).
  • Urine culture: In this test, a sample of urine is monitored to see if bacteria grow. This test is used to confirm a kidney or bladder infection.
  • Intravenous pyelogram (IVP): In this x-ray test, a dye (also called a contrast medium) is injected into an arm vein. The dye collects in the kidneys and is excreted in the urine, providing an outline of the entire urinary system. An IVP is particularly helpful for identifying kidney stones, though other problems, such as a tumour, can be detected with this test.
  • Ultrasound: This test uses sound waves to help establish whether a kidney mass is a noncancerous (benign), fluid-filled cyst or a solid mass, such as a cancerous tumour. Ultrasound also can identify kidney stones.
  • Computed tomography (CT) scan of the abdomen and pelvis: In a CT scan, a modified X-ray beam produces body images at different angles, offering a three-dimensional look at the inside of the kidneys, abdominal organs and pelvic organs. This test often is done with an injection of contrast dye, combining the features of an IVP and CT. When done this way, the test also is called a CT urogram.
  • Cystoscopy: In this test, the doctor inserts a flexible telescope into the urethra and passes it into the bladder to inspect the bladder lining for tumours or other problems. This test usually is done with local anaesthesia and sedation.
  • Blood tests: These can check for signs of urinary tract infection, renal failure, anemia (which often accompanies kidney problems), bleeding disorders, or abnormally high levels of blood chemicals that can encourage the formation of kidney stones. Additional testing for conditions causing kidney inflammation (such as auto-immune diseases) may be recommended, depending on the findings of the routine blood and urine tests.
Treatment: Treatment of oliguria will depend on the cause. Most causes of reduced urine production can be reversed, or at least improved. A catheter may be placed in the urinary bladder to relieve an obstruction and to assist with careful measurement of urine output. Some patients will need to be hospitalized for and given fluids through a drip if they are very dehydrated. Drugs which may be toxic to the kidneys may need to be stopped or changed. If there is a problem with the kidneys themselves, dialysis may be needed. Patients may need to be seen by the relevant specialists - the renal or urology doctors. Patients with oliguria secondary to obstruction, frequently require urological surgery, e.g. nephrostomy. Percutaneous nephrostomy is a simple technique for temporary drainage of an obstructed kidney. Under local anesthesia, a ureteric catheter is passed through a needle into the renal pelvis and is connected to a drainage bag. NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.  

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