Introduction
Critically ill patients often produce very little urine, a condition known as oliguria. It might be a sign of acute kidney injury (AKI) or a physiological reaction to hypovolemia (low body fluid levels), indicating intact glomerular and tubular function. It might also be caused by decreased glomerular filtration or tubular injury. Properly identifying and treating the cause of oliguria is crucial.
Oliguria has been defined in several different ways in the past. In the 1950s and 60s, severe oliguria was defined as producing less than 500 ml of urine in 24 hours. Since the 1970s, this threshold has been 400 ml in 24 hours.
Weight-based definitions also exist: less than 0.5 ml/kg/hour or less than 0.3 ml/kg/hour for at least 6 hours.
Although the relationship between ideal and actual body weight has not been thoroughly investigated, it is advised to use ideal body weight in order to prevent overdiagnosing AKI, especially in patients who are obese.1
From an epidemiological perspective, oliguria is defined by the Acute Dialysis Quality Initiative group as urine production of less than 0.3 ml/kg/h for a minimum of 24 hours. However, it appears that early clinical recognition of oliguria is important because any delay in treatment can result in a dangerous progression of acute kidney injury (AKI). Therefore, it is better to suspect oliguria when the urine flow rate is less than 0.5 ml/kg/h for two consecutive hours.2
Pathophysiology
It is important to determine if oliguria is the result of an underlying pathological process or a normal physiological response when examining its etiology. Causes include the following:
- Normal physiological response, with oliguria potentially arising from dehydration, fasting, or extreme physical exertion. Post-operative patients might experience short-term oliguria due to pain or nausea, which triggers hormone release that reduces urine output
- Physiological causes, which can be as a result of various factors, such as:
- Neuro-hormonal response, where stress activates the sympathetic nervous system, increasing hormones like vasopressin and aldosterone, which reduce urine production
- Reduced blood flow to the kidneys, which can be due to low blood volume or other haemodynamic issues
- Direct kidney damage, which can be caused by sepsis or other conditions that directly impair kidney function, causing blockage and reduced filtration3
Treatment by diet
A diet that is as high in carbohydrates as possible and as low in fat, potassium, and protein as is tolerable is provided to the patients. Dietary sodium restriction enables more accurate direct management of sodium. Because it helps prevent fat and protein breakdown as well as ketosis, carbohydrates are used instead of proteins and amino acids, which may have negative effects.
The patient's daily fluid allocation must be calculated taking into consideration the fluids that are part of their diet.4
The physiology of oliguiria
Any urine output value less than 0.5 milliliters per kilogram hour in adults is considered intraoperative oliguria. Urine output is influenced by more than just blood volume - it also responds to pain, nausea, surgery, and certain hormones, like antidiuretic hormone and aldosterone. In addition to volume depletion, other perioperative factors that can cause oliguria include physiological stress, intra-abdominal pressure, interstitial oedema, congestive heart failure, and medications. The degree of intraoperative oliguria is not always linked to a higher risk of postoperative AKI, despite the fact that oliguria is characterised by a continuum of decreasing urine output values.5
By understanding these aspects, healthcare providers can better diagnose and treat oliguria, improving patient outcomes.
Summary
Oliguria, or low urine output, is common in critically ill patients and can signal acute kidney injury (AKI) or other physiological conditions such as hypovolemia or stress responses. Defined as urine production of less than 0.5 ml/kg/hour for two consecutive hours, oliguria can be caused by dehydration, reduced kidney blood flow, or direct kidney damage. Treatment focuses on dietary adjustments, including low protein, sodium, and fat intake, with high carbohydrates to prevent further stress on the kidneys. Understanding the underlying causes and physiology of oliguria is crucial for timely diagnosis and treatment to prevent progression to AKI.
References
- Ostermann, M., Shaw, A. D., & Joannidis, M. (2023). Management of oliguria. Intensive care medicine, 49(1), 103–106. https://doi.org/10.1007/s00134-022-06909-5
- Rimmelé, T., & Kellum, J. A. (2010). Oliguria and fluid overload. Contributions to nephrology, 164, 39–45. https://doi.org/10.1159/000313719
- Klein, S. J., Lehner, G. F., Forni, L. G., & Joannidis, M. (2018). Oliguria in critically ill patients: a narrative review. Journal of nephrology, 31(6), 855–862. https://doi.org/10.1007/s40620-018-0539-6
- HOPPER, J. J., Jr, & PARTRIDGE, J. W. (1950). Anuria and oliguria; treatment by conservative means, case report, with determination of blood volume and Na24 space. California medicine, 73(1), 42–53.
- du Toit, L., & Biccard, B. M. (2019). The relationship between intraoperative oliguria and acute kidney injury. British journal of anaesthesia, 122(6), 707–710. https://doi.org/10.1016/j.bja.2019.03.008

