The management of acute renal failure (ARF) in critically ill patients can be divided into four major aspects:
1. prevention of ARF;
2. prevention of complications of ARF;
3. treatment with renal replacement therapy;
4. prevention of further injury to the kidney.
Each of these aspects requires separate detailed discussion. The prevention of acute renal failure
Critically ill patients are at particular risk of developing ARF. They are likely to experience hypotension because of sepsis, low cardiac output, major fluid losses, and hemorrhage. They often require treatment with drugs (aminoglycosides, amphotericin, non-steroidal anti-inflammatory drugs, radiocontrast agents, etc.) which can induce nephrotoxicity and which are often given under pathophysiological conditions which increase such toxicity. In addition, such patients are often in a state of immunological derangement which is associated with the release of renal vasoconstrictive substances and the induction of parenchymal inflammation. For these reasons, the intensivist and nephrologist must be extremely diligent in the treatment of all the above pathophysiological states and cautious in the prescription of drugs which may damage the kidney.
In this context, adequate fluid resuscitation and maintenance of a normal cardiac output are vital goals of resuscitation in all patients. In the intensive care unit (ICU), such resuscitation must always be guided by invasive monitoring techniques (central venous pressure and arterial pressure measurements at a minimum, and pulmonary artery occlusion pressure and thermodilution measurement of cardiac output in many cases).
While fluid resucitation is generally prompt in the ICU and support of cardiac output is equally aggressive, an important therapeutic goal in the prevention of renal failure, i.e. the maintenance of an adequate renal perfusion pressure, is commonly underemphasized. In fact, much experimental and clinical evidence indicates that global renal blood flow and glomerular filtration rate are 'pressure dependent' once they operate at values below their physiological autoregulation limits (mean arterial pressure of approximately 70-75 mmHg for renal blood flow and approximately 80-85 mmHg for glomerular filtration rate) ( Berstena^ Despite this well-established knowledge, lower levels of mean blood pressure are often tolerated unnecessarily in the ICU. Renal blood flow and glomerular filtration rate decrease precipitously once the mean arterial pressure falls below 75 to 80 mmHg. This decrease is not abrogated by the presence of a high cardiac output or the aggressive administration of intravenous fluids. More importantly, autoregulation of renal blood flow is lost once renal injury has occurred ( KeJieherefa/ 1987). Thus maintenance of an adequate renal perfusion pressure is even more important in the patient with early renal dysfunction ( Fig 1).
Fig. 1 The relationship between blood pressure and renal blood flow. The normal pressure-flow relationship (O) shows a steep increase in renal blood flow as the mean pressure rises to the autoregulation level. Once the autoregulation plateau is reached (mean arterial pressure of 75-80 mmHg), further increases in blood pressure do not increase blood flow to the kidney. If ARF develops, renal blood flow autoregulation fails and renal blood flow is even more dependent on adequate levels of perfusion pressure (o). As renal function recovers after ARF, the pressure-flow relationship begins to return to normal after 1 to 2 weeks (N).
While an adequate renal perfusion pressure can often be achieved with fluid resuscitation alone, several patients who have received adequate fluid resuscitation and have a high-normal to above-normal cardiac output remain hypotensive due to systemic vasodilatation and sepsis. These patients are at high risk of renal failure, and their blood pressure should be sustained to near-normal levels (> 80 mmHg) with vasoactive agents such as norepinephrine (noradrenaline), epinephrine (adrenaline), or a-dose dopamine. In addition, it is important to note that urine output and glomerular filtration rate appear to be preserved in some patients despite hypotension or a low cardiac output. These patients have maximum activation of compensatory mechanisms (afferent arteriolar vasodilatation and efferent arteriolar vasoconstriction). The administration of drugs that interfere with such compensatory mechanisms (e.g. non-steroidal anti-inflammatory drugs) can precipitate ARF.
The above physiological considerations are supported by all available clinical experience. Such experience suggests that vasopressor support in these patients results in improved renal function and increases urinary output ( Bersten .aD.d Holt, .. . 1.9.95). Animal data are also strongly suggestive of a beneficial effect of vasopressor treatment on renal blood flow during sepsis.
In all cases it is always important to consider whether increased intra-abdominal pressure may be responsible for inadequate renal perfusion pressure (renal perfusion pressure is the difference between mean arterial pressure and intra-abdominal pressure) despite adequate fluid and pressor support. Such pathophysiological increases in intra-abdominal pressure may be found in patients with intra-abdominal clot, severe unrelieved ileus, severe tense ascites, massive retroperitoneal hemorrhage, etc. Under these circumstances, renal failure will become inevitable unless such an increase in intra-abdominal pressure is relieved.
Once adequate resuscitation, maintenance of a normal cardiac output, and normalization of arterial blood pressure have been achieved, attention must be focused on making the correct diagnosis with regard to the etiology of the ARF.
If obstruction and parenchymal renal disease have been excluded, nephrotoxins have been removed, and so-called 'prerenal' renal failure has been diagnosed, attention is focused on whether additional therapeutic measures may benefit the kidney.
Such additional measures are typically thought to involve the administration of drugs with the intent of restoring renal blood flow to normal or near-normal levels or of maintaining glomerular filtration rate and urinary output, thus avoiding oliguric renal failure. Several drugs have been used and recommended for these purposes, including so-called low-dose dopamine, mannitol, furosemide (frusemide), and other loop diuretics. While there is controlled evidence that high-dose furosemide will increase urine output in patients with ARF, thus increasing the frequency of polyuric renal failure, there is no convincing evidence that any of these agents has a beneficial effect on the course of renal dysfunction.
A particular situation for the prevention of ARF is found in patients who already have renal dysfunction and are about to receive a radiocontrast agent. Radiocontrast agents are known to induce renal ischemia and medullary hypoxia, and are frequently needed for diagnostic purposes. A recent randomized controlled study
(SolomoneLaL 1994) clearly demonstrated that administration of saline to prevent intravascular volume depletion was superior to administration of saline plus mannitol or saline plus furosemide, adding further evidence against the use of so-called nephroprotective drugs.
The administration of potential nephrotoxins, such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, aminoglycoside antibiotics, glycopeptide antibiotics, amphotericin, cyclosporin A, and platinum-containing antineoplastic agents, must be closely monitored in all critically ill patients, and must occur only in situations where alternative drugs are not available and the benefit to the patient outweighs the associated risks.
Finally, the prevention of ARF requires close monitoring of renal function. Hourly urinary output measurements, daily serum creatinine and urea measurements, and regular monitoring of serum electrolytes are a mandatory part of the care of critically ill patients.
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