How to spot early warning signs of acute renal failure To prevent ARF, choose contrast agents (and contrast volumes) carefully by Deborah Gesensway
Published in the July 2008 issue of Today's Hospitalist
This is the second in a three-part update on critical care medicine for hospitalists
Because even mild renal failure can have devastating effects on critically ill patients, hospitalists need to be able to not only spot signs of trouble early on, but avoid making a bad situation worse through poor treatment choices.
At the Society of Hospital Medicine annual meeting this spring, Kathleen D. Liu, MD, who is assistant professor of medicine, nephrology and critical care at the University of California, San Francisco, painted a somber view of acute renal failure (ARF) in hospitals.
“A very small change in creatinine is associated with an increase in death.”
–Kathleen D. Liu, MD University of California, San Francisco
condition, also known as acute kidney injury, is so common in critically ill patients that up to 30% of patients may experience a 0.3 mg/dL or greater increase in serum creatinine during their hospitalization.
These patients have a six-fold higher mortality risk compared to patients who do not have acute renal failure. About 13% of patients experience an even higher—0.5 mg/dL—creatinine increase.
“What we think of as a very small change in creatinine,” said Dr. Liu, “is associated with an increase in death.”
To detect renal failure, Dr. Liu said that hospitalists need to first know a patient’s baseline creatinine level. They also need to remember that even “normal” levels may in fact be masking “significant renal insufficiency,” particularly in the elderly.
Another key, she said, is to remember that changes in creatinine reflect fluctuations in glomerular filtration rate (GFR), which is a late manifestation of renal injury.
While detecting and preventing renal failure is challenging, there are a number of strategies hospitalists can use to avoid hospital-acquired ARF. These include preventing hypoperfusion and steering clear of nephrotoxic medications when possible in patients at risk.
Nephrotoxic medications include NSAIDs, aminoglycosides, amphotericin, ACE inhibitors and angiotensin receptor blockers, but the area that presents the biggest challenge is radiocontrast dyes. According to Dr. Liu, contrast-induced nephropathy accounts for about 10% of all hospital-acquired ARF. And if the contrast-induced injury is so severe that dialysis is required, she said, in-hospital mortality rates spike above 35%.
Patients most at risk for developing contrast nephropathy include older individuals and people with chronic kidney disease, diabetes, hypertension or heart failure. While there may not be much you can do about these risk factors, your medical decisions can modify other potential sources of risk. You can avoid the use of ionic, high osmolality contrast agents, for example, and keep the volume of contrast to a minimum.
No clear evidence
Despite “a flurry of papers in the literature in the last five to seven years,” Dr. Liu said, experts still sharply disagree about what to do to avoid contrast nephropathy.
Studies of different interventions, including N-acetylcysteine and hydration with bicarbonate, have been promising. But those studies have all been small, she said. They’ve also relied on different definitions of ARF and looked at different patient populations.
The good news is that “most of the interventions seem to be relatively safe. They may also be most effective in reducing the risk of contrast nephropathy when used in combination.
A number of studies have found that giving patients doses of N-acetylcysteine with contrast can reduce risks of contrast nephropathy for many patients. But Dr. Liu pointed out that these studies have looked only at patients going for CT or cardiac catheterization who are not critically ill. It’s not clear what effect N-acetylcysteine has on other disease states such as sepsis.
In terms of administering IV fluids that contain bicarbonate for pre-contrast hydration, Dr. Liu cautioned that these fluids should be used carefully in patients with a respiratory or metabolic alkalosis and in those at risk for hypokalemia.
Limited treatment options
One reason that prevention is so critical, Dr. Liu said, is that treatment options for hospital-acquired ARF are limited. Treatments that have been tried but not shown to have much benefit include renal dose dopamine, atrial natriuretic peptide, insulin-like growth factor, fenoldopam, theophylline and calcium channel blockers.
Because loop and osmotic diuretics play an important role in managing volume overload, the thinking is that they also can help ARF patients. But as Dr. Liu explained, “there are no clinical trial data to base our practice on.” In addition, she said, two large observational studies of diuretic use in ARF “have been contradictory.”
In her personal practice, Dr. Liu sometimes uses diuretics to maintain fluid balance and prevent some complications of volume overload. But in the ICU, she said, “your threshold for initiating dialysis for volume overload in the setting of acute renal failure should be low.”
And if a patient’s renal failure is so bad that dialysis is called for, the newest data show that neither continuous nor intermittent hemodialysis works better than the other. Dr. Liu predicted that a new hybrid dialysis modality called slow low-efficiency daily dialysis (SLED) will find wider use in the ICU. “With SLED, fluid removal is slower than with intermittent dialysis,” she said, “yet the technique does not require 24-hour care like the continuous modalities.”
Deborah Gesensway is a freelance writer who covers U.S. health care from Toronto, Canada.
Revisiting the role of steroids in ARDS treatment
EXPERTS AT THE CRITICAL CARE PRESESSION held at the Society of Hospital Medicine annual meeting pointed out that there’s another area of critical care medicine where hospitalists can make a bad situation worse with poor treatment options: acute respiratory distress syndrome (ARDS).
With ARDS, the challenge is figuring out what to do. For 30 years, study after study has tried—and failed—to find a cure for the condition. “There are no magic bullets for this syndrome,” said B. Taylor Thompson, MD, associate professor of medicine at Harvard Medical School and director of the medical ICU at Massachusetts General Hospital.
And while physicians have in recent years looked to steroids to treat ARDS, the drugs have been overused. At the same time, results from the latest round of studies have led Dr. Thompson to have “diminished enthusiasm for steroids.”
He acknowledged that giving methylprednisolone to patients with ARDS—particularly early in its course—does seem to help in the short term, improving lung injury scores and helping patients come off ventilators faster. But these benefits tend to fade over time.
“Is this because steroids were tapered and ARDS came back and we need to give the drug longer?” asked Dr. Thompson. “Or did these patients suffer late complications of steroids such as neuromuscular weakness or secondary infections? I don’t think we know.”
In addition, Dr. Thompson wonders if steroids are “simply treating suboptimal practices,” such as the lung injury and inflammation from mechanical ventilation with high tidal volumes.
While steroids “improve some aspects of the disease,” he said, “they don’t appear to cure it.” If anything, he explained, the role of steroids is in early ARDS only. Starting the drugs after 14 days may actually increase patients’ risk of death.
That’s why Dr. Thompson recommended that hospitalists reserve steroids for “a subset of patients with severe ARDS who are free from infection and who are not responding to other forms of care.”