But there has been a significant change in thinking about this entire concept. Emergency clinicians are ordering more and more CT scans without IV contrast material for a number of reasons, first among them that the addition of IV contrast material does not aid one's diagnostic acumen in many cases and because of ongoing concern of kidney injury following the use of modern dyes. CT scanners also have become so adept that vascular structures do not always require dye to be evaluated.
CT scans take so little time if dye is not used. Hospitals now use nonionic contrast agents (osmolality 290-850 mosom/kg), and some newer dyes are actually iso-osmolar. Most still use second-generation agents, such iohexol (Omnipaque), a nonionic contrast material with a lower osmolality than the first-generation agents. The low-osmolar agents are thought to be associated with a decreased incidence of renal injury among high-risk patients. No specific treatment is available once contrast-induced nephropathy develops, and management is similar to any cause of acute kidney necrosis with a focus on maintaining fluid and electrolyte balance. The best treatment is prevention.
Of course, ultrasound and MRI, in addition to CT scanning without radio contrast agents, are becoming more and more common. A transient elevation in the serum creatinine of greater than 0.5 mg/dL or greater than a 25 percent increase above baseline at 48-72 hours post-injection is generally a standard method to define contrast-induced nephropathy. The actual clinical significance of these minor elevations is likely minimal.
The literature discusses the current newer understanding of contrast-induced acute kidney injury and the value of methodologies to prevent them from occurring in the first place. I was certainly schooled in this topic, and have changed my view of the previously blindly accepted great potential for renal harm from IV contrast. It seems that the adverse kidney effects of IV contrast material are not as straightforward as previously thought. In fact, there may be no real kidney risk for any patient given IV dye for a CT scan.
Does the Current Definition of Contrast-Induced Acute Kidney Injury Reflect a True Clinical Entity?
Sinert R, Brandler E, et al
Acad Emerg Med
This study compared the incidence of acute kidney injury in patients administered intravenous contrast with a cohort that was not exposed. The retrospective study included ED patients with normal renal function who received either contrast-enhanced abdominal or chest CT. A repeat creatinine performed 48 to 72 hours was used to define kidney injury. The traditional concern is that hospitalized patients who experience contrast nephropathy experience longer hospital stays and suffer significantly higher in-hospital and long-term mortality rates. Those who survive the renal insult are then touted to be predisposed to continued loss of kidney function.
This one-year retrospective study compared 773 contrast-exposed with 2,956 contrast-unexposed patients, and limited the study population to those with an initial pre-IV contrast serum creatinine less than 1.5 mg/dL or an estimated glomerular filtration rate greater than 60 ml/min. Patients with underlying renal dysfunction did not receive contrast material. The patients in each group were matched for age, diabetes, and anion gap/lactate.
No patient required dialysis, and mortality rates were similar in both groups. Older patients did not have an increased risk for renal failure. The authors conclude that it is safe to administer IV contrast for CT scans in patients with normal renal function because of a statistically greater incidence of acute kidney injury in the contrast-unexposed group compared with contrast-exposed patients (8.9% vs. 5.7% respectively).
In short, no evidence suggested that significant acute kidney injury resulted from contrast administration in patients with previously normal kidneys. The authors found no reason to withhold contrast material because of any concern of contrast-induced acute kidney injury in those patients who had a glomerular filtration rate of greater than 60 ml/min. They stated that the definition of acute contrast-induced kidney injury in patients with normal renal function may not represent a true clinical entity and that definition warrants revision. They posit that this belief was first extrapolated with data lacking from unexposed patients and without comparing unexposed patients experiencing similar decrease in renal function from other sources.
Comment: Patients ill with a variety of diseases and conditions frequently experience kidney failure while in the hospital. One study found that more than 50 percent of hospitalized patients not given contrast material developed an increase in creatinine of at least 25%. (AJR Am J Roentgenol 2008;191:376.) Many hospitalized individuals have received a contrast CT scan in the ED, and their change in kidney function has been thought to reflect kidney injury secondary to the dye. These authors found that this was not the case when their patients with normal renal function received contrast material. I note that no patient had mention of any ameliorating interventions, such as hydration, N-acetylcysteine, or bicarbonate, interventions thought to possibly lessen kidney damage from contrast material. This article would confirm the lack of kidney injury from modern contrast material in patients with normal kidney function. Note that these patients had primarily abdominal and chest CTs, not the cardiac studies that use greater amounts of contrast material, the subset from whom much of the concern has been gleaned.
Intravenous Contrast Material-Induced Nephropathy: Causal or Coincident Phenomenon?
McDonald RJ, McDonald JS, et al
These authors retrospectively reviewed their 10-year experience of 157,000 patients who received contrast material for abdominal or thoracic CT scans from 2000 to 2010. Those who received the scans were sorted into a low-, medium-, or high-risk subgroup based on baseline serum creatinine, with less than 1.5 mg/dL given a definition of low-risk, 1.5-2 mg/dL classified as medium-risk, and greater than 2 mg/dL defined as high-risk.
As in the prior study, a serum creatinine rise of more than 0.5 mg/dL above baseline was used as a definition of contrast-induced nephropathy. The authors pointed out that a causal link between IV contrast material and nephrotoxicity has recently come under scrutiny, though the adverse nephrogenic potential of iodinated contrast material is widely accepted in the medical literature.
These authors, after making some adjustments for differences in presumed risk for contrast nephropathy, found an equivalent risk for nephropathy in hospitalized patients who did not receive IV contrast compared with those who did, regardless of baseline renal function. Their results questioned the utility of serum creatinine as a marker for dye-induced kidney injury, and question the long-held relationship between administering IV contrast material and acute kidney injury.
A similar incidence of acute kidney injury after contrast-enhanced and unenhanced scans was found by the investigators, which presumably was unrelated to the administration of intravenous contrast material. The authors claimed their large sample size permitted the inclusion of risk factors and co-morbidity thought to raise the chance for nephropathy. These findings suggest that IV iodinated contrast material may not be a cause or even a relative factor in diminished renal function after contrast material administration. They also concluded that contrast-induced nephropathy cannot be accurately determined by creatinine-derived parameters, and that acute kidney injury following contrast material is clinically indistinguishable from contrast-independent nephropathy.
Comment: This article is a fascinating study that questioned the very entity of contrast-induced nephropathy. Even patients with a high serum creatinine level did not experience kidney failure more than those whose hospital course did not include IV contrast material. They usually used lower osmolality contrast material, and a decrease in contrast nephropathy is generally thought to be associated with the low-osmolar agents. This study utilized the iso-osmolar contrast agent (iodixanol/Visipaque) if the serum creatinine was greater than 2.0 mg/dL. All others received the low-osmolar agent, iohexol (Omnipaque 300). The volume of dye used was small, 80-200 ml, followed by a 50 ml saline flush.
The authors of this article also performed a systematic review and meta-analysis that further substantiated their conclusions. (See Radiology 2013;267:119.) They performed a literature search of all articles related to nephrotoxicity following IV contrast administration. They only reviewed articles where patients exposed to IV contrast were compared with the incidence of acute kidney in unexposed patients who underwent imaging based on serum creatinine level or glomerular filtration rate changes following a procedure.
The authors identified 13 nonrandomized studies representing more than 30,000 patients, and found no difference in acute kidney injury, death rates, or need for dialysis among patients who did or did not receive IV contrast material. This pattern was observed regardless of the IV contrast type or whether the patient had renal insufficiency or diabetes. They said the very well disseminated and universally accepted relationship between the administration of IV iodinated contrast and nephropathy remains controversial.
They also claimed that documented contrast nephropathy is derived from the literature from invasive cardiographic studies of intra-arterial contrast administration, and merely suggests a cause-effect relationship. But the true incidence and severity of contrast nephropathy following an IV contrast CT study is not well established. The lack of controlled studies likely obfuscated this issue for prior investigators, and led to an overestimation of contrast nephropathy. Simply stated, these authors believe that no difference exists in the incidence in acute injury in patients who receive IV contrast and patients who do not, and noted no association in patients with renal insufficiency and diabetes mellitus or in patients who receive high-osmolality contrast medium.
Comment: These authors present a rather controversial and very remarkable, if not almost counterintuitive, conclusion. Other investigators have found that hospitalized patients who are not exposed to contrast did have increases in serum creatinine levels that were similar to those associated with a reported incidence of contrast-induced nephropathy. (AJR Am J Roentgenol 2008;191:376). Various sources of renal dysfunction encountered by hospitalized patients include fluid restriction, hypotension, nephrotoxic medications, and hemorrhage.
So how does one clinically relate to these recently published studies? Most radiologists will balk at administering IV dyes to patients with baseline renal dysfunction. It seems reasonable to proceed with contrast administration for abdominal and chest CTs when the clinical benefit of using that material is obvious. More and more, however, radiologists are performing interpretation of CT scans without oral or intravenous contrast material.
Efforts to ameliorate kidney injury with contrast material have evaluated saline hydration, bicarbonate administration, and the use of N-acetylcysteine. Results are conflicting. One would intuit finding a readily obvious benefit if an intervention were protective, but multiple studies are inconclusive and even contradictory. Initial studies on the benefits of N-acetylcysteine prompted its use, but currently no strong recommendations can be made about it to decrease renal injury. Bicarbonate use has likely not been proven to reduce kidney injury from iodinated dyes.
Apparently the most readily available and seemingly best way to decrease renal dysfunction following IV dye is the hydration with saline before and after administration. Contrast levels are highest in the urine in the first hour. The optimal dose for saline administration is unclear, but pre-contrast volume expansion in dehydrated patients appears to be a reasonable ED intervention. The administration of 300 to 1200 mls of saline before, during, and after the procedure is suggested.
Important unresolved issues concerning contrast-induced nephropathy include the actual mechanism of action, a true understanding of the relative efficacies of various prophylactic strategies, and the relative nephrotoxicity of varying iodinated contrasting agents. The pathogenesis appears to be some type of acute tubular necrosis that is not well understood, possibly a result of renal vasoconstriction or other cytotoxic effects from contrast agents. Unlike other types of acute tubular necrosis, contrast nephropathy rapidly resolves. There could be some functional change in the renal epithelium rather than frank necrosis seen from other causes of acute tubular necrosis.
The general consensus appears to be an increased risk with IV iodinated agents, with further declines in glomerular filtration rate, but the actual GFR at which a clinically significant risk occurs is not well defined. Lower doses of contrast material, general less than 100 ml, have always been unlikely to cause any renal dysfunction, especially if the creatinine and GFR are normal. Recent studies question whether there is any risk of kidney dysfunction from IV dye in any patient. Most studies defining risk factors for contrast nephropathy include patients undergoing angiography for coronary arteriogram. The risk of nephropathy with an ED-ordered contrast abdominal CT scan is low. This is apparently even true for patients with chronic kidney disease.
It would appear reasonable to eschew the use of contrast material for CT scans whenever possible, but the use of IV contrast material is not as detrimental to kidney function as previously thought. Its use may actually be inconsequential in the development of clinically significant renal failure. Exactly what can occur following the use of contrast material cannot be known with certainty, and no prospective randomized trial has yet been undertaken. The medical field seems to have accepted the unwarranted serious potential for renal harm from IV contrast material with little real scientific analysis.
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Dr. Roberts: I found that it was quite easy when doing loop drainage for abscesses to pass the loop with alligator ear forceps. I insert the forceps through the first stab wound, and then pass these to the opposite side of the abscess, tenting the skin on the other side allowing a small incision there to bring the forceps to the surface. I then grasp the loop and deliver it through the abscess, as you instructed. (EMN 2013;35:16; http://bit.ly/12n4IpU.) Seems to work well. — William G. Bell, MD, Pittsburgh, PA
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