Cardiac Catheterization - Research Paper Example

? PREVENTION OF CONTRAST-INDUCED NEPHROPATHY DURING A CARDIAC CATHETERIZATION BY MARQUETTA HARDIMAN-RAVENELL OGMT-330 Prevention of Contrast-Induced Nephropathy during Cardiac Catheterization Cardiac catheterization is one of the most commonly performed medical procedures for evaluation and management of various cardiac ailments in a cardiology setting. This condition is however, fraught with several risks, one of which appears to be kidney failure, known as nephropathy (Rudnick, 2006). The nephropathy occurs because of the contrast-medium injected to study the arteries and the structure of the heart and hence is known as contrast-induced nephropathy or contrast-induced nephropathy. contrast-induced nephropathy is associated with several complications like morbidity, increased duration of stay in the hospital, hemodialysis risk, development of end-stage kidney disease and even death. Hence, it is very important to take all measures to prevent development of this condition in any patient undergoing cardiac catheterization. There has been ample research in this regard and several studies have been conducted to evaluate and ascertain various strategies that might be useful in preventing contrast-induced nephropathy at various stages of catheterization like before the procedure, after the procedure and during the procedure. In this essay, various preventive strategies for prevention of contrast-induced nephropathy during cardiac catheterization will be discussed through review of suitable literature. First of all, what is cardiac catheterization and how is it performed? Cardiac catheterization is one of the important and frequently performed medical procedures that is performed by interventional cardiologists to not only diagnose some heart-related conditions, but also treat them. The procedure involves insertion of a thin and long, but flexible tube called catheter through one of the major blood vessels from either groin, upper arm or neck, that is gradually threaded into the heart. Once the catheter is in the heart, a dye, known as contrast medium, is injected through the catheter into the heart. Once the dye reaches the heart, it flows through the coronary arteries, the arteries which supply blood to the heart. These arteries are then shown up in the X-ray. This test is actually known as coronary angiography and the procedure of performing coronary angiography is known as cardiac catheterization. Coronary angiography helps in identification of any blocked or narrowed arteries, thus establishing diagnosis and extent of coronary artery disease. The arteries can also be studied using ultrasound (NHLBI, 2009). This condition is fraught with several risks to the patient either due to the procedure itself, or due to the anaesthesia that is administered during the procedure or due to the contrast medium that is injected to study the heart. One such complication is contrast-induced nephropathy. Those who develop contrast-induced nephropathy are at increased risk of development of myocardial infarction and other complications like death (Rudnick, 2006). Infact, it appears to be the most common cause of hospital-acquired acute kidney failure. Contrast-induced nephropathy is a cause of concern for cardiologists especially in the cardiac catheterization arena, because interventional cardiologists use radiographic contrast media every day (Rudnick, 2006). Thus, it becomes obvious to minimise contrast-induced nephropathy associated with these contrast agents. Contrast-induced nephropathy may be defined as nephropathy induced because of contrast medium . It is one of the causes of acute renal failure and this clinical condition is gaining momemtum in various clinical settings, especially the cardiac intervention. The condition may be defined as "an increase in serum creatinine concentration of >0.5 mg/dL (>44 µmol/L) or 25% above baseline within 48 hours after contrast administration”(Rudnick, 2006). Normal creatinine value varies from age to age and in general it is less that img/dl (Rudnick, 2006). Contrast-induced nephropathy manifests are rise in serum creatinine levels 24- 48 hours after contrast medium exposure, gradually rises to a peak within 3-5 days and then finally, returns to baseline within 7- 10 days. Few patients may even need dialysis. What causes contrast-induced nephropathy? The exact mechanism of contrast-induced nephropathy is not yet fully understood. Some of the proposed mechanisms are increase in vasoconstriction related to certain substances in the body like endothelin, adenosine and free radicals and decrease in vasodilatation related to prostaglandin and nitric oxide. Vasoconstriction makes the arteries become smaller and thus causes decreased blood supply. Vasodilatation is the exact opposite of vasoconstriction. Both the mechanisms ultimately lead to ischemia. Other mechanisms include direct injury to some of the parts of the kidney leading to death of cells. There is evidence that after injection of a contrast media, there is transient increase in renal blood flow which decreases gradually over a long duration of time. This suggests that ischemia of the renal system is one of the major factors in the pathogenesis of contrast-induced nephropathy. The incidence of contrast-induced nephropathy is less than 2 percent in general population. In those with high risk conditions like chronic renal problems, diabetes mellitus, older age and congestive heart failure, the incidence can be higher, as much as 30 percent. contrast-induced nephropathy is not only associated with morbidity and mortality, but is also associated with increased stay in the hospital and increased healthcare. As of now, there is no proper treatment to either ameliorate or reverse contrast-induced nephropathy once it occurs; however, there is evidence that some prophylaxis before, during and after the procedure is possible. Infact, several preventive measures have been tried which are based on the pathogenetic mechanisms. Many of them have failed to show any benefits in well-defined, randomised controlled trials. Some of the drugs that have been widely studied for prevention are dopamine, mannitol, diuretics, endothelin receptor antagonists, atrial natriuretic peptide and fenoldopam (Rudnick, 2006). There is however, not much evidence to ascertain the role of these agents in the prevention of contrast-induced nephropathy (Rudnick, 2006). Here are some of the strategies which can be employed to prevent contrast-induced nephropathy during cardiac catheterization. 1. Estimation of risk of contrast-induced nephropathy and outcomes related to the patient Contrast agents can be high-osmolar or low osmolar. High osmolar agents have osmolality of about 2000 Osm/L and those that are low osmolar have osmolality of less than 1000 Osm/L. The low osmolar are of both types, non-ionic and ionic and both of them have less systemic side effects. There are several types of contrast media. Earlier, the contrast agents were basically ionic and contained a sodium atom which dissociated to ion form in water. Each molecule of the contrast agent had 3 iodine atoms and hence the osmolality of these agents were very high (2000mOsm/L) (Rudnick, 2006). Since 1980s, non-ionic form of contrast agents are being used and they have very less osmolality when compared to the ionic forms (600-900 mOsm/L) (Rudnick, 2006). The latest contrast agent, iodixanol has a very low osmolality (300mOsm/L) and is a nonionic dimer (Rudnick, 2006). There is sufficient evidence to state that low osmolar contrast agents are less dangerous to the kidneys when compared to high osmolar agents (Rudnick, 2006; Moore et al, 1992, Heinrich et al, 2005). The main predisposing factor for contrast-induced nephropathy is chronic kidney disease. The risk of development of contrast-induced nephropathy is related inversely to the estimated glomerular filtration rate. Glomerular filtration rate is the rate at which the kidneys allow water to be passed through specific filtering portions of the kidneys, known as glomeruli. Factors which increase the risk of development of contrast-induced nephropathy are congestive heart failure, age beyond 75 years, diabetes mellitus, hypotension, anemia, and chronic kidney disease which may be defined as increase in serum creatinine of more than 1.5 mg per dl or an eGFR of less than 60ml/kg/min/1.7m2 (Schweiger, 2007). The incidence of this condition is actually low in those with normal kidney function and it appears to be much higher in those with pre-existing kidney problems at the baseline. 2. Pre-procedural strategies for high-risk patient Currently, hydration is considered to be the most useful primary intervention for the contrast-induced nephropathy prevention during cardiac catheterization. Several trials have been conducted to ascertain the amount, type, duration and also route of volume replenishment for prevention of contrast-induced nephropathy. However, it has not been possible to compare the patient populations and the outcome aspects in these studies because of differences in the number and also the type of population. According to a study by Heinrich et al (2005), using isotonic normal saline for volume replenishment significantly decreased the incidence of contrast-induced nephropathy when compared to use of half normal saline for volume replenishment. Isotonic normal saline is 0.9 percent saline. It is similar to the sodium and water combination in the body and hence is called isotonic. Several other studies have agreed upon the importance of volume replenishment prior to the procedure in the prevention of contrast-induced nephropathy. Optimal volume repletion is what is recommended. What is strongly recommended is to administer atleast 1 litre of isotonic normal saline beginning atleast 3 hours before the initiation of procedure and then continuing this after the procedure for 6-8 hours. The infusion rates recommended are 100- 150 ml/hr (Solomon, 1994; Stevens, 1999). It is very important to exert caution in those patients with suspected or established decreased function of the left ventricle which is the left lower chamber of the heart. Thus, it is imperative that out-patient visits for patients with cardiac catheterizations must be scheduled in such a way that they have sufficient time for saline replenishment. Other than saline, even other fluids have been studied like sodium bicarbonate. In one particular study (cited in Rudnick et al, 2006), isotonic sodium bicarbonate has been found to be superior to saline in the prevention of contrast-induced nephropathy in patients with high risk. The recommended protocol is 3ml/kg/hr for 1 hour and 1ml/kg/ hr for 6 hours after the procedure. The rationale behind hydration is that adequate hydration decreases the renin-angiotensin activity, which is a specific hormone released from the kidneys, thus decreasing the levels of hormones like endothelin which have vasoconstrictive properties. This increases diuresis of sodium, leading to decreased tubuloglomerular feedback. Ultimately, tubular obstruction will be prevented and protection against reactive oxygen species can occur. All these amount to decrease in the direct nephrotoxic effect on the epithelium of the tubules. Several clinical studies have demonstrated the usefulness of hydration in preventing contrast-induced nephropathy, especially in high-risk patients. However, according to (Stevens et al, 1999), "as yet, no sufficiently powered, controlled, prospective trials have examined the minimally effective length of time, optimal rate, and fluid composition of intravenous hydration required before and after contrast administration in high-risk patients." It is very important to review medications of the patient before initiation of the procedure. Drugs of specific interest are aminoglycoside antibiotics (like azithromycin), non-steroidal anti-inflammatory drugs (like ibuprofen), anti-rejection medication (used in transplant patients), and angiotensin converting enzyme inhibitor (used to treat high blood pressure). Metformin is used to treat diabetes. It is also important to withold metformin until the status of renal function has been ascertained (Tepel, 2006). 3. Intraprocedural strategies for high-risk patient The volume of radiographic contrast material is one of the risk factors for contrast-induced nephropathy. Thus, lesser the amount of this material administered, lower is the risk for development of contrast-induced nephropathy. However, there are no definite studies that have actually evaluated this aspect. There is some evidence although, that a total dose of less than 30 ml for diagnostic studies and a dose of less than 100ml for interventional procedures decrease the risk of contrast-induced nephropathy (Mueller et al, 2002). Some of the measures which can be employed to decrease the volume of radiographic material that can be administered is small size of the catheter, coronary angiography in the biplane or rotational angle and avoidance of left ventriculography. As far as the type of contrast material is concerned, there is evidence that low-osmolar contrast material decreases the risk of contrast-induced nephropathy when compared to high-osmolar contrast material(Rudnick, 2006) . 4. Post-procedural strategies for high-risk patient In the post-procedural period volume replenishment is very important to decrease the risk of contrast-induced nephropathy. Adequate hydration status can be ensured by monitoring urine output. The preferred urine output is 150ml/hr. there is some evidence that hemodialysis removes contrast material but does not decrease the risk of contrast-induced nephropathy. Follow-up is also very important, especially in those with high risk. It is important to obtain serum creatinine values 48- 72 hours after administration of radiocontrast material (Mehran et al, 2004). Thus, contrast-induced nephropathy remains one of the concerns of interventional cardiologists and radiologists during catheterizations and measures need to be taken to prevent this. The most commonly recommended and employed measure is appropriate volume replenishment and hydration with normal saline during, before and after the procedure. References Heinrich, M.C., Kuhlmann, M.K., Grgic, A., Heckmann, M., Kramann, B., Uder, M. (2005). Cytotoxic effects of ionic high-osmolar, nonionic monomeric, and nonionic iso-osmolar dimeric iodinated contrast media on renal tubular cells in vitro. Radiology, 235, 843–849. Moore, R.D., Steinberg, E.P., Powe, N.R., Brinker, J.A., Fishman, E.K., Graziano, S., Gopalan, R. (1992). Nephrotoxicity of high-osmolality versus low-osmolality contrast media randomized clinical trial. Radiology, 182, 649–655. NHLBI. (2009). What Is Cardiac Catheterization? Retrieved on 5th Spetember, 2011 from http://www.nhlbi.nih.gov/health/health-topics/topics/cath/ Rudnick, M.R., Kesselheim, A., Goldfarb, S. (2006). Contrast-induced nephropathy: How it develops, how to prevent it. Cleveland Clinic Journal of Medicine, 73(1), 75- 87. Schweiger, M.J., Chambers, C.E., Davidson, C.J., Zhang, S., et al. (2007). Prevention of Contrast Induced nephropathy: Recommendations for the High Risk Patient Undergoing Cardiovascular procedures. Catheterization and Cardiovascular Interventions, 69, 135–140. Solomon, R., Werner, C., Mann, D., D’Elia, J., Silva, P. (1994). Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med., 331, 1416–1420. Stevens, M.A., McCullough, P.A., Tobin, K.J., et al. (1999). A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. Study. Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation. J Am Coll Cardiol., 33, 403–411. Tepel, M. (2006). Contrast-induced nephropathy. Circulation, 113, 1799- 1806. Read More