You are in: eMedicine Specialties > Radiology > VASCULAR/INTERVENTIONAL Contrast Medium Reactions, Recognition and TreatmentArticle Last Updated: Feb 11, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
 
Author: Nasir H Siddiqi, MBBS, MD, Consulting Staff, Department of Vascular and Interventional Radiology, Brigham and Women's Hospital Nasir H Siddiqi is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, and Radiological Society of North America Editors: Gary P Siskin, MD, Associate Professor, Department of Radiology, Albany Medical College; Chief, Division of Vascular and Interventional Radiology, Department of Radiology, Albany Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Douglas M Coldwell, MD, PhD, Professor of Interventional Radiology, Department of Radiology, University of Texas Southwestern Medical Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related keywords: iodinated contrast, radiographic contrast, organic radiographic iodinated contrast media, ICM, contrast agent, contrast material, contrast medium, adverse effects to contrast media, side effects of contrast media, hypersensitivity reaction(s) to contrast media INTRODUCTIONSection 2 of 12
 
Since their introduction in the 1950s, organic radiographic iodinated contrast media (ICM) have been among the most commonly prescribed drugs in the history of modern medicine. The phenomenon of present-day radiologic imaging would be lacking without these agents. ICM generally have a good safety record. Adverse effects from the intravascular administration of ICM are generally mild and self-limited; reactions that occur from the extravascular use of ICM are rare.1 Nonetheless, severe or life-threatening reactions can occur with either route of administration. Radiologists and other physicians must be aware of the risk factors for reactions to contrast media, use strategies to minimize adverse events, and be prepared to promptly recognize and manage any reactions to the contrast media.2, 3, 4 TYPES OF IODINATED CONTRAST MEDIASection 3 of 12
All currently used ICM are chemical modifications of a 2,4,6-tri-iodinated benzene ring (see Image 1).1 They are classified on the basis of their physical and chemical characteristics, including their chemical structure, osmolality, iodine content, and ionization in solution. In clinical practice, categorization based on osmolality is widely used. High-osmolality contrast mediaHigh-osmolality contrast media consist of a tri-iodinated benzene ring with 2 organic side chains and a carboxyl group. The iodinated anion, diatrizoate or iothalamate, is conjugated with a cation, sodium or meglumine; the result is an ionic monomer (see Image 1). The ionization at the carboxyl-cation bond makes the agent water soluble. Thus, for every 3 iodine atoms, 2 particles are present in solution (ie, a ratio of 3:2). The osmolality in solution ranges from 600 to 2100 mOsm/kg, versus 290 mOsm/kg for human plasma. The osmolality is related to some of the adverse events of these contrast media. Ionic monomers are subclassified by the percentage weight of the contrast agent molecule in solution (eg, 30% or 76%). In the United States, commonly used high-osmolality ICM are Renografin (diatrizoate anion; Bracco Diagnostics Inc, Princeton, NJ ) or Hypaque (diatrizoate anion; GE Healthcare, Inc, Princeton, NJ) and Conray (iothalamate anion; tyco Healthcare and Mallinckrodt Inc, St. Louis, Mo). Low-osmolality contrast mediaThere are 3 types of low-osmolality ICM: (1) nonionic monomers, (2) ionic dimers, and (3) nonionic dimers. Nonionic monomers In nonionic monomers, the tri-iodinated benzene ring is made water soluble by the addition of hydrophilic hydroxyl groups to organic side chains that are placed at the 1, 3, and 5 positions. Lacking a carboxyl group, nonionic monomers do not ionize in solution. Thus, for every 3 iodine atoms, only 1 particle is present in solution (ie, a ratio of 3:1). Therefore, at a given iodine concentration, nonionic monomers have approximately one half the osmolality of ionic monomers in solution. At normally used concentrations, 25-76%, nonionic monomers have 290-860 mOsm/kg. Nonionic monomers are subclassified according to the number of milligrams of iodine in 1 mL of solution (eg, 240, 300, or 370 mg I/mL). The larger side chains increase the viscosity of nonionic monomers compared with ionic monomers. The increased viscosity makes nonionic monomers harder to inject, but it does not appear to be related to the frequency of adverse events. Common nonionic monomers are iohexol (Omnipaque; GE Healthcare, Inc), iopamidol (Isovue; Bracco Diagnostics Inc), ioversol (Optiray; tyco Healthcare and Mallinckrodt Inc), and iopromide (Ultravist; Bayer HealthCare Pharmaceuticals Inc, Wayne, NJ). The nonionic monomers are the contrast agents of choice. In addition to their nonionic nature and lower osmolalities, they are potentially less chemotoxic than the ionic monomers. Ionic dimers Ionic dimers are formed by joining 2 ionic monomers and eliminating 1 carboxyl group. These agents contain 6 iodine atoms for every 2 particles in solution (ie, a ratio of 6:2). The only commercially available ionic dimer is ioxaglate (Hexabrix; tyco Healthcare and Mallinckrodt Inc). Ioxaglate has a concentration of 59%, or 320 mg I/mL, and an osmolality of 600 mOsm/kg. Because of its high viscosity, ioxaglate is not manufactured at higher concentrations. Ioxaglate is used primarily for peripheral arteriography. Nonionic dimers Nonionic dimers consist of 2 joined nonionic monomers. These substances contain 6 iodine atoms for every 1 particle in solution (ie, ratio of 6:1). For a given iodine concentration, the nonionic dimers have the lowest osmolality of all the contrast agents. At approximately 60% concentration by weight, these agents are iso-osmolar with plasma. They are also highly viscous and, thus, have limited clinical usefulness. Examples of nonionic dimers are iotrol and iodixanol (Visipaque; Amersham Health Inc, Princeton, NJ). ADVERSE REACTIONS TO ICMSection 4 of 12
Adverse reactions to ICM are classified as idiosyncratic and nonidiosyncratic.1, 3, 5, 6 The pathogenesis of such adverse reactions probably involves direct cellular effects; enzyme induction; and activation of the complement, fibrinolytic, kinin, and other systems. Idiosyncratic reactionsIdiosyncratic reactions typically begin within 20 minutes of the ICM injection, independent of the dose that is administered. A severe idiosyncratic reaction can occur after an injection of less than 1 mL of a contrast agent. Although reactions to ICM have the same manifestations as anaphylactic reactions, these are not true hypersensitivity reactions. Immunoglobulin E (IgE) antibodies are not involved. In addition, previous sensitization is not required, nor do these reactions consistently recur in a given patient. For these reasons, idiosyncratic reactions to ICM are called anaphylactic reactions. The symptoms of anaphylactic reaction can be classified as mild, moderate, and severe. Mild symptoms Mild symptoms include the following: scattered urticaria, which is the most commonly reported adverse reaction; pruritus; rhinorrhea; nausea, brief retching, and/or vomiting; diaphoresis; coughing; and dizziness. Patients with mild symptoms should be observed for the progression or evolution of a more severe reaction, which requires treatment. Moderate symptoms Moderate symptoms include the following: persistent vomiting; diffuse urticaria; headache; facial edema; laryngeal edema; mild bronchospasm or dyspnea; palpitations, tachycardia, or bradycardia; hypertension; and abdominal cramps. Nonidiosyncratic reactionsNonidiosyncratic reactions include the following: bradycardia, hypotension, and vasovagal reactions; neuropathy; cardiovascular reactions; extravasation; and delayed reactions. Other nonidiosyncratic reactions include sensations of warmth, a metallic taste in the mouth, and nausea and vomiting. Bradycardia, hypotension, and vasovagal reactions By inducing heightened systemic parasympathetic activity, ICM can precipitate bradycardia (eg, decreased discharge rate of the sinoatrial node, delayed atrioventricular nodal conduction) and peripheral vasodilatation. The end result is systemic hypotension with bradycardia. This may be accompanied by other autonomic manifestations, including nausea, vomiting, diaphoresis, sphincter dysfunction, and mental status changes. Untreated, these effects can lead to cardiovascular collapse and death. Some vasovagal reactions may be a result of coexisting circumstances such as emotion, apprehension, pain, and abdominal compression, rather than ICM administration. Nephropathy Contrast agent–related nephropathy is an elevation of the serum creatinine level that is more than 0.5 mg% or more than 50% of the baseline level at 1-3 days after the ICM injection. The elevation peaks by 3-7 days, and the creatinine level usually returns to baseline in 10-14 days. The incidence of contrast agent–related nephropathy in the general population is estimated to be 2-7%. As many as 25% of patients with this nephropathy have a sustained reduction in renal function, most commonly when the nephropathy is oliguric. The mechanism of this type of nephropathy is thought to be a combination of preexisting hemodynamic alterations; renal vasoconstriction, possibly through mediators such endothelin and adenosine; and direct ICM cellular toxicity. Cardiovascular reactions ICM can cause hypotension and bradycardia. Vasovagal reactions, a direct negative inotropic effect on the myocardium, and peripheral vasodilatation probably contribute to these effects. The latter 2 effects may represent the actions of cardioactive and vasoactive substances that are released after the anaphylactic reaction to the ICM. This effect is generally self-limiting, but it can also be an indicator of a more severe, evolving reaction. ICM can lower the ventricular arrhythmia threshold and precipitate cardiac arrhythmias and cardiac arrest. Fluid shifts due to an infusion of hyperosmolar intravascular fluid can produce an intravascular hypervolemic state, systemic hypertension, and pulmonary edema. Also, ICM can precipitate angina. The similarity of the cardiovascular and anaphylactic reactions to ICM can create confusion in identifying the true nature of the type and severity of an adverse reaction; this confusion can lead to the overtreatment or undertreatment of symptoms. Other nonidiosyncratic reactions include syncope; seizures; and the aggravation of underlying diseases, including pheochromocytomas, sickle cell anemia, hyperthyroidism, and myasthenia gravis. Extravasation Extravasation of ICM into soft tissues during an injection can lead to tissue damage as a result of direct toxicity of the contrast agent or pressure effects, such as compartment syndrome. Delayed reactions Delayed reactions become apparent at least 30 minutes after but within 7 days of the ICM injection. These reactions are identified in as many as 14-30% of patients after the injection of ionic monomers and in 8-10% of patients after the injection of nonionic monomers. Common delayed reactions include the development of flulike symptoms, such as the following: fatigue, weakness, upper respiratory tract congestion, fevers, chills, nausea, vomiting, diarrhea, abdominal pain, pain in the injected extremity, rash, dizziness, and headache. Less frequently reported manifestations are pruritus, parotitis, polyarthropathy, constipation, and depression. These signs and symptoms almost always resolve spontaneously; usually, little or no treatment is required. Some delayed reactions may be coincidental. INCIDENCE OF ADVERSE REACTIONS TO ICMSection 5 of 12
The incidence of any adverse reaction to ICM is about 15%. Most of these reactions are mild and require no treatment. Ionic ICM versus nonionic ICM In a large Japanese case series (337,647 cases), the overall risk of any adverse reaction was 12.66% with ionic ICM and 3.13% with nonionic ICM; the risk of a severe adverse drug reaction was 0.2% for ionic ICM and 0.04% for nonionic ICM; and the risk of a very severe adverse drug reaction was 0.04% for ionic ICM and 0.004% for nonionic ICM.7 In another large study, in which 6000 patients received ionic ICM, the incidence of mild adverse drug reactions was 2.5%; moderate reactions, 1.2%; and severe reactions, 0.4%.8 However, in 7170 patients who received nonionic ICM, the incidences were only 0.58% for mild reactions, 0.11% for moderate reactions, and 0% for severe reactions.9 High-osmolality ICM versus low-osmolality ICM A meta-analysis of the published data from 1980-1989 by Caro et al revealed that the risk of severe adverse reaction was 0.157% for high-osmolality ICM and 0.031% for nonionic ICM.11 The investigators found that the risk of death was 1 death in 100,000 patients with either type of agent. Other reports indicate that low-osmolality agents are somewhat less nephrotoxic in patients with azotemia than in other patients.12 Nonionic ICM are less likely than conventional ionic ICM to cause tissue damage when they are extravasated.13 Nonetheless, compartment syndromes and skin blistering are reported after the extravasation of nonionic agents. Some toxic effects of ICM, such as nausea and vomiting, are more common with ionic dimers than with nonionic monomers.14 Most authorities believe that the preponderance of evidence that supports the lower rate of adverse reactions with low-osmolality ICM compared with high-osmolality ICM is conclusive. The reason that low-osmolality ICM have not completely replaced the older high-osmolality ICM is the higher cost of the low-osmolality agents. Professional organizations have formulated guidelines regarding the selective use of low-osmolality ICM for certain high-risk patients. However, with the selective use of nonionic ICM, severe adverse contrast reactions are 3 times as likely in low-risk patients who receive conventional ionic agents (0.09%) than in high-risk patients who receive nonionic agents (0.03%). Thus, the single most important risk factor for an adverse reaction is the type of contrast agent that is chosen for injection. RISK FACTORS FOR ADVERSE REACTIONS TO ICMSection 6 of 12
Regarding the risk for ICM-related reactions, patients can be assigned to 3 categories, as follows: (1) those with an increased risk for idiosyncratic reactions, (2) those with an increased risk for contrast agent–induced nephropathy, and (3) those with an increased risk for nonidiosyncratic reactions. Risk factors related to idiosyncratic reactions Idiosyncratic reactions may occur in people with a previous reaction to ionic or nonionic ICM, asthma, and/or food or medication allergies. Previous reactions to ionic or nonionic ICM increase the relative risk of a repeat reaction 3.3- to 6.9-fold compared with the risk in the general population. Approximately 60% of patients who had hives after ICM administration in the past have hives with a repeat exposure. Similarly, facial edema has a recurrence rate in 68% of patients; difficulty breathing, 59%; and bronchospasm, 38%. Idiosyncratic reactions do not recur in all patients. Patients with a history of a reaction to ICM may report having undergone a recent contrast-enhanced study without adverse manifestations. Nevertheless, these patients still have a higher risk than that of the general population. People with asthma have 1.2-2.5 times the risk of such reactions than the general population. In addition, when the reactions occur, they are more likely to be severe. Severe reactions are 5-9 times more common in people with asthma than in others. Patients with allergies, including hay fever, are 1.5-3 times more likely to have an adverse reaction to ICM than other people. However, no consistent data warrant the use of any unique precautions in patients who have seafood or shellfish allergies. Risk factors related to contrast agent–induced nephropathy Patients with preexisting renal insufficiency have 5-10 times the risk of ICM-related nephropathy. Patients whose renal failure is the result of diabetic nephropathy are at the greatest risk. Azotemic diabetic patients also have the highest incidence of irreversible renal deterioration. In general, the higher the preexisting serum creatinine level, the greater the likelihood of contrast agent–induced nephrotoxicity. Other factors that are implicated in increasing the risk of renal failure after ICM administration include the following: American Heart Association class IV congestive heart failure, dehydration, hyperuricemia, concomitant use of nephrotoxic drugs such as aminoglycoside antibiotics and nonsteroidal anti-inflammatory agents (NSAIDs), advanced age, and large doses of ICM for a single study or multiple contrast-enhanced studies that are performed within a short period. Diseases that affect renal hemodynamics, such as cirrhosis and nephrotic syndrome, are also suspected of increasing a patient's susceptibility to renal damage from ICM. Diabetes mellitus alone is a controversial risk factor. Many authorities do not regard the presence of diabetes mellitus in the absence of renal failure as a risk factor for contrast agent–induced nephropathy. The risk of nephropathy is magnified when multiple risk factors are present in the same patient. Well-hydrated patients with myeloma who receive contrast material have a low incidence of 0.6-1.25% for subsequent renal failure. Risk factors related to nonidiosyncratic reactions ICM administration can aggravate diseases such as cardiac arrhythmias, angina, and pheochromocytoma. In patients who have received interleukin-2 immunotherapy for cancer, ICM administration increases the incidence and severity of delayed reactions. These reactions primarily include fevers, chills, rigors, flushing, dizziness, and, occasionally, hypotension. These reactions can occur even if immunotherapy is administered as long as 2 years before ICM administration. Metformin (Glucophage; Bristol-Myers Squibb Co, Princeton, NJ), an oral antihyperglycemic medication that is excreted predominantly by the kidneys, is not nephrotoxic per se, and it does not cause hypoglycemia in and of itself. If patients who receive metformin become azotemic, increased tissue levels of metformin may rarely induce life-threatening lactic acidosis. The drug should be discontinued in all patients at the time of or before any intravascular contrast-enhanced study is performed. Moreover, metformin administration should be withheld for at least 48 hours after the contrast-enhanced study, and its administration should be resumed only after the absence of renal dysfunction has been documented. Through their pharmacodynamic effects, beta-blockers can aggravate ICM-induced bradycardia, other cardiac arrhythmias, hypotension, and bronchospasm; these conditions can interfere with the treatment of ICM-related adverse events. When possible, the intravenous administration of contrast material should be avoided in pregnant women. Results of in vitro experiments have shown that contrast material is mutagenic to human cells; however, a few studies have failed to reveal a teratogenic effect in animals. Intravascular ICM crosses the placenta and can potentially produce transient fetal hypothyroidism. Lasting adverse effects on the fetus or neonates have not been identified. Nonetheless, nonionic agents are preferred to conventional ionic agents in pregnant women. PROPHYLAXIS FOR ADVERSE REACTIONS TO ICMSection 7 of 12
Prophylactic medications In a study by Lasser et al, methylprednisolone, 2 oral doses of 32 mg each administered at 12 and 2 hours before ICM administration, reduced the incidence of all adverse reactions to ionic ICM from 9% to 6.4%.8 The frequency of severe reactions that required treatment was also reduced from 2% to 1.2%. However, a single dose of 32 mg of methylprednisolone that was given 2 hours before ICM administration had virtually no effect. In the same study, oral corticosteroid premedication in 2 doses, one 6-24 hours before and the other 2 hours before ICM injection, significantly reduced the incidence of the total number of ICM-related adverse reactions from 5% to 2%.8 Studies of the potential role of H2 blockers, such as cimetidine, have shown a beneficial effect, no effect, or even adverse effects with the addition of H2 blockers to the premedication regimen. Recommended prophylactic regimens Methylprednisolone, one 32-mg tablet, may be orally administered at 12 and 2 hours before the study, or prednisone, one 50-mg tablet, may be orally administered 13 hours, 7 hours, and 1 hour before the contrast-enhanced study. If the patient had a previous moderate or severe reaction to ICM or one that included a respiratory component, an alternative study, such as ultrasonography or magnetic resonance imaging (MRI), should be considered. Otherwise, the following may be used: H1 antihistamines; diphenhydramine, one 50-mg tablet orally administered 1 hour before the study; H2-histamine receptor blockers, which is optional; cimetidine, 300 mg orally administered 1 hour before the study; and/or ranitidine 50 mg orally administered 1 hour before the study. Most authorities restrict corticosteroid pretreatment to patients in whom previous idiosyncratic adverse reactions to ICM were moderate or severe. Usually, corticosteroids are well tolerated and cause no adverse effects when only a few doses are administered. Although the utility of H2-receptor blockers is questionable, these agents are well tolerated and might be of benefit, particularly because they are effective in the treatment of at least some allergic cutaneous reactions to agents other than ICM. However, H2 blockers should not be used without H1 blockers. The treatment of the nonidiosyncratic adverse reactions of nausea and vomiting is not considered a routine indication for corticosteroid premedication or the use of nonionic ICM. Reducing the incidence of ICM nephropathy Other nephrotoxic drugs should be discontinued whenever possible, and the minimal amount of contrast material that is needed to perform a diagnostic study should be used. Nonionic agents are the ICM of choice. If multiple studies are required, time (as long as 5 days) should be allotted between the studies to allow the kidneys to recover fully from the ICM injection. Patients can be well hydrated until 12 hours before a contrast-enhanced study, and hydration should be continued for at least 2 hours after a contrast-enhanced procedure is performed.5 Other measures Use of mannitol or furosemide is not recommended, at least in patients with diabetic nephropathy. In several studies, these medications were not effective in reducing the incidence of ICM nephropathy. In other studies, the incidence of nephropathy was higher in patients who were given mannitol or furosemide. The use of mannitol or dopamine at renal vasodilatory doses or atrial natriuretic peptide reduced the incidence of ICM nephropathy in nondiabetic azotemic patients, compared with azotemic patients who received only hydration with sodium chloride solution. Several investigators have suggested that ICM nephrotoxicity can be reduced with the use of oral or intravenous theophylline, acetylcysteine, fenoldopam, or bosentan (an endothelin antagonist). Research with these agents is promising, but results are preliminary. Some prospective studies have suggested that prophylactic administration of 600 mg acetylcysteine twice daily in combination with hydration reduces the incidence of ICM nephrotoxicity.16 Prophylaxis in nonvascular studies Although rare, systemic reactions are reported after extravascular instillation of ICM (eg, during retrograde pyelography).13 When patients have had previous severe idiosyncratic or anaphylactic reactions to intravenous ICM, premedication with corticosteroids should be considered, even in nonvascular studies. Rate and temperature of ICM injection The perception that adverse reactions to ICM, particularly nausea and vomiting, are more common with a rapid rate of injection than with a slow injection has been refuted by findings from 2 studies.17, 18 Warming ICM to body temperature reduces their viscosity and may make the injection more comfortable for the patient. EVALUATING THE PATIENT BEFORE ICM ADMINISTRATIONSection 8 of 12
A pertinent patient medical history should be obtained, and the following elements should be stressed: history of allergies, asthma, diabetes mellitus, renal insufficiency, and/or cardiac diseases; currently or recently used medicines; possibility of pregnancy; and previous contrast agent administration. If the patient had a reaction in the past, the nature of the reaction must be determined. Also, serum creatinine levels should be determined. TREATMENT OF ADVERSE REACTIONSSection 9 of 12
Most acute severe adverse reactions to ICM occur within 20 minutes of injection. For this reason, the patient should be monitored for a minimum of 20 minutes after an ICM injection. Furthermore, any physician who is responsible for an imaging study that requires the use of ICM must be able to recognize and treat acute adverse reactions. Rooms in which contrast material is administered should be stocked with appropriate basic and advanced life support monitoring equipment and drugs. The equipment should be regularly checked. In the examination of a patient with an adverse reaction, a brief history should be obtained, including a summary of the current symptoms, any medical conditions (eg, heart disease), and the patient's medications. Vital signs should be assessed, and any patient with an adverse reaction should be closely monitored until the symptoms have stabilized or resolved. Assessment of the patient's airway, breathing, and circulation (ABCs) remain the cornerstone of the management of moderate or severe adverse reactions to ICM. In the treatment of adverse reactions, immediately discontinue ICM administration. Monitor the patient's cardiac rhythm, blood pressure, and oxygen saturation. Mild reactions are self-limiting and do not require treatment. However, the patient should be closely monitored until the symptoms resolve. Related Medscape topics: The treatment of most anaphylactic reactions, once they are recognized and differentiated from other types of reactions, is often straightforward. These are summarized below.
A respiratory component to an adverse reaction requires more aggressive therapy. Oxygen administration, 10-12 L/min via a partial nonrebreathing mask, should be considered in any patient with respiratory difficulty. If bronchospasm is accelerating or severe, if it does not respond to inhalers, or if an upper airway edema (including laryngospasm) is present, epinephrine should be injected promptly. Intravenous use of epinephrine is optional in normotensive patients, but it is necessary in hypotensive patients with respiratory reactions. Epinephrine must be administered with care to patients who have cardiac disease or those who are taking beta-blockers such as atenolol, propranolol, metoprolol, and nadolol, because the unopposed alpha effects of epinephrine in these patients may cause severe hypertension or angina. H1 antihistamines, such as diphenhydramine, and H2-receptor blockers, such as cimetidine, do not have a major role in the treatment of respiratory reactions, but they may be administered after epinephrine. Monitoring the vital signs can be helpful in determining the cause of the hypotension. Tachycardia (ie, heart rate more than 100 bpm) indicates that an anaphylactic reaction is more likely than other types of reactions. If the patient is bradycardic (ie, heart rate less than 60 bpm), a vasovagal reaction is probable, provided that the patient is not receiving beta-blockers. Hypotension resulting from an anaphylactic reaction is treated with an intravenous iso-osmolar fluid (ie, normal saline, Ringer lactate solution) in large volumes. Several liters of fluid may be required. If fluid and oxygen are unsuccessful in reversing the patient's hypotension, the use of vasopressors should be considered. The most specifically effective vasopressor is dopamine; at infusion rates of 2-10 mcg/kg/min, the cerebral, renal, and splanchnic vessels remain dilated, whereas the peripheral vessels constrict. Epinephrine is less useful, its results are less predictable, and it has more adverse effects. Treatment of nonidiosyncratic reactions Treatments for nonidiosyncratic reactions depend on the type of reaction.
SUMMARYSection 10 of 12
A basic understanding of ICM, the risks of their administration, the choice of the available agents, and premedication regimens for high-risk patients is beneficial in preparing patients for their contrast-enhanced imaging examinations. Radiologists are the primary physicians who administer contrast material. Because reactions to ICM may occur unexpectedly, radiologists should be able to recognize and treat the various types of possible adverse reactions, and they should seek clinical assistance as needed. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Contrast Medium Reactions, Recognition and Treatment excerpt Article Last Updated: Feb 11, 2008 | |||||||
