Contrast Media, Pharmacology, and Adverse Reactions
Core concepts
Understand iodinated contrast: ionic versus non-ionic, monomer versus dimer, osmolality, and viscosity. Higher osmolality drives chemotoxic effects; non-ionic low-osmolar agents reduce adverse reactions. Know the pathophysiology of contrast-induced acute kidney injury (CIN/PC-AKI): medullary hypoxia, vasoconstriction, and direct tubular toxicity; risk factors include pre-existing renal impairment, diabetes, dehydration, and volume of contrast. Learn the classic adverse reaction classification: mild (nausea, urticaria), moderate (bronchospasm, hypotension), severe (anaphylactoid). Understand pretreatment for prior reactions (corticosteroids plus antihistamine). Gadolinium: linear versus macrocyclic chelates, stability, and nephrogenic systemic fibrosis (NSF) risk with low eGFR and unstable linear agents. Understand barium versus water-soluble (iodinated) GI contrast and the risk of barium peritonitis with perforation. Know the mechanism of metformin and contrast interaction.
Traps
Distinguish anaphylactoid (non-IgE) from true anaphylaxis - most contrast reactions are anaphylactoid. Late reactions (rash) are often T-cell mediated. CIN is defined by creatinine rise at 48–72 hours, not immediately. NSF is linked to unstable linear agents in severe renal failure; macrocyclic agents are safer. Do not withhold metformin indefinitely - follow local guidance on renal function. Barium is contraindicated if perforation is suspected.
Rule of thumb
Use the lowest volume of low- or iso-osmolar contrast consistent with diagnostic quality, and hydrate high-risk patients. For severe reactions, epinephrine is first-line; antihistamines alone do not treat hypotension or bronchospasm.