Contrast Media
DR. MAHENDAR REDDY
IODINE
Most of the I.V. Contrast media contain Iodine
which has an atomic number of 53 and atomic
weight 127.
It’s preferred because
1) High contrast density due to high atomic
number. 2) Allows
firm binding to highly variable benzene ring
3) Low Toxicity
Conventional contrast Media/ High Osmolar
contrast media/ Ionic Monomers
 These are salts consisting of a sodium or meglumine cation and a
triodinated benzoate anion.
 Anions consisting of a benzoic acid molecule with three atoms of
iodine firmly attached at C2, C4 and C6.
 The C3 and C5 are connected to radicals CR3 and R5, which are
amines E-NH2 , and greatly reduce toxicity and increase solubility of
the molecules.
 Iodine particle ratio 3:2
 Sodium or meglumine acts as Cations
 Ex : Diatrizoic Acid ,Iothalamic Acid
Diatrizoic Acid
 The two side chains R3 and R5 in Diatrizoic acid
are replaced by ( NHCOCH3) . This
 Increases solubility
 Decreases plasma protein binding thereby
increasing its ability to be filtered in
glomerulus.
 Improves patient tolerance.
Disadvantages of conventional contrast
media
 Osmolar concentration(osmolality) is extremely
high up to 8times the physiological level of 300m
Osm/kg water.
 Osmolar challenge to every cell , tissue and fluid
in the body is responsible for their adverse
effects.
Useful facts to remember
 Osmolality is dependent on number of particles of
solute in solution.
 Radiopacity is dependent on the iodine concentration
of the solution and is therefore dependent on the
number of iodine atoms in each molecule of the
contrast media.
 High radiopacity and low osmolality are desirable
requirements.
 The ratio of the number of iodine atoms per
molecule to the number of particles per
molecule of solute in solution is therefore a
fundamental criterion.
 Iodine particle ratio for all is 3:2.
 Non- ionicity is essential for myelography and
reduces the reactions to I.V injection.
Additives used in contrast media
Stabilizer - Ca or Na EDTA.
BUFFERS – stabilizes pH during storage –
Na acid phosphates.
Preservatives: Generally not disclosed by
manufacturers.
Ideal contrast media should have
 High water solubility.
 Heat and chemical stability (shelf life). Ideally 3-5
years.
 Biological inertness ( non antigenic).
 Low viscosity.
 Low or iso-osmolar to plasma.
 Selective excretion, like excretion by kidney is
favourable.
Safety : LD50( lethal dose) should be
high.
Reasonable cost.
Points to remember
Contrast media used for myelography are
non- ionic contrast media.
 Contrast media used for cerebral angiography
are contrast media containing only meglumine
cation.
 Meglumine salts cause bronchospasm, so contra-
indicated in bronchial asthma.
Points to remember
Incidence of thrombo embolic
phenomenon is fairly high when
contrast media is mixed with blood.
So, meticulous heparinization is
required during angiography.
Toxicity
 Reactions unrelated to contrast media. 1)
Pyrogenic ( unsterile injection).
 2) vasovagal especially in anxious or
psychosomatic patient.
 3)Hypertensive attacks in patient with
pheochromocytoma.
 Excessive dehydration, hypoglycemia.
Toxicity: Hyper osmolarity
 This is due to high osmolarity of contrast media than
plasma. More with conventional contrast media. These
reactions include:
ERYTHROCYTE DAMAGE: Injection of
hyperosmolar contrast media > Loss of H20
from RBC > Dehydrated shrunken RBC >
Increased internal viscosity with loss of ability
of RBC to deform to traverse capillaries >
Obstruction of important capillary beds
(cerebral, coronary, renal, pulmonary).
Hyperosmolar Contrast media >
Shrinkage of endothelial cells >
Widening of intercellular gaps >
Capillary permeability.
Toxicity: Capillary endothelial damage
Toxicity: Vasodilation
 Vasodilatation of arteriolar beds, is a direct result of
perfusion with any hyperosmolar solution.
 Clinically, this is evident by marked vasodilatation
produced on peripheral arteriography.
 This produces a sensation of heat, which may be
uncomfortable and often accompanied by pain,
especially in hand and external carotid artery
territory.
Toxicity: Hypervolemia
 This is due to diffusion of extracellular fluid through capillary
walls into blood which occurs whenever large volumes of
hyperosmolar fluid are injected intravascularly.
 The extravascular fluid is drawn in so much that the blood
volume may increase by 10% within a few seconds.
 The increased capillary permeability due to endothelial
damage, permits intravascular fluid to escape from the
capillaries and soon reduces the blood volume towards its
original level.
Toxicity: Cardiovascular effects
 Peripheral vasodilatation.
 Decreased systemic blood pressure.
 Tachycardia.
 Cardiovascular insufficiency.
 Acute hypervolemia > Left ventricular stress.
 Selective arteriography induces bradycardia and moderate reduction in
cardiac output.
 Na edetate and Na citrate which are used as preservatives in the
contrast media chelate Ca2+, therefore leading to transient
hypocalcaemia. This causes negative ionotropic effect on heart.
Nephrotoxicity is due to:
 Decreased renal perfusion. (low B.P., peripheral
vasodilatation).
 Glomerular injury - manifest as proteinuria.
 Tubular injury - due to osmolarity, chemotoxicity,
ischaemia.
 Contrast media precipitation of Tamm Horsfall proteins
that block tubules.
 Swelling of renal tubular cells causing obstruction.
Immunological ( allergic)
Toxicity:Mechanisms
 Deactivation of angiotensin converting enzyme
 Incidence of adverse contrast media reactions to intra-arterial
injection is about l/3rd of incidence following intravenous
injection because the latter stimulate release of vasoactive
substances from mast cells or deactivates ACE in lung.
 ACE deactivates bradykinin, the concentration of which rises
with IV injection of Contrast media.
 Due to damage to the endothelium which initiates the activation
system which inturn may be responsible for many adverse
anaphylactoid reactions.
 Activation of complement, kinins, coagulation
and fibrinolytic systems.
 Inhibition of cholinesterase with consequent
vagal over stimulation > acetylcholine release
> collapse, bradycardia, bronchospasm.
 Release of vasoactive substances like
histamine, bradykinin,serotonin.
High risk group people
 Prior reactions to contrast media - 11 times more prone.
 History of allergy - 4 times more prone.
 Cardiac disease - 4 times more prone.
 Asthma - 5 times more prone.
 Diabetes - 4 times more prone.
 Old age - 4 times more prone.
 Neonates - 4 times more prone.
 Myelomatosis, polycythemia.
 Sickle cell anaemia, pheochromocytoma, homocystinuria.
Severity of Reactions
 Minor : 1 in 20 cases - 5% -Nausea, vomiting, mild rash, light
headache and mild dyspnoea. Needs no treatment, but requires
assurance.
 Intermediate l in 100 - 1% - Extensive urticaria, facial edema,
bronchospasm, laryngeal oedema, dyspnoea, mild chest pain or
hypotension. Requires treatment but generally there is no need
for hospitalization.
 Severe reactions (l in 2000 - 0.05%) - Circulatory collapse,
pulmonary oedema, severe angina, myocardial infarction,
convulsions, coma, cardiac or respiratory arrest. Requires
hospitalization and intensive care.
 Mortality - (l in 40,000 - 0.0025%).
Treatment if needed:
 No patient will have serious reaction after 60 mins of contrast
administration, so for first 60mins we need to monitor and
watch out for adverse reactions.
 Oxygen : Current recommendation for use of high dose
oxygen is at the rate of 10-12 L/min via face mask.•
 02 can be provided at up to 100% concentration.
 Currently it is recommended that high concentration of 02
shouldbe administered to any patient in respiratory distress,
regardless of his or her pre-existing condition.
Treatment
 Epinephrine: The most important medication
needed for Anaphylactoid reaction.
Thank you

contrast media copy.pptx

  • 1.
  • 4.
    IODINE Most of theI.V. Contrast media contain Iodine which has an atomic number of 53 and atomic weight 127. It’s preferred because 1) High contrast density due to high atomic number. 2) Allows firm binding to highly variable benzene ring 3) Low Toxicity
  • 5.
    Conventional contrast Media/High Osmolar contrast media/ Ionic Monomers  These are salts consisting of a sodium or meglumine cation and a triodinated benzoate anion.  Anions consisting of a benzoic acid molecule with three atoms of iodine firmly attached at C2, C4 and C6.  The C3 and C5 are connected to radicals CR3 and R5, which are amines E-NH2 , and greatly reduce toxicity and increase solubility of the molecules.  Iodine particle ratio 3:2  Sodium or meglumine acts as Cations  Ex : Diatrizoic Acid ,Iothalamic Acid
  • 6.
    Diatrizoic Acid  Thetwo side chains R3 and R5 in Diatrizoic acid are replaced by ( NHCOCH3) . This  Increases solubility  Decreases plasma protein binding thereby increasing its ability to be filtered in glomerulus.  Improves patient tolerance.
  • 7.
    Disadvantages of conventionalcontrast media  Osmolar concentration(osmolality) is extremely high up to 8times the physiological level of 300m Osm/kg water.  Osmolar challenge to every cell , tissue and fluid in the body is responsible for their adverse effects.
  • 8.
    Useful facts toremember  Osmolality is dependent on number of particles of solute in solution.  Radiopacity is dependent on the iodine concentration of the solution and is therefore dependent on the number of iodine atoms in each molecule of the contrast media.  High radiopacity and low osmolality are desirable requirements.
  • 9.
     The ratioof the number of iodine atoms per molecule to the number of particles per molecule of solute in solution is therefore a fundamental criterion.  Iodine particle ratio for all is 3:2.  Non- ionicity is essential for myelography and reduces the reactions to I.V injection.
  • 10.
    Additives used incontrast media Stabilizer - Ca or Na EDTA. BUFFERS – stabilizes pH during storage – Na acid phosphates. Preservatives: Generally not disclosed by manufacturers.
  • 11.
    Ideal contrast mediashould have  High water solubility.  Heat and chemical stability (shelf life). Ideally 3-5 years.  Biological inertness ( non antigenic).  Low viscosity.  Low or iso-osmolar to plasma.  Selective excretion, like excretion by kidney is favourable.
  • 12.
    Safety : LD50(lethal dose) should be high. Reasonable cost.
  • 13.
    Points to remember Contrastmedia used for myelography are non- ionic contrast media.  Contrast media used for cerebral angiography are contrast media containing only meglumine cation.  Meglumine salts cause bronchospasm, so contra- indicated in bronchial asthma.
  • 14.
    Points to remember Incidenceof thrombo embolic phenomenon is fairly high when contrast media is mixed with blood. So, meticulous heparinization is required during angiography.
  • 15.
    Toxicity  Reactions unrelatedto contrast media. 1) Pyrogenic ( unsterile injection).  2) vasovagal especially in anxious or psychosomatic patient.  3)Hypertensive attacks in patient with pheochromocytoma.  Excessive dehydration, hypoglycemia.
  • 16.
    Toxicity: Hyper osmolarity This is due to high osmolarity of contrast media than plasma. More with conventional contrast media. These reactions include: ERYTHROCYTE DAMAGE: Injection of hyperosmolar contrast media > Loss of H20 from RBC > Dehydrated shrunken RBC > Increased internal viscosity with loss of ability of RBC to deform to traverse capillaries > Obstruction of important capillary beds (cerebral, coronary, renal, pulmonary).
  • 17.
    Hyperosmolar Contrast media> Shrinkage of endothelial cells > Widening of intercellular gaps > Capillary permeability. Toxicity: Capillary endothelial damage
  • 18.
    Toxicity: Vasodilation  Vasodilatationof arteriolar beds, is a direct result of perfusion with any hyperosmolar solution.  Clinically, this is evident by marked vasodilatation produced on peripheral arteriography.  This produces a sensation of heat, which may be uncomfortable and often accompanied by pain, especially in hand and external carotid artery territory.
  • 19.
    Toxicity: Hypervolemia  Thisis due to diffusion of extracellular fluid through capillary walls into blood which occurs whenever large volumes of hyperosmolar fluid are injected intravascularly.  The extravascular fluid is drawn in so much that the blood volume may increase by 10% within a few seconds.  The increased capillary permeability due to endothelial damage, permits intravascular fluid to escape from the capillaries and soon reduces the blood volume towards its original level.
  • 20.
    Toxicity: Cardiovascular effects Peripheral vasodilatation.  Decreased systemic blood pressure.  Tachycardia.  Cardiovascular insufficiency.  Acute hypervolemia > Left ventricular stress.  Selective arteriography induces bradycardia and moderate reduction in cardiac output.  Na edetate and Na citrate which are used as preservatives in the contrast media chelate Ca2+, therefore leading to transient hypocalcaemia. This causes negative ionotropic effect on heart.
  • 21.
    Nephrotoxicity is dueto:  Decreased renal perfusion. (low B.P., peripheral vasodilatation).  Glomerular injury - manifest as proteinuria.  Tubular injury - due to osmolarity, chemotoxicity, ischaemia.  Contrast media precipitation of Tamm Horsfall proteins that block tubules.  Swelling of renal tubular cells causing obstruction.
  • 22.
    Immunological ( allergic) Toxicity:Mechanisms Deactivation of angiotensin converting enzyme  Incidence of adverse contrast media reactions to intra-arterial injection is about l/3rd of incidence following intravenous injection because the latter stimulate release of vasoactive substances from mast cells or deactivates ACE in lung.  ACE deactivates bradykinin, the concentration of which rises with IV injection of Contrast media.  Due to damage to the endothelium which initiates the activation system which inturn may be responsible for many adverse anaphylactoid reactions.
  • 23.
     Activation ofcomplement, kinins, coagulation and fibrinolytic systems.  Inhibition of cholinesterase with consequent vagal over stimulation > acetylcholine release > collapse, bradycardia, bronchospasm.  Release of vasoactive substances like histamine, bradykinin,serotonin.
  • 24.
    High risk grouppeople  Prior reactions to contrast media - 11 times more prone.  History of allergy - 4 times more prone.  Cardiac disease - 4 times more prone.  Asthma - 5 times more prone.  Diabetes - 4 times more prone.  Old age - 4 times more prone.  Neonates - 4 times more prone.  Myelomatosis, polycythemia.  Sickle cell anaemia, pheochromocytoma, homocystinuria.
  • 25.
    Severity of Reactions Minor : 1 in 20 cases - 5% -Nausea, vomiting, mild rash, light headache and mild dyspnoea. Needs no treatment, but requires assurance.  Intermediate l in 100 - 1% - Extensive urticaria, facial edema, bronchospasm, laryngeal oedema, dyspnoea, mild chest pain or hypotension. Requires treatment but generally there is no need for hospitalization.  Severe reactions (l in 2000 - 0.05%) - Circulatory collapse, pulmonary oedema, severe angina, myocardial infarction, convulsions, coma, cardiac or respiratory arrest. Requires hospitalization and intensive care.  Mortality - (l in 40,000 - 0.0025%).
  • 26.
    Treatment if needed: No patient will have serious reaction after 60 mins of contrast administration, so for first 60mins we need to monitor and watch out for adverse reactions.  Oxygen : Current recommendation for use of high dose oxygen is at the rate of 10-12 L/min via face mask.•  02 can be provided at up to 100% concentration.  Currently it is recommended that high concentration of 02 shouldbe administered to any patient in respiratory distress, regardless of his or her pre-existing condition.
  • 27.
    Treatment  Epinephrine: Themost important medication needed for Anaphylactoid reaction.
  • 28.