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CONTRASTS IN UROLOGY

INTRO …

Iodinated contrast media

Magnetic resonance contrast agents

Ultrasound micro bubble contrast agents

OPACIFY THE URINARY TRACT IN CONVENTIONAL


IMAGING TECHNIQUES

Used in intravenous pyelogram


contrast enhanced computed tomography
multi slice urography , ct angiography
contrast ultrasonography , mr angiography
INTRO…
Iodinated Contrasted Media
1930’s DI-IODINATED COMPOUNDS: LOW RADIOPACITY,
MODERATE TOXICITY

1950’ s TRI-IODINATED BENZOIC ACID DERIVATIVES

All derive from a 2, 4, 6- tri iodinated benzene ring,


with a carboxyl group at the 1-position.

Differing side chains at the 3 and 5 positions represent


different brands

advantages of urinary tract visualization, potential adverse


reactions are possible
APPLICATIONS :

INTEAVENOUS UROGRAPHY

CYSTO URETHROGRAPHY
STATIC CYSTOGRAPHY
VOIDING CYSTO URETHROGRAPHY
RETROGRADE URETHROGRAPHY

RETROGRADE PYELOGRAPHY

ANTEGRADE UROGRAPHY

LOOPOGRAPHY
Iv contrast administration
patients kept fasting for 4 hours before administration
of Iv contrast to reduce the risk of emesis and
aspiration.

BOWEL PREPARATION :
Some recommend a formal bowel preparation before
examination, although routine use is controversial.

clear liquids for 24 hours before examination and a


cathartic agent or enema.

Randomized studies : NO clear advantage in


visualization of the urinary tract with bowel
preparation, but prepared groups do have fewer
feces in their colon, which may have a subjective
impact on IVU efficacy

Bowel preparation should be considered in patients


with chronic constipation, such as patients with
neurologic deficits.
ROLE OF DEHYDRATION:

Dehydration may Improve imaging quality but has risks


necessity is controversial.

Dehydration induces an increase in antidiuretic


hormone, thus increasing tubular water resorption
and subsequent concentration of the contrast medium
( Talner, 1972 ).

Caution advised in patients with renal insufficiency,


because dehydration may exacerbate nephrotoxicity.

Overhydration should be avoided, because poor


visualization of the collecting system may
necessitate reexamination.

In practice, withholding fluids after midnight before


examination is sufficient to allow adequate
imaging.
Technique :

Initial scout radiograph is taken in the supine


position.

encompasses the field from the renal outlines to


the pubic symphysis: this is essential in revealing
renal outlines, calcifications, residual contrast
media, and positioning.

Oblique views may be taken if necessary to


allow better distinction of calcifications from
bony structures.

injection may be given as a bolus or drip


infusion, with bolus being the predominant
technique.

Fifty to 100 Ml of contrast medium is given


through an 18- or 19-gauge needle.
first few minutes after injection the nephrographic
phase produces images of the renal parenchyma.

Several tomograms may be taken to adequately


document the parenchymal outlines.

By 5 minutes the collecting system should opacify, and


imaging of the pyelographic phase commences.

A compression device may be attached, which


distends the collecting system and allows better
visualization of the pelvis and ureters.

After the 5-minute films, further imaging is


individualized to the patient, and subsequent images
should document the entire length of the ureter
for filling abnormalities
Certain accessory radiographs may be taken to
document special circumstances.

Oblique views may better visualize the calyceal


system or can allow clarification of filling
defects that may overlap in the routine ap views

Prone images place the ureter in a dependent


position and may be useful in distending and
imaging the ureter

Upright films can document renal ptosis or


layering of contrast media in severely
hydronephrotic systems.

postvoid film may be useful in evaluating


bladder outlet obstruction, diverticula, or
filling defects within the bladder
CT ANGIOGRAPHY

adequate IV access approximately 100 mL of contrast


material is given at the rate of 1.5 to 4.0 m L/s,
depending on the specific indication.

After contrast material is given, several phases of


renal enhancement occur.
optimize the scanning protocols and interpret the
findings intelligently.
1. The angiographic phase
occurs 15 to 40 seconds after injection
The number, location, and patency of the renal arteries
and the renal veins can be assessed.

2. The cortical phase


occurs between 25 and 80 seconds after
renal cortex is maximally enhanced, and the CORTICO
medullary differences are greatest

3. The nephrographic phase


usually begins 90 to 120 seconds after
characterized by the homogeneous enhancement
of the entire renal parenchyma

detection of renal lesions, particularly smaller is greatest.

4. The excretory or urographic phase


begins when contrast material is visualized in the
collecting system including calyces, infundibula, and
renal pelvis.
typically begins 3 to 5 minutes after injection and
persists for several minutes..
TYPES :
IONIC / HIGH OSMOLAR CONTRAST
NON IONIC / LOW OSMOLAR CONTRAST / organic

Hocm:
tri iodinated benzene ring with 2 organic side
chains and a carboxyl group

The ionic compounds are water-soluble salt


solutions THAT are hypertonic with an osmolality
2.5 to 6.0 times that of plasma

CATIONS: SODIUM OR MEGLUMINE ( METHYL GLUCAMINE)

ANIONS : DIATRIZOATE ( HYPAQUE , UROGRAFFIN)


IOTHALAMATE ( CONRAY )

The osmotic load of the HOCM has been associated


with an increased risk of complications
( varies from 600 to 2100 MOSM/KG )
low - osmolality ICM:

(1) non ionic monomers


3 types (2) ionic dimers
(3) non ionic dimers

Non ionic 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, non ionic 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).

at a given iodine concentration, non ionic monomers have


approximately one half the osmolality of ionic monomers
in solution
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).

Common nonionic monomers

Iohexol ( Omnipaque ) iopamidol ( Isovue )


ioversol ( Optiray ) iopromide ( Ultravist )

The nonionic monomers are the contrast agents of


choice.

In addition to their non ionic 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 (I .e; a ratio of 6 : 2).

The only commercially available ionic dimer is


ioxaglate ( HEXABRIX )

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
ioxaglate
Non ionic 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.( 280 MOSM/KG )

They are also highly viscous and thus, have limited


clinical usefulness.

Examples of nonionic dimers are


iotrol and iodixanol ( VISIPAQUE )
IONIC MONOMER NON IONIC MONOMER

IONIC DIMER NON IONIC DIMER


Advantages:
Cause fewer physiologic responses.

Produce less peripheral vasodilation

Less effect on myocardial contractility and cardiac


electrophysiology.

Non ionic agents can produce a urogram equal to or


better than ionic media

The lower osmolality and solute load allow the


non ionic agents to produce a denser pyelogram
with higher urinary iodine concentration

No significant difference in the nephrogram has


been noted .

Therefore using non ionic contrast does not


decrease the diagnostic efficacy of urography
Metabolism
Contrast material is almost entirely excreted by
glomerular filtration with little or no tubular
excretion.
Approximately 0.5% to 2.0% is excreted by the liver and
bowel. Most of this is excreted by the biliary system

small intestine, stomach, and salivary glands can


excrete small amounts.

Vicarious excretion is the term used when extrarenal


excretion is apparent on the radiograph

gallbladder and colon 24 hours after injection


in patients with decreased renal function, in whom
extra renal routes of excretion take on greater
importance.

also seen in patients with normal renal function after


they have received large doses of contrast mediuM
VICARIOUS EXCRETION
IN GALLBLADDER
The amount of contrast excretion by the kidney and
collecting system with resultant radiopacity is related to

plasma concentration
glomerular filtration rate (GFR)

Increasing the amount of contrast material will increase


the radiopacity of the urinary tract to a certain extent.

At doses greater than 2 mL/kg, the radiopacity will not


continue to increase significantly, but the risk of
toxicity is increased

The method of injection will also alter the quality


of the urogram.

PLASMA CONCENTRATION ACHIEVED BETTER WITH


BOLUS INJN. THAN DRIP INFUSION
The intensity of the nephrogram is related to
the plasma concentration
PHYSIOLOGICAL CONSIDERATIONS
subjective effects ( FOLLOWING IV INJN )

A sense of warmth and a “flushing” sensation universal


(misinterpreted as a reaction)

A metallic taste and circumoral tingling observed.

Sensations of pelvic and perineal warmth

These uncomfortable side effects are virtually


eliminated with nonionic contrast media

physiologic responses

mild and transient decrease in the systemic blood


pressure along with a transient decrease in the heart rate

Pulmonary arterial pressure has been found to be


transiently increased
Renal blood flow is initially increased 
decrease in renal blood flow proportional to the
dose administered

decreased myocardial contractility

secondary to calcium binding and a depressant


effect on the SA and AV nodes

Sub clinical bronchospasm

These effects are all transient


INCIDENCE :
overall incidence of contrast reactions of all types
5% to 8%

major respiratory or cardiovascular reactions


fewer than 1%

The reported frequency of fatal reactions ranges


between 1 in 14,000 and 1 in 75,000

the overall risk of any adverse reaction


2.66% with ionic ICM
3.13% with non ionic ICM

the risk of a severe adverse drug reaction


0.2% for ionic ICM
0.04% for nonionic ICM
the single most important risk factor for an adverse
reaction is
the type of contrast agent

Adverse reactions to ICM are classified as


idiosyncratic
non idiosyncratic

The pathogenesis involves

direct cellular effects enzyme induction

activation of the complement fibrinolytic, kinin. Sys.


Idiosyncratic Reactions

begin within 20 minutes of injection, independent


of the dose that is administered.

these are not true hypersensitivity reactions.

Immunoglobulin E (IgE) antibodies are not involved.


previous sensitization is not required
do not consistently recur in a given patient.

For these reasons, idiosyncratic reactions to ICM are


called anaphylactic reactions.

The symptoms
Mild moderate severe

In most series, 95% or more of all reactions are


classified as mild to moderate.
Mild reactions :
mild SCATTERED urticaria ( MC REPORTED )
Rhinorrhea , nausea, brief retching and/or vomiting;
diaphoresis , coughing DIZZINESS
Moderate REACTIONS:

persistent vomiting , diffuse urticaria,

HEADACHE facial edema,

laryngeal edema , mild bronchospasm or dyspnea,

palpitations, tachycardia or BRADYCARDIA

abdominal cramps

Severe reactions :

intense bronchospasm with laryngeal edema

along with potentially lethal cardiovascular responses


marked hypotension
pulmonary edema

ventricular arrhythmias  cardiovascular collapse.


Non idiosyncratic Reactions

include the following:


bradycardia hypotension and vaso vagal reactions

nephropathy ( cin ) cardiovascular reactions

extravasation delayed reactions

minor reactions include

sensations of warmth,
a metallic taste in the mouth,
nausea and vomiting.

Extravasation (during an injection )

Tissue damage as a result of


direct toxicity of the contrast agent
pressure effects such as compartment syndrome.
Delayed reactions

become apparent at least 30 minutes after but


within 7 days.

identified in
14 - 30% ionic monomers
8 - 10% nonionic monomers.

Common delayed reactions include

the development of flulike symptoms

fatigue, weakness, upper respiratory tract congestion,

fevers, chills, nausea, vomiting, diarrhea,

abdominal pain, pain in the injected extremity, rash,

dizziness, and headache


Risk factors for ICM reactions
for idiosyncratic reactions

previous reaction to ionic or non ionic ICM

Relative risk of a repeat reaction 3.3 to 6.9 folds greater

People with asthma

have 1.2- 2.5 times the risk of such reactions

reactions more likely to be severe.

Severe reactions are 5-9 times more common

Patients with allergies, including hay fever

1.5 - 3 times greater risk


no risk with sea food or shellfish allergies
for non idiosyncratic reactions.
Interleukin -2 immunotherapy for cancer

increases the incidence and severity of


delayed reactions.
can occur even if immunotherapy is administered
as long as 2 years before

Metformin
In azotemic pts, increased tissue levels of metformin
may rarely induce life-threatening lactic acidosis.

should be discontinued in all patients at the time of or


before any intravascular contrast-enhanced study
,
metformin administration should be withheld for at
least 48 hours after the contrast-enhanced study

administration should be resumed only after the absence


of renal dysfunction has been documented.
beta-blockers
can aggravate ICM-induced bradycardia, other cardiac
arrhythmias, hypotension, and bronchospasm

interfere with the treatment of ICM-related adverse events

pregnancy
mutagenic to human cells ( in vitro studies )

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 ICM
Prophylactic medications

methylprednisolone, 2 oral doses of 32 mg each


administered at 12 and 2 hours before ICM
administration (Lasser et al )

50 mg of oral prednisolone at 13 hours, 7 hours, and 1


hour before injection of the contrast material and 50
mg of oral diphenhydramine at 1 hour before ICM
injection (Greenberger et al )

single 100-mg tablet of hydroxyzine 12 hours before


the intravenous injection of the ionic dimer ioxaglate

H2 blockers, such as cimetidine, variable effect

ephedrine (sympathomimetic cardiac effects )


Recommended prophylactic regimens

Most authorities restrict corticosteroid pre


treatment to patients in whom previous idiosyncratic
adverse reactions to ICM were moderate or severe.

allergic reactions along with respiratory and


cutaneous component
H1 ( diphenhydramine ) and h2 blockers ( ranitidine )

corticosteroids are well tolerated and cause no


adverse effects when only a few doses are administered

The treatment of the non idiosyncratic adverse


reactions of nausea and vomiting is not considered a
routine indication for corticosteroid premedication
or the use of non ionic ICM
Treatment of Adverse Reactions
Overview

Most adverse reactions occur within 20 minutes of injection.


Should be monitored for a minimum of 20 minutes

physician who is responsible for an imaging study 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.

examination of a patient with an adverse reaction

brief history should be obtained

summary of the current symptoms


Any medical conditions (eg, heart disease)
the patient's medications.
Vital signs should be assessed

Closely monitored

Assessment of the patient's airway, breathing, and


circulation (ABCs) remain the cornerstone

Primary 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.
Treatment of Anaphylactic Reactions
RESPIRATORY DIFFICULTY

NEEDS more aggressive therapy.


O2 dministration, 10-12 L/min via a partial non
rebreathing mask

SEVERE bronchospasm AND upper airway edema


(including laryngospasm)

epinephrine should be injected promptly.

optional in normotensive patients, necessary in


HYpotensive patients respiratory reactions

administered with care to patients WITH cardiac


disease Or those who are taking beta-blockers
( RISK OF HYPERTENSION AND ANGINA )

NO MAJOR ROLE FOR ANTI HISTAMINES


Hypotension

*intravenous iso-osmolar fluid


(ie, normal saline, Ringer lactate solution in large
volumes.)

*Use of vasopressors should be considered.

Dopamine ( MOST EFFECTIVE )


infusion rates of 2-10 mcg/kg/min

*Epinephrine is less useful


( its results are less predictable, and it has more
adverse effects )
Urticaria
Asymptomatic: No treatment is needed.

Symptomatic, mild or moderate: Diphenhydramine 50 mg


may be administered orally, IM or IV

Severe: Treatment is as above;


consider adding IV H2 BLOCKERS

Bronchospasm
Mild: oxygen 10-12 L by face mask,
2 puffs of an albuterol or metaproterenol inhaler.

Moderate, without hypotension: Treatment is as above,


with epinephrine 1:1000, 0.1-0.3 mL given subcutaneously,
repeated every 10-15 minutes as needed until 1 mL is
administered.

Severe: Administer epinephrine 1:10,000 1 Ml slow


intravenous injection over approximately 5 minutes,
repeated every 5-10 minutes as needed
Laryngeal edema

Mild to moderate:
oxygen 10-12 L by face mask
epinephrine 1:1000 0.1-0.3 mL given subcutaneously,
repeated every 10-15 minutes as needed until 1 mL is
administered.

Moderate to severe:
Consider calling a code or intubating the patient.
Consider adding diphenhydramine 50 mg slow iv and
cimetidine 300 mg slow iv or ranitidine 50 mg slow iv

Isolated hypotension

Raise the patient's legs as much as possible while


preparing to administer intravenous fluids
.
The Trendelenburg position can also be
effective, but many radiographic tables do not tilt.

Oxygen should be administered in high doses


Hypotension with tachycardia
Mild to moderate:
Elevate the patient's legs.
Administer oxygen 10-12 L by face mask
intravenous isotonic fluid ( eg, 0.9% isotonic sodium
chloride solution, Ringer lactate solution).

Severe or unresponsive:
Treatment is as above, with dopamine 2-20 mcg/kg/min.
Call a code if no response occurs.

Vasovagal reaction
Mild to moderate reaction:
Elevate the patient's legs.
Administer oxygen 10-12 L by face mask
intravenous isotonic fluid (eg, 0.9% isotonic sodium
chloride solution, Ringer lactate solution).

Severe reaction or unresponsive patient:


intravenous atropine 0.6-1 mg, repeated every 3 - 5
minutes as needed until a total of 3 mg is
administered.
Treatment of Non idiosyncratic Reactions
depend on the type of reaction.

Vasovagal reaction

iso-osmolar fluid

bradycardia :
reversed with intravenous atropine 0.6-1 mg, repeated
every 3-5 minutes to a total dose of 3 mg, if needed.

Cardiac arrhythmias

A defibrillator should be obtained immediately, and


cardioversion or defibrillation should be performed.
Hypertensive reactions

nifedipine, a 10-mg tablet sublingually

No longer the favored drug

unpredictability of its response


its hemodynamic profile
the risk of reflex sympathetic hyperactivity.

Additional doses of the patient's usual


antihypertensive medications may be helpful.

Intravenous fenoldopam, labetalol, and nitroglycerin,


oral clonidine or captopril are reasonable choices

Intravenous furosemide 40 mg can also be used.


Seizure

hypoxia due to
respiratory insufficiency
intrinsic central nervous system (CNS)
response to the ICM.

Patients should be turned on their side


to prevent aspiration
high-dose oxygen should be administered.

When hypoxia is the cause of the seizure activity,


intubation may be required for adequate oxygenation.

In the case of primary CNS seizure activity, intravenous


diazepam 5 mg may be injected and repeated if necessary.

An emergency medical specialist should be consulted.


Pulmonary edema

elevate the patient's head

administering oxygen

intravenous injection of furosemide and


morphine 1-3 mg every 5-10 minutes as needed.

Angina
sublingual nitroglycerin and oxygen.

An electrocardiogram (ECG) may be obtained to assess


ischemic changes.

If the patient's symptoms persist or are new

cardiologist should be consulted, patient


transferred to an emergency department.
Delayed reactions

treated in a supportive manner,

analgesics are administered to treat headaches

antipyretics to treat high temperatures

meperidine to treat rigors; isotonic fluid to treat


hypotension

Extravasation injuries

elevate the affected extremity and apply cold


compresses.

if pain gradually increases over 2-4 hours,


If skin blistering or ulceration develops
If the circulation or sensation changes at or distal to
the level of the extravasation

Consult plastic surgeon


Contrast Induced Nephropathy ( C I N )
DEFN : ( esur )
an elevation of the serum creatinine level
more than 0.5 mg% or more than 25% of the baseline
level within 3 days after the ICM injection without
an alternative etiology .

The elevation peaks by 3 - 7 days

Creatinine level usually returns to baseline


in 10-14 Days.

The incidence is estimated to be 2 - 7 %.

Third most common cause of hospital acquired renal


failure ( hypoperfusion , drug induced )

25% of patients with this nephropathy have a


sustained reduction in renal function, most
commonly when the nephropathy is oliguric
less common following intravenous than intra arterial
administation

patho physiology :
Combination of toxic injury to tubules and ischemic injury
partly mediated by reactive OXYGEN species

Prolonged vasoconstriction and medullary ischemia

Increased perivascular hydrostatic pressure

INCREASED OSMOTIC LOAD  INCREASE IN PROXIMAL TUBULAR


PRESSURE- Gradual decrease in renal blood flow AND
moderate decrease in gfr

Afferent vasodilation and renin release counteracts the


fall in gfr ( lost in patients with diabetes and renal
failure )
Risk factors

preexisting renal insufficiency : 5-10 times MORE the risk

diabetic nephropathy  greatest risk

In general , the higher the pre existing serum creatinine


level, the greater THE nephrotoxicity.

Other factors
congestive heart failure ( NYHA CLASS IV )

dehydration hyperuricemia

concomitant use of nephrotoxic drugs


aminoglycoside antibiotics and NSAIDs

large doses of ICM for a single study or multiple


contrast -enhanced studies that are performed within
a short period.

advanced age

Cirrhosis and nephrotic syndrome ( ALTERED HEMODYNAMICS )


Clinical presentation

Most commonly : non oliguric and asymptomatic transient


decline in renal function

Acute renal failure requiring hemodialysis < 1 %

Complications like hematoma formation , pseudoaneurysms


stroke , coma , adult respiratory DISTRESS syndrome ,
pulmonary embolism
(in pts undergoing coronary intervention )

Hospital stay, complications , mortality depends upon gfr

Urinary epithelial cell casts, debris urate , calcium


oxalate crystals are

non specific and are not pathognomic


Reducing the incidence of ICM nephropathy

Other nephrotoxic drugs should be discontinued


whenever possible

the minimal amount of contrast material that is


needed to perform a diagnostic study should be used.
MAX 2ML / KG

CONTRAST LIMIT :
30 ML FOR DIAGNOSTIC STUDY
100 ML FOR INTERVENTIONAL PROCEDURE

Non ionic agents ( ISO OSMOLAR OR LOW OSMOLAR )


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.
ROLE OF HYDRATION

Patients can be well hydrated until 12 hours before a


contrast - enhanced study

hydration should be continued for at least 2 hours


after a contrast-enhanced procedure is performed.

HYDRATION AMELIORATE THE HARMFUL EFFECTS OF


CONTRAST AGENTS

INCREASE GFR BY PLASMA VOLUME EXPANSION AND


SUPPRESSING RAS  DOWNREGULATE TUBULO
GLOMERULAR FEEDBACK

USUALLY WITH NORMAL SALINE 1- 2 ML / KG / HR

1000 mEq /L OF SODIUM BICARBONATE IN 5% DEXTROSE AT


A RATE OF 3 ML / KG (ONE HR BEFORE TO 6 HRS AFTER)
FOUND TO BE BETTER CHOICE

ANTI OXIDANT FREE RADICAL SCAVENGING PROPERTY


ROLE OF N- ACETYL CYSEINE

THIOL CONTAINING ANTIOXIDANT

FREE RADICAL SCAVENGING EFFECT AND FORMATION OF


SULFHYDRL COMPOUNDS
NAC + NO  S- NITROTHIOSOL ( VASODILATOR )

INCREASE NO SYNTHASE  ENDOTHELIUM DEPENDENT


VASODILATION AND RENAL BLOOD FLOW INCREASE

BOTH ORAL AND IV PREPARATIONS

ORAL : 600 -- 1200 MG TWICE DAILY BEFORE AND AFTER


SHOULD BE STARTED 12 TO 24 HRS BEFORE
USEFUL IN CCF PATIENTS

IV : 500 - 1200 MG AS INFUSION IN 5 % DEXTROSE


1 - 2 HRS BEFORE TO 6 HRS AFTER

FOUND TO BE EFFECTIVE IN PREVENTING CIN IN VARIOUS META


ANALYSIS
ADENOSINE ANTAGONISTS

THEOPHYLLINE : NON SPECIFIC ADENOSINE RECEPTOR


ANTAGONIST

ADENOSINE ENHANCES THE RENAL HEMODYANAMIC


EFFECTS OF ICMRESULTING IN LOCAL RENAL
VASOCONSTICTION

MAXIMAL BENEFIT WITH DOSE 200 MG TWICE DAILY 24 HRS


BEFORE AND 48 HRS AFTER

NOT STRONGLY RECOMMENDED BY META ANALYSIS


STATINS IN CIN PREVENTION

AMELIORATION OF AT II MEDIATED ORGAN DAMAGE

INCREASED EXPRESSION OF INDUCIBLE NO SYNTHASE

STATINS PRIOR TO PROCEDURE ( IN RENAL IMPAIRED PTS )

DECREASED ACUTE RENAL FAILURE AFTER


ANGIOGRAPHIC STUDIES
OTHER AGENTS UNDER STUDY

TRIED BUT FOUND TO BE NOT USEFUL

•FENOLDOPAM : SPF . DOPAMINE – 1- RECEPTOR


( VASODILATION )

•DOPAMINE

•FRUSEMIDE: FOUND TO HAVE WORSE OUTCOME

• ILOPROST : PROSTAGLANDIN ANALOGUE: RISK OF


HYPOTENSION

•ATRIAL NATRIURETIC PEPTIDE

•ENDOTHELIN RECEPTOR ANTAGONIST : BOSENTAN

•CALCIUM CHANNEL BLOCKERS


MR contrast agents
first- generation MR contrast agents are “non-specific”

small molecular weight gadolinium chelates

Distribute in to the intravascular and interstitial


(extracellular) spaces

allows for physiological evaluation


of renal function, and kidney-specific anatomy
approach referred to as MR renography

Gadolinium diethylene triamine penta acetic acid


(Gd-DTPA) is mostcommonly used for this purpose.
GADOPENTATE GADODIAMIDE

GADOVERSATAMIDE

GADOTERATE GADOTERIOL
GADOBUTROL
tissue-specific contrast agents

hepatocyte specific
Reticulo endothelial system (RES) specific

characterization of focal liver lesions such as


metastases from urological cancer.

Hepatocyte specific agent

Gadobenate Dimeglumine distributes to the


extracellular space but is selectively taken up
by functioning hepatocytes and biliary excreted

Mangafodipir
manganese ion is a powerful T1 relaxation agent, and
an effective positive liver enhancer

small amount of agent (5μmol/kg) can


significantly improve contrast between focal liver
lesions and healthy parenchyma
RES- specific compounds
Largely super paramagnetic iron oxide (SPIO) particles

induce dramatic magnetic field disturbances, which


translate in to strong T2 effects.

These nanoparticles rapidly target the Kuppfer


cells of the liver causing a decrease in T2 signal
in healthy parenchyma, but not in metastases.

found increasing application as


intravenous MR lymphographic agents

In lymph nodes containing metastases, there is less


USPIO uptake, leading to relative hyperintensity
(i.e. ,no enhancement).

A focal area of relative signal hyperintensity may


represent an area of segmental malignant
infiltration within the node.
The optimal time for evaluation post-contrast is
24–36 hrs

allowS sufficient USPIO to accumulate within


the nodes ( early imaging result in a significant
false negative rate )

This has been evaluated to good effect in


prostate cancer, with the sensitivity of detection
of nodal metastases vastly superior to
conventional MR imaging
MR angiography (MRA) has increasing application,
particularly in surgical planning for urological cancer.

However, the extracellular agents rapidly pass out of


the I V SPACE, and so require rapid dynamic imaging in
order to provide a sufficient contrast to noise ratio
(vessel to background on MR).

Gadobutrol
newer extracellular agent currently licensed in
Europe but not IN the USA

Has double the concentration of gadolinium as


conventional extracellular agents
This has been shown to be efficacious in
pulmonary Imaging

Due to the reduced volume required for the


Same dose of gadolinium, it has been proposed as an
agent for MRA.
Caution …
The FDA recommends avoidance of all gadolinium
contrast media

in patients with SEVERE GRADES renal insufficiency


(GFR < 30 Ml / min per 1.73 m2)
OR
any grade of acute renal failure in liver
Transplantation patients.

On September 9, 2010, the FDA announced it is


requiring that gadolinium-based contrast agents
(GBCAs) carry new warnings on their labels about
the risk of nephrogenic systemic fibrosis (NSF) and
its association when administered to certain
patients with kidney disease
Nephrogenic systemic fibrosis (NSF)
Recently been reported in patients with advanced renal insufficiency (glomerular filtration rate [GFR] <30 mL/min).

Fibrosing disease of the skin, subcutaneous tissues, lungs, esophagus, heart, and skeletal muscles.
Initial symptoms typically include skin thickening and/or pruritus.

Symptoms and signs may develop and progress rapidly, with some affected patients developing contractures and joint
immobility within days of exposure.

Death may result in some patients, presumably as a result of visceral organ


involvement.

Onset of NSF varies between 2 days and 3 months.

Early manifestations include subacute swelling of distal extremities,


followed by severe skin induration and later even organ involvement.

Patients with chronic kidney disease (CKD) have a 1% to 7% chance of


developing NSF after MRI imaging with gadolinium agents
Ultrasound contrast agents : Micro bubbles

INTRODUCED IN 1990s.

less than 10 μ m in diameter so they can cross


capillary beds and are safe, effective echo
enhancers When administered intravenously

remain within the vascular compartment, unlike CT


and MR contrast agents

consist of a GAS (air or a per fluoro carbon) which is


stabilized by a SHELL (denatured albumin,
phospholipid or surfactant or cyanoacrylate)
Microbubbles produce marked augmentation of
the ultrasound signal for several minutes after an
intravenous bolus or for 15–20 min after an infusion
with enhancement in gray-scale and Doppler signals
of up to 25 dB
(greater than 300-fold increase).

The most widely used is Sonovue which is licensed in


Europe and Asia and consists of sulfur hexafluoride
SF6 gas surrounded by a phospholipid shell
MICROBUBBLES UNDER ELECTRON MICROSCOPY
Contrast-enhanced ultrasound (CEU)

uses gas-filled microbubbles as a tracer to assess


tissue perfusion with ultrasound.

microbubbles remain entirely within the


intravascular space and have a rheology similar to
that of RBC

IT IS hypothesized that measurements of their


renal tissue kinetics could be used TO Quantify
RBF as well as renal NBF.
APPLICATIONS..
useful in differentiating renal tumors from
pseudotumors such as a column of Bertin.

In pseudotumors the vasculature exhibits regular


and smooth branching compared to the chaotic
pattern seen in malignancy

useful in the assessment of renal cysts and can


reliably distinguish hemorrhagic and inflammatory
cysts from solid renal tumors

The presence of septal or mural nodular


enhancement is suggestive of malignancy.
useful to assess tumor vascularity and extent of
necrosis and to identify enhancement in tumor
thrombus.

In carcinoma of the prostate US contrast has shown


Promising results but its role in detection, staging,
and treatment is still under evaluation

HELPFUL IN CALCULATING MICRO CIRCULATORY FLOW RATE IN


RENAL TRANSPLANT PTS

by destroying microbubbles BY INTERMITTENT HIGH POWER


ULTRASOUND PULSES and measuring their tissue
replenishment with intermittent harmonic imaging.
THANK U

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