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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3591_Библиотеки_им_академика_М_И_Перельмана.pdf
24
S. Goswami et al.
Recommendations forPrevention
(i) The rst and also the most crucial step in the prevention
of renal injury is the identication of patients at risk for
risk stratication as well as justifying the need for the
administration of contrast media. Risk stratication
should be done based on eGFR/eCr, the presence of diabetes, AKI, and medications [3, 48].
(ii) Multiple contrast-enhanced studies involving the
administration of multiple ICM doses within a short
span of time are associated with an increased risk and
should be avoided [34, 35].
(iii) Intravenous normal saline for volume expansion can be
given to reduce the risk of developing AKI prior to contrast administration [49–55].
(iv) If eGFR/eCCr is <60, standard precautions include IV
hydration with normal saline and the use of low or isoosmolar contrast media. For intra-arterial administration, IOCM may be preferred based on patient tolerance
and reduced pain. N-acetyl cysteine administration to
prevent nephrotoxic effects is unproven and therefore
not recommended [3, 56].
(v) Bicarbonate is not considered superior to normal
saline for the prevention of CA-AKI and is not preferred due to a need for additional formulation preparation [3].
(vi) Nephrotoxic medications should be avoided if possible or
modied. In patients with AKI, severe chronic kidney disease (stage IV or V, eGFR <30) or those undergoing procedures with a risk of emboli to the renal arteries,
metformin should be temporarily stopped before the procedure and withheld for 48 hours afterwards. It should be
resumed only after renal functon is found to be normal on
reassessment [57, 58]. Nephrology consultation should be
sought for patients having eGFR/eCCr of <30. Efforts
should be made to reduce contrast doses during procedures. Interventional radiologists should be familiar with
the risk factors and diagnostic criteria of CA-AKI and
exercise various preventive strategies to minimize the risk.
4.3 Carbon Dioxide
phy during various interventions. As it is low in viscosity, with
appropriate use, CO
is less likely to cause tissue damage [61].
2
4.3.2 Contraindications
Despite having few advantages over more conventional contrast agents, CO2 angiography has certain contraindications
that need to be understood prior to its application. It is best to
not use CO2 in procedures above the diaphragm to minimize
the risk of cerebral air embolism whether it is due to a preexisting right-to-left cardiopulmonary shunt (cardiac septal
defect) or due to reux within a carotid or vertebral artery to
the brain [62]. To minimize this risk, Trendelenburg’s position
should be considered during procedures whenever possible. It
should be avoided when nitrous oxide is being used for sedation because it decreases the solubility of CO2 in blood and
prevents its excretion. It should be used with caution in patients
with pulmonary artery hypertension as it can potentially raise
the vascular bed pressure with over-administration.
4.3.3 Equipment
Currently, there is a single FDA-approved medical CO2
delivery system available consisting of a CO2 high-pressure
reservoir/delivery device and a low-pressure valve called the
K-valve [63]. Large medical-grade CO2 cylinders are not
FDA-approved. The entry and exit points of the system must
be sealed until the physician is ready to connect the system
to a catheter. It is imperative to have a trained technologist
for handling, setting up, and safely using the CO2 delivery
apparatus to ensure patient safety.
4.3.4 Preparation
Fluid (blood/saline) in the angiographic catheter must be
purged to prevent vessel dissection from explosive delivery
of uid during CO2 angiography [62].
CO2 is a negative contrast agent and can be used alternatively
in patients where iodinated contrast agents are contraindicated. It was used for the rst time in human subjects in 1956
by Barrera [59] via needle injection, and FDA-approved CO2
delivery systems are now available for administration.
4.3.1 Indication
CO2 is less viscous and a cheaper contrast which can be used to
the operator’s advantage. It can be used for arteriography,
wedged portal venography, e.g., during TIPS [60], and venogra-
4.3.5 Technique
An end-hole catheter is ideal for CO2 injection in large vessels like the aorta, IVC, and pulmonary arteries [62]. Multiple
options are available for CO2 delivery from the source, i.e.,
hand-injection, Bag reservoir delivery system,
CO2MMANDER/AngiAssist Portable system, automated
injectors, and CO2 Angioset [64]. While using hand injection, the use of a larger syringe (20–30mL) should be preferred to prevent explosive delivery into the vessel due to
compression in the syringe. Similar to conventional
CO
2
angiography, the CO2 injection rate is also determined by the
4 Contrast andDrugs inInterventional Radiology
25
caliber and diameter of the vessel as well as that of the capillary bed. The following volumes are considered sufcient for
corresponding vessels:
(i) 30–40 mL; up to 60 mL sufces for abdominal aorto-
gram/inferior vena cavogram
(ii) 20–30mL is sufcient for major aortic branches
(iii) 10–20mL for Wedged portal venography via the supe-
rior mesenteric artery
CO2 injections should be administered at least 2min
apart as CO2 dissolves within 30–60s.
Image optimization is crucial in successful CO2 angiography. It is highly susceptible to motion artifact, and therefore
various measures should be taken to reduce peristaltic and
respiratory motion, using mask imaging subtraction and
using higher frames per second, higher resolution, etc. [64].
It has been advised in various guidelines that monitoring of
CO2 retention with capnography (ETCO2) should be done
during conscious sedation procedures [65].
4.3.6 Complications
Air embolism during CO2 angiography is one of the most
serious complications that can potentially lead to amputation,
stroke, myocardial infarction, or in rare cases even death,
although the risk is reported to be less than 1% [62]. Other
commonly encountered side effects include paresthesia, nausea, and tenesmus. Mesenteric arteriography may cause
abdominal pain which can be controlled if the patient is
rotated from side to side. In case of non-resolving pain, vapor
lock should be suspected. It is a phenomenon occurring when
gas is trapped intra-arterially due to having a diffusion constant which prevents the gas from dissolving in blood and also
interrupts blood ow through the gas and eventually might
lead to mesenteric infarction if not treated. Mechanically dislodging the gas bubble through massage, patient rotation,
and/or catheter aspiration should be done. So far, CO2 poisoning has not been reported in the literature.
variability for estimation of caliber [67], and lower accuracy
for determining stenosis and even lesser visualization of infrapopliteal arteries [68]. There is a need to position the patient
accordingly for visualizing the posterior course of arteries as
CO2 tends to be lighter and remains on the surface of blood
are some of the disadvantages.
4.4 Anticoagulation andAntiplatelet
Medications
Prior to any IR procedure, planning and patient assessment are
the initial most crucial steps for ensuring a successful outcome
of the procedure. Risk stratication includes the type of procedure, assessment of coagulation parameters, and various anticoagulation medications that are indicated for prophylaxis and
treatment of vascular diseases (e.g., arterial and venous thrombosis, cerebral vascular disease, and ischemic heart disease).
The interventional radiologists need to decide on whether to
continue or hold the antiplatelet or anticoagulation medications.
Therefore, it is indispensable that interventional radiologists be
aware of the anticoagulation and antiplatelet medications, their
indications, adverse effects, and drug interactions.
Due to wide variations in the assessment of coagulation
parameters and subsequent management, society consensus
guidelines have been laid down by the Society of
Interventional Radiology (SIR) and the Cardiovascular and
Interventional Radiology Society of Europe (CIRSE) to
avoid these discrepancies [69–71]. Updated guidelines for
anticoagulation status assessment and management have
been published by SIR [72, 73].
4.4.1 Thrombolytics
Thrombolytics convert plasminogen into active plasmin,
which breaks down the blood clot to treat blockage [74].
These are safe and effective treatments for arterial ischemia,
venous thrombosis, massive pulmonary embolism, and acute
stroke. They may also be used to clear blocked catheters that
are used in long-term medical therapy.
4.3.7 Advantages
Due to lower viscosity, CO2 is more sensitive in situations
where there is a low ow system, e.g., arteriovenous stula,
slow GI hemorrhage, slow ow in a vessel (e.g., a bypass
graft), slow ow endoleak, and tumor blush [64].
4.3.8 Disadvantages
Inaccurate estimation of the vessel caliber when compared
with liquid contrast media [66] and a greater inter-observer
Table 4.2 Classication of thrombolytics
A.First generation (non-brin specic)
• Streptokinase
• Urokinase
B.Second generation (brin specic)
• Prourokinase
• Recombinant tissue plasminogen activator: Alteplase (Rt-PA)
C.Third generation (brin specic)
• Reteplase (r-PA)
• Tenecteplase (TNK-tPA)
• Desmopletase
26
S. Goswami et al.
4.4.1.1 Classication
Thrombolytic agents are classied into three generations of
drugs. The classication of thrombolytics is detailed in
Table4.2.
First-Generation Thrombolytic Agents
• Streptokinase: It is a non-brin selective plasminogen
activator and therefore degrades brinogen along with
other proteins that enhance its action.
• Urokinase: Unlike streptokinase, it activates plasminogen
directly and also lacks an antigenic response. However,
being a non-selective plasminogen activator, its use can
result in a severe lytic state [75].
• Dosage: Bolus—50,000U, Infusion—5000U/h for 12h.
Second-Generation Thrombolytic Agents
• Tissue plasminogen activator: It is a brinolytic agent
produced in vivo by endothelial cells and is a 527amino acid single-chain serine protease. It is involved
in maintaining the delicate intravascular balance of
thrombolysis and thrombogenesis [76]. It is brin
selective and does not activate free plasminogen in
blood. The binding of tPA and plasminogen to brin
accelerates the conversion of plasminogen to plasmin
which causes thrombolysis. Additionally, tPA also has
high brin afnity, i.e., it forms a strong bond with
brin. Off-label, it is also used for catheter-directed
venous and arterial thrombolysis.
• Alteplase (r-tPA) is a commercially available form of
tPA, produced with recombinant technology and
approved by the Food and Drug Administration (FDA)
[76] for acute myocardial infarction, acute stroke, massive pulmonary embolism, and central venous catheter
occlusion. The recommended dosage for catheterdirected thrombolysis: continuous, 0.5–1.0 mg/kg/h
(40mg maximum); bolus, 2–5mg bolus, then continuous infusion; pulse spray, 0.5mg/mL at 0.2 mL every
30–60s [77].
Third-Generation Thrombolytic Agents
• Tenecteplase, TNK-tPA, is developed by modifying enzymatic sites on tPA which improves the activity by increasing its brin specicity and prolonging its half-life [78].
Due to these, brinogen is depleted to a lesser extent, and
a longer half-life allows a single bolus administration
rather than continuous intravenous (IV) infusion [78].
Dosage: continuous, 0.125–0.25 mg/h; bolus, 1–5 mg,
then continuous infusion [79].
• Reteplase: Developed after several deletions of the
domain of tPA.It has a fourfold longer half-life (18min
vs. 4min for tPA) [80]. Dosage: continuous, 0.25–0.5U/h
(20units maximum); bolus, 2–5U bolus, then continuous
infusion [79].
4.4.1.2 Contraindications
Absolute contraindications for the use of thrombolytics are a
history of drug allergy and intracranial bleeding; active bleeding, hemorrhagic disorder, surgery within the past 10days,
serious GI bleeding within 3months, aortic dissection, and
hypertension with diastolic blood pressure>110mmHg are
some of the relative contraindications [74].
4.4.1.3 Adverse Eects
Adverse effects include bleeding complications at the catheterization site, and gastrointestinal and cerebral hemorrhages [81, 82]. Re-thrombosis can occur following
thrombolysis, and therefore, anticoagulants such as heparin
are usually co- administered and continued after thrombolytic therapy [83].
4.4.2 Anticoagulants
These include unfractionated heparin (UFH), low- molecularweight heparin (LMWH), and warfarin.
4.4.2.1 Unfractionated Heparin (UFH)
Heparin belongs to a heterogeneous group of linear polysaccharides of the glycosaminoglycan family. It is one of the
most commonly used and earliest anticoagulants [84].
Mechanism
It activates plasma serine protease inhibitor antithrombin
(AT) which inactivates thrombin (factor IIa) and factor Xa
[85, 86]. Apart from the anticoagulation effect, heparin also
has an antithrombotic effect through inhibition of the tissue
factor VIIa complex by inducing tissue factor pathway inhibitor secretion from vascular endothelial cells; this eventually
impedes thrombus formation.
The half-life of UFH is 60–90min. For high-risk procedures, UFH should be stopped 4–6h prior. Intravenous UFH
has an immediate antithrombotic effect, while the time to act
for subcutaneous injection is 60min.
Since UFH’s half-life and effects show variability, it is
recommended to monitor activated partial thromboplastin
time (aPTT) for monitoring therapy and adjusting the
dose [72, 87].
Indications
Heparin is used in treating acute peripheral arterial thromboembolism and ACS treatment. In the case of pulmonary
embolism and venous thrombosis, it is indicated for both
prophylaxis and treatment [85, 88, 89].
4.4.2.2 Low-Molecular-Weight Heparin (LMWH)
LMWH are fractions of heparin and obtained by various
methods and thereby heterogeneous in composition.
4 Contrast andDrugs inInterventional Radiology
27
Enoxaparin and dalteparin are commonly used LMWHs.
Bemiparin is a second-generation LMWH with the lowest
molecular weight and longest half-life [90].
Mechanism
Most of the LMWH acts mainly by inhibiting factor Xa
through antithrombin due to their smaller size and not
through AT-mediated thrombin inactivation. The half-life of
LMWHs is 4–6h [73, 87].
Indications
LMWHs are mainly used for venous thrombosis prophylaxis. Bemiparin is used for VTE prophylaxis and clot prevention during hemodialysis [91].
Special Considerations
Therapeutic doses of LMWH should be stopped 24h before
high-risk procedures. Only one dose of prophylactic
Enoxaparin needs to be held before a high-risk procedure
[73, 87].
4.4.2.3 Warfarin
Mechanism
An oral anticoagulant, it inhibits vitamin K-dependent coagulation factors (i.e., factor II, VII, IX, and X) and proteins C
and S synthesis in the liver by inhibiting vitamin K reductase
and epoxide reductase enzymes which are involved in the
pathway of formation of these factors [92].
4.4.3.1 Aspirin
Mechanism
It reduces the production of thromboxane A2 by irreversibly
inhibiting cyclooxygenase-1 (COX-1) which results in
reduced platelet aggregation. Due to its irreversible inhibition of COX-2, it acts for 7–10days (duration of lifespan of
platelets) [99].
Route andDose
For the antiplatelet effect, recommended doses of Aspirin are
80 mg and 325 mg. At higher doses, it also has an antiinammatory effect as it inhibits cyclooxygenase-2 (COX-2)
[99, 100].
Recommendations
It is recommended to stop Aspirin for 3–5days before procedures with a high risk of bleeding [72, 101]. Aspirin can be
resumed 24h after the procedure [102]. For low-risk procedures, Aspirin should not be stopped [103].
4.4.3.2 Clopidogrel
Mechanism
It belongs to the thienopyridines class of drugs which cause
irreversible inhibition of the P2Y12 adenosine diphosphate
(ADP) receptor that is present on the platelet surface and
thereby interrupting platelet aggregation and brinogen
binding [104, 105].
Indications
It is used for the treatment of venous thromboembolism and
for reducing the risk of death, thromboembolic events, or
recurrent myocardial infarction in patients with myocardial
infarction. In patients with atrial brillation, with mechanical heart valve, warfarin is used for prophylaxis [93].
Special Considerations
After 4–5 days of starting therapy, its full anticoagulation
effect (INR C 2.0) is achieved, while stopping therapy for
4–5 days ensures an INR of 1.2 in patients with a steadystate INR between 2.0 and 3.0 [94, 95].
For patients undergoing high-risk procedures, warfarin is
to be withheld 5 days before the procedure, which would
result in an INR of 1.5; whereas for patients undergoing lowrisk procedures, a shorter period (2–3days) is adequate for
an INR between 1.5 and 2 [96, 97].
Administration of oral 1mg vitamin K to normalize raised
INR on the day before surgery can be done [98].
4.4.3 Antiplatelet Drugs
These include aspirin, clopidogrel, and glycoprotein IIb/IIIa
inhibitors.
Route andDose
It is activated after being metabolized in the liver; its plasma
level peaks 1–2h after administration with a half-life of 6h
[104]. With the standard dose, i.e. 75mg/day, the maximum
effect is achieved 4–7days after the onset of therapy and in
4–6h of administration of a loading dose (300–600 mg) of
clopidogrel [106].
Ticlopidine (standard dose: 250mg twice daily) acts similarly [104]. Prasugrel is a newer thienopyridine antiplatelet
drug with similar properties; however, its active metabolite
peaks in the plasma approximately 30min after administration, and maximal effect is achieved in approximately 1h
with a loading dose of 20–60mg [107].
Since all these drugs have an irreversible effect on platelets, the duration of action is 7–10days [102].
Recommendations
Thienopyridines should be stopped 0–5days before a lowrisk procedure [71, 87, 108]. Ticlopidine should be stopped
7days prior to high-risk procedures while clopidogrel and
prasugrel should be withheld 5–7days before high-risk procedures. In order to assess adequate platelet function before
the procedure, platelet function tests may be done [71, 73,
87, 109].
28
S. Goswami et al.
Clopidogrel (regular dose) can be resumed in 6–12h, but
the loading dose of clopidogrel can be restarted after 24h. In
high-risk procedures, prasugrel can be restarted 24–48 h
later [72, 87, 109].
4.4.3.3 Glycoprotein IIb/IIIa Inhibitors (GPI)
Mechanism
Gp IIb-IIIa is integrin receptors on the platelets to which
brinogen binds; GPIs (abciximab, eptibatide, and tiroban) block this nal step in platelet aggregation [110].
Eptibatide and tiroban have a short half-life and act for
4–8h, but abciximab irreversibly binds to GP IIb-IIIa receptors and thus platelets regain function in 24–48h. These are
given intravenously.
Recommendations
For IR procedures, abciximab infusion should be stopped
24h prior and for at least 12h. Eptibatide/tiroban infusion
should be stopped for at least 4h before an IR procedure.
As GPIs are associated with a higher risk of thrombocytopenia, a platelet count should also be done. Patients undergoing PCI are administered with or without heparin.
4.4.4 Vasodilators
They are used in IR to enhance the opacication of distal
vessels by relieving arterial spasms. Two commonly used
drugs for this purpose are nitroglycerine and verapamil.
Blood pressure monitoring should be done with the use of
vasodilators [111–115].
4.4.4.1 Nitroglycerine
It is a rapidly acting vasodilator with an effect lasting for
several minutes depending on the dose.
Mechanism
It acts by releasing nitric oxide (NO) which activates intracellular cyclic GMP and leads to the relaxation of smooth muscle. It has a half-life of 1–4min and is excreted with urine.
Route andDose
They are administered as an intravascular bolus, between 50
and 300μg of 10μg/mL NG solution. At lower doses, it acts
upon systemic veins, and for arterial vasodilation, higher
dosage is required. At very high doses, arterioles or resistance vessels also dilate.
Indications
Periprocedural, it can be administered intravenously (IV) or
sublingually for the control of hypertension. It can also be
administered prophylactically to prevent arterial spasms.
4.4.4.2 Verapamil
It is a calcium channel blocker that acts by primarily dilating
the small resistance arterioles.
Mechanism
It binds and blocks calcium channels on vascular smooth
muscle cells which causes a reduction of intracellular calcium leading to smooth muscle relaxation and therefore
vasodilation [116].
Route andDose
It is administered as an intra-arterial bolus of 1–10mg in a
dilution of 10mL saline. It begins to act within 30s and the
effect lasts for approximately 6min [117].
Indications
They are preferred in mesenteric angiography and cerebral
arterial spasm.
Contraindications
It is contraindicated in patients with cardiac conduction disorders. They should not be used in elevated intracranial pressure, constrictive pericarditis, or pericardial tamponade.
Trendelenburg position should be done to improve cerebral
perfusion [111, 113].
Complications
A few adverse reactions such as systemic hypotension, headache, tachycardia, and nausea/vomiting are common to all
vasodilators.
4.4.5 Vasoconstrictors
One of the most commonly used vasoconstrictors is vasopressin. It is primarily used for acute gastroenterological
bleeding. It is an exogenous form of ADH (antidiuretic hormone) secreted from the posterior pituitary.
4.4.5.1 Mechanism
Vasopressin induces vascular smooth muscle contraction in
small arterioles, capillaries, and small venules through
cAMP mechanisms. Its half-life in plasma is 10–20 min
[111–113].
4.4.5.2 Route andDose
It is administered via the intra-arterial route. In cases of
GI bleeding where embolization is either not feasible or
not indicated, e.g., mucosal bleeding, vasopressin infusion is done with a catheter directly placed in the main
trunk. The initial dose is usually 0.2U/min, with repeat
doses administered if bleeding persists on repeat arteriograms. Doses above 0.4U/min are not recommended and
4 Contrast andDrugs inInterventional Radiology
29
alternate therapy is to be considered if bleeding cannot be
controlled. Once bleeding is controlled, the infusion is
continued for 12–24 h while tapering the dose by half
every 6–12h if there is no further bleeding. When the continuous infusion rate reaches 0.1 U/min for 6–12 h, the
infusion is switched to normal saline; the catheter can be
removed after 4–6h of no bleeding with normal saline
infusion [113, 114].
4.4.5.3 Indication
Vasopressin infusion is especially useful in lower GI bleeds,
up to 90% effective in the control of lower GI bleeding due
to various causes [118].
4.4.5.4 Complications andAdverse Eects
There is a considerable risk of rebleeding with the use of
vasopressin and it occurs in approximately 20% of cases
[119]. Common side effects are headache, abdominal
cramps, nausea, vomiting, and diaphoresis. In the presence
of atherosclerotic changes, vasopressin is less efcient due
to the impaired response of arterioles.
Adverse cardiovascular effects such as hypertension,
arrhythmias, and myocardial infarction occur in <5% of
cases. Ischemic effects on mesenteric vasculature may cause
bowel infarction in <1% of cases. Electrolyte imbalance,
oliguria, and hypertension can occur as delayed complications secondary to antidiuretic effects. Additional care
should be taken in patients with cardiac, renal, or hepatic
failure [120].
4.4.6 Prothrombotics
These include drugs for accelerating the natural clotting process. Thrombin is the most commonly used prothrombotic
which is a naturally occurring protein-serine protease synthesized by hepatocytes and an important component of the
clotting cascade. Bovine and recombinant human forms of
thrombin are available. Bovine thrombin is cheaper however
with a higher risk of allergic reactions. A lower dose of
human recombinant form is required to accomplish thrombosis [111–113].
4.4.6.1 Mechanism
It acts by converting soluble brinogen into insoluble
brin and therefore forming clots within seconds. Clot formation is directly related to the concentration of
thrombin.
4.4.6.2 Route andDose
It is available in powder form and needs to be reconstituted
with sterile normal saline immediately prior to injection.
Various concentrations and dosages have been recommended
which are based on the size and location of the injection site.
Standard practice is to use a thrombin concentration of
1000 IU/mL while the dosage for complete thrombosis is
between 0.3 and 3 mL (300–3000 IU). It is administered
under image guidance (ultrasound or CT) using a 19- to a
25-gauge needle in the center of the target; injected at a slow
and constant rate until the hypoechoic PSA turns to hyperechoic clot and the cessation of intraluminal blood ow
occurs on color doppler. If the complete occlusion is not
achieved or in case of recanalization, additional injections
should be administered [117].
4.4.6.3 Indications
The most common use of intravascular thrombin is for
PSA repair in peripheral vessels, with the aim to cause
thrombosis to prevent future rupture and decrease the risk
of distal embolization [121]. It is also used in the treatment of post- catheterization PSAs and found to be superior compared with compression in the treatment of
femoral PSAs [122]. Owing to its success in treating
peripheral vessels PSAs [122], it has been used to treat
visceral post-pancreatitis PSAs occurring in the splenic,
gastroduodenal, and superior mesenteric arteries by several authors [123–125].
4.4.6.4 Complications andContraindications
It has a low (<4%) complication risk [126], however with
serious consequences, and therefore, a careful patient
selection must be done. The highest reported serious complication is downstream thromboembolic events (0.8%)
[127]. A large aneurysmal neck size (>10mm) is associated with an increased risk of a distal thromboembolic
event. Local site infection is a contraindication to thrombin injection.
4.4.6.5 Special Considerations
An assessment of distal pulses and ankle-brachial indices
recording should be done preprocedural with postprocedural
follow-up recording immediately after and at 24h [117].
4.5 Conclusion
Various contrast agents and pharmaceutical agents are used
during IR procedures, and it is of paramount importance for
the radiologist to be aware of their properties, indications,
contraindications, and various drug interactions and adverse
effects in order to prevent and manage them efciently.
Selection of the appropriate contrast agent selection should
be done based on the patient prole, baseline renal function,
and other risk factors for the prevention of contrast-induced
30
S. Goswami et al.
renal injury and other side effects. Interventional radiologists
should be aware of the latest guidelines for various periprocedural and procedural continuation or discontinuation of
anticoagulants and antiplatelet drugs. Familiarity with these
agents, their indications, and contraindications will ensure a
favorable outcome.
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