Consensus Guidelines for Periprocedural Management of Coagulation Malloy

Consensus Guidelines for PeriproceduralManagement of Coagulation Status andHemostasis Risk in PercutaneousImage-guided Interventions

Patrick C. Malloy, MD, Clement J. Grassi, MD, Sanjoy Kundu, MD, Debra Ann Gervais, MD,Donald L. Miller, MD, Robert B. Osnis, MD, Darren W. Postoak, MD, Dheeraj K. Rajan, MD, David Sacks, MD,Marc S. Schwartzberg, MD, Darryl A. Zuckerman, MD, and John F. Cardella, MD, for the Standards of PracticeCommittee with Cardiovascular and Interventional Radiological Society of Europe (CIRSE) Endorsement

J Vasc Interv Radiol 2009; 20:S240–S249

Abbreviations: FFP � fresh-frozen plasma, INR � international normalized ratio, NSAID � nonsteroidal anti-inflammatory drug, PT � prothrombin time,PTT � partial thromboplastin time

THE membership of the Society ofInterventional Radiology (SIR) Stan-dards of Practice Committee repre-sents experts in a broad spectrum of

From the Division of Vascular and InterventionalRadiology, Jefferson Radiology, Hartford Hospital,85 Seymour St, Ste 200, Hartford, CT 06106 (P.C.M.);Department of Radiology, Boston Healthcare Sys-tem, VAMC Boston, Massachusetts (C.J.G.); Depart-ment of Medical Imaging, Scarborough GeneralHospital, Richmond Hill, Ontario, Canada (S.K.);Department of Radiology, GI/GU Division, Massa-chusetts General Hospital, Boston, Massachusetts(D.A.G.); Department of Radiology and RadiologicSciences, Uniformed Services University of theHealth Sciences and Department of Radiology, Na-tional Naval Medical Center, Bethesda, Maryland(D.L.M.); RADIA, Everett, Washington (R.B.O.); De-partment of Radiology, University of Florida,Gainesville, Florida (D.W.P.); Department of Medi-cal Imaging, Division of Vascular and InterventionalRadiology, University of Toronto, University HealthNetwork, Toronto, Ontario, Canada (D.K.R.); De-partment of Interventional Radiology, The ReadingHospital and Medical Center, West Reading, Penn-sylvania (D.S.); Radiology Associates of CentralFlorida, Mt Dora, Florida (M.S.S.); Mallinckrodt In-stitute of Radiology, St Louis, Missouri (D.A.Z.); andGeisinger System Radiology, Geisinger Health Sys-tem, Danville, Pennsylvania (J.F.C.). Received No-vember 18, 2008; accepted November 24, 2008. Ad-dress correspondence to P.C.M.; E-mail: [email protected]

P.C.M. is a paid consultant for Sirtex Medical.

© SIR, 2009

DOI: 10.1016/j.jvir.2008.11.027

S240

interventional procedures from boththe private and academic sectors ofmedicine. In general, Standards ofPractice Committee members dedicatethe vast majority of their professionaltime to performing interventional pro-cedures; as such they represent a validbroad expert constituency of the sub-ject matter under consideration forstandards production.

Technical documents specifying theexact consensus and literature reviewmethodologies as well as the institu-tional affiliations and professional cre-dentials of the authors of this docu-ment are available upon request fromSIR, 3975 Fair Ridge Dr, Ste 400 North,Fairfax, VA 22033.

METHODOLOGY

SIR produces its Standards of Prac-tice documents by using the followingprocess. Standards documents of rele-vance and timeliness are conceptual-ized by the Standards of Practice Com-mittee members. A recognized expertis identified to serve as the principalauthor for the standard. Additionalauthors may be assigned dependentupon the magnitude of the project.

An in-depth literature search is per-formed by using electronic medical
literature databases. Then, a critical re-
view of peer-reviewed articles is per-formed with regard to the study meth-odology, results, and conclusions. Thequalitative weight of these articles is as-sembled into an evidence table, which isused to write the document such that itcontains evidence-based data with re-spect to content, complication rates, out-comes, and thresholds for promptingquality assurance reviews.

When the evidence of literature isweak, conflicting, or contradictory,consensus for the parameter is reachedby a minimum of 12 Standards ofPractice Committee members by usinga Modified Delphi Consensus Method(Appendix) (1). For purposes of thesedocuments, consensus is defined as80% Delphi participant agreement ona value or parameter.

The draft document is critically re-viewed by the Standards of PracticeCommittee members, either by tele-phone conference calling or face-to-face meeting. The finalized draft fromthe Committee is sent to the SIR mem-bership for further input/criticismduring a 30-day comment period.These comments are discussed bythe Standards of Practice Committee,and appropriate revisions are madeto create the finished standards doc-
ument. Before its publication, the
mailto:[email protected]

mailto:[email protected]

ced

Malloy et al • S241Volume 20 Number 7S

document is endorsed by the SIR Ex-ecutive Council.

INTRODUCTION ANDBACKGROUND

The hematologic management ofthe patient undergoing percutaneousimage-guided intervention is complexdue to the wide range of proceduresand equally wide range of patient de-mographics and co-morbidities. Aconcurrent increase in the use of bothshort- and long-term anticoagulation,as well as the increasing use of anti-platelet agents, further complicates thepreprocedural management of thesepatients. Despite the continuing in-crease in the volume of percutaneousimaging-guided procedures, there is ageneral paucity of data regarding theperiprocedural management of the pa-tient with abnormal coagulation pa-rameters. In the absence of data, clini-cians may respond to the patient withabnormal coagulation parameters bycanceling or postponing the proce-dure, altering an otherwise indicatedprocedure, or infusing blood productssuch as fresh-frozen plasma (FFP)or platelets. Recommendations fromopen surgical experience may not beapplicable to interventional proce-dures because of direct visualizationand the ability to obtain prompt vas-cular control in open cases. Finally,medicolegal factors may influence themanagement of the patient, as clini-cians feel the need to “correct” an ab-normal coagulation factor, despite thefact that studies of bleeding complica-tions in percutaneous procedures havenot shown correlation between mild to

Table 1Tests of Hemostasis

Test Indicatio

INR/PT Extrinsic pathway (I,Oral anticoagulant thLiver disease

Activated PTT Intrinsic pathway (VIIntravenous heparin tvon Willebrand diseaFactor VIII, IX, or XI

Platelet count Known or suspectedthrombocytopenia

Bleeding time No current indicationimaging-guided pro

moderate abnormality of preprocedural

coagulation parameters and a higher in-cidence of bleeding complications.

The coagulation status of patientsundergoing imaging-guided interven-tions should be assessed whenever theprocedure involves direct entry intothe arterial or venous system as ananticipated part of the procedure orwhenever there is a possibility of in-advertent entry into the arterial or ve-nous system with significant sized in-terventional devices or tools. Patientsare at increased risk for delayed detec-tion of postprocedural hemorrhagewhen the site of the intervention is noteasily assessed and poorly controllable(eg, percutaneous intraperitoneal pro-cedures). Coagulation status is com-plex; components of the intrinsic andextrinsic coagulation cascade andplatelet function figure integrally intohuman hemostasis. The componentsof coagulation are evaluated by multi-ple tests of hemostasis. These tests andthe component of coagulation functionthey assess are described below andsummarized in Table 1, along withnormal values for each test.

DEFINITIONS

Coagulation Parameters

Prothrombin time (PT).—The PT testmeasures the clotting time upon acti-vation of the extrinsic coagulationpathway. It is used for monitoring oralanticoagulant therapy and is nowwidely reported as an internationalnormalized ratio (INR). The degree ofprolongation of the clotting time cor-relates with the degree of deficiency orinhibition of extrinsic or common

Normal Range

, VII, X) INR, 0.9–1.1y

X, XI, XII) Activated PTT, 25–35 secapy

iciency150,000–450,000/�L

foreures

pathway clotting factors I (fibrinogen),

II (prothrombin), V, VII, and X, whichare synthesized by the liver. When anyof these factors is deficient, the PT isprolonged and the INR is elevated.The PT in a healthy adult is approxi-mately 11–14 seconds. There is varia-tion depending on the reagent used inthe test (2).

INR.—The INR is an expression ofthe results of a PT in a standardizedtesting environment. It is calculated byusing an international standard thatcorrects for laboratory variation. TheINR allows for universal standardiza-tion anticoagulant therapy. In the fol-lowing calculation, the ISI is the Inter-national Sensitivity Index of thethromboplastin reagent used in the as-say: INR � (patient PT/control PT)ISI.

In this test, the patient’s plasma ismixed with a PT reagent containingthromboplastin and calcium chloride.The time to clot formation is mea-sured. The degree of prolongation ofthe clotting time correlates with thedegree of deficiency or inhibition ofextrinsic or common pathway clottingfactors I (fibrinogen), II (prothrombin),V, VII, and X, which are synthesizedby the liver. When any of these factorsis deficient or inhibited, the PT is pro-longed and the INR is elevated. TheINR in a normal patient not undergo-ing warfarin therapy is 0.9–1.1.

A prolonged PT and elevated INRoccur with vitamin K deficiency, lupusanticoagulants, extrinsic pathwaycoagulation factor deficiencies, liverdisease, disseminated intravascularcoagulation bile duct obstruction, mal-absorption, and other conditions.Hirudin, argatroban, and heparin mayprolong the PT.

The degree of prolongation of theclotting time correlates with the de-gree of deficiency or inhibition of ex-trinsic or common pathway clottingfactors I (fibrinogen), II (prothrombin),V, VII, and X, which are synthesized bythe liver. When any of these factors isdeficient, the PT is prolonged and theINR is elevated. The coagulation factorsare synthesized in the liver, and the PTis elevated with severe liver failure andacute liver injury (3,4).

Activated partial thromboplastin time(PTT).—The activated PTT measuresthe clotting time upon activation of theintrinsic coagulation pathways. In thistest, the patient’s plasma is mixed with

n

II, Verap

II, Ihersedef

be

reagent containing an activator, phos-

S242 • Guidelines for Coagulation Status and Hemostasis Risk July 2009 JVIR

pholipid, and calcium chloride. Thetime to clot formation is measured.

A normal activated PTT in an adult isapproximately 25–35 seconds. A thera-peutic ratio of 1.5–2.5 times the controlvalue is frequently employed in heparintherapy; however, this range varies de-pending on the reagent.

A prolonged PTT occurs with factordeficiencies (especially of factors VIII,IX, XI, and/or XII), inhibitors (lupusanticoagulants), liver disease, dissem-inated intravascular coagulation, vita-min K deficiency, or therapeutic anti-coagulants such as heparin, hirudin,or argatroban). The PTT is not usefulin monitoring warfarin therapy (5).

Thrombin time.—Thrombin time pro-vides an assay for fibrinogen concen-tration indirectly by measuring exog-enous thrombin-activated clottingtimes (6).

Bleeding time.—Originally intro-duced in 1901 by Milian, the bleedingtime has been used to diagnose plate-let disorders, assess patients for clini-cally significant bleeding tendenciesbefore invasive procedures, and assessthe effects of various therapies onbleeding tendencies and platelet func-tion. The bleeding time has largelyfallen out of favor in modern clinicalpractice as an assessment for bleedingtendencies because of conflicting dataon its usefulness (7).

Platelet count.—The platelet count isgenerally measured as a standard partof the complete blood count. It is usedto diagnose and follow bleeding disor-ders, thrombocytopenia, drug-inducedthrombocytopenia, disseminated intra-vascular coagulation, and neoplasticdisorders and to evaluate the responseto platelet tranfusions. A normal adultplatelet count is approximately150,000–450,000 platelets per microli-ter of blood. A platelet count of lessthan 20,000/�L is a life-threateningevent in which spontaneous bleedingmay occur.

A small number of patients receivingheparin (including low-dose heparin)develop thrombocytopenia. Drugs andchemicals associated with thrombocy-topenia include chemotherapeuticagents, chloramphenicol, colchicine,H2 blocking agents, heparin, hydral-azine, indomethacin, isoniazid, quini-dine, streptomycin, sulfonamide, thia-zide diuretic, and tolbutamide.Estrogen and oral contraceptives may
cause elevated platelet levels.
Anticoagulants

Warfarin.—Warfarin (Coumadin;Bristol-Myers Squibb, New York, NewYork) antagonizes the production ofthe vitamin K–dependent clotting fac-tors (II, VII, IX, X) in the liver. Theclinical effect is measured with theINR, which reflects antagonism of fac-tor VII, which has the shortest half-lifeof approximately 6 hours. TherapeuticINR values may vary by indication foranticoagulation but most often rangefrom 2.2 to 2.8. Patient co-morbiditiesmay significantly alter the effect ofCoumadin. Congestive heart failure,malignancy, malnutrition, diarrhea,unsuspected vitamin K deficiency,and concomitant antibiotic use may allenhance the response to Coumadin.

Heparin (unfractionated).—Unfrac-tionated heparin potentiates the actionof antithrombin III, is dosed accordingto weight, and is administered bymeans of continuous intravenous infu-sion. Therapeutic response is moni-tored by activated PTT, which is tar-geted at 1.5–2.5 times normal.

Platelet count is monitored after theadministration of heparin for the pos-sibility of heparin-induced thrombo-cytopenia, which is defined as a plate-let count of less than 150,000/�L or a50% decrease in platelet count within5–10 days of the start of therapy. Thereare two types of thrombocytopenia:type I is a benign self-limited disorderwhere the platelet count is rarely lessthan 100,000/�L and type II is a pos-sibly life-threatening disorder withplatelet counts often less than75,000/�L and often seen in associa-tion with acute arterial and/or venousplatelet rich “white” thrombi.

Low-molecular-weight heparin.—Low-molecular-weight heparin is adminis-tered subcutaneously and often dosedby weight. It does not affect the valuesof the INR or activated PTT. Thera-peutic dosing (ie, treatment of acutedeep venous thrombosis) is at 12-hourintervals, whereas prophylactic dosing(ie, postoperative deep venous throm-bosis prophylaxis) is at 24-hourintervals.

Hemostatic Agents

FFP.—The effect of FFP is variabledue to the variable concentration ofvitamin K dependent clotting factors.
On average, at least 10 mL/kg is
needed to effectively raise plasma pro-tein levels. Common dose ranges from15–30 mL/kg. In practice, in the pa-tient with an INR in the 2.5 range, 2units of FFP may be effective in revers-ing the effect of Coumadin. Patientswith higher INR levels should bedosed accordingly, with possible con-comitant use of vitamin K (8–11).

Platelets.—Fractionated blood prod-uct used in the setting of thrombocy-topenia or platelet dysfunction. Oftendosed as 4–6 units (random donors)or as one single donor unit (12).

Protamine.—Protamine may be usedin emergency situations when rapid re-versal of heparin is needed before aprocedure or when heparin reversal isdesired before the removal of arterialcatheters or sheaths. Protamine has arapid onset of action within 10 min-utes after administration. Its half-life,however, is short and ranges from 5 to7.5 minutes, which can lead to “para-doxical” re-anticoagulation after pro-tamine administration. Protamine dos-ing strategies vary considerably. A“neutralizing dose” of protamine is 2mg/kg. Protamine may also be dosedaccording to the amount of heparingiven, on a 1-mg protamine to 100-unitheparin ratio. To reverse commonlygiven intraprocedural doses of hepa-rin (3,000–5,000 IU), we often give atotal of 50-mg protamine in an adult.Protamine should be given by meansof slow intravenous push or infusionover 5–10 minutes. Side effects includehypotension, bradycardia, pulmonaryarterial hypertension, decreased oxy-gen consumption, and anaphylactoidreactions (13–17).

Vitamin K (phytonadione).—VitaminK may be given orally, intravenously,or subcutaneously depending on thevalue of the INR and the desired time-frame for anticoagulant reversal. TheAmerican College of Chest Physicianshas published evidence-based guide-lines for the use of vitamin K in man-aging elevated INRs and/or clinicalbleeding in patients receiving oral an-ticoagulation (18). In stable, electivepatients without active bleeding, oraladministration (5–10 mg in adults) ispreferred. Although intravenous ad-ministration of vitamin K is associatedwith a risk of anaphylactoid reaction,it has a more rapid effect than the sub-cutaneous route and may be moreeffective in the truly emergent pa-
tient. The U.S. Food and Drug Ad-


ministration has issued a black boxwarning for the subcutaneous, intra-venous, and intramuscular routes ofadministration due to reports of se-vere reactions, including fatalities(19,20).

Cryoprecipitate.—Cryoprecipitate isused in acquired or hereditary defi-ciencies of fibrinogen. Ten bags willtypically increase the fibrinogen levelby 75 mg/dL in a 70-kg patient (21).

Recombinant factor VIIa.—Recombi-nant factor VIIa is used in hemophiliain patients with inhibitors to factor 8or in severe, nonhemophiliac-relatedbleeding such as acute trauma (22).

Desmopressin.—Desmopressin (1-deamino-8-D-arginine vasopressin[DDAVP]) is a synthetic analogue ofantidiuretic hormone. DDAVP actsthrough an unclear mechanism to en-hance the plasma levels of factor VIIIand von Willebrand factor (23). A doseof 0.3 �g/kg is given intravenously,usually diluted in 100 mL of normalsaline and infused over 20–30 min-utes. A single dose can be expected toraise the factor VIII level 3–6 fold. Ad-verse effects may include mild hypo-natremia. Tachyphylaxis has been re-ported in patients who have receivedmultiple treatments. There are case re-ports of vascular thrombosis and myo-cardial ischemia after intravenous ad-ministration (24).

DDAVP may be indicated beforeimage-guided procedures in patientswith hemophilia, von Willebrand dis-ease, and acquired platelet disordersdue to uremia, liver disease, or anti-platelet agents (25).

Transfusion Management

FFP.—The most common interven-tion before imaging-guided proce-dures is transfusion of FFP. In theUnited States, more than 3 millionunits of FFP are transfused each year.Dzik and Rao (26) reported in a3-month audit of FFP usage at theMassachusetts General Hospital thatthe most common reason for prescrib-ing FFP was to prepare the patientwith an elevated INR for an invasiveprocedure. This indication accountedfor one-third of all requests for FFP.Stanworth et al (27) reported a reviewof 57 randomized controlled trials in-vestigating the efficacy of FFP to pre-vent hemorrhagic complications over
a wide variety of indications and clin-
ical settings, including cardiac sur-gery. They found the data insufficientto recommend or refute the prophy-lactic use of FFP. Due to the lack ofdata, percutaneous procedures werenot included in this comprehensive re-view. There is a clear need for addi-tional investigation of the use of FFPwith imaging-guided procedures (27).

Segal and Dzik (28) recently re-ported an analysis of 25 studies ana-lyzing the ability of abnormal coagu-lation parameters to predict bleedingassociated with invasive bedside orimage-guided procedures. Of the 25studies available for analysis, one wasa clinical trial (comparison of trans-jugular liver biopsy to percutaneousbiopsy with tract plugging [29]). Theremaining studies were case series.The studies included patients under-going bronchoscopy with biopsy, cen-tral vein cannulation, femoral angiog-raphy, liver biopsy, kidney biopsy,paracentesis, thoracentesis, and lum-bar puncture. Overall, the authors con-cluded that elevated coagulation pa-rameters provide little to no predictivevalue for bleeding complications fromimaging-guided interventions. Theyassert that, in the absence of random-ized, controlled studies, mild to mod-erate elevation of coagulation timesshould neither be assumed to repre-sent an increased risk for periproce-dural bleeding nor be used as an indi-cation for transfusion of FFP orclotting factor concentrates. Literaturedata on preprocedural coagulationtesting for specific procedures aresummarized below.

Angiography.—In a prospectivestudy of 1,000 patients undergoing ar-teriography via common femoral ar-tery access, Darcy et al (30) identified85 patients with abnormal coagulationparameters, defined as a PT greaterthan 15 seconds (range, 15–20.8 sec-onds; normal, 13 seconds). Majorbleeding, defined as a groin hema-toma larger than 4 cm, was found in1.2% (one of 85) of patients with ab-normal coagulation parameters and1.6% (15 of 915) of patients with nor-mal coagulation parameters. Mostprocedures were performed with 5-Fcatheters (72%) or 6–7-F catheters(23%). There was, however, a correla-tion of a higher incidence of hema-toma with a platelet count less than100,000/�L (P � .002). The study con-
cluded that, in the absence of an overt
history of bleeding and an expectedPT of less than 18 seconds, preproce-dural testing with PT and activatedPTT is not warranted (30).

Liver biopsy.—In a laparoscopicstudy, Ewe (31) was able to directlyvisualize the liver biopsy site forbleeding. He found that 4.3% of pa-tients with a PT longer than 13.5 sec-onds bled for more than 12 minutesafter biopsy, in comparison to 4.6% ofpatients with normal coagulation pa-rameters. He was unable to draw anycorrelation between the degree of ab-normality of preprocedural coagula-tion parameters and the length of ob-served bleeding.

Central venous catheter placement.—Fisher and Mutimer (32) evaluated 580patients with an INR greater than 1.5undergoing central venous catheter-ization. All procedures were per-formed with a 16- or 18-gauge needle.Most patients (83%) had a plateletcount less than 150,000/�L. One pa-tient (0.2%) had major bleeding due toinadvertent puncture of the carotid ar-tery. The authors concluded that cen-tral venous access can be performedsafely by experienced physicians inthe presence of abnormal coagulationparameters. Other studies have sup-ported these results (33,34).

Morado et al (35) reported a caseseries of 15 patients with hemophiliaand inhibitors who underwent a totalof 34 catheter insertions. The mean pa-tient age was 8.8 years (range, 16months to 39 years); all patients hadfactor VIII/IX inhibitors. Pericatheterbleeding was seen in seven catheterinsertions in six patients and requiredsubstantive treatment for several days.

Central Venous Catheter Removal

There is some controversy and lackof consensus over the management ofpatients undergoing the removal oftunneled catheters. There is no evi-dence of the value of pre-removal co-agulation parameters or platelet countin the management of these patients.Stecker et al (36) reported a study of180 patients with tunneled cuffed cen-tral venous catheters. Time to hemo-stasis was 5 minutes for 166 patients,with 14 patients requiring more than 5minutes of manual compression at theinsertion site (range, 10–35 minutes).Only one patient required more than
15 minutes of pressure. In the 14 pa-


tients with prolonged (�5 minutes)time to hemostasis, statistically signif-icant factors included the use of anti-platelet agents, renal failure, the use ofhigh-flow hemodialysis catheter, andoperator experience. They concludedthat pre-removal laboratory evalua-tion was not warranted and that plate-let dysfunction was a more importantfactor than platelet number in pro-longing time to hemostasis, but thatthe degree of prolongation was un-likely to be clinically relevant.

Nephrostomy Tube Placement

Martin et al (37) reported a series of160 patients who underwent percuta-neous nephrostomy tube placementby an experienced operator. One hun-dred fifty-three patients had normalcoagulation tests; seven patients hadan abnormal PT or activated PTT(mean PT, 13.9 seconds; mean acti-vated PTT, 30.3 seconds). No patientsin the study experienced bleedingcomplications associated with ne-phrostomy tube placement. The au-thors concluded that screening coagu-lation studies are not necessary inpatients before nephrostomy tubeplacement (37,38).

PLATELET TRANSFUSIONS

Severe thrombocytopenia may re-sult in an increased bleeding risk withimaging-guided interventions andopen surgery, although the recom-mended threshold for platelet transfu-sion varies between procedures. Aswith the use of FFP, the literature datafor platelet use are mostly from caseseries, retrospective case reviews, andconsensus data (39–43). There aremany etiologies of thrombocytopeniaand significant variation in plateletfunction associated with patient co-morbidities and medication use. Thedecision for platelet transfusion beforepercutaneous procedures, therefore, isbased on multiple variables, includingplatelet count, etiology of thrombocy-topenia, platelet function, type of pro-cedure, operator expertise and experi-ence, and concurrent coagulopathiesand other co-morbidities.

Ewe (31) reported a series of 200consecutive patients in whom liverbleeding time was observed with lapa-roscopy after percutaneous biopsy.
Liver bleeding time and patient out-
come did not correlate with preproce-dural coagulation parameters or plate-let count. The author concluded thatstandard measures of evaluation of co-agulation and platelet count were notuseful in determining bleeding risk as-sociated with percutaneous liver bi-opsy.

Shiffer et al (44) reported recom-mendations for platelet transfusionsin cancer patients. With respect toperiprocedural management, the au-thors concluded that, on the basis ofseveral consensus statements, in theabsence of coexisting coagulation ab-normalities a platelet count of 40,000–50,000/�L is sufficient for the safe per-formance of major invasive procedures.The consensus statements included datafrom both major operative proceduressuch as laparotomy or craniotomy tomore minor invasive procedures such ascentral line placement, transbronchialbiopsy, and bone marrow biopsies.They noted that certain procedures,such as bone marrow aspiration and bi-opsy, are routinely performed safely atplatelet levels of 20,000/�L or less.There were some data suggesting thatcoexisting coagulopathies resulted inhigher periprocedural blood loss in thesetting of thrombocytopenia. Theynoted the relative lack of studies evalu-ating the safety and efficacy of invasiveprocedures in thrombocytopenic pa-tients. Posttransfusion platelet countswere strongly recommended in all pa-tients receiving platelet transfusions be-fore invasive procedures (44).

With respect to percutaneous trans-abdominal liver biopsy, McVay andToy (45) reported an incidence of clin-ically significant bleeding of 3.4% in291 consecutive patients with mildthrombocytopenia, as defined byplatelet counts between 50,000 and99,000/�L. There was no difference inbleeding incidence in comparison withpatients with normal platelet counts.Underlying malignancy appeared tobe an independent risk factor forbleeding. Wallace et al (46) reported aseries of 50 patients with hematologicmalignancies and moderate to severethrombocytopenia who underwenttransjugular liver biopsy. The meanpreprocedure, pretransfusion plateletcount was 17,000/�L. Patients re-ceived prophylactic platelet transfu-sions before the procedure, with post-transfusion platelet counts ranging
from 5,000 to 105,000/�L (mean
38,000/�L). The platelet count wasless than 30,000/�L in 24 patients. Pa-tients received a mean of 11 units ofplatelets. No clinically significantbleeding was encountered. The au-thors concluded that a platelet countof 30,000/�L represents a safe level fortransjugular liver biopsy (46).

Multiple studies have evaluated therisk of bleeding with the placement ofcentral venous access devices in thesetting of thrombocytopenia. In a pro-spective study of 105 patients, Ray andShenoy (47) evaluated the effect ofvarious levels of thrombocytopenia onthe incidence of bleeding complica-tions necessitating intervention. Pa-tients were divided into three groups:(a) those with moderate thrombocyto-penia (platelet count �50,000/�L), (b)those with mild thrombocytopenia(platelet count 50,000–100,000/�L),and (c) those with platelet countsgreater than 100,000/�L. Patients inthe first group received platelet trans-fusions during the procedure, al-though the mean increase in plateletcount was only 11,500/�L. There wereno significant bleeding complicationsrequiring intervention in patients withthrombocytopenia (47). Other studieshave shown similar results in patientswith both thrombocytopenia and anelevated INR, with a low incidence ofbleeding complications (1%–2%) andno deaths due to periproceduralbleeding complications (21).

Multiple studies have investigatedthe incidence of bleeding complica-tions with lumbar puncture in the set-ting of thrombocytopenia. In 1974,Edelson et al (48) reported spinal sub-dural hematomas after lumbar punc-ture in eight patients with thrombocy-topenia, five of whom had plateletcounts of less than 20,000/�L. In 1982,Breuer et al (49) reported significantspinal subarachnoid hematomas intwo of 13 patients with platelet countsless than 20,000/�L who did not un-dergo preprocedural platelet transfu-sion. None of the seven patients withthis degree of thrombocytopenia whoreceived platelet transfusions devel-oped significant bleeding complica-tions. In 2000, Howard et al (50) retro-spectively reviewed the results of4,309 lumbar punctures performed in959 children with acute lymphocyticleukemia. Three hundred seventy-eight procedures were performed in
patients with platelet counts of less


than 25,000/�L. There were no signif-icant bleeding complications in anypatients, although a higher incidenceof traumatic lumbar puncture ap-peared to be associated with worsen-ing thrombocytopenia. Vavricka et al(51) reported the results of 195 lumbarpuncture procedures in 66 adult pa-tients with acute leukemia. There wereno significant bleeding complications,although the authors reported a statis-tically significant trend in the occur-rence of traumatic procedures in pa-tients with the lowest platelet counts.Each of the above authors recom-mended a threshold level of 20,000/�Lfor platelet transfusion before lumbarpuncture, and most noted the effect ofincreased operator experience in reduc-ing hemorrhagic complications andtraumatic procedures.

Many of these authors have ex-pressed the opinion that severe coagu-lopathies and severe thrombocytopeniashould be corrected before percutane-ous nephrostomy tube placement, al-though specific recommendations forthreshold values vary or many times arenot specified.

ANTIPLATELET AGENTMANAGEMENT

Antiplatelet therapy has beenshown to be effective in patients withcoronary artery disease. Due to theprevalence of coronary artery disease,antiplatelet agents are commonly onthe list of medications of patients pre-senting for noncardiac image-guidedprocedures. Two of the most com-monly prescribed medications includeaspirin and clopidogrel (Plavix; Bris-tol-Myers Squibb). Fox et al (52) re-ported the results of the Clopidogrelin Unstable Angina to Prevent Recur-rent Ischemic Events (CURE) trial, inwhich 12,562 patients with unstableangina were randomized to clopi-dogrel or placebo. Of the study pa-tients undergoing bypass surgery (n �1,015), the rates of life-threateninghemorrhage were 4.2% in the placebogroup and 5.6% in the clopidogrelgroup (relative risk � 1.30, not signif-icant). The authors reported an excessof seven patients requiring transfusionand a trend for four patients to expe-rience a life-threatening hemorrhagein the clopidogrel group. They recom-mended stopping clopidogrel for 5
days before coronary artery bypass
graft placement for nonemergent sur-gery (52). There have been reports ofserious and, in one case, fatal bleedingfollowing lumbar sympathetic block inpatients undergoing lumbar blockprocedures (53). Hussain et al (54) re-ported a case control study of 40 pa-tients undergoing endoscopic sphinc-terotomy. Most of their study patientswho were receiving antiplatelet ther-apy were taking aspirin. The authorsconcluded that, after adjustment forelevated INR and cholangitis, anti-platelet agents do not increase the riskof clinically significant bleeding asso-ciated with endoscopic sphincterot-omy.

Both clopidogrel and aspirin resultin irreversible platelet inhibition. Inpatients with normal bone marrowfunction and reserve, the platelet lifes-pan is approximately 10 days. Takinginto account variabilities in drug clear-ance, withholding antiplatelet agentsfor 5 days will, therefore, result in ap-proximately 30%–50% of platelets atthe time of the procedure to have nor-mal function.

Nonsteroidal anti-inflammatory drugs(NSAIDs) can inhibit platelet aggrega-tion. The effect of NSAIDs on plateletaggregation, unlike aspirin, is revers-ible and will decay along with clear-ance of drug levels from the circula-tion. In general, NSAIDs do not causesignificant bleeding problems exceptin patients with existing coagulopa-thies such as hemophilia, von Wille-brand disease, or severe thrombocyto-penia. Paradoxically, NSAIDs tend todiminish the antiplatelet effect of aspi-rin when given concomitantly and,therefore, should not be given to pa-tients receiving aspirin therapy forcardiovascular disease (55,56).

RECOMMENDATIONS FORPREPROCEDURE TESTINGAND MANAGEMENT

Assessment and preparation of thepatient before imaging-guided proce-dures will vary according to the pro-cedure to be performed in conjunctionwith a comprehensive assessment ofthe patient’s co-morbidities. Althoughimage guidance is likely to make min-imally invasive procedures more accu-rate, for example, in their ability totarget lesions or to put effector devicessuch as needles or catheters in optimal
position, by their very nature these
procedures preclude the operatorfrom direct visualization of postproce-dure bleeding. The lack of availablerandomized, controlled studies spe-cific to imaging-guided percutaneousprocedures has resulted in consider-able variety in clinical practice. Fur-thermore, it is doubtful that one canextrapolate the results from open sur-gical procedures to minimally inva-sive procedures due to the aforemen-tioned separation of the operator fromdirect assessment of bleeding (and theassociated ability to control it) at thesite of the procedure.

Recommendations for patient eval-uation and general indications for theuse of blood products and other hemo-static agents are outlined in Tables2–4. Where reliable data was lacking,recommendations were derived byDelphi consensus of a panel of expertpractitioners. Tables 2–4 represent theresults of the Delphi consensus panel,which were derived for the manage-ment of a patient with a single hemo-static defect. A total of 18 Certificate ofAdded Qualification–certified interven-tional radiologists participated in afour-round Delphi process. Althoughrepresentative procedures were placedinto one of three categories of risk, asoutlined in Tables 2–4, the panel be-lieved there was significant potentialvariability in risk from procedure toprocedure within each category, de-pending on the individual patient co-morbidities and possible multiple con-comitant hemostatic defects. It must bestressed, therefore, that specific assess-ment of bleeding risk and consider-ations for the use of blood products orother hemostatic agents must be indi-vidualized to the patient at the total dis-cretion of the performing physician,who must, at the time of the procedure,make clinical decisions on the basis ofan often complex array of patient vari-ables, co-morbidities, and concomitanthemostatic defects. With respect to thecategories in Tables 2–4, any individualprocedure might possibly be treated ata higher risk level, depending on theseindividual patient factors. In addition,for the purposes of this document, theDelphi consensus panel treated theprocedures as elective, with a singlehemostatic defect. Emergency indica-tions, multiple concomitant hemo-static defects, and the use of topical orintravascular/perivascular closure de-
vices were not specifically addressed.

ula

ula


Emergency or highly urgent proce-dures, where the risk of proceduraldelay may outweigh the potentialhemorrhagic risk, may not afford thetime for equivalent correction of he-mostatic defects as may be achieved inelective procedures. The physicianmust take into account pathophysio-

Table 2Category 1: Procedures with Low Risk o

Procedures

VascularDialysis access interventionsVenographyCentral line removalIVC filter placementPICC line placement

NonvascularDrainage catheter exchange (biliary,

nephrostomy, abcess catheter)ThoracentesisParacentesisSuperficial aspiration and biopsy (exclu

intrathoracic or intraabdominal sites)thyroid, superficial lymph node

Superficial abscess drainage

There was an 80% consensus for each ofThe management recommendations for ethat no other drug that might affect coag

Table 3Category 2: Procedures with Moderate R

Procedures

VascularAngiography, arterial intervention with

size up to 7 FVenous interventionsChemoembolizationUterine fibroid embolizationTransjugular liver biopsyTunneled central venous catheterSubcutaneous port device

NonvascularIntraabdominal, chest wall, or retroper

abcess drainage or biopsyLung biopsyTransabdominal liver biopsy (core needPercutaneous cholecystostomyGastrostomy tube: initial placementRadiofrequency ablation: straightforwaSpine procedures (vertebroplasty, kyph

lumbar puncture, epidural injection,

There was an 80% consensus on each of tThe management recommendations for ethat no other drug that might affect coag

logic, psychosocial, medicolegal, and

religious variables in coming to anoverall assessment of the patient. Forexample, periprocedural managementfor percutaneous liver biopsy mayvary significantly between one patientwith an INR of 1.7 with no co-morbid-ities and a second patient with an INR1.7 and concomitant renal failure and

leeding, Easily Detected and Controllabl

Preprocedure Laboratory Testing

s

INR: Routinely recommended for patiereceiving warfarin anticoagulation owith known or suspected liver disea

Activated PTT: Routinely recommendefor patients receiving intravenousunfractionated heparin.

Platelet count: Not routinely recommenHematocrit: Not routinely recommend

se recommendations unless otherwise statecoagulation defect and drug assume that

tion status has been administered.

of Bleeding

Preprocedure LaboratoryTesting

cess

eal

lasty,et block)

INR: RecommendedActivated PTT: Recommended in

patients receiving intravenousunfractionated heparin

Platelet count: Not routinelyrecommended

Hematocrit: Not routinelyrecommended

e recommendations unless otherwise statecoagulation defect and drug assume that


cirrhosis. Although the recommenda-

tions given in the tables attempt todivide the spectrum of imaging-guided procedures into categories ofrisk, only the practicing physician canadequately assess risk at the point ofcare and, therefore, the potential needfor treatment in the individual patient.

Because there is no evidence to sup-

Management

d

INR �2.0: Threshold for treatment(ie, FFP, vitamin K)

PTT: No consensusHematocrit: No recommended

threshold for transfusionPlatelets: Transfusion recommended

for counts �50,000/ULPlavix: Do not withholdAspirin: Do not withholdLow-molecular-weight heparin

(therapeutic dose): Withhold onedose before procedure

DDAVP: Not indicated

other coagulation defect is present and

Management

R: Correct above 1.5 (89% consensus)ctivated PTT: No consensus (trendtoward correcting for values �1.5 timescontrol, 73%)

latelets: Transfusion recommended forcounts �50,000/uLematocrit: No recommended thresholdfor transfusion

lavix: Withhold for 5 d before procedurespirin: Do not withholdow-molecular-weight heparin (therapeu-tic dose): Withhold one dose beforeprocedureDAVP: not indicated


f B e

de:

ntsrsed

deed

the d.ach no

isk

ac

iton

le)

rdopfac

INA

P

H

PAL

D

hes d.ach no

port the use of bleeding times before

ula


minimally invasive procedures, theDelphi consensus panel did not ad-dress the use of this test. In addition,the use of recombinant factor VIIa wasnot addressed. NSAID use was notspecifically addressed by the panel. Asmentioned earlier, although NSAIDscan inhibit platelet function, the effectis reversible with clearance of thedrug. Furthermore, NSAIDs tend tocause bleeding mostly in patients withpre-existing coagulopathies. Low-mo-lecular-weight heparin was consid-ered by the panel with respect to ther-apeutic dosing.

CONCLUSION

In this document, we attempt tosummarize some of the available liter-ature regarding periprocedural sur-veillance and management of hemo-static defects in patients undergoingpercutaneous, imaging-guided proce-dures. Because of the lack of random-ized, controlled studies or other high-level evidence on this topic, a Delphipanel of experts constructed a set ofconsensus guidelines to hopefullyserve as a reference for the practicinginterventionalist in constructing theirindividual practice guidelines. Al-though it is likely that individual prac-tice parameters will vary from thisdocument, each practitioner shouldmonitor outcomes and look for trends,both positive and negative, that maysuggest modifications or adjustmentsto these parameters. Outlining bleed-ing complication rates for specific pro-

Table 4Category 3: Procedures with Significant

Procedures

VascularTransjugular intrahepatic porto-

systemic shuntNonvascular

Renal biopsyBiliary interventions (new tract)Nephrostomy tube placementRadiofrequency ablation: com-

plex

INAc

thn

PlaHe

There was an 80% consensus on each of tThe management recommendations for ethat no other drug that might affect coag

cedures is beyond the scope of this

document and, in many cases, may bedifficult or impossible to accurately ac-complish due to the lack of high leveldata. Where external benchmarks arenot available, practitioners maychoose to benchmark against theirown historical data as part of an over-all quality improvement program.

The periprocedural management ofpatients undergoing imaging-guidedprocedures is a continually evolvingparadigm. Local factors such as proce-dure types and patient selection willinfluence management. In addition,advances in technology and imageguidance may have a significant effecton periprocedural management. Theuse of closure devices, smaller gaugecatheters and biopsy devices, adjuncthemostatic measures such as postbi-opsy tract plugging, and color flowultrasonography or computed tomo-graphic fluoroscopy all have the po-tential to effect the incidence ofperiprocedural bleeding complica-tions, although further studies will beneeded to accurately assess their im-pact.

Acknowledgments: Dr. Patrick C. Mal-loy authored the first draft of this docu-ment and served as topic leader during thesubsequent revisions of the draft. Dr.Clement J. Grassi was chair of the SIR Stan-dards of Practice Committee during thedevelopment of this document. Dr. SanjoyKundu is now chair. Dr. John F. Cardella isCouncilor of the SIR Standards Division.Other members of the Standards of Prac-tice Committee and SIR who participatedin the development of this clinical practice

eding Risk, Difficult to Detect or Contro

Preprocedure Laboratory Testing

outinely recommendedted PTT: Routinely recommended in pa-

ts receiving intravenous unfractionatedarin infusion. No consensus on patientsreceiving heparint count: Routinely recommended

tocrit: Routinely recommended

e recommendations unless otherwise statecoagulation defect and drug assume that


guideline are (listed alphabetically): John

“Fritz” Angle, MD, Ganesh Annamalai,MD, Curtis W. Bakal, MD, Stephen Balter,PhD, Daniel B. Brown, MD, Danny Chan,MD, Timothy W.I. Clark, MD, MSc, BairbreL. Connolly, MD, Horacio D’Agostino,MD, Brian D. Davison, MD, Peter Drescher,MD, S. Nahum Goldberg, MD, Manraj K.S.Heran, MD, Maxim Itkin, MD, Sanjeeva P.Kalva, MD, Arshad Ahmed Khan, MD,Neil M. Khilnani, MD, Curtis A. Lewis,MD, MBA, JD, J. Kevin McGraw, MD, TimMcSorley, BS, RN, CRN, Philip M. Meyers,MD, Steven F. Millward, MD, Charles A.Owens, MD, Anne C. Roberts, MD, StevenC. Rose, MD, Tarun Sabharwal, MD, CindyKaiser Saiter, NP, Nasir H. Siddiqu, MD,LeAnn Stokes, MD, Timothy L. Swan, MD,Patricia E. Thorpe, MD, Richard Towbin,MD, Aradhana Venkatesan, MD, Louis K.Wagner, PhD, Prof, Michael J. Wallace,MD, Bret N. Wiechmann, MD, Joan Wojak,MD, and Kenneth S. Rholl, MD.

APPENDIX: SIR STANDARDSOF PRACTICE COMMITTEE

Consensus Methodology

Consensus guidelines reported inthis document were obtained by usinga modified Delphi technique (1). Eigh-teen CAQ-certified members of theSIR Standards of Practice Committeeparticipated through four rounds ofthe Delphi to reach consensus as re-ported.

References1. Fink A, Kosefcoff J, Chassin M, Brook

RH. Consensus methods: characteris-tics and guidelines for use. Am J Public

Management

R: Correct above 1.5 (95% consensus)ctivated PTT: Stop or reverse heparinfor values �1.5 times control)

latelets �50,000: Transfuseematocrit: No recommended thresholdfor transfusion

lavix: Withhold for 5 d before procedurespirin: Withhold for 5 dactionated heparin: withhold for 24 hor up to two dosesDAVP: Not indicated


Ble l

R: Rtivaienepottelema

INA

PH

PAFr

D

hes dach no

Health 1984; 74:979–998.


2. Hyers TM, Agnelli G, Hull RD, et al.Antithrombotic therapy for venousthromboembolic disease. Chest 2001;119(1 suppl):176S–193S.

3. O’Grady JG, Alexander GJM, HayllarKM, et al. Early indicators of progno-sis in fulminant hepatic failure. Gastro-enterology 1989; 97:439–445.

4. Lee WM. Acute liver failure. N EnglJ Med 1993; 329:1862–1872.

5. Pilsczek FH, Rifkin WD, Walerstein S.Overuse of prothrombin and partialthromboplastin coagulation tests inmedical inpatients. Heart Lung 2005;34:402–405.

6. Clauss A. A rapid physiological co-agulation method for the determina-tion of fibrinogen. Acta Haematol 1957;17:237–240.

7. Rodgers RP, Levin J. A critical reap-praisal of the bleeding time. SeminThromb Hemost 1990; 16:1–20.

8. Hellstern P, Muntean W, Schramm W,Seifried E, Solheim B. Practical guide-lines for the clinical use of plasma.Thromb Res 2002; 107(suppl 1):S53.

9. Escobar MA. Reversal of coumarin-induced over-anticoagulation. Br JHaematol 2002; 118:925–926, discus-sion 926.

10. Wilson SE, Douketis JD, Crowther MA.Treatment of warfarin-associated co-agulopathy: a physician survey. Chest2001; 120:1972–1976.

11. Jacobs LG, Nusbaum N. Periopera-tive management and reversal of anti-thrombotic therapy. Clin Geriatr Med2001; 17:189–202.

12. O’Connell BA, Lee EJ, Schiffer CA.The value of 10-minute post transfu-sion platelet counts. Transfusion 1988;26:66–67.

13. Butterworth J, Lin YA, Prielipp RC,Bennett J, Hammon JW, James RL.Rapid disappearance of protamine inadults undergoing cardiac operationwith cardiopulmonary bypass. AnnThorac Surg 2002; 74:1589–1595.

14. Butterworth J, Lin YA, Prielipp R, Ben-nett J, James R. The pharmacokineticsand cardiovascular effects of a singleintravenous dose of protamine in nor-mal volunteers. Anesth Analg 2002; 94:514–522.

15. Brooks JC. Noncardiogenic pulmo-nary edema immediately followingrapid protamine administration. AnnPharmacother 1999; 33:927–930.

16. Wright SJ, Murray WB, Hampton WA,Hargovan H. Calculating the prota-mine-heparin reversal ratio: a pilotstudy investigating a new method.J Cardiothorac Vasc Anesth 1993; 7:416–421.

17. Lowenstein E. Lessons from studyingan infrequent event: adverse hemody-namic response associated with prota-
mine reversal of heparin anticoagula-
tion. J Cardiothorac Anesth 1989;3:99–107.

18. Ansell J, Hirsh J, Poller L, et al. Thepharmacology and management of thevitamin K antagonists. Chest 2004; 126(suppl 3):204S–233S.

19. Raj G, Kumar R, McKinney WP. Timecourse of reversal of anticoagulant ef-fect of warfarin by intravenous andsubcutaneous phytonadione. Arch In-tern Med 1999; 159:2721–2724.

20. Byrd DC, Stephens MA, Hamann GL,Dorko C. Subcutaneous phytonadi-one for reversal of warfarin-inducedelevation of the international normal-ized ratio. Am J Health Syst Pharm1999; 56:2312–2315.

21. Konkle B. Percutaneous interven-tions in the coagulopathic patient. Se-min Intervent Radiol 2005; 22:88–94.

22. Pusateri AE, Park MS. Mechanisticimplications for the use and monitor-ing of recombinant activated factor VIIin trauma. Critical Care 2005, 9(suppl5):S15–S24.

23. Mannucci PM, Ruggeri Z, Pareti F,Capitanio A. 1-deamino-8-argininevasopressin: a new pharmacologicalapproach to the management of hae-mophilia and von Willebrands disease.Lancet 1977; 1:869–872.

24. Mannucci PM, Bettega D, Cattaneo M.Patterns of development of tachphy-laxis in patients with haemophilia andvon Willebrand disease after repeateddoses of desmopressin (DDAVP). Br JHaematol 1992; 82:87–93.

25. Mannucci PM. Desmopressin: a non-transfusional form of treatment forcongenital and acquired bleeding dis-orders. Blood 1988; 72:1449–1455.

26. Dzik W, Rao A. Why do physiciansrequest fresh frozen plasma? Transfu-sion 2004; 44:1393.

27. Stanworth SJ, Brunskill SJ, Hyde CJ,McClelland D, Murphy MF. Is freshfrozen plasma clinically effective? Asystematic review of randomized con-trolled trials. Br J Haematol 2004; 126:1139.

28. Segal JB, Dzik WH. Transfusion Med-icine/Hemostasis Clinical Trials Net-work. Paucity of studies to supportthat abnormal coagulation test resultspredict bleeding in the setting of inva-sive procedures: an evidence-based re-view. Transfusion 2005; 45:1413–1425.

29. Sawyerr AM, McCormick PA, Tenny-son GS, et al. A comparison of trans-jugular and plugged-percutaneousliver biopsy in patients with impairedcoagulation. J Hepatol 1993; 17:81–85.

30. Darcy MD, Kanterman RY, KleinhofferMA, et al. Evaluation of coagulationtests as predictors of angiographicbleeding complications. Radiology
1996; 198:741–744.
31. Ewe K. Bleeding after liver biopsydoes not correlate with indices of pe-ripheral coagulation. Dig Dis Sci 1981;26:388–393.

32. Fisher NC, Mutimer DJ. Central ve-nous cannulation in patients with liverdisease and coagulopathy: a prospec-tive audit. Intensive Care Med 1999;25:5.

33. Doerfler ME, Kaufman B, GoldenbergAS. Central venous catheter place-ment in patients with disorders of he-mostasis. Chest 1996; 110:185–188.

34. Stellato TA, Gauderer MW, LazarusHM, et al. Percutaneous isoelasticcatheter insertion in patients withthrombocytopenia. Cancer 1985; 56:2691–2693.

35. Morado M, Jimenez-Yuste V, Villar A,et al. Complications of central venouscatheters in patients with haemophiliaand inhibitors. Haemophilia 2001; 7:551–556.

36. Stecker M, Johnson M, Ying J, et al.Time to hemostasis after traction re-moval of tunneled cuffed central ve-nous catheters. J Vasc Interv Radiol2007; 18:1232–1239.

37. Martin JH, Rosser CJ, Linebach RF, Mc-Cullough DL, Assimos DG. Are coag-ulation studies necessary before percu-taneous nephrostomy? Tech Urol 2000;6:205–207.

38. Zagoria RJ, Dyer RB. Do’s and don’tsof percutaneous nephrostomy. AcadRadiol 1999; 6:370–377.

39. Platelet transfusion therapy. NationalInstitutes of Health Consensus Confer-ence. Transfusion Med Rev 1987; 1:195–200.

40. Norfolk DR, Ancliffe PJ, Contreras M,et al. Consensus conference on plate-let transfusion. Royal College of Physi-cians of Edinburgh, 27–28 November1997. Br J Haematol 1998; 101:609–617.

41. Bishop JF, Schiffer CA, Aisner J, et al.Surgery in acute leukemia: a review of167 operations in thrombocytopenicpatients. Am J Hematol 1987; 26:147–155.

42. Chu DZJ, Shivshanker K, Stroehlein JR,et al. Thrombocytopenia and gastro-intestinal hemorrhage in the cancer pa-tient: prevalence of unmasked lesions.Gastrointest Endosc 1983; 29:269–272.

43. Weiss SM, Hert RC, Gianola FJ, et al.Complications of fiberoptic bronchos-copy in thrombocytopenic patients.Chest 1993; 104:1025–1028.

44. Schiffer CA, Anderson KC, Bennett CL,et al. Platelet transfusion for patientswith cancer: clinical practice guidelinesof the American Society of Clinical On-cology. J Clin Oncol 2001; 19:1519–
1538.


45. McVay PA, Toy PT. Lack of increasedbleeding after liver biopsy in patientswith mild hemostatic abnormalities.Am J Clin Pathol 1990; 94:747–753.

46. Wallace M, Narvios A, Lichtiger B, etal. Transjugular liver biopsy in pa-tients with hematologic malignancyand severe thrombocytopenia. J VascInterv Radiol 2003; 14:323–327.

47. Ray CEJ, Shenoy SS. Patients withthrombocytopenia: outcome of radio-logic placement of central venous ac-cess devices. Radiology 1997; 204:97–99.

48. Edelson RN, Chernik NL, Posner JB.Spinal subdural hematomas complicat-ing lumbar puncture. Arch Neurol1974; 31:134–137.

49. Breuer AC, Tyler R, Marzewski DJ, etal. Radicular vessels are the most

blood in lumbar puncture. Cancer1982; 49:2168–2172.

50. Howard SC, Gajjar A, Ribeiro RC, et al.Safety of lumbar puncture for childrenwith acute lymphoblastic leukemiaandthrombocytopenia.JAMA2000;284:2222–2224.

51. Vavricka SR, Walter RB, Irani S, HalterJ, Schanz U. Safety of lumbar punc-ture for adults with acute leukemia andrestrictive prophylactic platelet trans-fusion. Ann Hematol 2003; 82:570–573.

52. Fox KA, Mehta SR, Peters R, et al.Benefits and risks of the combinationof clopidogrel and aspirin in patientsundergoing surgical revascularizationfor non–ST-elevation acute coronarysyndrome: the Clopidogrel in UnstableAngina to Prevent Recurrent IschemicEvents (CURE) Trial. Circulation 2004;

53. Maier C, Gleim M, Weiss, T, StachetzkiU, Nicolas V, Zenz M. Severe bleed-ing following lumbar sympatheticblockade in two patients under medi-cation with irreversible platelet aggre-gation inhibitors. Anesthesiology 2002;97:740–743.

54. Hussain N, Alsulaiman R, Burtin P, etal. The safety of endoscopic sphinc-terotomy in patients receiving anti-platelet agents: a case-control study.Alimentary Pharmacol Ther 2007; 25:579–584.

55. Schafer AI. Effects of nonsteroidalantiinflammatory drugs on plateletfunction and systemic hemostasis.J Clin Pharmacol 1995; 35:209–219.

56. Schafer AL. Effects of nonsteroidalanti-inflammatory therapy on platelets.

probable source of needle induced 110:1202–1208. Am J Med 1999; 106(suppl 5b):25S–36S.

SIR DISCLAIMER

The clinical practice guidelines of the Society of Interventional Radiology attempt to define practice principles thatgenerally should assist in producing high quality medical care. These guidelines are voluntary and are not rules. Aphysician may deviate from these guidelines, as necessitated by the individual patient and available resources. Thesepractice guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of carethat are reasonably directed towards the same result. Other sources of information may be used in conjunction withthese principles to produce a process leading to high quality medical care. The ultimate judgment regarding theconduct of any specific procedure or course of management must be made by the physician, who should consider allcircumstances relevant to the individual clinical situation. Adherence to the SIR Quality Improvement Program will notassure a successful outcome in every situation. It is prudent to document the rationale for any deviation from thesuggested practice guidelines in the department policies and procedure manual or in the patient’s medical record.

Documents

Consensus Guidelines for Periprocedural Management of Coagulation Malloy