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• W2912402179 abstract "THE membership of the Society of Interventional Radiology (SIR) Standards of Practice Committee represents experts in a broad spectrum of interventional procedures from both the private and academic sectors of medicine. In general, Standards of Practice Committee members dedicate the vast majority of their professional time to performing interventional procedures; as such they represent a valid broad expert constituency of the subject matter under consideration for standards production.SIR DisclaimerThe clinical practice guidelines of the Society of Interventional Radiology attempt to define practice principles that generally should assist in producing high quality medical care. These guidelines are voluntary and are not rules. A physician may deviate from these guidelines, as necessitated by the individual patient and available resources. These practice guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of care that are reasonably directed towards the same result. Other sources of information may be used in conjunction with these principles to produce a process leading to high quality medical care. The ultimate judgment regarding the conduct of any specific procedure or course of management must be made by the physician, who should consider all circumstances relevant to the individual clinical situation. Adherence to the SIR Quality Improvement Program will not assure a successful outcome in every situation. It is prudent to document the rationale for any deviation from the suggested practice guidelines in the department policies and procedure manual or in the patient's medical record.Technical documents specifying the exact consensus and literature review methodologies as well as the institutional affiliations and professional credentials of the authors of this document are available upon request from SIR, 3975 Fair Ridge Dr, Ste 400 North, Fairfax, VA 22033.MethodologySIR produces its Standards of Practice documents by using the following process. Standards documents of relevance and timeliness are conceptualized by the Standards of Practice Committee members. A recognized expert is identified to serve as the principal author for the standard. Additional authors may be assigned dependent upon the magnitude of the project.An in-depth literature search is performed by using electronic medical literature databases. Then, a critical review of peer-reviewed articles is performed with regard to the study methodology, results, and conclusions. The qualitative weight of these articles is assembled into an evidence table, which is used to write the document such that it contains evidence-based data with respect to content, complication rates, outcomes, and thresholds for prompting quality assurance reviews.When the evidence of literature is weak, conflicting, or contradictory, consensus for the parameter is reached by a minimum of 12 Standards of Practice Committee members by using a Modified Delphi Consensus Method (Appendix) (1Fink A. Kosefcoff J. Chassin M. Brook R.H. Consensus methods: characteristics and guidelines for use.Am J Public Health. 1984; 74: 979-998Crossref PubMed Scopus (1358) Google Scholar). For purposes of these documents, consensus is defined as 80% Delphi participant agreement on a value or parameter.The draft document is critically reviewed by the Standards of Practice Committee members, either by telephone conference calling or face-to-face meeting. The finalized draft from the Committee is sent to the SIR membership for further input/criticism during a 30-day comment period. These comments are discussed by the Standards of Practice Committee, and appropriate revisions are made to create the finished standards document. Before its publication, the document is endorsed by the SIR Executive Council.Introduction and BackgroundThe hematologic management of the patient undergoing percutaneous image-guided intervention is complex due to the wide range of procedures and equally wide range of patient demographics and co-morbidities. A concurrent increase in the use of both short- and long-term anticoagulation, as well as the increasing use of antiplatelet agents, further complicates the preprocedural management of these patients. Despite the continuing increase in the volume of percutaneous imaging-guided procedures, there is a general paucity of data regarding the periprocedural management of the patient with abnormal coagulation parameters. In the absence of data, clinicians may respond to the patient with abnormal coagulation parameters by canceling or postponing the procedure, altering an otherwise indicated procedure, or infusing blood products such as fresh-frozen plasma (FFP) or platelets. Recommendations from open surgical experience may not be applicable to interventional procedures because of direct visualization and the ability to obtain prompt vascular control in open cases. Finally, medicolegal factors may influence the management of the patient, as clinicians feel the need to “correct” an abnormal coagulation factor, despite the fact that studies of bleeding complications in percutaneous procedures have not shown correlation between mild to moderate abnormality of preprocedural coagulation parameters and a higher incidence of bleeding complications.The coagulation status of patients undergoing imaging-guided interventions should be assessed whenever the procedure involves direct entry into the arterial or venous system as an anticipated part of the procedure or whenever there is a possibility of inadvertent entry into the arterial or venous system with significant sized interventional devices or tools. Patients are at increased risk for delayed detection of postprocedural hemorrhage when the site of the intervention is not easily assessed and poorly controllable (eg, percutaneous intraperitoneal procedures). Coagulation status is complex; components of the intrinsic and extrinsic coagulation cascade and platelet function figure integrally into human hemostasis. The components of coagulation are evaluated by multiple tests of hemostasis. These tests and the component of coagulation function they assess are described below and summarized in Table 1, along with normal values for each test.Table 1Tests of HemostasisTestIndicationNormal RangeINR/PTExtrinsic pathway (I, II, V, VII, X)INR, 0.9–1.1Oral anticoagulant therapyLiver diseaseActivated PTTIntrinsic pathway (VIII, IX, XI, XII)Activated PTT, 25–35 secIntravenous heparin therapyvon Willebrand diseaseFactor VIII, IX, or XI deficiencyPlatelet countKnown or suspected thrombocytopenia150,000–450,000/μLBleeding timeNo current indication before imaging-guided procedures Open table in a new tab DefinitionsCoagulation ParametersProthrombin time (PT)The PT test measures the clotting time upon activation of the extrinsic coagulation pathway. It is used for monitoring oral anticoagulant therapy and is now widely reported as an international normalized ratio (INR). The degree of prolongation of the clotting time correlates with the degree of deficiency or inhibition of extrinsic or common pathway clotting factors I (fibrinogen), II (prothrombin), V, VII, and X, which are synthesized by the liver. When any of these factors is deficient, the PT is prolonged and the INR is elevated. The PT in a healthy adult is approximately 11–14 seconds. There is variation depending on the reagent used in the test (2Hyers T.M. Agnelli G. Hull R.D. et al.Antithrombotic therapy for venous thromboembolic disease.Chest. 2001; 119: 176S-193SCrossref PubMed Scopus (602) Google Scholar).INRThe INR is an expression of the results of a PT in a standardized testing environment. It is calculated by using an international standard that corrects for laboratory variation. The INR allows for universal standardization anticoagulant therapy. In the following calculation, the ISI is the International Sensitivity Index of the thromboplastin reagent used in the assay: INR = (patient PT/control PT)ISI.In this test, the patient's plasma is mixed with a PT reagent containing thromboplastin and calcium chloride. The time to clot formation is measured. The degree of prolongation of the clotting time correlates with the degree of deficiency or inhibition of extrinsic or common pathway clotting factors I (fibrinogen), II (prothrombin), V, VII, and X, which are synthesized by the liver. When any of these factors is deficient or inhibited, the PT is prolonged and the INR is elevated. The INR in a normal patient not undergoing warfarin therapy is 0.9–1.1.A prolonged PT and elevated INR occur with vitamin K deficiency, lupus anticoagulants, extrinsic pathway coagulation factor deficiencies, liver disease, disseminated intravascular coagulation bile duct obstruction, malabsorption, and other conditions. Hirudin, argatroban, and heparin may prolong the PT.The degree of prolongation of the clotting time correlates with the degree of deficiency or inhibition of extrinsic or common pathway clotting factors I (fibrinogen), II (prothrombin), V, VII, and X, which are synthesized by the liver. When any of these factors is deficient, the PT is prolonged and the INR is elevated. The coagulation factors are synthesized in the liver, and the PT is elevated with severe liver failure and acute liver injury (3O'Grady J.G. Alexander G.J.M. Hayllar K.M. et al.Early indicators of prognosis in fulminant hepatic failure.Gastroenterology. 1989; 97: 439-445Abstract PubMed Google Scholar, 4Lee W.M. Acute liver failure.N Engl J Med. 1993; 329: 1862-1872Crossref PubMed Scopus (553) Google Scholar).Activated partial thromboplastin time (PTT)The activated PTT measures the clotting time upon activation of the intrinsic coagulation pathways. In this test, the patient's plasma is mixed with reagent containing an activator, phospholipid, and calcium chloride. The time to clot formation is measured.A normal activated PTT in an adult is approximately 25–35 seconds. A therapeutic ratio of 1.5–2.5 times the control value is frequently employed in heparin therapy; however, this range varies depending on the reagent.A prolonged PTT occurs with factor deficiencies (especially of factors VIII, IX, XI, and/or XII), inhibitors (lupus anticoagulants), liver disease, disseminated intravascular coagulation, vitamin K deficiency, or therapeutic anticoagulants such as heparin, hirudin, or argatroban). The PTT is not useful in monitoring warfarin therapy (5Pilsczek F.H. Rifkin W.D. Walerstein S. Overuse of prothrombin and partial thromboplastin coagulation tests in medical inpatients.Heart Lung. 2005; 34: 402-405Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar).Thrombin timeThrombin time provides an assay for fibrinogen concentration indirectly by measuring exogenous thrombin-activated clotting times (6Clauss A. A rapid physiological coagulation method for the determination of fibrinogen.Acta Haematol. 1957; 17: 237-240Crossref PubMed Scopus (2967) Google Scholar).Bleeding timeOriginally introduced in 1901 by Milian, the bleeding time has been used to diagnose platelet disorders, assess patients for clinically significant bleeding tendencies before invasive procedures, and assess the effects of various therapies on bleeding tendencies and platelet function. The bleeding time has largely fallen out of favor in modern clinical practice as an assessment for bleeding tendencies because of conflicting data on its usefulness (7Rodgers R.P. Levin J. A critical reappraisal of the bleeding time.Semin Thromb Hemost. 1990; 16: 1-20Crossref PubMed Scopus (590) Google Scholar).Platelet countThe platelet count is generally measured as a standard part of the complete blood count. It is used to diagnose and follow bleeding disorders, thrombocytopenia, drug-induced thrombocytopenia, disseminated intravascular coagulation, and neoplastic disorders and to evaluate the response to platelet tranfusions. A normal adult platelet count is approximately 150,000–450,000 platelets per microliter of blood. A platelet count of less than 20,000/μL is a life-threatening event in which spontaneous bleeding may occur.A small number of patients receiving heparin (including low-dose heparin) develop thrombocytopenia. Drugs and chemicals associated with thrombocytopenia include chemotherapeutic agents, chloramphenicol, colchicine, H2 blocking agents, heparin, hydralazine, indomethacin, isoniazid, quinidine, streptomycin, sulfonamide, thiazide diuretic, and tolbutamide. Estrogen and oral contraceptives may cause elevated platelet levels.AnticoagulantsWarfarinWarfarin (Coumadin; Bristol-Myers Squibb, New York, New York) antagonizes the production of the vitamin K–dependent clotting factors (II, VII, IX, X) in the liver. The clinical effect is measured with the INR, which reflects antagonism of factor VII, which has the shortest half-life of approximately 6 hours. Therapeutic INR values may vary by indication for anticoagulation but most often range from 2.2 to 2.8. Patient co-morbidities may significantly alter the effect of Coumadin. Congestive heart failure, malignancy, malnutrition, diarrhea, unsuspected vitamin K deficiency, and concomitant antibiotic use may all enhance the response to Coumadin.Heparin (unfractionated)Unfractionated heparin potentiates the action of antithrombin III, is dosed according to weight, and is administered by means of continuous intravenous infusion. Therapeutic response is monitored by activated PTT, which is targeted at 1.5–2.5 times normal.Platelet count is monitored after the administration of heparin for the possibility of heparin-induced thrombocytopenia, which is defined as a platelet count of less than 150,000/μL or a 50% decrease in platelet count within 5–10 days of the start of therapy. There are two types of thrombocytopenia: type I is a benign self-limited disorder where the platelet count is rarely less than 100,000/μL and type II is a possibly life-threatening disorder with platelet counts often less than 75,000/μL and often seen in association with acute arterial and/or venous platelet rich “white” thrombi.Low-molecular-weight heparinLow-molecular-weight heparin is administered subcutaneously and often dosed by weight. It does not affect the values of the INR or activated PTT. Therapeutic dosing (ie, treatment of acute deep venous thrombosis) is at 12-hour intervals, whereas prophylactic dosing (ie, postoperative deep venous thrombosis prophylaxis) is at 24-hour intervals.Hemostatic AgentsFFPThe effect of FFP is variable due to the variable concentration of vitamin K dependent clotting factors. On average, at least 10 mL/kg is needed to effectively raise plasma protein levels. Common dose ranges from 15–30 mL/kg. In practice, in the patient with an INR in the 2.5 range, 2 units of FFP may be effective in reversing the effect of Coumadin. Patients with higher INR levels should be dosed accordingly, with possible concomitant use of vitamin K (8Hellstern P. Muntean W. Schramm W. Seifried E. Solheim B. Practical guidelines for the clinical use of plasma.Thromb Res. 2002; 107: S53Abstract Full Text Full Text PDF PubMed Scopus (74) Google Scholar, 9Escobar M.A. Reversal of coumarin-induced over-anticoagulation.Br J Haematol. 2002; 118 (discussion 926.): 925-926PubMed Google Scholar, 10Wilson S.E. Douketis J.D. Crowther M.A. Treatment of warfarin-associated coagulopathy: a physician survey.Chest. 2001; 120: 1972-1976Crossref PubMed Scopus (23) Google Scholar, 11Jacobs L.G. Nusbaum N. Perioperative management and reversal of antithrombotic therapy.Clin Geriatr Med. 2001; 17: 189-202Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar).PlateletsFractionated blood product used in the setting of thrombocytopenia or platelet dysfunction. Often dosed as 4–6 units (random donors) or as one single donor unit (12O'Connell B.A. Lee E.J. Schiffer C.A. The value of 10-minute post transfusion platelet counts.Transfusion. 1988; 26: 66-67Crossref Scopus (80) Google Scholar).ProtamineProtamine may be used in emergency situations when rapid reversal of heparin is needed before a procedure or when heparin reversal is desired before the removal of arterial catheters or sheaths. Protamine has a rapid onset of action within 10 minutes after administration. Its half-life, however, is short and ranges from 5 to 7.5 minutes, which can lead to “paradoxical” re-anticoagulation after protamine administration. Protamine dosing strategies vary considerably. A “neutralizing dose” of protamine is 2 mg/kg. Protamine may also be dosed according to the amount of heparin given, on a 1-mg protamine to 100-unit heparin ratio. To reverse commonly given intraprocedural doses of heparin (3,000–5,000 IU), we often give a total of 50-mg protamine in an adult. Protamine should be given by means of slow intravenous push or infusion over 5–10 minutes. Side effects include hypotension, bradycardia, pulmonary arterial hypertension, decreased oxygen consumption, and anaphylactoid reactions (13Butterworth J. Lin Y.A. Prielipp R.C. Bennett J. Hammon J.W. James R.L. Rapid disappearance of protamine in adults undergoing cardiac operation with cardiopulmonary bypass.Ann Thorac Surg. 2002; 74: 1589-1595Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar, 14Butterworth J. Lin Y.A. Prielipp R. Bennett J. James R. The pharmacokinetics and cardiovascular effects of a single intravenous dose of protamine in normal volunteers.Anesth Analg. 2002; 94: 514-522Crossref PubMed Scopus (47) Google Scholar, 15Brooks J.C. Noncardiogenic pulmonary edema immediately following rapid protamine administration.Ann Pharmacother. 1999; 33: 927-930Crossref PubMed Scopus (9) Google Scholar, 16Wright S.J. Murray W.B. Hampton W.A. Hargovan H. Calculating the protamine-heparin reversal ratio: a pilot study investigating a new method.J Cardiothorac Vasc Anesth. 1993; 7: 416-421Abstract Full Text PDF PubMed Scopus (13) Google Scholar, 17Lowenstein E. Lessons from studying an infrequent event: adverse hemodynamic response associated with protamine reversal of heparin anticoagulation.J Cardiothorac Anesth. 1989; 3: 99-107Abstract Full Text PDF PubMed Scopus (15) Google Scholar).Vitamin K (phytonadione)Vitamin K may be given orally, intravenously, or subcutaneously depending on the value of the INR and the desired timeframe for anticoagulant reversal. The American College of Chest Physicians has published evidence-based guidelines for the use of vitamin K in managing elevated INRs and/or clinical bleeding in patients receiving oral anticoagulation (18Ansell J. Hirsh J. Poller L. et al.The pharmacology and management of the vitamin K antagonists.Chest. 2004; 126: 204S-233SCrossref PubMed Scopus (1072) Google Scholar). In stable, elective patients without active bleeding, oral administration (5–10 mg in adults) is preferred. Although intravenous administration of vitamin K is associated with a risk of anaphylactoid reaction, it has a more rapid effect than the subcutaneous route and may be more effective in the truly emergent patient. The U.S. Food and Drug Administration has issued a black box warning for the subcutaneous, intravenous, and intramuscular routes of administration due to reports of severe reactions, including fatalities (19Raj G. Kumar R. McKinney W.P. Time course of reversal of anticoagulant effect of warfarin by intravenous and subcutaneous phytonadione.Arch Intern Med. 1999; 159: 2721-2724Crossref PubMed Scopus (104) Google Scholar, 20Byrd D.C. Stephens M.A. Hamann G.L. Dorko C. Subcutaneous phytonadione for reversal of warfarin-induced elevation of the international normalized ratio.Am J Health Syst Pharm. 1999; 56: 2312-2315PubMed Google Scholar).CryoprecipitateCryoprecipitate is used in acquired or hereditary deficiencies of fibrinogen. Ten bags will typically increase the fibrinogen level by 75 mg/dL in a 70-kg patient (21Konkle B. Percutaneous interventions in the coagulopathic patient.Semin Intervent Radiol. 2005; 22: 88-94Crossref PubMed Scopus (9) Google Scholar).Recombinant factor VIIaRecombinant factor VIIa is used in hemophilia in patients with inhibitors to factor 8 or in severe, nonhemophiliac-related bleeding such as acute trauma (22Pusateri A.E. Park M.S. Mechanistic implications for the use and monitoring of recombinant activated factor VII in trauma.Critical Care. 2005; 9: S15-S24Crossref PubMed Scopus (31) Google Scholar).DesmopressinDesmopressin (1-deamino-8-D-arginine vasopressin [DDAVP]) is a synthetic analogue of antidiuretic hormone. DDAVP acts through an unclear mechanism to enhance the plasma levels of factor VIII and von Willebrand factor (23Mannucci P.M. Ruggeri Z. Pareti F. Capitanio A. 1-deamino-8-arginine vasopressin: a new pharmacological approach to the management of haemophilia and von Willebrands disease.Lancet. 1977; 1: 869-872Abstract PubMed Scopus (490) Google Scholar). A dose of 0.3 μg/kg is given intravenously, usually diluted in 100 mL of normal saline and infused over 20–30 minutes. A single dose can be expected to raise the factor VIII level 3–6 fold. Adverse effects may include mild hyponatremia. Tachyphylaxis has been reported in patients who have received multiple treatments. There are case reports of vascular thrombosis and myocardial ischemia after intravenous administration (24Mannucci P.M. Bettega D. Cattaneo M. Patterns of development of tachphylaxis in patients with haemophilia and von Willebrand disease after repeated doses of desmopressin (DDAVP).Br J Haematol. 1992; 82: 87-93Crossref PubMed Scopus (159) Google Scholar).DDAVP may be indicated before image-guided procedures in patients with hemophilia, von Willebrand disease, and acquired platelet disorders due to uremia, liver disease, or antiplatelet agents (25Mannucci P.M. Desmopressin: a nontransfusional form of treatment for congenital and acquired bleeding disorders.Blood. 1988; 72: 1449-1455PubMed Google Scholar).Transfusion ManagementFFPThe most common intervention before imaging-guided procedures is transfusion of FFP. In the United States, more than 3 million units of FFP are transfused each year. Dzik and Rao (26Dzik W. Rao A. Why do physicians request fresh frozen plasma?.Transfusion. 2004; 44: 1393Crossref PubMed Scopus (65) Google Scholar) reported in a 3-month audit of FFP usage at the Massachusetts General Hospital that the most common reason for prescribing FFP was to prepare the patient with an elevated INR for an invasive procedure. This indication accounted for one-third of all requests for FFP. Stanworth et al (27Stanworth S.J. Brunskill S.J. Hyde C.J. McClelland D. Murphy M.F. Is fresh frozen plasma clinically effective? A systematic review of randomized controlled trials.Br J Haematol. 2004; 126: 1139Crossref Scopus (343) Google Scholar) reported a review of 57 randomized controlled trials investigating the efficacy of FFP to prevent hemorrhagic complications over a wide variety of indications and clinical settings, including cardiac surgery. They found the data insufficient to recommend or refute the prophylactic use of FFP. Due to the lack of data, percutaneous procedures were not included in this comprehensive review. There is a clear need for additional investigation of the use of FFP with imaging-guided procedures (27Stanworth S.J. Brunskill S.J. Hyde C.J. McClelland D. Murphy M.F. Is fresh frozen plasma clinically effective? A systematic review of randomized controlled trials.Br J Haematol. 2004; 126: 1139Crossref Scopus (343) Google Scholar).Segal and Dzik (28Segal J.B. Dzik W.H. Transfusion Medicine/Hemostasis Clinical Trials Network Paucity of studies to support that abnormal coagulation test results predict bleeding in the setting of invasive procedures: an evidence-based review.Transfusion. 2005; 45: 1413-1425Crossref PubMed Scopus (532) Google Scholar) recently reported an analysis of 25 studies analyzing the ability of abnormal coagulation parameters to predict bleeding associated with invasive bedside or image-guided procedures. Of the 25 studies available for analysis, one was a clinical trial (comparison of transjugular liver biopsy to percutaneous biopsy with tract plugging [29Sawyerr A.M. McCormick P.A. Tennyson G.S. et al.A comparison of transjugular and plugged-percutaneous liver biopsy in patients with impaired coagulation.J Hepatol. 1993; 17: 81-85Abstract Full Text PDF PubMed Scopus (85) Google Scholar]). The remaining studies were case series. The studies included patients undergoing bronchoscopy with biopsy, central vein cannulation, femoral angiography, liver biopsy, kidney biopsy, paracentesis, thoracentesis, and lumbar puncture. Overall, the authors concluded that elevated coagulation parameters provide little to no predictive value for bleeding complications from imaging-guided interventions. They assert that, in the absence of randomized, controlled studies, mild to moderate elevation of coagulation times should neither be assumed to represent an increased risk for periprocedural bleeding nor be used as an indication for transfusion of FFP or clotting factor concentrates. Literature data on preprocedural coagulation testing for specific procedures are summarized below.AngiographyIn a prospective study of 1,000 patients undergoing arteriography via common femoral artery access, Darcy et al (30Darcy M.D. Kanterman R.Y. Kleinhoffer M.A. et al.Evaluation of coagulation tests as predictors of angiographic bleeding complications.Radiology. 1996; 198: 741-744PubMed Google Scholar) identified 85 patients with abnormal coagulation parameters, defined as a PT greater than 15 seconds (range, 15–20.8 seconds; normal, 13 seconds). Major bleeding, defined as a groin hematoma larger than 4 cm, was found in 1.2% (one of 85) of patients with abnormal coagulation parameters and 1.6% (15 of 915) of patients with normal coagulation parameters. Most procedures were performed with 5-F catheters (72%) or 6–7-F catheters (23%). There was, however, a correlation of a higher incidence of hematoma with a platelet count less than 100,000/μL (P = .002). The study concluded that, in the absence of an overt history of bleeding and an expected PT of less than 18 seconds, preprocedural testing with PT and activated PTT is not warranted (30Darcy M.D. Kanterman R.Y. Kleinhoffer M.A. et al.Evaluation of coagulation tests as predictors of angiographic bleeding complications.Radiology. 1996; 198: 741-744PubMed Google Scholar).Liver biopsyIn a laparoscopic study, Ewe (31Ewe K. Bleeding after liver biopsy does not correlate with indices of peripheral coagulation.Dig Dis Sci. 1981; 26: 388-393Crossref PubMed Scopus (285) Google Scholar) was able to directly visualize the liver biopsy site for bleeding. He found that 4.3% of patients with a PT longer than 13.5 seconds bled for more than 12 minutes after biopsy, in comparison to 4.6% of patients with normal coagulation parameters. He was unable to draw any correlation between the degree of abnormality of preprocedural coagulation parameters and the length of observed bleeding.Central venous catheter placementFisher and Mutimer (32Fisher N.C. Mutimer D.J. Central venous cannulation in patients with liver disease and coagulopathy: a prospective audit.Intensive Care Med. 1999; 25: 5Crossref PubMed Scopus (137) Google Scholar) evaluated 580 patients with an INR greater than 1.5 undergoing central venous catheterization. All procedures were performed with a 16- or 18-gauge needle. Most patients (83%) had a platelet count less than 150,000/μL. One patient (0.2%) had major bleeding due to inadvertent puncture of the carotid artery. The authors concluded that central venous access can be performed safely by experienced physicians in the presence of abnormal coagulation parameters. Other studies have supported these results (33Doerfler M.E. Kaufman B. Goldenberg A.S. Central venous catheter placement in patients with disorders of hemostasis.Chest. 1996; 110: 185-188Crossref PubMed Scopus (134) Google Scholar, 34Stellato T.A. Gauderer M.W. Lazarus H.M. et al.Percutaneous isoelastic catheter insertion in patients with thrombocytopenia.Cancer. 1985; 56: 2691-2693Crossref PubMed Scopus (18) Google Scholar).Morado et al (35Morado M. Jimenez-Yuste V. Villar A. et al.Complications of central venous catheters in patients with haemophilia and inhibitors.Haemophilia. 2001; 7: 551-556Crossref PubMed Scopus (48) Google Scholar) reported a case series of 15 patients with hemophilia and inhibitors who underwent a total of 34 catheter insertions. The mean patient age was 8.8 years (range, 16 months to 39 years); all patients had factor VIII/IX inhibitors. Pericatheter bleeding was seen in seven catheter insertions in six patients and required substantive treatment for several days.Central Venous Catheter RemovalThere is some controversy and lack of consensus over the management of patients undergoing the removal of tunneled catheters. There is no evidence of the value of pre-removal coagulation parameters or platelet count in the management of these patients. Stecker et al (36Stecker M. Johnson M. Ying J. et al.Time to hemostasis after traction removal of tunneled cuffed central venous catheters.J Vasc Interv Radiol. 2007; 18: 1232-1239Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar) reported a study of 180 patients with tunneled cuffed central venous catheters. Time to hemostasis was 5 minutes for 166 patients, with 14 patients requiring more than 5 minutes of manual compression at the insertion site (range, 10–35 minutes). Only one patient required more than 15 minutes of pressure. In the 14 patients with prolonged (>5 minutes) time to hemostasis, statistically significant factors included the use of antiplatelet agents, renal failure, the use of high-flow hemodialysis catheter, and operator experience. They concluded that pre-removal laboratory evaluation was not warranted and that platelet dysfunction was a mo" @default.
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• W2912402179 title "Consensus Guidelines for Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous Image-guided Interventions" @default.
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• W2912402179 doi "https://doi.org/10.1016/j.jvir.2008.11.027" @default.
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