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Endoscopic procedures in patients with disorders of hemostasis

Author: Patrick S Kamath, MD

Section Editor: John R Saltzman, MD, FACP, FACG, FASGE, AGAF
Deputy Editor: Kristen M Robson, MD, MBA, FACG

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2018. | This topic last updated: Mar 14, 2018.

INTRODUCTION — Gastroenterologic procedures are commonly performed in patients with abnormal

hemostasis. However, there are limited data assessing the bleeding risk of specific procedures in these
settings.

This topic will review the bleeding risks associated with endoscopic procedures, the risk of thromboembolic
complications associated with various conditions, and the periprocedural management of patients with von
Willebrand's disease, hemophilia, renal failure, liver failure, and thrombocytopenia. The management of
patients taking anticoagulants or antiplatelet agents is discussed elsewhere. (See "Management of
anticoagulants in patients undergoing endoscopic procedures" and "Management of antiplatelet agents in
patients undergoing endoscopic procedures".)

SOCIETY GUIDELINES — The American Society for Gastrointestinal Endoscopy (ASGE) has issued official
guidelines based upon the available evidence and consensus opinion [1]. The recommendations in this topic
review are consistent with the ASGE guidelines. In addition, this topic review also addresses disorders of
hemostasis not covered by the ASGE guidelines. This topic is also addressed in reviews from the American
Journal of Gastroenterology and the Journal of the American College of Cardiology, which make similar
recommendations [2,3].

PROCEDURE-RELATED BLEEDING RISK — The ASGE classifies the risk of bleeding from endoscopic
procedures in patients with normal coagulation status as either high or low (table 1) (see appropriate topic
reviews).

● High-risk procedures (risk of bleeding 1 to 6 percent) include:

• Colonoscopic or gastric polypectomy

• Biliary or pancreatic sphincterotomy

• Treatment of varices

• Percutaneous endoscopic gastrostomy (PEG) tube placement

• Therapeutic balloon-assisted enteroscopy

• Endoscopic ultrasound (EUS) with fine-needle aspiration (FNA)

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• Tumor ablation

• Cystgastrostomy

• Ampullary resection

• Endoscopic mucosal resection

• Endoscopic submucosal dissection

• Pneumatic or bougie dilation

• Percutaneous endoscopic jejunostomy placement

● Low-risk procedures (bleeding risk <1 percent) include:

• Diagnostic upper endoscopy, flexible sigmoidoscopy, and colonoscopy (including biopsies)

• Diagnostic endoscopic retrograde cholangiopancreatography

• Biliary stent insertion without endoscopic sphincterotomy

• Papillary balloon dilation (without sphincterotomy)

• EUS without FNA

• Push enteroscopy and diagnostic balloon-assisted enteroscopy

• Enteral stent deployment (controversial)

• Argon plasma coagulation

• Barrett's ablation

In some cases, the risk varies depending on whether antithrombotic therapy is being used. PEG tube
placement is considered low risk for patients on aspirin or clopidogrel (but not those on dual antiplatelet
therapy), and EUS-FNA of solid masses is considered low risk in patients taking aspirin or NSAIDs.

Among patients undergoing colonic polypectomy, the size of the polyp influences the risk of bleeding, and it
may be more appropriate to categorize polyps less than 1 cm in size as low risk for bleeding [4-7]. In some
cases, endoscopic techniques can be used to decrease the risk of bleeding. For example, in patients
undergoing polypectomy, hemoclips may be placed at the polypectomy site. (See "Bleeding after colonic
polypectomy", section on 'Prevention of immediate bleeding' and "Bleeding after colonic polypectomy",
section on 'Prevention of delayed bleeding'.)

RISK OF THROMBOEMBOLIC COMPLICATIONS — The probability of a thromboembolic complication

following reversal or discontinuation of anticoagulation or antiplatelet agents depends upon the preexisting
condition for which the medication was prescribed (table 2 and table 3). The approach to estimating
thromboembolic risk is discussed in detail elsewhere. (See "Perioperative management of patients receiving
anticoagulants", section on 'Estimating thromboembolic risk' and "Antithrombotic therapy for prosthetic heart
valves: Management of bleeding and invasive procedures", section on 'Management of antithrombotic therapy
for invasive procedures'.)

PATIENTS TAKING ANTICOAGULANTS — The management of patients taking anticoagulants is reviewed

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in detail elsewhere. (See "Management of anticoagulants in patients undergoing endoscopic procedures".)

PATIENTS TAKING ANTIPLATELET AGENTS — The management of patients taking antiplatelet agents is
reviewed in detail elsewhere. (See "Management of antiplatelet agents in patients undergoing endoscopic
procedures".)

INHERITED DISORDERS OF HEMOSTASIS — A number of inherited disorders of hemostasis may increase

the risk of bleeding with gastrointestinal procedures and require specific preventive measures. We suggest
consultation with an expert in coagulation disorders before performing endoscopic procedures in these
patients.

von Willebrand disease — von Willebrand disease is the most common inherited bleeding disorder, with an
estimated prevalence in the general population of 1 percent [8]. Although it is primarily a congenital disorder,
there are also acquired forms of the disease. (See "Classification and pathophysiology of von Willebrand
disease".)

von Willebrand factor (VWF) performs two critical functions in hemostasis: It acts as a bridging molecule for
normal platelet adhesion and aggregation, and it acts as a carrier for factor VIII in the circulation, increasing
the half-life of factor VIII fivefold [9]. von Willebrand disease occurs when VWF is deficient or qualitatively
abnormal.

Three types of the inherited form of von Willebrand disease have been recognized [10] (see "Classification
and pathophysiology of von Willebrand disease"):

● Type I is the most common form and is due to reduced functional VWF

● Type II is caused by a qualitative abnormality, resulting in defective interaction of VWF with platelets and
the vessel wall

● Type III is the most severe form, caused by markedly reduced levels of VWF in the plasma

Treatment depends upon the type of von Willebrand disease and the procedure being performed.

● DDAVP – For diagnostic procedures and mucosal biopsies in patients with Type I disease, treatment with
DDAVP (desmopressin) is usually sufficient. DDAVP can cause vasospasm and should be used
cautiously in patients with coronary artery disease. Patients should also be monitored for the
development of hyponatremia. (See "Treatment of von Willebrand disease", section on 'Desmopressin
(DDAVP)'.)

● von Willebrand factor – For therapeutic procedures in patients with Type I disease, and for all procedures
in patients with Types II and III disease, replacement of VWF is required. Products available that contain
VWF in high concentrations include factor VIII concentrates, purified VWF concentrates, and
cryoprecipitate. Replacement therapy should be continued for two to three days in patients who had a
mucosal biopsy. For patients who underwent a therapeutic procedure, replacement should continue for
up to two weeks. (See "Treatment of von Willebrand disease", section on 'VWF replacement therapy'.)

Hemophilia A and B — Hemophilia A is an x-linked recessive disorder due to congenital factor VIII
deficiency. Hemophilia B is less common, is also x-linked recessive, and is due to congenital factor IX
deficiency. Patients with these disorders should be prepared for endoscopy as if they were having a life-
threatening hemorrhage.

In patients with factor VIII deficiency, the factor VIII activity should be raised by infusion of a factor VIII

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concentrate one hour before the procedure. Baseline and post infusion levels should be measured to
determine that the response has been adequate.

Guidelines are lacking with regard to factor replacement for endoscopic procedures. However, in patients
undergoing major surgical procedures, an initial factor level of 60 to 100 percent is achieved for hemostasis
[11]. A prophylactic level of 30 to 50 percent is then maintained until the wound has healed (typically 10 to 14
days).

The principles are the same for patients with factor IX deficiency.

ACQUIRED DISORDERS OF HEMOSTASIS — Renal failure, liver failure, and thrombocytopenia may all
predispose to procedure-related bleeding. von Willebrand disease can also exist in an acquired form. (See
'von Willebrand disease' above.)

Renal failure — An increased tendency to bleed is present in both acute and chronic renal failure [12,13].
This is most often manifested by skin hemorrhage and by bleeding at sites of surgery or trauma. (See
"Platelet dysfunction in uremia".)

Uremic bleeding appears to correlate most closely with prolongation of the bleeding time, due primarily to
impaired platelet function [14-16]. Other coagulation parameters are generally intact in uremia [12]. The
platelet count is usually normal or only slightly reduced, and there is no prolongation of the prothrombin or
partial thromboplastin times.

The risk of bleeding with gastrointestinal endoscopic procedures cannot be accurately predicted from the
bleeding time, and there are relatively few data to guide optimal treatment to prevent bleeding. As a general
rule, patients should be treated as though their risk of bleeding is increased, and preventive measures should
be guided by the clinical situation. Options for improving platelet function include DDAVP, dialysis, estrogens,
and correction of anemia, which are discussed in detail separately. (See "Platelet dysfunction in uremia".)

Liver failure — Patients with liver failure have a number of derangements in hemostasis. (See "Hemostatic
abnormalities in patients with liver disease".)

Causes of coagulopathy — Prolongation of the prothrombin time (PT) and partial thromboplastin time
usually indicates impaired hepatic synthesis of coagulation factors or vitamin K deficiency.

Other coagulation abnormalities are commonly present in patients with liver failure. Low fibrinogen levels may
be due to the presence of structurally abnormal fibrinogen, increased fibrinolysis, and disseminated
intravascular coagulation. Patients may also have thrombocytopenia and qualitative platelet dysfunction (see
'Thrombocytopenia' below). Administration of DDAVP may be beneficial in patients with qualitative platelet
dysfunction.

Evaluation — Because the liver makes coagulation factors as well as anticoagulant proteins, liver disease
can lead to a hypocoagulable state or a hypercoagulable state. The relative balance or imbalance of these
factors is not reflected in conventional indices of coagulation, such as the prothrombin time, activated partial
thromboplastin time, or international normalized ratio (INR). (See "Hemostatic abnormalities in patients with
liver disease", section on 'Effects of hepatic dysfunction'.)

Because conventional indices of coagulation are not helpful in determining a patient's bleeding risk, patients
who require an invasive procedure that is at moderate or high risk for bleeding may need additional testing,
such as a determination of fibrinogen levels, thromboelastography, or thromboelastometry to guide
management. This approach needs further study before being recommended as routine pre-procedure

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assessment of bleeding risk. In general, in patients with liver disease, procedure-related bleeding risk cannot
be assessed accurately pre-procedure.

Treatment — While plasma is commonly given to patients with chronic liver disease and an elevated INR
prior to invasive procedures, plasma infusion may have adverse effects on portal vein pressures and
collateral vessel flow. In addition, the traditional dose of two units of plasma is unlikely to significantly alter
coagulation factor levels. (See "Clinical use of plasma components", section on 'Plasma products' and
"Hemostatic abnormalities in patients with liver disease", section on 'Common clinical problems'.)

The management of patients with chronic liver disease who require an invasive procedure may depend on
factors such as fibrinogen levels and global assays of hemostasis (eg, thromboelastography, or
thromboelastometry). This is discussed in detail elsewhere. (See "Hemostatic abnormalities in patients with
liver disease", section on 'Invasive procedure'.)

Thrombocytopenia — No large prospective studies have established optimal strategies for giving
prophylactic platelet transfusions in patients with thrombocytopenia. One set of recommendations suggests
increasing the platelet count to greater than 50,000 platelets/microL before high-risk therapeutic procedures
[10]. A platelet count of more than 20,000 platelets/microL may be adequate for low-risk procedures. In a
retrospective series of 395 patients with platelet counts less than 75,000/microL who underwent 617
endoscopic procedures, the risk of bleeding following biopsy was 1.5 percent (6 of 398 endoscopies) and
following polypectomy was 4 percent (2 of 45 polypectomies) [17]. (See 'Procedure-related bleeding risk'
above and "Approach to the adult with unexplained thrombocytopenia", section on 'General management
principles' and "Clinical and laboratory aspects of platelet transfusion therapy", section on 'Preparation for an
invasive procedure'.)

The situation is more complex in patients who have disorders associated with platelet destruction such as
immune thrombocytopenia. In such patients, elective procedures should be postponed until therapy
addressing the underlying condition has been instituted. In emergency settings, platelet infusions should be
given to maintain a platelet count of at least 20,000 to 30,000/microL. Further infusions should be given if
there is evidence of bleeding. Glucocorticoids and immunoglobulin may also be beneficial. (See "Immune
thrombocytopenia (ITP) in adults: Initial treatment and prognosis" and "Clinical and laboratory aspects of
platelet transfusion therapy", section on 'Immune thrombocytopenia (ITP)'.)

SUMMARY AND RECOMMENDATIONS

● The risk of bleeding from endoscopic procedures can be classified as high or low. In general, diagnostic
procedures are low risk, whereas therapeutic procedures are high risk (table 1). (See 'Procedure-related
bleeding risk' above.)

● The probability of a thromboembolic complication following reversal or discontinuation of anticoagulation

or antiplatelet agents depends upon the preexisting condition for which the medication was prescribed
(table 2 and table 3). (See 'Risk of thromboembolic complications' above.)

● Disorders of hemostasis that may require treatment prior to gastrointestinal procedures include von
Willebrand disease, hemophilia A and B, renal failure, liver failure, and thrombocytopenia. (See 'von
Willebrand disease' above and 'Hemophilia A and B' above and 'Renal failure' above and 'Liver failure'
above and 'Thrombocytopenia' above.)

● The management of patients taking anticoagulants is reviewed in detail elsewhere. (See "Management of
anticoagulants in patients undergoing endoscopic procedures".)

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● The management of patients taking antiplatelet agents is reviewed in detail elsewhere. (See
"Management of antiplatelet agents in patients undergoing endoscopic procedures".)

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REFERENCES

1. ASGE Standards of Practice Committee, Acosta RD, Abraham NS, et al. The management of
antithrombotic agents for patients undergoing GI endoscopy. Gastrointest Endosc 2016; 83:3.
2. Kwok A, Faigel DO. Management of anticoagulation before and after gastrointestinal endoscopy. Am J
Gastroenterol 2009; 104:3085.
3. Becker RC, Scheiman J, Dauerman HL, et al. Management of platelet-directed pharmacotherapy in
patients with atherosclerotic coronary artery disease undergoing elective endoscopic gastrointestinal
procedures. J Am Coll Cardiol 2009; 54:2261.
4. Sawhney MS, Salfiti N, Nelson DB, et al. Risk factors for severe delayed postpolypectomy bleeding.
Endoscopy 2008; 40:115.
5. Rosen L, Bub DS, Reed JF 3rd, Nastasee SA. Hemorrhage following colonoscopic polypectomy. Dis
Colon Rectum 1993; 36:1126.
6. Kim HS, Kim TI, Kim WH, et al. Risk factors for immediate postpolypectomy bleeding of the colon: a
multicenter study. Am J Gastroenterol 2006; 101:1333.
7. Friedland S, Sedehi D, Soetikno R. Colonoscopic polypectomy in anticoagulated patients. World J
Gastroenterol 2009; 15:1973.
8. Rodeghiero F, Castaman G, Dini E. Epidemiological investigation of the prevalence of von Willebrand's
disease. Blood 1987; 69:454.
9. Brinkhous KM, Sandberg H, Garris JB, et al. Purified human factor VIII procoagulant protein:
comparative hemostatic response after infusions into hemophilic and von Willebrand disease dogs. Proc
Natl Acad Sci U S A 1985; 82:8752.
10. Van Os EC, Kamath PS, Gostout CJ, Heit JA. Gastroenterological procedures among patients with
disorders of hemostasis: evaluation and management recommendations. Gastrointest Endosc 1999;
50:536.
11. Srivastava A. Dose and response in haemophilia--optimization of factor replacement therapy. Br J
Haematol 2004; 127:12.
12. Eberst ME, Berkowitz LR. Hemostasis in renal disease: pathophysiology and management. Am J Med
1994; 96:168.
13. Lutz J, Menke J, Sollinger D, et al. Haemostasis in chronic kidney disease. Nephrol Dial Transplant
2014; 29:29.
14. Steiner RW, Coggins C, Carvalho AC. Bleeding time in uremia: a useful test to assess clinical bleeding.
Am J Hematol 1979; 7:107.
15. Escolar G, Cases A, Bastida E, et al. Uremic platelets have a functional defect affecting the interaction
of von Willebrand factor with glycoprotein IIb-IIIa. Blood 1990; 76:1336.
16. Gawaz MP, Dobos G, Späth M, et al. Impaired function of platelet membrane glycoprotein IIb-IIIa in end-
stage renal disease. J Am Soc Nephrol 1994; 5:36.

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17. Krishna SG, Rao BB, Thirumurthi S, et al. Safety of endoscopic interventions in patients with
thrombocytopenia. Gastrointest Endosc 2014; 80:425.

Topic 2553 Version 16.0

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GRAPHICS

Procedure-related bleeding risk from gastrointestinal procedures

Higher-risk procedures
Polypectomy*

Biliary or pancreatic sphincterotomy

Treatment of varices

PEG placement ¶

Therapeutic balloon-assisted enteroscopy

EUS with FNA Δ

Endoscopic hemostasis

Tumor ablation

Cystgastrostomy

Ampullary resection

EMR

Endoscopic submucosal dissection

Pneumatic or bougie dilation

PEJ

Low-risk procedures
Diagnostic (EGD, colonoscopy, flexible sigmoidoscopy) including mucosal biopsy

ERCP with stent (biliary or pancreatic) placement or papillary balloon dilation without sphincterotomy

Push enteroscopy and diagnostic balloon-assisted enteroscopy

Capsule endoscopy

Enteral stent deployment (controversial)

EUS without FNA

Argon plasma coagulation

Barrett's ablation

EGD: esophagogastroduodenoscopy; ERCP: endoscopic retrograde cholangiopancreatography; PEG: percutaneous

endoscopic gastrostomy; EUS: endoscopic ultrasound; FNA: fine-needle aspiration; EMR: endoscopic mucosal resection;
PEJ: percutaneous endoscopic jejunostomy.
* Among patients undergoing colonic polypectomy, the size of the polyp influences the risk of bleeding, and it may be
more appropriate to categorize polyps less than 1 cm in size as low-risk for bleeding.
¶ PEG on aspirin or clopidogrel therapy is low risk. Does not apply to dual antiplatelet therapy.
Δ EUS-FNA of solid masses on aspirin/nonsteroidal anti-inflammatory drugs is low risk.

Reproduced from: ASGE Standards of Practice Committee, Acosta RD, Abraham NS, et al. The management of
antithrombotic agents for patients undergoing GI endoscopy. Gastrointest Endosc 2016; 83:3. Table used with the
permission of Elsevier Inc. All rights reserved.

Graphic 50700 Version 7.0

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Perioperative thrombotic risk

Indication for anticoagulant therapy

Risk stratum
Mechanical heart valve Atrial fibrillation VTE

Very high thrombotic risk*
Any mitral valve prosthesis
Any caged-ball or tilting
disc aortic valve prosthesis
Recent (within six months)
stroke or transient
ischemic attack
CHA 2 DS 2 -VASc score of Recent (within three
≥6 months) VTE
(or CHADS 2 score of 5-6) Severe thrombophilia (eg,
Recent (within three deficiency of protein C,
months) stroke or protein S, or antithrombin;
transient ischemic attack antiphospholipid
antibodies; multiple
Rheumatic valvular heart
abnormalities)
disease

High thrombotic risk
Bileaflet aortic valve
prosthesis and one or
more of the of following
risk factors: atrial
fibrillation, prior stroke or
transient ischemic attack,
hypertension, diabetes,
congestive heart failure,
age >75 years
CHA 2 DS 2 -VASc score of VTE within the past 3 to 12
4-5 or CHADS 2 score of months
3-4 Nonsevere thrombophilia
(eg, heterozygous factor V
Leiden or prothrombin
gene mutation)
Recurrent VTE
Active cancer (treated
within six months or
palliative)

Moderate thrombotic risk
Bileaflet aortic valve
prosthesis without atrial
fibrillation and no other
risk factors for stroke
CHA 2 DS 2 -VASc score of VTE >12 months previous
2-3 or CHADS 2 score of and no other risk factors
0-2 (assuming no prior
stroke or transient
ischemic attack)

Refer to UpToDate topics on perioperative anticoagulation management for details.

VTE: venous thromboembolism; CHADS 2 : congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, and
stroke or transient ischemic attack; CHA 2 DS 2 -VASc: congestive heart failure, hypertension, age ≥75 years (2 points),
diabetes mellitus, prior stroke or transient ischemic attack or thromboembolism (2 points), vascular disease (peripheral
artery disease, myocardial infarction, or aortic plaque), age 65-74 years, sex category female.
* Very high risk patients may also include those with a prior stroke or transient ischemic attack occurring >3 months
before the planned surgery and a CHA 2 DS 2 -VASc score <6 (or CHADS 2 score <5), those with prior thromboembolism
during temporary interruption of anticoagulation, or those undergoing certain types of surgery associated with an
increased risk for stroke or other thromboembolism (eg, cardiac valve replacement, carotid endarterectomy, major
vascular surgery).

Modified from Douketis JD, Spyropoulos AC, Spencer FA, et al. Perioperative management of antithrombotic therapy:
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based
Clinical Practice Guidelines. Chest 2012; 141(2 Suppl):e326S. Copyright © 2012. Reproduced with permission from the
American College of Chest Physicians.

Graphic 86930 Version 4.0

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Comparison of the CHADS2 and CHA2DS2-VASc risk stratification scores for

subjects with nonvalvular AF

Definition and scores for CHADS 2 and Stroke risk stratification with the
CHA 2 DS 2 -VASc CHADS 2 and CHA 2 DS 2 -VASc scores
CHADS 2 acronym Score CHADS 2 acronym Unadjusted ischemic stroke
rate (% per year)*
Congestive HF 1
0 0.6%
Hypertension 1
1 3.0%
Age ≥75 years 1
2 4.2%
Diabetes mellitus 1
3 7.1%
Stroke/TIA/TE 2
4 11.1%
Maximum score 6
5 12.5%
CHA 2 DS 2 -VASc acronym Score
6 13.0%
Congestive HF 1
CHA 2 DS 2 -VASc Unadjusted ischemic stroke
Hypertension 1
acronym rate (% per year)*
Age ≥75 years 2
0 0.2%
Diabetes mellitus 1
1 0.6%
Stroke/TIA/TE 2
2 2.2%
Vascular disease (prior MI, PAD, or aortic 1
3 3.2%
plaque)
4 4.8%
Age 65 to 74 years 1
5 7.2%
Sex category (ie, female sex) 1
6 9.7%
Maximum score 9
7 11.2%

8 10.8%

9 12.2%

AF: atrial fibrillation; CHADS 2 : Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus, Prior Stroke or
TIA or Thromboembolism (doubled); CHA 2 DS 2 -VASc: Congestive heart failure, Hypertension, Age ≥75 years (doubled),
Diabetes mellitus, Prior Stroke or TIA or thromboembolism (doubled), Vascular disease, Age 65-74 years, Sex category;
HF: heart failure; LV: left ventricular; MI: myocardial infarction; PAD: peripheral artery disease; TE: thromboembolic; TIA:
transient ischemic attack.
* These unadjusted (not adjusted for possible use of aspirin) stroke rates were published in 2012 [1]. Actual rates of stroke
in contemporary cohorts might vary from these estimates.

Reference:
1. Friberg L, Rosenqvist M, Lip GY. Evaluation of risk stratification schemes for ischaemic stroke and bleeding in 182
678 patients with atrial fibrillation: the Swedish Atrial Fibrillation cohort study. Eur Heart J 2012; 33:1500.
Original figure modified for this publication. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the
Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2014. DOI:
10.1016/j.jacc.2014.03.022. Table used with the permission of Elsevier Inc. All rights reserved.

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Contributor Disclosures
Patrick S Kamath, MD Nothing to disclose John R Saltzman, MD, FACP, FACG, FASGE,
AGAF Consultant/Advisory Boards: Iterative scopes [Artificial intelligence (AI) applied to polyp detection
during colonoscopy]. Kristen M Robson, MD, MBA, FACG Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

Conflict of interest policy

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