Hemostatic evaluation before abdominal interventions: an overview and proposal.

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233

Perspective

Hemostatic Evaluation Before An Overview and Proposal Stuart

G. Silverman,1’2

Peter

R. Mueller,1

and Richard

Abdominal

Interventions:

C. Pfister1

Despite many years of routine interventional practice, no specific guidelines exist on how to evaluate a patient’s hemostatic function before a procedure. In many institutions, patients are often tested for prothrombin time (PT), partial thromboplastin time (PTT), and platelet count with little regard for the type of procedure planned or the patient’s history. Clearly, not all patients need to undergo these tests routinely. In a complex climate of increasing litigation and rising healthcare costs, how can we best identify the unsuspected bleeder or evaluate the suspected bleeder? No published radiologic studies have specifically examined these questions. A prospective randomized investigation of a large number of patients needs to be performed, whereby numerous factors including patient’s history, procedure performed, techniques used, and laboratory tests all would be examined and compared with specific outcomes. Using nonvascular abdominal interventions as a model, we propose specific guidelines on how to evaluate a patient’s hemostatic function before an interventional procedure. The recommendations are based on Rapaport’s preoperative assessment of 1983 [1] and modified for interventional radiology. The basic idea is that the extent of the laboratory evaluation is determined by the patient’s medical history and the procedure planned. This allows minor procedures to be done in healthy patients without laboratory testing, and a thorough laboratory evaluation can be done both before invasive procedures and in patients whose history suggests a bleeding disorder. We hope these guidelines will someday serve as a template for prospective study or at least provide

a working guide to the interventional radiologist in everyday practice. Basic mechanisms of normal hemostasis, laboratory tests, and disorders of coagulation are reviewed first. Abdominal interventions are then divided into two groups, minor and major, according to bleeding potential. Finally, the preprocedural hemostatic assessment is formulated on the basis of the screening history and the procedure planned.

Basic Laboratory Hemostasis

Tests in Normal and Abnormal

Normal hemostasis has two basic components [2]: primary hemostasis is the formation of a platelet plug, and secondary hemostasis is the formation of fibnn as a result of a cascade of interactions of the plasma coagulation system. Effective primary hemostasis occurs after platelet adhesion, platelet granule release, and platelet aggregation. The platelet count is the basic test of primary hemostasis. The normal platelet count ranges from 150,000 to 450,000 platelets per cubic millimeter of blood. The propensity to bleed generally correlates with the platelet count. Patients with platelet counts between 50,000 and 100,000 may bleed after severe trauma. In patients with platelet counts less than 50,000, cutaneous ecchymosis may develop after minor trauma [3]. The risk of spontaneous bleeding becomes significant at platelet counts less than 10,000-20,000. Because of its frequency, thrombocytopenia should be excluded first as the cause of abnor-

Received May 16, 1989; accepted after revision July 10, 1989. Department of Radiology, Massachusetts General Hospital, 32 Fruit St., Boston, MA 02114. Address reprint requests address: Department of Radiology, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115.

to P. A. Mueller.

2

AJR 154:233-238,

February

1990 0361 -803X/90/1

542-02330

American

Roentgen

Ray Society This

One

SILVERMAN


234

mal bleeding. The causes of thrombocytopenia are many and include bone marrow replacement (tumor) or failure (drugs, aplastic anemias); hypersplenism; and increased destruction of platelets from nonimmune causes (sepsis, vasculitis, vascular prostheses), disseminated intravascular coagulation, or immune causes (systemic lupus erythematosus, drugs) [3]. A more stringent measure of primary hemostasis is the bleeding time which, although more difficult to determine, can be used to screen for abnormal platelet function, which may be due to a platelet deficiency or abnormal platelets. The bleeding time is the interval required for hemostasis after a standardized superficial incision (1 -2 mm deep, 5 mm long) in the forearm skin while venous pressure is maintained at 40 mm Hg. A normal result is between 4 and 7 mm, but the time varies slightly depending on the method used [4]. Isolated qualitative platelet abnormalities (normal platelet count, abnormal bleeding time) are usually due to the ingestion of certain drugs, such as aspirin and other nonsteroidal antiinflammatory agents, or to uremia [5]. The hemostatic defect due to aspirin is usually minor: 1 .5-2 mm prolongation of the bleeding time [6]. Restoration of platelet function usually takes 3-4 days after the last dose of aspirin [6], but may take as long as 7-1 0 days [5]. The defect can be magnified, however, by virtually any other abnormality in hemostasis. Ingestion of aspirin before surgery is actually quite common. In one study, 42% of patients used aspirin within 72 hr of an unexpected operation. Thirty-six percent of these patients had abnormal bleeding times (up to 1 6 mm) but had no increased perioperative blood loss [7]. Other studies have shown an increased risk of bleeding after a variety of surgical procedures [8, 9]. The significance of antiplatelet drug ingestion before procedures is therefore controversial [5]. Although the bleeding time can be used to evaluate the severity of the aspirininduced hemostatic defect, the predictive value of the bleeding time before surgery or interventional procedures has not been defined. Secondary hemostasis is the formation of fibrin. Fibrin is the end product of a series of enzymatic reactions, summarized in Figure 1 involving the plasma coagulation factors [2]. The figure emphasizes the two pathways by which the coagulation scheme can be activated. The intrinsic pathway is measured by the partial thromboplastin time (PU) and the extrinsic pathway by the prothrombin time (PT). After factor X is activated by either pathway, there is a common sequence whereby factor II (prothrombin) is converted to thrombin, which in turn results in the formation of fibrin. This last step, the conversion of fibrinogen to fibrin, is measured with the thrombin clotting time (TCT). Factor XIII, not shown in Figure 1, is necessary to stabilize the fibrin clot. The PU is prolonged whenever there is significant reduction of one or more of the factors in the intrinsic pathway. The PT is prolonged whenever the amount of one or more of the factors in the extrinsic pathway is reduced significantly. Both the PT and the PU are prolonged when deficiencies occur in factors X and V, prothrombin, and fibrinogen because these are common to both pathways. An isolated abnormality of TCT is seen if only abnormalities of the conversion of fibrinogen to fibrin occur. The screening tests are normal in the rare patient with factor XIII deficiency, which can be ,

ET AL.

r

surface

XII

AJR:154,

February

1990

contact

XIIa

Xis

tissue

factor

PTT intrinsic pathway

iXa Viii PL,

L

Vita

Vii

caJ

PT extrinsic pathway

Xa V.

Ca

PL

Fibrinogen

Fig. 1.-Summary of plasma pathway is measured by partial way is measured by prothrombin by thrombin clotting time (TcT). factors. PL = phospholipid; Ca

us

Fibrin

TCT

coagulation sequence. Note that intrinsic thromboplastin time (PU), extrinsic pathtime (PT), and fibrinogen-fibrin conversion Lower case “a” designates the activated calcium.

detected with a clot solubility test. This test will show that the clot is soluble in 5 mol/l urea or 1 % monochloroacetic acid if factor XIII is deficient [1 1 0, 1 1 ]. Table 1 is a diagnostic guide to analyzing the results of these basic tests of hemostasis [2]. Patients most likely to present with hemostatic problems to the interventional radiologist include those taking anticoagulants and those with underlying clinical conditions that affect primary or secondary hemostasis (Table 2) [2]. Warfarinlike drugs (e.g., coumarin) inhibit the vitamin K-dependent factors II, VII, IX, and X, thus affecting PT predominantly. Heparin accelerates the action of antithrombin, an important regulator of coagulation. The effect of heparin is generally a prolonged PU; however, a milder prolongation of PT can be observed [1 2]. The combination of a prolonged TCT and a normal reptilase time is a strong indication that a prolonged PU is the result of heparin [13]. In addition to the diseases listed in Table 2, a wide variety of conditions may result in abnormal hemostasis known as disseminated intravascular coagulation (DIC). These include overwhelming infection, severe physical trauma, diffuse hemolysis, disseminated malignant disease (particularLy prostatic carcinoma and leukemia), obstetric complications such as placental abruption and amniotic fluid embolism, and ischemic gangrene [6, 14]. These conditions are thought to cause bleeding by triggering diffuse coagulation through the release of powerful thrombogenic materials. This results in the consumption of platelets and coagulation factors so that they become depleted. Prolongation of PT and PU, thrombocytopenia, hypofibrinogenemia, and increased levels of fibrin degradation products may be observed. ,

Procedure

Risk Groups

The proper preprocedural hemostatic evaluation depends on many factors. In this section, we consider only the factors related to the procedure, including instruments used, target structure, and target location. We do not consider the operator or the image-guidance technique. If there is a spectrum

PREPROCEDURE

AJR:154, February 1990


TABLE

1: Screening

Absent Present Present

Laboratory

PIT

PT

ABN ABN ABN

NL NL ABN

HEMOSTATIC

Tests

in Selected

TCT NL NL NL

235

EVALUATION

Hemostatic

Bi;rr19

Pa0t::t

NL NL NL

NL NL NL

Disorders

Possible

Defects

Factor Xli, lupus anticoagulant XI, IX, VIII (Hemophilia) V, X, II, coumann, vitamin K

deficiency, ease

mild hepatic dis-

Present Present Present Present Present Present Present

NL ABN ABN NL NL NL ABN

ABN NL ABN NL NL NL ABN

NL NL ABN NL NL NL ABN

NL ABN ABN ABN ABN NL ABN

NL NL NL ABN NL NL ABN

VII von Willebrand diseasea Afibrinogenemiab Thrombocytopenia Qualitative platelet disorders Factor XIII Disseminated intravascular co-

Variable

NL

NL

ABN

NL

NL

Present

ABN

NL

ABN

NL

NL

Dysfibnnogenemia, fibnn degradation Heparinc

agulation,

Note-Modified from White et al. [2]. PU = partial thromboplastin time; PT clotting time; ABN = abnormal; NL = normal. a Variable partial thromboplastin time and bleeding time. b May have a normal bleeding time. C High plasma concentration associated with a long prothrombin time.

TABLE

2:

Acquired

Hemostatic

Defects

Underlying Clinical Condition Liver disease

Renal disease Malabsorption Acute leukemia

Myeloproliferative

disease

Associated

with

lymphocytic

Dysproteinemia

Factor deficiency Fibrinolysis Thrombocytopenia Thrombocytopenia Multiple factor deficiency Thrombocytopenia Disseminated intravascular coagulation (DIC) Platelet defect Thrombocythemia/throm-

Systemic

lupus

Underlying

myeloma, products

time; TCT

Clinical

=

thrombin

Conditions

Cause Decreased Decreased

synthesis clearance

of activators

Splenic sequestration Retained metabolites Vitamin K Decreased megakaryocytopolesis Increased cellular procoagulant activity Abnormal thrombopoiesis Hyperplastic or replaced marrow,

splenic sequestration

Decreased von Willebrand factor Low factor VIII Thrombocytopenia Thrombocytopenia Prolonged thrombin ting time Factor X deficiency Capillary fragility Factor deficiency

Amyloidosis

prothrombin

=

Type of Hemostatic Defect

bocytopenia Lymphoma/chronic leukemia

Selected

liver failure

clot-

Adsorption onto tumor, body Autoantibody

Marrow

replacement,

autoanti-

splenic

sequestration Decreased production Inhibition of fibrin Adsorption by amyloid Vascular infiltration Autoantibodies to coagulation

proteins Thrombocytopenia/throm-

bocytopathia Note-Modified

Autoantibodies

to platelet

glyco-

proteins

from White et al. [2].

of percutaneous interventions that differ according to bleeding potential, we can divide all procedures into two groups, one comprising procedures with negligible bleeding risk, the other comprising procedures with significant hemorrhagic potential. We believe there are some procedures in interventional radiology that may proceed without laboratory testing if performed in healthy patients. This group of “minor” interventions, hereafter referred to as procedure risk group (PRG) 1, includes fine-needle (20 gauge or smaller) aspirations of fluid

collections such as cysts, pseudocysts, abscesses, lymphoceles, hematomas, bilomas, and urinomas. Fine-needle aspiration of these fluid collections may be either external to or within an organ in which, based on the knowledge of the patient’s anatomy from prior imaging studies, no major yessels will be traversed. Although the location of major vessels may not always be certain, their presence is often unlikely, particularly with superficial targets. Puncture of cysts and aspiration of superficial fluid collections have a negligible


236

SILVERMAN

bleeding potential [1 5]. The O.6% incidence of minor bleeding in a series of over 5000 patients after renal cyst puncture would be even lower if anteriorly located cysts were excluded. Hence, although traversing renal parenchyma with a fine needle would appear to increase the risk of bleeding, all renal cyst punctures and antegrade pyelography (1 0% macroscopic hematuria) are included in PRG 1 [16]. PRG 2 includes all other abdominal interventions, such as tissue biopsy, transhepatic cholangiography, and all catheter placements. Within this group, even the least “invasive” procedure, percutaneous biopsy with a fine (23 to 20 gauge) needle, has a small but finite risk of hemorrhage. A series of 1 1 ,700 patients had only seven patients (0.06%) with “major” or “moderate” hemorrhage after fine-needle abdominal biopsies [1 7]. However, in a more recent series of 360 patients undergoing abdominal mass biopsy, mostly with 22-gauge needles, 2.5% had a drop in hematocrit of 3% or more [18]. The same article reviewed the biopsy literature and reported an overall hemorrhagic complication rate of 1 -5% [18-20]. Although it is tempting to postulate that significant hemorrhage is more likely with larger needles (1 8 gauge or greater) and hypervascular tumors (e.g., hemangioma [1 8, 1 9] and hepatoma [20, 21]), these hypotheses have not been proved. Large-diameter needles may be necessary to obtain diagnostic tissue. The practical significance of an increased risk of performing biopsies on hypervascular lesions is suspect because a priori knowledge of the presence of a hypervascular tumor is not always possible. Significant bleeding with smaller (20 and 22 gauge) needles is probably unavoidable. In a large questionnaire sampling 63,1 08 biopsies, only 27 patients required blood transfusions; however, three deaths resulted from biopsies with 22-gauge needles (adrenal angiosarcoma, myeloma, liver metastasis from lung primary) in patients with normal hemostatic parameters at the time of the procedure [22]. Given this experience, there is a low but finite incidence of significant hemorrhagic complications, and therefore all tissue biopsies, regardless of technique and lesion, are placed in PRG 2. Hemorrhage associated with catheter drainage of abscess and fluid collections occurs in approximately 4% of patients and is usually minor [23]. This series of 250 patients included two who had “major hemorrhages” and one who died from direct laceration of a mesenteric vessel with a 16-gauge needle. Transient hematuria (500 ml) bleeding and a 1 % mortality rate directly attributed to hemorrhage in 200 patients [29, 30]. Although a 22-gauge needle often is used, transhepatic cholangiography is placed in this category. On the basis of a large survey of 2000 patients, the incidence of bleeding after transhepatic cholangiography, including one death due to intraperitoneal hemorrhage, was 1% [31], but may be as high as 4% [32]. Significant gastrointestinal bleeding has been reported in approximately 1 % of patients after percutaneous feeding gastrostomy, although this is a relatively new procedure in interventional radiology [33]. Table 3 summarizes the categorization of abdominal interventions into PRG 1 and PRG 2. Preprocedural

Hemostatic

Assessment

The primary means for identifying a potential bleeder is the patient’s clinical history (Table 4). Although the history is significant, it alone is not adequate to screen all patients. Subclinical defects or alterations that may have developed since an uneventful surgical or interventional procedure may be missed if one considers the history alone. Patients who are unreliable historians, or who are too ill to give a history, also need laboratory testing as part of the evaluation. On the basis of the screening history, a patient can be considered tentatively as having no hemostatic defect or as possibly having a bleeding disorder. This knowledge, coupled with the PRG, will determine which tests, if any, are necessary. On the basis of Rapaport’s preoperative recommendations [1], we have formulated similar guidelines for interventional radiologic procedures; PRG 1 procedures are the minor group and PRG 2 procedures are the major group. Four possible levels of categorization then exist (Table 5). Level

1

The patient has no history of a hemostatic defect, and the planned procedure is in PRG 1. No laboratory tests are

TABLE 3: Procedure Risk Groups (PRG): Stratification Nonvascular Abdominal Interventions According to Bleeding Potential

Procedures PRG 1: Significant Fine-needle Tissue

fluid aspiration

biopsy

PRG 2: Significant Catheter

placement

Examples bleeding potential

minimal

Fluid collection Paracentesis Cyst puncture Suprapubic voiding cystourethrography Antegrade pyelography bleeding

potential

low but finite

All tissues Fluid/abscess drainage Nephrostomy Nephrostolithotomy

Biliary drainage Gastrostomy Miscellaneous

of

Transhepatic

cholangiography

PREPROCEDURE

AJR:154, February 1990


TABLE

4: Screening

HEMOSTATIC

History

1 . Have you ever bled or developed a swollen tongue or mouth after cutting or biting your tongue, cheek, or lip? 2. Do you develop bruises larger than a silver dollar without being able to remember when or how you injured yourself? If so, how big was the largest of the bruises? 3. How many times have you had teeth pulled and what was the longest time you bled after an extraction? Has bleeding ever

started up again the day after an extraction? 4. What operations or prior radiologic procedures including minor surgery these procedures ever unusual bruising in the 5. Have you had a medical a doctor’s care? If so,

6. What medications

including

aspirin

or any other

headaches, colds, menstrual cramps, arthritis, you taken within the past 7-9 days. 7. Has any blood relative had a problem with

bleeding after surgery? trol the bleeding? Note-Modified

from

have you had,

such as skin biopsies? Was bleeding after hard to stop? Have you ever developed skin around the area of surgery or injury? problem within the past 5 years requiring what was its nature? pains have

unusual

bruising

required to con-

Laboratory

Tests

1

Normal

1

2

Normal

2

3

Possible defect

1, 2

PU, PT, platelet count, BT, clot solubility test

4

Probable

1, 2

PU,

defect

None PU, platelet

Level

3

This category includes all patients whose screening history raises the possibility of a hemostatic defect. In addition to measuring platelet count and PU, bleeding time and PT measurements are recommended. The clot solubility test can be performed to screen for factor XIII deficiency [1 1 0, 1 1]. If results are normal, as Rapaport suggests, the screening history is not abnormal enough to warrant further testing. ,

Level 4

[1].

PRG

defects are not performed; we rely instead on the absence of underlying predisposing conditions such as uremia or myeloproliferative disorders (Table 2).

or

TABLE 5: Suggested Preprocedural Hemostatic Evaluation Based on Screening History and Procedure Risk Groups

Level

237

for

or other

Were blood transfusions

Rapaport

remedies

EVALUATION

count

PT, platelet

clot solubility

count,

BT,

test, BT

after 600 mg ASA, clotting factor assays, thrombin time, inhibitor assays Note.-PAG = procedure risk group; PU = activated partial thromboplastin time; PT = prothrombin time; BT = bleeding time; ASA = acetylsalicylic acid.

required. Rapaport argues that the cumulative costs to society of screening tests before minor surgery (e.g., dental extraction, excisional biopsy) outweigh the rare but non-lifethreatening bleeding in a patient with a mild bleeding disorder not detected with the history alone. No laboratory tests are required before minor surgical procedures if the screening history is normal. Similarly, we believe no laboratory testing is necessary in otherwise healthy patients undergoing fineneedle fluid aspirations.

All of these patients have a history that raises serious suspicion or certainty of a hemostatic defect. This creates the need for a full diagnostic evaluation regardless of the procedure planned. The initial evaluation of patients in this group is the same as for patients in level 3. If these tests yield an abnormal result, then further workup is dictated by those abnormalities. If the level 3 tests are normal, then the following additional tests are recommended: (1) Bleeding time can be measured after an oral dose of 600 mg of aspirin to detect a mild qualitative platelet disorder [34]. If the planned procedure is urgent, however, this test should not be done because the deleterious effect of aspirin on platelet function may increase the risk of bleeding and necessitate delaying the procedure. (2) Specific assays for clotting factors VIII and IX can be done to detect a rare patient with mild hemophilia A or B presenting with a normal PU. (3) Measurement of thrombin clotting time may reveal a rare case of dysfibrinogenemia or an anticoagulant. (4) If these results are normal, specific assays for circulating inhibitors such as alpha2-antiplasmin may be performed. Alpha2-antiplasmin is the main inhibitor of fibrinolysis, and thus a rare inherited deficiency will result in a bleeding tendency because of unopposed lysis of fibrin [35]. Within these broad guidelines, special circumstances may arise. An occasional level 2 patient will be found to have a prolonged PU caused by the lupus anticoagulant or a deficiency of factor XII, neither of which will increase bleeding tendency. The lupus anticoagulant is an acquired anticoagulant initially described in patients with systemic lupus erythematosus and subsequently found to occur with other autoimmune disorders, drugs, neoplasm, or as an isolated finding [36]. Factor XII (Hageman factor), as shown in Figure 1 is the first protein in the intrinsic pathway of coagulation and also participates in the inflammatory response and fibrinolysis. Levels of factor XII may vary with ethnic and racial background [37]. The recognition of these disorders of hemostasis, while allowing the interventional procedure to be performed without concern for hemorrhage, may contribute to the diagnosis of an underlying disorder. The importance of identifying this subset of patients is further emphasized by evidence that suggests that both groups of patients are at increased risk for thrombotic events, particularly those patients with the lupus anticoagulant [36, 38]. ,

Level

2

The screening history is normal, but a PRG 2 procedure is planned. Measurements of PU and platelet count are suggested. Rapaport recommends obtaining only PU and platelet count for patients with a normal history, which includes prior surgical tests of hemostasis, about to undergo major surgery (e.g., cholecystectomy and bowel resection). These laboratory examinations will detect an unsuspected anticoagulant, thrombocytopenia, or occult DIC (moderate thrombocytopenia,

short

or long PU).

Tests

for qualitative

platelet


The issue of the use of aspirin and other nonsteroidal antiinflammatory agents is controversial [6, 7], and therefore specific recommendations are not given. When an elective procedure is planned in patients receiving antiplatelet drugs, the radiologist has several choices. The most conservative approach would be to delay the procedure, regardless of the category, and wait the necessary 3-1 0 days after the last dose of aspirin before performing the procedure [5, 6]. One may choose to do so only before PRG 2 procedures. Or one may simply accept the hemostatic defect, relying on the absence of any evidence of concomitant defects, a modified less invasive technique, and the statistical likelihood that a significant hemorrhagic complication as a result of aspirin alone is probably very low. It can be argued that if minor surgery is allowed to proceed in a healthy patient without laboratory testing, then all percutaneous procedures should follow in the same path. This assumes however, that all percutaneous procedures are at the same or lower risk compared with minor surgery, when in fact they may not be. The fundamental disadvantge of interventional radiology in this regard is that intraprocedural hemostasis cannot always be actively maintained. A potential site of bleeding can go temporarily unrecognized, and even if it is recognized, it cannot be treated immediately as it can during surgery. The ideas expressed herein are only a suggested proposal. We believe that patients should be managed individually and that physicians have the right and the responsibility to deviate from guidelines if the clinical situation warrants it, particularly in the case of emergent or life-saving procedures. In summary, the hemostatic evaluation depends first and foremost on the patient’s history, which if normal, allows many percutaneous procedures to proceed without laboratory testing. If a more invasive procedure is planned, the normal history allows us to tailor the laboratory evaluation. More importantly perhaps, these broad guidelines provide for a thorough investigation of patients who are at significant risk of bleeding. Implementation of these guidelines could reduce health-care costs while preventing hemorrhagic complications.

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The reader’s

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is directed

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Cooling interventions for athletes: An overview of effectiveness, physiological mechanisms, and practical considerations.

An overview of disparities and interventions in pediatric kidney transplantation worldwide.

Erratum to: Behavior change interventions and policies influencing primary healthcare professionals' practice-an overview of reviews.

Acceptability of healthcare interventions: an overview of reviews and development of a theoretical framework.

Formative research methods for designing culturally appropriate, integrated child nutrition and development interventions: an overview.

Interventions to Improve Neonatal Health and Later Survival: An Overview of Systematic Reviews.

Comprehensive evaluation of a Thorotrast patient: an overview.

Evaluation Frameworks, Part 1: An Overview.

Overview of platelet physiology: its hemostatic and nonhemostatic role in disease pathogenesis.

Are multifaceted interventions more effective than single-component interventions in changing health-care professionals' behaviours? An overview of systematic reviews.