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Year : 2014  |  Volume : 6  |  Issue : 2  |  Page : 143-150

Bleeding disorders in dental practice: A diagnostic overview


1 Final Year Post Graduate Trainees, Department of Pedodontics and Preventive Dentistry, Guru Nanak Institute of Dental Sciences and Research, Kolkata, India
2 Professor and Head, Department of Pedodontics and Preventive Dentistry, Guru Nanak Institute of Dental Sciences and Research, Kolkata, India
3 Professor, Department of Oral and Maxillofacial Surgery, Guru Nanak Institute of Dental Sciences and Research, Kolkata, India
4 Professor and Head, Department of Cardiac Anaesthesiology, Institute of Post Graduate Medical Education and Research and SSKM Hospital, Kolkata, India

Date of Web Publication28-Oct-2014

Correspondence Address:
Abhirup Goswami
M. C. Lahiri Street, Chatra. (Serampore-4), Hooghly - 712 204, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0754.143529

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   Abstract 

Dental health care workers are increasingly called upon to provide quality dental care to individuals whose bleeding and clotting mechanisms have been altered by inherited or acquired diseases. This provides an opportunity for the dentist who is trained in the recognition of oral and systemic signs of altered hemostasis to assist in the diagnosis of the underlying condition. A number of dental procedures result in the risk of bleeding that can have serious consequences, such as severe hemorrhage or possibly death, for the patient with a bleeding disorder. Oral care providers must be aware of the impact of bleeding disorders on the management of their patients. These disorders must be recognized from history, clinical examinations, and laboratory investigations, if indicated, prior to surgical procedures including those in dental surgery to prevent bleeding related complications. Safe dental care may require consultation with the patient's physician, systemic management, and dental treatment modifications. The purpose of this article is how to identify these patients with bleeding disorders.

Keywords: Bleeding disorders, coagulation disorder, diagnosis


How to cite this article:
Goswami A, Bora A, Kundu GK, Ghosh S, Goswami A. Bleeding disorders in dental practice: A diagnostic overview . J Int Clin Dent Res Organ 2014;6:143-50

How to cite this URL:
Goswami A, Bora A, Kundu GK, Ghosh S, Goswami A. Bleeding disorders in dental practice: A diagnostic overview . J Int Clin Dent Res Organ [serial online] 2014 [cited 2018 Dec 17];6:143-50. Available from: http://www.jicdro.org/text.asp?2014/6/2/143/143529


   Introduction Top


Bleeding disorders are due to altered ability of blood vessels, platelets, and coagulation factors to maintain haemostasis. These may be inherited due to genetic transmission or acquired secondary to diseases affecting vascular wall integrity, platelets, and coagulation factors or due to drugs, radiation or chemotherapy. Most of the bleeding disorders are iatrogenic.

The most common inherited bleeding disorder is von Willebrand disease affecting approximately 1% of the population in the United States while Hemophilia A is the most common inherited coagulation disorders with an overall prevalence of 1case for every 20000 people in the United States. [1]

Normal control of bleeding

The three phases of haemostasis for controlling bleeding are vascular, platelet and coagulation phases. The coagulation phase is followed by fibrinolytic phase that dissolves the clot.

Vascular phase (In Seconds) [1],[2]

Any injury triggers vascular phase, which consists of:

  1. Vasoconstriction of arteries and veins in the area of injury.
  2. Retraction of cut arteries.
  3. Build-up of extra vascular pressure by blood lost from cut vessels.


Platelet phase (primary hemostasis-in seconds) [1],[2]

  1. Platelets and vessel walls become sticky.
  2. Mechanical plugs of platelets seal off openings of cut vessels.


Coagulation phase (secondary haemostasis-in minutes) [Figure 1] [1],[2]
Figure 1: Coagulation cascade

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  1. Blood lost into surrounding areas coagulates through extrinsic and common pathways.
  2. Blood in vessels in areas of injury coagulates through intrinsic and common pathways.
  3. Takes place more slowly than other phases.


Fibrinolytic/Metabolic phase [Figure 2] [1],[2]
Figure 2: Fibrinolytic system

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  1. It is activated simultaneously with the coagulation and functions to maintain fluidity of blood during coagulation.
  2. It also serves in clot lysis once tissue repair begins.
  3. Anti-thrombotic agents are released.
  4. Spleen and liver destroy these anti-thrombotic agents.


The coagulation cascade

The fundamental reaction of formation of the blood clot is conversion of the soluble protein fibrinogen into insoluble fibrin under the action of thrombin. The conversion of prothrombin to thrombin involves a series of plasma serine proteases (collectively referred to as clotting factors) that normally exist in inactive, pro enzyme forms, becoming activated in cascade sequence as shown in [Figure 1]. [3]

The anticlotting mechanism and fibrinolysis

In vivo , there is a natural tendency for blood to clot. This is balanced by various naturally occurring anticoagulants. The most important of these is antithrombin III, which inhibits the activity of factors IX, X, XII as well as thrombin. This inhibition is greatly facilitated by heparin. Coagulation is also inhibited by thrombomodulin, secreted by intact endothelial cells and binds thrombin. The thrombomodulin-thrombin complex then activates a proenzyme protein C, found in plasma, to its enzymatic form and this, together with co-factor, protein S, in plasma, results in inactivation of activated factors V and VIII.

Fibrinolysis (dissolution of fibrin) occurs mainly through the action of plasmin, which degrades fibrin and fibrinogen into fibrin degradation products [Figure 2]. Plasmin is present as an inactive precursor, plasminogen. Its conversion to plasmin is brought about primarily by tissue-type plasminogen activator (t-PA), a protein released from endothelium. [3]

Modern concept of coagulation

The classical separation of coagulation into extrinsic and intrinsic pathways is overly complicated and now not thought to occur in vivo. Instead there is a common pathway of initiation [Figure 3]. Tissue factor from damaged vascular beds combines with factor VIIa and activates factors IX and X which leads to generation of small amounts of thrombin (IIa), followed by amplification. This then activates further factors (V and VIII), leading to massive production of thrombin and generation of fibrin from fibrinogen. [4] Classification of bleeding disorders as detailed in [Table 1]. [1],[5],[8]
Figure 3: Coagulation cascade (modern concept)

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Table 1: Classifi cation of bleeding disorders

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   Identifying patients at risk of bleeding Top


History of:

  • Bleeding problems in relatives.
  • Bleeding problems after surgery, tooth extraction and trauma.
  • Medications: Aspirin, anticoagulants, long term antibiotics.
  • Illnesses associated with bleeding problems: Leukemia, congenital heart disease, liver disease, hemophilia
  • Spontaneous bleeding


Clinical findings:

  • Jaundice, pallor
  • Spider angiomas
  • Ecchymoses, petechiae
  • Oral ulcers
  • Hyperplastic gingival tissue
  • Hemarthrosis


Screening laboratory tests:

  • Platelet count
  • Ivy bleeding time (BT)/PFA*
  • Prothrombin Time (PT)&INR
  • Activated partial thromboplastin time (aPTT)
  • Thrombin time (TT)


[*Platelet function analysis may ultimately replace BT] [1],[5],[6]


   Screening laboratory tests for platelet abnormalities Top


Quantitative (Platelet Count): [7]

  1. Normal Platelet Count-150,000~440,000/mm 3
  2. Thrombocytopenia-Platelet <150,000/mm 3
  3. Severe intraop bleeding-Platelet <40,000~70,000/ mm 3
  4. Spontaneous bleeding-Platelet <20,000/mm 3
  5. Minimal recommended preop platelet >75,000/mm 3


However, qualitative difference makes it unwise to rely solely on platelet count

Qualitative (platelet function): [1]

  1. Ivy Bleeding Time-Normally 1~6 mins
  2. Closure Time from PFA 100-Normally 60~120 seconds


Ivy bleeding time

In the Ivy method [Figure 4], a blood pressure cuff is placed on the upper arm and inflated to 30 mm of Hg. A lancet or scalpel blade is used to make a stab wound on the underside of the forearm. An automatic, spring-loaded blade device is most commonly used to make a standard-sized cut. The area stabbed is selected so that no superficial or visible veins are cut. As these veins, because of their size, may have longer bleeding times, especially in people with bleeding defects. The time from when the stab wound is made until all bleeding has stopped is measured and is called the bleeding time. Every 30 seconds, filter paper or a paper towel is used to draw off the blood. The test is finished when bleeding has stopped completely.
Figure 4: Ivy bleeding time: Method

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No two wounds are the same, so the test does not reproduce well.

Platelet function analysis

The "Platelet Function Analyzer" [Figure 5] is an in vitro system for the detection of platelet dysfunction. It provides a quantitative measures of platelet function in anticoagulated whole blood. The system consists of a microprocessor-controlled instrument and a disposable test cartridge containing a biologically active membrane. [1]
Figure 5: Platelet function analyzer

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Generally 2 types of disposable test cartridges are used

A standard cartridge containing collagen-ADP

A cartridge containing collagen-epinephrine

The instrument aspirates blood sample under constant vacuum from the sample reservoir through a capillary and a microscopic aperture cut into the membrane, that has been coated with collagen and with either ADP or epinephrine (EPI). The presence of either ADP or EPI and the high shear rates generated under the standardised flow condition result in platelet attachment, activation, and aggregation which slowly builds to a stable platelet plug of the aperture. The time required to obtain full occlusion of the aperture is reported as "closure time" (CT). An initial screen is done with collagen/EPI. If the CT is normal, it is unlikely that a platelet dysfunction exists. The collagen/ADP test is run to confirm an abnormal collagen/EPI test. If both tests are abnormal, it is likely that the patient has a platelet dysfunction and further testing for inherited or acquired bleeding disorders is indicated. If the collagen/ADP test is normal, then the abnormal collagen/EPI test may be due to aspirin ingestion. This is the most frequently encountered abnormal collagen/EPI result as a single dose of aspirin can affect platelet function for about 10 days. [1]


   Screening laboratory tests for coagulation disorders Top


Prothrombin time (PT) and International normalized ratio (INR)

PT-Activated by tissue thromboplastin.

It tests extrinsic and common pathways.

INR: It is a mathematical 'correction' of the PT ratio (patient PT/mean normal PT) for differences in the sensitivity of thromboplastin reagents. It relies upon "reference" thromboplastins with known sensitivity to antithrombotic effects of oral anticoagulants (ISI). INR is the PT ratio one would have obtained if the "reference" thromboplastin had been used.

It allows for comparison of results between laboratories that is, T ratio) orrection"d as closure timebuilds to a stable platelet plug of the apperture tachments and standardizes reporting of the prothrombin time.

Equation for calculation of INR:

INR = (patient PT/mean normal PT) ISI

ISI = International Sensitivity Index, assigned to the test system

Normal values:

PT = 11-15 secs, INR = 1.0-1.2

Activated partial thromboplastintime (aPTT)

Initiated by phospholipid platelet substitute and activated by addition of contact activator (kaolin)

Tests intrinsic and common pathways

  • Normal value: 25-35 secs


Thrombin time (TT):

Tests the common pathway, thus the ability to form initial clot from fibrinogen.

  • Normal Value: 9-13 secs


[Control should be run for all the above mentioned tests]

  • Characteristic changes in Inherited Coagulapathies: [Table 2]
  • Characteristic changes in Acquired Coagulapathies: [Table 3]
Table 2: Characteristic changes in Inherited Coagulapathies[6,7]

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Table 3: Characteristic changes in Acquired Coagulapathies[6,7]

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   Recent advances in diagnosing bleeding disorders Top


Thromboelastography (TEG)

Thromboelastograph is an instrument that measures the development of blood clot viscoelastic strength over time. A rotating piston is suspended in a cuvette filled with heated blood. As clot formation proceeds, the rotation of the piston is affected and characteristic curves are generated [Figure 6]a and b.

TEG assesses the whole blood clotting system. The measurements are displayed as a graph from the beginning of clot formation to fibrinolysis [Figure 7]. [7],[8]
Figure 6: (a) Working principles of TEG (b) Working principles of TEG

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Figure 7: Thromboelastogram, normal parameters

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TEG provides information about the kinetics, strength and stability of the blood clot. The shape of the graph is determined by the viscoelastic properties of the blood and functional activity of the blood components. Its interpretation requires comprehensive knowledge.

Thromboelastogram- normal parameters

There are five parameters of the TEG tracing [7] :

  1. R: Period of time from the initiation of the test to initial fibrin formation
  2. K: Time from the beginning of clot formation until the amplitude of TEG reaches 20 mm, representing the dynamics of clot formation.
  3. α angle: Angle between the line in the middle of the TEG tracing and the line tangential to the developing body of the tracing, representing the kinetics of fibrin cross linking.
  4. MA (maximum amplitude): Reflexes the strength of the clot, which is dependent on the No. and function of platelets and their interaction with fibrin.
  5. A60: Measures the rate of amplitude reduction 60 min after MA, representing the stability of the clot.


The etiology of the coagulopathy may be obtained by analyzing the thromboelastograms [Figure 8].
Figure 8: TEG patterns in some coagulation disorders

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Portable systems for rapid measurementof PT and INR

Portable systems for rapid measurement of PT and INR [Figure 9] have been specifically designed for healthcare professionals and their patients to enable on-the-spot analysis of coagulation levels (PT/INR) during mobile emergency treatment or for routine follow-up in a hospital ward and/or at their general practice. These systems are easy-to-use reflectance photometers, portable and battery-powered devices for rapid measurement of Prothrombin Time (PT) and International Normalized Ratio (INR). It has always been a challenge to health care professionals and to their patients which involves a venous blood sample or the patient themselves being sent to a laboratory. This is time-consuming and patient's compliance can be limited, as it often requires a second appointment with the healthcare professional. These systems provide accurate results from a single drop of capillary blood from the fingertip within one minute improving compliance.
Figure 9: Portable systems for rapid measurement of PT and INR

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  • Systemic diseases which cause bleeding during procedure, their causes and their resulting coagulation defects: [Table 4]. [8]
  • Treatment protocols in short: Principal Products for Systemic Management of
  • Patients with Bleeding Disorders: [9] [Table 5].
Table 4: Systemic diseases which cause bleeding during procedure, their causes and their resulting coagulation defects

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Table 5: Principal products for systemic management of patients with bleeding disorders

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Patients on dual antiplatlet therapy

The combination of clopidogrel plus asprin is mainly used in patients with percutaneous coronary stent intervention (coronary stents), in order to prevent thrombotic complications following placement. While the combination of aspirin and clopidogrel has been associated with bleeding risk with coronary artery bypass graft (CABG) surgery, there have been no studies to examine whether an increased risk of bleeding exists in the dental setting following extractions compared to more invasive surgical procedures (such as a CABG). Of significance however, is that a recent Science Advisory from the American Heart Association, American College of Cardiology, American College of Surgeons and the American Dental Association recommended continuing aspirin and clopidogrel therapy for minor dental surgical procedures in patients who have coronary artery stents or delaying treatment until the prescribed antiplatelet regimen is completed and warned of the significant thrombotic risks if therapy was discontinued. [10]

According to the European school of thought, a literature review and guideline development process conducted by the Oral Medicine and Oral Surgery Francophone Society. They found that, based on agreement among professionals in the field, interruption of aspirin or thienopyridine therapy before dental procedures is unnecessary. Most such procedures carry a low risk of bleeding, and any bleeding that occurs can usually be controlled by local homeostasis. Oral, periodontal, and implant dental surgery are not associated with high rates of bleeding. Any bleeding that occurs can usually be controlled locally, so discontinuation of anti-platelet therapy is not recommended. [11],[12],[13]

According to the recently published POISE-2 study on aspirin in patients undergoing noncardiac elective surgery; "Administration of aspirin before surgery and throughout the early postsurgical period had no significant effect on the rate of a composite of death or nonfatal myocardial infarction but increased the risk of major bleeding." [14]


   Conclusion Top


  • A number of surgical procedures including those performed in dentistry may cause bleeding. Normally these procedures carry very little risk; however, this is compounded in the presence of bleeding disorders.
  • Once the patient with bleeding problem has been identified from history, clinical examination, and laboratory diagnostic tests; steps can be taken, to greatly reduce the risk associated with these procedures.


 
   References Top

1.
Little JW, Falace DA, Miller CS, Rhodus NL, editors. Dental Management of the Medically Compromised Patient. 8 th ed.; 2012.  Back to cited text no. 1
    
2.
Morgan GE Jr, Mikhail MS, Murray MJ, editors: Clinical Anaesthesiology. 5 th ed. Lange; 2013.  Back to cited text no. 2
    
3.
Minors DS. Haemostasis, blood platelets and coagulation. Anaesth Intensive Care Med 2004;1:11-3.  Back to cited text no. 3
    
4.
Allman KG, Wilson IH, editors. Oxford Handbook of Anaesthesia. 3 rd ed. Oxford: Oxford University Press; 2010.  Back to cited text no. 4
    
5.
Brown V. Clinical aspects of coagulation. Anaesth Intensive Care Med 2004;1:14-7.  Back to cited text no. 5
    
6.
Gupta A, Epstein JB, Cabay RJ. Bleeding disorders of importance in dental care and related patient management. J Can Dent Assoc 2007;73:77-83.  Back to cited text no. 6
    
7.
In: Duke J, editor. Anesthesia Secrets. 4 th ed. Elsevier; 2010.  Back to cited text no. 7
    
8.
Yao FF, editor. Anaesthseiology Problem-Oriented Patient Management. 7 th ed. Lippincott-Raven; 2011.  Back to cited text no. 8
    
9.
Greenberg Martin S. Glick Michael: Burket's Oral Medicine. 11 th ed. McGraw-Hill Medical; 2011.  Back to cited text no. 9
    
10.
Henry RG. Dental management of patients taking antiplatelet medications. Tex Dent J 2009;126:608-16.  Back to cited text no. 10
    
11.
Oral Medicine and Oral Surgery Francophone Society. Management of patients under anti-platelet agents' treatment in odontostomatology.  Back to cited text no. 11
    
12.
Verma G. Dental extraction can be performed safely in patients on aspirin therapy: A timely reminder. ISRN Dent 2014;2014:463684.  Back to cited text no. 12
    
13.
Bertrand ME. When and how to discontinue antiplatelet therapy. Eur Heart J Suppl 2008;10 (Supplement A):A35-41.  Back to cited text no. 13
    
14.
Aspirin in Patients Undergoing Noncardiac Surgery: POISE-2 clinical trial (Perioperative ischemic evaluation study). Gov number, NCT01082874. Published online on March 31, 2014, at NEJM.org.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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