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| IMC Wiki | Haemorrhagic diatheses

Haemorrhagic diatheses

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Definition

Bleedings are:
  • too long
  • too strong
  • without appropriate cause
Bleeding disorders may be caused by:
  1. Platelets: thrombocytopathies, thrombocytpenias
  2. Blood vessels: vaskulopathies
  3. Plasma factors: Koagulopathies
2/3 of all haemorrhagic diatheses are related to disorders of platelets.
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Types of bleeding disorders



Coagulopathies
  • Large surface bleedings with sharp edges (no petecchyae)
  • Muscle bleeding
  • Bleeding into joints with arthropathies
#pic#

The primary haemostasis is normal, secondary bleeding is typical


Diatheses related to platelet or blood vessel disorders
  • Petechiae: punctual bleeding (do’nt disappear upon pressure)
  • Purpura: Exanthema from petechiae

Diagnosis



If there is suspect of bleeding disorder:
  1. medical history and clinical performance (type of bleeding!)
  2. consult treating physician
  3. laboratory studies
#pic#

Platelet count
  • normal range: 150.000–400.000/µl.
Bleeding time
Prolonged bleeding time signalises vascular or platelet-related disorders
Assessment accordin to Ivy:
  • a blood pressure cuff is inflated to 40 mm Hg around the upper arm
    #pic#
  • a 5-mm deep incision is made on the flexor surface of the forearm
    #pic#
  • in all 30 sec blood drop is swabbed by filter and the time is measured to cessation of bleeding
    #pic#
  • Normal result: 3-6 min
    Results are within normal range in:
    Haemophilia A and B
    Hepatic disorders
    following heparin administration
    following marcumar administration
Quick´s prothrombin test
A low Quick value is indicative of coagulopathy.
  • Extrinsic coagulation pathway screen
  • Lower values in deficiency of clotting factors: I, II, V, VII, X
  • for monitoring anticoagulation therapy of the vitamin-K-dependent factors: II, VII, IX, X
  • Normal value > 70%
INR (International Normalised Ratio)
An increased INR value is indicative of a coagulopathy.
The INR is not a novel test method, but an international normalisation of the Quick-value relative to the laboratory test used.
  • normal range: 0,8–1,15
  • therapeutic range: 2,0-3,5
An example from our laboratory for the relationship between Quick- and INR values:
INR 2,0 2,5 3,0 3,5 4,0 4,5
Quick 38% 29% 24% 20%   15%


PTT (Partial Thromboplastin Time)
An increased PTT-value is indicative of coagulopathy
  • intrinsic coagulation pathway screen
  • increased value with deficiency of clotting factors: I, II, V, VII-XII
  • for monitoring heparin therapy
  • test is not standardised, reference values are laboratory


Rumpel-Leede-Test
indicator of vascular haemorrhagic disorders, angiopathies and thrombocytopathies.
  • Test of capillary resistancy
  • After 5 minutes congestion caused by an inflated blood pressure cuff around the upper arm, petechiae appear at the lower arm 20 mm Hg below the systolic pressure in positive cases.

Overview

  Quick test PTT Platelet count Bleeding time
Working diagnosis        
Vascular haemorrhagic diatheses normal normal normal normal
Heparin-therapy normal prolonged normal normal
Kumarin (Marcumar® )-therapy
Vit.K-deficiency
decreased prolonged normal normal
Hepatic disorders decreased prolonged decreased prolonged
Thrombozytopenia normal normal decreased prolonged
Thrombozytopathy normal normal normal prolonged

Coagulopathies

Coagulopathies related to clotting factor deficiency

1. Hereditary deficiencies:

Haemophilia A
  • lack of or reduced activity of factor VIII
Haemophilia B
  • lack of or reduced activity of factor IX
von Willebrand’s disease [von-Willebrand-Jürgens-Syndrom (vWS)]
  • deranged platelet adhesion by reduced vWF in serum and
  • deranged factor VIII activity, because vWF stabilizes factor VIII in circulation
2. Aquired deficiencies

The majority of clotting and fibrinolytic system factors are synthesised in the liver, in which the synthesis of the following factors is vitamin K-dependent:
  • II, VII, IX, X
  • Protein C and protein S
Causes of reduction in Vitamin K-dependent clotting factors:
  • Impaired synthesis in liver
  • Vitamin-K-deficiency
  • Vitamin-K-antagonists (Kumarine, z. B. Marcumar® Falithrom®, Phenopro-ratiopharm®)

Immunocoagulopathies

Result from development of antibodies secondary to substitution of specific factors (most commonly platelets) or in autoimmune diseases

Thrombocytopenias

Thromocytopenia is the most common cause of heamorrhagic diatheses.
Platelet count is < 140.000/µl.

Generally, there is no risk of spontaneous bleeding, but for performing small dental interventions, the count of fully functional platelets should be > 70.000/µl along with intact plasmatic coagulation and vessel functions.


Causes
  • Decreased production of platelets in bone marrow:
    • Injuries to bone marrow (radiation, cytostatics, immunosuppressiva)
    • Infections (viral hepatitis, tuberkulosis, malaria)
    • Deficiencies (Vitamin B12, folic acid, iron)
  • Increased peripheral turnover
    • Idiopathic thrombozytopenic purpura (ITP; Morbus Werlhof)
    • Drug-induced immune thrombozytopenia
    • Drug-associated-toxic (Heparin)
  • Mechanical destruction by prosthetic valves

Defective platelet functions (Thrombocytopathies)

Congenital thrombocytopathies are rare.
The aquired thrombocytopathies are clinically relevant.

Therapy with platelet aggregation inhibitors

Acetyl salicylic acid
  • Inhibits the enzyme cyclooxygenase and suppresses the synthesis of prothrombotic thromboxanes (and antithrombotic prostacyclins)
  • Platelet function normalises in 7-10 days after cessation of therapy
    (cyclooxygenase inhibiton is irreversible, but new platelets can fully function)
Ticlopedin (Ticlyd®)
  • Inhibits platelet aggregation by suppressing the ADP-related step in the process.
Clopidrogel (Plavix®)
  • Inhibits platelet aggregation by suppressing the ADP-related step in the process.
Glycoprotein-IIb/IIa-Antagonists (Integrilin®)
  • Inactivates the fibrinogen receptor of platelets
Further causes of defective platelet function can be:
  • Uraemia
  • Dextran
Diagnosis

Prolonged bleeding time in association with normal platelet count.

Vascular haemorrhagic diatheses

This form has a heterogeneous clinical presentation.
Bleeding time can facultatively be prolonged.
The Rumpel-Leede test is positive (decreased capillary resistency)

Congenital disorders



  • Morbus Osler
    • Autosomal dominant malformation of vessel with focally diluted and convoluted venules and capillaries
    • Common localisation:
      nasal mucosa
      lip
      gingiva
      tongue
      palate
      fingertips
    #pic#
    #pic#
    #pic#
    #pic#
    #pic#

Aquired disorders

  • Henoch-Schönlein purpura (allergic vasculitis)
  • Vitamin C deficiency (impaired collagen synthesis)
  • Senile purpura (increased vessel fragility)
  • Morbus Cushing (long-term treatmetn with corticosteroids)
  • Diabetes mellitus (microangiopathies)

Treatment in dental practice

Patients on anticoagulant therapy or with vascluar haemorrhagic diathesis can be treated in the frame of dental care in the dental practice after thorough preparation and by using local haemostyptical therapy.
Anticoagulants are administered on vital indication and must not be discontinued without consulting the treating haematologist!

Treatment in hospital

All patients who possibly or necessarily require transfusion of blood products (e.g. fresh frozen plasma, platelet concentrates) are treated in a specialist clinic.
Could the anticoagulant therapy not be reduced owing to vital indication, it will be changed to heparin, possibly temporarily, in hospital.
Anticoagulation with heparin is easier to handle due to rapid onset of the effect and shorter half-time.

Wound treatment in bleeding disorders

Single tooth extraction:
  • INR 2,0–3,5
Extended restoration:
  • INR 1,6-1,9
Prophylaxis:
  • Only small incisions
  • Only one tooth per sitting
  • Always provide qualified medical aid
Treatment:
  • Tight wound closure!!!
    Incision of the periosteum only in exceptional cases!!!


  • Splint
  • Local haemostyptical treatment

Local haemostyptic preparations

Collagen

Effect on plateletes
  • Platelet adhaesion to collagen fibres
  • Release of vasoactive amines
  • Activation of prostaglandin metabolism
Plasmatic coagulation
  • Activation of factor XII
  • Activation of factor XI

Oxycellulose

Haemostasis is achieved by pressure and stabilisation of the clot.
Tabotamp - a resorbable haemostyptical preparation

Gelatine sponge

Haemostasis is achieved by pressure and stabilisation of the clot.

Gelastypt – porcine gelatine
Spongostan

Alpaslan et al. (1997) compared the biocompatibility of implanted oxycellulose, gelatine- and collagen sponges in soft tissues in rat. All materials were well tolerated and seemed not to influence wound healing.

Bone wax

  • Bone wax
    It is an effective material for haemostasis, but prolongates bone healing and triggers antibody reaction (Mattsson et al 1990, Solheim et al 1992, Allison 1994)

Fibrin glue

#pic#

Antifibrinolytic preparations

Tranexamic acid (Anvitoff®, Cyclokapron®)

Effect:
Antifibrinolytic via blockading the effect of plasmin

Application:
Direct postoperatively:
rinsing the operation wound with an ampule of tranexamic acid solution diluted in 1:2 with 0.9% NaCl
Several days postoperatively:
rinsing the operation wound with 5% tranexamic acid solution 4x daily

Treatment summary



Grade Clinics Treatment
I Strong bleedings in anamnesis,
no abnormal clotting test
Tight suture
Close postoperative monitoring
II Known bleeding disorder,
mild deviances from the normal
(INR, Quick, PTT, BT)
e.g. Patients on anticoagulant therapy
Collagen fleece
Tight suture
Fakultatively:
  • (Quick: 25%)-Fibrin glue
  • splints
  • Antifibrinolyticum
  • III Highly abnormal bleeding tests
    e.g. Haemophilia A or B, von-Willebrand-Jürgens-syndrom
    Collagen fleece
    Tight suture
    Fibrin glue
    Substitution therapy, if indicated


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    sources

    • Allison RT (1994)   Foreign body reactions and an associated histological artefact due to bone wax   Br J Biomed Sci 51:14-7
    • Alpaslan C, Alpaslan GH, Oygur T (1997)   Tissue reaction to three subcutaneously implanted local hemostatic agents   Br J Oral Maxillofac Surg 35:129-32
    • DGZMK (2001)   Zahnärztliche Chirurgie bei Patienten mit Antikoagulantientherapie  
    • Mattsson T, Anderssen K, Koendell PA, Lindskog S (1990)   A longitudinal comparative histometric study of the biocompatibility of three local hemostatic agents   Int J Oral Maxillofac Surg 19:47-50
    • Solheim E, Pinholt EM, Bang G, Sudmann E (1992)   Effect of local hemostatics on bone induction in rats: a comparative study of bone wax, fibrin-collagen paste, and bioerodible polyorthoester with and without gentamicin