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1. PRESENTED BY
Dr. DEBRAJ SAMANTA
Department of oral and maxillofacial surgery
HIDSAR

2. INTRODUCTION
 The concept of Dyscrasia was
developed by the Greek physician
Galen (130-199 AD) who elaborated a
model of health and disease as a
structure of elements, qualities,
humors, organs, and temperaments.

3. BLOOD
 Blood is a bodily fluid that delivers necessary substances such as
nutrients and oxygen to the cells and transports metabolic waste
products away from cells.

4. ERYTHROCYTES/RBCs
 Circular biconcave cell
 Doesn’t contain nucleus, ribosomes
or mitochondria.
 Contain Hb which is interwoven in
stroma.

5. LEUKOCYTES/WBCs
Leukos=white +cytes=cells
FUNCTION-
Provide defence against:
Bacteria
Virus
Fungi
Parasites
Remove debries(dead cells) and foreign protein.
Produce chemicals that produce inflammation.

6. CLASSIFICATION

7. RED CELL DISORDERS

8. ERYTHROCYTS
(RED BLOOD
CELLS)

9. ANAEMIA

10. IRON DEFICIENCY ANAEMIA
 Most common anaemia
 Microcytic hypochromic type of
anaemia
 Women are affected 4 times more
frequently than men
CAUSES
 Nutritional deficiency
 Chronic blood loss
 Malaria

11. IRON METABOLISM

12. Systemic features
 None in the early stages
Cardiorespiretory
 Dyspnoea
 Tachycardia
 Palpitations
Cutaneous
 Pallor
 Koilonychia-spoon shaped nails

13. Oral Manifestations

14. Investigations
 RBC number- decreases
 Serum Fe-decreases
 Serum ferritin level-decreases( most sensitive &specific test)
 Transferrin saturation –decreases
 Total iron binding capacity-increases
 MCV-decreases
 RDW(red cell distribution index)-increases

15. General Management
 Administration of 300 mg ferrous sulphate orally, 3 times daily for 10
days.
 Mild gastrointestinal intolerance is the side effect.
 Takes 10 to 20 days for the hematocrit to normalize.
 Parenteral administration reserved for patients who do not respond to
oral therapy.

16. Dental Considerations
 Local Anesthesia adequate for pain
control.
 Atrophic glossitis-soreness of tongue
with depapillation or colour change-
best known effect of severe anaemia.
 Candidiasis may be a presenting
feature caused by candida albicans
which may be promoted by anaemia
itself.

17. Vitamin B12
Deficiency
Anaemia

18. Causes
 Auto immune-pernicious
anaemia(due to atrophy of gastric
mucosa).
 Poor intake-specially vegeterians
 Malabsorption
Congenital
Gastrectomy
ileal disease

19. General features
Slow to develop because liver stores last
upto 3 years.
Weakness
Fatigue
Light-headedness
Rapid heartbeat
Rapid breathing
Pale color to the skin
Neurological symptoms particularly
paresthesiaof extremities

20. Oral manifestations
A physically normal ,sore or burning tongue
can be caused by early vitamin B12
deficiency.
Tongue may appear fiery or beefy red and
the tip and margins show papillary atrophy.
Candidiasis can be precipitated by anaemia.
Apthous stomatitis

21. DIAGNOSIS
 No. of RBC –decreases
 MCV-increases
 MCHC-normal
 MCH-increases
 Hb- decreases
 Neutrophil-Hypersegmented
 SCHILLING’S TEST-

22. General Management
 Parenteral course of vitamin B12 sufficient to provide daily requirement
of 2 to 5 microgram until abnormality is corrected.
 This regimen is followed by monthly intra muscular injections (50 to 100
microgram)for rest of the patients life.

23. Dental Considerations
 Local anaesthesia satisfactory
 Conscious sedation –Nitrous oxide is contraindicated.
 General anaesthesia should be postponed until a low haemoglobin
has been remedied.

24. PERNICIOUS ANAEMIA

25. Folic Acid Deficiency Anaemia
Needed by the body to-
-Synthesize and breakdown
amino acids
-Synthesize DNA/RNA
-Essential for maturation of
erythrocytes
Laboratory picture is that of
megaloblastic anaemia

26. CAUSES
 Mostly dietary deficiency
 Malabsorption
coeliac disease and crohn’s disease
 Increased demands
pregnancy
patients under going long term renal dialysis
 Drugs-
Alcohol-interfare with metabolism and absorption of folic acid
Barbiturates
Phenytoin

27. General Features
Folate deficiency leads to anaemia
 Fatigue
 Dizziness
 Feeling cold
 Headache
 Difficulty breathing
 Pale skin
 GI symptoms such as-
Nausea,vomiting
Abdominal pain
Diarrhea, especially after meals
 Anorexia also common

28. General Management

29. Dental Consideration
 Local anaesthesia is satisfactory.
 Conscious sedation can be given if the haemoglobin level is only
moderately depressed and supplemental oxygen can be given.
 General anaesthesia should be postponed until a low haemoglobin has
been remedied.

30. Aplastic Anaemia
 Pancytopania with a non functioning
bone marrow
 Rare disease causing leucopenia,
thrombocytopenia and refrectory
anaemia
CAUSES
 Idiopathic
 Chemicals such as benzene
 Drugs
 Hepatic viruses

31. Criteria for Diagnosis
3 major-
 Neutrophils count less than 500/mm3
 Platelets count less than 20,000/microlitre
 Reticulocytes less than 1%
1 minor-
 Severe hypoplasia of bone marrow

32. General features
Features of anaemia
 Purpura-usually the first manifestation
 Suseptibility to infection
 Reticulocytosis and spleenomegaly not
seen in aplastic anaemia

33. Oral Manifestations
 Ulceration
 Haemorrhagic tendencies
 Suseptibility to infections
 Oral lichenoid reactions

34. Dental Considerations
 Local anaesthesia is satisfactory.
 Conscious sedation can be given if the haemoglobin level is only
moderately depressed and supplemental oxygen can be given.
 General anaesthesia should be postponed until a low haemoglobin has
been remedied.

35. DISORDER IN RBC
MEMBRANE

36. HEREDITORY SPHEROCYTOSIS

37. GENERAL FEATURES
Signs and symptoms are highly
variable
 Include mild pallor
 Intermittent jaundice
 splenomegaly

40. Haemoglobinopathies
 They are genetically determined disorders of haemoglobin production.
 Each of the haemoglobin peptide (globin) chains has an unique amino
acid sequence that can be altered as a result of DNA mutations.
 Mostly seen in non-caucasians.

41. Sickle cell Anaemia
 It is an autosomal recessive
disorder.
 HbS haemoglobin present
instead of HbA.
 In beta chains in position 6,
valine instead of glutamic acid
is present.

42. General Features

43. Lab diagnosis
 Normocytic normochromic RBC
In blood smear-
 sickled RBC
 HOWELL JOLLY BODIES
 TARGET RBC & basophillic
stipling
 IN MRI-GAMMA GANDY BODIES
seen in spleen
 X Ray finding-
 hair on end appearance in skull x ray

44. Dental Considerations
 Sickle cell anaemia with Hb less than 11 gm/dl presents a hazard for
general anaesthesia.
 Local anaesthesia is the preferred mode for pain control.
 Conscious sedation can be used safely.
 Preferable to avoid prilocarpine which in overdose may cause
methaemoglobinemia.
 Aspirin is best avoided –may cause acidosis in large doses.
 Prophylactic antibiotics should be given and infection may be treated
vigorously.

45. THALASSEMIA
 The thalassemia syndromes are a
heterogeneous group of disorders caused by
inherited mutations that decrease the
synthesis of adult hemoglobin, HbA
(α2β2).
 The two α chains in HbA are encoded by
an identical pair of α-globin genes on
chromosome 16.
 the two β chains are encoded by a single
β-globin gene on chromosome 11.

46. Beta Thalassemias

47. Oral manifestations
 Marked overdeveloped of maxilla and mandible
The osseous changes causes-
 prominent cheek bones
 sunken roots of nose
 labial inclination of maxillary incisors
 inadequate lip seal
 CHIPMUNK OR RODENT FACIES

48. Dental considerations
 Patients undergoing repeated treansfusions are at a risk of hepatiti B, C
and HIV carriage.
 Local anaesthesia is safe.
 Conscious sedation may be given with oxygen levels not less than 30%
 General anaesthesia may be complicated by enlargement of
maxilla(difficulty in intubation)

49. WBC DISORDERS

50. Classification

51. Leukemias
 Leukemias are potentially lethal diseases in which there is neoplastic
proliferation of bone marrow WBCs.
 They are classified by:
Clinical course-acute or chronic
Cell of origin-lymphoblast or non lymphoblast
 Dental management of such patients is often complicated by bleeding
tendencies and susceptibility to infection.

52. Acute lymphoblastic leukemia
 Most common malignant disease of children.
Causes
 Ionizing radiation
 Exposure of benzene
Clinical features-
Anaemia
Spleenomegally
Lymphadenopathy
Infection
Bleeding tendencies

53. Oral manifestations
 Oral bleeding and petechiae are
typical manifestation
 Oral pallor
 Gingival swelling
 Mucosal or gingival ulceration
 Pericoronitis
 Cervical lymphadenopathy
 Candidiasis caused by candida
albicans

54. Dental consideration
 Preventive oral health care is essential and conservative dental
treatment may be possible.
 Surgery should be deferred except in emergency.
 Regional local anaesthesia contraindicated if there is severe
hemorrhagic tendencies.
 Conscious sedation is usually possible.
 Aspirin and NSAIDs should not be given since they can aggrevate
bleeding.

55. Acute myeloid leukemia
 Most common leukemia in adult.
Causes-
 Anaemia
 Lymphadenopathy
 Spleenomegally
 Infection
 Bruising and bleeding tendencies

56. Oral Manifestation
 Oral bleeding and petechiae are
typical manifestation
 Oral pallor
 Gingival swelling
 Mucosal or gingival ulceration
 Pericoronitis
 Cervical lymphadenopathy

57. Chronic Lymphocytic Leukemia
 Primary disease of older persons
CLINICAL FEATURES
 Fatigue
 Fever
 Weight loss
 Anorexia
 lymphadenopathy

58. Oral manifestation
 Oral bleeding and petechiae are
typical manifestation
 Oral pallor
 Oral ulceration
 Candidiasis is common

59. Dental Consideration
 Local anaesthesia is satisfactory.
 Consious sedation may be given
 General anaesthesia should be carried out in a hospital.

60. Hodgkin’s Lymphoma
 It is a neoplastic disorder
originating in lymphoid tissue.
 The disease classically begins as a
painless, enlarging mass that
appears in the neck or
mediastinum of adults.
 Characterized by a neoplastic
proliferation of large multi
nucleated reticulum cells known as
Reed Sternberg Cells.

61.  Progressive painless swelling of
the cervical lymph nodes.
 Generalized itching
 Chills and night sweats
 Weight loss

62. Non-Hodgkin’s Lymphoma
 Produce numerous atypical lymphocytes that obliterate normal lymph
nodal architecture.
General Features-
 Painless lymphadenopathy –presenting feature
 Enlarged lymph nodes are firm, rubbery and mobile.
 Rapid nodal growth may impair lymphatic drainage, resulting in
lymphoedema, pain, paraesthesia.

63. Dental Considerations
 Preventive dental measures are most important in patients with
lymphoma.
 Patients with acute signs or symptoms of lymphoma should receive only
conservative emergeny dental care.
 Patient undergoing chemotherapy or radiation therapy should be
observed for xerostomia or radiation caries.

64. DISORDER OF
HAEMOSTASIS

65. HAEMOSTASIS
 Normal haemostasis (bleeding
cessation) depends on the
interaction of blood vessels,
platelets, fibrin coagulation and
deposition, and fibrinolytic
proteins.
Three reactions –
 Primary-vascular & platelet
phase
 secondary –coagulation phase
 tertiary –Fibrinolytic phase

66. PRIMARY HAEMOSTASIS

67. Abnormalities in primary haemostasis
 Abnormal platelet number or function
 Abnormal vWF
 Defects in the blood vessel wall
CLINICAL FEATURES-
 haemorrhage from mucosal surfaces
 epistaxis, gingival bleeding
 melaena
 haematuria
 petechial or ecchymotic haemorrhages.

68. SECONDARY HAEMOSTASIS

69. Abnormalities in the coagulation cascade
 Bleeding into cavities (chest, joints and cranium)
 Subcutaneously (haematomas)
 main coagulation inhibitor-
 antithrombin(AT; also called antithrombin III,or ATIII)
 liver alpha2-globulin that inhibits thrombin (factor IIa)

70. TERTIARY HAEMOSTASIS (FIBRINOLYSIS)
Plasminogen activator
inhibitors (PAI-1 and PAI-2) are
released by endothelial cells and
limit plasmin generation by
binding to t-PA

71. HAEMOSTASIS SCREENING TESTS
 full blood count, film & PLATELET COUNT
 Activated partial thromboplastin time (APTT)-The APTT measures the
intrinsic pathway and factors V, VIII, IX, X and XI . Normal APTT values range
between 25 ± 10 seconds.
 prothrombin time (PT) and international normalized ratio (INR)-The
activity of the extrinsic coagulation pathway (factors II, V, VII and X) is measured
by the PT. normal values ranging between 12 and 15 seconds.
 Thrombin time(TT)-normally 9 to 13 seconds
 The INR is the PT ratio of a test sample compared to a normal PT corrected for the
sensitivity of the thromboplastin used. Normal INR values are about 1.0.
 An INR of 2–3 is the usual therapeutic range for patients on anticoagulants used to
treat deep vein thrombosis.
 INR of up to 3.5 is required for patients with prosthetic heart valves.

72. General Features
Deep haemorrhage into muscles,
Joints or skin.
Bleeding from and into mucosa and
Skin (bruising )-suggests purpura.

73. ACQUIRED BLEEDING DISORDER
 Bleeding disorder are conditions that alter the ability of blood vessels
,platelets, and coagulation factors to maintain hemostasis.
 Acquired bleeding disorder may occur as the result of diseases, drugs,
radiation, chemotherapy for cancer in which vascular wall integrity,
platelet production or function or coagulation factors are impaired.

74. THROMBOTIC THROMBOCYTOPENIC PURPURA(TTP)
 ADAM TS13 deficiency
THE TERRIBLE PENTAD(TTP)
 THROMBOCYTOPENIA
 RENAL FAILURE
 FEVER
 MICROANGIOPATHIC
HEMOLYTIC ANAEMIA
 DECREASE NEUROLOGICAL
FUNCTION

75. TREATMENT PROTOCOL
Main stage
therapy –plasma
exchange
therapy

76. IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)
 TYPE 2 HYPERSENITIVITY REACTION
 petechiae, ecchymoses and postoperative
haemorrhage.
 No SPLEENOMEGALY
 NO HEPATOMEGALY
 NO LYMPHADENOPATHY
Eltrombopag and romiplostin are thrombopoietin
receptor agonists which stimulate platelet
production and used to treat ITP.
 Dental extractions can be covered by these agents

77. Treatment Protocol
 Acute ITP-NO TREATMENT
 CHRONIC ITP-
 If platelet count >50k-no treatment
 20k-50k-prednisolon
 <20k-immunoglobulin
 Romiplostin (Thrombopoietin analogue)

78. Disseminated Intravascular Coagulation(DIC)
 Multiple coagulation factor defects
 Increased CT, PT, aPTT
 Increased BT (due to platelet count decreased)
 Increased TT (due to fibrinogen decreased)
 Increased FDP (D-DIMER TEST)

79. DENTAL MANAGEMENT
 4 METHODS FOR PATIENT IDENTIFICATION
 A Thorough History
 Physical Examination
 Screening Clinical lab tests
 Observation of excessive bleeding after surgical procedures

80. Antithrombotic agents
 Aspirin –orally 75-325 mg once daily
 Aspirin + dipyridamole(Aggrenox)-orally aspirin 50 mg b.i.d;
dipyridamole 200mg
 NSAIDs(ibuprofen)-orally 400 mg once daily
 ADP inhibitors- clopidogrel 75 mg once daily; ticlopidine 250 mg bid
 Fibrinogen receptor inhibitors(GPIIb/IIIa)-Tirofiban, abciximab
 Tirofiban IV 0.4 microgram/kg/min for 30 mins, then 0.1
microgram/kg/min untill steady state achieved.

81. TOPICAL HEMOSTATIC AGENTS
 GAUZE-indicated for immediately after extraction.
 GELFOAM-
 HEMCON dental dressing

82.  Cellulose (surgicel and oxygel)
 Collagen
 THROMBIN-Thrombostat, thrombinar
 Tranexamic acid
 Aminocaproic acid(amicar)

83. Consideration in patient taking warfarin
ANALGESICS- avoid aspirin , NSAIDs
 Acetaminophen with or without codeine is suggested for most of the
patients.
 DRUGS- avoid all drugs that may cause bleeding-
NSAIDs, metronidazole, Erythromycine
Barbiturates, steroids, naficillin that antagonize the action of warfarin
should be avoided.

84. Congenital Bleeding Disorder
 Clotting factor deficiency resulting deep muscle bleeding.
 BT-Normal
 PT,APTT,CT-Increases
 Haemophilia A
 Haemophilia B
 Hemophilia C
 Von willebrand disease

85. HAEMOPHILIA A
 Deficiency of factor VIII
 X linked recessive disorder
 aPTT-increased
 CT-Increased
 PT,BT-Normal
 Management-desmopresin
 Aminocaproic acid
 Factor VIII

86. HAEMOPHILIA B
 Christmas disease
 X linked recessive
 Factor IX deficiency
 Management-desmopressin
 Aminocaproic acid
 Factor IX

87. VON WILLEBRAND DISEASE
Inherent autosomal disorder involving
chromosome 12
Decreased platelet adhesion--increased BT,CT
Intrinsic pathway problem--aPTT increases
PT Normal
Management-Desmopresin
Aminocaproic acid
Factor VIII

88. LAB FINDINGS-
Prolonged activated partial
thromboplastin time
 Low levels of von Willebrand
factor (factor VIIIR:Ag)
 Low factor VIIIC levels
 Reduced platelet aggregation in
the presence of ristocetin

89. Conclusion
 Recording a proper history including past medical and dental history
and family history of the patient goes a long way in helping the clinician
in managing patients with bleeding disorders.
 Knowledge of signs and symptoms , both oral and systemic of these
diseases enable the clinician in diagnosing cases in which the patient
does not have any information about the presence of such diseases.

90. THANK YOU