Haemostasis and Bleeding in Dental Practice Lecture - Dr Allameddine Allemedine
Page 1: Introduction
Subject: Medicine & Surgery 2023
Instructor: Prof. Mark Greenwood
Focus Area: Haematology
Page 2: Anaemia
Definition: Low Hemoglobin (Hb) due to decreased red cell mass
Normal Range:
Female: 110-180 g/l
Male: 130-180 g/l
Page 3: Normal FBC Appearance
Components:
Platelets
Neutrophils
Red cells
Page 4: Iron Deficiency Anaemia
Characteristics:
Hypochromic, microcytic red blood cells
Low Hemoglobin (Hb)
Low Mean Corpuscular Volume (MCV)
Low Serum Ferritin levels
Page 5: FBC - Normal Values
Haemoglobin:
Male: 130-180 g/l
Female: 110-180 g/l
Haematocrit: 0.35-0.50
Mean Corpuscular Volume (MCV): 77-87 fl
Mean Corpuscular Hemoglobin (MCH): 25-33 pg
White Cell Count: 4.5-10 x 10^9/l
Platelets: 150-400 x 10^9/l
Page 6: Terminology
Terms:
Cytosis: Too many cells
Paenia: Not enough cells
Examples:
Platelets: Too many = Thrombocytosis; Not enough = Thrombopaenia
Page 7: Main Types of Anaemia
Categories:
Microcytic hypochromic (Iron deficiency)
Normocytic (Chronic disease)
Macrocytic (B₁₂, Folate deficiency)
Page 8: Causes of Iron Deficiency
Factors:
Dietary Deficiency
Malabsorption
Chronic Blood Loss (GI Tract, Menorrhagia)
Page 9: B12 and Folate Deficiency
Impact: Leads to Macrocytic Anaemia
Folate Supply:
Approx. 4 months' supply in the body (found in leafy greens, liver, fruits)
Absorbed in small intestine
B12 Supply:
2-6 years' supply in the body (found in animal proteins)
Requires intrinsic factor for absorption in the terminal ileum
Page 10: Folate Deficiency Causes
Causes Include:
Reduced Intake (e.g., Elderly)
Alcoholism
Increased Requirements (e.g., pregnancy, haemolysis)
Malabsorption (e.g., Coeliac disease)
Drugs (e.g., Methotrexate)
Page 11: B12 Deficiency Aetiology
Factors:
Inadequate Intake
Low Gastric Acid (10-30% patients post-gastrectomy)
Intrinsic Factor Antibodies (Pernicious Anaemia)
Abnormal absorption in terminal ileum
Page 12: Pernicious Anaemia
Definition: Malabsorption of vitamin B12 due to decreased intrinsic factor
Associations: Thyroid disease, Vitiligo, Addison's disease
Symptom: Decreased Hemoglobin (Hb)
Page 13: Diagnosis of B12 and Folate Deficiency
Tests:
Red Cell Folate Levels
Serum Vitamin B12 Levels, Intrinsic Factor Antibodies
Treatment:
Identify underlying cause
Oral Folate Replacement or lifelong injections of Vitamin B12 every 3 months
Page 14: Other Causes of Macrocytic Anaemia
Drug-related (e.g., Methotrexate)
Alcohol
Myelodysplasia
Page 15: Blood Transfusions
Recommendation: Avoid if possible
Indication for Transfusion: Hb < 70 g/l or symptomatic
Blood Matching:
O Rhesus negative = Universal Donor
AB positive = Universal Recipient
Page 16: White Cell Count
Normal Values: 4.5-10 x 10^9/l
Page 17: Neutrophils
Increase: Bacterial infections, Trauma, Surgery
Decrease: Viral infections, Certain drugs
Page 18: Lymphocytes
Increase: Viral infections, Chronic Lymphocytic Leukaemia (CLL)
Decrease: Steroid treatment, Systemic Lupus Erythematosus (SLE)
Page 19: Eosinophils
Increase: Observed in some allergic disorders
Page 20: Platelet Abnormalities
Normal Platelet Count: 150-400 x 10^9/l
Thrombocytopaenia:
Count <50 x 10^9/l is a concern
Associated with Von Willebrand's disease
Page 21: Petechiae
Signifies reduced number of platelets
Page 22: Causes of Petechiae
Primary Causes:
Immune Thrombocytopenia (ITP)
Disseminated Intravascular Coagulation (DIC)
Page 23: Additional Causes of Petechiae
Recent Infections
Infectious Mononucleosis
Bone Marrow Infiltration
Acute Leukaemia
Bone Marrow Failure Syndromes (e.g., Aplastic Anaemia, Myelodysplastic Syndromes)
Page 24: Sickle Cell Anaemia
Types:
Homozygote = Disease
Heterozygote = Trait
Mechanism: Cells sickle under low oxygen tension leading to infarction
Page 25: Sickle Cell Depiction
Page 26: Thalassaemias
Definition: Group of disorders with decreased production of one or more globin chains
Types: Alpha and Beta types refer to decreased Alpha and Beta chain production respectively
Page 27: Care with Sickle Cell/Thalassaemia
Consideration: Increased care during decreased oxygen tension, particularly in sedation/GA
Page 28: Leukaemia
Definition: Cancer of blood cells; type depends on affected cells (bone marrow or lymphatic system)
Prevalence: Most common in adults; prevalent cancer in children; some forms are now treatable
Page 29: Types of Leukaemia
Progression Speed:
Acute: Blast cells, fast progression
Chronic: More mature cells, slow progression
Cell Type Affected:
Lymphocytic
Myelogenous (affects RBC, WBC, platelets)
Page 30: Symptoms of Acute Leukaemias
Presentation:
Short history of bruising, bleeding, infection, sometimes skin rash
Lymphadenopathy, gingival hypertrophy, recurrent nosebleeds
Page 31: Additional Symptoms of Acute Leukaemias
Symptoms:
Fever, chills, weakness, fatigue, unintentional weight loss
Enlarged lymph nodes, liver, and/or spleen
Page 32: Treatment of Acute Leukaemia
Dependent on Subtype: Often involves clinical trials
Options: May include bone marrow transplantation
Survival: 30-70% at five years depending on leukaemia type and treatment; prognosis worse in elderly
Page 33: Bone Marrow Failure
Outcome: Leads to pancytopaenia
Myeloma: Plasma cell neoplasm leading to marrow infiltration and osteolytic deposits
Page 34: Myelodysplastic Syndrome (MDS)
Pathophysiology: Immature cells fail to mature into useful blood cells
Discovery: Often found on blood tests while asymptomatic
Symptoms: May present with signs of anaemia
Management: Control rather than treatment; use of stem cell transplants, chemotherapy, and other therapies as needed
Page 35: Multiple Myeloma
Characteristics: Plasma cells in bone marrow
Common Treatment: Nearly all patients use bisphosphonates
Median Age: 67 years at presentation
Symptoms: Anaemia, bone pain, infection, constipation, stomach issues due to hypercalcaemia
Page 36: Multiple Myeloma Findings
Types of Anaemia: Normochromic normocytic anaemia
Detection: Paraprotein (Bence Jones protein) in urine
Indicators: Raised ESR, non-specific
Page 37: (Empty Page)
Page 38: Lymphoma
Definition: Cancer of the lymphatic system
Types:
Non-Hodgkin lymphoma
High-grade lymphoma
Low-grade lymphoma
Hodgkin lymphoma characterized by Reed-Sternberg cells
Page 39: Symptoms of Lymphoma
Common Signs:
Painless lymph node swelling (often in neck)
Fever, fatigue
Night sweats, pruritus
Unexplained weight loss
Page 40: Non-Hodgkin Lymphoma (NHL)
Incidence: 3-4 times as common as Hodgkin’s lymphoma
Trend: Increasing incidence
Varieties: Around 50 different subtypes
Importance: Expert pathology service is crucial
Page 41: NHL Treatment
Options: Chemotherapy, radiotherapy, monoclonal antibody treatment, stem cell transplants
Page 42: Bleeding/Coagulation Problems
Types of Disorders: Inherited and acquired
Page 43: Bleeding Disorders
Categories:
Vascular Defects (congenital or acquired)
Platelet Disorders
Page 44: Coagulation Disorders
Examples:
Haemophilia A: Factor VIII replacement, DDAVP
Haemophilia B: Factor IX replacement
Anti-fibrinolytics: Tranexamic acid
Page 45: Haemophilia A
Characteristics: Factor VIII deficiency, X-linked inheritance
Symptoms: Range in severity; prolonged APTT, normal PT
Treatment:
Factor VIII replacement (or support)
Possible use of Desmopressin (DDAVP) in mild cases
Tranexamic acid may be recommended
Page 46: Haemophilia B (Christmas Disease)
Characteristics: Factor IX deficiency; similar inheritance to A
Symptoms: Range in severity; prolonged APTT, normal PT
Treatment: May need Factor IX; DDAVP ineffective
Page 47: von Willebrand Disease (VWD)
Definition: Most common inherited bleeding disorder (1% UK population)
Cause: Deficiency of von Willebrand Factor (vWF)
Inheritance: Usually autosomal dominant; can be sex-linked recessive or acquired (e.g., autoimmune disorder)
Page 48: VWD Mechanism
Function: vWF is present in platelets and endothelial cell walls; affects platelet adhesion and migration (primary platelet plug formation)
Page 49: VWD Subtypes
Range of Severity: Varying clinical significance
Subtypes:
1: Mildest and most common (autosomal dominant)
2: Normal amount of vWF but dysfunctional
3: No vWF and low Factor VIII levels
Page 50: VWD Management
Dependent on: Severity, planned procedures, previous history, subtype
Possibilities: DDAVP, VWF factor replacement, Factor VIII supplementation, antifibrinolytic drugs
Page 51: Factor V Leiden Thrombophilia
Mechanism: Hypercoagulability due to abnormal Factor V
Prevalence: Affects about 5% of Europeans; inherited
Page 52: Principles of Management
Considerations: Range from no intervention needed to factor replacement
Collaboration: Maintain liaison with a haematologist
Local Measures: Suturing, resorbable oxidized cellulose, tranexamic acid mouthwash
Page 53: Bleeding Disorders and Medications
Contraindications: Avoid NSAIDs
Types of Bleeding Disorders: Inherited (e.g., Haemophilia A, B, von Willebrand’s Disease) and acquired (e.g., liver disease causing deficiencies in various clotting factors, anticoagulant therapy)
Page 54: Liver Problems
Impact: Decreased Vitamin K leads to reduced clotting factors II, VII, IX, and X
Page 55: X-linked Conditions
Overview: Congenital deficiencies in Factor VIII (Haemophilia A) and Factor IX (Haemophilia B)
Consequences: Inability to stabilize the platelet plug
Page 56: Patient Management in Haemophilia
Close liaison with Haemophilia Centre
DDAVP infusion for mild haemophilia
Factor VIII/IX replacement for moderate/severe cases (check levels)
Page 57: Continuing Management
Atraumatic techniques
Local haemostatic measures
Oral tranexamic acid or mouthwash
Page 58: Management of VWD Patients
Liaison with Haemophilia Centre
DDAVP infusion for type I VWD
VWD replacement
Atraumatic technique
Local haemostatic measures
Oral tranexamic acid or mouthwash
Page 59: Managing Low Platelet Counts
Approach: Determine underlying cause and assess reversibility
Surgery:
Delay non-urgent surgery if platelet count is <50 x 10^9/l
Functional Defects: May need treatment like platelet transfusions or DDAVP
Page 60: Management of Platelet Abnormalities
Close liaison with Haemophilia Centre
Potential need for platelet transfusion or DDAVP
Atraumatic techniques
Local haemostatic measures
Oral tranexamic acid or mouthwash
Page 61: Drug Management
Warfarin: Maintain INR at 4 or less with local haemostatic measures
Heparin: Measured by APTT
Low Molecular Weight Heparins: Monitor as appropriate
Page 62: Direct Oral Anticoagulants (DOACs)
Page 63: Dabigatran
Function: Thrombin inhibitor
Monitoring: Not reflected in INR, linear dose-response
Page 64: Other DOACs - Rivaroxaban
Mechanism: Direct Factor Xa inhibitor
Page 65: DOACs - Low Risk Procedures
Recommendations: Safe for simple extractions, incision and drainage, perio exams, restorations with sub-gingival margins
Page 66: DOACs - Higher Risk Procedures
Considerations: Higher risk during complex/adjacent extractions, flap raising, gingival re-contouring, biopsies
Page 67: Higher Risk Management - Dabigatran
Treatment: If twice daily, miss morning dose and give evening dose >4 hours after haemostasis
Page 68: Higher Risk Management - Rivaroxaban
Dosage: Delay morning dose, give >4 hours post-haemostasis
Page 69: Evening Dosing for Rivaroxaban
Process: For evening doses, give at regular timing if >4 hours from haemostasis
Page 70: Erythrocyte Sedimentation Rate (ESR)
Definition: Non-specific indicator of disease presence
Age-dependent calculations:
Men: Age divided by 2
Women: (Age + 10) divided by 2
Page 71: Summary
Conclusion: Haematological issues impact dental practice; liaison with haematologist is crucial during uncertain cases.