This document summarizes a seminar on bleeding disorders. It begins with an introduction to hemostasis and the coagulation cascade. It describes the roles of platelets, coagulation factors, and the intrinsic and extrinsic pathways. It discusses specific coagulation factor deficiencies like hemophilia A, hemophilia B, and von Willebrand disease. The document outlines approaches to evaluating patients for bleeding disorders, including history, physical exam, and laboratory tests like complete blood count, bleeding time, prothrombin time, and factor assays. Overall, the seminar provides a comprehensive overview of hemostasis and classification of bleeding disorders.
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
Bleeding Disorders: Causes, Types, and Diagnosis Dr Medical
https://userupload.net/wxvqfbo7ywqu
A bleeding disorder is a condition that affects the way your blood normally clots. The clotting process, also known as coagulation, changes blood from a liquid to a solid. When you’re injured, your blood normally begins to clot to prevent a massive loss of blood. Sometimes, certain conditions prevent blood from clotting properly, which can result in heavy or prolonged bleeding.
Bleeding disorders can cause abnormal bleeding both outside and inside the body. Some disorders can drastically increase the amount of blood leaving your body. Others cause bleeding to occur under the skin or in vital organs, such as the brain.
Bleeding disorders Causes, Types, and DiagnosisDr Medical
https://userupload.net/v3l4i8jsk7wq
Factor II, V, VII, X, or XII deficiencies are bleeding disorders related to blood clotting problems or abnormal bleeding problems. Von Willebrand's disease isthe most common inherited bleeding disorder. It develops when the blood lacks von Willebrand factor, which helps the blood to clot.
INTRODUCTION
• Blood must be maintained in a fluid state in order to function as a transport system, but must be able to solidify to form a clot following vascular injury.
• Successful haemostasis is achieved by complex interactions between vascular endothelium, platelets, coagulation factors etc.
HAEMOSTASIS
• The term haemostasis is derived from the Greek word haem= blood and stasis=halt.
• Process of stoppage of bleeding after blood vessels are punctured , cut , or otherwise damaged.
• It is a complex natural physiological response.
• Bleeding disorders are due to altered ability of blood vessels, platelets , and coagulation factors to maintain haemostasis.
• Steps of natural haemostasis:
• Pre-injury conditions-> Early haemostatic response-> Fibrin clot formation-> Limiting clot formation-> Fibrinolysis
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
Bleeding Disorders: Causes, Types, and Diagnosis Dr Medical
https://userupload.net/wxvqfbo7ywqu
A bleeding disorder is a condition that affects the way your blood normally clots. The clotting process, also known as coagulation, changes blood from a liquid to a solid. When you’re injured, your blood normally begins to clot to prevent a massive loss of blood. Sometimes, certain conditions prevent blood from clotting properly, which can result in heavy or prolonged bleeding.
Bleeding disorders can cause abnormal bleeding both outside and inside the body. Some disorders can drastically increase the amount of blood leaving your body. Others cause bleeding to occur under the skin or in vital organs, such as the brain.
Bleeding disorders Causes, Types, and DiagnosisDr Medical
https://userupload.net/v3l4i8jsk7wq
Factor II, V, VII, X, or XII deficiencies are bleeding disorders related to blood clotting problems or abnormal bleeding problems. Von Willebrand's disease isthe most common inherited bleeding disorder. It develops when the blood lacks von Willebrand factor, which helps the blood to clot.
INTRODUCTION
• Blood must be maintained in a fluid state in order to function as a transport system, but must be able to solidify to form a clot following vascular injury.
• Successful haemostasis is achieved by complex interactions between vascular endothelium, platelets, coagulation factors etc.
HAEMOSTASIS
• The term haemostasis is derived from the Greek word haem= blood and stasis=halt.
• Process of stoppage of bleeding after blood vessels are punctured , cut , or otherwise damaged.
• It is a complex natural physiological response.
• Bleeding disorders are due to altered ability of blood vessels, platelets , and coagulation factors to maintain haemostasis.
• Steps of natural haemostasis:
• Pre-injury conditions-> Early haemostatic response-> Fibrin clot formation-> Limiting clot formation-> Fibrinolysis
Von Willebrand Disease is the most common hereditary bleeding disorder; roughly 1 in every 100 people suffers from the disease. People who suffer from VWD have blood that does not clot properly.
Normally when a person is injured and starts to bleed, the von Willebrand factor in the blood attaches to small blood cells called platelets. This helps the platelets stick together to form a clot at the site of the injury and stop bleeding. When a person has VWD, the clot might take longer to form or not form the way it should and bleeding might take longer to stop. This can lead to heavy, hard-to-stop bleeding. Although rare, the bleeding can be severe enough to damage joints or internal organs, or even be life-threatening.
http://www.nlm.nih.gov/medlineplus/plateletdisorders.html#cat1
http://www.cdc.gov/ncbddd/vwd/facts.html
Von Willebrand Disease is the most common hereditary bleeding disorder; roughly 1 in every 100 people suffers from the disease. People who suffer from VWD have blood that does not clot properly.
Normally when a person is injured and starts to bleed, the von Willebrand factor in the blood attaches to small blood cells called platelets. This helps the platelets stick together to form a clot at the site of the injury and stop bleeding. When a person has VWD, the clot might take longer to form or not form the way it should and bleeding might take longer to stop. This can lead to heavy, hard-to-stop bleeding. Although rare, the bleeding can be severe enough to damage joints or internal organs, or even be life-threatening.
http://www.nlm.nih.gov/medlineplus/plateletdisorders.html#cat1
http://www.cdc.gov/ncbddd/vwd/facts.html
Hemostasis definition, types and steps.
Hemostasis and coagulation physiology and pathology in steps and illustrated in simple way by diagrams.
Intrinsic and extrinsic pathways are mentioned in details.
Platelet function as a corner stone hemostasis in case of endothelial injury or another pathology taht affect endothelium or blood vessels.
Some pharmacological notes about drugs related to hemostasis and its clinical significance.
A detailed description of various stages in blood coagulation, clotting factors involved, the role of calcium, vitamin K, thrombin, phospholipids in blood coagulation, various tests for blood clotting, the significance of bleeding disorders in the treatment of periodontal disease and management.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Hemostasis is normal physiological mechanism by which blood in fluid state in vascular system normally and prevention of bleeding by Hemostasis by complex interactions of blood vessels wall, plasma proteins and platelets.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
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Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Bleeding disorders
1. Seminar presented by : Dr. Manishpala Meda
MDS IInd Year
Dept. of Pedodontics and Preventive Dentistry
2. Introduction
History
Hemostasis
Platelet activation
Coagulation cascade
Phases of coagulation
Role of each coagulation factor
Anti thrombolytic mechanism
Approach to child with bleeding disorder
Laboratory investigations
Classification of bleeding disorders
PART I
3. Bleeding disorders are usually taken to mean coagulopathies with reduced
clotting of the blood.
Bleeding disorders characterised by abnormal platelet function or blood
vessel walls that result in increased bleeding.
Bleeding disorders may result from faults at many different levels in the
coagulation cascade.
4. 1828 - Term “haemorrhaphilia” first used.
Later shortened to “haemophilia.”
Hemophilia is sometimes referred to as “the royal disease,” because it affected
the royal families of England, Germany, Russia and Spain in the 19th and
20th centuries. Queen Victoria of England, who ruled from 1837-1901, is
believed to have been the carrier of Hemophilia B, or factor IX deficiency.
5. HEMOSTASIS: The ability of the body to control the flow of blood following
vascular injury is paramount to continued survival.
The process of blood clotting and then the subsequent dissolution of the clot,
following repair of the injured tissue.
It is composed of 4 major events that occur in a set order following the loss of
vascular integrity:
Coagulation and Bleeding Disorders: Review and Update
Douglas A. Triplett: Clinical Chemistry 46, No. 8(B), 2000
6.
7. Vascular constriction -limits the flow of blood to the area of injury.
Platelet aggregation –Blood platelets clump when binding to collagen that
becomes exposed following rupture of the endothelial lining of vessels.
-Blood platelets become activated and aggregate at the site of injury .
-Upon activation, platelets release ADP and TXA2 (which activate
additional platelets).
Clot formation -To insure stability of the initially loose platelet plug, a
fibrin mesh (also called the clot) forms and entraps the plug.
Fibrinolysis -The clot must be dissolved in order for normal blood flow to
resume following tissue repair. The dissolution of the clot occurs through
the action of plasmin
8. Normally platelets do not adhere to intact vascular endothelium.
Subsequent to the vascular injury, platelets adhere to collagen and vWF in
the subendothelial tissue and undergo a morphological change by assuming
irregular surface, forming numerous pseudopods thus drastically increasing
their surface area.
9. The formation of the platelet plug involves a series of steps:
Platelet adhesion
After vascular injury VWf acts as a bridge between endothelial collagen and
platelet surface receptors GpIb and promotes platelet adhesion.
The platelet glycoprotein complex I (GP-Ib) is the principal receptor for vWF.
Text book of Platelet-Vessel Wall Interactions in Hemostasis and Thrombosis
Rolando E. Rumbaut and Perumal Thiagarajan.
10. Platelet secretion
After adhesion, degranulation from both types of granules takes place with the
release of various factors.
Release of calcium occurs here. Calcium binds to the phospholipids that appear
secondary to the platelet activation and provides a surface for assembly of various
coagulation factors.
Text book of Platelet-Vessel Wall Interactions in Hemostasis and Thrombosis
Rolando E. Rumbaut and Perumal Thiagarajan.
11. Platelet aggregation:
Thromboxane A2 produced by activated platelets
provide stimulus for further platelet aggregation.
TxA2 along with ADP enlarge this platelet aggregate
leading to the formation of the platelet plug, which
seals off vascular injury temporarily.
ADP binding also causes a conformational change in
GpIIb/IIIa receptors presents on the platelet surface
causing deposition of fibrinogen.
Thrombin generation also catalyses the conversion of
this fibrinogen to fibrin which adds to the stability of
the platelet plug and is now known as secondary
haemostasis.
12.
13.
14. It is based on cell based theory of coagulation
Intiation phase : The initiation phase is localized to the cells that express TF.
The FVIIa/TF complex activates small amounts of FIX and FX.
FXa associates with its cofactor, FVa, and forms a prothrombinase complex
on the surface of the TF-bearing cell.
Theories of Blood Coagulation: James P. Riddel Jr, MS, RN, CPNP Bradley E. Aouizerat, PhD Christine
Miaskowski, RN, PhDDavid P. Lillicrap, MD, FRCPC:Journal of Pediatric Oncology Nursing, Vol 24, No 3
(May-June), 2007: pp 123-131
15. Amplification phase: A small amount of thrombin generated on the
TFbearing cell has several important functions.
A major function is the activation of platelets, exposing receptors and binding
sites for activated clotting factors.
As a result of this activation, the platelets release partially activated forms of
FV onto their surfaces.
Thrombin activates platelets, cofactor FVA and FVIII on the platelet surface
and FXI on platelet surface.
16. Propagation Phase: As large numbers of platelets are recruited to the site of
injury, the propagation phase of clot formation occurs on the surface of
activated platelets.
First, FIXa activated during the initiation phase can now bind to FVIIIa on the
platelet surface.
Theories of Blood Coagulation: James P. Riddel Jr, MS, RN, CPNP Bradley E. Aouizerat, PhD Christine
Miaskowski, RN, PhDDavid P. Lillicrap, MD, FRCPC:Journal of Pediatric Oncology Nursing, Vol 24, No 3
(May-June), 2007: pp 123-131
17. Termination Phase:
Once a fibrin platelet clot is formed over an area of injury, the clotting process
must be limited to avoid thrombotic occlusion in surrounding normal areas of
the vasculature
Three types of natural anticoagulants regulate clotting: antithrombin (ATIII)
inhibits the activity of thrombin and other serine proteases, such as FIXa, FXa,
FXIa, and FXIIa.
18.
19. Fibrinogen (factor I): consists of three polypeptide
chains - alpha, beta and gamma.
It is converted to fibrin (factor Ia) by thrombin
(factor IIa).
Fibrin forms a mesh around the wound ultimately
leading to blood clot.
The inherited disorders caused due to mutations in
fibrinogen include: Afibrinogenemia (complete lack
of fibrinogen), Hypofibrinogenemia (reduced levels
of fibrinogen) Hyperfibrinogenemia (dysfunctional
fibrinogen).
These individuals suffer from thromboembolism.
The gene for factor I is located on the fourth
chromosome.
Overview of the coagulation system: Sanjeev Palta, Richa singh:
Indian journal of anesthesia; vol 25 sept-0ct 2014
20.
21. Tissue factor (factor III) :
It is also called as platelet tissue factor.
It is found on the outside of blood vessels and is not exposed to the
bloodstream.
It initiates the extrinsic pathway at the site of injury.
It functions as a high-affinity receptor for factor VII.
It acts as a cofactor in the factor VIIa-catalyzed activation of factor X to FXa.
The gene for tissue factor is located on the first chromosome.
22. Factor V :
Is also referred to as proaccelerin or labile factor.
It is enzymatically inactive and acts as a cofactor to the serine protease FXa,
which in the presence of calcium ions and an appropriate phospholipid (PL)
membrane surface enhances the activation of prothrombin to thrombin.
Factor V Leiden mutation causes factor V deficiency or parahemophilia, which is
a rare bleeding disorder.
It may also lead to myocardial infarction and deep vein thrombosis.
The gene for factor V is located on the first chromosome (1q21-q25).
23. Factor VII:
Vitamin K-dependent serine protease.
It initiates coagulation by activating factors IX and X simultaneously with tissue
factor in the extrinsic pathway.
Its deficiency may lead to epitaxis, menorrhagia, hematomas, hemarthrosis,
digestive tract or cerebral haemorhages.
The gene for factor VII is located on the thirteenth chromosome (13q34-qter).
24. Factor VIII:
Is also known as anti-hemophilic factor (AHF).
It is a cofactor in the activation of factor X to FXa, which is catalyzed by factor
IXa in the presence of calcium and phospholipids.
Mutations in the factor VIII gene results in Hemophilia A. It is also called
classical hemophilia, an X-linked recessive coagulation disorder.
It is the most common type of hemophilia. Pateints suffer from clinical
manifestations in their early childhood; spontaneous and traumatic bleeds
continue throughout their life.
The gene for factor VIII is located on the long arm of X chromosome (Xq28).
25. Factor IX:
Is also known as Christmas factor.
It is a proenzyme serine protease, which in the presence
of calcium activates factor X.
Its deficiency cause Hemophilia B or Christmas disease.
Although, the clinical symptoms of hemophilia A and B
are similar, hemophilia B is less severe than hemophilia
A.
High antigen or activity levels of factor IX is associated
with an increased risk of thromboembolism.
The gene for factor IX is located on the X chromosome
(Xq27.1-q27.2).
26. Factor X:
Is also known as Stuart-Prower factor.
In the presence of calcium and phospholipid, it functions in
both intrinsic and extrinsic pathway of blood coagulation.
Factor X is activated to FXa by factors IX and VII. It is the
first member of the common pathway of blood coagulation.
FXa cleaves prothrombin to thrombin.
Its deficiency may cause bleeding diathesis and
hemorrhages.
Patients commonly suffer from epitaxis, gastrointestinal
bleeds and hemarthrosis. Women with factor X deficiency
may be susceptible to miscarriages.
The gene for factor X is located on the thirteenth
chromosome (13q32-qter).
27. Factor XI :
Is also known as plasma thromboplastin antecedent.
It is a serine protease zymogen which is activated to factor XIa
by factor XIIa.
Deficiency in factor XI causes injury-related bleeding.
The disorder is sometimes referred to as Hemophilia C.
Individuals with severe deficiency do not show excessive
bleeding conditions and hemorrhage normally occurs after
trauma or surgery.
Female patients may experience menorrhagia and prolonged
bleeding after childbirth.
The gene for factor XI is located on the distal end on the
long arm of fourth chromosome (4q35).
28. Factor XII :
Is a plasma protein, also known as Hageman factor.
It is the zymogen form of factor XIIa, which
activates factor XI and prekallikrein.
Its deficiency does not cause excessive hemorrhage
due to lack of involvement of factor XIIa in
thrombin formation.
However, it may increase the risk of thrombosis,
due to inadequate activation of the fibrinolytic
pathway.
The gene for factor XII is located on the tip of the
long arm of the fifth chromosome (5q33-qter).
29. Factor XIII or fibrin stabilizing factor:
It is the proenzyme form of plasma transglutaminase.
It is activated by thrombin into factor XIIIa in presence of
calcium.
It forms ε-(γ-glutamyl)-lysyl bonds between the fibrin
chains and stabilizes the blood clot.
Thus, it reduces the sensitivity of the clot to degradation by
proteases.
Genetic defects in the factor XIII gene leads to lifelong
bleeding diathesis.
Patients may also suffer from intercranial bleeding and
death.
The gene for F13A is located on the sixth chromosome
(6p24-25). The F13B gene is located on the long arm of
first chromosome (1q32-32.1)
30. Von Willebrand factor (VWF):
Is a multimeric glycoprotein involved in hemostasis.
It supports binding of platelets to the site of injury by forming a bridge
between collagen matrix and platelet-surface receptor complex.
Hereditary or acquired defects of vWF lead to von Willebrand disease.
Patients may suffer from bleeding diathesis, menorrhagia and gastrointestinal
bleeding.
The gene for vWF is located on short arm of the twelfth chromosome
31.
32. It is therefore important that the endothelial
surface provides several proteins and receptors
that inhibit thrombin and counteract the progress
of coagulation.
The potent thrombin inhibitor antithrombin III
binds to specific heparan sulfates of
proteoglycans in the glycocalyx that covers the
endothelial surface .
Inadequate antithrombin III activity is
accompanied by severe thrombotic complications.
Furthermore, a triad of endothelial receptors is
involved in the generation the important anti-
coagulant activated protein C (aPC), which can
interrupt the coagulation cascade by cleavage of
factors Va and VIIIa
33. The history should determine:
The site or sites of bleeding, the severity and
duration of hemorrhage, and the age at onset.
Was the bleeding spontaneous, or did it occur
after trauma?
Was there a previous personal or family
history of similar problems?
If a child or adolescent has had surgery that
affects the mucosal surfaces, such as a
tonsillectomy or major dental extractions, the
absence of bleeding usually rules out a
hereditary bleeding disorder
34. PHYSICAL EXAMINATION
The P/E should focus on whether bleeding symptoms are associated primarily
with the mucous membranes or skin (mucocutaneous bleeding) or with the
muscles and joints(deep bleeding).
The examination should determine the presence of petechiae, ecchymoses,
hematomas, hemarthroses, or mucous membrane bleeding.
Patients with defects in platelet-blood vessel wall interaction (VWD or
platelet function defects) usually have mucocutaneous bleeding.
Individuals with a clotting factor deficiency of factor VIII or IX (hemophilia A
or B) have symptoms of deep bleeding into muscles and joints.
Individuals with disorders of the collagen matrix and vessel wall may have
loose joints and lax skin associated with easy bruising (Ehlers-Danlos
syndrome).
35. Blood count and film
show the number and morphology of platelets and any blood disorder such
as leukaemia or lymphoma.
The normal range for the platelet count is 150- 400 × 109/L
Bleeding time
measures platelet plug formation in vivo
normally between 3 and 10 minutes
Prolonged bleeding times are found in patients with platelet function
defects
TEXT BOOK of medical physiology: Guyton and hall :12 th Edition
36. Prolonged bleeding times are found in patients with platelet function
defects.
Performed using blood collected into citrate, which neutralizes
calcium ions and prevents clotting.
The prothrombin time (PT)
The partial thromboplastin time (PTT)
The thrombin time (TT)
Correction tests
Factor assays
Special tests of coagulation
37. Coagulation tests
The prothrombin time (PT)
Time needed for the plasma to clot in the presence of tissue
thromboplastin and calcium
Evaluates the ability of blood to clot properly
Normal time for clotting is 10-14s
Prolong PT results from def of:
Factor V
Factor VII
Factor X
Prothrombin
Fibrinogen
38. Seminar presented by : Dr. Manishpala Meda
MDS IInd Year
Dept. of Pedodontics and Preventive Dentistry
PART II
39. Types of bleeding disorders
Coagulation factor deficiencies
Hemophillia A
Hemophillia B
Von willibrands disease
Vitamin k deficiency
Liver disease
Platelet disorders/ coagulation factor deficiencies
DIC
Conclusion
References
40. Coagulation factor deficiencies:
Congenital
Hemophilia A and B
Von Willebrand’s disease
Other factor deficiencies (rare)
Acquired
Liver disease
Vitamin K deficiency, warfarin use
Disseminated intravascular coagulation
45. Hemophilia A is due to a deficiency of clotting factor VIII or antihemophilic
factor or Hemophilia B is due to deficiency of clotting factor IX (hemophilia B).
Inherited X-link disorder
Prevelance 1 in 5000 in male population.
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the hemophiliac: Is there a
protocol in place? Indian J Dent Res 2007;18:48-54
46.
47. Clinical features
Atypical profuse bleeding at circumcision
Bruising at neonatal vaccines
Joints and soft tissue bleeds and excessive bleeding when they start to
be active
Prolonged bleeding after teeth extraction
Recurrent painful hemarthrosis
Muscle haemoatomas
Spontaneous haematouria
GIT hemorrhage
Spontaneous intracranial hemorrhage (rare)
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the
hemophiliac: Is there a protocol in place? Indian J Dent Res 2007;18:48-54
48.
49. Clinical features
The clinical severity depend on the level of factor VIII:C = severity of
condition
Severe = factor level < 1%
Moderate = factor level 1 – 5%
Mild = factor level > 5 %
50. Severe disease – factor level < 1%
Frequent spontaneous bleeding from early life
Haemarthroses are common and may lead to joint deformity
Bleeding into muscles is also common
Moderate disease – factor level 1 – 5 %
Post traumatic Bleeding
Occasional apparently spontaneous episodes
Mild disease – factor level > 5 %
Usually with bleeding only after injury or surgery
Diagnosis in this group is often delayed until quite late in life
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the
hemophiliac: Is there a protocol in place? Indian J Dent Res 2007;18:48-54
51. Laboratory finding – investigations
Coagulation testing
Prolonged activated partial thromboplastin time (APTT)
Normal prothrombin time (PT)
Normal bleeding time (BT)
Factor assay (reduced level of factor VIII)
52. Also known as Christmas disease
Caused by a deficiency of factor IX
The inheritance and clinical features are identical to hemophilia A
Only can be distinguished by specific coagulation factor assays
The incidence is only about 1 in 30 000 males
Hemophilia B is treated with factor IX concentrates
53. General Management
1. Factor replacement
Bleeding is treated by administration of factor VIII concentrate by intravenous infusion.
Minor bleeding: the factor VIII:C level should be raised to 20-30%
Severe bleeding: the factor VIII:C should be raised to at least 50%
Major surgery: the factor VIII:C should be raised to 100% preoperatively and
maintained above 50% until healing has occurred.
The following formulas were applied for calculating the factor dose:
Dosage (units) = body weight (kg) × desired factor VIII rise (IU/dL or % of
normal) × 0.5
Dosage (units) = body weight (kg) × desired factor IX rise (IU/dL or % of
normal)x 0.5
54. 2. Synthetic vasopressin (Desmopressin)
An analogue of vasopressin
Intravenous, subcutaneous or intranasal
Produces a rise in factor VIII:C in mild hemophilia
It avoids the complications associated with blood products
It is ineffective in severe haemophilia
55. 3.Tranexamic acid is a synthetic derivative of lysine, available for topical and
systemic usage. However, nausea is a common adverse effect.
4.The anti-fibrinolytic agent Epsilon amino caprioic acid (EACA) given
orally of IV is a potent inhibitor of initial clot dissolution. A regimen of 50
mg/kg body weight EACA given orally as a 25% oral rinse every six hours
for seven to ten days appears adequate as an adjunct.
Still tranexamic acid is 10 times more potent than EACA with fewer side-
effects.
56. Difficulties in the management of a hemophiliac dental patient include the
following:
Dental neglect necessitating frequent extractions
Trauma and surgery
Factor VIII inhibitors (recombinant FVIIa is an alternative Solution)
Hazards of anesthesia and injections
Risk of hepatitis B and liver disease and HIV infection
Aggravation of bleeding by drugs
Anxiety and drug dependence
Scully C, Cawson RA. Medical problems in dentistry. 5th ed. Elsevier: London; 2005.
57. The bleeding tendency can be aggravated by NSAIDs. Safer alternatives for
pain control are acetaminophen, codeine and Cox-2 inhibitors.
Local anesthetic regional blocks, lingual infiltrations or injections into the
floor of the mouth must not be used in the absence of Factor VIII replacement
because of the risk of hemorrhage hazarding the airway and being life-
threatening.
If FVIII replacement therapy has been given, regional LA can be used
provided the FVIII level is maintained above 30%.
Infiltrations, intraligamentary, intraosseous or intrapulpal injections are still
safer.
58. Restorative treatment can be undertaken routinely providing care is taken to
protect the mucosa. There is a risk of bleeding with the use of matrix bands or
wooden wedges. This can be controlled by local means or the application of
topical agents.
Cotton rolls should be wetted before removal.
High-speed vacuum aspirators and saliva ejectors can cause hematomas.
Trauma from the saliva ejector can be minimized by resting it on a gauze
swab in the floor of the mouth.
Brewer A, Correa ME. Guidelines for dental treatment of patients with inherited bleeding disorders.
Treatment of hemophilia. 2006; 40.
59. Avoiding instrumentation through the periapex is of prime importance in
endodontic therapy.
The presence of bleeding in the canal is indicative of pulp tissue remaining
in the canal.
Sodium hypochlorite should be used for irrigation in all cases, followed by
the use of calcium hydroxide paste to control the bleeding.
Formaldehyde-derived substances may also be used in cases where there is
persistent bleeding or even before the pulpectomy.
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
60. Isolation with rubber dam provides retraction of gingiva and improves
visibility.
It also minimizes the potential for laceration of the buccal mucosa and lips.
Notches may be placed in buccal and lingual surfaces with a fissure bur
into which clamp prongs will fit tightly.
Brewer A, Correa ME. Guidelines for dental treatment of patients with inherited bleeding disorders.
Treatment of hemophilia. 2006; 40.
61. Mild hemophiliacs requiring surgeries can be managed usually without factor
replacements.
Desmopressin and tranexamic acid are primary alternatives.
Desmopressin can be as a slow intravenous infusion over 20 min of 0.3-0.5
µg/kg, 30 to 60 min prior to the surgical procedure.
This results in a two- to threefold rise in Factor VIII activity with a mean half-
life of 9.4h.
Borea G, Montebugnoli L, Capuzzi P, Magelli C. Tranexamic acid as a mouthwash in anticoagulant-
treated patients undergoing oral surgery. An alternative method to discontuing anticoagulant therapy. Oral
Surg Oral Med Oral Pathol 1993; 75: 29-31
62. Intranasal administration as a spray of 1.5 mg per ml with each 0.1 ml pump
spray is an alternative, limiting treatment to those hemophiliac patients whose
basal factor levels are sufficiently high.
Tranexamic acid significantly reduces blood loss and can be given topically
or systemically
Borea G, Montebugnoli L, Capuzzi P, Magelli C. Tranexamic acid as a mouthwash in anticoagulant-
treated patients undergoing oral surgery. An alternative method to discontuing anticoagulant therapy. Oral
Surg Oral Med Oral Pathol 1993; 75: 29-31
63. Healthy periodontal tissue is essential to prevent bleeding and tooth loss.
If oral hygiene is poor treatment must start as soon as possible after the patient
has had a dental examination and treatment plan formulated to prevent
additional damage to the periodontal tissues.
In cases of severe periodontal disease, it may be necessary to carry out
supragingival scaling initially along with oral hygiene education.
Subgingival scaling can start as soon as the inflammation has decreased. The
treatment may need to be carried out over several visits to prevent excessive
blood loss.
In addition, chlorhexidine gluconate mouthwash can be used to control
periodontal problems.
Antibiotics may be required to help reduce the initial inflammation.
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the hemophiliac: Is there
a protocol in place? Indian J Dent Res 2007;18:48-54
64. Dental pain can usually be controlled with a minor analgesic such as
paracetamol (acetaminophen). Aspirin should not be used due to its inhibitory
affect on platelet aggregation.
The use of any non-steroidal anti-inflammatory drug (NSAID) must be
discussed beforehand with the patient's hematologist because of their effect on
platelet aggregation
A buccal infiltration can be used without any factor replacement. It will
anesthetize all the upper teeth and lower anterior and premolar teeth.
65. Contact the hemophilia unit and consider using additional factor concentrate.
Inspect the site of the bleed.
If there is any evidence of a tear in the gingiva or other obvious bleeding point
this should be treated using local measures.
Instruct the patient to sit up and bite on a damp gauze swab for at least 10
minutes.
Use a 10% solution of tranexamic acid or EACA to dampen the swab or as a
mouthwash if the bleeding is difficult to stop.
Monitor the patient’s blood pressure as it may increase due to worry and pain.
Brewer A, Correa ME. Guidelines for dental treatment of patients with inherited bleeding disorders.
Treatment of hemophilia. 2006; 40.
66. In some hemophilia centres, fibrin glue is used as a local hemostatic measure,
along with an oral antifibrinolytic agent, to achieve hemostasis and reduce the
need for clotting factor replacement therapy.
All fibrin glue contains human or animal components, which has made a
number of physicians and patients being hesitant to use this treatment
particularly for patients who are receiving recombinant factor concentrates or
have never received blood products derived from humans.
Brewer A, Correa ME. Guidelines for dental treatment of patients with inherited bleeding disorders.
Treatment of hemophilia. 2006; 40.
67. A 7-year and 3-month-old known mild hemophilic child who
was under the regular care of a hematologist and a
pediatrician in a private hospital in Jeddah, Saudi Arabia.
Medical History :
The patient had no other medical disorders or history of
surgeries.
The patient had multiple incidents of nasal bleeding that
required admission to the same hospital.
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
68. The intraoral examination revealed the following:
Missing teeth, numbers 51 and 52 due to normal shedding
Decayed teeth, numbers 55, 74, 46 and 85
Badly decayed and infected teeth, numbers 54, 64 and 84
Potential for crowding in the lower anterior segment
The treatment plan included the following:
Composite resin restoration for teeth numbers 55, 74, 46 and 85
Pulpotomy (ferric sulfate) and steel crowns for teeth numbers 65 and 75
Extraction for teeth 54, 64 and 84
Chairside ready-made space maintainers in place of teeth 54, 64 and 84
Mesial slicing of the lower canines for temporary relief of crowding in the
lower incisor region
Sealant applications for teeth 16, 26 and 36
Topical fluoride application
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
69. The child was admitted to the hospital 48 hours prior to the operation for factor VIII
replacement therapy using the following formula:
FVIII dose (IU/kg) = (desired increase in FVIII IU/dl) ÷ 2 to maintain an FVIII
level of 70 IU/dl.
This level was recommended by the hematologist based on the type of teeth to be
removed (primary or permanent) and the anticipated amount of trauma that might be
exerted during the dental procedures as stated by the pediatric dentist.
The preoperative blood investigation results were taken. The child was advised and
educated to perform gentle brushing with a soft toothbrush and to use a povidone
iodine mouthwash after meals.
The parents were instructed to stop meals for at least 6 hours prior to the time of
surgery.
Preoperative complete blood counts showed low hemoglobin (10.6 g/dl); other
values were within the normal range according to the patient’s age group
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
70. Oral intubation in a small child requires good intraoral
Space management for proper accessibility and vision.
During the course of the dental treatment, the mouth probe was inserted in a
reversed position to allow good retraction of the tube, which was
accommodated inside the probe to economize the use of the intraoral space
Use of local anesthesia, even for patients undergoing treatment under general
anesthesia, to minimize postoperative pain and aid patient homeostasis during
surgery.
The current case was not an exception to this routine. Nerve block injections
were avoided to lower the risk of hematoma and/or internal bleeding
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
71. Positioning the Child
Children with hemophilia can suffer from internal bleeding of the joints and
muscles should these tissues become strained.
Adequate support for the knees and neck is routinely provided for all children
undergoing dental care under general anesthesia, with special concern for
hemophilic children.
Hygoformic saliva ejectors (Orsing Co.) were used to minimize possible
trauma and subsequent bleeding risk . The suction holes of these tips were
directed away from mucosal tissue.
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
72. Extractions
Avoiding unnecessary trauma was a primary concern.
The following were considered:
1. Elective root division was used, and each root was extracted individually .
2. Plastic instrumentation was used to remove broken down teeth instead of
root elevators to minimize the use of excessive force.
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
73. Postoperative Care
The patient was hospitalized for 48 hours, during which he continued factor
VIII replacement as proposed by his hematologist and pediatrician.
Oral amoxicillin and clavulanic acid postoperative antibiotics (457 mg/5 ml )
were administered every 12 hours for 7 days.
For postoperative pain control, the preferred drug was acetaminophen 200 mg,
administered every 8 hours for 3 days.
Batawi HYE. Minimizing the risk of perioperative bleeding in a child with hemophilia A during dental
rehabilitation under general anesthesiia: a case report. Int J Clin Ped Dent 2013; 6(3): 217-222.
74. Dental management of hemophiliac child under general anesthesia JOURNAL OF INDIAN SOCIETY
OF PEDODONTICS AND PREVENTIVE DENTISTRY | Jan - Mar 2011 | Issue 1 | Vol 29 |
A 4-year-old boy came along with the parents the exclusive child specialty
dental center with the complaints of pain in the right upper back tooth
region
75. Hereditary coagulation abnormality caused by either:
Reduced level of vWF
Abnormality in vWF
Due to Point mutation or Major deletion
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
76. Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
77. Vwf is a protein plays two role in action:
It promote adhesion of platelets to the endothelium
It is a carrier molecule for factor VIII, protecting it from premature
destruction
So in Vwd :
Defective platelet function
Factor VIII:C deficiency
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
78. CLASSIFICATION OF VWD:
3 TYPES:
TYPE I:
Characterized by a mild reduction in VWF
usually inherited as an autosomal dominant.
TYPE II:
Loss of high-molecular-weight multimers, and it too is usually inherited as an
autosomal dominant
TYPEIII:
Characterized by severe reduction in VWF and usually inherited as
autosomal recessive.
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
79. Clinical features
Typically there is mucus membrane bleeding (epistaxis, menorrhage...)
The severity of symptoms are variable with types
Type 1, 2 usually mild symptoms
Type 3 severe symptoms
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
80. Laboratory Investigations:
The bleeding time is prolonged
APTT is prolonged
Factor VIII is low
VWF is usually low (type 1,2)
Platelets count is normal
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
81.
82. Treatment
Depends on the severity of the condition.
May be similar to that of mild haemophilia, including the use of
Desmopressin where possible.
Factor VIII or Von Willebrand factor concentrates should be used to treat
bleeding or to cover surgery in patients who require replacement therapy.
Guidance on the dental management of patients with haemophilia and congenital bleeding disorders J. A.
M. Anderson,*1 A. Brewer,1 D. Creagh,1 S. Hook,1 J. Mainwaring,1 A. McKernan,1 T. T. Yee1 and C. A.
YeungBRITISH DENTAL JOURNAL VOLUME 215 NO. 10 NOV 23 2013
83. Factor XI deficiency
Rare
Seen mainly in Ashkenazi Jews
Caused bleeding only after trauma
Treated by factor XI
Factor XII deficiency
Usually cause no bleeding
84. Acquired coagulation disorders
More common than inherited disorders
Usually multiple clotting factors
Includes
Vitamin K deficiency
Liver disease
Coagulation disorders caused by antibodies
Massive transfusion syndrome
85. Vitamin K is a fat soluble vitamin
Obtained from green vegetables and bacterial synthesis in the gut
Important on coagulation factors II, VII, IX and X and on proteins C and S.
Without it, these factors cannot bind calcium.
Hemorrhagic disease of the newborn
Biliary obstruction
Malabsorption of vitamin K
Vitamin K antagonist drugs
86. Biliary obstruction results in malabsorption of vitamin K and therefore
decreased synthesis of factors II, VII, IX and X.
Also there are decreased in factor V and fibrinogen.
Dysfibrinogenemia.
Thrombocytopenia.
Functional abnormalities of platelets.
Hypersplenism associated with portal hypertension.
DIC.
87. There is widespread deposition of fibrin within blood vessels with
consumption of coagulation factors and platelets occurs as a
consequence of many disorders which release procoagulant material
into the circulation or diffuse endothelial damage or generalized
platelet aggregation
Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta,
BDS; Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007,
Vol. 73, No. 1 •
88. • Infections
– Gram neg septicemia
– Septic abortion
• Malignancy
– Widespread mucin secreting
adeno-carcinoma
– Acute promyelocytic
leukemia
• Hypersensitivity reactions
– Anaphylaxis
– Incompatible blood
transfusion
• Obstetric complications
– Amniotic fluid embolism
– Eclampsia, retained
placenta
• Widespread tissue damage
– Following surgery/trauma
– After severe burns
• Miscellaneous
– Liver failure
– Severe burns
– Hypothermia
– Snake venoms
– Acute hypoxia
Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta,
BDS; Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007,
Vol. 73, No. 1 •
89. DIC may triggered by the entry of procoagulant material into circulation:
Amniotic fluid embolism
APML
Premature separation of placenta
Initiated by widespread endothelial damage and collagen exposure:
Septicemia
Severe burns
Widespread intravascular platelet aggregation
Some bacteria, viruses and immune complexes may have direct effect
on platelets.
Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta,
BDS; Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007,
Vol. 73, No. 1 •
90. Clinical features
Bleeding, particularly from venipuncture
Purpura
Generalized bleeding in GIT, oropharynx,
lungs, urogenital tract, vaginal bleeding
Less frequently, microthrombi may cause
skin lesions, renal failure, gangrene of
fingers
91. Laboratory finding
The platelet count is low
Fibrinogen low
Thrombin time is prolonged
High level of fibrin degradation products (FDP)
PT and APTT are prolonged in acute syndromes
Blood film
Fragmentation of red cells
Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta,
BDS; Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007,
Vol. 73, No. 1 •
92. Treatment
Treat underlying cause
Supportive therapy with fresh frozen plasma (FFP) and platelets
concentrates
Cryoprecipitate may also required
Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta,
BDS; Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007,
Vol. 73, No. 1 •
93. If there is active bleeding, consultation with a hematologist may be
considered to assist with definitive diagnosis and, for patients who are
ultimately diagnosed with a bleeding disorder, individualized long-term
hemostatic management.
Treatment planning is essential for good outcome and should involve liaison
between the dentist and the haemophilia centre.
Consideration should be given to careful scheduling of invasive dental
procedures to minimise re-exposure to factor concentrate.
Written post-procedural instructions should be provided and must include
emergency contact numbers.
94. Bleeding Disorders of Importance in Dental Care and Related Patient Management Anurag Gupta, BDS;
Joel B. Epstein, DMD, MSD, FRCD(C); Robert J. Cabay, MD, DDSJCDA • • February 2007, Vol. 73, No.
1 •
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