This document discusses coagulopathy, which refers to medical disorders involving abnormal blood clotting due to deficiencies or issues with platelets, clotting factors, or the fibrinolytic system. It defines various bleeding disorders and coagulation tests. Specific conditions covered include immune thrombocytopenic purpura (ITP), von Willebrand disease, hemophilia A/B, and disseminated intravascular coagulation (DIC). Treatment involves replacing the deficient clotting factor, managing underlying causes, or administering medications depending on the condition causing the coagulopathy. Complications can include excessive bleeding, joint damage, and transmission of infections.
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
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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
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
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
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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In the DSM-5, all types of substance abuse and dependence have been
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AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
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the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
www.agostodourado.com
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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2. Contents
• Hemostasis
• Coagulation Process
• Definition of Bleeding disorders
• Definition & Extent of Coagulopathy
• Medical Conditions under Coagulopathy with their
Management
• Pre operative preparation for the patients with
coagulopathy
3. Hemostasis
• It is the process to maintain the blood in a clot free
state, as well as formation of blood clot at the site of
vascular injury to arrest or limit the extent of
bleeding
12. • Bleeding Time (BT):
– time for the formation of platelet plug
• Clotting Time (CT):
– time for the formation of fibrin polymer
(intrinsic + common pathway)
• Prothrombin Time (PT):
– time for the formation of prothrombin to thrombin
(Extrinsic + common pathway)
• Activated Partial Thromboplastin Time (APTT):
– time for the formation of fibrin monomer
(intrinsic + common pathway)
14. What is bleeding disorder?
• Disorders associated
with abnormal bleeding
due to platelet defect,
clotting factor defect or
vessel wall defect
Bleeding disorder
Clotting
factor
defect
platelet
defect
vessel wall
defect
15. Definition of Coagulopathy
Group of medical disorders where derangement of
hemostasis occur due to any of the following
condition:
• Deficiency/inadequate function of platelet, or
• deficiency of clotting factor or
• excessive activity of fibrinolytic system
Ref: de gruchy 5th
19. Disorders of coagulation defect
Congenital Causes
• Hemophilia A
• Hemophilia B
• Von willebrands Disease
• Other specific factor
deficiency
Acquired Causes
• Liver disease
• DIC
• Vitamin K deficiency
• Massive blood transfusion
• Anticoagulant drugs
•Coagulation defect Can be due to single factor deficiency or Multiple factor deficiency
20. We will focus on following conditions
Platelet defect
• ITP
• Secondary
Thrombocytopenia
Coagulation defect
• Hemophilia
• Von Willebrands
Diseases
Both Platelet &
coagulation defect
• DIC
• TIC
21. Primary Thrombocytopenia(ITP)
• Antiplatelet auto-antibody(IgG) is formed against
membrane glycoprotein IIb-IIIa
• This Antigen-Antibody complex dose not causes direct
lysis of platelet by activating complement system
• Rather it causes premature removal of platelets by
Mononeuclear phagocyte system
• Most common in children and young adults
• Females are more affected (2:1 female:male ratio)
22. • In children often precipitated
by viral infection
• Muco-Cutaneous bleeding
o Petechi,Pupura,Echymoses
o Epistaxis
o Gum bleeding
o GIT Bleeding
• Bleeding from internal organ
may occur
• Often self limiting
1. Platelet count < 10,000/ml
2. BT > 30 minutes or longer
3. CT normal
4. Tourniquet test positive in
most cases
5. PBF:
• abnormal platelet may be
found
6. Bone marrow:
• megakaryocytes & their
precursor are normal
7. Anti-platelet Ab(IgG) may be
demostrated
Clinical features Lab findings
Clinical and Lab findings
23. Treatment
• Treatment
1. Prednisolon 1-2 mg/kg/day
2. IV Immunoglobulin 1gm/kg/day for 2-3 days
3. Danazole 600mg/day (response rate is 50%)
4. Immunosuppressive drugs (e.g. Vincristine,
Vinblastin,Azathioprine,Cyclophosphamide)
5. Splenectomy (for steroid non responders)
• Prognosis
– Good if disease is initially controlled with prednisolone
– Splenectomy is definite Rx
24. Secondary Thrombocytopenia
Etiology
1. Decreased bone marrow production
a. Aplastic anemia
b. Leukemias
c. Lymphoma
d. Multiple Myeloma
e. Secondary Metastesis
f. Infections (Dengue,HIV)
2. Increased platelet destruction
a. Drugs (cytotoxic, sulphonamide, trimethoprime, chloramphenicol,
chloroquine)
b. Hyperspleenism
c. Post transfusion Alloimune thrombocytopeina
3. Increased platelet consumption
a. DIC
b. Septicemia
25. Clinical features
Superficial Bleeding
• Petechi,Pupura,Echymoses
• Epistaxis
• Gum bleeding
• GIT Bleeding
• Bleeding from internal
organ may occur
Lab findings
– Platelet count ↓
– BT ↑↑
– CT normal
– PT normal or ↑
– PBF:
• abnormal platelet may be
found
– Bone marrow:
• megakaryocytes & their
precursor are reduced
Clinical and Lab findings
27. Von Willebrand’s Disease
• Autosomal dominant disease
– gene for vWF located in chromosome 12
• vWF is synthesized by
– endothelial cells &
– megakaryocytes.
• It acts as
– Adhesive protein
• bridges collagen to platelet receptor GP1b
– Carrier protein
• for Factor VIII (anti hemophilic factor)
30. Why platelet transfusion is discouraged in
dengue hemorrhagic fever??
Dengue haemorrhagic fever
↓ADAMTS
(vWF cleaving
protease)
↑vWF
multimer
(active form)
↑ platelet
adhesion &
consumption
↑bleeding &
microthromb
us
31. Clinical and Lab findings
Clinical feature
• Mainly superficial bleeding:
– Bruising
– Epistaxis
– Gum bleeding
– Hematemesis,Malena
– Hematuria
– Menirrhagia
• Rarely Deep tissue bleeding
haematoma,haemarthrosis are
only seen in patients with marked
concomitant factor VIII deficit.
Lab findings
• Platelet count Normal
• BT ↑↑
• CT ↑↑
• APTT ↑↑
• Normal PT
• vWF assay : vWF ↓
• vWF Ristocetin cofactor
activity ↓
• Factor VIII assay: Factor VIII ↓
32. Treatment
• For mild to moderate hemorrage
(vWF Ristocetin cofactor 10-40 IU/dl)
Desmopressin (DDAVP: 1-desamino-8d arginine vasopressin)
– Not applicable for Children <3 years old
– Intranasal spray (for home treatment)
• 300 µgm
– For Pre operative prophylaxis
• .3 µgm/kg in 50-100 ml N/S IV over 30-60 minutes
• vWF level usually raised 3 units within 90 minutes
• For Severe haemorrhage
(vWF Ristocetin cofactor <10 IU/dl)
Factor VIII transfusion
33. Haemophilia
• X linked recessive disorder
• Usually Male are affected
• Female are Carrier
• But female can be affected also
34. Types
Hemophilia A
• Deficiency of Factor VIII
(anti hemophilic factor)
Hemophilia B
• Deficiency of Factor IX
(Christmas factor)
II
XII
XI
IX
VIII VII
X
V
I
XIII
Stable clot
According to deficiency of clotting factors
According to severity
Mild : 5%-30% of normal level
Moderate: 1-5% of normal level
Severe: <1% normal level
37. Clinical Features
Female may show symptoms in
• When Carrier mother crosses with hemophilic
father
• Turner syndrom (45 X0)
Deep tissue bleeding (80-90%)
• Hemarthrosis 70-80%
• Hematomas 10-20%
subcutaneous or intramuscular
Superficial bleeding(10-20%)
Muco-cutaneous Bleeding from-
Nasal mucosa,GIT mucosa,Intra-abdominal organs
Heavy bleeding after minor cut injury
38. Lab findings
• Platelet count Normal
• BT normal
• CT ↑↑
• APTT ↑↑
• Normal PT
• Factor VIII/IX assay:
– Factor VIII ↓ in Hemophila A
– Factor IX ↓ in hemophilia B
• Factor VIII/IX inhibitor assay
39. Management of hemophilia
• Treatment for the patient
• Genetic counselling for the parents
– For subsequent pregnancy
– Chorionic villous sampling on 10th week of
gestation for early detection
– Amniocentesis on 16th week of gestation
40. Treatment of Haemophilic patient
• Factor VIII or Factor IX Prophylaxis
– prophylaxis is primary Rx
– therapy is started in patients as young as 1 y and continues into adolescence
– usually requires the administration of FVIII 3 times per week, FIX every 10 days
interval
• Other options:
– Monoclonal Ab(Rituximab)
– Desmopressin (can ↑ fVIII upto 4 fold in mild hemorrhagic episodes only)
– Antifibrinolytics (Tranexamic acid) are useful in acute hemorrhagic episodes
• Rx of Factor VIII or Factor IX inhibitors
– aPCC(activated prothombin complex concentrate)
– Monoclonal Ab(Emicizumab) bridges between FIX & FX
– Activated factor VII
• Rx & rehabilitation for hemophilia synovitis
– Radio-synovectomy (by Yittrium 90 & Rhenium 186) ↓hemarthrosis, ↓joint
damgae, prevent arthropathy
– Arthroplasty
41. Factor VIII maintenance
• Mild hemorrhages (early hemarthrosis, epistaxis, gingival bleeding)
– Maintain an FVIII level of 30%
• Major hemorrhages (hemarthrosis or muscle hematoma with pain,
prophylaxis after head trauma with negative findings on
examination):
– Maintain an FVIII level of 50%
• Life-threatening bleeding episodes (major trauma or surgery,
advanced or recurrent hemarthrosis):
– Maintain an FVIII level of >80 %
– after stabilization, maintain levels above 40-50% for a minimum
of 7-10 days
Factor VIII maintenance
• Mild hemorrhages (early hemarthrosis, epistaxis, gingival bleeding)
– Maintain an FVIII level of 30%
• Major hemorrhages (hemarthrosis or muscle hematoma with pain,
prophylaxis after head trauma with negative findings on
examination):
– Maintain an FVIII level of 50%
• Life-threatening bleeding episodes (major trauma or surgery,
advanced or recurrent hemarthrosis):
– Maintain an FVIII level of >80 %
– after stabilization, maintain levels above 40-50% for a minimum
of 7-10 days
42. Complication
• Complication due to Rx
– Development of Antibodies against clotting factors
– Transmission of Viral Diseases like HBV,HCV,HIV.
• Complication due to haemorrhage
– Synovitis of large joints, Arthropathy
– Muscular atrophy due to hematoma
– Entrapment mononeuropathy due to pressure from
hematoma
43. Hemophilia is a life long disease
• A person born with
haemophilia will have it for
life.
• The level of factor VIII or IX in
his blood usually stays the
same throughout his life.
44. Surgery in a child with Hemophilia
For Minor Surgery
Factor VIII should be >50% than normal predicted
value
For Major Surgery
Factor VIII should be >80% of normal predicted
value
It should be transfused just before surgery and
repeat 12 hours after initial dose to pass the
reactionary phase
Half life is 8-12 hours
45. Calculation
• One unit of Factor VIII or Factor IX:
– the amount of FVIII & FIX in 1 mL of plasma (1 U/mL or 1%)
– FVIII 1 U/kg increases FVIII plasma levels by 2%
– FIX 1 U/kg increases FVIII plasma levels by 2%
• The volume of distribution
– FVIII is that of plasma, approximately 50 mL/kg
– FIX is approximately 100 mL/kg
• Units Factor VIII = (weight in kg) x (50 mL plasma/kg) x
(1 U FVIII/mL plasma) x (desired FVIII level - native FVIII level)
• Units factor IX = (weight in kg) x (100 mL/kg) x
(1 U Factor IX/mL) x (desired factor IX level - native Factor IX level)
46. Disseminated Intravascular Coagulation (DIC)
• It is a Thrombo-hemorrhagic disorder which
apperas as a complication of several
conditions
• There is rapid consumption of platelet &
clotting factors leading to thrombosis
• As well as activation of plasminogen causing
fibrinolysis that leads to bleeding
49. Clinical features & Lab findings
Clinical Features
• Clinical manifestations
include the manifestations
of underlying causes
• There may be signs of
concealed or revealed
bleeding
• Also signs of systemic
thrombosis may be present
Lab findings
• Platelet count ↓
• BT ↑↑
• CT ↑↑
• PT ↑↑
• APTT ↑↑
• Factor II,V,VII,X - ↓
• FDP/D-dimer- ↑
51. Trauma Induced Coagulopathy (TIC)
• Combination of tissue trauma (e.g. Major
surgery) & hypovolemic shock leads to
development of an endogenous coagulopathy
called Acute traumatic coagulopathy(ATC)
• ATC is associated with 4 fold increase in
mortality
• ATC is the component of TIC
53. Pathophysiology of TIC
1. trauma → haemorrhage → Shock→ hypoperfusion →anaerobic
glycolysis →Metabolic acidosis → decrease coagulation protease
function→ Further bleeding occurs
2. trauma → haemorrhage → Shock → under perfused muscle/exposed
body cavity → unable to generate heat →hypothermia → poor
coagulation function at low temperature → Further bleeding ensues
3. trauma → ↓ plasminogen activator inhibitor(PAI) →hyper fibrinolysis
→ Further bleeding occurs
4. trauma → haemorrhage →loss of clotting factors due to
bleeding/dilution of clotting factors due to massive infusion or
transfusion → Further bleeding ensues
54. Management of TIC
According to ATLS protocol
1. Primary survey & simultaneous resuscitation
• c= Control of active bleeding
• A= Airway maintenance with cervical spine protection
• B= Breathing by oxygen
• C= Circulation maintenance by blood/fluid
• D= Disability or Neurological status
• E= Exposed adequately in a controlled environment
2. Secondary survey (head to toe examination)
3. Definitive treatment
• Control of bleeding & definite surgery for trauma
• Correction of hypovelemia
• correction acidosis
• Control of hypothermia
• Antibiotics
• Tetanus IG
• Rx of complication