This document provides an overview of thrombocytopenia, including:
1. A brief history of the identification and study of platelets.
2. Normal platelet kinetics such as production, lifespan, and circulating counts.
3. Causes of thrombocytopenia including decreased production, increased destruction, and sequestration.
4. Evaluation and management of common causes like ITP and TTP, focusing on correlating bleeding risk with platelet counts and treatment options.
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
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
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
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
aplastic anemia pediatrics
It compromises a group of disorders of the hematopoietic stem cells resulting in the suppression of one or more of erythroid, myeloid and megakaryotic cell lines.
thrombocytopenia
Current Standards and New Directions in the Treatment of Acquired Thrombotic ...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.
Gain insight and expertise in this presentation on acquired thrombotic thrombocytopenic purpura. Spero Cataland, MD, Professor of Clinical Internal Medicine and Director of Benign Hematology at The Ohio State University, will provide guidance on current treatment standards and will discuss emerging therapies with the potential to improve patient outcomes in aTTP.
STATEMENT OF NEED
Acquired thrombotic thrombocytopenic purpura (aTTP) is a rare, life-threatening thrombotic microangiopathy with a rapid onset and progression and a mortality rate of 10% to 20% with prompt treatment. Onset of aTTP is characterized by severe thrombocytopenia, microangiopathic hemolytic anemia, and a constellation of associated symptoms including hemorrhage, neurologic and renal manifestations, cardiac abnormalities, and mesenteric ischemia (Joly et al, 2017). Survivors of first aTTP events tend to have relapse events which need to be controlled. Rapid recognition and immediate appropriate treatment are critical for achieving optimized outcomes in aTTP. In this activity chaired by Spero Cataland, MD, Professor of Clinical Internal Medicine and Director of Benign Hematology at The Ohio State University, expert faculty will provide insightful guidance on current treatment standards and will discuss emerging therapies with the potential to improve patient outcomes in aTTP.
TARGET AUDIENCE
Hematology fellows, attending faculty, and other health care professionals involved in the treatment of patients with acquired thrombotic thrombocytopenic purpura (aTTP).
LEARNING OBJECTIVES
Upon completion of this activity, participants should be able to
Evaluate the clinical and laboratory features of aTTP that can inform timely and accurate diagnosis
Discuss how ADAMTS13 activity can be used to guide the management of aTTP
Assess the mechanism of action, efficacy, and safety of novel anti-von Willebrand factor nanobodies in aTTP as elucidated by recent clinical trials
Evaluate novel treatment combinations and sequences with the potential to improve the outcomes of patients with aTTP
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
aplastic anemia pediatrics
It compromises a group of disorders of the hematopoietic stem cells resulting in the suppression of one or more of erythroid, myeloid and megakaryotic cell lines.
thrombocytopenia
Current Standards and New Directions in the Treatment of Acquired Thrombotic ...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.
Gain insight and expertise in this presentation on acquired thrombotic thrombocytopenic purpura. Spero Cataland, MD, Professor of Clinical Internal Medicine and Director of Benign Hematology at The Ohio State University, will provide guidance on current treatment standards and will discuss emerging therapies with the potential to improve patient outcomes in aTTP.
STATEMENT OF NEED
Acquired thrombotic thrombocytopenic purpura (aTTP) is a rare, life-threatening thrombotic microangiopathy with a rapid onset and progression and a mortality rate of 10% to 20% with prompt treatment. Onset of aTTP is characterized by severe thrombocytopenia, microangiopathic hemolytic anemia, and a constellation of associated symptoms including hemorrhage, neurologic and renal manifestations, cardiac abnormalities, and mesenteric ischemia (Joly et al, 2017). Survivors of first aTTP events tend to have relapse events which need to be controlled. Rapid recognition and immediate appropriate treatment are critical for achieving optimized outcomes in aTTP. In this activity chaired by Spero Cataland, MD, Professor of Clinical Internal Medicine and Director of Benign Hematology at The Ohio State University, expert faculty will provide insightful guidance on current treatment standards and will discuss emerging therapies with the potential to improve patient outcomes in aTTP.
TARGET AUDIENCE
Hematology fellows, attending faculty, and other health care professionals involved in the treatment of patients with acquired thrombotic thrombocytopenic purpura (aTTP).
LEARNING OBJECTIVES
Upon completion of this activity, participants should be able to
Evaluate the clinical and laboratory features of aTTP that can inform timely and accurate diagnosis
Discuss how ADAMTS13 activity can be used to guide the management of aTTP
Assess the mechanism of action, efficacy, and safety of novel anti-von Willebrand factor nanobodies in aTTP as elucidated by recent clinical trials
Evaluate novel treatment combinations and sequences with the potential to improve the outcomes of patients with aTTP
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
Simple way to explain primary haemostatic anomalies
Easy to teach
Platelet function as well as disorders of granules and their release reaction. A reader will find a few better resources.
Outline is from introduction to explanation of every single anomaly. Happy reading
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.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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.
- 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
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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.
2. The granular appearance of the platelets helps to distinguish them from artifact in the
peripheral smear
3. Brief history of the platelet
• Osler, Hayam, and Bizzozero identified small particles in the
blood, these were believed to be either bacteria or red cell
fragments
• James Homer Wright “Wright Stain” identified platelets as a
distinct hematopoetic component arising from
megakaryocytes
• William Duke in 1910 described 3 patients with low platelet
counts that had hemorrhagic disease
• Duke created a venous shunt from a normal donor to a
thrombocytopenic recipient and showed that the platelet
count could rise and the bleeding would cease
4.
5. Figure ; Platelets can be seen as individual structures forming on the periphery of this
megakaryocyte
6. Platelet Kinetics
• Normal circulating platelet count
– 150K to 400K (150,000/ul to 400,000/ul )
– 90 to 300 K in people of Mediterranean descent
• 1/3 of platelets are sequestered in the spleen
• lifespan of a platelet is 7 to 10 days
• 15 to 45 K platelets are produced daily to maintain
steady state
7. .
EDTA may produce this effect causing a spurious decrease in the platelet count
8.
9. Thrombopoietin (TPO)
• TPO is the primary regulatory protein in the
production of platelets
• TPO gene is on chromosome 3
• TPO is expressed in the liver, kidneys, and smooth
muscle cells
• Has a plasma half life of 30 hours
• The receptor for TPO is c-MPL which is present on
the megakaryocytes and platelets
• TPO rises with platelet fall and declines as the megakaryocyte
and platelet mass increase
10. why we are worried about
Thrombocytopenia ?
• 1/3 of all Hematology Consults in a General Hospital are for
thrombocytopenia
• 5 -10% of all hospital patients are thrombocytopenic
• 35% patients in the ICU are thrombocytopenic
• Thrombocytopenic patients in the hospital suffer a two fold
greater mortality rate than those who are not
11. Practical Importance of Assessing
Thrombocytopenia..
The primary reason for evaluating
thrombocytopenia is
• To assess the risk of bleeding
• To assess the presence of serious underlying
disorders (malignancy ,TTP, HIT )
12. Relation of bleeding risk and platelet
count
– < 20 K …..increased risk of bleeding
– 20 – 50 K ….. rarely have increase risk of spontaneous
bleeding but increase risk of bleeding from procedures
– 50 --100 K ……no increased risk of spontaneous bleeding
and can undergo most procedures
13. Clinical manifestations of thrombocytopenia
• Petechiae (not seen in haemophilia or VWD)
• Pupura
• Echymoses
• Mucosal bleeding
• Menorrhagia
• Intracranial bleeding (uncommon but the most feared)
14. Clinical manifestations of thrombocytopenia
• Some times
thrombosis
Infact low platelet is a manifestation of
thrombosis
15. Petechiae
Do not blanch with pressure
(cf. angiomas)
Not palpable
(cf. vasculitis)
(typical of platelet disorders)
16.
17. Thrombocytopenia
sequestration
in spleen
• Production
– Marrow
Damage
• Aplasia
• Drugs
• Malignancy
– Congenital
Defects
– Ineffective
Production
• B12 def
• Folic acid def
• Destruction
– Non
Immune
• DIC
• TTP
• HELLP
– Immune
• ITP
• HIT
• SLE, AIDS
• TTP
20. Congenital Thrombocytopenia
• Reasons to Suspect
• Persistence of neonatal thrombocytopenia
• onset of bleeding symptoms in childhood
• Family history of thrombocytopenia or mucocutaneous
bleeding
• Platelet count unresponsive to typical treatments for ITP
21. Congenital Thrombocytopenia
Low MPV Normal MPV Large MPV
W A S (X linked) FPD/AML Bernard Soulier
TAR Platelet type vWD
AT/RS MYH9
CAT Grey Platelets
11q- disorder GATA1
Treatment of Bleeding
• platelets
• DDAVP
• Recombinant FVIIa
23. ITP
(Immune Thrombocytopenic Purpura)
• Isolated thrombocytopenia with no clinically
apparent associated conditions or other causes of
thrombocytopenia
• high prevalence disease
• 16 to 27 per million per year
• Incidence increases with age
• Female predominance at age < 60 but not over the
age of 60
• It is generally abrupt in onset with children
• It can have an insidious onset.
24. Types of ITP according to etiology
• ITP..(idiopathic)
• Neonatal Thrombocytopenia
Associated with Maternal ITP( transfer of IgG),Drug-Related
• Drug Induced
Quinidine, Quinine, Sulfa, Gold Salts, Abx (Vanco etc), Heparin
• Lymphoma associated
• Autoimmune disorders
Thyroiditis, SLE, Colitis, Sarcoidosis
• Infections
HIV, Rubella, viral Hepatitis, CMV,
• Pos-transfusion Purpura
25. Types of ITP according to clinical
presentation
• Acute ITP
• Chronic ITP
• Resistant ITP
• Refractory ITP
26.
27. Pathogenesis of ITP
• Increased platelet destruction caused by antiplatelet
antibodies
• +
• Lack of compensatory response by megakaryocytes
due to suppressive effect of antiplatelet antibodies
28. Features of Acute ITP
• Peak age Children (2-6 yrs)
• Female:male 1:1
• Antecedent infection Common
• Onset of symptoms Abrupt
• Platelet count at presentation <20,000
• Duration 2-6 weeks
• Spontaneous remission Common
29. Features of Chronic ITP
• Peak age Adults (20-40 yrs)
• Female:male 3:1
• Antecedent infection Rare
• Onset of symptoms Abrupt-indolent
• Platelet count at presentation <50,000
• Duration Long-term
• Spontaneous remission Uncommon
30. Diagnosis of ITP
• Features consistent with the diagnosis of ITP
– Thrombocytopenia with normal or slightly large platelets
– Normal RBC morphology and number (may have
associated iron def or thallasemia etc.)
– Normal white cell number and morphology
– Splenomegaly rare
• Features not consistent with the diagnosis of ITP
– Giant platelets
– RBC abnormalities ie schisotocytes
– Leukocytosis or Leukopenia
31. Laboratory evaluation of ITP
• Not Much !!!!!!!
– Platelet associated immunoglobulin reflect
plasma concentration
– Bone Marrow not very helpful as initial test
• May be helpful in patient over 50 years and concerned
about MDS
• If patient has failed initial treatment and diagnosis is in
question
– TSH and HIV test helpful,
– Peripheral Smear helpful
32. Management of ITP
• Most patients with ITP do not have clinically
significant bleeding
– Risk of intracranial bleed 0.1 to 1% (This is an
overestimate)
– Wet Purpura ie epistaxis, gingival bleeding is a risk
factor for major bleeding
In asymptomatic patients with platelets counts
greater then 20 K observation is reasonable
33. Management of Acute ITP
• First line therapy
1. Steroids
– Prednisone 1mg/kg/day , tapering over 2 months
– Decadron 40 mg/day x 4 days
– Solumedrol 1 gram/day x 3 days
2. Antibodies
– IVIG 1 gram/day x 2 days
– Anti-D 50 mcg/kg IV x1
34. Management of Acute ITP
• Second line therapy
1. Immunomodulation .
a. anti CD 20. 375mg/m2/week x 4 injections
b. Azathioprine 50-200 mg /d
c. Cyclosporine 50-200 mg/d
d. Danazol 200-800 mg/d
e. Vincritine 2mg /week x3 injections
2. Splenectomy
3. Eltrombopag 25-75 mg /day
35. Management of Chronic ITP
• Splenectomy
– Immunize with Pneumovax, Hib, Meningococcal
• Chronic Anti-D therapy
– Does not put the disease in remission
• Immunomodulation eg Rituximab
• Eltrombopag ,TPO analogue
• Observation
36. Management in pregnancy
• Gestational Thrombocytopenia
– Platelet count >70K, occurs late in gestation, not
associated with fetal thrombocytopenia, resolves
after pregnancy
• ITP in pregnancy
– Treat if symptoms, intermittent IVIG, Prednisone,
anti-D
– Epidural anesthesia appears safe if platelet count
> 50K
– Monitoring for neonatal thrombocytopenia
39. Lab findings of TTP
• Severe thrombocytopenia <30 K to 75 -100 K
• Hemolytic anemia with several fragmented red cells
in high power oil (>1% total number of RBC
• Renal Abnormalities ,may be subtle ,initially
• Markedly elevated LDH
• Initially coagulation studies are normal
40. Figure 1. Peripheral smear showing microangiopathic hemolytic features with numerous RBC
fragments (helmet cells/schistocytes)
41. Figure 2. Peripheral smear showing RBC fragmentation consistent with a microangiopathic
hemolytic process
43. Treatment of TTP
• Daily plasma exchange with either FFP or
cryopoor FFP (45 to 55 cc/kg/day) reduces
mortality from 100% to 20%
• Steroids
• Platelet tx …?
• no …..why?????
44. Heparin Induced Thrombocytopenia
• Described in 1958 by Rodger Weismann and
Richard Tobin after extracting platelet fibrin
thrombi that formed after 1 to 2 week course
of heparin
• HITT is the presence of a multimolecular
complex between platelet factor 4, and
heparin
• HITT is associated with thrombosis despite
profound thrombocytopenia
45.
46. Clinical Features of HITT
• Timing
– Onset between days 5 and 10 after heparin
initiation
– Rapid onset if previously exposed to heparin
• Thrombocytopenia nadir between 15 to 150 K
• >50% develop a new thrombosis both venous and
arterial
• Absence of petechia
47. Diagnosis of HITT
• Clinical Suspicion (ie greater then 50% drop in
platelets in the setting of heparin use)
• Laboratory Studies
– Platelet Activation Studies (Complicated and
physiologic)
– PF4/Polyanion Studies (Less time consuming but
not necessarily physiologic)
• Even without evidence of thrombosis patient should
get lower extremity dopplers
48. Treatment of HITT
• Removal of all Heparin products
• Begin direct thrombin inhibitor (DTI) (Argatroban or
Refludan)
• Treat with DTI until platelet count normalizes then
may begin anticoaguation with warfarin
• Fondaparinux (Arixtra) is a reasonable agent to use
for DVT prophylaxis in patient with history of HIT
54. Treatment
• FFP and platelet transfusions in bleeding
• Trigger for prophylactic platelet tx is higher
than in ITP
• Why ?
55. Macrovascular thrombosis
• Macrovascular thrombosis eg DVT is also a
cause of low platelet s
• D dimer
• Doppler studies
• Anticoagulation with careful monitoring of
counts
• Rise in plt count is indicater of …..
56. Practical Aspects for the management of
thrombocytopenia
• What is an adequate platelet count for procedures?
– Routine Dentistry >10K
– Dental Extraction >30K
– Regional Dental Block >30K
– Minor Surgery >50K
– Major Surgery>80K
– Epidural is okay at platelet count 50K for patient with ITP
• The target platelet count for a bleeding patient is
generally >40K
• Prophylactic platelet transfusions trigger is < 10K
57. Treatment options for the Bleeding Patient
• Red blood cells
• Platelet transfusions
• Fresh frozen plasma
• Cryoprecipitate
• Amicar
• DDAVP
• Recombinant Human factor VIIa
58. 1.PRBC tx
• Laminar blood flow is disturbed at HCT <30%,
• so It is important to raise HCT by PRBC tx ,in
severely anemic and thrombocytopenic
patients.
60. Platelet transfusions - complications
• Transfusion reactions
– Higher incidence than in RBC transfusions
– Related to length of storage/leukocytes/RBC mismatch
– Bacterial contamination
• Platelet transfusion refractoriness
– Alloimmune destruction of platelets (HLA antigens)
– Non-immune refractoriness
• Microangiopathic hemolytic anemia
• Coagulopathy
• Splenic sequestration
• Fever and infection
• Medications (Amphotericin, vancomycin, ATG, Interferons)
61. Aminocaproic acid (Amicar)
• Mechanism
– Prevent activation plaminogen → plasmin
• Dose 50mg/kg po or IV q 4 hr
• Uses
– Primary menorrhagia
– Oral bleeding
– Bleeding in patients with thrombocytopenia
– Blood loss during cardiac surgery
• Side effects GI toxicity,Thrombi formation
63. message
• Treatment of thrombocytopenia is according to cause
• It is important to know spleen size of thrombocytopenic
patient
• Look at LDH
• Every thrombocytopenia is not ITP
• Every ITP does not need tm