DOCSLIB.ORG

Immune Thrombocytopenic Purpura an Overview for School Professionals

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Immune Thrombocytopenic Purpura an Overview for School Professionals Immune Thrombocytopenic Purpura An overview for school professionals Immune Thrombocytopenic Purpura (ITP) is an acquired bleeding disorder that is caused by abnormally low levels of platelets, which are necessary for normal blood clotting. What are some common symptoms of ITP? Easy bruising of skin, mouth, gums Petechiae (red dots on the skin from broken capillaries) Nose bleeding, bleeding gums Prolonged bleeding after cuts or surgery Bleeding with dental work Blood in urine or stool What type of support plan is appropriate for a student with ITP? Students with ITP may require an Individual Healthcare Plan or a 504 Plan. In the event that a 504 Plan in required, the diagnosis of ITP gives reasonable cause to bypass the SST process, which will allow you to provide immediate accommodations to the student. All teachers who provide instruction for your student should be made aware of these accommodations. What accommodations are necessary for a student with ITP? ATTENDANCE: The medical management of ITP may require frequent visits to the doctor’s office or hospital for evaluations, laboratory testing and possibly treatments. Please consider the following attendance accommodations: suspension of attendance requirements for absences due to medical appointments and illness, including allowances for student to participate in extra-curricular programs and events without penalty due to absences. partial-day attendance, as necessary ASSIGNMENTS: In the event that a student is absent, it is important for teacher and parents to ensure that student receive assignments in a timely manner so student does not get further behind. a system for providing advance assignments to the parent or student for absences due to planned medical appointments a system for providing make-up assignments in a timely manner when patient is absent due to illness or hospitalization extra time to make up missed assignments ACTIVITY RESTRICTIONS: Student’s with ITP may attend school and participate in most activities. They may participate in sports that are of low risk for bleeding such as physical education, walking, light jogging, light calisthenics, swimming. However, they should be excused from all contact sports and all activities that involve high risk of traumatic injury, such as football, basketball, gymnastics, hockey, etc. BLEEDING PRECAUTIONS: Student’s with ITP are at an increased risk for bleeding. Minor cuts or scrapes: Give routine First Aid as for any other child for minor external bleeding such as a small cut or scrap and clean with soap and water, apply pressure and ice for 5-20 minutes, elevate and cover. If bleeding continues or a lump forms despite above, call the parents as further treatment may be indicated. Oozing from a Cut in the Mouth or from around a Tooth: Apply gloves and use crushed ice to make an ice compress and apply continuous pressure for 20 minutes. One may also apply a wet tea bag to the area as a compress for 20 minutes. If no response, call the parents as further treatment may be necessary. Nosebleeds: o Tilt head slightly forward and have the child sit down. o Apply firm pressure by pressing the sides of the nose together. It may require up to 20 minutes of uninterrupted pressure to stop the bleed. o A small ice pack may also be applied to the bridge of the nose. o If continues for > 20 minutes call the parents. o Vomiting may occur if blood is ingested. Severe Traumatic Injury: If a student has had a head, abdominal or other severe injury, s/he should be brought to the nearest emergency department for STAT CT scan. The list of accommodations above is not meant to be exhaustive; each student's unique needs will dictate the appropriate accommodations to be listed in his/her healthcare plan. 2 .
Load more

Recommended publications
  • Urticarial Vasculitis Associated with Essential Thrombocythaemia
    Acta Derm Venereol 2014; 94: 244–245 SHORT COMMUNICATION Urticarial Vasculitis Associated with Essential Thrombocythaemia Annabel D. Scott, Nicholas Francis, Helen Yarranton and Sarita Singh Dermatology Registrar, Department of Dermatology, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, United Kingdom. E-mail: [email protected] Accepted Apr 3, 2013; Epub ahead of print Aug 27, 2013 Urticarial vasculitis is a form of leucocytoclastic vas- prednisolone 30 mg once daily, which controlled her culitis whereby the skin lesions resemble urticaria. It is symptoms. associated with systemic lupus erythematosus, Sjögren’s A biopsy was taken from an uticarial lesion on the syndrome, hepatitis B and C viruses (1). Rarely it is asso- arm. Histology showed numerous perivascular neutro- ciated with an underlying haematological disorders and, phils and eosinophils with margination of neutrophils to the best of our knowledge, has never been reported in in the lumen of vessels and some leucocytoclasis with association with essential thrombocythaemia. We present red cell extravasation in keeping with an urticarial a case report of urticarial vasculitis associated with es- vasculitis (Fig. 2). sential thrombocythaemia. Blood tests revealed an erythrocyte sedimentation rate of 47 mm/h (normal range 1–12), a platelet count of 1,098 × 109/l (normal range 135–400) and an eosi- CASE REPORT nophilia of 1.0 × 109/l (normal range 0–0.2). Comple- A 32-year-old woman presented with a several month ment levels, thyroid function, serum iron, haemoglobin, history of recurrent urticaria without angioedema, 4 C-reactive protein, anti-nuclear antibody, anti-nuclear months post-partum.
    [Show full text]
  • 081999 Disseminated Intravascular Coagulation
    The New England Journal of Medicine Current Concepts Systemic activation+ of coagulation DISSEMINATED INTRAVASCULAR COAGULATION Intravascular+ Depletion of platelets+ deposition of fibrin and coagulation factors MARCEL LEVI, M.D., AND HUGO TEN CATE, M.D. Thrombosis of small+ Bleeding and midsize vessels+ ISSEMINATED intravascular coagulation is and organ failure characterized by the widespread activation Dof coagulation, which results in the intravas- Figure 1. The Mechanism of Disseminated Intravascular Coag- cular formation of fibrin and ultimately thrombotic ulation. occlusion of small and midsize vessels.1-3 Intravascu- Systemic activation of coagulation leads to widespread intra- lar coagulation can also compromise the blood sup- vascular deposition of fibrin and depletion of platelets and co- agulation factors. As a result, thrombosis of small and midsize ply to organs and, in conjunction with hemodynam- vessels may occur, contributing to organ failure, and there may ic and metabolic derangements, may contribute to be severe bleeding. the failure of multiple organs. At the same time, the use and subsequent depletion of platelets and coag- ulation proteins resulting from the ongoing coagu- lation may induce severe bleeding (Fig. 1). Bleeding may be the presenting symptom in a patient with disseminated intravascular coagulation, a factor that can complicate decisions about treatment. TABLE 1. COMMON CLINICAL CONDITIONS ASSOCIATED WITH DISSEMINATED ASSOCIATED CLINICAL CONDITIONS INTRAVASCULAR COAGULATION. AND INCIDENCE Sepsis Infectious Disease Trauma Serious tissue injury Disseminated intravascular coagulation is an ac- Head injury Fat embolism quired disorder that occurs in a wide variety of clin- Cancer ical conditions, the most important of which are listed Myeloproliferative diseases in Table 1.
    [Show full text]
  • What Everyone Should Know to Stop Bleeding After an Injury
    What Everyone Should Know to Stop Bleeding After an Injury THE HARTFORD CONSENSUS The Joint Committee to Increase Survival from Active Shooter and Intentional Mass Casualty Events was convened by the American College of Surgeons in response to the growing number and severity of these events. The committee met in Hartford Connecticut and has produced a number of documents with rec- ommendations. The documents represent the consensus opinion of a multi-dis- ciplinary committee involving medical groups, the military, the National Security Council, Homeland Security, the FBI, law enforcement, fire rescue, and EMS. These recommendations have become known as the Hartford Consensus. The overarching principle of the Hartford Consensus is that no one should die from uncontrolled bleeding. The Hartford Consensus recommends that all citizens learn to stop bleeding. Further information about the Hartford Consensus and bleeding control can be found on the website: Bleedingcontrol.org 2 SAVE A LIFE: What Everyone Should Know to Stop Bleeding After an Injury Authors: Peter T. Pons, MD, FACEP Lenworth Jacobs, MD, MPH, FACS Acknowledgements: The authors acknowledge the contributions of Michael Cohen and James “Brooks” Hart, CMI to the design of this manual. Some images adapted from Adam Wehrle, EMT-P and NAEMT. © 2017 American College of Surgeons CONTENTS SECTION 1 3 ■ Introduction ■ Primary Principles of Trauma Care Response ■ The ABCs of Bleeding SECTION 2 5 ■ Ensure Your Own Safety SECTION 3 6 ■ A – Alert – call 9-1-1 SECTION 4 7 ■ B – Bleeding – find the bleeding injury SECTION 5 9 ■ C – Compress – apply pressure to stop the bleeding by: ■ Covering the wound with a clean cloth and applying pressure by pushing directly on it with both hands, OR ■Using a tourniquet, OR ■ Packing (stuff) the wound with gauze or a clean cloth and then applying pressure with both hands SECTION 6 13 ■ Summary 2 SECTION 1: INTRODUCTION Welcome to the Stop the Bleed: Bleeding Control for the Injured information booklet.
    [Show full text]
  • Using Tourniquets to Stop Bleeding
    JAMA PATIENT PAGE | Trauma Using Tourniquets to Stop Bleeding After the April 15, 2013, Boston Marathon bombings, 27 patients with life-threatening bleeding were saved by placement of tourniquets by people at the scene. What Is a Tourniquet? Applying a tourniquet with a windlass device A tourniquet is a device that is placed around a bleeding arm or leg. Apply direct pressure 1 Place a 2-3” strip of material Tourniquets work by squeezing large blood vessels. The squeezing to the wound for about 2” from the edge helps stop blood loss. at least 15 minutes. of the wound over a long bone between the wound and the heart. Use a tourniquet only How Do I Put a Tourniquet On? when bleeding cannot be stopped and Tourniquets can be made out of any available material. For ex- is life threatening. ample, you can use a bandage, strip of cloth, or even a t-shirt. The material should be at least 2 to 3 inches wide. The material should also overlap itself. Using thin straps or material less than 2 inches wide can rip or cut the skin. Tourniquets often use a windlass device to increase tighten- 2 Insert a stick or other strong, straight ing. Inflated tourniquets (for example, those made from blood pres- item into the knot to act as a windlass. sure cuffs) can work well. But they must be carefully watched for small leaks. The injured blood vessel is not always right below the skin wound. Place the tourniquet between the injured vessel and the heart, about 2 inches from the closest wound edge.
    [Show full text]
  • ER Guide to Bleeding Disorders
    Bleeding disorders ER guide to bleeding disorders 1 Table of contents 4 General Guidelines 4–5 national Hemophilia Foundation guidelines 5–10 Treatment options 10 HemopHilia a Name:__________________________________________________________________________________________________ 10–11 national Hemophilia Foundation guidelines Address:________________________________________________________________________________________________ 12 dosage chart Phone:__________________________________________________________________________________________________ 14–15 Treatment products 16 HemopHilia B In case of emergency, contact: ______________________________________________________________________________ 16 national Hemophilia Foundation guidelines Relation to patient:________________________________________________________________________________________ 17 dosage chart 18 Treatment products 19 HemopHilia a or B with inHiBiTors Diagnosis: Hemophilia A: Mild Moderate Severe 20 national Hemophilia Foundation guidelines Inhibitors Inhibitors Bethesda units (if known) ____________________________________ 21 Treatment products Hemophilia B: Mild Moderate Severe 22–23 Von willeBrand disease Inhibitors Inhibitors Bethesda units (if known) ____________________________________ 23–24 national Hemophilia Foundation guidelines von Willebrand disease: Type 1 Type 2 Type 3 Platelet type 25 Treatment products 27 Bibliography Preferred product:_________________________________________________________________________________________ Dose for life-threatening
    [Show full text]
  • Appendix Search Strategy Treatment of Hemophilia.Pdf
    Appendix Search strategies Hemophilia – general aspects PubMed (NLM) September 2009 Von Willebrand disease (TiAb) AND Controlled clinical trial (PT) NOT Purpura, Thrombocytopenic (Me) Angiohemophilia (TiAb) Meta analysis (PT) Blood coagulation disorders (Me) Randomized controlled trial (PT) Hemophilia (TiAb) Systematic (SB) Haemophilia (TiAb) Bleeding disorder (TiAb) Random* (Ti) Bleeding disorders (TiAb) OR Control* (Ti) NOT Medline (SB) ("controlled clinical trial"[Publication Type] OR "meta analysis"[Publication Type] OR "randomized controlled trial"[Publication Type] OR systematic[sb] OR ((random*[Title] OR control*[Title]) NOT Medline[sb])) AND ("von Willebrand Disease"[title/abstract] OR "angiohemophilia"[title/Abstract] OR "Blood Coagulation Disorders"[Mesh terms] OR "hemophilia"[title/abstract] OR "haemophilia"[title/abstract] OR "bleeding disorder"[title/abstract] OR "bleeding disorders"[Title/abstract]) NOT "Purpura, Thrombocytopenic"[MeSH Terms] 211 Hemophilia – general aspects Embase.com (Elsevier) September 2009 Blood clotting factor deficiency (Exp,MJR) AND Clinical trial (Exp) NOT Thrombocytopenic purpura (Exp) Von Willebrand disease (Ti) Intervention study (De) Angiohemophilia (Ti) Longitudinal study (De) Angiohaemophilia (Ti) Prospective study (De) Hemophilia (Ti) Meta analysis (De) Haemophilia (Ti) Systematic review (De) Bleeding disorder (Ti) Random* (Ti) Bleeding disorders (Ti) Control* (Ti) ('blood clotting factor deficiency'/exp/mjOR 'von willebrand disease':ti OR 'angiohemophilia':ti OR 'angiohaemophilia':ti OR 'hemophilia':ti
    [Show full text]
  • Immune Thrombocytopenic Purpura with Subsequent Development of JAK2 V617F-Positive Essential Thrombocythemia: Case Report
    ISSN: 2640-7914 DOI: https://dx.doi.org/10.17352/ahcrr CLINICAL GROUP Received: 13 July, 2021 Case Report Accepted: 03 August, 2021 Published: 04 August, 2021 *Corresponding author: Marisabel Hurtado-Castillo, Immune thrombocytopenic PGY-3, Internal Medicine, Department of Medicine at NYU, 536 Ovington Avenue Apartment 3, Brooklyn NYC 11209, USA, Tel: 718-312-9641; purpura with subsequent Email: Keywords: Immune thrombocytopenic purpura; development of JAK2 Essential thrombocythemia; JAK-STAT signaling path- way; JAK2(V617F) mutation V617F-positive essential https://www.peertechzpublications.com thrombocythemia: Case Report Marisabel Hurtado-Castillo1*, Brian Flaherty2 and Morris Jrada2 1PGY-3, Internal Medicine, Department of Medicine at NYU, Brooklyn, NY, USA 2Clinical Assistant Professor, Department of Medicine at NYU Grossman School of Medicine, Brooklyn, NY, USA Abstract The sequential occurrence of Immune Thrombocytopenic Purpura (ITP) and Essential Thrombocythemia (ET) has been reported in the literature on a few occasions, as these are two hematologic disorders with distinct etiologies and patients usually have contrasting clinical presentations. Our case highlights the sequential occurrence of ITP, followed by Janus kinase 2 (JAK2) (V617F)-positive ET in a 64-year-old white woman, after four years of follow-up. The pathophysiology relating to these two conditions is incompletely understood, however, JAK2(V617F) mutation has been found in all the cases reported. Early identifi cation of JAK2(V617F) mutation in a patient with a
    [Show full text]
  • Thrombocytopenia.Pdf
    THROMBOCYTOPENIA DIFFERENTIAL DIAGNOSIS FALSELY LOW PLATELET COUNT In vitro platelet clumping caused by EDTA-dependent agglutinins Giant platelets COMMON CAUSES OF THROMBOCYTOPENIA Pregnancy (gestational thrombocytopenia, preeclampsia) Drug-induced thrombocytopenia (i.e., heparin, quinidine, quinine, and sulfonamides) Viral infections (ie. HIV, rubella, infectious mononucleosis) Hypersplenism due to chronic liver disease Dilutional (massive transfusion) OTHER CAUSES OF THROMBOCYTOPENIA Myelodysplasia Congenital thrombocytopenia Thrombotic thrombocytopenic purpura (TTP) -hemolytic-uremic syndrome (HUS) Chronic disseminated intravascular coagulation (DIC) Autoimmune diseases, such as systemic lupus erythematosus-associated lymphoproliferative disorders (CLL and NHL) Sepsis Idiopathic thrombocytopenic purpura (ITP)* DIFFERENTIAL FOR THROMBOCYTOPENIA BASED ON CLINICAL SETTING CLINICAL SETTING DIFFERENTIAL DIAGNOSES Cardiac surgery Cardiopulmonary bypass, HIT, dilutional thrombocytopenia, PTP Interventional cardiac Abciximab or other IIb/IIIa blockers, HIT procedure Sepsis syndrome DIC, ehrlichiosis, sepsis, hemophagocytosis syndrome, drug-induced, misdiagnosed TTP, mechanical ventilation, pulmonary artery catheters Pulmonary failure DIC, hantavirus pulmonary syndrome, mechanical ventilation, pulmonary artery catheters Mental status TTP, ehrlichiosis changes/seizures Renal failure TTP, Dengue, HIT, DIC, HUS Continuous hemofiltration HIT, consumption by filter and tubing Cardiac failure HIT, drug-induced, pulmonary artery catheter Post-surgery
    [Show full text]
  • Ten Patient Stories Illustrating the Extraordinarily Diverse Clinical Features of Patients with Thrombotic Thrombocytopenic Purpura and Severe ADAMTS13 Deficiency
    Journal of Clinical Apheresis 27:302–311 (2012) Ten Patient Stories Illustrating the Extraordinarily Diverse Clinical Features of Patients With Thrombotic Thrombocytopenic Purpura and Severe ADAMTS13 Deficiency James N. George,* Qiaofang Chen, Cassie C. Deford, and Zayd Al-Nouri Department of Biostatistics and Epidemiology, College of Public Health, Department of Medicine, College of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma Patients with thrombotic thrombocytopenic purpura (TTP) and severe ADAMTS13 deficiency are often consid- ered to have typical clinical features. However, our experience is that there is extraordinary diversity of the pre- senting features and the clinical courses of these patients. This diversity is illustrated by descriptions of 10 patients. The patients illustrate that ADAMTS13 activity may be normal initially but severely deficient in subse- quent episodes. Patients with established diagnoses of systemic infection as the cause of their clinical features may have undetectable ADAMTS13 activity. Patients may have a prolonged prodrome of mild symptoms with only microangiopathic hemolytic anemia and thrombocytopenia or they may have the sudden onset of critical ill- ness with multiple organ involvement. Patients may die rapidly or recover rapidly; they may require minimal treatment or extensive and prolonged treatment. Patients may have acute and severe neurologic abnormalities before microangiopathic hemolytic anemia and thrombocytopenia occur. Patients may have concurrent TTP and systemic lupus erythematosus. Patients may have hereditary ADAMTS13 deficiency as the etiology of their TTP rather than acquired autoimmune ADAMTS13 deficiency. These patients’ stories illustrate the clinical spectrum of TTP with ADAMTS13 deficiency and emphasize the difficulties of clinical diagnosis. J. Clin.
    [Show full text]
  • Modern Management of Traumatic Hemothorax
    rauma & f T T o re l a t a m n r e u n o t J Mahoozi, et al., J Trauma Treat 2016, 5:3 Journal of Trauma & Treatment DOI: 10.4172/2167-1222.1000326 ISSN: 2167-1222 Review Article Open Access Modern Management of Traumatic Hemothorax Hamid Reza Mahoozi, Jan Volmerig and Erich Hecker* Thoraxzentrum Ruhrgebiet, Department of Thoracic Surgery, Evangelisches Krankenhaus, Herne, Germany *Corresponding author: Erich Hecker, Thoraxzentrum Ruhrgebiet, Department of Thoracic Surgery, Evangelisches Krankenhaus, Herne, Germany, Tel: 0232349892212; Fax: 0232349892229; E-mail: [email protected] Rec date: Jun 28, 2016; Acc date: Aug 17, 2016; Pub date: Aug 19, 2016 Copyright: © 2016 Mahoozi HR. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Hemothorax is defined as a bleeding into pleural cavity. Hemothorax is a frequent manifestation of blunt chest trauma. Some authors suggested a hematocrit value more than 50% for differentiation of a hemothorax from a sanguineous pleural effusion. Hemothorax is also often associated with penetrating chest injury or chest wall blunt chest wall trauma with skeletal injury. Much less common, it may be related to pleural diseases, induced iatrogenic or develop spontaneously. In the vast majority of blunt and penetrating trauma cases, hemothoraces can be managed by relatively simple means in the course of care. Keywords: Traumatic hemothorax; Internal chest wall; Cardiac Hemodynamic response injury; Clinical manifestation; Blunt chest-wall injuries; Blunt As above mentioned the hemodynamic response is a multifactorial intrathoracic injuries; Penetrating thoracic trauma response and depends on severity of hemothorax according to its classification.
    [Show full text]
  • Acute Immune Thrombocytopenic Purpura in Children
    Turk J Hematol 2007; 24:41-51 REVIEW ARTICLE © Turkish Society of Hematology Acute immune thrombocytopenic purpura in children Abdul Rehman Sadiq Public School, Bahawalpur, Pakistan [email protected] Received: Sep 12, 2006 • Accepted: Mar 21, 2007 ABSTRACT Immune thrombocytopenic purpura (ITP) in children is usually a benign and self-limiting disorder. It may follow a viral infection or immunization and is caused by an inappropriate response of the immune system. The diagnosis relies on the exclusion of other causes of thrombocytopenia. This paper discusses the differential diagnoses and investigations, especially the importance of bone marrow aspiration. The course of the disease and incidence of intracranial hemorrhage are also discussed. There is substantial discrepancy between published guidelines and between clinicians who like to over-treat. The treatment of the disease ranges from observation to drugs like intrave- nous immunoglobulin, steroids and anti-D to splenectomy. The different modes of treatment are evaluated. The best treatment seems to be observation except in severe cases. Key Words: Thrombocytopenic purpura, bone marrow aspiration, Intravenous immunoglobulin therapy, steroids, anti-D immunoglobulins 41 Rehman A INTRODUCTION There is evidence that enhanced T-helper cell/ Immune thrombocytopenic purpura (ITP) in APC interactions in patients with ITP may play an children is usually a self-limiting disorder. The integral role in IgG antiplatelet autoantibody pro- American Society of Hematology (ASH) in 1996 duction
    [Show full text]
  • Painless Purple Streaks on the Arms and Chest
    PHOTO CHALLENGE Painless Purple Streaks on the Arms and Chest Tiffany Alexander, MD; Bernard Cohen, MD A 10-year-old boy presented with painless purple streaks on the arms and chest of 2 months’ duration. The rash recurred several times per month and cleared without treatment in 3 to 5 days. There was no history of trauma or medication exposure, and he was growing and developing normally.copy WHAT’S THE DIAGNOSIS? a. child maltreatment syndrome b. notfactitial purpura c. Henoch-Schönlein purpura d. idiopathic thrombocytopenic purpura Doe. meningococcemia PLEASE TURN TO PAGE E9 FOR THE DIAGNOSIS CUTIS Dr. Alexander was from the University of Maryland, Baltimore, and currently is from the Department of Dermatology, Duke University Medical Center, Durham, North Carolina. Dr. Cohen is from the Department of Dermatology, Division of Pediatric Dermatology, Johns Hopkins University School of Medicine, Baltimore. The authors report no conflict of interest. Correspondence: Bernard Cohen, MD, Johns Hopkins University School of Medicine, Division of Pediatric Dermatology, David M. Rubenstein Child Health Bldg, Ste 2107, 200 N Wolfe St, Baltimore, MD 21287 ([email protected]). E8 I CUTIS® WWW.MDEDGE.COM/DERMATOLOGY Copyright Cutis 2019. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. PHOTO CHALLENGE DISCUSSION THE DIAGNOSIS: Factitial Purpura actitial dermatologic disorders are characterized by the state of one’s health and life span.4 Cupping is per- skin findings triggered by deliberate manipulation formed by placing a glass cup over a painful body part. F of the skin with objects to create lesions and feign A partial vacuum is created by flaming, mechanical with- signs of a dermatologic condition to seek emotional drawal, or thermal cooling of the entrapped air under the and psychological benefit.1 The etiology of the lesions is cup.
    [Show full text]