Perinatal/Neonatal Case Presentation
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Crofab Brochure
Control With Confidence The only antivenom derived from native US pit vipers to treat envenomations from all species of North American pit vipers1 CroFab is the only antivenom Derived from geographically and clinically relevant US snakes for comprehensive coverage of all North American pit viper envenomations1 Designed with small, venom-specific protein (Fab) fragments for rapid neutralization of venom toxins throughout affected tissue1,2 With Level 1 evidence in the treatment of copperhead envenomation3 Manufactured to yield the highest level of quality, purity, and safety1 With a proven efficacy and safety profile, backed by >20 years of clinical experience1 Reliably supplied throughout the United States4 CroFab meets World Health Organization (WHO) guidelines for effective antivenom, utilizing venom from 4 clinically relevant pit viper species native to the United States.1,5 Indication CroFab® Crotalidae Polyvalent Immune Fab (Ovine) is a sheep-derived antivenin indicated for the management of adult and pediatric patients with North American crotalid envenomation. The term crotalid is used to describe the Crotalinae subfamily (formerly known as Crotalidae) of venomous snakes which includes rattlesnakes, copperheads and cottonmouths/water moccasins. Important Safety Information Contraindications Do not administer CroFab® to patients with a known history of hypersensitivity to any of its components, or to papaya or papain unless the benefits outweigh the risks and appropriate management for anaphylactic reactions is readily available. Warnings and Precautions Coagulopathy: In clinical trials, recurrent coagulopathy (the return of a coagulation abnormality after it has been successfully treated with antivenin), characterized by decreased fibrinogen, decreased platelets, and elevated prothrombin time, occurred in approximately half of the patients studied; one patient required re-hospitalization and additional antivenin administration. -
Mutation in the Prothrombin Gene G20210A As a Cause of Cerebral Venous Thrombosis
Hindawi Publishing Corporation Case Reports in Medicine Volume 2012, Article ID 828050, 3 pages doi:10.1155/2012/828050 Case Report Mutation in the Prothrombin Gene G20210A as a Cause of Cerebral Venous Thrombosis Jorge A. Arroyave1 and Jairo Quinones˜ 2 1 Internal Medicine, Universidad CES, Medell´ın, Colombia 2 Neuroinmunology, Clinical Neurology, Fundacion´ Cl´ınica Valle del Lili, Cali, Colombia Correspondence should be addressed to Jorge A. Arroyave, [email protected] Received 8 February 2012; Accepted 21 February 2012 Academic Editor: Mamede de Carvalho Copyright © 2012 J. A. Arroyave and J. Quinones.˜ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Cerebral venous sinus thrombosis (CVST) is a rare form of cerebrovascular disease, which may manifest clinically by a wide variety of signs and symptoms. It has been associated with multiple risk factors including genetic or acquired blood disorders, infections, and trauma. Case Report. Man of 17 years who presented with 10 days of intense global headache with nausea and vomiting and subsequent onset of mild hemiparesis and hypoesthesia in right hemibody. Studies show venous thrombosis of the superior longitudinal sinus. It was identified a gene mutation in prothrombin G20210A as a probable cause of the thrombosis. Conclusions. Substitution of guanine for adenine at nucleotide 20210 in the coding region of the prothrombin gene is the second most common primary thrombophilia. Multiple cases of CVST have been associated with this mutation. In the presence of CVST must be considered the primary studies for thrombophilia gene mutations, including prothrombin G20210A. -
Haemostatic Problems in Liver Disease
Gut: first published as 10.1136/gut.27.3.339 on 1 March 1986. Downloaded from Gut, 1986, 27, 339-349 Progress report Haemostatic problems in liver disease The liver plays a major role in the control of coagulation and as a result haemostatic problems are detected in approximately 75% of patients with liver disease.1 The coagulation abnormalities are both complex and multifactorial and depend on the balance between hepatic synthesis and clearance of activated coagulation proteins and their inhibitors; the presence or absence of dysfibrinogenaemia; thrombocytopenia, abnormal platelet function, and disseminated intravascular coagulation. Some patients will present with petechiae, ecchymosis or epistaxis, but most patients are asymptomatic or only bleed after venepuncture or liver biopsy. Alternatively haemorrhage may be life threatening and patients may die from variceal bleeding or from disseminated intravascular coagulation. The reasons for this disparity are not yet clear, but after the introduction of newer techniques, in particular the development of immunological assays for the antigens of coagulation proteins, our understanding of these problems has improved. The normal coagulation and fibrinolytic systems are depicted in Figures 1 and 2 while the major .__Intrinsic___ _ pathwY http://gut.bmj.com/ Kallikrein.o- PK | HMWKq 8t XII -*xiiXIIa_4------- ATIII ~ ~ 'I L1HMWK - XI* Xla %' xC-a; --------- -- on September 28, 2021 by guest. Protected copyright. IX - IXa VII -e'VIIca Extrinsic pathway [X VIII a Ce X P'okin C ATIII Ca+ XIII Common mI ~V PL II a pathway I XIIIa Fibrinogen - Fibrin Fig. 1 The coagulation cascade. HMWK=high molecular weight Kinogen, PK=Pre-Kallikrein, A TIII=antithrornbin III, PL=platelets, Ca" = Calcium, TF=tissue factor, -t- =proteolytic activation, -+=conversion ofcoagulation protein, -- -+=inhibition by plasma inhibitors, tit =crosslinking, a=activated coagulation enzyme. -
The Underrecognized Prothrombotic Vascular Disease of COVID-19
Journal Articles 2020 The underrecognized prothrombotic vascular disease of COVID-19. KP Cohoon G Mahé AC Spyropoulos Zucker School of Medicine at Hofstra/Northwell, [email protected] Follow this and additional works at: https://academicworks.medicine.hofstra.edu/articles Part of the Internal Medicine Commons Recommended Citation Cohoon K, Mahé G, Spyropoulos A. The underrecognized prothrombotic vascular disease of COVID-19.. 2020 Jan 01; 4(5):Article 6487 [ p.]. Available from: https://academicworks.medicine.hofstra.edu/articles/ 6487. Free full text article. This Article is brought to you for free and open access by Donald and Barbara Zucker School of Medicine Academic Works. It has been accepted for inclusion in Journal Articles by an authorized administrator of Donald and Barbara Zucker School of Medicine Academic Works. For more information, please contact [email protected]. Received: 6 May 2020 | Revised: 16 May 2020 | Accepted: 21 May 2020 DOI: 10.1002/rth2.12396 LETTER TO THE EDITOR The underrecognized prothrombotic vascular disease of COVID-19 We have read with interest “COVID-19-associated coagulopathy around elevated markers of hypercoagulability, including D-dimer, and thromboembolic disease: Commentary on an interim expert tissue factor expression, fibrinogen levels, factor VIII levels, guidance” recently provided by Cannegieter and Klok.1 This com- short-activated partial thromboplastin time, platelet binding, and mentary exemplifies the importance that venous thromboembolism thrombin formation.8 Based on well-defined clinical and laboratory (VTE) and atheroembolism may be underrepresented and a cause parameters, a proposal for staging COVID-19 coagulopathy may for increased morbidity and mortality among coronavirus disease provide treatment algorithms stratified into 3 stages.9 However, 2019 (COVID-19) patients. -
Guidelines for the Management of Haemophilia in Australia
Guidelines for the management of haemophilia in Australia A joint project between Australian Haemophilia Centre Directors’ Organisation, and the National Blood Authority, Australia © Australian Haemophilia Centre Directors’ Organisation, 2016. With the exception of any logos and registered trademarks, and where otherwise noted, all material presented in this document is provided under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Australia (http://creativecommons.org/licenses/by-nc-sa/3.0/au/) licence. You are free to copy, communicate and adapt the work for non-commercial purposes, as long as you attribute the authors and distribute any derivative work (i.e. new work based on this work) only under this licence. If you adapt this work in any way or include it in a collection, and publish, distribute or otherwise disseminate that adaptation or collection to the public, it should be attributed in the following way: This work is based on/includes the Australian Haemophilia Centre Directors’ Organisation’s Guidelines for the management of haemophilia in Australia, which is licensed under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Australia licence. Where this work is not modified or changed, it should be attributed in the following way: © Australian Haemophilia Centre Directors’ Organisation, 2016. ISBN: 978-09944061-6-3 (print) ISBN: 978-0-9944061-7-0 (electronic) For more information and to request permission to reproduce material: Australian Haemophilia Centre Directors’ Organisation 7 Dene Avenue Malvern East VIC 3145 Telephone: +61 3 9885 1777 Website: www.ahcdo.org.au Disclaimer This document is a general guide to appropriate practice, to be followed subject to the circumstances, clinician’s judgement and patient’s preferences in each individual case. -
Spontaneous Deep Vein Thrombosis in Hemophilia A: a Case Report Murat Bicer, Murat Yanar* and Oktay Tuydes
Open Access Case report Spontaneous deep vein thrombosis in hemophilia A: a case report Murat Bicer, Murat Yanar* and Oktay Tuydes Address: Department of Cardiac Surgery, Kalp Damar Cerrahisi Anabilim Dali Görükle Yerles¸kesi, Nilüfer Bursa 16059, Turkey Email: MB - [email protected]; MY* - [email protected]; OT - [email protected] * Corresponding author Received: 4 March 2009 Accepted: 5 July 2009 Published: 11 September 2009 Cases Journal 2009, 2:6390 doi: 10.4076/1757-1626-2-6390 This article is available from: http://casesjournal.com/casesjournal/article/view/6390 © 2009 Bicer et al.; licensee Cases Network Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Venous thromboembolus is an important cause of hospital acquired morbidity and mortality. Venous thrombosis is a very rare occurrence in patients with haemophilia A. The thrombosis originated from the right main and external iliac veins, and effects the cranial segments of the main, deep and superficial femoral veins as an acute phase thrombus. Neither any local anatomic compression nor any predisposing thrombophilic risk factors were identified. We treated the patient with enoxaparine 1 mg/kg twice a day subcutaneously and then started oral anticoagulation with warfarin. Introduction was warmer and 2 cm larger than the left lower extremity in Venous thromboembolus is an important cause of hospital circumference. According to the visual analog scale, the acquired morbidity and mortality [1]. Hemophilia A is pain score was 6. -
Thrombosis and Coagulopathy Guidance in COVID-19
Thrombosis and Coagulopathy Guidance in COVID-19 The risk of thrombosis in COVID-19 Patients with COVID-19 are at risk of venous thromboembolism (VTE), which is a deep vein thrombosis (DVT) or pulmonary embolism (PE). It is still unknown if this risk is higher in comparison to non-COVID acutely ill patients. How to interpret a D-dimer level in COVID-19 An elevated or rising D-dimer level is commonly seen in patients with COVID-19 (~50%) and is because of a profound inflammatory state. An elevated D-dimer alone does not warrant investigation for VTE unless there is also a high clinical suspicion for DVT and/or PE. Pulmonary embolism should be considered in admitted patients with COVID-19 who have unexplained worsening respiratory status/hypoxia, unexplained hypotension or tachycardia, or signs of DVT. If the D-dimer is normal, this has the ability to rule out VTE. Although the false negative rate of D-dimer testing (i.e. DVT/PE is present but the result is normal) is unknown in COVID-19 patients, low rates of 1- 2% using highly sensitive D-dimer assays have been reported in other high risk populations. Therefore, a normal level D-dimer level provides reasonable confidence that VTE is not present. Prevention of thrombosis All hospitalized patients with suspected or confirmed COVID-19 should receive pharmacologic thromboprophylaxis, preferably with low-molecular-weight heparin (LMWH). LMWH prophylaxis should be held if the patient is bleeding or has a platelet count <30 x 109/L. In patients where anticoagulation is contraindicated, use mechanical thromboprophylaxis (e.g. -
PROTEIN C DEFICIENCY 1215 Adulthood and a Large Number of Children and Adults with Protein C Mutations [6,13]
Haemophilia (2008), 14, 1214–1221 DOI: 10.1111/j.1365-2516.2008.01838.x ORIGINAL ARTICLE Protein C deficiency N. A. GOLDENBERG* and M. J. MANCO-JOHNSON* *Hemophilia & Thrombosis Center, Section of Hematology, Oncology, and Bone Marrow Transplantation, Department of Pediatrics, University of Colorado Denver and The ChildrenÕs Hospital, Aurora, CO; and Division of Hematology/ Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA Summary. Severe protein C deficiency (i.e. protein C ment of acute thrombotic events in severe protein C ) activity <1 IU dL 1) is a rare autosomal recessive deficiency typically requires replacement with pro- disorder that usually presents in the neonatal period tein C concentrate while maintaining therapeutic with purpura fulminans (PF) and severe disseminated anticoagulation; protein C replacement is also used intravascular coagulation (DIC), often with concom- for prevention of these complications around sur- itant venous thromboembolism (VTE). Recurrent gery. Long-term management in severe protein C thrombotic episodes (PF, DIC, or VTE) are common. deficiency involves anticoagulation with or without a Homozygotes and compound heterozygotes often protein C replacement regimen. Although many possess a similar phenotype of severe protein C patients with severe protein C deficiency are born deficiency. Mild (i.e. simple heterozygous) protein C with evidence of in utero thrombosis and experience deficiency, by contrast, is often asymptomatic but multiple further events, intensive treatment and may involve recurrent VTE episodes, most often monitoring can enable these individuals to thrive. triggered by clinical risk factors. The coagulopathy in Further research is needed to better delineate optimal protein C deficiency is caused by impaired inactiva- preventive and therapeutic strategies. -
Canine and Feline Coagulopathies Office News Michelle Fulks, DVM, Virginia Sinnott, DVM, DACVECC William B
Monthly Update August 2013 Issue Contributors: Michelle Fulks, DVM, Virginia Sinnott, DVM, DACVECC, William B. Henry DVM, DACVS Editor: William B. Henry DVM, DACVS Canine and Feline Coagulopathies Office News Michelle Fulks, DVM, Virginia Sinnott, DVM, DACVECC William B. Henry, Jr. DVM, DACVS Canine and Feline Coagulopathies Bleeding disorders are considered a potential life-threatening emergency in small animal practice. It is crucial to recognize the potential for a coagulation disorder through history and physical exam findings, pursue appropriate diagnostic tests and then treat appropriately in order to prevent massive bleeding in these patients. Three areas of the hemostatic system may be affected to cause coagulopathies: Amanda Spencer, CVT joined our surgery team in late 2012. She has 10 1. Disorders of Primary Hemostasis years experience in surgery and 2. Disorders of Secondary Hemostasis emergency care. Her sole focus at BVS 3. Disorders of Fibrinolysis is with the surgical practice. Her skills, dedication to excellence, and caring Primary hemostasis is the formation of the initial platelet plug. Decreases in attitude towards our clients and platelet number, platelet function, or reduced von Willebrand factor (VWF) can all patients, has been outstanding. Her cause disorders of primary hemostasis and lead to mucosal bleeding or calm upbeat personality makes our bruising. Secondary hemostasis is the formation of a stable fibrin clot via cascade days together as a team more of enzymes that ultimately convert fibrinogen to fibrin. Defects in coagulation enjoyable. She is one of those staff factors can lead to severe bleeding diatheses. Fibrinolysis is the breakdown of the members "behind the public eye" who fibrin clot by plasmin. -
Thrombocytopenia and Intracranial Venous Sinus Thrombosis After “COVID-19 Vaccine Astrazeneca” Exposure
Journal of Clinical Medicine Article Thrombocytopenia and Intracranial Venous Sinus Thrombosis after “COVID-19 Vaccine AstraZeneca” Exposure Marc E. Wolf 1,2 , Beate Luz 3, Ludwig Niehaus 4 , Pervinder Bhogal 5, Hansjörg Bäzner 1,2 and Hans Henkes 6,7,* 1 Neurologische Klinik, Klinikum Stuttgart, D-70174 Stuttgart, Germany; [email protected] (M.E.W.); [email protected] (H.B.) 2 Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, D-68167 Mannheim, Germany 3 Zentralinstitut für Transfusionsmedizin und Blutspendedienst, Klinikum Stuttgart, D-70174 Stuttgart, Germany; [email protected] 4 Neurologie, Rems-Murr-Klinikum Winnenden, D-71364 Winnenden, Germany; [email protected] 5 Department of Interventional Neuroradiology, The Royal London Hospital, Barts NHS Trust, London E1 1FR, UK; [email protected] 6 Neuroradiologische Klinik, Klinikum Stuttgart, D-70174 Stuttgart, Germany 7 Medical Faculty, University Duisburg-Essen, D-47057 Duisburg, Germany * Correspondence: [email protected]; Fax: +49-711-278-345-09 Abstract: Background: As of 8 April 2021, a total of 2.9 million people have died with or from the coronavirus infection causing COVID-19 (Corona Virus Disease 2019). On 29 January 2021, the European Medicines Agency (EMA) approved a COVID-19 vaccine developed by Oxford University Citation: Wolf, M.E.; Luz, B.; and AstraZeneca (AZD1222, ChAdOx1 nCoV-19, COVID-19 vaccine AstraZeneca, Vaxzevria, Cov- Niehaus, L.; Bhogal, P.; Bäzner, H.; ishield). While the vaccine prevents severe course of and death from COVID-19, the observation of Henkes, H. Thrombocytopenia and pulmonary, abdominal, and intracranial venous thromboembolic events has raised concerns. Objec- Intracranial Venous Sinus Thrombosis after “COVID-19 Vaccine tive: To describe the clinical manifestations and the concerning management of patients with cranial AstraZeneca” Exposure. -
Disseminated Intravascular Coagulation and Coagulation Disorders Carl-Erik Dempfle
Disseminated intravascular coagulation and coagulation disorders Carl-Erik Dempfle Purpose of review Abbreviations An update on recent developments in diagnosis and treatment aPTT activated partial thromboplastin time of disseminated intravascular coagulation. DAA drotrecogin a (activated) DIC disseminated intravascular coagulation Recent findings FRM fibrin-related marker Disseminated intravascular coagulation is defined as a typical ISTH International Society for Thrombosis and Hemostasis disease condition with laboratory findings indicating massive # coagulation activation and reduction in procoagulant capacity. 2004 Lippincott Williams & Wilkins 0952-7907 Clinical syndromes associated with the condition are consumption coagulopathy, sepsis-induced purpura fulminans, and viral hemorrhagic fevers. Consumption coagulopathy is Introduction observed in patients with sepsis, aortic aneurysms, acute The diagnosis of disseminated intravascular coagulation promyelocytic leukemia, and other disseminated malignancies. (DIC) is based on the combination of a disease condition Sepsis-induced purpura fulminans is characterized by with laboratory findings indicating massive coagulation microvascular occlusion causing hemorrhagic necrosis of the activation and reduction in procoagulant capacity (Table skin and organ failure. Viral hemorrhagic fevers result in 1). Current scoring systems include elevated fibrin- massively increased tissue factor production in monocytes and related markers (FRMs), prolonged prothrombin time, macrophages, inducing microvascular -
OFC Vol. 17/4
CLINICAL PRACTICE ○○○○○○○○○○○○○○○○○ Prevalence of Factor V Leiden, Prothrombin G20210A, and MTHFR C677T Mutations in 200 Healthy Jordanians SUHAIR S EID, GHADA RIHANI ○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○ Thrombophilia is now considered a multi-causal condition, Ghada Rihani is Chief Officer Immunology and Molecular with interplay of acquired genetic risk factors. In order to Laboratory, King Hussein Medical Centre, Jordan. estimate the frequency of the factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations in the Jorda- Address for correspondence: Suhair S Eid, PO Box 143 855, nian population, we screened 200 healthy Jordanian indi- Amman 11814, Jordan. (+9626) 581-8531, (+9626) 566- Downloaded from viduals. 40% were females. Mean age was 32.1 years for males 2260 (fax). [email protected] and 30.0 years for female participants. A PCR method de- tected 15.0% factor V Leiden (87% heterozygous, 13% ho- Thrombosis risk factors predispose towards thrombosis but, mozygous), 2% prothrombin G20210A (100% heterozy- due to the episodic nature of thrombosis, interaction with gous), and 24% MTHFR C677T (67% heterozygous, 33% other components is required before onset of the clinical homozygous). disorder. A well-established genetic predisposition to throm- http://hwmaint.clsjournal.ascls.org/ bosis is a single point mutation in the gene encoding coagu- We conclude that the prevalence of factor V Leiden and lation factor V (G1691A) leading to factor V Leiden (FVL) MTHFR C677T is elevated in this population of Jordani- which was identified as the molecular basis for the pheno- ans. However the incidence of G20210A is relatively low. type of activated protein C resistance (APC-R) in the ma- jority of affected individuals.1,2 This mutation is associated Quantification of these genetic thrombosis risk factors in vari- with a five- to ten-fold risk for heterozygotes and 80-fold ous populations will contribute to a better understanding of risk for homozygotes.3 the interaction of genetic and environmental risk factors.