Management of Select Thrombocytopenias

2019 ◽  
Vol 30 (2) ◽  
pp. 165-180
Author(s):  
Thomas A. VanDruff
Keyword(s):  
Immune Thrombocytopenia ◽  
Treatment Options ◽  
Diagnostic Testing ◽  
Management Strategies ◽  
Laboratory Evaluation ◽  
Thrombotic Microangiopathies ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
Patient Presentation ◽  
Specific Management

Evaluating, diagnosing, and managing patients with consumptive thrombocytopenia is challenging because of the overlapping nature of many of the diseases that reduce platelet counts. Immune thrombocytopenia (and its variations), drug-induced immune thrombocytopenia, and heparin-induced thrombocytopenia result from autoimmune antibody-mediated destruction of platelets. Thrombotic thrombocytopenia (both congenital and acquired) and the hemolytic uremic syndromes (both typical and atypical) are thrombotic microangiopathies associated with platelet aggregation and consumption along with anemia and renal dysfunction. Rapid history taking, physical assessment, and laboratory evaluation are crucial to accurately managing patients with these disorders. Platelet-associated coagulopathies are infrequently encountered by most providers, and limited exposure to these types of patients, combined with the wide variety of treatment options for reversing bleeding or thrombotic sequelae, makes management difficult. This article reviews the pathophysiology, patient presentation, diagnostic testing, and specific management strategies and challenges of these thrombocytopenias.

Drug-Induced Immune Thrombocytopenia

2014 ◽  
Vol 27 (5) ◽  
pp. 430-439 ◽  
Author(s):  
Teresa Kam ◽  
Maurice Alexander
Keyword(s):  
Data Collection ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Immune Thrombocytopenia ◽  
Treatment Options ◽  
Diagnosis And Treatment ◽  
Drug Induced ◽  
Laboratory Findings ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated

Thrombocytopenia is commonly seen in laboratory findings, especially in critically ill patients. Although the incidence is rare, drug-induced immune thrombocytopenia (DITP) is a serious complication that is often overlooked as a cause of thrombocytopenia. Over the last century, extensive research and data collection have been done in an attempt to better characterize DITP. Heparin-induced thrombocytopenia is the most common DITP and has distinct pathogenesis, diagnosis, and treatment options. However, other offending medications are less well known and have triggered many questions and constant search for answers. This review will discuss both drug-induced immune-mediated and nonimmune-mediated thrombocytopenias, with a focus on immune-mediated processes. Thrombocytopenia caused by chemotherapy will not be discussed in this article.

Heparin-induced Thrombocytopenia: Towards Consensus

1998 ◽  
Vol 79 (01) ◽  
pp. 1-7 ◽  
Author(s):  
Theodore Warkentin ◽  
Beng Chong ◽  
Andreas Greinacher
Keyword(s):  
Adverse Reaction ◽  
Treatment Approach ◽  
Diagnostic Testing ◽  
Optimal Treatment ◽  
Drug Induced ◽  
Danaparoid Sodium ◽  
Heparin Induced Thrombocytopenia ◽  
Thrombin Inhibition ◽  
Common Drug ◽  
Thrombotic Complications

SummaryHeparin-induced thrombocytopenia (HIT) is a drug-induced, immunoglobulin-mediated thrombocytopenic disorder that is important for at least three reasons. First, it is a relatively common drug-induced immunohematologic adverse reaction. Second, it is frequently complicated by life- and limb-threatening thrombotic complications. And third, there remains uncertainty about the optimal treatment approach for these patients. Recently, there has emerged increasing consensus on such important issues as the frequency, pathogenesis, and diagnostic testing, which we will summarize here. Further, a greater appreciation of the activation of the coagulation pathways in this syndrome indicate a rationale to treatment approaches that emphasize thrombin inhibition (eg. danaparoid sodium; hirudin and its analogues).

Piperacillin–Tazobactam-Induced Immune Thrombocytopenia: A Case Report

2021 ◽  
pp. 089719002110481
Author(s):  
Shangwe Kiliaki
Keyword(s):  
Laboratory Testing ◽  
Immune Thrombocytopenia ◽  
Drug Discontinuation ◽  
Patient Case ◽  
Platelet Destruction ◽  
Drug Induced ◽  
Diabetic Ulcer ◽  
Heparin Induced Thrombocytopenia ◽  
Common Drug ◽  
Drug Dependent

Drug-induced immune thrombocytopenia is an isolated thrombocytopenia caused by accelerated platelet destruction from drug-dependent, platelet-reactive antibodies. Heparin-induced thrombocytopenia is the most common drug-induced immune thrombocytopenia. Common implicated antibiotics for drug-induced immune thrombocytopenia include ceftriaxone, trimethoprim–sulfamethoxazole, vancomycin, and penicillin. The platelet nadir can be less than 20 × 10 (9)/L and typically occurs within 1 to 2 weeks of exposure to the inciting drug. Although rare, drug-induced immune thrombocytopenia can be fatal. Diagnosis is made by excluding other causes of thrombocytopenia. Laboratory testing for drug-dependent antiplatelet antibodies is often helpful but not required. Thrombocytopenia typically improves within 1 to 2 days of drug discontinuation and platelet count returns to normal within a week. Identifying and discontinuing the implicated medication is key to prevention of serious complications. A patient case of drug-induced immune thrombocytopenia is described after initiation of empiric piperacillin–tazobactam for refractory right foot cellulitis in the setting of right fourth toe diabetic ulcer.

scholarly journals Drug-Immune Thrombocytopenia with Thrombosis versus Heparin-Induced Thrombocytopenia: A Critical Clinical Controversy

2015 ◽  
Vol 5 (2) ◽  
pp. 152-159
Author(s):  
Hassan Al-Jafar ◽  
Anas Al-Yousef ◽  
Somaya Al-Shatti ◽  
Khalifa Al-Banwan
Keyword(s):  
Immune Thrombocytopenia ◽  
Recurrent Infection ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Clinical Issue ◽  
Heparin Induced Thrombocytopenia ◽  
Vein Thrombosis ◽  
Below The Knee ◽  
Febrile Episodes ◽  
End Stage

Heparin-induced thrombocytopenia (HIT) is a type of drug-induced immune thrombocytopenia (DITP). DITP is a rare and challenging clinical issue, especially when it is associated with thrombosis. A 62-year-old woman was admitted to our institution with end-stage renal failure. She received heparin for hemodialysis. Six days later, she became febrile and was treated with vancomycin and amikacin antibiotics. Two days after starting the vancomycin, she developed severe thrombocytopenia with extensive gangrenous deep vein thrombosis in her right leg, which required a below-the-knee amputation. The HIT test yielded positive results when heparin was already stopped, but her platelet count did not regenerate even after 3 months of heparin-free treatment. Courses of vancomycin treatment were given during several febrile episodes over the long period of severe thrombocytopenia. The patient was given both anti-immune thrombocytopenia and anticoagulant treatments because of both severe persistent thrombocytopenia and recurrent thrombotic episodes. The patient died as a result of severe thrombocytopenia, recurrent infection, and blood loss from the amputation site. Vancomycin is known to cause DITP, thrombosis, and immune complexes. DITP is a bleeding disorder, whereas HIT is a controversial thrombotic disorder. HIT tests can be influenced by cross-reacting antibodies and many other factors. Thus, there is no single method that can be considered 100% effective in confirming the HIT diagnosis. Anticoagulants must be used with great caution in patients with suspected DITP. Treatment of HIT-positive cases requires both clinical correlation and experience rather than reliance on HIT tests alone.

scholarly journals Interprofessional Management of Allergic Conjunctivitis

2018 ◽  
Vol 80 (3) ◽  
pp. 11-27 ◽  
Author(s):  
C. Lisa Prokopich ◽  
Michael Lee-Poyb ◽  
Harold Kimc
Keyword(s):  
Daily Living ◽  
Allergic Conjunctivitis ◽  
Treatment Options ◽  
Management Strategies ◽  
Treatment Algorithm ◽  
Current Treatment ◽  
Inflammatory Drugs ◽  
Patient Presentation ◽  
Symptoms And Signs

Ocular allergies affect a large and increasing number of people in North America. Canada’s statistics are likely to mirror those of the U.S., where up to 40% of the population is affected by ocular allergies. The symptoms and signs of ocular allergies can greatly affect productivity and have a dramatic effect on overall quality of life (QoL). Over the years, many effective treatments have been developed for the management of ocular allergies. For allergic conjunctivitis, topical ophthalmic agents include antihistamines, mast-cell stabilizers, dual-activity agents, steroids, nonsteroidal anti-inflammatory drugs, and other immune-modulating drugs. Oral antihistamines are commonly chosen by patients for all forms of allergy, including allergic conjunctivitis. This review provides a summary of the forms of ocular allergy, with a particular focus on the symptoms and signs, diagnosis, current treatment options, and impact on QoL. More importantly, through multidisciplinary collaboration, a simplified treatment algorithm is proposed for Canadian clinical practice. This algorithm provides practitioners the best possible management strategies based on an individual patient presentation, thereby maximizing treatment efficacy and minimizing the effects on tasks of daily living and QoL.

scholarly journals Recent advances in understanding and management of acquired thrombocytopenia

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 68 ◽  
Author(s):  
Srikanth Nagalla ◽  
Ravindra Sarode
Keyword(s):  
Bone Marrow ◽  
Immune Thrombocytopenia ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Diagnostic Testing ◽  
Thrombocytopenic Purpura ◽  
Heparin Induced Thrombocytopenia ◽  
Mortality And Morbidity ◽  
Splenic Sequestration ◽  
The Past ◽  
Uremic Syndrome

There are numerous congenital and acquired causes of thrombocytopenia. Thrombocytopenia could be a result of decreased bone marrow production, increased consumption, increased destruction, splenic sequestration or a combination of these causes. In this review, we have focused on some of the serious acquired causes of thrombocytopenia. There have been some significant advances in our understanding of the pathophysiology, diagnostic testing, and treatment of immune thrombocytopenia, heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura, and atypical hemolytic uremic syndrome over the past five years. These advances have resulted in a significant decrease in mortality and morbidity of patients with these disorders. Despite these advances, we are still faced with numerous unanswered questions in the pathophysiology and management of these complex thrombocytopenic disorders.

Congenital and Acquired Thrombocytopenia

Hematology ◽  
2004 ◽  
Vol 2004 (1) ◽  
pp. 390-406 ◽  
Author(s):  
Douglas B. Cines ◽  
James B. Bussel ◽  
Robert B. McMillan ◽  
James L. Zehnder
Keyword(s):  
Natural History ◽  
Management Strategies ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
History Of ◽  
Thrombotic Complications ◽  
Antibody Determination

Abstract The diagnosis and management of thrombocytopenia is a growing component in the practice of hematology. The frequency with which hematologists are called in consultation for thrombocytopenia continues to increase with the advent of routine automated platelet determinations and the introduction of new medications. For most patients, such as those with inherited and auto-immune thrombocytopenia, emphasis is focused on efforts to treat or forestall bleeding without excess drug-induced toxicity or burden to the patient. However, in disorders such as heparin-induced thrombocytopenia (HIT), avoidance of thrombotic complications is the key to management. In this chapter, we provide the pediatric and adult hematologist with new insights into the pathogenesis and recognition of congenital inherited thrombocytopenias (CTP), a hitherto difficult to comprehend constellation of clinical entities. We also highlight new approaches to the diagnosis and treatment of two of the more common thrombocytopenic conditions encountered in practice, autoimmune or idiopathic thrombocytopenic purpura (ITP) and HIT. In Section I, Dr. James Bussel discusses CTPs and their distinction from childhood ITP. He emphasizes the clinical features that enable the pediatrician and hematologist to suspect the diagnosis of CTP and those that are of use to subcategorize the various entities, where possible. He also emphasizes newer molecular markers that afford definitive diagnosis in some cases and provide insight into platelet production. This section highlights the characteristic associated findings and differences in the natural history and approaches to management of the various entities. In Section II, Dr. Robert McMillan discusses adult chronic ITP. He revisits the utility of platelet antibody determination in diagnosis and review new insights into pathogenesis. The role of Helicobacter pylori infection and the timing of splenectomy in the management of acute and emergent ITP are examined. New insights into the natural history of ITP post-splenectomy and management strategies for patients with severe, chronic, refractory ITP are discussed. In Section III, Dr. James Zehnder updates us on HIT. He emphasizes new insights into the clinical presentation and pathogenesis of this condition. He critically reviews the utility of laboratory testing for heparin-dependent antibodies. Recent studies on the use of direct thrombin inhibitors are examined and the management of cardiopulmonary bypass surgery in patients with HIT is discussed.

Autoimmune and Paraneoplastic Myelopathies

2018 ◽  
Vol 38 (03) ◽  
pp. 278-289 ◽  
Author(s):  
Nicholas Zalewski ◽  
Eoin Flanagan
Keyword(s):  
Patient Outcomes ◽  
Treatment Plan ◽  
Treatment Options ◽  
Management Strategies ◽  
Management Plan ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Diagnostic Information ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Paraneoplastic Diseases ◽  
Specific Management

AbstractPrompt recognition of an inflammatory myelopathy is critical, as a specific diagnosis and management plan allows for optimal patient outcomes. Many treatment options are now available for autoimmune and paraneoplastic myelopathies, but specific management strategies and expected prognosis vary widely depending on the underlying etiology. An understanding of the relevant clinical details, imaging findings, and other diagnostic information that can help achieve a specific myelopathy diagnosis and treatment plan is essential for all neurologists, given the variety of contexts in which myelopathies are encountered. We provide an outline of the diagnostic evaluation and treatment of various inflammatory myelopathies seen in autoimmune and paraneoplastic diseases, including multiple sclerosis, aquaporin-4 immunoglobulin G (IgG) seropositive neuromyelitis optica spectrum disorder, sarcoidosis, myelin oligodendrocyte glycoprotein IgG associated disease, and other rare inflammatory myelopathies; we also highlight common mimickers of inflammatory myelopathies.

Acute Renal Failure and the Critically Ill Patient

2002 ◽  
Vol 15 (2) ◽  
pp. 158-166 ◽  
Author(s):  
Earnest Alexander ◽  
Bradley A. Boucher
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Current Knowledge ◽  
Treatment Options ◽  
Management Strategies ◽  
Critically Ill Patient ◽  
Drug Induced ◽  
Investigational Therapies

Acute renal failure (ARF) is a complication frequently observed in critically ill patients. This review provides details regarding the epidemiology and overall care of the ARF patient. ARF is defined and classified based on etiology. These classifications are prerenal azotemia, ischemic ARF, and postrenal azotemia. Examples of drug-induced nephrotoxicity are also outlined. Clinical presentation and diagnostic criteria of ARF are differentiated among the major ARF classes, and management strategies are outlined. These management strategies include preventive, supportive, pharmacologic, and nonpharmacologic interventions. Current standards of practice and investigational therapies are also discussed. Pharmacokinetic monitoring and dosing regimen adjustments in ARF patients with and without renal replacement therapy are reviewed. Finally, a prognostic evaluation of ARF in critically ill patients is provided based on current knowledge of the disease state and treatment options.

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