scholarly journals Heparin-induced thrombocytopenia: An Update

1970 ◽  
Vol 3 (2) ◽  
pp. 187-199
Author(s):  
LA Sayami ◽  
M Ullah
Keyword(s):  
Morbidity And Mortality ◽  
Diagnosis And Treatment ◽  
Significant Morbidity ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
Recent Advances ◽  
Immune Mediated

Heparin-induced thrombocytopenia (HIT) is the most important and most frequent drug-induced, immune-mediated type of thrombocytopenia. It is associated with significant morbidity and mortality if unrecognized. In this review, we briefly discuss the main features of heparin-induced thrombocytopenia, particularly analyzing the most recent advances in the pathophysiology, diagnosis and treatment of this syndrome. Keywords: Heparin; Thrombocytopenia DOI: http://dx.doi.org/10.3329/cardio.v3i2.9189 Cardiovasc. J. 2011; 3(2): 187-199

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: when a low platelet count is a mandate for anticoagulation

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel
Keyword(s):  
Platelet Count ◽  
Heparin Therapy ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Number Of Patients ◽  
Increased Risk ◽  
Antibody Levels

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.

Disseminated intravascular coagulation in paediatrics

2016 ◽  
Vol 102 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Revathi Rajagopal ◽  
Jecko Thachil ◽  
Paul Monagle
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Diagnostic Tests ◽  
Early Life ◽  
Clinical Manifestations ◽  
Review Article ◽  
Morbidity And Mortality ◽  
Significant Morbidity ◽  
Intravascular Coagulation ◽  
Management Algorithm ◽  
Recent Advances

Disseminated intravascular coagulation (DIC) in paediatrics is associated with significant morbidity and mortality. Although there have been several recent advances in the pathophysiology of DIC, most of these studies were done in adults. Since the haemostatic system is very different in early life and changes dramatically with age, creating a variety of challenges for the clinician, delay in the diagnosis of DIC can happen until overt DIC is evident. In this review article, we report the aetiology, pathophysiology, clinical manifestations, diagnostic tests and a management algorithm to guide paediatricians when treating patients with DIC.

scholarly journals TROMBOSITOPENIA PADA PENGOBATAN DENGAN HEPARIN

2018 ◽  
Vol 13 (3) ◽  
pp. 114
Author(s):  
B. Mulyadi,* ◽  
J. Soemarsono
Keyword(s):  
Side Effect ◽  
Heparin Therapy ◽  
Morbidity And Mortality ◽  
Severe Side Effect ◽  
Drug Induced ◽  
Platelet Factor ◽  
Platelet Surface ◽  
Heparin Induced Thrombocytopenia

Heparin induced thrombocytopenia (HIT), a well known side effect of heparin therapy, occurs in 1–5% of adults exposed to heparin.Unlike other drug induced thrombocytopenia, HIT does not usually cause bleeding, but instead cause thrombosis about 50% of HIT.The thrombosis in HIT can lead to limb gangrene or even death. The Importance to know the HIT is the wide use of heparin led tothe increasing recognition of untoward complications including HIT, relatively uncommon but severe side effect of heparin therapy,unpredictable, and difficulty in diagnosing and treating HIT. HIT is mediated by an antibody that recognizes an epitope on the plateletfactor (PF4)-heparin complex. The platelet factor (PF4)-heparin complex binds to FcgRII receptor on the platelet surface and crosslinksthereceptors.Thisinducesintenseplateletactivationandaggregationandsimultaneouslyactivatesbloodcoagulationpathways,thesechangesareprobablythebasisofthethrombosiseventsinHIT.HITwasclassifiedintotype1and2baseonthepathogenesisandtheseverityofHIT.RegularplateletcountmonitoringisbestsuitedforearlydiagnosisofHIT.Functional(serotoninrelease,plateletaggregationtest)andantigenassays(solidphaseenzymeimmunoassay,fluidphase,andparticlegelimmunoassay)areavailabletoconfirmHIT.HITwasmadebaseontheclinicalfindingandlaboratoryexamination.OnceHITisclinicallysuspected,heparinshouldbestoppedimmediatelyandtreatmentwithanalternativeanticoagulant,waitingforlaboratoryconfirmationmaybecatastrophic.Earlydiagnosisof HIT will decrease the morbidity and mortality.

scholarly journals DRESS syndrome in the setting of oxacillin therapy—a call for better patient preparedness: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Hawa Ozien Abu ◽  
Sajjadh M. J. Ali ◽  
Anil Phuyal ◽  
Akil Sherif ◽  
Gregory T. Williams ◽  
...  
Keyword(s):  
Emergency Department ◽  
Staphylococcus Aureus ◽  
Drug Reaction ◽  
Early Recognition ◽  
Elevated Serum ◽  
Morbidity And Mortality ◽  
Significant Morbidity ◽  
Drug Induced ◽  
Life Threatening ◽  
Systemic Symptoms

Abstract Background Drug reaction with eosinophilia and systemic symptoms syndrome is a rare but severe and potentially life-threatening hypersensitivity reaction, with significant morbidity and mortality. The clinical presentation of drug reaction with eosinophilia and systemic symptoms may include extensive skin rash, fever, lymphadenopathy, internal organ involvement, eosinophilia, and atypical lymphocytosis, most commonly due to drug-induced reaction. Our case is a rare occurrence of drug reaction with eosinophilia and systemic symptoms syndrome in the setting of oxacillin therapy. Case presentation A 55-year-old Caucasian male presented to the emergency department on account of acute onset, 2-day history of generalized pruritic rash with associated fever, occurring 3 weeks after commencing therapy with intravenous oxacillin for methicillin-sensitive Staphylococcus aureus bacteremia. He had no known drug allergies. Two days prior to hospitalization, he had a telehealth visit with the infectious diseases specialist on account of his rash, and was recommended to use oral diphenhydramine. However, with the onset of fever and persistence of his rash, he was advised to discontinue the oxacillin and present to the emergency department. On examination, he was febrile at 101.2 °F and had a generalized blanchable maculopapular and morbilliform rash involving the face, trunk, upper and lower extremities, but sparing the palms, soles, and oral mucosa. He had palpable nontender lymph nodes in the cervical and inguinal regions bilaterally. Laboratory studies revealed atypical lymphocytosis, eosinophilia, neutrophilia, and elevated serum transaminases. He was started on intravenous diphenhydramine and admitted to the in-patient medical service. On the second day of hospitalization, his fever resolved. However, his rash was persistent and generalized, as well as elevated transaminases and an abnormal cell count on the second day of hospitalization. To complete his 6-week course of antibiotics for methicillin-sensitive Staphylococcus aureus bacteremia, he was switched to an alternative therapy with cefazolin, and he was scheduled for weekly follow-up assessments following hospital discharge. Conclusions Healthcare providers should increasingly be aware of the significant morbidity and mortality attributable to drug reaction with eosinophilia and systemic symptoms syndrome and the potential medications which may incite such life-threatening reactions. Early recognition of drug reaction with eosinophilia and systemic symptoms syndrome and prompt institution of management strategies can promote improved clinical outcomes. Enhanced patient–provider communication strategies should be implemented to better prepare patients for the likelihood of such drug reactions, with the goal of improving patient-centered care and adherence with treatment strategies.

Heparin-Induced Thrombocytopenia with Thrombosis

2017 ◽  
Author(s):  
Young Kim ◽  
Brent T Xia ◽  
Christopher A Droege ◽  
Kristen E Carter ◽  
Timothy A Pritts
Keyword(s):  
Adverse Drug Reaction ◽  
Clinical Suspicion ◽  
Type Ii ◽  
Significant Morbidity ◽  
Heparin Induced Thrombocytopenia ◽  
Functional Assays ◽  
High Clinical Suspicion ◽  
Immune Mediated ◽  
Laboratory Confirmation ◽  
Key Words Heparin

Heparin-induced thrombocytopenia type II (HIT II) is an immune-mediated adverse drug reaction to heparin and heparinoid compounds. Unlike other etiologies of thrombocytopenia, HIT II frequently manifests with arterial or venous thromboemboli, leading to significant morbidity and mortality. Diagnosis of HIT II requires a high clinical suspicion, pretest probability scoring, and laboratory confirmation through immunologic and functional assays. Moderate probability for HIT II should be met with discontinuation of the offending agent and initiation of an alternative anticoagulant. Key words: heparin-induced thrombocytopenia, heparin-induced thrombocytopenia with thrombosis, HIT II, HITT

scholarly journals The Therapeutic Challenges in Treating Duodenal Injury

2013 ◽  
Vol 2 (3) ◽  
pp. 126-133
Author(s):  
Charles E Lucas
Keyword(s):  
Critical Care ◽  
Morbidity And Mortality ◽  
Diagnosis And Treatment ◽  
Significant Morbidity ◽  
Duodenal Injury ◽  
Duodenal Injuries

ABSTRACT Duodenal injuries pose many challenges in diagnosis and treatment. Unless suspected, pursued vigorously and treated by a well-designed plan, can cause significant morbidity and mortality. How to cite this article Lucas CE. The Therapeutic Challenges in Treating Duodenal Injury. J Trauma Critical Care Emerg Surg 2013;2(3):126-133.

scholarly journals Commentary on Pedal Revascularization: Extending the Limits of Endovascular or Surgical Means to Prevent Amputation

2021 ◽  
Vol 6 (2) ◽  
pp. 1-4
Author(s):  
Richard F Neville ◽  
Keyword(s):  
Limb Salvage ◽  
Critical Limb Ischemia ◽  
State Of The Art ◽  
Limb Ischemia ◽  
Arterial Disease ◽  
Morbidity And Mortality ◽  
Significant Morbidity ◽  
Below The Knee ◽  
Recent Advances ◽  
Primary Amputation

Critical limb ischemia carries risk of significant morbidity and mortality and revascularization is particularly challenging in patients with tibial and pedal arterial disease. Recent advances in both endovascular therapies and open revascularization techniques have expanded our ability to treat patients with below the knee disease who may otherwise be subject to amputation. This commentary briefly reflects on emerging endovascular and open revascularization techniques for limb salvage in complex below knee arterial disease in order to raise awareness and minimize primary amputation without attempts at these “state of the art” modalities.

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