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

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.

2017 ◽  
Vol 117 (10) ◽  
pp. 1868-1874 ◽  
Author(s):  
Jo-Ann Sheppard ◽  
Theodore Warkentin ◽  
Andrew Shih

SummaryOne of the standard distinctions between type 1 (non-immune) and type 2 (immune-mediated) heparin-induced thrombocytopenia (HIT) is the transience of thrombocytopenia: type 1 HIT is viewed as early-onset and transient thrombocytopenia, with platelet count recovery despite continuing heparin administration. In contrast, type 2 HIT is viewed as later-onset (i. e., 5 days or later) thrombocytopenia in which it is generally believed that platelet count recovery will not occur unless heparin is discontinued. However, older reports of type 2 HIT sometimes did include the unexpected observation that platelet counts could recover despite continued heparin administration, although without information provided regarding changes in HIT antibody levels in association with platelet count recovery. In recent years, some reports of type 2 HIT have confirmed the observation that platelet count recovery can occur despite continuing heparin administration, with serological evidence of waning levels of HIT antibodies (“seroreversion”). We now report two additional patient cases of type 2 HIT with platelet count recovery despite ongoing therapeutic-dose (1 case) or prophylactic-dose (1 case) heparin administration, in which we demonstrate concomitant waning of HIT antibody levels. We further review the literature describing this phenomenon of HIT antibody seroreversion and platelet count recovery despite continuing heparin administration. Our observations add to the concept that HIT represents a remarkably transient immune response, including sometimes even when heparin is continued.


2020 ◽  
Vol 4 (4) ◽  
pp. 776-783 ◽  
Author(s):  
Leslie Skeith ◽  
Lisa Baumann Kreuziger ◽  
Mark A. Crowther ◽  
Theodore E. Warkentin

Abstract Identifying the cause(s) of postoperative thrombocytopenia is challenging. The postoperative period includes numerous interventions, including fluid administration and transfusion of blood products, medication use (including heparin), and increased risk of organ dysfunction and infection. Understanding normal thrombopoietin physiology and the associated expected postoperative platelet count changes is the crucial first step in evaluation. Timing of thrombocytopenia is the most important feature when differentiating causes of postoperative thrombocytopenia. Thrombocytopenia within 4 days of surgery is commonly caused by hemodilution and increased perioperative platelet consumption prior to thrombopoietin-induced platelet count recovery and transient platelet count overshoot. A much broader list of possible conditions that can cause late-onset thrombocytopenia (postoperative day 5 [POD5] or later) is generally divided into consumptive and destructive causes. The former includes common (eg, infection-associated disseminated intravascular coagulation) and rare (eg, postoperative thrombotic thrombocytopenic purpura) conditions, whereas the latter includes such entities as drug-induced immune thrombocytopenia or posttransfusion purpura. Heparin-induced thrombocytopenia is a unique entity associated with thrombosis that is typically related to intraoperative/perioperative heparin exposure, although it can develop following knee replacement surgery even in the absence of heparin exposure. Very late onset (POD10 or later) of thrombocytopenia can indicate bacterial or fungal infection. Lastly, thrombocytopenia after mechanical device implantation requires unique considerations. Understanding the timing and severity of postoperative thrombocytopenia provides a practical approach to a common and challenging consultation.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1957-1957
Author(s):  
Udhayvir Singh Grewal ◽  
Shiva Jashwanth Gaddam ◽  
Sahith Reddy Thotamgari ◽  
Tyiesha Brown ◽  
Kavitha Beedupalli ◽  
...  

Abstract Background: Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Both clinical probability and laboratory testing are needed for establishing a diagnosis of HIT. The 4Ts clinical scoring system, due to a very high negative predictive value when low, offers a robust means to exclude a diagnosis of HIT. However, these strategies are under-employed in clinical practice and limited evidence indicates a high prevalence of over-testing for HIT. Methods: This retrospective analysis was conducted to identify patients who underwent heparin/PF4 antibody testing over a period of 12 months. The testing was performed using an ELISA-based IgG anti-heparin/PF4 antibody assay and an optical density (OD) of 0.4 was used as a cut-off for a positive value. Electronic medical records were reviewed for 4T score documentation, anti-PF4 results, SRA testing and 4T scores were retrospectively calculated for all the patients. SAS v9.4 (Cary, NC) was used for statistical analysis. Results: A total of 105 patients who underwent anti-PF4 antibody testing were included for analysis. Majority of the patients in our cohort were admitted in an intensive care unit setting (75/105,71.4%). On chart review, only 17 patients (16.2%) were noted to have documentation of 4T score. Based on the retrospectively calculated 4T scores, 60 patients (57.1%) had low pre-test probability, 41 (39%) had intermediate pre-test probability and 4 (3.8%) patients were noted to have high pre-test probability. Anti-PF4/heparin antibodies were positive in 9 patients, of which 5 (55.5%) patients did not undergo concomitant SRA testing. Out of 9, 4 (44.4%) had weakly positive (0.4-1.0 OD units), 2 (21.1%) had strongly positive (1.0-2.0 OD units) and 2 (21.1%) patients had very strongly positive (>2 OD units) anti-PF4 antibody titers. Out of 105 patients, SRA was tested in 11 patients (10.5%) and was noted to be positive in 1 (0.95%). Overall, 2 patients were diagnosed and treated for HIT, out of which the diagnosis was not confirmed with SRA in 1 patient (due to high pre-test probability and very strong anti-PF4 titers). In the remaining patients, sepsis (48, 46.6%) and drug-induced thrombocytopenia (29, 28.2%) emerged as the most common possible causes of thrombocytopenia. Conclusion: Among hospitalized patients, over-testing for HIT is common. Practices to promote 4T score documentation and evidence-based anti-PF4 testing may help prevent unnecessary costs associated with serological testing and costly alternate anticoagulants. To improve overall outcomes, clinicians should also attempt to identify and treat other more likely causes of thrombocytopenia, especially in patients with low pre-test probability for HIT. Disclosures No relevant conflicts of interest to declare.


Author(s):  
B. Mulyadi,* ◽  
J. Soemarsono

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.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Payel Datta ◽  
Fuming Zhang ◽  
Jonathan S. Dordick ◽  
Robert J. Linhardt

Abstract Background This is a review article on heparin-induced thrombocytopenia, an adverse effect of heparin therapy, and vaccine-induced immune thrombotic thrombocytopenia, occurring in some patients administered certain coronavirus vaccines. Main body/text Immune-mediated thrombocytopenia occurs when specific antibodies bind to platelet factor 4 /heparin complexes. Platelet factor 4 is a naturally occurring chemokine, and under certain conditions, may complex with negatively charged molecules and polyanions, including heparin. The antibody-platelet factor 4/heparin complex may lead to platelet activation, accompanied by other cascading reactions, resulting in cerebral sinus thrombosis, deep vein thrombosis, lower limb arterial thrombosis, myocardial infarction, pulmonary embolism, skin necrosis, and thrombotic stroke. If untreated, heparin-induced thrombocytopenia can be life threatening. In parallel, rare incidents of spontaneous vaccine-induced immune thrombotic thrombocytopenia can also occur in some patients administered certain coronavirus vaccines. The role of platelet factor 4 in vaccine-induced thrombosis with thrombocytopenia syndrome further reinforces the importance the platelet factor 4/polyanion immune complexes and the complications that this might pose to susceptible individuals. These findings demonstrate, how auxiliary factors can complicate heparin therapy and drug development. An increasing interest in biomanufacturing heparins from non-animal sources has driven a growing interest in understanding the biology of immune-mediated heparin-induced thrombocytopenia, and therefore, the development of safe and effective biosynthetic heparins. Short conclusion In conclusion, these findings further reinforce the importance of the binding of platelet factor 4 with known and unknown polyanions, and the complications that these might pose to susceptible patients. In parallel, these findings also demonstrate how auxiliary factors can complicate the heparin drug development.


Hematology ◽  
2018 ◽  
Vol 2018 (1) ◽  
pp. 576-583 ◽  
Author(s):  
Tamam Bakchoul ◽  
Irene Marini

Abstract Many drugs have been implicated in drug-induced immune thrombocytopenia (DITP). Patients with DITP develop a drop in platelet count 5 to 10 days after drug administration with an increased risk of hemorrhage. The diagnosis of DITP is often challenging, because most hospitalized patients are taking multiple medications and have comorbidities that can also cause thrombocytopenia. Specialized laboratory diagnostic tests have been developed and are helpful to confirm the diagnosis. Treatment of DITP involves discontinuation of the offending drug. The platelet count usually starts to recover after 4 or 5 half-lives of the responsible drug or drug metabolite. High doses of intravenous immunoglobulin can be given to patients with severe thrombocytopenia and bleeding. Although in most cases, DITP is associated with bleeding, life-threatening thromboembolic complications are common in patients with heparin-induced thrombocytopenia (HIT). Binding of antiplatelet factor 4/heparin antibodies to Fc receptors on platelets and monocytes causes intravascular cellular activation, leading to an intensely prothrombotic state in HIT. The clinical symptoms include a decrease in platelet counts by >50% and/or new thromboembolic complications. Two approaches can help to confirm or rule out HIT: assessment of the clinical presentation using scoring systems and in vitro demonstration of antiplatelet factor 4/heparin antibodies. The cornerstone of HIT management is immediate discontinuation of heparin when the disease is suspected and anticoagulation using nonheparin anticoagulant. In this review, we will provide an update on the pathophysiology, diagnosis, and management of both DITP and HIT.


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4077-4077 ◽  
Author(s):  
John L. Francis ◽  
Alane Drexler ◽  
Gage Gwyn ◽  
Rebecca Moroose

Abstract Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin therapy. As thrombosis occurs in 50% of untreated patients, prompt treatment with a direct thrombin inhibitor (DTI) is recommended. Lepirudin and argatroban are currently approved for the treatment of HIT. However, their use is complicated by antibody formation with potential for anaphylactic shock (lepirudin), effects on the PT/INR that complicate transition to coumadin (argatroban), and significant dose adjustments in patients with renal (lepirudin) or liver (argatroban) impairment. The effectiveness of bivalirudin, another DTI, as a replacement for heparin has been well documented in percutaneous coronary intervention, but there are little published data on its use in treating HIT. We now report our experience with bivalirudin in 52 patients with clinical suspicion of HIT, or at increased risk of this complication. HIT was suspected on the basis of a falling platelet count and/or thrombosis in the setting of current or recent heparin therapy (n=49). Patients were considered at increased risk of HIT if they required ongoing intravenous anticoagulation in a setting associated with a high incidence of heparin-platelet factor 4 (HPF4) antibodies (n=3). Data were collected by retrospective chart review, and patients classified according to whether HIT was very likely (n=13), likely (n=17), unlikely (n=11) or very unlikely (n=11). Bivalirudin was given by intravenous infusion, typically at an initial dose of 0.15 - 0.20 mg/kg/h and adjusted to achieve an APTT of approximately 1.5–2.5 x baseline. Twenty-one patients had moderate or severe renal impairment. The infusion rate was significantly lower for patients with severe renal insufficiency, but was not different in those with mild renal dysfunction. ELISA-detectable HPF4 antibodies were present in 43/52 cases. Twenty-seven patients were significantly thrombocytopenic (<100,000 x 109/L) and 22 had thrombosis before therapy. Transition to warfarin was achieved in 44/52 patients with a median overlap of therapy of 4 (0.5–14) days. Bivalirudin therapy was continued for an average of 8.0 (3–47) days, and had a relatively minor impact on the PT/INR. The mean INR on monotherapy was 1.50 (1.23–2.18) with a mean change in INR due to bivalirudin therapy of 0.33 ± 0.22. Therapeutic APTTs were achieved in all patients, with approximately 92.5% of tests in the desired range. The average time to platelet recovery was 3.0 (1–10) days. There were no cases of major bleeding, no deaths attributable to HIT, and no patient required amputation. We conclude that bivalirudin provides safe and effective anticoagulation for patients with suspected HIT, as well as for those with an increased risk of HIT that require intravenous anticoagulation. Potential advantages of bivalirudin include the relatively minor effect on the PT, which facilitates transition to warfarin therapy, and its short half-life in patients at high risk of bleeding or who require invasive procedures at short notice.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 56-56 ◽  
Author(s):  
Michael P. Reilly ◽  
Scott K. Dessain ◽  
Scott M. Taylor ◽  
M. Anna Kowalska ◽  
Mortimer Poncz ◽  
...  

Abstract Heparin-induced thrombocytopenia/thrombosis (HIT/T), the most frequent drug-induced immune thrombocytopenia, is a common cause of life- and limb-threatening thrombosis. Although heparin/platelet factor 4 (PF4) antibodies are detected in many patients treated with heparin, there is little understanding of why only a subset of patients develops thrombosis. We recently produced and characterized the first mouse model that recapitulates the salient features of the disease. A second generation model, designated IIA/hPF4-mPF4KO, expresses human FcγRIIA and PF4 but lacks endogenous mouse PF4. These models allow systematic investigations of factors that contribute to pathogenic consequences of HIT/T antibodies. In the current study, we hypothesize that hypercholesterolemia, a known stimulus for atherosclerosis, endothelial dysfunction, and platelet hyperreactivity, would augment thrombosis in our mouse model of HIT/T. Age and sex-matched IIA/hPF4-mPF4KO mice were fed an atherogenic diet (Paigen diet) (AD; 15% cocoa butter, 1% cholesterol, 0.5% cholate) (n=10) or maintained on standard diet (SD; 4.5% fat, no cholate) (n=10). Mice fed the AD for only 4 weeks had significantly increased cholesterol levels (173 ± 29 mg/dl vs. 50 ± 18 mg/dl for SD-fed; p < 0.0001). Mice were then injected with 30 U heparin and KKO, a mouse monoclonal heparin/PF4 antibody. The mean nadir platelet count in AD-fed mice was 34.6% ± 9.1 lower than that in the SD-fed mice (p< 0.0001). Thrombin-anti-thrombin III (TAT) levels, which reflect thrombin generation in vivo, in the AD-fed mice increased from 32 ± 5 μg/at baseline to 79 ± 16 μg/l (p < 0.0001) coincident with the platelet nadir. In contrast, SD-fed mice, with a less profound fall in platelets, showed no increase in TAT. Histological examination showed multiple platelet-fibrin thrombi in lungs and livers of AD-fed mice, whereas the SD-fed mice showed no histological evidence of thrombosis. Thus, in our mouse model, short-term diet-induced hyperlipidemia significantly increases the severity of heparin/PF4 antibody-mediated thrombocytopenia and thrombosis. Our studies provide evidence that a specific host factor can enhance the pathologic effects of heparin/PF4 antibodies in vivo and contribute to thrombotic risk in patients with HIT/T. An increased understanding of the contribution of prothrombotic factors not only will facilitate identification of patients with heparin/PF4 antibodies who are at increased risk of thrombosis, but also provide novel approaches to treatment of HIT/T.


Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2757-2757
Author(s):  
Ishac Nazi ◽  
Donald M Arnold ◽  
James W Smith ◽  
Theodore E. Warkentin ◽  
Jane C Moore ◽  
...  

Abstract Background: Heparin-induced thrombocytopenia (HIT) is a common drug reaction that causes arterial or venous thrombosis as a result of heparin therapy. Platelet-activating antibodies, against complexes of platelet factor 4 (PF4) and heparin, cause intense platelet activation, ultimately leading to an increased risk of thrombosis, limb-loss and even death. Most patients exposed to heparin will produce non-pathogenic anti-PF4/heparin antibodies while only a small number will produce platelet-activating and HIT-causing antibodies (pathogenic HIT antibodies). Among HIT tests, the functional assays, such as the serotonin release assay (SRA), correlate best with the disease because they can specifically identify the pathogenic HIT antibodies whereas the enzyme immunoassays (EIAs) cannot. We have previously shown that anti-PF4/heparin antibody production precedes thrombocytopenia in HIT patients (Warkentin et al., Blood 2009 113: 4963-4969) possibly indicating the need for a threshold plasma level of pathogenic HIT antibody, among other factors, to cause the disease. The objective of this study was to investigate the presence of low levels of pathogenic HIT antibodies in samples from patients suspected of HIT who had detectable anti-PF4/heparin antibodies in the EIA (EIA-positive), but who did not have platelet-activating antibodies in the standard SRA (SRA-negative). Methods: We used an in-house IgG-specific EIA to detect the presence of anti-PF4/heparin antibodies (EIA-positive: OD405nm> 0.45) and the standard SRA to detect the presence of heparin-dependent platelet-activating antibodies (SRA-positive: release >20% with 0.1-0.3 IU/mL of unfractionated heparin). We developed an enhanced SRA (eSRA) by adding increasing concentrations of exogenous PF4 (0-100 μg/mL) to detect sub-threshold levels of platelet activating antibodies undetectable in the standard SRA (eSRA-positive: release >20%). Samples tested were referred for HIT testing by the McMaster Platelet Immunology Laboratory (Hamilton, Canada). Results: Sera from healthy individuals (n=10) and from suspected HIT patients with a negative anti-PF4/heparin EIA (n=15) did not demonstrate platelet activation in the eSRA at any dose of exogenous PF4 added. SRA-positive sera (n = 7), diluted sufficiently that they were non-reactive in the standard SRA, demonstrated PF4 dose-dependent platelet activation in the eSRA. This confirmed the increased sensitivity of the eSRA in detecting low-titre platelet-activating antibodies. Reactivity in the eSRA was inhibited by high heparin (100 U/mL) and by blocking the platelet FcgRIIa receptor with the monoclonal antibody IV.3. We then tested samples (n=24) referred for HIT testing that were positive in the anti-PF4/heparin EIA (optical densities OD405nm 0.7 to 2.4) but negative in the standard SRA. Heparin-dependent platelet activation (20-99% release) was demonstrated in 11 of 24 (46%) in the eSRA. This reactivity directly correlated with the amount of PF4 added to the platelets (optimal concentration of PF4 12.5 - 100 μg/mL) but not with the strength (OD405nm) of the anti-PF4/heparin EIA. In further investigations, we concentrated (4-fold) 7 of the 11 eSRA-positive samples in an attempt to increase the concentration of the antibodies. Of those 7 samples, 5 (71%) became positive in the standard SRA upon testing of the concentrated sample. Conclusions: These data indicate that low-titre platelet-activating antibodies may be found in some patients suspected of having HIT that test negative in the standard SRA irrespective of the strength (OD405nm) of the anti-PF4/heparin EIA. The immune response during heparin therapy can produce both families of pathogenic and non-pathogenic anti-PF4/heparin antibodies but it is the titre of the pathogenic antibody that may be necessary for platelet activation. Perhaps under permissive clinical conditions and with patient-specific factors, the titre of the pathogenic HIT antibodies may increase and lead to HIT. Disclosures Warkentin: Pfizer Canada: Honoraria; Instrumentation Laboratory: Honoraria; GlaxoSmithKline: Consultancy, Research Funding; W.L. Gore: Consultancy, Research Funding.


1998 ◽  
Vol 32 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Aditya K Gupta ◽  
Michael J Kovacs ◽  
Daniel N Sauder

OBJECTIVE To highlight the importance of heparin-induced thrombocytopenia (HIT), a potentially fatal adverse effect of heparin therapy. CASE SUMMARY: There are two types of HIT with a distinct etiology. Type 1 HIT is a relatively mild thrombocytopenia of early onset that generally resolves with ongoing heparin therapy. Clinical complications are uncommon. Type 2 HIT, which is more severe, is the main focus of this report. Five patients receiving heparin therapy developed type 2 HIT, which in some cases resulted in complications that required limb amputation, or eventuated in death. DISCUSSION: In a patient receiving heparin therapy, the development of thrombocytopenia should alert the caregiver to the possible development of HIT. Prompt management of HIT can help prevent complications. HIT usually manifests 5–8 days after starting heparin therapy. The platelet count usually decreases to less than 100 times 103/mm3. It generally normalizes within 5–7 days after discontinuing heparin therapy. In spite of the thrombocytopenia, thrombosis or disseminated intravascular coagulation can occur. The management may be subdivided into three clinical situations: mild-to-moderate asymptomatic thrombocytopenia, severe thrombocytopenia with a platelet count of less than 50 times 103/mm3, and thrombosis or embolism complicating HIT. CONCLUSIONS Heparin-induced thrombocytopenia is an uncommon but potentially serious, and sometimes lethal, complication of heparin therapy. Therefore, it is important to be aware of the possibility of the development of HIT with heparin therapy, to recognize it early, and to manage it appropriately before the manifestation of adverse effects. OBJETIVO Establecer la importancia de la trombocitopenia inducido por heparina (TIH), lo cual representa un posible efecto adverso fatal associado con la terapia de este medicamento. RESUMEN DEL CASO Existen dos tipos de TIH con etiologias distintas. TIH del tipo I representa trombocitopenia que es relativamente leve y de occurrencia temprana y que se resuelve generalmente con la terapia continua de heparina. Complicaciones clínicas son infrequentes. TIH del tipo II es más severa y representa el foco principal de este reporte. Se describe cinco pacientes que recibieron terapia con heparina que desarrollaron TIH del tipo II y cuyos casos resultaron en complicaciones que necesitaron amputaciones en las extremidades o que aveces resultaron en condiciones fatales. DISCUSSIÓN En pacientes que reciben terapia con heparina, el desarrollo de trombocitopenia debe alertar el médico al posible desarrollo de TIH. El manejo inmediato de TIH puede prevenir estas complicaciones. Después de la primera exposición a la heparina, TIH se manifiesta 5–8 días después del inicio del tratamiento. En estos casos, el número de plaquetas usualmente se disminuye a menos de 100 times 103/mm3 y generalmente se normalisa dentro de 5–7 días al descontinuarse la heparina. A pesar de la trombocitopenia, trombosis y coagulación intravascular deseminada puede desarrollarse en estos pacientes. El manejo de éstas complicaciones puede ser subdividido en tres situaciones clínicas: trombocitopenia asintomático leve o moderada, trombocitopenia severa con un conteo de plaquetas de menos de 50 times 103/mm3 o complicaciones de trombosis y embolismo debido al TIH. CONCLUSIONES TIH es una complicación infrequente, pero este puede resultar en complicaciones serias y a veces letales debido a la terapia de heparina. Como resultado, es importante estar al tanto del posible desarrollo de TIH asociado con el tratamiento de heparina, reconocer esta complicación lo más pronto posible, y manejarlo apropriadamente antes de las manifestaciones de los efectos adversos. OBJECTIF Souligner l'importance de la thrombocytopénie induite par l'héparine (TIH), un effet indésirable potentiellement fatal de l'héparine. RÉSUMÉ DU CAS Il existe deux types de TIH, présentant des étiologies distinctes. Le type I se définit comme une thrombocytopénie légère, d'apparition précoce et qui se résout généralement malgré la poursuite du traitement à l'héparine. Les complications cliniques de ce premier type sont inhabituelles. Le type II est plus grave et il sera le point de mire du présent article. Cinq patients recevant de l'héparine ont développé une TIH de type II ayant résulté, dans certains cas, en des complications menant à l'amputation d'un membre ou même, à la mort. DISCUSSION Chez un patient recevant de l'héparine, le développement de thrombocytopénie devrait alerter l'équipe soignante à la possibilité de TIH. Le traitement rapide de la TIH peut aider à prévenir les complications. Suivant une première exposition à l'héparine, la TIH se manifeste généralement 5–8 jours après le début du traitement. Le décompte plaquettaire diminue habituellement à moins de 100 times 103/mm3. Par la suite, il se normalise en 5–7 jours après l'arrêt du traitement à l'héparine. Malgré la thrombocytopénie, une thrombose ou de la coagulation intravasculaire disséminée peuvent se produire. Le traitement peut se subdiviser selon trois situations cliniques: thrombocytopénie légère à modérée asymptomatique, thrombocytopénie grave avec un compte de plaquettes moins de 50 times 103/mm3, et TIH compliquée de thromboembolie. CONCLUSIONS La TIH est une complication rare, potentiellement grave, et parfois fatale de l'héparinothérapie. Ainsi, lorsqu'un patient reçoit de l'héparine, le clinicien doit surveiller l'apparition de TIH, afin de la reconnaître de façon précoce et de la traiter adéquatement avant l'apparition de complications graves.


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