scholarly journals Heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation and the role of a heparin-bonded circuit

Perfusion ◽  
2019 ◽  
Vol 34 (7) ◽  
pp. 584-589 ◽  
Author(s):  
Dirk Pabst ◽  
Jacqueline B Boone ◽  
Behzad Soleimani ◽  
Christoph E Brehm

Background: In patients supported with extracorporeal membrane oxygenation, and who develop heparin-induced thrombocytopenia, there is no clear evidence to support changing to a non-heparin-coated extracorporeal membrane oxygenation circuit. Our goal was to evaluate clinical outcomes of patients who were continued on heparin-bonded circuits despite diagnosed heparin-induced thrombocytopenia. Methods: We completed a single-center retrospective study of all patients who underwent extracorporeal membrane oxygenation support from July 2008 to July 2017 and were tested heparin-induced thrombocytopenia positive while on extracorporeal membrane oxygenation support. After diagnosis of heparin-induced thrombocytopenia, mean platelet count (k/µL) was measured on consecutive days for 14 days. Results: Out of 455 patients, 14 (3.1%) had a diagnosis of heparin-induced thrombocytopenia by serotonin release assay and systemic heparin treatment was discontinued in every case. In total, 11 of the heparin-induced thrombocytopenia patients (78.6%) survived to discharge. The overall survival of all 455 extracorporeal membrane oxygenation patients was 54.1%. Platelets counts after discontinuation of systemic heparin in the heparin-induced thrombocytopenia patients increased from a mean of 59.8 k/µL at time of heparin-induced thrombocytopenia diagnosis to a mean of 280.2 k/µL at 14 days after discontinuation of heparin despite continuation of the heparin-bonded circuit. Platelet count increased in heparin-induced thrombocytopenia patients on extracorporeal membrane oxygenation support after discontinuation of systemic heparin even if maintained on the heparin-bonded circuit. Conclusion: Discontinuation of systemic heparin but continuation of heparin-coated extracorporeal membrane oxygenation circuits appeared to be an appropriate response for our extracorporeal membrane oxygenation–supported patients who developed heparin-induced thrombocytopenia. Survival in this group was not significantly different to those patients on extracorporeal membrane oxygenation without heparin-induced thrombocytopenia. Larger studies should evaluate the safety of heparin-bonded extracorporeal membrane oxygenation systems in heparin-induced thrombocytopenia patients.

2017 ◽  
Vol 24 (6) ◽  
pp. 944-949 ◽  
Author(s):  
Shinya Motohashi ◽  
Takefumi Matsuo ◽  
Hidenori Inoue ◽  
Makoto Kaneko ◽  
Shunya Shindo

Heparin-induced thrombocytopenia (HIT) is one of the serious complications in patients who undergo cardiac surgery. However, there remains a major problem in diagnosing HIT because the current immunological assays for detection of HIT antibody have limitations. Furthermore, the clinical course of thrombocytopenia in this surgery makes it increasingly difficult to diagnose HIT. We investigated the relationship between platelet count and HIT antibody in 59 patients who underwent cardiac surgery using cardiopulmonary bypass (CPB). The number of postoperative HIT antibody-positive patients evaluated using enzyme-linked immunosorbent assay kit (polyanion IgG/IgA/IgM complex antibodies/antiplatelet factor 4 enhanced) was 37 (62.7%). In contrast, platelet activation by HIT antibody was evaluated using the serotonin release assay (SRA). More than 20% and 50% release of serotonin was obtained from 12 patients (20.3%) and 8 patients (13.6%), respectively. The levels of d-dimer were significantly different on postoperative day 14 between SRA-positive and SRA-negative groups; however, postoperative thrombus complication was not detected using sonography in the patients with positive serotonin release at all. After being decreased by the operation, their platelet count recovered within 2 weeks in both groups equally. In our study, although the patients were positive in the platelet activating HIT antibody assay, they remained free from thrombosis and their platelet count recovered after early postoperative platelet decrease. Therefore, in addition to the SRA, monitoring of platelet count might be still considered an indispensable factor to facilitate the prediction of HIT thrombosis prior to manifestation in the patients undergoing cardiac surgery using CPB.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tia C Kohs ◽  
Vikram Raghunathan ◽  
Patricia Liu ◽  
Ramin Amirsoltani ◽  
Michael Oakes ◽  
...  

Introduction: Extracorporeal membrane oxygenation (ECMO) is used to provide circulatory support and facilitate gas exchange via cardiopulmonary bypass. The relationship between ECMO and the incidence of severe thrombocytopenia (platelet count <50 x 10 9 /L) and subsequent clinical consequences are ill defined. We aimed to identify the risk factors for the development of thrombocytopenia and its clinical implications. Methods: This is a single-center retrospective cohort study of adults who received venoarterial (VA) ECMO. We examined consecutive platelet counts while on ECMO. Univariate logistic regression was used to determine if mean platelet count, platelet count range, or severe thrombocytopenia were predictors of overall survival, hemorrhage and thrombosis. A multivariate logistic regression model was used to identify factors that contribute to the development of the aforementioned patient outcomes. Results: In our cohort, 33 patients were included with a mean age of 55 years and duration of ECMO of 5.9 days. All patients received heparin, 33.3% received antiplatelet therapy and 45.5% developed severe thrombocytopenia. In univariate, analysis the development of severe thrombocytopenia increased the odds of major bleeding by 450% (OR 5.500, 95% CI 1.219 - 24.813, P -value 0.027), and the odds of surviving hospitalization decreased 84.1% (OR 0.159, 95% CI 0.033 - 0.773, P -value 0.023). Multivariate logistic regression controlling for additional clinical variables found no significant association between the development of severe thrombocytopenia and rates of thrombosis, hemorrhage, or overall survival. Platelet count decreased over time while on ECMO. Conclusions: Nearly half of the patients requiring VA-ECMO developed severe thrombocytopenia, which was associated with an increased risk of hemorrhage and in-hospital mortality. Additional studies are required to clarify the clinical implications of severe thrombocytopenia in ECMO patients.


Perfusion ◽  
2019 ◽  
Vol 35 (5) ◽  
pp. 378-383 ◽  
Author(s):  
Jaclyn Sullivan ◽  
Erica Bak ◽  
Mary Jane Sullivan ◽  
Payal K. Gurnani

There are currently no scoring tools validated for use in predicting heparin-induced thrombocytopenia in patients receiving extracorporeal membrane oxygenation. This study aims to determine the predictive value of the Warkentin 4T score, Lilo-Le Louet score, and the heparin-induced thrombocytopenia expert probability score in detecting heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation. This was a single center, retrospective, observational cohort study of patients at Rush University Medical Center. Heparin-induced thrombocytopenia–positive patients were defined as those with an optical density greater than or equal to 0.4, consistent with a positive anti-platelet 4 heparin antibody. Out of 39 patients on extracorporeal membrane oxygenation with suspected heparin-induced thrombocytopenia, six (15.4%) were found to be anti-platelet 4–positive. A heparin-induced thrombocytopenia diagnosis was confirmed by serotonin-release assay in two patients (5.1%). The 4T, heparin-induced thrombocytopenia expert probability, and Lilo-Le Louet scoring tools all demonstrated a low positive predictive value (21.4%, 16.7%, and 6.7%, respectively), with the 4T and heparin-induced thrombocytopenia expert probability scores demonstrating the highest specificity (66.7% and 84.8%, respectively) and lowest sensitivity (50% and 16.7%, respectively). The Lilo-Le Louet score had high sensitivity (100%) and low specificity (12.5%) in post-cardiopulmonary bypass patients. Based on the findings of this study, all three scoring tools have limited utility for predicting heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation.


2019 ◽  
Vol 119 (07) ◽  
pp. 1138-1146 ◽  
Author(s):  
Caroline Vayne ◽  
Marc-Antoine May ◽  
Thierry Bourguignon ◽  
Eric Lemoine ◽  
Eve-Anne Guery ◽  
...  

Introduction/Objectives Extracorporeal membrane oxygenation (ECMO) provides circulatory support in patients with severe heart failure, but the frequent use of unfractionated heparin exposes patients to high risk of heparin-induced thrombocytopenia (HIT). We prospectively evaluated the development and clinical impact of platelet factor 4 (PF4)-specific antibodies (Abs) during ECMO and whether specific biological characteristics could predict HIT. Materials and Methods From 2014 to 2018, we studied 57 adults who underwent an ECMO for at least 5 days. The plasma samples collected daily were tested for PF4-specific Abs using immunoassays to detect immunoglobulin (Ig) G, A, and M isotypes or only IgG. Serotonin release assay was performed without and with PF4 to detect pathogenic Abs. Results Twenty-nine patients (50%) were positive for PF4-specific Abs (IgG, A, M), with IgG in 17/57 (30%) and 16 of them (94%) were immunized within 10 days. PF4-specific IgG Abs did not affect the clinical or biological course of most patients. HIT was suspected in only two patients with ECMO circuit dysfunction and unexpected platelet count decrease after day 5. High levels of PF4-specific IgG were detected in both patients, and HIT was confirmed by a serotonin release assay, which was also more sensitive when exogenous PF4 was present. Conclusion PF4-specific Abs are common during ECMO but are mostly non-pathogenic and not associated with a less favorable prognosis. However, an abnormal platelet count evolution, in particular if associated with ECMO circuit dysfunction, should prompt the search for pathogenic PF4-specific IgG.


1998 ◽  
Vol 79 (03) ◽  
pp. 523-528 ◽  
Author(s):  
Raphaël Saffroy ◽  
Dominique Lasne ◽  
Gilles Chatellier ◽  
Martine Aiach ◽  
Francine Rendu ◽  
...  

SummaryHeparin-induced thrombocytopenia (HIT) involves heparin-dependent antibodies which induce platelet activation. In the present study, we searched for a relationship between the polymorphism of the Fc receptor (FcγRIIa) and the development of HIT. In this purpose, all the donors were genotyped for their FcγRIIA and HIT patients were selected on the basis of at least one positive answer by 14C-serotonin release assay (SRA). The frequency distribution of the FcγRIIa polymorphism in the HIT patient group was similar to that observed in the healthy control group. Moreover, a statistical analysis taking into account our results and those of 3 previously published studies, suggested at most only a weak association between HIT and the FcγRIIa-131 polymorphism.Laboratory tests used to diagnose HIT rely on the activation of normal donor platelets but fail to detect every HIT positive patient. We determined the role of FcγRIIa-131 polymorphism on the reactivity of control platelets to HIT plasmas. When control platelet FcγRIIa-131 was of Arg/Arg form, only 47% of the HIT plasmas were positive by SRA, compared to 81% and 74% for His/His or His/Arg forms, respectively. We also compared the level of anti PF4/heparin antibodies in the HIT plasmas with the response obtained by SRA. The mean anti PF4/heparin antibodies level in HIT plasma was significantly lower in negative SRA than in positive tests when using control platelets from FcγRIIa-Arg/Arg131 and heterozygous donors. Thus, the variability of control platelets to respond to HIT plasmas in the SRA test is related to both the FcγRIIa-131 polymorphism, and to the amount of anti PF4/heparin antibodies.


Author(s):  
P Malla

Background: This is the first report of Heparin induced thrombocytopenia (HIT) presenting as bilateral carotid thrombi and multiple cerebral infarcts. Methods: 54 year old woman presented with sudden onset of right arm numbness and weakness two days after discharge from hospital. During her hospitalization 9 days prior, she underwent colovesicular fistula repair, received heparin subcutaneously for DVT prophylaxis and had normal platelet counts. Results: On this admission, MRI Brain showed scattered multiple acute infarcts within the cortex of bilateral cerebral hemispheres. CT angiography head /neck showed non-occlusive thrombi at the carotid bifurcations bilaterally. Platelet count on admission was 267 K/uL q which decreased to 125 K/uL the next day, after which heparin was started for the carotid thrombi. The platelet count rapidly decreased further to 79 K/uL leading to suspicion for HIT and switching to Argatroban. HIT and serotonin release assay were positive confirming the diagnosis of HIT. CT chest and tranthoracic echocardiogram was normal. Venous Duplex of bilateral upper and lower extremities were negative for DVTs.Hypercoaguable evaluation was negative. Conclusions: This case highlights the importance of identifying HIT as a cause of arterial thrombosis and stroke even with normal platelet counts in the clinical setting of recent heparin use.


2005 ◽  
Vol 10 (1) ◽  
pp. 26-35
Author(s):  
Marcia L. Buck

The use of extracorporeal membrane oxygenation (ECMO) requires maintaining a delicate balance between the prevention of thrombosis and the avoidance of hemorrhage. Anticoagulation is necessary to maintain circuit flow. It counteracts the activation of clotting mechanisms that occurs as a result of the interaction between circulating blood and the foreign surfaces of the ECMO equipment as well as endothelial damage within the vasculature. Heparin remains the anticoagulant of choice; however, the difficulty in adjusting dosages and the risk of developing heparin-induced thrombocytopenia have led to the use of alternative therapies such as argatroban and lepirudin. In addition, thrombolysis with alteplase is now being used in patients who develop clots despite anticoagulation. Aminocaproic acid has been used for more than a decade to manage or prevent hemorrhage in patients on ECMO, but a new report suggests that activated recombinant factor VII may also be useful as a hemostatic agent. Over the next decade, it is likely that the role of these newer agents will grow, making them important tools in the management of patients on ECMO.


2020 ◽  
Vol 8 ◽  
pp. 232470962094409 ◽  
Author(s):  
Prasanth Lingamaneni ◽  
Sriram Gonakoti ◽  
Krishna Moturi ◽  
Ishaan Vohra ◽  
Maryam Zia

COVID-19 (coronavirus disease-2019) infection is a highly prothrombotic state, resulting from a dysregulation of the coagulation cascade. Therefore, thromboprophylaxis is strongly recommended in these patients, with some experts even advocating for therapeutic dosing to prevent thromboembolic events. Heparin-induced thrombocytopenia (HIT) is a well-known complication of heparin therapy. In this article, we report a case of HIT in a patient with COVID-19. A 63-year-old male presented with 1 week of dry cough and diarrhea. He had a positive nasopharyngeal COVID-19 reverse-transcriptase–polymerase chain reaction. On admission, the platelet count and liver function tests were within normal limits. During his hospitalization, he developed a right femoral deep venous thrombosis and was started on therapeutic anticoagulation. Due to worsening respiratory failure, he was intubated and mechanically ventilated. Between days 11 and 12 of hospitalization, platelet count dropped from 304 000 to 96 000 cells/µL. He had a high pretest probability for HIT with a 4T score of 6 and a positive anti-PF4/heparin antibody. Heparin drip was discontinued and was switched to argatroban. The serotonin release assay eventually returned positive, which confirmed the diagnosis of HIT. We also discuss potential overdiagnosis of HIT in COVID-19 through 4 cases with false-positive HIT antibodies.


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