"Spontaneous" Heparin-Induced Thrombocytopenia and Thrombosis After Total Knee Arthroplasty: A Report of 2 Cases.
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ABSTRACT:
SUBMITTER: Olevsky OM
PROVIDER: S-EPMC8121995 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Heparin-induced thrombocytopenia syndrome is an acquired potentially life-threatening prothrombotic disorder caused by antibodies that recognize complexes of platelet factor 4 bound to heparin or heparin-like molecules. It typically occurs after exposure to unfractionated heparin, to a lesser extent after exposure to low-molecular-weight heparins, and rarely after exposure to fondaparinux. Herein, we report the case of a 48-year-old woman who developed severe thrombocytopenia, bilateral pulmonary embolism, and bilateral adrenal hemorrhages after total knee arthroplasty without evidence of heparin exposure. Antibodies to the heparin-platelet factor 4 complex and serotonin-release assay were positive. Spontaneous heparin-induced thrombocytopenia syndrome should be considered in patients with unexplained thrombocytopenia after knee replacement surgery even without heparin exposure, and a high index of suspicion for adrenal hemorrhage is needed in patients with fever, abdominal pain, and shock.
| S-EPMC4956682 | biostudies-literature
Project description:Background:Heparin-induced thrombocytopenia (HIT) typically responds to heparin termination. Some types of HIT can persist after heparin discontinuation. Case summary:A 95-year-old woman was referred to the cardiology from orthopaedics because of acute limb ischaemia (ALI) 1?day after surgery of a femoral neck fracture. Despite thrombectomy, ALI relapsed the next day. She had been treated with intravenous antibiotics with a diagnosis of aspiration pneumonia for 1?week until 3?days before surgery, together with heparin flush twice a day. Of note, no intra-/post-operative heparin was administered, no cell salvage device, central venous, nor arterial catheters were used before development of ALI. The patient and her family refused reattempting invasive therapies; consequently, the patient continued to worsen and died on post-operative day 3. Diagnosis of autoimmune HIT, which was prompted by surgery without re-exposure to heparin, was confirmed posthumously. Discussion:This case emphasizes the significance of suspecting autoimmune HIT in any patient presenting with thrombosis, even if the heparin exposure dates back more than a few days or even without heparin exposure.
| S-EPMC7180709 | biostudies-literature
Project description:BackgroundHeparin-induced thrombocytopenia (HIT) is a rare complication of heparin therapy. Its pathogenesis includes thrombotic events that can rarely affect the coronary arteries.Case summaryWe report a 67-year-old woman who presented with extensive lower extremities deep venous thrombosis. After being treated with heparin, she developed an ST-elevation myocardial infarction secondary to an acute thrombus formation. The patient's platelets dropped within 6 days from the procedure and her heparin-PF4 IgG antibody and serotonin release assay were positive confirming the diagnosis of HIT.DiscussionProthrombotic states, such as HIT, are associated with increased risk for coronary thrombosis and ischaemia. Heparin-induced thrombocytopenia can cause coronary complications usually in previously disrupted coronary vessels and bypass grafts. Here, we demonstrate that spontaneous thrombosis can occur in a previously untreated native coronary artery in a patient with HIT.
| S-EPMC6426051 | biostudies-literature
Project description:Background:Total knee arthroplasty (TKA) in the setting of a prior contralateral above-knee amputation (AKA) represents a rare scenario with limited reported outcomes. As such, it is difficult for surgeons to effectively counsel these patients relative to risks and expected outcomes after TKA. We report outcomes for a series of 10 such patients. Methods:We retrospectively reviewed all patients at our institution from 2005 to 2018 who underwent a primary TKA and prior contralateral AKA and had a minimum 12-month follow-up. Data regarding complications, ambulatory status, reported pain, patient demographics, length of follow-up, and comorbidities were obtained. Results:Ten patients met criteria. Follow-up ranged from 1 to 8 years. Six reported no pain or improved pain with weight-bearing. Ambulatory status worsened for 5 patients, remained unchanged for 3, and improved for 2. Five patients had significant postoperative complications: infection requiring repeat surgery (3), quadriceps tendon rupture (1), and revision for implant failure and instability (1). Patients in this cohort had a median of 3 medical comorbidities known to affect postoperative outcomes and complication rates. Conclusions:While a contralateral AKA is not an absolute contraindication to TKA, these results should influence patient counseling. Most of our cohort benefited from improved pain, but only 2 of 10 had improved ambulation and half had significant complications. Medical comorbidities may have contributed to these complications. Surgeons contemplating TKA in this situation might consider modified postoperative recovery protocols and aggressive preoperative optimization of medical comorbidities to lower the risk of complication in this high-risk population.
| S-EPMC7476212 | biostudies-literature
Project description:Ischaemic preconditioning is a method of protecting tissue against ischaemia-reperfusion injury. It is an innate protective mechanism that increases a tissue's tolerance to prolonged ischaemia when it is first subjected to short burst of ischaemia and reperfusion. It is thought to provide this protection by increasing the tissue's tolerance to ischaemia, therby reducing oxidative stress, inflammation and apoptosis in the preconditioned tissue. We used microarrays to investigate the genomic response induced by ischaemic preconditioning in muscle biopsies taken from the operative leg of total knee arthroplasty patients in order to gain insight into the ischaemic preconditioning mechanism. Patients undergoing primary knee arthroplasty were randomised to control and treatment (ischaemic preconditioning) groups. Patients in the treatment group received a preconditioning stimulus immediately prior to surgery. The ischaemic preconditioning stimulus consisted of three five-minute periods of tourniquet insufflation on the lower operative limb, interrupted by five minute periods of reperfusion. All patients had a tourniquet applied to the lower limb after the administration of spinal anaesthesia, as per normal protocol for knee arthroplasty surgery. Muscle biopsies were taken from the quadriceps muscle of the operative knee at the immediate onset of surgery (T0) and at 1 hour into surgery (T1). Total RNA was extracted from biospies of four control and four treatment patients and hybridised to the Affymetrix Human U133 2.0 chip.
2010-04-12 | E-GEOD-21164 | biostudies-arrayexpress
Project description:Background and purpose - The number of primary, highly constrained knee arthroplasty implants has increased with a theoretically increased risk of early failure. Therefore we analyzed the risk of all revision following total knee arthroplasty (TKA) in patients receiving a hinged or condylar constrained knee (CCK) compared with a conventional unconstrained TKA. Patients and methods - The analyses included 401 primary highly constrained or hinged implants from 1994 to 2017. Kaplan-Meier survival curves were used to evaluate time to first revision with a maximum follow-up of 20 years. Cox regression was used to calculate hazard ratio (HR) comparing condylar constrained knee (CCK), hinged, and unconstrained TKA. Results - Kaplan-Meier estimated prosthesis survival after 2 years was 94.8% (95% CI 91.4-98.2) and 93.5% after 5 years for the primary CCK and 91.0% (CI 86.6-95.4) after 2 years and 85.5% after 5 years for the primary hinged TKA. Adjusted for sex, age groups, diagnosis, time period, previous surgery, and surgery time HR was 1.4 (CI 0.8-2.3) for the CCK and 2.4 (CI 1.6-3.7) for the hinged implants. The most common cause of revision in hinged implants was infection: 14 of 22 revisions. When excluding infection as revision cause, there were no differences in survival between the implant types. Estimated survival excluding infection revisions at 5 years was 96% for unconstrained, CCK, and hinged primary TKA implants. Interpretation - Primary rotating hinge total knee arthroplasty had a higher risk of revision compared with conventional TKA after 2 and 5 years' follow-up. Infection was the most common cause of revision. When excluding infection revisions from the survival analysis, hinged and CCK implants had similar performance to unconstrained TKA.
| S-EPMC6746286 | biostudies-literature
Project description:Ischaemic preconditioning is a method of protecting tissue against ischaemia-reperfusion injury. It is an innate protective mechanism that increases a tissue's tolerance to prolonged ischaemia when it is first subjected to short burst of ischaemia and reperfusion. It is thought to provide this protection by increasing the tissue's tolerance to ischaemia, therby reducing oxidative stress, inflammation and apoptosis in the preconditioned tissue. We used microarrays to investigate the genomic response induced by ischaemic preconditioning in muscle biopsies taken from the operative leg of total knee arthroplasty patients in order to gain insight into the ischaemic preconditioning mechanism.
2010-04-02 | GSE21164 | GEO
Project description:This study investigates the relationship between intraoperative extreme flexion and tibia-femoral dislocation during total knee arthroplasty on the prevalence of postoperative deep venous thrombosis. Knees were randomized into two groups. The control group underwent the procedure according to normal protocol, which kept the knee in extreme flexion and maintained dislocation for the duration of the exposure, whereas the variable group underwent the procedure modified to minimize the total amount of time the knee was hyperflexed and dislocated. Venograms were positive in 42% (39/92) of the control knees and 38% (30/79) of the modified group (p = 0.6). Proximal deep venous thrombosis were found in 12% (11/92) of the control knees and in 16% (13/79) of the modified knees (p = 0.4). No statistical difference could be detected between the two techniques in regards to the incidence of deep venous thrombosis.
| S-EPMC2488169 | biostudies-other
Project description:Heparin-induced thrombocytopenia (HIT) is associated with severe and potentially lethal thrombotic complications. NETosis was recently shown to be an important driver of thrombosis in HIT. We investigated the role of reactive oxygen species (ROS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and their contributions to thrombus development in HIT. We showed that neutrophil activation by HIT immune complexes induced ROS-dependent NETosis. Analysis of thrombi formed in a microfluidics system showed ROS production in both platelets and neutrophils, and abundant neutrophil extracellular traps (NETs) and ROS distributed throughout the clot. Neutrophil-targeted ROS inhibition was sufficient to block HIT-induced NETosis and thrombosis using human blood. Inhibition of NOX2 with diphenyleneiodonium chloride or GSK2795039 abrogated HIT-induced thrombi in vivo using FcγRIIa+/hPF4+-transgenic mice. Thrombocytopenia in mice remained unaffected by ROS inhibition. Increased ROS production in activated neutrophils was also confirmed using fresh blood from patients with active HIT. Our findings show that ROS and NOX2 play a crucial role in NETosis and thrombosis in HIT. This enhances our understanding of the processes driving thrombosis in HIT and identifies NOX2 as a potential new therapeutic target for antithrombotic treatment of HIT.
| S-EPMC9153028 | biostudies-literature
Project description:Heparin-induced thrombocytopenia/thrombosis (HIT) is a serious immune reaction to heparins, characterized by thrombocytopenia and often severe thrombosis with high morbidity and mortality. HIT is mediated by IgG antibodies against heparin/platelet factor 4 antigenic complexes. These complexes are thought to activate platelets leading to thrombocytopenia and thrombosis. Here we show that HIT immune complexes induce NETosis via interaction with FcγRIIa on neutrophils and through neutrophil-platelet association. HIT immune complexes induce formation of thrombi containing neutrophils, extracellular DNA, citrullinated histone H3 and platelets in a microfluidics system and in vivo, while neutrophil depletion abolishes thrombus formation. Absence of PAD4 or PAD4 inhibition with GSK484 abrogates thrombus formation but not thrombocytopenia, suggesting they are induced by separate mechanisms. NETs markers and neutrophils undergoing NETosis are present in HIT patients. Our findings demonstrating the involvement of NETosis in thrombosis will modify the current concept of HIT pathogenesis and may lead to new therapeutic strategies.
| S-EPMC6428879 | biostudies-literature