Department of Neurological Surgery, Mayo Clinic, Rochester, MN, USA.
Mayo Clinic Alix School of Medicine, Rochester, MN, USA.
J Thromb Thrombolysis. 2021 Oct;52(3):952-961. doi: 10.1007/s11239-021-02484-6. Epub 2021 Jun 5.
Heparin-induced thrombocytopenia (HIT) causes thrombosis and thrombocytopenia, usually due to prior heparin exposure, so-called classical HIT. However, in the autoimmune form, the signs and symptoms of HIT occur without prior heparin exposure. Development of cerebral venous sinus thrombosis (CVST) secondary to HIT is a rare occurrence, with relatively few reports in the literature. There is a need to better understand the clinical presentation and treatment paradigms in these rare cases. Therefore, we present the first systematic review of CVST occurring in classical and autoimmune HIT. Cases of HIT-induced CVST were identified through a systematic search of Pubmed from the date of inception to March 2021. Literature search revealed 21 cases of HIT and associated CVST with six cases (28.6%) of autoimmune HIT. Patients presented with signs and symptoms consistent with increased intracranial pressure, intracerebral hemorrhage (ICH), and/or focal neurologic deficits. Headache was the most common symptom with 12 patients (60.0%) presenting as such. 10 patients (47.6%) included in the study developed ICH. Non-heparin anticoagulants, especially direct thrombin inhibitors, were the first-line treatment for the majority of patients (55.6%). Intravenous immunoglobulin (IVIG) was used as treatment for select patients (16.7%) with autoimmune HIT. Few patients received surgical intervention for CVST (14.3%) or ICH (30.0%). Four patients had a full recovery, four patients had residual deficits, and seven patients ultimately expired. Symptoms of HIT-induced CVST are often related to CNS dysfunction. Non-heparin anticoagulants are important to treat CVST, even when patients have concomitant ICH, and may be supplemented with IVIG if treating autoimmune HIT. Rapid identification and treatment of HIT-induced CVST is imperative in order to prevent morbidity and mortality.
肝素诱导的血小板减少症(HIT)可导致血栓形成和血小板减少症,通常是由于先前暴露于肝素,即所谓的经典型 HIT。然而,在自身免疫形式中,HIT 的体征和症状发生在没有先前肝素暴露的情况下。继发于 HIT 的脑静脉窦血栓形成(CVST)是一种罕见的情况,文献中的报道相对较少。需要更好地了解这些罕见病例的临床表现和治疗方案。因此,我们对经典型和自身免疫型 HIT 中发生的 CVST 进行了首次系统综述。通过对 Pubmed 从成立日期到 2021 年 3 月的系统搜索,确定了 HIT 引起的 CVST 病例。文献检索显示有 21 例 HIT 伴 CVST,其中 6 例(28.6%)为自身免疫性 HIT。患者表现出与颅内压升高、脑出血(ICH)和/或局灶性神经功能缺损一致的体征和症状。头痛是最常见的症状,有 12 例患者(60.0%)表现为头痛。研究中有 10 例患者(47.6%)发生 ICH。大多数患者(55.6%)的一线治疗是非肝素抗凝剂,特别是直接凝血酶抑制剂。静脉注射免疫球蛋白(IVIG)被用于治疗部分自身免疫性 HIT 患者(16.7%)。少数患者(14.3%)接受了 CVST 或 ICH(30.0%)的手术干预。4 名患者完全康复,4 名患者留有残余缺陷,7 名患者最终死亡。HIT 引起的 CVST 的症状通常与中枢神经系统功能障碍有关。非肝素抗凝剂对治疗 CVST 很重要,即使患者同时伴有 ICH,并且如果治疗自身免疫性 HIT,可能需要补充 IVIG。快速识别和治疗 HIT 引起的 CVST 对于预防发病率和死亡率至关重要。