4.3 Article

Snakebite-associated thrombotic microangiopathy: an Australian prospective cohort study [ASP30]

期刊

CLINICAL TOXICOLOGY
卷 60, 期 2, 页码 205-213

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/15563650.2021.1948559

关键词

Snakes; thrombotic microangiopathies; acute kidney injury; hemolysis; schistocytes

资金

  1. National Health and Medical Research Council (NHMRC) [1154503]
  2. NHMRC Clinical Centre for Research Excellence [1110343]
  3. Menzies School of Health Research
  4. Charles Darwin University
  5. National Health and Medical Research Council of Australia [1154503, 1110343] Funding Source: NHMRC

向作者/读者索取更多资源

Snakebite-associated thrombotic microangiopathy (TMA) is characterized by anemia with schistocytosis and thrombocytopenia or >25% drop in platelet count. Most TMA patients develop acute kidney injury (AKI), with a subset requiring dialysis, and long-term risk of chronic kidney disease (CKD) is present for half of the cases. Therapeutic plasma-exchange (TPE) did not show benefit in TMA cases with dialysis-dependent AKI.
Background Snakebite-associated thrombotic microangiopathy (TMA) occurs in a subset of patients with venom-induced consumption coagulopathy (VICC) following snakebite. Acute kidney injury (AKI) is the commonest end-organ manifestation of TMA. The epidemiology, diagnostic features, outcomes, and effectiveness of interventions including therapeutic plasma-exchange (TPE), in snakebite-associated TMA are poorly understood. Methods We reviewed all patients with suspected or confirmed snakebite recruited to the Australian Snakebite Project (2004-2018 inclusive), a prospective cohort study, from 202 participating Australian hospitals across the country. TMA was defined as anemia with schistocytosis. Results 2069 patients with suspected snakebite were enrolled, with 1158 (56.0%) systemically envenomed, of which 842 (72.7%) developed VICC, from which 104 (12.4%) developed TMA. Of those systemically envenomed, TMA occurred in 26% (13/50) taipan, 17% (60/351) brown, and 8% (16/197) tiger snakebites. Thrombocytopenia was present in 90% (94/104) of TMA cases, and a further eight (8%) had a > 25% decrease in platelets from the presentation. Patients with TMA were significantly older than non-TMA patients with VICC (53 [35-61] versus 41 [24-55] years, median [IQR], p < 0.0001). AKI developed in 94% (98/104) of TMA patients, with 34% (33/98) requiring dialysis (D-AKI). There were four deaths. In D-AKI TMA cases, eventual dialysis-free survival (DFS) was 97% (32/33). TPE was used in five D-AKI cases, with no significant difference in DFS or time to independence from dialysis. >90-day follow-up for 25 D-AKI cases (130 person-years) showed no end-stage kidney disease but 52% (13/25) had >= stage 3 chronic kidney disease (CKD). Conclusion Our findings support a definition of snakebite-associated TMA as anemia with schistocytosis and either thrombocytopenia or >25% drop in platelet count. AKI occurring with snakebite-associated TMA varied in severity, with most achieving DFS, but with a risk of long-term CKD in half. We found no evidence of benefit for TPE in D-AKI.

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