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

Abstract

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 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.

Snake envenomation: not your average acute kidney injury

“…1 TMA occurs in 9% of snake envenomation in Australia, occurring only in the subset of patients who develop VICC. 2 This case was a severe example, with the degree of AKI, thrombocytopenia and anaemia being much outside the medians reported by a recent Australian series of snake envenomation with 104 cases of TMA. 2 The series reported a median creatinine of 362 μmol/L, nadir haemoglobin of 95 g/L and nadir platelet count of 55 Â 10 9 /L.…”

“…2 This case was a severe example, with the degree of AKI, thrombocytopenia and anaemia being much outside the medians reported by a recent Australian series of snake envenomation with 104 cases of TMA. 2 The series reported a median creatinine of 362 μmol/L, nadir haemoglobin of 95 g/L and nadir platelet count of 55 Â 10 9 /L. 2 AKI occurred in 94% cases of TMA, of which 34% required dialysis.…”

“…2 The series reported a median creatinine of 362 μmol/L, nadir haemoglobin of 95 g/L and nadir platelet count of 55 Â 10 9 /L. 2 AKI occurred in 94% cases of TMA, of which 34% required dialysis. 2 All patients were independent of dialysis at 90 days, with 52% having residual stage 3 or 4 CKD.…”

A review of 91 canine and feline red‐bellied black snake (Pseudechis porphyriacus) envenomation cases and lessons for improved management

“…It is interesting to note that the fatal complications documented in these cases do not seem to occur in people where the RBBS toxidrome is limited to a localised bite-site reaction, subclinical coagulopathy and occasional myotoxicity. 23,27 Reasons for this are unclear but may include physiological and/or behavioural differences between species (e.g. dogs may fight back and get bitten multiple times, whereas humans may retreat immediately following the first bite).…”

The Unusual Metalloprotease-Rich Venom Proteome of the Australian Elapid Snake Hoplocephalus stephensii

“…The toxin responsible for in vitro post-synaptic neurotoxic activity is a short-chain three-finger toxin (3FTx), with a molecular mass of 6.66 kDa and has been named Hostoxin-1 [ 16 ]. The main clinical feature of bites by H. stephensii is venom-induced consumption coagulopathy (VICC), and rarely thrombotic microangiopathy, but not neurotoxicity or myotoxicity [ 17 , 18 ].…”