Delayed onset of myotoxicity following red-bellied black snake envenoming: a case report

Abstract

Background

Myotoxicity is an important and recognized effect of red-bellied black snake envenoming that remains poorly understood but can result in severe illness. Prior observational data have shown that myotoxicity develops less frequently and later than other envenoming effects, including systemic symptoms and anticoagulant coagulopathy, which are likely to coexist in an envenomed victim. Current recommendations for managing snake bite victims in Australia include serial clinical and laboratory assessments for envenoming for at least 12 hours post-bite.

Case presentation

We report the case of an 18-year-old white male individual with red-bellied black snake envenoming who developed delayed-onset myotoxicity. His symptoms included abdominal pain, vomiting, and generalized myalgias. Myotoxicity occurred after the standard 12-hour post-bite observation period, with serum creatine kinase remaining less than 1000 U/L at 17.5 hours post-bite before increasing to a peak of 93,790 U/L at 57 hours post-bite. He developed myalgia and myoglobinuria at 22 hours post-bite without associated renal impairment. He did not receive antivenom. He was treated with intravenous fluids and was discharged on day 4 with declining creatine kinase levels and made a full recovery.

Conclusion

Our case of red-bellied black snake envenoming with delayed-onset myotoxicity was managed successfully without antivenom. Cases of delayed myotoxicity may warrant prolonged observation with supportive care.

Background

Myotoxicity is a recognized but poorly understood effect of red-bellied black snake (Pseudechis porphyriacus) envenoming, which can result in severe illness [1]. The onset of myotoxicity may be delayed well beyond other clinical or laboratory features of envenoming, including after standard observation recommendations for snake bite victims in Australia, which include serial laboratory and clinical evaluations for envenoming [2–4]. We report a case of red-bellied black snake envenoming with delayed-onset myotoxicity.

Case presentation

An 18-year-old caucasian male presented after a red-bellied black snake bite to his lower leg while bushwalking in Western Sydney, Australia. He had no preexisting medical conditions. The snake was visually identified by the victim and bystanders. He presented to the emergency department by private transport 90 minutes after the bite, with a visible bite mark on his right lower leg (Fig. 1). A pressure bandage was applied to the entire lower limb and the limb immobilized. At presentation, he had no symptoms, including no bite-site pain or myalgia. On clinical assessment, he had no features of bleeding, neurotoxicity, or cardiovascular compromise. Laboratory investigations were performed periodically in accordance with Australian protocols at presentation up to 12 hours after the bite, then subsequently as dictated by clinical need [3, 4]. At 9 hours after the bite, the patient developed nausea and abdominal pain. At 22 hours after the bite, he reported myalgias in his arms and legs and developed myoglobinuria (Fig. 2). The relevant pathology results are shown in Figs. 3, 4, and 5. The activated partial thromboplastin time (aPTT) was prolonged above the reference range at 4 hours after the bite. Myotoxicity is typically defined with a peak serum creatine kinase (CK) level > 1000 U/L, and at 17.5 hours after the bite, CK remained below this threshold [4]. At 26 hours after the bite, the CK increased to 8851 U/L, peaking at a level of 93,790 U/L at 57 hours. Renal function remained normal, with an estimated glomerular filtration rate (eGFR) > 90 mL/minute/1.73 m². Antivenom was not administered. The patient was admitted to hospital and treated with intravenous fluids. He was discharged home on day 4 with declining CK levels and improving myalgia and made a full recovery with resolution of symptoms 1 week post-bite.

Fig. 1.

Bite site on right lower leg

Fig. 2.

Urine specimen at 24 hours post-bite, demonstrating myoglobinuria

Fig. 3.

Creatine kinase levels

Fig. 4.

Activated partial thromboplastin time levels

Fig. 5.

International normalized ratio levels

Discussion

The red-bellied black snake is a common cause of snake bite in Australia, particularly on the south-east coast. Myotoxicity is a recognized effect of red-bellied black snake envenoming that occurs in approximately 20% of reported cases [5]. More common effects include local envenoming (in 96%), systemic symptoms (in 95%), and an anticoagulant coagulopathy with elevated aPTT (in 61%). Myotoxicity generally develops more slowly than other venom effects and lasts up to 7 days post-bite. The Australian Snakebite Project (ASP-11) reported that the occurrence of myotoxicity was associated with increased length of hospital stay (3 days versus 21 hours without myotoxicity), with a small number of victims requiring intensive care unit admission owing to muscle weakness. A prospective cohort study of Australian snake bite victims with envenoming confirmed by serum venom analysis observed that CK levels generally begin to rise at 2–12 hours, peak at 1–3 days, and decline after 3–5 days [6]. Our case is consistent with these data, as CK levels did not surpass 1000 U/L until well beyond 12 hours post-bite.

As per current snakebite guidelines, envenoming is generally considered to be excluded if no clinical or laboratory evidence is observed after 12 hours post-bite. In practice, additional features of envenoming, including systemic symptoms and anticoagulant coagulopathy, occur more commonly than myotoxicity and are likely to be simultaneously present, reducing the risk of missed envenoming. Our patient developed a mild elevation in aPTT during this period, and while this may have been an early sign of envenoming, myotoxicity did not develop until well after 12 hours post-bite. Antivenom was not administered as systemic symptoms and myotoxicity developed in a delayed fashion [7]. The strengths of this case include the availability of serial laboratory testing that demonstrates the delayed rise in CK levels. Limitations include the absence of serum venom levels to confirm red-bellied black snake envenomation. The observed delayed rise in CK levels highlights the importance of repeated clinical assessment when caring for snake bite patients as laboratory evidence of envenoming may occur after the routinely recommended 12-hour timeframe post-bite, and symptoms may precede laboratory abnormalities. Future research further exploring how symptom onset aligns with laboratory abnormalities in envenomed patients may yield valuable insights.

Conclusion

Our patient with red-bellied black snake envenoming developed delayed-onset myotoxicity and myoglobinuria that was managed without antivenom. Cases of delayed myotoxicity may warrant prolonged observation and supportive care with intravenous fluid therapy.

Abbreviations

CK

Creatine kinase

APTT

Activated partial thromboplastin time

U/L

Units/liter

eGFR

Estimated glomerular filtration rate

ASP

Australian Snakebite Project

INR

International normalized ratio

Author contributions

All authors were involved in writing and revising the manuscript. All authors read and approved the final manuscript.

Funding

No funding was obtained for the completion of this case report.

Data availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Declarations

Ethics approval and consent to participate

Formal human research ethics committee (HREC) approval is not required for case reports in Western Sydney Local Health District.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.