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Acute kidney injury secondary to Eastern Brown snake (Pseudonaja textilis) bite: a case study.


The Eastern Brown snake (Pseudonaja textilis) is the second most venomous snake in the world (Women's and Children's Hospital [WCH], 2014). In Australia each year there are approximately 3000 incidents of snake bite, resulting in 1-4 deaths despite the wide availability of first aid, intensive care and antivenom (Isbister et al., 2007; Therapeutic Guidelines, 2012). Of Australian snakebite fatalities, 60% are caused by brown snake envenomation (Isbister, 2006). It is the purpose of this article to describe a case of envenomation by an Eastern Brown snake, which resulted in acute kidney injury (AKI) requiring haemodialysis (HD). This case study will examine the pathophysiology of the effects of the envenomation, explaining the mechanism of AKI whilst relating to the clinical presentation of the patient. This article will also reflect on the treatment of this patient, including HD, antivenom and first aid, and provide comment on the lessons that can be learned from this individual case.

Case report

A 45-year-old male (Mr X) with no significant previous medical history was bitten on the right index finger by an unidentified snake in his home in a residential suburb of south-east Queensland. As the painless bite left only a minor scratch on the finger, Mr X disregarded his injury. Mr X did not realise that the Eastern Brown snake has rather small fangs and often leaves barely a trace that its prey has been bitten, while it has potentially injected a potent concentration of toxic, rapid-acting venom (WCH, 2014). Unaware of his risk, Mr X transported the snake to the local veterinary clinic to be identified. Upon arrival to the veterinary clinic, Mr X did not disclose that he had been bitten, and collapsed, suffering a deep laceration above his left eye and incontinence of urine. Mr X was immediately transported by ambulance to the nearest hospital. A snake expert had verified the identity of the snake: Pseudonaja textilis--the Eastern Brown.

Upon arrival at the hospital, Mr X was alert with a Glasgow Coma Scale of 15. A splint and bandage had been applied to the snake bite, and pressure was being applied to the head laceration as it had been bleeding profusely. Sutures were applied to the laceration and pathology revealed alarming coagulation results: INR > 10, APTT > 200 (Table 1).

Brown snake antivenom was administered via intravenous infusion, but Mr X responded with a hypotensive anaphylactic reaction, requiring the administration of adrenaline. Tiger snake antivenom was then administered, resulting in the same reaction, once again corrected by adrenaline. Mr X was transferred to the intensive care unit, where more antivenom was administered at a slower rate, this time with success.

Meanwhile, Mr X's head laceration was bleeding through the sutures, so it was infiltrated with adrenaline and lignocaine and re-sutured. Various blood products and coagulation factor concentrates were administered to combat the coagulopathy (Tables 1 and 2). A large proportion of snake envenomation-related deaths occur due to bleeding complications such as intracranial haemorrhage, which can occur due to coagulopathy, and Mr X's head trauma put him at significant risk (Chaisakul et al., 2013; WCH, 2014). While a CT scan of the head revealed a large left frontal subgaleal haematoma, there was no sign of intracranial haemorrhage.

The clinical situation had not yet stabilised, however, as Mr X's renal function began to plummet (Table 3). Mr X rapidly developed anuric AKI, requiring the initiation of HD treatment.

Venom-induced consumptive coagulopathy (VICC)

Mr X's less-than-optimal coagulation profile (Table 1) can be explained by complete defibrination caused by venom-induced consumptive coagulopathy (VICC), which can manifest within 30 minutes of envenomation (Therapeutic Guidelines, 2012; WCH, 2014). The venom of the Eastern Brown snake contains group C prothrombin activator toxin, which converts prothrombin to thrombin, activating the coagulation cascade, leading to the complete consumption of clotting factors (Chaisakul et al., 2013; Isbister et al., 2007; Isbister et al., 2010; Ministry of Health, NSW, 2013). This results in an initial thrombotic state that can potentially cause significant complications such as pulmonary and coronary thrombi (Chaisakul et al., 2013; Currie, 2004; WCH, 2014). As coagulation factors become exhausted, coagulopathy develops, resulting in uncontrollable bleeding. Within two hours of envenomation, factors V, VIII, protein C, plasminogen and fibrinogen are significantly depleted (Isbister, 2006; Isbister et al., 2010; Ministry of Health, NSW, 2013). As was observed in Mr X, this results in INR, prothrombin time, APTT and D-Dimer elevation beyond detection (Isbister, 2006; Ministry of Health, NSW, 2013; Therapeutic Guidelines, 2012; White, 2013). This places the victim at extreme risk of life-threatening haemorrhage (WCH, 2014). VICC usually resolves within 12-48 hours of venom neutralisation, once clotting factors are resynthesised (Chaisakul et al., 2013; Isbister, 2006; Isbister et al., 2013; Whyte & Buckley, 2012).

Microangiopathic haemolytic anaemia and AKI

Mr X's full blood count at the time was suggestive of thrombotic microangiopathy, resulting in microangiopathic haemolytic anaemia and thrombocytopaenia (Table 2). Haemolysis was confirmed by the detection of marked numbers of schistocytes, moderate numbers of spherocytes and mild polychromasia on blood film, and elevated serum lactate dehydrogenase and bilirubin (Figures 1 and 2). Haptoglobin levels were unable to be produced due to specimen haemolysis.

Microangiopathic haemolytic anaemia was brought about by the combination of two mechanisms (Figure 3), and resulted in AKI. Firstly and most significantly, as VICC develops, strands of fibrinogen form in the blood vessels. As red blood cells pass through these fibrinogen strands they become fragmented (Schrier, 2013). Secondly, Eastern Brown snake venom contains phospholipase A2 (Chaisakul et al., 2013), which lyses the phospholipid cell membranes of red blood cells (Birrell et al., 2006; Fry, 1999; Kholi & Sakhuja, 2003). The haemolysis that occurs as a result of each of these mechanisms causes haemoglobin to be released into the plasma from the haemolysed red blood cells (Schrier, 2013). The haemoglobin is then filtered by the glomerulus into the urinary space, releasing haem pigment. Haem pigment is toxic to the kidneys in three ways: tubular obstruction; direct proximal tubular cell injury; and vasoconstriction, resulting in reduction in blood flow in the outer medulla (Eustace & Kinsella, 2013).

Haemodialysis (HD)

Mr X developed anuric AKI and required the initiation of HD treatment during his hospital stay, which was continued for a short period of time after he was discharged. HD treatment was commenced using a percutaneous, non-tunnelled, non-cuffed HD catheter; however, this was replaced by a tunnelled, cuffed HD catheter when it became apparent that HD may be required for a longer period.

One of the obvious challenges encountered when dialysing a patient with such severe coagulopathy was the risk of coagulation of the extracorporeal circuit. Initially Mr X was dialysed with no anticoagulant and the extracorporeal circuit was vigilantly monitored for signs of coagulation. For subsequent HD sessions, as Mr X's coagulation profile and blood count normalised, heparin was gradually introduced. The introduction of heparin also had to be monitored very closely, in order to reduce the risk of coagulation, or conversely, bleeding. It was extremely important to avoid either of these adverse events, as Mr X was already severely anaemic.



The other major challenge faced by the clinicians involved in the care of Mr X was the maintenance of an optimal fluid status. In the absence of urine output, it was clearly important to avoid fluid overload. Therefore, Mr X was placed on a 750 mL daily fluid restriction, strict fluid balance chart, and was being weighed daily. Similarly, avoiding dehydration was also of high importance, as this could have worsened Mr X's renal function. For this reason, extreme caution was required with ultrafiltration. Ultrafiltration goals were calculated, based on thorough assessments of Mr X's fluid status and were adjusted as needed, based on continuous assessment throughout the HD treatment. Close collaboration and teamwork between the HD nurses, nephrologists and registrars within the renal dialysis unit, as well as with the multidisciplinary team of the general medical ward, was crucial.


Brown snake antivenom

Both brown and tiger snake antivenoms were administered to Mr X in the hours following his envenomation. Mr X reacted with hypotensive anaphylactic reactions (systolic blood pressure 75 mmHg), with erythema to the chest and arms. While these reactions are alarming, such reactions to antivenom are well documented and acknowledged to be a common occurrence, due to the antivenom being prepared from the plasma of horses injected with the venom of the brown snake (MIMS Australia, 2014; Whyte & Buckley, 2012). Immediate-type hypersensitivity reactions are known to occur in one-quarter, and severe hypotensive reactions in 5% of patients receiving antivenom (Isbister et al., 2008; Therapeutic Guidelines, 2012). In fact, the incidence of severe adverse reaction is so common that the recommended standard of practice is to have a syringe already loaded with 1:1000 adrenaline available during antivenom therapy, and to administer the antivenom in an intensive care unit if possible (MIMS Australia, 2014). Adverse reactions to antivenom are best avoided by only administering antivenom in the presence of clinical evidence of systemic envenomation, and by administering the drug via a slow intravenous infusion at an adequate dilution (MIMS Australia, 2014). After having anaphylactic reactions to both brown and tiger snake antivenoms, Mr X was able to successfully complete the dose of tiger snake antivenom when the infusion rate was significantly reduced.

One vial of brown snake antivenom is intended to neutralise the average yield of brown snake venom, as demonstrated in vitro (MIMS Australia, 2014; Whyte & Buckley, 2012). In recent years there has been a lot of controversy as to the optimal dose of antivenom that is required. Frequently patients have been administered three or more vials of antivenom, and the administration of up to 13 vials has been recorded (MIMS Australia, 2014). Increasing amounts of antivenom have particularly been administered to patients with venom-induced consumptive coagulopathy, based on the number of doses required before coagulation normalised. In order for coagulopathy to resolve, however, clotting factors must be resynthesised by the liver, which can take 12-48 hours once venom has been neutralised (Chaisakul et al., 2013; Isbister, 2006; Isbister et al., 2013; Whyte & Buckley, 2012). Therefore, current guidelines recommend that one vial of antivenom is sufficient to neutralise all circulating venom and that the administration of further doses will not speed up the recovery processes (Chaisakul et al., 2013; Ministry of Health, NSW, 2013; Therapeutic Guidelines, 2012; White, 2013; Whyte & Buckley, 2012). Involvement of an expert clinical toxicologist is crucial (Therapeutic Guidelines, 2012).

Did the administration of antivenom help Mr X's overall renal outcome? Clinical evidence of systemic envenomation was apparent long before Mr X presented to hospital, as he had collapsed and VICC was present. Therefore, antivenom was indicated (Therapeutic Guidelines, 2012). The administration of antivenom would have had benefits in terms of short-term complications and other effects associated with venom (for example, if any neurotoxicity symptoms such as paralysis were present), and would certainly have helped resolve VICC (Therapeutic Guidelines, 2012). Antivenom, however, would not likely have had any effect on Mr X's resultant AKI and requirement for dialysis (Therapeutic Guidelines, 2012), as Eastern Brown snake venom is not known to contain direct nephrotoxins (Australian Venom and Research Unit, 2014; Birrell et al., 2006; Currie, 2000; Fry, 1999; WCH, 2014). The strands of fibrinogen were already in place to destroy the red blood cells, and at this stage Mr X's AKI was likely inevitable. If there was less delay in Mr X's presentation to hospital, or had adequate first aid been administered sooner, perhaps Mr X could have avoided dialysis.


There are many lessons that can be learned from the case of Mr X. Failing to realise the significance of his snake bite and seek appropriate medical assistance, Mr X prolonged the length of time until his health care was received. Current recommendations for the first aid treatment of snake bites in Australia are to employ the pressure-immobilisation technique. This technique involves applying firm bandaging all the way along the affected limb from below the bite site upward, and applying a splint or sling to comfortably immobilise the limb (Australian Venom and Research Unit, 2007; Therapeutic Guidelines, 2012). This prevents the spread of venom throughout the lymphatic system by compressing the lymphatic vessels (Australian Venom and Research Unit, 2007). Pressure-immobilisation should remain in place until venom has been neutralised or envenomation has been ruled out (Stewart, 2003; Therapeutic Guidelines, 2012). From review of the clinical notes, it is apparent that pressure-immobilisation was not applied until the arrival of an ambulance to the veterinary clinic, by which point a significant amount of time had passed since the bite occurred at Mr X's house. Furthermore, Mr X's movement after his bite not only put him at risk of serious injury when he collapsed, but may have expedited the systemic spread of venom. It is recommended that snake bite victims are placed in a position of rest and participate in minimal movement (Stewart, 2003; Therapeutic Guidelines, 2012).


Mr X continued dialysis throughout his hospital stay and as an outpatient, until eventually, three weeks after envenomation, dialysis was no longer required.

Snake bite envenomation is quite uncommon in Australia, and resultant AKI is even rarer. Therefore, this case study has taken the opportunity to share this experience with the wider renal community, and in doing so add one more account to the limited collection of literature on this topic. This case study has attempted to describe the complex mechanisms by which one patient developed VICC, microangiopathic haemolytic anaemia and AKI as the result of envenomation by an Eastern Brown snake.

From this case study we are reminded of the importance of adequate first aid and early intervention. Specific to the HD specialty, this case study provides an account of an interesting and rare case, and reflects upon some of the challenges experienced within the HD setting. I hope the contribution made by this case study to the limited body of evidence surrounding snake bite envenomation and resultant AKI is able to improve the knowledge and preparedness of health professionals for similar cases that may present. Furthermore, perhaps by reflecting on this case it will serve as a reminder of the importance of current first aid recommendations, and assist in reducing snake bite-related fatality.


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Chaisakul, J., Isbister, G., Kuruppu, S., Konstantakopoulos, N., & Hodgson, W. (2013). An examination of cardiovascular collapse induced by eastern brown snake (Pseudonaja textilis) venom. Toxicology Letters, 221, 205-211.

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Submitted: 10 December 2014, Accepted: 2 February 2015

Brendan Zornig Clinical Facilitator (Haemodialysis), Logan Hospital, QLD, Australia

Renal Dialysis Unit, Building 2, Logan Hospital, Cnr Armstrong & Loganlea Roads, Meadowbrook, QLD 4131, Australia Email
Table 1: Coagulation profile

Date, time          INR       Prothrombin   APTT (s)   Fibrinogen
                              Time (s)                 (g/L)

25/10/2013, 05:30   1.2       13            30         4.3
24/10/2013, 06:20   1.2       12            32         3.0
23/10/2013, 20:00   1.3       14            46         1.6
23/10/2013, 12:30   1.6       17            93         1.0
23/10/2013, 05:55   2.0       22            150        1.0
23/10/2013, 00:45   >10.0     >100          >200       <0.4
22/10/2013, 14:50   >10.0     >100          >200       <0.4
Reference range     0.9-1.2   10-13         26-41      1.7-4.5

Table 2: Blood count

Date, time          Haemoglobin   White blood cell   Platelets
                    (g/L)         count              (x [10.sup.9]/L)
                                  (x [10.sup.9]/L)

27/10/2013, 08:45   86            13.5               37
26/10/2013, 18:15   79            11.6               40
26/10/2013, 12:30   86            9.2                49
26/10/2013, 05:55   67            9.6                21
25/10/2013, 12:30   75            7.7                55
25/10/2013, 05:30   67            8.3                17
24/10/2013, 06:20   85            9.0                52
23/10/2013, 20:00   84            8.1                59
23/10/2013, 12:30   73            7.3                43
23/10/2013, 05:55   60            7.3                64
23/10/2013, 00:45   93            10.1               122
22/10/2013. 14:50   152           13.4               191
Reference range     135-180       4.0-11.0           140-400

Table 3: Renal function

Date, time          Urea (mmol/L)   Creatinine       EGFR (mL/min/L)

28/10/2013, 10:55   27.6            759              7
27/10/2013, 08:45   17.9            495              11
26/10/2013, 05:55   3.5             120              63
25/10/2013, 05:30   13.1            433              13
24/10/2013, 06:20   15.9            467              12
23/10/2013, 12:30   9.7             229              29
23/10/2013, 05:55   6.7             131              56
23/10/2013, 00:45   5.0             104              74
22/10/2013, 14:50   4.0             94               84
Reference range     2.1-7.1         73-108           >60
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Author:Zornig, Brendan
Publication:Renal Society of Australasia Journal
Article Type:Clinical report
Geographic Code:8AUST
Date:Jul 1, 2015
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