aka Toxicology Conundrum 052
A 30 year-old man was walking alone in rural New South Wales, Australia.
He was startled by a brown-coloured snake and stepped backwards into a nearby bush. He didn’t see the snake bite him, but as it slithered away he noticed blood oozing from a scratch on his leg.
He anxiously walked to his car, and drove to the nearest hospital, arriving 45 minutes later.
Q1. Would you apply a pressure immobilization bandage (PIB) on arrival at the hospital?
Yes – there is little to lose.
This patient has been moving around for 45 minutes after a possible snakebite. Chances are that applying a PIB at this point won’t do much in terms of decreasing systemic absorption of snake venom – probably a case of shutting the gate after the horse has bolted.
Exactly how long after a bite a PIB will be effective is debatable, and probably depends on how mobile the patient was in the interim. Some snakebite experts have suggested that PIB may be ineffective if applied after 30-45 minutes in most settings.
However there is an argument that any potential snakebite, whatever the time of presentation (within reason) should have PIB applied. This helps to:
- (perhaps) limit ongoing systemic absorption of venom from the bite site and the nearby lymphatics.
- maintain skills in PIB application among staff
- reinforce its importance to staff, the patient and the general public that PIB is a useful first aid measure
The patient is anxious and feels nauseated. A small amount of blood is oozing from the scratch mark near his right ankle. His right inguinal lymph nodes are mildly tender. There is no evidence of bleeding from other sites and his cranial nerve exam is normal.
His blood tests show the following:
Q2. Describe and interpret these blood results. Given the clinical context, what Australian snakes, if any, are these results consistent with?
There is evidence of venom-induced consumptive coagulopathy (VICC):
- Immeasurably high INR and aPTT with an unmeasurable fibrinogen and positive D-dimer.
- This cannot be anticoagulation due to a black snake, because fibrinogen would be normal.
The presence of VICC limits the possible snake envenoming syndromes to those of brown snakes, tiger snakes and taipans. The latter can be supposedly excluded based on geography (there may be areas of NSW where the Inland Taipan is present – bites by this, the snake with the most lethal venom of any in the world, are extremely rare). An inland taipan bite in NSW featured in the news recently.
The full blood count is suggestive of thrombotic microangiopathy resulting in microangiopathic hemolytic anemia (Hb 95) and thrombocytopenia (plt 60). Further tests are needed to confirm hemolysis (e.g. blood film, LDH, Hb in urine, haptoglobin). Leucocytosis (WBC 12.3) is a non-specific finding in possible snakebite.
Any of the snakes that cause VICC can cause MAHA. It is rare, but when present is usually in the context of delayed presentations (unlike this scenario!).
The UEC, with an elevated creatinine (Cr 190) is consistent with . This could be due to direct nephrotoxicity (thought to occur in brown snake envenoming, and possibly Tigers and Taipans), due to myotoxicity resulting in rhabdomyolysis (this would exclude brown snake envenoming), or due to MAHA.
MAHA is the most likely cause of renal impairment in this setting. Most patients will require renal replacement therapy but most will recover after a few weeks.
The combination of VICC with thrombotic microangiopathy mimics disseminated intravascular coagulation (DIC).
Based on geography and the available clinical and laboratory data the patient has evidence of systemic envenoming by a Brown Snake or a Tiger snake.
Q3. What is the role of the snake venom detection kit (VDK) in the assessment and management of the possible snakebite patient?
The VDK does NOT indicate that a patient is envenomed.
Envenoming is determined by the presence of characteristic clinical and laboratory features, that are clearly present in this case (see Q2).
The VDK result can help decide which antivenom to give, IF the patient is envenomed.
Antivenom selection is based on:
- Geography (different snakes have different geographic distributions)
- Clinical and laboratory features (consistent with the specific envenoming syndromes of different types of snake)
- VDK result
In my opinion, the VDK is the LEAST important of the three.
Except in rare circumstances (e.g. when a recognized snake expert is available), snake identification plays no role in antivenom selection. Brown snakes can have stripes and Tiger snakes can be brown…
There is no clinical or laboratory evidence of rhabdomyolysis due to myotoxicity (which may or may not occur in Tiger snake envenoming).
A VDK is performed using a bite site swab. Well 2 turns rapidly turns strongly blue, and is soon followed by Well 7, then after a couple of minutes, Well 1.
Q4. What antivenom would you give, and how much?
Brown snake antivenom — the brown snake well is strongly positive and is consistent with the geography, clinical and laboratory features.
It is not unusual for other wells to change colour as well. For this reason it is important that the VDK is observed closely. It is best performed by a laboratory technician rather than a doctor in a busy ED!
If the VDK result doesn’t match the geography, clinical and laboratory data – don’t believe the VDK. Remember Osler, who told us to listen to the patient as he will tell us the diagnosis!
Give brown snake antivenom as follows:
- Administer 1 ampoule in 500 mL normal saline over 20 minutes in a resuscitation area.
- Ensure that the patient has 2 working IV lines and that adrenaline is immediately available in case of antivenom anaphylaxis.
Finally, I recommend discussing Australian snake bite cases with a toxicologists via the Poisons Information Center and enrolling patients in the Australian Snakebite Project (ASP). The dose of snake antivenom remains controversial, be guided by a toxicologist.
Journals and Textbooks
- Canale E, Isbister GK, Currie BJ. Investigating pressure bandaging for snakebite in a simulated setting: bandage type, training and the effect of transport. Emerg Med Australas. 2009 Jun;21(3):184-90. PubMed PMID: 19527277.
- Isbister GK, Little M, Cull G, McCoubrie D, Lawton P, Szabo F, Kennedy J, Trethewy C, Luxton G, Brown SG, Currie BJ. Thrombotic microangiopathy from Australian brown snake (Pseudonaja) envenoming. Intern Med J. 2007 Aug;37(8):523-8. PubMed PMID: 17640187.
- Isbister GK. Snakebite doesn’t cause disseminated intravascular coagulation: coagulopathy and thrombotic microangiopathy in snake envenoming. Semin Thromb Hemost. 2010 Jun;36(4):444-51. Epub 2010 Jul 7. Review. PubMed PMID: 20614396.
- Murray L, Daly FFS, Little M, and Cadogan M. Toxicology Handbook (2nd edition), Elsevier Australia 2011. [Google Books Preview]
- Sutherland SK, Coulter AR, Harris RD. Rationalisation of first-aid measures for elapid snakebite. Lancet. 1979 Jan 27;1(8109):183-5. PubMed PMID: 84206.
- Sutherland SK, Harris RD, Coulter AR, Lovering KE. Simple method to delay the movement from the site of injection of low molecular weight substances. Med J Aust. 1980 Jan 26;1(2):81. PubMed PMID: 6767176.