CSL Antivenom Handbook

CSL Antivenom Handbook Medical Treatment of Bites and Stings General Principles Bites/stings by some animals are potentially lethal, such as snakebite, funnel web spider bite, paralysis tick bite, blue ringed octopus bite, cone shell sting and box jellyfish sting. Any patient presenting with a possible or definite bite/sting by these organisms should be given high priority in triage and assessed as quickly as possible. In some cases a delay of even minutes may be crucial in affecting outcome. Bites/stings by some other animals, notably the red back spider, stonefish, and stingrays may result in severe problems, equally demanding urgent attention. Diagnosis of bites and stings may be straightforward, but often is less than easy, and occasionally quite difficult. In the latter case, rapid accurate diagnosis may be critical to the outcome for the patient and this requires doctors to maintain a high index of suspicion for envenoming in certain situations. This will be discussed more fully below (section on "Diagnosis"). Where available, antivenom is virtually always the best treatment for envenoming, but is usually only needed if there is significant systemic envenoming. Not every snake bitten patient needs antivenom! Never assume that medical or nursing staff know what to look for in observing a patient with envenoming. Instruct them on what to look for, particularly specific signs, such as ptosis, dysarthria and weakness (ie paralysis in snakebite, blue ringed octopus bite and tick bite), persistent bleeding from bite site or venepuncture wounds (ie coagulopathy in snakebite), dark urine due to myoglobin (ie myolysis) or haematuria in snakebite, profuse sweating (ie red back spider bite), profuse salivation, lachrymation and piloerection with muscle twitching (ie funnel web spider bite). Frequent detailed and specific observations are the rule for most cases of possible envenoming. Any bite may be the source of secondary infection and this may include tetanus, so ensure tetanus prophylaxis and watch for developing cellulitis.

Diagnosis The diagnosis and identification of the animal causing the bite/sting may be obvious, particularly if the offending animal is presented with the patient, but it more often is less clear. The patient may present with marks that may or may not be due to a bite/sting by organism unknown. If they have symptoms, signs or laboratory test results indicative of

envenoming then this will clarify the situation, but sometimes all of these are non specific and may point to a variety of possible aetiologies, of which envenoming is just one. Most worrying is the patient who presents with no history of a bite/sting, in whom the constellation of symptoms, signs and laboratory test results may not immediately suggest envenoming. In such cases it is essential to do the right tests to confirm or exclude envenoming. To elaborate on all possible scenarios would exceed the scope of this publication. Some specific pointers for particular venomous animals are noted in the clinical sections for each antivenom, later in this book. A few important case situations are given in the general information for snakes, then basic details on various animal groups including clinical features of envenoming. Major envenoming is a condition treated only rarely by most doctors, who therefore will have little opportunity to develop or maintain current knowledge or skills appropriate for these cases. Never delay or be hesitant in seeking expert advice in management of envenoming. Such advice from doctors trained in the management of envenoming is available through CSL (03 9389 1911) and also through the National Poisons Centre Network (131 126) - ask to speak to the Duty Medical Toxicologist.

Treatment The treatment of a case of envenoming will be determined by both animal and patient factors. Not all patients bitten/stung by dangerously venomous animals will be envenomed. Antivenom is not needed in every case. Rates of antivenom use will vary from animal to animal. Amongst those cases requiring antivenom therapy, there will be a considerable variation in the amount of antivenom needed. The information given in this book can be a guide only. Every case needs to be individually assessed.

Basics Any patient presenting for treatment of a suspected bite/sting should be rapidly triaged and if there is significant impairment of cardiovascular or respiratory function, management of this takes priority. For potentially life threatening bites/stings (eg snakebite, funnel web spider bite, box jellyfish stings) it is important to obtain good venous access early, with a catheter or drip set, and this is a good opportunity to take initial blood samples for laboratory tests, if indicated (particularly in snakebite). If there is a pressure immobilisation bandage in use as first aid, leave it on until ready to treat envenoming. For potentially life threatening envenoming (eg snakebite, funnel web spider bite, blue ringed octopus bite, box jellyfish sting) the first aid should never be removed to inspect the wound if antivenom and treatment facilities are not immediately available.

Snake Venom Detection General Principles This only applies for suspected snakebite (in Australia). The CSL Snake Venom Detection Kit (SVDK) is produced specifically to identify the presence and type of Australian snake venom. It is very practical in design, giving results which relate directly to the most appropriate antivenom to use.The best sample for testing is a swab from the bite site and it can detect nanogram quantities of venom. Even a bite site that has been washed may yield a positive result. If the patient already has systemic envenoming, then venom may be present in the urine and this is then a useful alternative for sampling. Unfortunately, because of non specific binding with plasma proteins, blood is not a reliable sample and is only recommended if a bite site swab or urine is unavailable. If a blood sample is used, the snake venom detection kit product information should be carefully read before proceeding. If a dead snake is available, a swab from the fangs may yield a positive result, if a bite site is not available, but beware finger prick envenoming from the fangs. Everything needed to perform a SVDK is provided in the kit, with the following exceptions. The kit does not provide a source of running water for the washing phase, nor a container for waste. If the kit is to be used in transit in a medical retrieval plane or ambulance, then also carry a squeeze bottle of water for washing and a waste liquid container. Each SVDK box contains three test kits and three sample bottles, but the substrate reagents and sample well holder are common to all 3 test kits.

How to perform a Snake Venom Detection test Interpretation of the Snake Venom Detection test • Locate the bite site (cut off bandage over the bite site only to gain access, if there is first aid in place). Make sure no-one washes it! Alternatively, if there is clearly systemic envenoming and the bite site is of poor quality, test urine. • Take one of the cotton bud swab sticks provided in the kit and an unused "Yellow Sample Diluent" bottle. Unscrew the cap off the bottle, revealing the dropper cap. Lever this off, using a finger nail and put it to one side.

• Put the swab stick into the sample diluent fluid to thoroughly moisten it. • Rotate and rub the moistened swab stick vigorously over the bite site and adjacent skin, to pick up venom on the skin around the bite and from just beneath the surface of the bite marks. • Place the swab stick back in the "Sample Diluent" bottle and twirl it around, to get any venom off into solution, then remove the swab stick and replace the dropper cap. You are now ready to start the test procedure. • Open a pack containing test wells (silver like pack), remove the enclosed set of 8 joined wells and place them in the holder. There is a lug at one end to enable easy placement in the right orientation. Remove the cover from the wells. • Place 2 drops of the sample diluent you have prepared into each well. • Leave to stand for 10 minutes. • Gently wash all wells under gently running water 7 times (blood is not a recommended sample in envenomed humans but if used requires at least 15 washings), then invert and gently shake out excess water (don't try and dry the inside of the wells with anything). • Now add the 2 substrate reagents, one drop to each well of the "Peroxide" and the "Chromogen". • Allow to incubate for 10 minutes, watching the whole time, against a white background, for colour change. It is vital to observe the kit throughout this final phase, as the time sequence of colour change may be crucial. • There should be a blue colour develop in well 7 (positive control), usually within 23 minutes. There should be no colour change in well 6 (negative control). A colour change in any of wells 1 to 5 indicates the presence of snake venom. The number of the well changing colour first indicates the type of snake venom and corresponding CSL snake antivenom. If there is no snake venom detected, then wells 1 to 5 will not change colour.

• Once the kit has been read, remember to put common reagent tubes, the white well holder, instructions, unused swab sticks and well packets back in the box and then put this back in the fridge. The reagents may quickly deteriorate if left out at room temperature too long!

Interpretation of the Snake Venom Detection test How to perform a Snake Venom Detection test Interpretation of the SVDK is often simple. Always remember that a positive result for venom from the bite site does not mean the patient has been significantly envenomed. A positive SVDK from the bite site is not an indication to give antivenom. It is an indication of the type of antivenom to give if, on clinical or laboratory grounds, the patient needs antivenom therapy. • Well 6 must not change colour and well 7 must change to blue for the test to be valid. • If wells 1 to 5 show no colour change, then no venom has been detected.

Only well 7 positive: No snake venom detected. This result does not exclude snakebite.

• If well 1 changes to blue first, then the patient has been bitten by either a tiger snake or rough scaled snake, or possibly a copperhead, broad-headed snake or Stephen's banded snake. Envenoming from all these snakes respond to CSL Tiger Snake Antivenom.

Wells 7 & 1 positive: If systemic effects include defibrination, paralysis ± myolysis, suggests tiger snake or rough scaled snake bite. If systemic effects defibrination only, consider bite by broad-headed, pale-headed or Stephen's banded snake. If systemic effects are confined to paralysis, without defibrination, consider possibility of copperhead bite.

• If well 2 changes to blue first, then the patient has been bitten by a brown snake. CSL Brown Snake Antivenom will then be the right choice.

Wells 7 & 2 positive: Most likely a brown snake bite. If systemic envenoming develops, expect defibrination coagulopathy, ± renal damage. Paralysis is unlikely and myolysis should not occur.

• If well 3 changes to blue first, then the patient has been bitten by a mulga snake (king brown), red bellied black snake, spotted black snake or Collett's snake. All these respond to CSL Black Snake Antivenom, but this is best reserved for bites by the mulga snake and Collett's snake, as all the others respond well to CSL Tiger Snake Antivenom (which is lower volume and cost effective).

Wells 7 & 3 positive: Most likely a bite by a mulga snake (king brown) or Collett's snake; if systemic envenoming, expectmyolysis, extensive swelling of bitten limb, ± anticoagulant coagulopathy, ± renal damage, OR possibly a bite by a red-bellied or blue-bellied (spotted) black snake; if systemic envenoming. expect only mild myolysis, no coagulopathy, paralysis or renal damage.

• If well 4 changes to blue first, then the patient has been bitten by a death adder, and CSL Death Adder Antivenom will be the most appropriate choice.

Wells 7 & 4 positive: Death adder bite; if systemic envenoming, expect post-synaptic paralysis, no coagulopathy, significant myolysis or renal damage.

• If well 5 changes to blue first, then the patient has been bitten by a taipan or inland taipan, and CSL Taipan Antivenom or CSL Polyvalent Antivenom is the appropriate choice.

Wells 7 & 5 positive: Taipan or inland taipan bite; systemic envenoming very likely. Expect defibrination coagulopathy, paralysis, ± myolysis, ± renal damage.

• If wells 1 and 3 change to blue at the same time, then the patient has been bitten by either a copperhead, a red bellied black snake, a spotted black snake or possibly a Collett's snake. CSL Tiger Snake Antivenom is the appropriate choice, except for Collett's snake where CSL Black Snake Antivenom is preferable.

Wells 7, 1 & 3 positive: This pattern is sometimes seen with bites by several species. If a copperhead bite, if there is systemic envenoming, expect paralysis, without coagulopathy. If a red-bellied or blue-bellied (spotted) black snake bite, if there is systemic envenoming, expect only mild myolysis, no coagulopathy, paralysis or renal damage. If a Collett's snake bite, if there is systemic envenoming, expect myolysis, possibly anticoagulant coagulopathy, ± renal damage.

• If some other combination occurs please ring CSL for advice (03) 9389 1911

No wells positive: Indicates kit failure. Re-test with a new kit.

Note: 1. Sea snake venoms are not reliably detected by the SVDK. 2. Some other species of venomous Australian land snakes, not known to cause medically significant envenoming, may occasionally give a positive SVDK result. Notable examples of this phenomenon are the whip snakes. Remember, a positive SVDK result does NOT mean the patient requires antivenom.

Diagnostic Flowcharts Determining the most likely snake based on clinical findings, if venom detection is not available or fails.

General Principles Australia's venomous snakes are all Elapid (cobra type) snakes, with small to medium sized paired fangs at the front of the mouth. The venom glands are posterior to the eye and it appears the snake can control venom ejection, so that it is possible for the snake to bite, leave bite marks or scratches, yet not inject any venom (the "dry bite"). Each group of snakes has distinctive venom, causing typical local and general effects, but there is always the potential for variability in venom action within a single species of snake, depending on geographic variation and individual variation. Some key components of Australian snake venoms are listed below. Not all species have all components (see details for each group under respective antivenoms).

Neurotoxins These act at the skeletal neuromuscular junction (NMJ), either pre or postsynaptically, causing progressive paralysis of voluntary and respiratory muscle. Because the venom must first reach the NMJ and then fix to target tissues, the first effects of these toxins are not seen in less than 1 hour after the bite and usually the earliest signs take 2-4 hours or more to develop. Complete paralysis, which is not common, even in untreated cases, may take from 3 to greater than 18 hours to develop, but breathing difficulty due to paralysis of the tongue and pharynx may develop much earlier than full respiratory paralysis and require intubation and ventilation.

Bilateral ptosis

Key early signs include; ptosis, partial ophthalmoplegia with diplopia, dysarthria and loss of facial expression. Ptosis alone may be seen with severe envenoming by mulga snakes. Key laboratory tests; there are none which are diagnostic but pulse oximetry may be helpful in documenting deteriorating respiratory function. Key species; tiger snakes, taipans, death adders, rough scaled snake, copperheads, and only rarely brown snakes. Value of antivenom treatment: for post-synaptic only paralysis ( eg. Death adders), even late antivenom may reverse paralysis, but established, severe presynaptic paralysis (eg. tiger snakes, taipans, rough-scaled snake) will not be reversed by antivenom.

Myotoxins These are often related to the neurotoxins structurally (ie phospholipase A2 ) and they bind to the muscle fibres, causing progressive destruction of the muscle cells with release of breakdown products. It is likely this process takes hours to become evident, by which time irreversible damage has been done. The result is progressive muscle weakness and pain on movement, with myoglobinuria and possible secondary renal failure and hyperkalaemia (which can be severe, intractable and lethal).

Red discolouration of urine due to myolysis, resulting in myoglobinuria.

Key early signs include; pain on contracting muscles against resistance, muscle weakness (may mimic paralytic signs, as above) and dark urine which tests positive for blood on dipstix.

Key laboratory tests; plasma CK, urinary myoglobin (qualitative only; positive "ward test" for blood), plasma potassium levels and renal function. Key species; tiger snakes, mulga snake, taipans, rough scaled snake, sea snakes. Value of antivenom treatment: limited clinical experience suggests that antivenom, even given several days after the bite, may sometimes cause a rapid resolution of symptoms (muscle pain) and a fall in CK.

Procoagulants These potent coagulants act as prothrombin converters, resulting in consumption of fibrinogen. This may result in rapid complete defibrination (within 30 minutes of the bite), with resulting bleeding tendency, though platelet function and numbers are usually normal, at least initially. In some species, unless adequate antivenom is given, the coagulopathy may be prolonged (eg brown snakes, taipans), while in others it may be initially severe, yet resolve spontaneously within 12 to 18 hours without antivenom treatment (eg tiger snakes). In the latter situation there may be residual raised fibrin(ogen) degradation products present up to 24 hours after the bite, giving a clue to what has occurred. Major haemorrhage associated with snakebite coagulopathy is not very common, nor is it rare, with intracranial bleeding a particular worry.

Extensive haematoma associated with attempted insertion of jugular venous line in a patient with snake bite coagulopathy.

Key early signs include; persistent ooze from the bite site or venepuncture sites and signs of cerebral irritation (if intracranial haemorrhage). Key laboratory tests; prothrombin time/INR (International Normalised Ratio), APTT, complete blood picture (platelet count), fibrinogen level, fibrin(ogen) degradation products (such as XDP = d-dimer), TCT (thrombin clotting time). If in a country hospital without ready access to laboratory facilities, a whole blood clotting time is useful (see details of test). Key species; brown snakes, tiger snakes, taipans, rough scaled snake, broad-headed snake, Stephen's banded snake, pale-headed snake.

Value of antivenom treatment: antivenom is the only effective treatment of snakebite defibrination coagulopathy and sometimes many vials of antivenom may be required. It is important to wait at least 3 hours after a dose before deciding to give further antivenom, as the key measure of effective treatment, a rise in fibrinogen (not returning to normal), will take at least this long to become apparent.

Anticoagulants Potent anticoagulants in a few snake venoms may cause rapidly reversible coagulopathy, without defibrination. Key early signs include persistent ooze from bite site or venepuncture sites. Key laboratory tests; prothrombin time/INR, aPTT, fibrinogen levels (should remain normal), fibrin(ogen) degradation products (should be absent). Key species; mulga snake, Collett's snake. Value of antivenom treatment: only effective treatment, rapid response.

Nephrotoxins While there are no isolated nephrotoxins in any Australian snake venom, they are known from some exotic snake venoms and kidney damage is not rare in Australian snakebite. The mechanisms are unclear, but may include both direct toxic effects on the kidney and secondary damage as a result of hypotension, myolysis or coagulopathy. Kidney damage may develop early, is uncommon in children, but much more likely if the patient has consumed significant amounts of alcohol prior to the bite. Key early signs include; oliguria or anuria (but neither are common). Key laboratory tests; urea, creatinine, potassium. Key species; any snake but particularly brown snakes, tiger snakes, mulga snakes, taipans, rough scaled snake. Value of antivenom treatment: uncertain.

Local Cyototoxins Again, not clearly demonstrated in Australian snake venoms. Major local skin damage at the bite site is rare in Australia. However, moderate to marked local swelling is seen following bites by mulga snakes, red bellied black snakes and other members of this genus. Mild local swelling with ecchymosis and pain is common after bites by tiger snakes. Brown snakes usually cause minimal or no local pain, redness and swelling, with

bite marks or scratches which are hard to see in some cases. Taipans cause variable local effects, usually less severe than for tiger snakes. Death adders usually cause mild swelling but marked pain.

Suggested Laboratory Tests for Snakebite Patients in Major Hospitals • Snake venom detection (CSL Kit) on bite site (or urine if there is systemic envenoming). • Coagulation studies. Prothrombin time/INR and APTT and if these are prolonged do fibrinogen, fibrin(ogen) degradation products and possibly TCT (Thrombin Clotting Time). • Complete blood picture (platelet count). • Plasma/serum electrolytes and renal function (especially K+, creatinine and urea). • CK. • Urine (ward test=dipstix looking for blood=?myoglobin or ? true haematuria microscopy required to look for red cells). All tests should be performed on first presentation and at intervals thereafter, the frequency depending on the results and the patient's condition.

Suggested Laboratory Tests for Snakebite Patients in Major Hospitals • Snake venom detection (CSL Kit) on bite site (or urine if there is systemic envenoming). • Coagulation studies. Prothrombin time/INR and APTT and if these are prolonged do fibrinogen, fibrin(ogen) degradation products and possibly TCT (Thrombin Clotting Time). • Complete blood picture (platelet count). • Plasma/serum electrolytes and renal function (especially K+, creatinine and urea). • CK. • Urine (ward test=dipstix looking for blood=?myoglobin or ? true haematuria microscopy required to look for red cells).

All tests should be performed on first presentation and at intervals thereafter, the frequency depending on the results and the patient's condition.

Suggested Laboratory Tests for Snakebite Patients in Country Hospitals • Snake venom detection (CSL Kit) on bite site (or urine, only if there is systemic envenoming). • Coagulation studies. Whole blood clotting time (5-10mL venous blood in a glass test tube and measure time to clot; >12min suspicious of coagulopathy; >20min and no clot very suspicious of severe coagulopathy). If possible, run a normal control using blood from a staff volunteer (ensure that they are not on anticoagulant drugs). Also take blood for laboratory tests performed at the regional hospital laboratories and send off as soon as possible (eg prothrombin time/INR and APTT and if these are prolonged do fibrinogen, fibrin(ogen) degradation products and TCT), complete blood picture (platelet count), plasma/serum electrolytes and renal function (especially K+, creatinine and urea) and CK. • Urine (ward test=dipstix looking for blood=?myoglobin or ? true haematuria microscopy required to look for red cells). All tests should be performed on first presentation and at intervals thereafter, the frequency depending on the results and the patient's condition.

Snakebite treatment flowchart

Some problem presentations for snakebite There are a number of ways in which a snake bitten patient may present without snakebite being an obvious diagnosis. In small children, no history of a bite may be given. The child may run inside crying, collapse and possibly have a grand mal convulsion. Unless bite marks are obvious and looked for, the parents may not suspect snakebite and the child may be presented to the doctor as a case of convulsions. Again, in children, if development of envenoming is less precipitate as in the previous example, but again with no history of a bite, the child may be presented to the doctor as becoming progressively unwell, lethargic, with vomiting, mild fever, and possibly apparent neck stiffness and fixed dilated pupils. If checked, the urine may be dark and showing "haematuria", with abdominal pain. Careful examination in such cases may show progressive paralysis, notably ptosis. The "haematuria" usually is myoglobinuria. The neck stiffness is due to myolysis and the fixed dilated pupils due to the effect of neurotoxins. Even adults may be unaware of being bitten by a snake, such as when walking through long grass, and may present later with headache, nausea and vomiting, or worse still, collapse and be presented unconscious, again, with no history of a bite. An unnoticed bite might also cause renal failure, presenting a day or more after the bite. These are but a few of the many cryptic presentations for snakebite. Also remember that snakes can, and do, enter houses and unnoticed snakebites can occur inside the patient's house!

Types of antivenoms Basic Information Used for neutralising systemic envenoming by members of the Australian brown snake group. It is made from horse IgG. Each ampoule contains 1000 units of neutralising capacity against the target venoms. One unit of antivenom activity should neutralise 0.01mg of dried venom from the species of animal against which the antivenom has been raised. Average volume per ampoule is 4.5-9mL. The immunising venom used is common brown snake venom.

Information about the snakes covered by this antivenom The species Brown snakes are the most common cause of snakebites and snakebite deaths in Australia. The fangs are small; average fang length in adults is only 2.8mm. Compared to many other dangerous snakes, they generally produce little venom, though the venom is

very potent. There are several species, the most important medically being the eastern or common brown, the western brown or gwardar and the dugite. They vary in length up to 2m, rarely more. Colouration is very variable; they may be brown, orange-red, grey, almost black, unbanded, speckled, banded, or black headed. Juveniles have distinctive head and neck markings, with a black mark on the top of the head, followed by a brown to orange band, then a black band. These baby brown snakes typically hatch around February/March and are about 25cm long.

Eastern brown snake Pseudonaja textilis

Spotted brown snake Pseudonaja guttata

Peninsula brown snake Pseudonaja (no map) inframacula

Western brown snake Pseudonaja nuchalis

Western brown snake Pseudonaja nuchalis

Western brown snake Pseudonaja nuchalis

Dugite Pseudonaja affinis

Juvenile brown snake Pseudonaja textilis

Ingram's brown snake Pseudonaja ingrami

(no photo)

Distribution Brown snakes are common throughout mainland Australia, in essentially all habitats, including urban areas. They are not present in Tasmania or the islands off the southern coast of Australia, such as Kangaroo Island (SA). They are relatively common in some urban and metropolitan areas. Hundreds of brown snakes are removed from houses and other properties each year in some capital cities and >10% of these snakes are found inside the house!

Venom composition The venom is multicomponent and includes powerful presynaptic neurotoxins, procoagulants and possibly both cardiotoxins and direct nephrotoxins. There is no myolytic activity. The venom of the common brown snake is the second most potent snake venom in the world.

Clinical effects Perhaps because of their small fangs and relatively small amount of venom available, many brown snake bites are minor, not requiring antivenom therapy. Of course, this is not known initially, so all bites should be treated as potentially lethal. In the days prior to antivenom therapy less than 10% of brown snake bites were fatal. However, this low rate of lethality is more than compensated by the frequency of bites and when a brown snake does inject plenty of venom, it is both very toxic and rapid acting. A typical brown snake bite is either painless or almost painless. The tiny fangs often leave only faint puncture or scratch marks, without local redness, bruising or swelling. Indeed, the bite can be hard to see without a magnifying glass. Do not be fooled; even such an apparently trivial looking bite can result in lethal envenoming, particularly in young children. If a significant amount of venom has been injected, then the patient may develop local draining lymph node tenderness/swelling, a persistent ooze from the bite site, headache, nausea/vomiting, abdominal pain, severe coagulopathy and sometimes, kidney damage. Paralysis is also possible but is only rarely seen, even with otherwise severe envenoming. Myolysis does not occur. In young children and occasionally in adults, early collapse ± grand mal convulsions may occur. In cases where there has been massive envenoming such as with multiple bites, the early collapse may be associated with cardiac arrhythmias and even cardiac arrest, probably secondary to short-lived coronary vessel occlusion by thrombi generated by venom procoagulants. However, it is coagulopathy which is the hallmark of brown snake envenoming. There is consumption of circulating fibrinogen, with production of breakdown products. The defibrination may be total within 30 mins of the bite. Fortunately, platelets are often not affected, at least initially. In these patients with complete defibrination, the INR will be >12 (actually infinity), the fibrinogen unmeasurably low and degradation products massively elevated. The patient is at risk of major haemorrhage and fatal intracerebral haemorrhages do occur. Anything causing hypertension is to be avoided. Antivenom is the best way to reverse this devastating coagulopathy but large amounts may be required. FFP is usually not needed and is contraindicated until all circulating venom has been neutralised with adequate antivenom, except if there is severe, life threatening haemorrhage.

For brown snake bites, the majority of patients will not need antivenom. However, if there is any evidence of either coagulopathy or kidney damage, antivenom is required. If systemic symptoms and coagulopathy are only mild (say INR >1.5 but <2.0), then an initial dose of 2 vials of CSL Brown Snake Antivenom may be sufficient. If, however, there is major coagulopathy, commence with 4 vials of antivenom and expect to give 2 to 6 more vials over the next few hours, titrated against coagulation results. Wait 3 hours before definitive retesting of coagulation to determine if more antivenom is required. Kidney damage is the other major clinical problem of brown snake bite. It is mostly seen in adults, especially if they have had alcohol prior to the bite. Causation is uncertain, probably multifactorial, but may include direct nephrotoxic action of the venom, though this is, as yet, unproved. Early generous iv hydration in all cases of brown snake bite may reduce the chance of major kidney damage.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Brown Snake Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each vial/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field.

What to do if there is an immediate untoward reaction to the antivenom (This section is common to most antivenoms) What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for

review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. If several bottles of antivenom have been given to the patient (eg >4) it may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

CSL Tiger Snake Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian tiger snake group and also copperheads, the rough scaled snake, the broad-headed snake, the paleheaded snake, Stephen's banded snake and many members of the black snake group (but not the mulga or king brown snake or Collett's snake). It is also effective against many sea snake bites. It is made from horse IgG. Each ampoule contains 3000 units of neutralising capacity against the target venoms. Average volume per ampoule is 9-12mL. The immunising venom is common tiger snake venom.

Information about the snakes covered by this antivenom The species Tiger snakes are a common cause of snakebites and the second most common cause of snakebite deaths in Australia. Adult fangs in the common tiger snake are about 3.5mm long. They produce a moderate amount of very toxic venom. They vary in length up to 1.5m, though some sub species of black tiger snake may exceed 2m, with correspondingly longer fangs and more venom. Coloration for the common (mainland) species is variable, though most specimens show banding. However, unbanded brown or black colour phases are seen. The black tiger snake is usually coloured as its name suggests, though juveniles may show faint banding. The common copperhead is similar in size to the common tiger snake, but has a russet sheen on the sides of the body and is not banded. There are typical pale cream or white edging to the scales of the upper and lower lips in all copperheads, a useful diagnostic feature. The highland copperhead is similar to the common copperhead, though generally smaller. The pygmy copperhead is smaller and grey in colour. The rough scaled snake, also known as the Clarence River tiger snake, is up to 1.2m long, with banding on the body. The broad-headed snake, pale-headed snake and Stephen's banded snake, all of the genus Hoplocephalus, are generally nocturnal, and small in size. Colouration depends on species.

The black snakes are also mentioned under the section on black snake antivenom, although CSL Tiger Snake Antivenom is often the preferred choice for treatment. Two of the species recognised in Australia; the red bellied black snake, a uniformly black coloured snake with a deep red belly; and the blue bellied or spotted black snake, with a black or dark grey-brown body with black specks and a dark to black belly, respond to CSL Tiger Snake Antivenom. Note that there are three other members of this genus in Australia, the mulga snake (king brown), Butler's mulga snake and Collett's snake. The former two are large brown coloured snakes from arid Australia, which respond best to CSL Black Snake Antivenom and are discussed in detail in the section on that antivenom, along with Collett's snake.

Common tiger snake Notechis scutatus

Common tiger snake Notechis scutatus

Black tiger snake Notechis ater

Rough scaled snake Tropidechis carinatus

Common copperhead Austrelaps superbus

(no photo)

Highland copperhead Austrelaps ramsayi

Pygmy copperhead Austrelaps labialis

Broad-headed snake Hoplocephalus bungaroides

Pale-headed snake Hoplocephalus bitorquatus

Stephen's banded snake Hoplocephalus stephensi

Red bellied black snake Pseudechis porphyriacus

Spotted black snake Pseudechis guttatus

Distribution Tiger snakes are moderately common in wetter areas of southern and coastal eastern Australia, particularly near water courses or swamps. The copperheads are also found in wetter areas of south eastern Australia. The rough scaled snake is found in wetter areas in selected parts of eastern Australia. The broad-headed snake is increasingly rare, confined to rocky areas of parts of the great Divide, NSW. The pale-headed and Stephen's banded snakes have a wider range in NE NSW, through to SE Queensland. The Black snakes are found in a variety of habitats in eastern Australia. The commonest species, the red bellied black snake prefers wetter areas, often near water. The blue bellied black snake is more common in dryer habitats, notably in rocky areas.

Venom composition Tiger snake venom is very potent and contains neurotoxins, both pre and post-synaptic, myolysins, and procoagulants. Kidney damage may occur, but is probably a secondary phenomenon. Copperhead venom is less well characterised but contains neurotoxins and may cause myolysis. Coagulopathy is less certain. Rough scaled snake venom has effects very similar to those of tiger snake venom. Broad-headed snakes, pale-headed snakes and Stephen's banded snake venom contain a procoagulant, but not neurotoxins or myolysins of clinical significance.

Black snake venoms are less toxic and do not contain major neurotoxins, myolysins or procoagulants, though minor myolysis may occur.

Clinical effects Prior to the development of antivenom, nearly 50% of all tiger snake bites were fatal. This snake is still an important cause of snakebite deaths. Unlike brown snake bites, most tiger snake bites will result in systemic envenoming, so most patients will need antivenom therapy. A typical tiger snake bite is felt, is locally painful and often there is local redness, swelling, and bruising at the bite site. Occasionally there is a small area of skin damage. Fang puncture or scratch marks are usually visible to the naked eye. The venom will cause the usual features of systemic envenoming, such as headache, nausea/vomiting, abdominal pain and sometimes collapse. In children early collapse and grand mal convulsions may occur. Draining lymph nodes may be tender. Paralysis is a common feature of tiger snake bites. The earliest sign is usually ptosis, which develops from 1 to several hours after the bite. It may be followed by progressive paralysis of ocular, facial, peripheral and glossopharyngeal muscles, the latter imperilling the airway. Full paralysis of respiratory muscles may eventually develop, if no antivenom is given. Presynaptic paralysis by this venom is not reversed by antivenom, therefore it is essential that early signs of paralysis be noted and antivenom given then, prior to development of major paralysis. If the patient presents many hours after the bite, with major paralysis requiring intubation and ventilation, it may be necessary to continue this for days, weeks, very occasionally even over a month! Severe myolysis can occur with tiger snake bites, particularly if treatment is delayed or inadequate. The usual signs may occur, including muscle weakness and movement pain, myoglobinuria (red/brown urine that looks like haematuria and tests positive for blood) and later development of muscle wasting. Secondary kidney failure may occur, as may severe hyperkalaemia, a potentially fatal complication requiring heroic measures, including dialysis. Defibrination coagulopathy is a common feature of tiger snake bites, may be profound as with brown snake bites, and lethal cerebral haemorrhages have occurred. However, unlike brown snake bite defibrination, which is slow to resolve without antivenom therapy, tiger snake bite defibrination often completely resolves spontaneously after 15 to 18 hours, even without antivenom therapy. Thus a tiger snake bite seen very late may have apparently normal clotting, but degradation products will still be raised, as evidence of the earlier oagulopathy. Given the danger of major haemorrhage, letting the coagulopathy resolve spontaneously is definitely not a clinical option, and it should be treated, if present, with antivenom. Usually at least 3-4 vials of CSL Tiger Snake

Antivenom will be needed. FFP is generally not needed and should not be used if there is still circulating venom, except if there is major, life threatening haemorrhage. Kidney damage does occur, though less commonly than with brown snake bites, and causation is multifactorial, due to secondary factors such as myolysis and coagulopathy. Copperhead bites are only infrequently reported and there is a paucity of good clinical data. From available information it appears that the common copperhead can cause severe envenoming, with paralysis and possibly myolysis, but defibrination type coagulopathy is unlikely, though secondary kidney damage might occur. Bites are likely to cause local pain and swelling. Bites by the highland copperhead are likely to be similar to those of the common copperhead. For the pygmy copperhead in SA, all bites so far recorded have been minor, with minimal local pain or swelling and no significant systemic effects. However, this does not imply that every bite will be minor. Bites by the broad-headed snake, pale-headed snake and Stephen's banded snake can cause severe defibrination coagulopathy, but not paralysis or myolysis. Clinically they behave similarly to brown snake bites, with which they may be confused. Rough scaled snake bites can be severe, with local pain and swelling, paralysis, myolysis, defibrination coagulopathy and secondary kidney damage. Bites by black snakes are rarely life threatening and do not cause paralysis, defibrination coagulopathy or major myolysis. They are discussed in more detail below, in indications for antivenom use.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Tiger Snake Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the

Product Information be read before use and if necessary contact be made with a specialist in the field. For tiger snake bites, the majority of patients will need antivenom. Any evidence of paralysis, myolysis, coagulopathy or kidney damage, or clear general symptoms of envenoming, such as vomiting or collapse, mandate the early use of antivenom. Start with at least 2 vials of CSL Tiger Snake Antivenom, or 4 if there is coagulopathy, severe paralysis, a multiple bite or the bite was by one of the larger subspecies of black tiger snake. Be prepared to give further doses to reverse the coagulopathy, or reduce the degree of severe myolysis. The extent and resolution of coagulopathy can be used to guide antivenom dosage. For copperhead bites, the proportion of bites requiring antivenom therapy is less certain. For bites by the common copperhead and highland copperhead, it may be similar to tiger snake bites, but for the pygmy copperhead in SA, very few bites will require antivenom therapy (in fact no confirmed cases so far). For the common copperhead and highland copperhead, start with at least 1 vial of CSL Tiger Snake Antivenom, but use more than 2-4 vials if it is a multiple bite or the patient is already severely envenomed. As coagulopathy is probably not a major feature of bites by this snake, its extent and resolution cannot be used to guide antivenom dosage. For rough scaled snake bites follow the guidelines for tiger snake bites, which are very similar in clinical effects. The extent and resolution of coagulopathy can be used to guide antivenom dosage. For bites by the broad-headed snake, pale-headed snake and Stephen's banded snake, antivenom is required if there is a coagulopathy, probably present in at least 50% of bites. Start with 2-4 vials, however further doses may be required to reverse severe defibrination. For bites by the red bellied black snake and the blue bellied black snake (=spotted black snake), antivenom is often less important, as these bites are rarely life threatening, though they may be distressing for the patient. Certainly, only cases with major systemic envenoming should be considered for antivenom therapy. As paralysis and coagulopathy do not occur, they cannot be used as criteria of envenoming. Myolysis, if present at all, is generally very mild, with peak CK of <2000IU. This does not, by itself, warrant antivenom therapy. If the patient is a young child or elderly or infirm, then antivenom therapy should be considered more actively. Apart from these patients, in ormal healthy adults, antivenom is best reserved for severe envenoming with recurrent vomiting, major abdominal pain or headache, or where there are other significant symptoms or signs. Transient headache, vomiting or abdominal pain are not sufficient to commence antivenom therapy following bites by these snakes. If antivenom is to be used, CSL Tiger Snake Antivenom is effective and is preferred to CSL Black Snake Antivenom for two reasons; it is lower volume, therefore safer, and it is cheaper.

One vial will often be sufficient, though occasionally 2 or more vials are needed to resolve all symptoms.

What to do if there is an immediate untoward reaction to the antivenom (This section is common to most antivenoms) What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. If several bottles of antivenom have been given to the patient (eg. >4) it may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

CSL Black Snake Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian black snake group. It is made from horse IgG. Each ampoule contains 18000 units of neutralising capacity against the target venoms. Average volume per ampoule is 30-50mL. The immunising venom is mulga snake venom. The main species for which this antivenom is used are the mulga snake (=king brown), Butler's mulga snake, Collett's snake and the Papuan black snake. It is also effective for bites by other members of this genus, namely the red bellied black snake and the blue bellied black snake (=spotted black snake). However, CSL Tiger Snake Antivenom is usually used in preference for treating bites by these latter three species. For this reason, details about these snakes is given in the section on CSL Tiger Snake Antivenom.

Information about the snakes covered by this antivenom The species The mulga snake or king brown is a large land snake which may exceed 2.5m in length. It has moderately large fangs and produces more venom than any other Australian snake. It is fortunate that this venom is less toxic than some of the other species. It is brown to red brown in body colour, with cream coloured belly scales. The body scales have distinctive

colouration, being paler brown or cream on the inner aspect, darkening towards the margin of each scale. This gives the snake a subtle reticulated appearance, but is easily mistaken for a uniform brown colour. The head is large and triangular in shape, compared to the true brown snake. Butler's mulga snake is similar except it has more distinct yellow or cream markings on the body, producing a speckled pattern in some specimens.The appearance of the other species is listed in the section on CSL Tiger Snake Antivenom. Collett's snake may exceed 2.5m in length. It is brown with pinkish specs on the body which is almost banded in some specimens.

Mulga or king brown snake Pseudechis australis

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Butler's mulga snake Pseudechis butleri

Collett's snake Pseudechis colletii

Distribution The mulga snake is common in arid and semi arid areas through to tropical areas in northern Australia. It is found in some urban areas in central and northern Australia. Butler's mulga snake is restricted to inland areas of thesouthern half of WA. Collett's snake is found in a restricted area of central Queensland.

Venom composition Mulga snake venom contains several potent phospholipase toxins that are either myotoxins or neurotoxins. There is also an anticoagulant toxin, but no procoagulant is present. Butler's mulga snake is presumed to have a similar venom. Collett's snake has venom similar to the mulga snake.

Clinical effects It is not known what proportion of mulga snake bites would be lethal if no treatment were given, though a figure of 30% has been estimated. Because of the size of these snakes and the large amount of venom available, it may be expected that most cases will be envenomed. Locally, bites cause pain and extensive swelling, which may involve much of the bitten limb, however tissue damage is rare and the swelling usually subsides over 2-4 days. The principal clinical problem with mulga snake bites is myolysis, which may be severe, with potential for secondary kidney failure and hyperkalaemia. The usual clinical features of myolysis may be expected, including myoglobinuria (red to brown urine testing positive for blood), skeletal muscle weakness and pain on movement. Defibrination coagulopathy is not seen, but there may be slight elevation of clotting times due to anticoagulants in the venom. Because there are neurotoxins in the venom, paralysis might be predicted theoretically, but in clinical practice, neuromuscular paralysis of clinical significance is rarely seen (except for ptosis), though there may be detectable muscle weakness secondary to muscle damage. Occasionally there may be an anticoagulant coagulopathy, with prolonged prothrombin time and aPTT, but normal fibrinogen and no fibrin(ogen) degradation products. Collett's snake and probably Butler's mulga snake cause similar clinical effects.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Black Snake Antivenom should only be given if there is clear evidence of envenoming. See potential complications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes.Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have

adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary, contact be made with a specialist in the field. The antivenom of choice for envenoming by mulga snakes is CSL Black Snake Antivenom. It should be used in every case where there is evidence of systemic envenoming. Because whole blood clotting time is unlikely to be prolonged greatly in mulga snake bites, it is not a useful measure of systemic envenoming in these cases. Therefore, in any case of mulga snake bite, Collett's snake bite or Butler's mulga snake bite, if there are general symptoms of envenoming present, such as persistent headache with nausea/vomiting or abdominal pain, it is generally advisable to give 1 vial of antivenom. If there is already severe myolysis established at the time of presentation, it may be necessary to give a second vial of antivenom. For bites by the red bellied black snake and the blue bellied black snake (=spotted black snake), see the section on CSL Tiger Snake Antivenom. Should this antivenom be unavailable, then the initial dose of CSL Black Snake Antivenom for bites by these species requiring antivenom therapy (many bites don't need antivenom), is often listed as 1/3 to 1/2 a vial. Except in smaller children, where volume is an issue, in practice it is probably best to give a full vial. This ensures a very adequate dose is given and avoids wastage of antivenom. It may increase the risk of serum sickness, but this is a lesser consideration.

What to do if there is an immediate untoward reactio to the antivenom (This section is common to most antivenoms) What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. It may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

CSL Death Adder Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian death adder group. It is made from horse IgG. Each ampoule contains 6000 units of neutralising capacity against the target venoms. Average volume per ampoule is 25-26mL. The immunising venom is from the common death adder.

Information about the snakes covered by this antivenom The species Death adders are distinctive snakes, with triangular heads, squat bodies, and thin tails, sometimes used as a lure. They are the only dangerous Australian venomous snake habitually nocturnal, though most other species will be active on hot nights. They are also known as "deaf" adders, with good reason. Like all snakes, they lack external ears and so rely on vibration rather than hearing to detect the approach of large animals, including humans. All other dangerous Australian snakes will usually try and move away from a potential threat. Death adders often rely on camouflage, burrowing deeper into leaf litter or other ground debris, rather than moving out of the way. If stepped on they will bite rapidly and effectively. It is therefore fortunate that death adders seem to have adjusted poorly to human encroachment on their environment. In many parts of southern Australia, at least, their range is contracting. They are a rather infrequent cause of bites now.

Common death adder Acanthophis antarcticus

Desert death adder Acanthophis pyrrhus

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Northern death adder Acanthophis praelongus

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Pilbara death adder Acanthophis wellsii

Distribution Death adders are found in a variety of habitats, both arid and temperate to tropical, but in most parts of their current range, they are infrequently encountered. In some areas this is due to contracting populations of these snakes, but in other areas it is more likely due to their cryptic habits. They are not found in Tasmania or the islands off the southern coast.

Venom composition Death adders have large fangs, producing a considerable quantity of toxic venom. However, in humans, the only major effect of this venom appears to be post synaptic neurotoxic paralysis. The venom does not contain either procoagulants or myolysins of significance.

Clinical effects 50 to 100 years ago, death adder bites were greatly feared, carrying a 50% mortality rate, due to profound paralysis. With current medical facilities, paralysis should be a nonlethal complication of snakebite in all but the most exceptional of cases, therefore death adders should no longer be considered near the top of the list of Australia's dangerous

snakes. Current statistics tend to confirm this view. Many bites should result in systemic envenoming, but in practice, at least in urban areas, nearly all bites are from captive specimens and usually are trivial. Where venom has been injected, there is often local pain and mild swelling, followed by progressive development of paralysis over the next few hours, starting with ptosis, then affecting other cranial nerves, peripheral muscles, and finally, if untreated, respiratory muscles. Major respiratory paralysis can occur within 6 hours of the bite. Defibrination coagulopathy, myolysis and major kidney damage do not occur, although the latter might conceivably occur as a secondary complication.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Death Adder Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg. saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field. The indication for antivenom therapy in death adder bite is relatively simple; at the earliest sign of paralysis (usually ptosis), antivenom should be given. The specific antivenom is CSL Death Adder Antivenom, and 1 vial is often sufficient. If the paralysis progresses despite the initial dose, give a second vial. Because the neurotoxins in this venom are post synaptic, non-antivenom treatments for paralysis may also be effective if antivenom is not readily available. Specifically, anticholinesterases (eg neostigmine) may retard or even reverse development of paralysis by making more acetylcholine available as transmitter at the neuromuscular junction, allowing the post synaptic blockade to be overcome.

What to do if there is an immediate untoward reactio to the antivenom (This section is common to most antivenoms)

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. It may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

CSL Taipan Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian taipan snake group. It is made from horse IgG. Each ampoule contains 12,000 units of neutralising capacity against the target venoms. Average volume per ampoule is 43-50mL. The immunising venom is from the common taipan.

Information about the snakes covered by this antivenom The species The taipans are, at least in theory, amongst the most deadly snakes in the world, combining very potent venom, large amounts of venom and long fangs with accurate strike. The common taipan may exceed 2.5m in length and is found in mixed habitats. It often has a pale head with olive to brown body and is a swift moving snake. The inland taipan (=western taipan; small scaled snake; fierce snake) has a more restricted natural distribution, but is also a large snake, sometimes exceeding 2.5m. Colour is variable, some specimens having a shiny black sheen to the head at some times of the year.

Common taipan Oxyuranus scutellatus

Inland taipan Oxyuranus microlepidotus

Distribution The common taipan is found across the top of Australia and part way down the east coast, and may enter urban areas. The inland taipan is restricted to arid areas, mostly black soil plains country in part of central inland Australia, including some of the Lake Eyre drainage basin. It is only rarely encountered, but is possibly common within its range, where it may spend much of the time beneath the surface, in the deep cracks in the soil. Because of their reputation, both taipans are much sought after by reptile collectors, and a considerable number of these snakes are kept alive in both public and private collections in capital cities and some rural towns, thus bites may present well outside of the natural range for these snakes.

Venom composition Taipan venom is amongst the most potent of all snake venoms. Inland taipan venom is the most toxic snake venom known. Both species of taipans have similar venom components, including both pre and post-synaptic neurotoxins, powerful procoagulants, myolysins, and clinically, kidney damage may occur, though this may be secondary. The common taipan may have fangs >1cm in length, capable of penetrating a leather boot! This, coupled with the large quantity of venom produced, has helped fuel the fearsome reputation of these snakes.

Clinical effects Prior to the development by CSL of specific taipan antivenom in 1956, taipan bite was nearly always fatal. There were only two reported survivors of taipan bite in the years before 1956. Nearly all taipan bites are likely to result in life threatening envenoming, with the exception of bites by juveniles in captivity, where current experience suggests that the rate of major bites may be lower. There is often pain and swelling at the bite site, though this is not always so and a trivial looking bite site does not imply a trivial bite. There may be rapid development of major

systemic envenoming, including headache, nausea/vomiting, collapse, convulsions (especially in children), paralysis, defibrination coagulopathy, myolysis and kidney damage. The paralysis may be severe, with major respiratory paralysis developing within 2 to 6 hours of the bite in some cases. The coagulopathy is often profound, with complete defibrination within an hour of the bite and a potential for major haemorrhage, including cerebral haemorrhage. The myolysis, if present, is often not as severe as seen with some tiger snake and mulga snake bites. The kidney damage is by no means a constant feature of taipan bite but does occur sometimes, possibly as a secondary phenomenon. There is one case of renal cortical necrosis following taipan bite.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Taipan Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary, contact be made with a specialist in the field. Given the high potential for severe envenoming with taipan bites, antivenom therapy should be considered as soon as there is any suggestion of systemic envenoming, such as headache, nausea/vomiting, abdominal pain, or clinical evidence of paralysis (eg ptosis), coagulopathy (eg bleeding from the bite or gums), or myolysis (eg muscle pain or myoglobinuria). Initial dose in even a mild case should be 1 vial of CSL Taipan Antivenom. If there is severe defibrination, then start with at least 3 vials of antivenom and be prepared to give more, up to 5 to 8 in total (only rarely would more be needed). In areas of Australia where the taipan is only found as captive specimens, which includes most capital cities, then CSL Taipan Antivenom may not be readily available. In this circumstance, CSL Polyvalent Snake Antivenom is a very good alternative. It is only slightly higher in volume and price than the taipan specific antivenom. Bites by inland taipans should be handled in the same way as for the common taipan.

What to do if there is an immediate untoward reaction to the antivenom (This section is common to most antivenoms)

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. It may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

CSL Polyvalent Snake Antivenom Basic Information Used for neutralising systemic envenoming by all dangerous Australian snakes. It is made from horse IgG. Each ampoule contains 1,000 units of neutralising capacity against brown snake venom, 3,000 units against tiger snake venom, 18,000 units against mulga snake venom, 6,000 units against death adder venom and 12,000 units against taipan venom. It is therefore equivalent in neutralising power, to giving the patient 1 ampoule of each of the five "monovalent" snake antivenoms. Average volume per ampoule is high, as expected, about 46-50mL.

Information about the snakes covered by this antivenom The species CSL Polyvalent Snake Antivenom covers all dangerous Australian snakes. For details see the previous sections on "monovalent" snake antivenoms. There is some clinical experience suggesting that this antivenom may also be effective for the treatment of envenoming by the New Guinea small-eyed snake (Micropechis ikaheka).

Distribution See relevant specific snake antivenom pages.

Venom composition See relevant specific snake antivenom pages.

Clinical effects See relevant specific snake antivenom pages.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Polyvalent Snake Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/ dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field. Because of its higher volume and cost, CSL Polyvalent Snake Antivenom should only be used if it is not possible to use a specific or "monovalent" snake antivenom. This will occur in several circumstances: • The type of snake cannot be identified, because venom detection has failed or is not available, and the range of possible snakes would require mixing of 3 or more "monovalent" snake antivenoms. • The patient is very severely envenomed, and waiting for venom detection results would cause unacceptable delay in starting antivenom treatment, and the range of possible snakes would require mixing of 3 or more "monovalent" snake antivenoms. • CSL Polyvalent Snake Antivenom is the only antivenom available in the hospital able to cover the type of snake which caused the bite. • Stocks of appropriate "monovalent" antivenom have all been used and the patient requires further antivenom before restocking supplies arrive. Never overlook polyvalent antivenom as a back up in this situation. If the patient is not severely envenomed and it is possible to determine the type of snake involved, and appropriate "monovalent" antivenom is available, then do not use CSL

Polyvalent Snake Antivenom as it is both higher volume (= higher risk of adverse reactions) and higher cost than the "monovalent" antivenom. In some parts of Australia, the range of snake species is limited. If all likely species are covered by just 2 "monovalent" snake antivenoms, then it is better to give these as a mixture, rather than use polyvalent antivenom. Examples of this would be the greater metropolitan areas of Melbourne and Adelaide, where all naturally occurring snake species would be covered by just CSL Brown Snake Antivenom and CSL Tiger Snake Antivenom. Similarly, in Tasmania, only CSL Tiger Snake Antivenom would be required. The same applies to Kangaroo Island in SA. Detailing such options for every part of Australia is beyond the scope of this publication.

What to do if there is an immediate untoward reaction to the antivenom (This section is common to most antivenoms)

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy, if this has not been given prophylactically. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. It may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).

First Aid for Bites and Stings Basic Principles There are several important principles of first aid for bites and stings that should guide decisions on what is, and as importantly, what is not good first aid. • • •

First aid should do no harm! First aid should be practical and achievable. First aid should be supported by both clinical and scientific evidence of effectiveness.

Older "first aid" methods for snakebite are classic examples of techniques with the potential to cause the patient harm. Indeed, the use of tourniquets and "cut and suck" have resulted in numerous cases of permanent and severe injury to patients, even deaths.

The Pressure Immobilisation Method The Pressure Immobilisation Method This important first aid method was developed by Dr. Struan Sutherland and colleagues at CSL and first published in 1978 in the prestigious international journal, "The Lancet". It is based on knowledge of the structure of important snake and spider toxins and previous clinical and experimental experience. It has been known for many years that the lymphatic system plays a key role in transport of toxins from the periphery to the circulation. In the case of snake venom toxins this is easily explained by the large size of these toxins. Clinically, adenopathy in nodes draining the bite site is often an early sign of absorption of venom, and in those tragic cases ending fatally, Sutherland was able to show high concentrations of venom in regional nodes. The aim of this method is therefore to retard venom transport via the lymphatic system. This is achieved in a dual approach. Firstly the lymphatic vessels at the bite site are compressed by bandaging, extended to much of the rest of the bitten limb as possible. Secondly, proximal movement of lymph in the vessels is slowed or stopped by splinting the limb, thus also stopping the "muscle pump" effect of muscle movement. Correctly applied, this technique can virtually stop venom movement into the circulation until removed, up to hours later, without any threat to limb tissue oxygenation, which is just one of the major problems in using tourniquets. It must be remembered, however, that

this method is only first aid. It is not definitive medical treatment for envenoming. Once in a hospital equipped to treat the bite with antivenom, if necessary, then all first aid should be removed after initial tests and precautions are taken. The details of these may be found in the following section on "Medical Treatment of Bites and Stings". In summary, the pressure immobilisation method of first aid is: • Apply a firm broad bandage or similar (even clothing strips or pantyhose will do in an emergency) over the bite site, at the same pressure as for a sprain. Do not occlude the circulation. • Apply further bandage over as much of the rest of the bitten limb as practical. Ensure fingers or toes are covered to immobilise them. It is often easiest to go over the top of clothing such as jeans, rather than move the limb to remove clothing. • Ensure the bitten limb is kept motionless by applying a splint and instructing the patient to cease all use of the limb and any general activity.

The pressure immobilisation method of first aid is ideal for Australian snakebite by all species, as well as bites from suspected funnel web spiders and mouse spiders, and for bites by the blue ringed octopus and cone. It is not appropriate for bites from the red back spider, other spiders, scorpions or centipedes or stings from venomous fish.

First Aid for Snakebite • Keep the patient still and reassure them. • Maintain vital functions, if imperilled (e.g. "ABC") • Immediately apply a pressure immobilisation bandage.

• Try and maintain the patient as still as possible and bring transport to them. • Always seek medical help at the earliest opportunity. • If the snake has been killed, bring it with the patient, but do not waste time, risk further bites and delay application of pressure bandage and splint by trying to kill the snake. • Do not wash the wound. • Do not use a tourniquet. • Do not cut or suck the wound. • Do not give alcohol to the patient. • Do not give food and only non-alcoholic clear fluids may be used for drinks.

First Aid for Funnel Web Spider Bite • As for snakebite, using pressure immobilisation method. • Always try and bring the spider with the patient, for identification at the hospital.

CSL Funnel Web Spider Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian funnel web spider group. It is made from rabbit IgG. Each ampoule contains 125 units of neutralising capacity against the target venoms. This is a freeze dried preparation. Re-constitute with approximately 6.3mL of Water for Injections BP. The immunising species is the Sydney funnel web spider.

Information about the spiders covered by this antivenom The species CSL Funnel Web Spider Antivenom was originally developed to treat cases of bites by the Sydney funnel web spider, but has proved effective in bites by a variety of other species of funnel web spiders as well. There are at least 35 species of funnel web spiders, in 2 genera, Atrax and Hadronyche. All are medium to large, robust spiders, mostly dark or black in colour, with stout legs and large fangs. Both males and females build silk tube retreats, usually in the ground. Males leave these retreats in search of female mates, a process which may increase the chance of adverse interaction with people, as the

wandering males may get underfoot, into shoes, boots or clothing left on or near the floor. There is experimental evidence suggesting that this antivenom may also be effective in treating severe envenoming by mouse spiders (Missulena).

Distribution Funnel web spiders have a wide distribution throughout south east Australia, including Tasmania. However, species so far proven dangerous to humans have a more limited range, largely limited to eastern parts of NSW and SE Queensland. The only proven killer, the Sydney funnel web spider, is restricted to the Sydney region and adjacent areas to the north and south of the city, including Gosford.

Venom composition Funnel web spider venom is multicomponent, but a protein toxin, robustoxin, is considered to be the principal component responsible for severe envenoming in humans. It is interesting to note that most mammals are relatively unaffected by funnel web spider venom, but humans are very sensitive. Robustoxin causes stimulation of the nervous system at a variety of synapse types, with rapid and devastating effect.

Clinical effects Despite its fearsome reputation, there are only 14 recorded deaths due to funnel web spider bite, and experience has shown that many bites do not result in significant envenoming. However, when the spider does inject a dangerous quantity of venom, the effects can be rapid and severe, and death within an hour may occur. The bite is usually painful, both due to large fangs and acidic venom and the spider is usually seen. If envenoming occurs, it will develop early, starting with tingling around the lips, twitching of the tongue, then profuse salivation, lachrymation, sweating, piloerection and muscle twitching/spasms. Hypertension and tachycardia occur, and respiratory distress due to rapid development of pulmonary oedema, which may be very severe and potentially lethal. In the early stages it may be mistaken for organo-phosphate poisoning. Convulsions may occur.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Funnel Web Spider Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur, though with envenoming by funnel web spider anaphylaxis is unlikely because of the "catecholamine storm" effect of the venom. Specifically, have adrenaline ready to give, though it is very unlikely to be required. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field. At the first sign of systemic envenoming due to suspected funnel web spider bite, it is advisable to give 2 vials of CSL Funnel Web Spider Antivenom, and be prepared to give another 2 to 4 vials. If envenoming is already severe, start with 4 vials. Any patient who has been bitten by a spider which is possibly a funnel web spider, and who develops excessive salivation or lachrymation or twitching of the tongue or respiratory distress should be assumed to have systemic envenoming and treated with antivenom. If there has been an initial response, followed by later return of respiratory distress without other features of envenoming (such as salivation and lachrymation), it is quite possible this is due to further venom entering the circulation, and more antivenom may be needed. Another possible explanation in this situation, at least in children, is that they are developing pulmonary oedema due to overload of IV fluids. Unless the latter is clearly the explanation, err on the side of further venom effect. If the respiratory impairment is mild, it might be reasonable to try a diuretic, such as frusemide, as first line therapy, but if this does not work, or respiratory distress worsens or is severe, use antivenom.

What to do if there is an immediate untoward reaction to the antivenom If there is either a sudden fall in blood pressure or bronchospasm, after starting the antivenom infusion, then temporarily stop the antivenom and give adrenaline by subcutaneous injection(1:1000 solution), give 100% O2 and IV fluids (such as Haemaccel®, but be cautious of fluid overload). Once the untoward antivenom reaction is thus controlled, cautiously recommence antivenom infusion.

Adrenaline dose; for adults give 0.5mL (0.5mg) initially; for children give 0.01mg/kg initially. Repeat as necessary and try IM injection if no response to SC injection. If bronchospasm is the major problem, try nebulised adrenaline, 2mL of 1:1000 solution.

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later, though this appears to be rare with CSL Funnel Web Spider Antivenom. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming.

First Aid for Red Back Spider Bite • Reassure the patient that their life is not at major risk. • Apply an ice pack to the bite area. • Seek medical advice. • Bring the spider with the patient if possible. • Do NOT use a pressure immobilisation bandage.

CSL Red Back Spider Antivenom Basic Information Used for neutralising systemic envenoming by Australian red back spiders, which are members of the black widow spider group found world-wide. It is made from horse IgG. Each ampoule contains 500 units of neutralising capacity against the target venom. Average volume per ampoule is 1-1.5mL. The immunising species is the Australian red back spider.

Information about the spiders covered by this antivenom The species Although this antivenom is developed purely for use against bites by the Australian red back spider, there is evidence it is effective against bites by any black widow spider. It may also be effective against bites by related Theriid spiders, such as the cupboard spider, Steatoda spp.. Red back spiders usually build webs under objects, with droplines

to the ground or other flat surface, thus they may commonly be found under lower shelves, the bottom rails of fence lines, in refuse areas, especially old car bodies, even on the underside of seats left outside and in the recesses of cupboards indoors! Only the female is dangerous to humans. As they tend not to wander, most bites occur when the person comes in contact with the web structure.

Distribution Red back spiders are found throughout Australia, in essentially all habitats, from very arid through to tropical, and they are common in urban areas, where most bites occur.

Venom composition The venom is multicomponent, with a family of protein toxins, the latrotoxins, most prominent. One of these, a-latrotoxin, is effective in mammals, including humans, causing stimulation of neural synapses throughout the body with wide ranging effects.

Clinical effects The clinical features of major envenoming by red back spiders are sometimes Herculean in extent, but rarely lethal. Less than 20% of bites actually result in significant envenoming, and it is only in this latter group that antivenom therapy should be considered. The classic effective red back spider bite is felt as a mild sting only, with little to see at the bite site. Between 10 and about 40 minutes later, the bite site becomes painful. The pain becomes severe, over a variable timeframe, extending proximally and involving draining lymph nodes in the axilla or groin. There is often local sweating. The pain may then spread to the abdomen, chest, neck or head, often associated with profuse sweating, either localised or general, mild to severe hypertension, and malaise with nausea. Many other symptoms or signs may occur, but the forgoing are clinically most consistent and useful for diagnosis. The progression from local to generalised pain may occur within 1 to 3 hours, or take up to 24 hours. In infants, general miserableness, refusal of feeds, inconsolable crying, and sometimes a non specific erythematous rash are key features of red back spider bite. Occasionally the initial bite may not have been noticed and the patient may present with abdominal or chest pain. In such cases, careful

questioning will usually elicit a history of possible exposure to spider bite and initial localised pain, pointing to the true diagnosis. In pregnancy, the generalised abdominal pain of red back spider bite may appear similar to onset of premature labour. Usually a clear history of a bite with initially local pain will be available.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Red Back Spider Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intramuscularly in most cases, not IV. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field. Because of its low volume, CSL Red Back Spider Antivenom has a very low incidence of adverse reactions and this has allowed a lowering of the threshold for using it. Any patient with symptoms consistent with significant envenoming by a red back spider, such as local then generalised pain, sweating, ± hypertension, should be considered for a trial of the antivenom, even if no spider was seen. Give 1 vial of CSL Red Back Spider Antivenom IM. If there is a complete or partial resolution of symptoms, the patient's distress has been alleviated and the diagnosis confirmed. If the initial response to antivenom is incomplete or a relapse occurs, give a further vial of antivenom. Occasionally it is necessary to give a third vial, but only rarely more than this, except if treatment has been delayed more than 24 hours, when higher doses are frequently required. Red back spider bite is one of the few cases where antivenom may be effective days after the bite. If the symptoms fit red back spider bite, it is quite acceptable to try a dose of antivenom a week, or more, after the original bite occurred. Multiple doses may be required. If, after 3 ampoules of antivenom, either early or late, there has been no improvement at all in symptoms, then reconsider the diagnosis. Patients in whom antivenom treatment has been delayed more than 24 hours occasionally require higher doses of antivenom, but it is often adviseable to extend the time between doses and consider the IV route. CSL Red Back Spider Antivenom has been given to pregnant women on a number of occasions, without detriment to the mother or foetus, with a normal infant delivered at term being the outcome.

What to do if there is an immediate untoward reaction to the antivenom If there is either a sudden fall in blood pressure or bronchospasm, after giving the antivenom, give adrenaline by subcutaneous injection, give 100% O2 and IV fluids (Haemaccel®). If adrenaline is to be given by subcutaneous injection, use a 1:1000 solution. For adults give 0.5mL (0.5mg) initially. For children give 0.01mg/kg initially. Repeat as necessary and try IM injection if no response to SC injection.If bronchospasm is the major problem, try nebulised adrenaline, 2mL of 1:1000 solution.

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later, but this is quite rare for CSL Red Back Spider Antivenom. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for envenoming by red back spiders.

First Aid for Other Spider Bites • As for red back spider bite. NOTE: For Mouse Spiders, first aid as per Funnel Web Spiders.

Spiders Necrotic Arachnidism This condition encompasses a broad spectrum of responses to spider bite, from very mild local skin damage through to major skin damage and systemic illness. It is a phenomenon seen in many parts of the world, but particularly in the Americas, where it is caused by the recluse spiders (Loxosceles reclusa, L. laeta, L. gaucho and others; "Loxoscelism"). In Australia local skin damage following presumed spider bite is not rare, with probably hundreds of cases each year. Most of these are minor, with ulcers of less than 2cm in size, but there are a few cases with large areas of skin loss requiring prolonged hospitalisation and ultimately, skin grafting. Several spiders have been suggested as causes of these ulcers (eg. white tailed spider) but until recently, none was proven. Recently in South Australia there have been cases where the spider was caught at the time of biting and in these cases it was a relative of the recluse spiders (fiddleback spider; Loxosceles rufescens). This spider is not native to Australia but has been accidentally introduced and

is establishing itself in metropolitan areas. However, it cannot be said that all cases of "necrotic arachnidism" in Australia are due to this spider. Indeed, it is likely that in many cases the cause of the ulcer is secondary infection. A typical case of necrotic arachnidism will present with a small, often painful, area of skin, usually found in the morning. It is presumed the bite occurred overnight while the patient was asleep. They often have erythema and a central blister at the presumed bite site. Over the next few days this may either resolve or develop a central ulcer, which is both painful and slow to heal. Secondary infection may occur and warrant treatment. The wound should be kept clean and the patient regularly reviewed. They should be told that this ulcer may take weeks or even months to fully heal. Occasionally the local lesion is more alarming, with extensive blistering and darkening of the skin. The darkened skin, which may be deep blue to black, may well become fully necrotic, leaving a large area of painful full thickness skin loss. Such cases require hospitalisation, bed rest, careful cleaning, antibiotics (after culture), and DELAYED surgical debridement. There is limited evidence that hyperbaric oxygen may assist in the healing process, which in any case, may be prolonged.

Some notable spiders & other arthropods The white tailed spider, Lampona cylindrata The white tailed spider, Lampona cylindrata This common hunting spider, found in houses, has been linked with necrotic arachnidism, often tenuously. Experience with definite bites by this spider has generally been that both pain and local reactions were mild to moderate, with very few cases where ulceration developed. Venom research has failed to confirm that this spider damages skin. While the white-tailed spider cannot yet be excluded as a cause of necrotic arachnidism, there is no evidence to suggest that it is the major cause. Bites by organisms unknown, causing ulceration, should NOT be labelled as "white-tailed" spider bites.

The black house spider, Badumna insignis A robust black spider found in untidy webs with a tube retreat. Common in urban habitats. Its bite can cause moderate local pain, with erythema and swelling, and occasionally mild systemic symptoms. The black house spider ia a likely candidate for causing some cases of necrotic arachnidism.

The huntsman spiders There are many species, common inside houses, but bites are generally very mild, with short lived pain. A few species can occasionally also cause mild systemic symptoms, notably headache and nausea.

The wolf spiders Many species of these ground hunting spiders are common in gardens, sometimes entering houses. Few bites are recorded and on this limited evidence, it appears bites are minor.

Orb weaving spiders These common spiders, with many species, build "typical" spider webs in the garden at night. People walking into the web and crushing the spider against their body may be bitten, resulting in mild local pain and a small red lump, lasting about 24 hours. These spiders may also hide in clothing left outside overnight, on washing lines. The next person to put the clothing on may be bitten!

Trapdoor spiders Again, a number of species of robust, ground dwelling, burrowing spiders, with very large fangs. They are often dug up in gardens. Bites appear to cause surprisingly mild pain, given the spider's size, and no systemic problems.

Mouse spiders Ground dwelling spiders with large fangs, and venom which is reported to be more toxic than that of the funnel web spider (in tests involving mice). Apart from a single case from Queensland, all reported bites by these spiders have been minor. The Queensland case had some similarity to envenoming by a funnel web spider. There is a growing body of research suggesting that this spider could cause major envenoming, similar to that of the funnel-web spider, and is likely to be responsive to CSL Funnel Web Spider Antivenom, although this is not yet an approved indication.

Centipedes These have fangs and venom glands at the head end and bites may cause severe local pain. Infection sometimes occurs, which is occasionaly severe.

Scorpions None of the many species of Australian scorpions is dangerous to humans but most cause intense local pain when they sting. This usually lasts only a short while, and systemic symptoms rarely occur and are never severe.

Ticks The most important ticks are those which cause paralysis, discussed under the section on tick antivenom. Many other ticks may bite humans causing a variety of local reactions, usually local irritation or pruritis. A few may sometimes cause a mild systemic illness, including malaise, nausea or headaches. It should be noted that ticks do transmit a variety of diseases, both in Australia and overseas. A discussion of this problem is beyond the scope of this publication, but some of these tick borne diseases can be severe.

Jellyfish and Other Marine Animals General Principles There are many species of jellyfish which can affect humans. The major Australian box jellyfish, Chironex fleckeri , is the only proven lethal species, for which there is an antivenom, and will be discussed in that section. There are several other species which can cause severe, maybe lethal, reactions. All jellyfish sting using individual stinging cells (nematocysts), and millions of these may discharge into a patient in a major jellyfish sting. Some of this venom may directly enter capillaries, so systemic envenoming can be very rapid indeed. Much less commonly, the venom may cause "allergic" type reactions in some people. Pain is not a universal diagnostic feature of all jellyfish envenoming, though it is the most common symptom. •

Irukandji syndrome • Jimble • Morbakka • Bluebottle • Sea nettle • Mauve stinger • Hair jelly • Cone shells

•

Blue ringed octopus • Stingrays • Stinging fish • Toxic fish • Sea snakes

Irukandji syndrome This important response to stings by several probably related species of small and virtually invisible, tropical jellyfish (including Carukia barnesii) is typified by mild local pain, usually without skin marks. About 30 to 40 minutes later there may develop the typical syndrome of cramping muscle, back and abdominal pains, prostration, hypertension and occasionally, pulmonary or cardiac complications, notably pulmonary oedema. This is a most unpleasant condition and is potentially lethal. There is no antivenom. Hospitalisation is essential for the full blown syndrome. Early vinegar application is recommended for nematocyst inhibition.

Jimble, Carybdea rastoni A small 4 tentacled box jellyfish found commonly (but not exclusively) in southern Australian waters in summer, often in swarms. The sting is painful, with an angry red mark. Significant systemic effects are recently being reported from tropical waters.

Morbakka, Tamoya sp. A large 4 tentacled box jellyfish from tropical waters, which causes a very painful sting which may show cross hatching skin marks (as seen with Chironex fleckeri). Systemic envenoming may occur, including collapse, but there are no recorded deaths. There is no antivenom and vinegar is effective as first aid.

Bluebottle, Physalia sp. A medium sized "jellyfish" causing stings in northern and eastern Australian waters mainly, often in swarms. There is immediate pain lasting an hour or more, with typical elliptical blanched wheals and surrounding erythema. Mild or no systemic symptoms are usual, but a musclepain syndrome may occur. There is no antivenom. Vinegar or water discharges adherent nematocysts.

Sea nettle, Chrysaora sp. Moderate sized jellyfish which causes mild to moderate local pain, lasting up to several hours. Allergic reactions can occur. There is no antivenom and there is currently no substance which appears useful in first aid to inactivate nematocysts. Vinegar is not effective.

Mauve stinger, Pelagia sp. Large jellyfish, sometimes found in swarms, causing painful stings with wheals, pruritis and swelling. Appears to have allergenic venom. There is no antivenom.

Hair jelly, Cyanea sp. Very large jellyfish, causing moderate pain and redness of short duration, without systemic envenoming. There is no antivenom, vinegar is ineffective as first aid and should not be used.

Cone shells, Conus sp. Only a few cone shells, from tropical waters, are known to be hazardous to humans. Their venom contains a complex mixture of varied toxins, noteably the conotoxins. The envenoming occurs usually when the shell is picked up, and may result in local pain, potentially followed by systemic envenoming, with progressive paralysis and collapse requiring respiratory support. There is no antivenom.

Blue ringed octopus, Hapalochlaena sp. There are two species, found in all Australian coastal waters, often commonly. These are small octopuses which, when alarmed, develop vivid blue to purple rings on the body and tentacles. The saliva contains a potent neurotoxin, tetrodotoxin. Bites virtually never occur unless the octopus is removed from the water and placed on exposed skin. The bite may not be painful. Not every bite results in systemic envenoming, but paralysis, including respiratory paralysis, may develop quickly in severe cases, requiring urgent respiratory support on the beach. More often, the envenoming is less severe, with tingling around the mouth and mild weakness. There is no antivenom.

Stingrays Stingray injuries mostly occur when a person steps on the ray, either when climbing out of a boat in shallow sandy water or when running into such water. The stingray whips its poison barbed tail around, lacerating the foot or lower leg, sometimes leaving a portion of the barb behind. The mechanical injury can be severe, with fatal cases due to direct heart or bowel puncture or transection of major limb vessels. Nerve or tendon damage can occur. The venom causes intense local pain, which is heat susceptible, hence the value of hot water immersion as first aid. Always check the wound for foreign bodies, allow to close by secondary intention and consider prophylactic antibiotics. The severe local pain may require major analgesia or regional nerve block. There is no antivenom.

Stinging fish Many fish have venomous spines, which can cause severe local pain and occasionally, as in the case of stonefish, possible systemic symptoms. Hot water immersion, medical analgesia, removal of residual spine(s) and consideration of prophylactic antibiotics and tetanus immunisation are the mainstays of treatment. There is an antivenom for stonefish stings.

Toxic fish There are a number of toxins found in fish, some of which are potentially lethal. The best known is tetrodotoxin (Fugu poisoning) found in pufferfish and some related species. Eating these fish may result in classic neurotoxic poisoning, as seen with blue ringed octopus bites. Removal of fish from the stomach and cardiorespiratory support are the main modes of treatment in severe cases. Ciguatera is the other common and well known fish toxin, probably produced by microorganisms (dinoflagellates) and concentrated via the food chain, so that people eating large fish may be poisoned. The toxic fish appear and taste normal, the first indication of problems being the development of "food poisoning", with vomiting and diarrhoea, but also muscle cramps, joint pain and parasthesiae. In severe cases there may be prostration and these patients usually feel miserable and very weak. There is no antivenom and treatment is controversial. Support with iv fluids is usually helpful and there is some clinical support for the early use of iv mannitol, which appears to greatly moderate symptoms in severe cases.

Sea snakes There are many species of sea snakes in northern Australian waters, though bites are uncommon, as these purely aquatic snakes are generally inoffensive. They are front fanged and have potent venoms acting systemically. Both paralysis and severe myolysis with secondary renal failure may occur, depending on the species of snake involved. More details are given under the section on CSL sea snake antivenom.Coagulopathy is not observed.

Medications and Antivenom Anticoagulants

Patients on anticoagulants can be expected to have abnormal

coagulation test results which may hinder interpretation of these tests in relation to snake bite. Bet Blockers Patients on beta blockers, especially propranolol, may be far less responsive to adrenaline, thus may be difficult to resuscitate if they have an anaphylactic reaction to antivenom. While never documented with antivenom, this adverse effect of beta blockers has been reported with some other causes of anaphylaxis, with potentially lethal consequences. This should be considered before deciding to commence antivenom therapy. If in doubt, seek expert advice. Though less clear, a similar situation may apply to ACE inhibitors.

First Aid for Scorpion and Centipede Stings/Bites • Apply an ice pack to the bite area. • If pain is severe and prolonged, seek medical help. • If the patient has not had tetanus immunisation booster within the last 5 years, ensure this is given by the local doctor. • If the wound becomes more red and painful after 24 hours seek medical help (possible secondary infection).

First Aid for Tick Bites • Carefully remove the tick using alcohol to irritate it and pry it off the patient using tweezers on either side of the mouth parts. Do not hold it by the body and pull it off as this may leave mouth parts embedded in the skin. • If the patient has, or develops, any symptoms of paralysis, such as gait disturbance or other muscle weakness, immediately seek medical help.

• If the patient has not had tetanus immunisation booster within the last 5 years, ensure this is given by the local doctor. • If the wound becomes more red and painful after 24 hours seek medical help (possible secondary infection).

CSL Paralysis Tick Antivenom Basic Information Used for neutralising systemic envenoming by members of the Australian paralysis tick group. It is made from dog IgG. Each ampoule contains 1,000 units of neutralising capacity against the target venoms. This is a freeze dried preparation. Re-constitute with approximately 6.3mL of Water for Injections BP. The immunising venom is common paralysis tick (Ixodes holocyclus) venom (salivary gland extract).

Information about the ticks covered by this antivenom The species Current experience suggests that all Ixodes paralysis tick venoms will respond to CSL Tick Antivenom, though it was principally developed for bites by the common paralysis tick. These are robust "hard bodied" ticks.

Distribution The common paralysis tick is found in eastern Australia.

Venom composition The saliva contains a presynaptic neurotoxin, holocyclotoxin, active at the skeletal neuromuscular junction causing progressive flaccid paralysis.

Clinical effects Paralysis is not the most common effect of bites by paralysis ticks, which more usually cause local skin irritation. Multiple bites may leave an effect like a rash. Particularly in children, an adult female tick feeding over several days may cause the classical paralysis, usually first noticed as an ataxic gait with general malaise. Untreated, this can progress to full respiratory paralysis, the cause of most fatalities. Once the tick is removed, it might be expected that the effects of the toxin would quickly dissipate, but this is not the case. Indeed, the extent of paralysis may worsen for up to 48 hours after removal of all ticks.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Tick Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field. CSL Tick Antivenom should be considered in every case of significant systemic envenoming by paralysis ticks in Australia, the hallmark of which will be progressive and major paralysis. If paralytic features are only minor, then removal of the tick will usually be sufficient.

What to do if there is an immediate untoward reaction to the antivenom If there is either a sudden fall in blood pressure or bronchospasm, after starting the antivenom infusion, then temporarily stop the antivenom and give adrenaline by subcutaneous injection, give 100% O2 and IV fluids (Haemaccel®). If there is an infusion pump set up, then commence cautious IV infusion of 6mg/100mL adrenaline dilution, (at about 10mL/hr), increasing the rate if there is no response in a few minutes, and decreasing the rate as soon as a sufficient response is obtained. Once the untoward antivenom reaction is thus controlled, cautiously recommence antivenom infusion. If adrenaline is to be given (by subcutaneous injection), use a 1:1000 solution. For adults give 0.5mL (0.5mg) initially. For children give 0.01mg/kg initially. Repeat as necessary and try IM injection if no response to SC injection. If bronchospasm is the major problem, try nebulised adrenaline, 2mL of 1:1000 solution.

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness,

such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming.

First Aid for Marine Bites and Stings First Aid for Stonefish Sting • If the patient is still in the sea, immediately remove from the water. • Immerse the stung limb in hot water, ensuring first that it is not so hot that skin damage may occur. • If the patient has not had tetanus immunisation booster within the last 5 years, ensure this is given by the local doctor. • Seek medical help.

CSL Stonefish Antivenom Basic Information Used for neutralising envenoming by the Australian stonefish, Synanceia trachynis. It is made from horse IgG. Each ampoule contains 2000 units of neutralising capacity against the target venoms. Average volume per ampoule is 1.5-3mL. The immunising species is the stonefish, Synanceia trachynis.

Information about the fish covered by this antivenom The species The stonefish is a rather unattractive squat fish with a most irregular "skin" which assists its superb camouflage as it sits on old coral or debris. There are a series of erectile dorsal spines, which, with the associated venom glands, are the means of envenoming potential predators.

Distribution Stonefish are found throughout northern Australian waters, especially in association with coral reefs. They are mostly encountered in shallow water, where, owing to their excellent camouflage, they may be stepped on by accident, or picked up by the unwary.

Venom composition The venom is multicomponent, with neurotoxic, myotoxic, cardiotoxic and cytotoxic effects in experimental animals. A presynaptic neurotoxin has been described from the venom. While the venom can cause haemolysis, this is not a significant problem in people envenomed by the stonefish. The venom may also cause vascular leakage.

Clinical effects Most stonefish stings occur when the fish is stepped on, or less commonly, when picked up incautiously. No confirmed deaths from stonefish sting have occurred in Australia, but deaths are reported for some stonefish in the Indo-Pacific. Instant and severe pain is a constant feature of stings, followed by local swelling, which may be marked, tenderness and a blue discolouration of skin surrounding the sting penetration site. Dizziness, nausea, hypotension, collapse, cyanosis and pulmonary oedema have been described, though are by no means common. Tissue necrosis at the sting site is not seen.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Stonefish Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given only IM, not IV. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. In any significant stonefish sting, with severe local pain, it is worth considering antivenom

therapy. For 1 to 2 spine puncture wounds, give 1 vial of CSL Stonefish Antivenom IM. For 3 to 4 spine puncture wounds give 2 vials of CSL Stonefish Antivenom IM. For more than 4 spine puncture wounds give 3 vials of CSL Stonefish Antivenom. The use of CSL Stonefish Antivenom in stings by other species of scorpionfish is not clearly recommended, but there is limited evidence that it may be beneficial (eg possibly bullrout stings, Notesthes robusta). The potential risks of immediate and delayed adverse reactions to antivenom should be carefully considered before using this antivenom for other than stonefish stings. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field.

What to do if there is an immediate untoward reaction to the antivenom If there is either a sudden fall in blood pressure or bronchospasm, after giving the antivenom, then give adrenaline by subcutaneous injection, give 100% O2 and IV fluids (Haemaccel®). If adrenaline is to be given (by subcutaneous injection), use a 1:1000 solution. For adults give 0.5mL (0.5mg) initially. For children give 0.01mg/kg initially. Repeat as necessary and try IM injection if no response to SC injection. If bronchospasm is the major problem, try nebulised adrenaline, 2mL of

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. For patients receiving multiple ampoules of CSL Stonefish Antivenom, it may be helpful to give a short course of oral steroids as prophylaxis. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming.

First Aid for Other Fish Stings • If the patient is still in the sea, immediately remove from the water.

• Immerse the stung limb in hot water, ensuring first that it is not so hot that skin damage may occur. • If the patient has not had tetanus immunisation booster within the last 5 years, ensure this is given by the local doctor. • If the wound becomes more red and painful after 24 hours seek medical help (possible secondary infection).

First Aid for Stingray Injuries • If the patient is still in the sea, immediately remove from the water. • Staunch any profuse bleeding with application of local pressure bandage. • Immerse the stung limb in hot water, ensuring first that it is not so hot that skin damage may occur. • Unless the wound is a trivial one confined to a limb, medical help should be sought urgently. • If the patient has not had tetanus immunisation booster within the last 5 years, ensure this is given by the local doctor. • If the wound becomes more red and painful after 24 hours seek medical help (possible secondary infection).

First Aid for Blue ringed octopus bites • If the patient is still in the sea, immediately remove from the water. • Maintain vital functions, especially respiration; if impaired (use of "ABC"). • Apply a pressure immobilisation bandage, as for snakebite. • Seek urgent medical help. • If the wound becomes more red and painful after 24 hours seek medical help (possible secondary infection).

First Aid for Box Jellyfish Stings • If the patient is still in the sea, immediately remove from the water, avoiding further stings (use caution as the tentacles may be difficult to see).

• Immediately douse the stung area with copious quantities of household vinegar. • Some authorities recommend that if the sting involves more than half of one limb in area, then apply a pressure immobilisation bandage and douse with further copious vinegar. There is recent evidence suggesting a pressure immobilisation bandage may actually worsen envenoming. This question is currently unresolved. • Maintain vital functions, if impaired (use of "ABC"). If the patient has no pulse then use external cardiac compression and keep this going, if necessary, for a prolonged period, with an optimistic outlook. • Urgently seek medical help. • Cold packs are often helpful for pain relief.

CSL Box Jellyfish Antivenom Basic Information Used for neutralising envenoming by the major Australian box jellyfish (=sea wasp), Chironex fleckeri. It is made from sheep IgG. Each ampoule contains 20,000 units of neutralising capacity against the target venoms. Average volume per ampoule is 1.5-4mL. The immunising species is the box jellyfish, Chironex fleckeri.

Information about the jellyfish covered by this antivenom The species Chirodropids (eg Chironex fleckeri) are large, tropical virtually transparent jellyfish, with an approximately square shaped body, with tentacles draping from each of the four corners. Each tentacle contains millions of individual stinging cells, nematocysts, each of which can deliver venom via an everting stinging device. A proportion of this venom may be injected into capillaries just beneath the skin surface. This explains the very rapid development of severe systemic envenoming in major box jellyfish stings. A number of other box jellyfish species occur in Australian coastal waters but none has been definitely associated with fatal envenoming.

Distribution Chirodropids (eg Chironex fleckeri) are confined to tropical Australian waters, including offshore islands, where they are found year round, but are most commonly encountered in the summer months and near outflows from estuaries.

Venom composition The venom is multicomponent and difficult to collect, so is incompletely understood. It has components which can cause local pain and necrosis, and in high doses, components that can affect cardiac function and respiration.

Clinical effects The extent of envenoming by Chirodropids (eg Chironex fleckeri) is essentially dependent on the area of discharging tentacle contact. Involvement covering > 10% of total skin area is a potentially lethal envenoming especially in children. Systemic envenoming in such cases can occur within minutes of the sting, with cardiac dysfunction or arrest possible within 5 mins after a major sting. This emphasises the importance of rapid effective first aid. At every point of skin contact with tentacles there will be immediate excruciating pain, usually with linear red whelts. These affected areas of skin may go on to develop blistering and/or necrosis. Incoherence due to pain may occur. Shortly after, in severe stings, there may be the cardiac problems mentioned earlier. Respiratory dysfunction may occur later, sometimes associated with pulmonary oedema, but a central respiratory depressant effect has also been suggested.

When to use this antivenom, how much to use and how to give it CSL Box Jellyfish Antivenom should be given as soon as possible if there is evidence of life threatening envenoming, such as collapse or cardiac dysfunction /arrest (3 vials recommended). See potential contraindications. It should ideally be given intravenously, through a drip set, but speed is of the essence in severe envenoming and it has proved efficacious and safe, given IM on the beach or in the ambulance, by paramedical staff. In a situation of persisting collapse or life threatening cardiac dysfunction/arrest, up to 6 vials of antivenom may be given consecutively IV (preferably diluted). Other indications for antivenom are severe pain, persisting despite cold packs and parenteral narcotics and a potential but unproven benefit to cosmetic outcome. Again, ideally, prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. In practice, however, anaphylaxis has not yet resulted with this antivenom, and the need for early administration in severe cases may well outweigh the need to be fully prepared to treat anaphylaxis. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field.

What to do if there is an immediate untoward reaction to the antivenom If there is either a sudden fall in blood pressure or bronchospasm, after starting the antivenom infusion and clearly due to an adverse reaction to antivenom rather than an effect of the venom, then temporarily stop the antivenom and give adrenaline by subcutaneous injection, give 100% O2 and IV fluids (Haemaccel®). Once the untoward antivenom reaction is thus controlled, cautiously recommence antivenom infusion. If adrenaline is to be given (by subcutaneous injection), use a 1:1000 solution. For adults give 0.5mL (0.5mg) initially. For children give 0.01mg/kg initially. Repeat as necessary and try IM injection if no response to SC injection. If bronchospasm is the major problem, try nebulised adrenaline, 2mL of 1:1000 solution.

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming.

First Aid for Other Jellyfish Stings This is more controversial and dependant on species, but for some, notably the bluebottle (Portuguese man-o-war) vinegar is not appropriate. Water (even ice water) should not be used on any jellyfish sting, as this may increase envenoming. Application of a cold pack is always useful.

First Aid for Sea Snake Bites As for other snake bites, using pressure immobilisation method.

CSL Sea Snake Antivenom Basic Information Used for neutralising systemic envenoming by all species of sea snakes. It is made from horse IgG. Each ampoule contains 1000 units of neutralising capacity against the target venoms. Average volume per ampoule is 15-35mL. The immunising species are the beaked sea snake, Enhydrina schistosa and the Australian tiger snake, Notechis scutatus. The antivenom has been shown to be effective, to varying degrees, in neutralising a wide variety of sea snake venoms, including olive sea snake Aipysurus laevis, Stoke's sea snake Astrotia stokesii, olive headed sea snake Disteira (Hydrophis) major, banded sea snake Hydrophis cyanocinctus, elegant sea snake Hydrophis elegans, Daudin's sea snake Hydrophis nigrocinctus, narrow banded sea snake Hydrophis spiralis, Gunther's sea snake Hydrophis stricticollis, spine-bellied sea snake Lapemis hardwickii, banded sea krait Laticauda semifasciata and needle-headed sea snake Microcephalophis gracilis.

Information about the snakes covered by this antivenom The species There are 31 species of sea snake in northern Australian waters alone. All are possibly dangerous to humans, but relatively few of these have caused bites of significance. Sea snakes are closely related to the venomous Australian land snakes of the family Elapidae, but are currently classified in a separate family, Hydrophiidae. Two subfamilies have been listed in the past, the sea kraits, Laticaudinae, and the true sea snakes, Hydrophiinae, though recent work suggests this subfamilial division may be inappropriate. All spend some (sea kraits) or all (sea snakes) of their life in the sea. Most are fish eaters. They may be inquisitive but are not usually aggressive unless threatened, such as when caught in a fishing net. A description of all species is clearly beyond the scope of this publication.

Distribution Sea snakes are found predominantly in the northern waters of Australia, though storms may carry the occasional specimen southward, with authenticated bites from Sydney. They are not likely to be found in waters off the southern coast of Australia, where alleged sea snake bites are essentially always due to some other organism, usually an eel.

Venom composition Sea snake venoms have been the subject of much research, because of their post synaptic neurotoxins, many of which have been sequenced. The other important component of some sea snake venoms is myotoxin, which may dominate the clinical picture.

Clinical effects Sea snake bite is usually felt, with small but distinct teeth marks visible, which may be multiple, mostly from non-fang teeth. Pain at the bite site is not a major feature, nor swelling. The important effects, seen in only some cases, are systemic, either paralysis and/or myolysis. If envenoming has occurred, then one of these latter two effects may be expected within 6 hours in most cases, manifested as either early paralysis (eg ptosis, ophthalmoplegia, limb or respiratory weakness) or myolysis (eg myoglobinuria, muscle pain and weakness). Secondary kidney damage may occur if there is major myolysis and there may also be severe hyperkalaemia. Coagulopathy is not seen.

When to use this antivenom, how much to use and how to give it As with most antivenoms, CSL Sea Snake Antivenom should only be given if there is clear evidence of envenoming. See potential contraindications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes. Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started. The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary contact be made with a specialist in the field.

If there is evidence of either paralysis or myolysis then the patient should receive antivenom. CSL Sea Snake Antivenom is the first choice, starting with an initial dose of 1 to 3 vials, depending on the severity and rapidity of onset of envenoming. Up to 10 vials have been used in severe cases. If CSL Sea Snake Antivenom is either not available, or inadequate stocks are to hand, then CSL Tiger Snake Antivenom may be used; as a rough guide, 1 vial of CSL Sea Snake Antivenom is equivalent to 2 to 4 vial of CSL Tiger Snake Antivenom. CSL Polyvalent snake antivenom may be used if no sea snake or tiger snake antivenom is available.

What to do if there is an immediate untoward reaction to the antivenom (This section is common to most antivenoms)

What to do prior to discharge Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. If several bottles of antivenom have been given to the patient (eg >2) it may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).