TOxicon, Supp1.3, pp.493-496, 1983.

Pergamon Press Ltd.Printed in Great Britain,

IACAL TISSUS DESTRUCTION AND AUSTRALIAN 8IJIPID SDIVEN(Y~4~TION

Julian White

Poisons Centre, Adelaide Children's Hospital, North Adelaide, South Australia 5006,Australia.

INTRODUCTION

i~ocal tissue injury is a common feature of snakebite in many regions of the world andis aesocaitad with bites by both viperid and Elapid snakes . Sore elapid snakes,particularly the Cobras, frequently cause severe local tissue injury, in addition toproblems caused by systemically active venom casq~onents each ae neuroto:ina . However,snakebite it Australia is apparently rarely associated with significant local tissueinjury, for local problems are virtually never mentioned in published cases of snakebitefrom Australia. (WHITE, 1981) . Australian elapid venoms are more potent than venoms ofelapid snakes elsewhere, and contain a variety of systemically active toxins includingpreaynaptic neurotoxins, postaynaptic neurotoxins, myotoains, haemolyains, andprothrombin activators .

They also contain a variety of enzymes which may potentiallycause local tissue injury, although the precise enzyme composition of these venoms is notknown . However, the lethal activity of these vanome lies in the systemically activecomponents .

The venom delivery apparatus of elapid snakes is not as sophisticated as that ofviperid snakes . While the modified maxilla can rotate slightly, it cannot movesufficiently to fold the fang, so fang length ie restricted . In some Australian species,fang length is very short, with an average of only 2.8mm for the Brown Snake, which ieone of the moat important species implicated in snakebites . Another important species,the Tiger Snake, has an average fang length of 3.5mm . Those Australian species withlarger fangs are lees caamionly implicated in snakebite.

The quantity of venom deliveredmatches imperfectly to fang length, but those species with large fangs do produce morevenom on average than those with smaller fangs . FAIRLSY (1929) studied the bite mechanismof Australian elapid snakes, and delineated four phases of the bite . The first is thestrike . The fangs are rotated forward at contact, to mazimum elevation .

The mouth thencloses with fang entry and venom inoculation. The maxillae and fangs then rotate back-wards leaving a track of venom beneath the akin .

This latter movement may be responsiblefor linear marks on the akin rather than a single puncture wound.

It would also assistin drawing small prey items into the snakes mouth .

The range of similarly coloured potentially dangerous snakes in most regions ofMainland Australia, has made the treatment of snakebite difficult, and necessitated thefrequent use of Polyvalent Antivenom, which has a significantly higher incidence ofcomplications than monovalent antivenoms .

(SUTHERLAND and IAVERING, 1979) . TheCommonwealth Serum Laboratories have recently produced an ELISA (Enzyme Linked immunoSorbent Assay) Kit to allow identification of species from venom swabbed from the victim .This will substantially ia~rove treatment of snakebite in Australia, if it becomes widelyutilized . Nevertheless, if clinical differences in the signs and sXmptoms between speciesexist, this may be very useful in allowing the use of monovalent antivenom when theELISA is not available . However, little attempt has been made to delineate suchdifferences in the past . PEARN and COVACEVICH (1981) published a brief "Atlas of SkinLesions in Snake Bites", and WSITS (1981) reviewed a lnrga personal series of snakebitesfrom South Australia which included comments on local tissue appearances .

Ae the rangeof systemic problems is similar in most Australian elapida, differences in localappearances may be more useful as differentiatore.

MATSRTLTR AND METHODS

Casen of snakebite admitted to the Adelaide Children's Hospital (1968-1982), RoyalAdelaide Hospital (1970-1982) and the Flindera Medical Centre (1976-1980) were reviewed .Other snakebites in the author's personal series were also reviewed . Photographs of thebite site were reviewed where available .

493

RESULTS AND DISCUSSION

Hites by members of the Brown Snake group, and in particular the Common Brown Snake(Pseudonaja textiZia) and the western Brown Snake (Paeudonaja nuehaZis) are the moatcommon in South Australia. (WHITE, 1982)

They are usually associated with minimal oreven no local pain, oedema, or erythema . The only local sign is usually one or morefaint scratch marks which are often visible only under a magnifying glass at the time ofthe bite . They become more readily visible over the following hour . Even in the presenceof severe defibrination syndrome bleeding from the bite is not seen, although venepuncturesites may ooze persistently . Multiple bites may occur, often in close Proximity to eachother . .

Rarely, the site of the bite may be tender to palpation . There are no reportsof local tissue destruction.

Tiger Snakes(Notechis aoutatus) are probably responsible for more snakebites than anyother species in Australia (SUTHERLAND, 1982) . They have larger fangs and injectsignificantly more venom than Brown Snakes .

Local scratch marks from the fang are oftenseen and may be multiple and patchy ; even in a single bite . There may be prolonged oozefrom the bite, even in the absence of a documented defibrination syndrome . Oedema anderythema are usually seen, and an area of superficial tissue necrosis may be seen .This will initially manifest as an area of darkly discoloured skin which will usuallycontract in size over the subsequent 24 hours or more before final delineation of theactual area of necrosis .

This area of necrosis may be quite small, and often healsspontaneously over the following weeks without need for surgical intervention . The biteie usually acutely painful and an area of associated hypo and hyperaestheaia isfrequently found if looked for.

The Red Bellied Black Snake (Pseudechis pgrphyrRticus)and the congeneric Mulga Snake(Pseudeahis austraZis) are both relatively large snakes, especially the Mulga Snake, whichdelivers more venom on average milking than any other Australian species. However thereare relatively few reports of bites frown these species, especially the Mulga Snake. Bitesby the Red Bellied Black Snake usually are painful, sometimes intensely so, and areassociated with extensive oedema and some erythema . Fang marks are usually scratches,and oozing may occur . Oedema may involve the whole bitten limb and may be slow to subsideSmall areas of local necrosis or subcuticular haemorrhage are seen, and these may becomesecondarily infected . One case had a deep vein thrombosis in the bitten arm.

Bites by the Mulqa Snake cause similar problems which may be more severe .

In a fatalcase there was gross oedema and diacolouration of the bitten hand and arm, with severesubcutaneous oedema, haemorrhage and infiltration with polymorphs at autopsy (ROWLANDSet al, 1969) . Another non-fatal case had necrosis of the thumb distal to the bite andthis will be discussed further later . Local pain is a prominent feature of Mulga Snakebite, as is extensive local oedema which may involve the whole limb .

Paraesthesiaassociated with the bite site may occur . Same days after the bite the surface layers ofakin around the bite peel off .

Death Adders (Aoanthophis antaz~aticus) are notreaponaible for many bites in Australia,but have a reputation for severe and often fatal enveno~mation . Death Adder bites areusually associated with very little local oedema or erythema, but considerable local pain .Where significant bites have occurred on fingers, the finger is usually tight : rather thangrossly oedematous, and there is severe local tenderness and almost total limitation ofjoint movement due to pain and tlsaue tightness . This local tenderness, pain, andlimitation of joint movement may persist for days or even several months, without evidenceof infection .

Ooze from the bite site is not seen, and the fang marks are usuallyscratches .

The Taipan (Ckeyurmtus scuteZlatus) and Inland Taipan or Small Scaled Snake(0 . microZepidotus) are potentially the moat lethal annkes in the world. They have longfangs and produce large quantities of a very potent venom. The Taipan has longer fangsand produces more venom than the more toxic inland Taipan . Local reactions to bites bythese species are not well documented . There may be local pain with extensive oedema andlocal subcuticular haemorrhages, although some significant bites are apparently painlessand without local tissue reaction . At the other extreme, local tissue necrosis following

Taipan bite has been described (BENN, 1951) .

Elapid Envenomation and Tissue Destruction

495

There ie little clinical information reported about Copperhead bites, althoughSIITHFrtr.nun (1982) suggests that at least in Victoria, bites by the Common Copperhead(AustreZapa superbea) are often associated with significant local reactions includingtissue necrosis, and presumably pain and oedema . Bites by the as yet undescribed speciesof Copperhead from the Adelaide Hills region in South Australia do not cause significantclinical problems . All confirmed cases so far have had no local pain or oedema, andfang marks are usually slight scratches on even classic punctures.

Bites by the Rough Scaled Snake (Propedechis carinatus) are usually not associatedwith local problems, although one reported case developed oedema and urticaria (TRINCAet aZ, 1971) . There are no reports of local tissue necrosis .

Though not thought to be dangerous to man, the Yellow-faced Whip Snake (DemaneiapacmmOphis) is responsible for a number of snakebites . Systemic problems are notsignificant, but extensive local oedema with some pain, usually not severe, is described,and appears to be the most common reaction to bites by this species . The oedema may takea week or more to subside .

It can be seen there are real differences in local reactions to the bites ofvarious Australian elapid species, and when an ELISA is unavailable, this could be usedto determine the monovalent antivenom required . Excapt in those areas where the Taipanand Inland Taipan occur, a bite by a large brown coloured snake will moat probably bedue to a Brown Snake or Western Brown if no local oedema, or a Mulga Snake if extensivelocal oedema .

The Death Adder is sufficiently distinct in appearance to be readilyidentified from a description by the victim . Of the other species, moat will producesome local reaction, and will respond to monovalent Tiger Snake antivenom which iseffective for Tiger Snake, Copperhead, Rough-scaled Snake and Red Bellied Black Snakebites.

Severe local tissue injury in non-fatal cases of snakebite has only been describedfollowing Mulga Snake bite and Tiger Snake bite . The worst such injury was in an amateursnake keeper bitten by a large Mulga Snake while putting the snake in a bag . He wasbitten just prozimal to the base of the right thumb, and applied a tight tourniquet . Onarrival at hospital the hand was tense, swollen and blue-white in colour . The tourniquetwas released and he was given one ampoule of polyvalent antivenom i.v . The oedemaincreased, spreading to the chest wall, and 24 hours later the distal phalanx of thethumb was gangrenous . 24 hours later, though the rest of the oedema was subsiding, therest of the thumb became gangrenous . The thumb was later amputated and attempts atreconstruction were not wholly successful . Another amateur snake keeper bitten by a petTiger Snake developed an area of skin necrosis surrounding the bite on his left hand, inthe first web space .

He had also used a tourniquet which. was both far too tight, andleft on too long . The area of necrosis subsequently required skin grafting . FRUST(1981) has described another case of Tiger Snake bite, to the calf, which resulted in anarea of akin necrosis requiring susequent akin grafting . The lymphatic pressure bandagereco~uended by SUTFIERLAND (1979) was used in this case s but was not applied until 45minutes after the bite and was left on for 12 boars.

This last case has prompteddiscussion in the Australian Medical press about the length of time the lymphaticpressure bandage is left in place.

in all three cases there was immobilization of venom in the bitten limb for asignificant period by the first aid measures.

This may have allowed more local effect tooccur that would have been the case if the venom was able to move normally from the bitesite . These local affects could be due to aytotoxic enzymes, and also due to localiachaeemi.a secondary to microemboli caused by prothrambin converters in the venom.

Thislatter mechanism has been suggested by DUNCAN and TIHBALS (1982) as the reason fornecrosis in FRDST'S (1981) case . Both Mulga Snake and Tiger Snake venoms have coagulantaction, as do nearly all Australian elapid venams (WHITE, 1982) . Hoarever, some species,such ae the Brown Snake, which has potent direct pro+-h~hin convertors, do not havesignificant local effects at the bite site, even in cases where first aidmobilization has been used .

It is possible therefore, that some other venom component

496

J. WHITE

is responsible for local tissue destruction, and that this is present in only somaAustralian elapid venoms, such as Mulqa Snake, Tiger Snake and Red Bellied Black Snakevenom. The myotoxic potential of these venoms is interesting in this regard, and furtherbasic research into these venoms may answer the questions here raised .

REFERENCES

1. BENN, R.M . (1951) . Med.J.Aust. _1 ;147 .2 . DUNCAN, A.W., TTnnnr.rs , J, (1982) . Med.J.AUet. _l1155 .3 . FAIRLEY, N .H . (1929) . Med .J .Auat. _l :313 .4 . FROST, J . (1981) . Med .J .AUSt. _2v579 .5 . PEARN, J ., COVACEVICH, J . (1981) . Med.J.Auat . _l1568 .6 . ROWLAI~S, J .H ., MASTAGLIA, F .L., RAKULAS, H.A., HAINSWORTH, D. (1969) . Med.J.Aust .

_lx226 .7 . SUTHERLAND, S .K . (1982) . Pera.Com.8 . SUTHERLAND, S .K., COULTER, A.R., HARRIS, R.D . (1979) Lancet _l ;183 .9 . SUTHERLAND, S .R., IAVERING, K .E . (1979) Med.J.Aust . _2l671 .lO.TRINCA, J.C ., GRAYDON, J.J., COVACEVICH, J ., LIl~US, C . (1971) Med.J.AUSt . _2v80111 .WHITE, J. (1981) . Rec.Adelaide Child .Hosptl. _2(3) ;311-421 .12 .WHITE, J. (1982) . Proceedings of 7th World Congresa on Animal, Plant and Microbial

Toxins .13 .WHITE, J. (1982) Ibid .

The author gratefully acknowledges the administrators and medical staff of theAdelaide Children's Hospital, Royal Adelaide Hospital and Flinders Medical Centre forpermission to review case records ; Hrian Fotheringham for reviewing the draft of the pape>:Jeremy Frost for detailed information on a case of Tiger Snake bite ; the Department ofClinical Photography, A .C .H . for assistance in preparing illustrations; and MaureenBooth for typing the manuscript .

BROfPNSNAKE RITE

HROWN SNARE BITESingle linear fang mark on Multiple linear fang marksaide of foot . No oedema .

on finger . No oedema .

DEATH ADDER HITEFang entry on side of indexfinger . Slight but tense swell-ing of bitten finger only .

TIGER SNARE BITE

RED HELLIED BLACK SNARE BITS

MUrrn SNARE BITESingle bite in first web space,

Multiple bite to indez finger . Necrosis of thumb afterwith local early necrosis and

Extensive oedema of hand .

bite to thenar eminence.oedema of hand .