Bites And Stings Poisonous Animals Valuable Source

Bites and stings from animals, venomous and non-venomous, cause an unknown number of injuries per year, but statistics from a few key groups of venomous animals indicate that there are millions of cases annually, with at least 125,000 deaths. While in most cases of venomous animal injury, the primary problem is direct venom toxicity effects, there may also be significant local tissue injury and non-venomous animals will principally cause direct trauma. Because of the global magnitude of human injury, morbidity and mortality from venomous animal bites and stings, this area will be dealt with in some detail, even though it encompasses more than just primary physical trauma. Venomous animals Venomous animals are found in most groups or classes of the Animal Kingdom and in most habitats, both terrestrial and marine, reflecting the selective advantage venom may bestow, in both acquiring prey and deterring predators. In this section of the chapter, the types of animals, the types of venoms, clinical effects and general comments on management will be covered. This is followed by a more detailed look at individual types of animals and their effects on humans. Overview of venomous animals Of the approximately 26 Phyla of animals, at least 6 contain species that use venom or internal poison, as either pure defense, or both for offence and defense (Figure 1). A few groups, however, account for the vast majority of cases of human envenoming or poisoning by animals: •

Venomous snakes – >125,000 deaths/year.

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Scorpions – approximately 5,000 deaths/year.

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Stinging insects – hundreds of deaths/year due to anaphylactic reactions to venom.

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Puffer fish – several hundred deaths/year.

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Jellyfish – possibly scores of deaths/year.

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Spiders – perhaps 10-50 deaths/year.

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Stinging fish – perhaps 1-10 deaths/year.

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Venomous molluscs – perhaps 1-10 deaths/year.

Taxonomy considerations Fundamental to the understanding of trauma from venomous animals is a knowledge of the taxonomy of these animals, for without a reliable way of identifying an animal, it will not be possible to accurately record cause and effect, essential in elucidating epidemiology, etiology, pathophysiology, and clinical management. It is beyond the scope of this chapter to detail the taxonomy of all venomous animals. A simplified scheme is outlined in Figure 1. Overview of venoms Venoms are nearly always complex mixtures of varied biologically active substances (toxins) which may work independently or synergystically and each of which may have one or more quite distinct target sites and actions. In many venoms a single component or group of closely related components may be responsible for most or all major effects in envenomed humans, but in other venoms, particularly snake venoms, a multitude of diverse components may each cause distinct major effects, resulting in a complex, multisystem disease process.

Venoms have evolved principally because they benefit the venomous animal, giving it some competitive advantage over related non-venomous species. In many species the venom has evolved from digestive juices, especially enzymes, the venom gland being a highly evolved digestive gland. It is not surprising therefore that many venomous animals use their venom principally to aid digestion, explaining many of the rather unpleasant effects on envenomed humans. At some point in evolution some venomous animals have evolved venom with rather different effects, designed to assist acquiring prey or as a defense against predators. It is this latter group of venom toxins that often cause the major systemic effects of envenoming in humans. Often these toxins may have evolved from digestive enzymes, but their principal action is not related to enzymic activity. Indeed, there may be no significant residual enzymic activity, despite considerable sequence homology with the original enzyme. Classic examples of this are the phospholipase A2 (PLA2) toxins that are so prominent in snake venoms and have evolved into potent toxins such as neurotoxins, myotoxins, procoagulants, anticoagulants, platelet-active toxins and necrotoxins. There are many methods of classifying venom components and types of toxins. The method used herein is based on clinical effect. A single toxin may be active within several categories.

Neurotoxins Neurotoxins are classic venom components causing potentially lethal envenoming in humans. There are many types, widely distributed amongst venomous animals. Some cause flaccid paralysis, others cause hyperstimulation of portions of the nervous system.

Paralysing neurotoxins Presynaptic neuromuscular junction neurotoxins These toxins act at the neuromuscular junction (NMJ) in humans, damaging the terminal axon, resulting in a brief period of neurotransmitter release, followed by cessation of all neurotransmitter release, resulting in irreversible paralysis. This manifests clinically as progressive flaccid paralysis. Antivenom therapy cannot reverse such paralysis, which may persist for days, weeks or occasionally months, but if given at the earliest sign of paralysis, may prevent progression to widespread severe paralysis. As these toxins affect the skeletal NMJ, they affect skeletal muscle only, including respiration, but not cardiac or smooth muscle. They have evolved from PLA2 toxins, but some are complex multicomponent molecules without residual enzymatic activity. These toxins are particularly found in some snake venoms.

Postsynaptic neuromuscular junction neurotoxins Like the presynaptic neurotoxins, these toxins act principally at the skeletal muscle NMJ, causing progressive flaccid paralysis, but act extracellularly by reversibly binding to the acetylcholine receptor on the muscle end plate. Their effect is therefore reversible with sufficient antivenom therapy and may also be at least partially overcome by the use of anticholinesterases, such as neostigmine, though this often requires ongoing dosing. These toxins are also particularly found in some snake venoms.

Presynaptic and postsynaptic synergystic neuromuscular junction neurotoxins These toxins are found in African mamba snake venoms. The dendrotoxins act presynaptically to increase release of the neurotransmitter, acetylcholine, flooding the NMJ and causing overstimulation of the muscle. This action is synergystically compounded by the second set of toxins in mamba venoms, the fasciculins, which act as anticholinesterases, preventing removal of the acetylcholine, thus increasing the neurotransmitter concentration and adding to the flooding effect, resulting in muscle fasciculation and effective paralysis of skeletal muscle.

Sodium channel neurotoxins There are a variety of these toxins, the best known of which is tetrodotoxin (TTX), found in such diverse animals as the Australian blue ringed octopus (in its saliva) and the flesh of puffer fish (fugu). A small molecule, TTX causes rapid, reversible short-lived flaccid paralysis of skeletal muscle principally by blocking nerve transmission, through action on the sodium channels of axons.

Potassium channel neurotoxins A variety of channel blocking toxins exist in venoms, most notably in some scorpion venoms and cone shell venoms. A variety of potassium channels may be affected, the usual clinical effect being flaccid paralysis, though hypertonic paralysis may also occur.

Excitatory neurotoxins A number of excitatory neurotoxins have been reported from venoms, especially arthropod venoms such as from spiders and scorpions. These toxins may target diverse parts of the human nervous system, often as an unfortunate biproduct of toxicity designed to immobilise prey species, mostly other arthropods. A good example is the Australian funnel web spider, the principal toxin of which will affect arthropod prey, but not most mammals, an unfortunate exception being humans, who are exquisitely susceptible to this venom. Some of these toxins affect neuronal ion channels, though mechanisms of action are still uncertain in many cases.

Autonomic neurotoxins A number of neurotoxins from venoms may affect part or all of the autonomic system, either primarily or secondarily. This includes neurotoxins from the previously mentioned classes, especially the excitatory and ion channel toxins.

Myotoxins There are two principal types of myotoxic action in venoms; local, at the bite/sting area and systemic. The latter is of most clinical significance. Systemic myolysins are particularly important in some snake venoms, which in humans may result in potentially lethal myolysis of skeletal muscle. These latter myotoxins are PLA2 toxins and in some cases are the same toxin as presynaptic neurotoxins (an example is notexin from Australian tiger snake venom), mediating myotoxicity through a part of the molecule distinct from the neurotoxic active site. Myotoxins cause

extensive membrane and intracellular damage to individual muscle cells, commencing within 60 minutes of reaching their target site and by 24 hours (in experimental models) cell destruction is complete. However, the basal lamina remains intact, so that after about 3 days cellular reconstruction commences, completing around 28 days. There is some evidence that only slow fibres regenerate, not fast fibres. In the process of muscle cell degeneration there is release of cell contents into the circulation, most notably myoglobin, creatine kinase (CK) and potassium. The former may cause secondary renal damage or failure; the latter cardiac arrhythmia or arrest. Cardiac and smooth muscle appear largely unaffected by venom myolysins.

Cardiotoxins There are a number of PLA2 “cardiotoxins” described from some snake venoms, but these are mostly just general cellular toxins which cause cell damage and tissue necrosis. There are, however, a variety of toxins which can directly or indirectly affect the myocardium. These are found in a variety of venoms, notably snake venoms, but indirect cardiac effects are prominent in envenoming by some arthropods (especially scorpions) and marine animals (some jellyfish and cone shells). The mechanisms of action and structural identity of such toxins are diverse and beyond the scope of this chapter.

Coagulopathic Toxins Many snake venoms have actions on the human haemostatic system. A broad outline of modes of action is given in Table 1 and Figure 3.

Procoagulants While the name procoagulant accurately depicts the primary action of these venom toxins, the clinical effects in humans are more complex and subtle. In normal haemostasis the formation of a blood clot by crosslinking fibrin occurs in a protective platelet plug at the site of haemorrhage. It is therefore protected from dissolution by the fibrinolytic system until vessel wall repair has occurred. Venom procoagulants act outside this structured environment. Fibrinogen is rapidly converted to fibrin, which starts to crosslink, but fibrinolysis is also rapidly activated, so that within minutes of the venom causing microclotting, there is hyperfibrinolysis, causing fibrin to be destroyed as rapidly as it is formed. So powerful is this reaction with some venom procoagulants, notably the prothrombin convertors of some Australian Elapid snake venoms, that all circulating fibrinogen can be consumed within 5-15 minutes, rendering the patient profoundly anticoagulated and at risk of haemorrhage. If envenoming is severe, there may be a brief period at the outset of procoagulant action, before fibrinolysis is established, where substantial thrombi will form and potentially embolise. These may cause diverse and potentially catastrophic effects, notably coronary occlusion leading to cardiac arrhythmia or arrest. Subsequent fibrinolysis will quickly remove such thrombi, so that they will not be evident at autopsy in fatal cases. This mechanism is postulated as a cause of the rapid collapse and cardiac problems seen particularly with envenoming by the Australian brown snake. Venom procoagulants are usually multicomponent molecules, sometimes quite large, as seen in some prothrombin convertors, and generally their structure mimics normal components of human haemostasis, particularly part or all of the “prothrombinase” complex (factor Xa, Va, phospholipid, Ca). The specific types of procoagulants are listed in Table 1.

Anticoagulants Some venoms contain true anticoagulants, components that directly inhibit portions of the clotting cascade, resulting in prolonged clotting times. While such effects can increase a bleeding tendency, in general the likelihood of major haemorrhage as a result of these direct anticoagulants is less than with the action of the powerful procoagulants mentioned earlier. The precise mechanism of action of the anticoagulants varies between venoms, as does component structure (see Table 1).

Fibrinolytic agents Fibrinolytic proteinases occur in a number of Viperid snake venoms. or both sets of fibrinogen

or B Fibrinolytic

enzymes split off eiher the A splitting enzymes are principally metalloproteinases,αfibrinopeptides. A particularly zinc metalloproteinases (metzincin family), which are inactive in splittingβthe venom gland and activated by cysteine release prior to a bite. B enzymes are mostly serine proteases, closely related to thrombin-like, protein c activating and kallikrein activating snake venom enzymes. The other group of fibrinolytic venom agents are the plasminogen activators, often closely related to the prothrombin activators. Some of the latter also have plasminogen activating activity. The result of all these related agents is rapid thrombus removal and often, consumption of fibrinogen, thus effectively causing anticoagulation.

Platelet active agents Snake venoms in particular contain a number of components with actions on platelets, either promoting platelet aggregation, or more commonly inhibiting aggregation, through a variety of direct and indirect mechanisms. In clinical terms, both types of action are of importance, in either causing thrombocytopenia, with secondary increased bleeding tendency, or causing inhibition of platelet aggregation, with similar clinical effects. The platelet aggregation inducers are a diverse group of toxins, widely represented in viperid snake venoms; serine proteases, lectins, convulxins, aggregoserpentins, aggretins, von Willebrand factor agents (botrocetin, bitiscetin, alboaggregins) and the flavocetins. Platelet aggregation inhibitors in snake venoms fall into 4 -fibrinogenases, PLA2, 5’-nucleotidases, and fibrinogen receptorαclasses; antagonists (disintegrins). The latter group, disintegrins, are the focus of considerable research, because of their many therapeutic possibilities (treating thrombosis & DVT,reducing CVA damage, platelet protection during heart bypass surgery, potent antineoplastic agents and inhibiting bone resorption). 2 subfamilies (fibrinogen 1 and βThey specifically inhibit integrins of the receptor GIIb/IIIa; vitronectin receptor; fibronectin receptor) and are found principally in viperid snake venoms.

Haemorrhagins Direct and indirect haemorrhagic activity is a prominent feature of many viper venoms. The viperid zinc metalloproteinases are amongst the best characterised. They cause capillary leakage by degrading blood vessel basement membranes., resulting in haemorrhagic necrosis. They are related to the disintegrins, containing a disintegrin-like domain, allowing binding to collagen receptors.

SERPIN inactivators SERPIN (plasma SERine Protease Inhibitors) inactivators are found in some viperid and colubrid snake venoms. SERPINs are important controlling enzymes for haemostasis, making up 10% of all plasma proteins (eg antithrombin 1-proteinase inhibitor) and their inactivation removes checks onαIII, thrombosis, clearly synergistic with other haemostatically active venom components.

Nephrotoxins Renal damage from envenoming is not a rare event and may follow envenoming by a wide range of venomous animals, as a secondary effect of venom induced hypotension, causing renal hypoxic damage, or by deposition of byproducts of venom induced coagulopathy or myolysis. However, at least a few snakes appear to possess primary nephrotoxins in their venom, which can induce severe renal failure. There are also instances, following snakebite, of permanent major renal injury, notably renal cortical necrosis, the etiology of which is uncertain and probably multifactorial.

Necrotoxins A variety of venomous animals can cause local tissue necrosis at the bite/sting site, through a variety of mechanisms. Some snakes (eg many vipers, pit vipers, some cobras) commonly cause major local tissue injury, as a result of a variety of different venom effects, including the effects of cytolytic phospholipase A2 toxins. A few spiders cause local necrosis as the most prominent feature of envenoming (eg recluse spiders; Loxosceles spp.). A few jellyfish may also cause local necrosis along the tracks of stings (eg box jellyfish).

Other venom components There are many other components found in venoms, most of which may have little clear clinical effect, but some, such as hyaluronidase, may enhance other venom actions, while others, such as histamine, serotonin and 5HT, may have potent, if short lived actions. These latter components are particularly prominent in arthropod venoms, notably those of stinging hymenoptera, which also contain specialised small peptides such as apamin and melitin (eg honey bee venom), which have potent cardiovascular actions. In addition these peptides may also be highly allergenic, resulting in anaphylaxis on subsequent exposure in sensitive individuals. This is a common problem with honey bee venom, but also with a variety of other bee and wasp venoms and is particularly common with some of the Australian primitive stinging ant venoms (eg hopper and inch ants, Myrmecia spp.).

Pharmacodynamics of envenoming The way venoms are introduced by a bite or sting, the depth of injection, quantity involved, the size and action of venom components, size, age, pre-existing disease and post envenoming activity of the victim will all influence the rate of absorption, clinical effectiveness and elimination of venom. With a range of quite different venom components all working at once, in different ways, understanding the pharmacodynamics of envenoming can be difficult. In general terms, however, the speed of onset of action of a particular component will be determined by its size and target tissue location. Thus necrotoxins and other locally active toxins may commence clinical effects almost

immediately after the bite or sting, as they are already at their target site, while systemically active toxins must first reach the bloodstream (Figure 4). Toxins active within the bloodstream will rapidly exert their effect, but toxins with extravascular targets, such as neurotoxins and myotoxins, will generally have a more delayed onset. The rapidity of effect will also be influenced by any latency period, between time of binding to the target tissue, and onset of detectable action. As an example, presynaptic neurotoxins may have a latency period of 60 minutes, while postsynaptic neurotoxins may have almost no latency period; these differences are relected in the speed of onset of neurotoxic symptoms and signs. However, in real clinical circumstances, assessment is rarely so simple, for a single venom will contain a diverse array of toxins. Again, using the neurotoxins as an example, the venom may well contain both pre- and postsynaptic neurotoxins, so there will be a continuous onset and development of paralysis, as each type of neurotoxin exerts its effect. Many venoms are eliminated by the kidneys, explaining why testing urine for venom can be rewarding and this renal excretion may commence as soon as venom reaches the circulation. Thus blood levels of venom reflect not just the quantity of venom absorbed, but the rate of absorption and of excretion. In most cases, when venom is injected by a sting or bite, it will be deposited subcutaneously or intradermally. Some snakes such as large vipers, with long fangs, may occasionally inject deeper, even into muscle. While direct injection into blood vessels can occur, it seems a rare event, except for some jellyfish, notably species such as the lethal box jellyfish. The precise mechanism of venom introduction will be discussed later, but these jellyfish may inject a major part of their venom directly into subdermal capillaries, resulting in very rapid, devastating and sometimes lethal envenoming. Clinical effects of venoms With such a wide array of venomous animals and venom components, the range of clinical effects might be considered immense. However, a few major themes of venom action dominate, so that there just a few major classes of clinical effect, with classic symptoms, signs and laboratory findings. It must be remembered that venomous animals are not evolutionarily frozen; their venoms may still be evolving, so that effects may also evolve and change. This is clearly true for venomous snakes. Both the nature of venom components and the snakes abundance, geographical range and even diet are the subject of rapid change. It follows that whatever may presently be stated as the effects, range, habits etc for a given species of venomous animal must be continuously reinterpreted as the animals change, and the unexpected should always be looked for.

Neurotoxic paralysis Neurotoxic paralysis is usually a result of neuromuscular junction pre- and/or postsynaptic neurotoxins which act systemically rather than locally, affecting voluntary and respiratory muscle. It is a classic effect of many snake venoms, but is also seen with envenoming by other animals such as paralysis ticks and a few marine animals, notably cone shells and blue ringed octopuses. These latter marine animals may rapidly induce paralysis, with clinically apparent effects in 10-30 minutes, but neurotoxic snakes usually cause a more delayed onset paralysis, which may take 1 to 12 or more hours to become evident, while for ticks it may take days to become apparent. In all cases, however, it is a progressive flaccid paralysis, often first seen in the cranial nerves, where it is easily missed if not sought by careful examination. Ptosis, partial, then complete ophthalmoplegia, loss of facial tone, dysarthria and dysphagia are all common early signs of paralysis (Figures 5, 6). The pupils may become dilated and unresponsive to light. Progressive weakness of limbs and bulbar function may follow, the latter often mandating intubation and

ventilation to protect the airway. Accessory muscles of respiration may become prominent and the patient more agitated or drowsy as hypoxia develops. The diaphragm is often the last muscle to be paralysed and may not be fully affected for up to 24 hours after a neurotic snakebite. If the neurotoxin is extracellular, such as snake postsynaptic neurotoxins, tetrodotoxin, conotoxins, then the paralytic effect may last only a few hours or may be reversible with treatment, such as antivenom or anticholinesterase, but presynaptic paralysis usually involves damage to the terminal axon, so reversal must await regeneration, which may take days, weeks or months.

Exicitatory neurotoxin effects Excitatory neurotoxins, as found in some arachnid (spider) and related arthropod (scorpion) venoms, usually cause very rapid onset of clinical effects, with potentially catastrophic effects possible within 10 to 30 minutes of a sting or bite. So rapidly are these toxins absorbed, transported and bound to target tissues, that antivenom therapy is frequently administered too late to have optimal effect. The clinical effect will vary with species, but commonly includes local pain, rapid onset of anxiety, hypertension, tachycardia, and in some species, dyspnoea and pulmonary oedema (eg Australian funnel web spiders) or cardiac arrhythmias (eg some scorpions) or muscle fasciculation (some scorpions, spiders). There is often evidence of autonomic excitation, such as piloerection, priapism (banana spider), sweating, lachrymation, hypersalivation, in addition to the cardiovascular manifestations.

Cardiotoxin effects In many cases, cardiovascular effects are secondary to other venom actions, but direct cardiovascular effects, such as hyper- or hypotension, brady- or tachycardia, cardiac arrhythmias can occur, particularly in scorpion venoms and a few jellyfish venoms (eg box jellyfish), as well as a few snake venoms (eg gabboon viper).

Myotoxin effects Local myotoxins will cause local tissue damage, resulting in local effects such as pain and swelling and secondary effects, such as compartment syndrome and hypovolaemic shock. Systemic myotoxins, such as those in some snake venoms, will cause progressive myolysis of skeletal muscle, resulting in muscle pain, tenderness, weakness, that may mimic paralysis, and secondary effects, notably myoglobinaemia, myoglobinuria (with potential secondary renal failure) (Figure 7), hyperkalaemia (with potential secondary cardiac arrhythmia) and rise in serum enzymes, especially creatine kinase (CK), which may reach extraordinary levels. Myoglobinuria gives the classic red to black urine that is dipstix positive for “blood”.

Haemostasis effects The wide variety of haemostatically active venom components, particularly present in many snake venoms, may give rise to a variety of clinical disorders of haemostasis, distinguishable by detailed coagulation and platelet function studies. However, just three basic syndromes are generally evident; incoagulable blood with bleeding tendency, poorly coagulable or incoagulable blood without clinically apparent bleeding tendency, and thrombotic tendency. The latter is unusual, but is clearly present in envenoming by a few Central American vipers, where DVT is a common sequelae of envenoming. Those with bleeding tendency may exhibit no clinical signs other than persistent bleeding

from the bite site (Figure 8), but more commonly there is also bleeding from the gums, and GIT bleeding (manifest as haematemesis or malaena) and haematuria may also occur. Bleeding into a major organ or space (eg intracranial) will produce classic signs, but more localised bleeding, such as into the pituitary (Sheehan’s syndrome following Burmese Russell’s viper bite) may produce more subtle or delayed signs. Any artificial breach of vascular integrity, such as insertion of canulae, may result in prolonged and significant bleeding. This has obvious management implications.

Haemorrhagin effects The effects of haemorrhagins are similar to the more severe effect of haemostatically active toxins, in that they will produce clinically apparent bleeding. As the two groups of toxins are usually present together and are synergistic, bleeding can be major. There may be marked bleeding in the bitten area (Figures 9, 10), as other venom components assist tissue breakdown and allow extravasation of blood from vessels damaged by haemorrhagins.

Nephrotoxin effects Nephrotoxins, primary or secondary, will exert their effect somewhat silently at first, the first indication of problems often being a rapidly falling urine output, accompanied by rising creatinine and urea. In an case of envenoming where renal failure is possible, such as many snakebites, it is therefore advisable to carefully monitor fluid input and output and give an initial IV fluid load.

Other systemic effects A variety of specific systemic effects may be induced by envenoming by certain species. Of particular note is haemolysis, seen with some snakebites and with severe envenoming by recluse spiders. Liver damage may also occur, following bites or stings by many animals, but is rarely of major significance. Pancreatitis can be induced by some scorpion stings.

Necrotoxin effects These may be rapidly evident, as is seen with some snakebites (eg many vipers, pit vipers, some cobras), as progressive swelling, blistering, ecchymosis and darkening of skin, or liquefaction of skin (Figure 10). Over 24 to 48 hours this may progress to clear skin necrosis, resulting in deep ulceration, sometimes involving muscle and other deeper tissues. Pain is present in most cases. Spider necrotoxins may cause more insidious effects, particularly recluse spiders. The bite may go unnoticed, frequently occurring at night while the victim is asleep. This is followed by local redness, sometimes, but not always associated with local pain. Blisters may form after 12 to 48 hours, or areas of ecchymosis (Figure 11), becoming darker and more clearly necrotic over the next 1 to 7 days, eventually developing a full thickness skin ulcer or ulcers, which may occupy an area far greater than the original bite region. Jellyfish necrotoxins, such as those in box jellyfish venom, are associated with major envenoming. The sting is intensely painful, with wheal formation, with necrosis taking several days to become evident.

Other local effects The local effects of envenoming, dependent on both species and dose, may include pain, swelling, blistering, ecchymosis, necrosis, persistent bleeding, blanching, wheal formation, or almost no visible effect at all, even in the presence of life threatening systemic envenoming. Some elapid snakes and a variety of other animals can envenom sufficient to cause major systemic effects, yet leave little evidence locally, not even significant pain.

General systemic effects The range of general systemic effects of envenoming is considerable and variable. Snakebite often is associated with headache, nausea, vomiting and abdominal pain. Diarrhoea may also occur. Collapse and even convulsions may occur as early manifestations of major envenoming, especially in children.

First aid for envenoming First aid for envenoming is often controversial and frequently based on inadequate experimental or clinical research. The first principle should always be “do no harm”. As a general rule immobilisation of the bitten limb is a useful technique to reduce venom transport, as many venom components are of moderate to large molecular weight and lymphatic flow is important in their transport. The use of compression bandaging (Figure 12) is more controversial, but is apparently beneficial for certain types of snake and spider bite and a few major marine toxins (box jellyfish, cone shells, blue ringed octopus). Application of a cold pack to the wound area is a useful technique for many types of envenoming by marine invertebrates, especially jellyfish, and some terrestrial invertebrates, but is not applicable for envenoming by vertebrates (snakes, fish). For fish with venomous spines and for stingrays, immersion of the stung limb in hot water is effective in reducing local pain (be sure the water is not so hot it may cause thermal injury). There are some first aid methods which are known to be either of no value or potentially harmful and so should not be used. These include tourniquets, cutting and suction of the wound, application of chemicals such as condy’s crystals, use of cryotherapy and electric shock to the bite site. All these methods are still used in various regions of the world, most commonly for snakebite, despite the evidence that they frequently cause harm, without conferring benefit. Of these techniques, the use of medically supervised tourniquets has merit in certain circumstances, where the bite is from a lethal species and transport time to a hospital with appropriate antivenom is less than 30 minutes. The use of proprietory suction devices to remove venom is advocated by their manufacturers, but studies of efficacy do not inspire confidence in the technique, as even in optimal circumstances, at least 70% of the venom will be left in the victim. Cryotherapy has been clearly shown to be harmful. Electric shock for snakebite, though still promoted by manufacturers of these devices, has been shown to offer no benefit and its use may delay more appropriate first aid. Medical management of envenoming Most doctors will see few cases of significant envenoming, thus acquiring and maintaining skills in management is problematic. It is therefore advisable, when faced with a case of major envenoming, to seek expert advice at the earliest opportunity, either from a regional expert or from a regional poisons information centre, the staff of which may facilitate referral to an appropriate expert.

Diagnosis Diagnosis is no less crucial in effective management, than in other areas of medicine, yet is often far from simple. Patients may present with a clear history of a bite or sting and either a good description of their assailant or the assailant itself. The latter may introduce further problems if it is still alive (such as an angry venomous snake!). In this situation, while the diagnosis may be clear, some expertise may be required to determine the true identity of the assailant, sometimes crucial in determining which type of antivenom to consider. Equally, the extent of envenoming may not be immediately apparent, and some major types of envenoming, such as paralysis, myolysis, coagulopathy and renal damage may not be initially evident from examination, or require appropriate laboratory investigation. Given these obstacles to early accurate diagnosis, where the assailant is clearly known, the situation becomes far more complex when the assailant is most uncertain, as is frequently the case. Children may be unable to give a history of a bite or sting and may present with advanced envenoming, manifest as symptoms and signs that could point to a miriad of diagnoses. Beware the child with unexplained collapse and convulsions, which might be indicative of major envenoming by a snake, scorpion or spider. Adults may also be unaware of being bitten, as some bites (eg by certain snakes, blue ringed octopuses, ticks) may be painless. They will later present with symptoms that might indicate a wide range of diagnoses and the lack of a noted bite may erroneously point the diagnostic process away from envenoming. Envenoming should be considered in otherwise unexplained collapse, convulsions, flaccid paralysis, autonomic stimulation, myolysis, coagulopathy, thrombosis (DVT), haemorrhage, renal failure, chest pain, abdominal pain, regional pain, muscle fasciculation, excessive sweating, nausea and vomiting, headache, local swelling, ecchymosis, blistering, ulceration, cardiac arrhythmias and pulmonary oedema. This list covers only some of the more common effects of envenoming.

History The mix of the following points in history taking will be determined by the circumstances and the nature of the assailant. •

Precise date and time of the incident that might have involved a bite or sting.

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Geographic location at the time of the incident (to narrow down potential assailant fauna).

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A description of the assailant, if possible.

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A detailed description of how the bite or sting occurred, including how many bites or stings (multiple bites or stings are generally more severe), or the patients activity at the time an unnoticed bite or sting might have occurred.

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What first aid, if any, was used, its timing after the bite or sting, and patient physical activity both before and after first aid applied (physical activity may decrease first aid effectiveness).

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A list of symptoms observed by the patient and their time of onset and cessation. Specifically ask for symptoms indicative of envenoming by likely assailant species.

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A list of any signs noted by those with the patient, including timing of onset and cessation.

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Relevant past medical history, including allergy, particularly to animals used to produce antivenom (eg horses, sheep, rabbits) and any medications used by the patient. Also inquire about recent use of alcohol or recreational drugs that might affect symptoms or signs.

Examination It is easy to detect many signs of envenoming if looked for, but even easier to miss them if not considered during examination. Envenoming frequently evolves over time, so repeated examination may be vital in detecting important signs. This is particularly true for systemic effects of envenoming (see Figures 5 – 11). •

Check bite or sting site for evidence of bite/sting marks (is there a sting left behind – consider honey bee), distance between bite marks (may indicate mouth size for snakebite), multiple bites or stings, local effects such as erythema, oedema, blistering, ecchymosis, necrosis, physical trauma (eg lacerations following sting ray injury).

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Check regional lymph nodes for evidence of venom spread (swelling or tenderness).

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Check general systemic function (BP, pulse, respiration).

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Look for specific venom effects:

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Flaccid paralysis – ptosis, ophthalmoplegia (partial or complete), pupil dilation, loss of facial tone, limited mouth opening or tongue extrusion, palatal paresis, drooling, limb weakness, gait disturbance, accessory respiratory muscle use, depressed or absent deep tendon reflexes, depressed or absent response to painful stimuli (note the patient still feels the pain, but cannot withdraw due to paralysis, so consideration for patient distress is important), cyanosis, signs of hypoxia, including confusion.

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Excitatory neurotoxic effects – anxiety, restlessness, hyperreflexia, piloerection, increased sweating, salivation, lacchrymation, muscle fasciculation, confusion, hypoxia, pulmonary oedema, uncontrolled random limb movements (some scorpion stings).

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Myotoxicity – muscle tenderness, pain on contraction against resistance, weakness (may mimic paralysis), muscle spasm, rarely compartment syndrome signs due to massive muscle swelling. Also check ECG for evidence of hyperkalaemic effects.

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Cardiotoxicity – cardiac arrhythmias, arrest, ECG abnormalities (various).

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Coagulopathy and haemorrhagins – persistent ooze of blood from bite site, venepuncture sites, bleeding gums, bruising, occasionally signs consistent with a bleed into an internal organ/space (eg intracranial etc).

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Nephrotoxicity – usually little to find, check for oliguria or anuria.

Laboratory tests The extent and nature of laboratory tests will be determined by the likely type and extent of envenoming and the availability of laboratory resources.

Basic health facility: •

Urine output – check for haematuria or myoglobinuria (red or black urine; dipstix test positive for blood; simple microscopy for red cells).

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Coagulopathy – 20 minute whole blood clotting test (if poor or absent clot, indicates coagulopathy; requires only needle, syringe and glass tube or container).

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Venom detection (Australia only) – simple commercial ELISA based test for Australian snake venoms (Figure 13). Best sample is the bite site. If there is systemic envenoming, then urine could be tested, but blood is unreliable as a sample. A positive result indicates both that a snakebite has occurred and the most appropriate antivenom, but is not an indication to give antivenom, as venom can be on the skin, without significant systemic envenoming. A negative result does not exclude snakebite, so is of little diagnostic help.

Fully resourced hospital •

Urine output - check for haematuria or myoglobinuria (red or black urine; dipstix test positive for blood; simple microscopy for red cells).

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Blood tests:

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Extended coagulation studies - (prothrombin time/INR; aPTT; fibrinogen level; fibrin(ogen) degradation products).

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Complete blood picture – raised WCC suggestive of envenoming or infection; absolute lymphopenia suggestive of certain types of snake envenoming; Hb level (look for evidence of haemolysis); thrombocytopenia may indicate direct or indirect effect of some snake venoms or secondary DIC.

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Electrolytes and renal function – look for hyperkalaemia if there is myolysis or renal failure.

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Creatine kinase (CK) – elevated, sometimes to extreme levels, in presence of myolysis.

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Liver function tests – enzyme levels may be elevated if there is myolysis.

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Arterial blood gas – relevant only if advanced respiratory failure due to neurotoxic paralysis or pulmonary oedema.

•

Venom detection (Australia only) – simple commercial ELISA based test for Australian snake venoms (Figure 13). Best sample is the bite site. If there is systemic envenoming, then urine could be tested, but blood is unreliable as a sample. A positive result indicates both that a snakebite has occurred and the most appropriate antivenom, but is not an indication to give antivenom, as venom can be on the skin, without significant systemic envenoming. A negative result does not exclude snakebite, so is of little diagnostic help.

Critical Care

Major envenoming is often optimally managed in an intensive care setting. The major requirement for intensive care will be respiratory support for cases with advanced neurotoxic flaccid paralysis or severe pulmonary oedema. Respiratory support, including intubation and ventilation, may be needed only for a few hours, but for some snake species, may be required for days, weeks or months, until the neuromuscular junction regenerates. Intubation and ventilation is often required to maintain airway safety, long before there is full respiratory paralysis. Tracheostomy should be avoided until there is complete resolution of any coagulopathy or haemorrhagic tendency (some snakebite cases); all invasive procedures with the potential to cause bleeding should be avoided for similar reasons. In cases of cardiac arrest or severe dysfunction following envenoming by cardiotoxic species, notably the Australian box jellyfish, prolonged cardiac support may be required.

Antivenoms Antivenoms are the treatment of choice, where available, for most forms of major envenoming, particularly systemic envenoming. Old aphorisms suggesting antivenom is more dangerous than envenoming are generally ill-founded and inappropriate. Nevertheless, antivenom therapy carries certain risks and should only be used when clearly indicated. However, for many venomous animals and in many less developed regions, antivenom is either unavailable or economically impractical. Antivenoms are specific antidotes to venoms. Virtually all are whole or fractionated animal IgG raised against a target whole venom, not specific venom components. Antivenoms are polyclonal and may contain far more neutralising activity against some venom components than others. To produce antivenoms, a source of venom for immunising must be determined. The choice of venoms may strongly influence the clinical efficacy of an antivenom; if only a narrow range of species or species from a small part of a geographic range is used, then the antivenom may lack efficacy against bites from a wider range of species or against bites from the target species from other parts of its geographic range. Antivenoms may be truly monovalent (raised against the venom of a single species of animal), “monovalent” to genus level (cover all or several species within a genus, or ocasionally closely related genera) or polyvalent (raised against a venoms from a variety of species, usually unrelated apart from a common geographic range). Most commonly, the animal used for immunising is the horse, but sheep, goats, rabbits and even chicken egg yolk have been used. Horse based antivenoms, in particular, have a generally high incidence of adverse reactions, but the rate of reactions will also be determined by the degree and quality of refining, particularly removal of non-IgG components such as albumin and where IgG has been fractionated, removal of FC fragment contaminents. The three major types of antivenom, based on the degree of fractionation are; whole IgG, F(ab)2 and Fab (Figure 14). Their individual characteristics are listed in Table 2. Principles of antivenom therapy The first principle of antivenom therapy is to tailor the dose to the individual situation. From this it follows that just as the degree of envenoming varies from nil (“dry bite”) to severe systemic, so the amount of antivenom required will vary from none to potentially large quantities. The quantity required will therefore be determined by the assailant venomous animal and not the size of the patient; there are no paediatric doses of antivenom; children require the same amount as adults. Determining how much antivenom to administer requires considerable clinical judgement. For some regions there are guidelines covering common species of venomous animal, notably snakes. This information is not always available in product literature. It is beyond the scope of this chapter to detail how much of

each antivenom to give in any possible clinical case. Consultation with regional, national or international experts is advised if the dose required is unclear. In the past, most failures of antivenom therapy can be attributed to inadequate dosage, or wrong choice of antivenom. The second principle of antivenom therapy is to give as soon as possible, once it is indicated. From this it follows that in most situations of acute envenoming, the IV route is preferred, but there are exceptions, which will be noted for particular animals as they apply. The third principle is to monitor carefully for the effect of antivenom therapy. This includes monitoring both effectiveness in counteracting envenoming and observing for adverse effects of therapy. It is frequently the case that an initial dose of antivenom may be insufficient and that follow up doses may be required. Some venom may be sequestrated at the bite site, being released over a period of hours or days, necessitating ongoing antivenom therapy. Equally, the type of antivenom will influence clearance as well as compartmental distribution. Fab antivenoms are more rapidly cleared than F(ab)2 or whole IgG antivenoms, so are more likely to require continuous infusion or regular repeated doses.

Complications of antivenom therapy The principle complications of antivenom therapy are: •

Acute adverse reactions.

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Anaphylaxis and related early reactions.

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Rash.

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Febrile reactions (usually related to toxin contamination).

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Delayed adverse reactions.

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Serum sickness.

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Failure of efficacy.

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Incorrect antivenom.

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Inadequate dose.

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Inappropriate route of administration (IM or local when IV was required).

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Therapy commenced too late.

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Out of date antivenom or poorly stored antivenom (ie refrigerated antivenom that has been exposed to prolonged heat).

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Poor quality antivenom.

Several methods have been employed to minimise the chance of adverse effects from antivenom therapy. •

Skin sensitivity testing prior to administration. This method is flawed in both theory and practice. Such sensitivity testing will delay treatment, fail to reliably predict major adverse

reactions (eg anaphylaxis), potentially sensitise the patient to antivenom should it be required in the future and may precipitate an anaphylactic reaction. For these reasons skin sensitivity testing is not recommended, even though it is advised by a number of antivenom producers and is routinely used in some countries (eg USA). •

Premedication prior to antivenom therapy. This is controversial and is not widely accepted or used. Antihistamines and steroids have been shown to have no real benefit in preventing acute antivenom reactions. In addition, antihistamines may induce drowsiness or occasionally, hyperexcitability, both potentially dangerous in major envenoming. Epinephrine (adrenaline) has been shown to reduce the likelihood of adverse reactions for certain high risk antivenoms (those that are poorly refined, with a high rate of adverse reactions) in a single trial, but its benefit for other antivenoms is uncertain and it carries clear risks that may outweigh any potential benefits. This is particularly true if the envenoming causes increased bleeding, as seen with many snakebites. Premedication is not currently recommended by antivenom producers. Future studies may better define its role, if any.

•

Use of diluted antivenom infusions. Most antivenoms should be given IV. Many experts recommend dilution of the antivenom up to 1:10 in a suitable diluent for IV use, such as normal saline or Hartmans solution. The degree of dilution will be limited by the volume of antivenom and the size of the patient. While this technique may be useful, it is not strictly necessary, as studies have shown that IV push neat antivenom does not carry a higher incidence of acute adverse effects. In addition, the latter technique requires the doctor to stay with the patient throughout the antivenom infusion, which increases the chances of rapidly and effectively responding to acute adverse events.

Antivenom should always be given in the expectation that anaphylaxis may occur, even though this complication is rare with good quality antivenoms. Thus epinephrine (adrenaline) should always be ready in a syringe or set up as an infusion, prior to commencing antivenom therapy and both staff and equipment for resuscitation should be on hand.

Sourcing antivenoms For antivenoms required for local species there will usually be a common source, often a regional or national antivenom producer. There are significant areas of the world with moderate to high rates of envenoming where antivenom is either in short supply, very expensive, or completely unavailable. There are many venomous animals for which there is either no specific antivenom or no useable antivenom. For exotic venomous animals, such as venomous snakes in zoos or private collections, appropriate exotic antivenoms may be unavailable or difficult to source in reasonable time and quantity. A number of major zoos with reptile houses in both North America and Europe stock a range of exotic antivenoms. Poisons information centres may also have lists of institutions stocking exotic antivenoms, as well as experts in clinical toxinology who may be consulted on the management of envenoming by exotic animals. There are several published lists of antivenoms and antivenom producers globally and similar lists may be available on the internet.

Non-antivenom treatments While antivenom is often the preferred treatment of significant envenoming, it is not available for all animals, nor in all areas of the world. Non-antivenom treatments may be effective as adjuncts to antivenom or as alternatives in some situations.

Pharmaceutical Apart from the standard range of pharmaceuticals used in a wide array of diseases, a few agents have specific roles in certain forms of envenoming. •

Anticholinesterases: Useful for flaccid neurotoxic paralysis due to post-synaptic snake neurotoxins. They may be used as an adjunct to antivenom or as sole therapy where antivenom is unavailable. First perform a tensilon test to determine efficacy.

•

Dapsone: Potentially useful for reducing necrosis in known recluse spider bites, if used early, but toxic and controversial.

•

Fresh frozen plasma: Of value in replacing depleted clotting factors after snakebite coagulopathy, but potentially hazardous if given prior to neutralisation of all circulating antivenom.

Surgical Surgical intervention is rarely appropriate in acute envenoming, with the exception of injuries causing acute significant local trauma, such as some stingray injuries or where a portion of the biting or stinging apparatus remains in the wound and requires urgent removal. Some surgical manouvres are worthy of particular comment. •

Fasciotomy: This technique for releasing local tissue pressure is generally only warranted to relieve proven (by intracompartmental pressure manometry or by doppler) intracompartmental syndrome, where failure to do so would be likely to result in significant long term ischaemic injury. Even in this latter, uncommon situation, most likely encountered with some forms of snakebite, any coagulopathy should first be under control. Unwarranted fasciotomy in snakebite, used mearly because of extensive tissue swelling, frequently results in long term cosmetic and functional deformity and is to be avoided.

•

Bite or sting site wound excision: There is no substantial evidence to suggest that excising the area of immediate envenoming is likely to be a useful procedure and it may often result in short and long term complications. For necrotic arachnidism it is clear that early debridement of the necrotic region (within the first 4-5 weeks) may actually extend the area of necrosis.

Other •

Hyperbaric oxygen therapy: This has been used for necrotic arachnidism to both reduce the associated pain and to accelerate healing. There is limited clinical evidence in support and the

therapy is controversial, but may be useful in at least some patients. Guidelines for use in envenoming are not yet established.

Complications of envenoming Of the many potential complications of envenoming that may occur, a few particularly common or important varieties are discussed here, most pertaining to snakebite.

Paralysis Flaccid neurotoxic paralysis is a potentially lethal complication of major envenoming by a variety of venomous animals (see Table 3). It may develop very rapidly (eg envenoming by the blue ringed octopus) or be more gradual and insidious in onset. The latter may result in missing early signs, so that diagnosis is not made until paralysis is advanced. The three principle manouvers available to manage significant paralysis are: •

Intubation and ventilation.

•

Antivenom. Only effective for postsynaptic type paralysis.

•

Anticholinesterases. Only effective for postsynaptic type paralysis.

A fully paralysed snakebite patient may appear severely cerebrally injured, with fixed dilated pupils, absent reflexes, flaccid tone and no response to painful stimuli, yet throughout an examination to establish these signs, may be awake, terrified and well able to feel painful stimuli. Great care and consideration is required in managing such patients. By manually opening their eyes and moving their head around, they will be able to see their environment and those caring for them. Often it is possible to find at least some residual muscle movement which can be used to establish communication, even if just indicating “yes” and “no”. Aspiration pneumonia and secondary infections are also significant risks in these patients. If the paralysis is presynaptic, then assisted ventilation may be required for weeks or months, necessitating consideration of tracheostomy after 1-2 weeks.

Myolysis Major myolysis is particularly a feature of snakebite by some species (see Table 4). Myolysis is most problematic when systemic. Even late administration of antivenom may sometimes speed resolution. Early and maintained good renal throughput, by ensuring adequate hydration, may reduce the chance of secondary renal damage. Hyperkalaemia is always a risk in these cases and should be actively sought and vigorously treated if present. At least in the early stages, over the first 1-10 days, when muscle breakdown is peaking, it is advisable to avoid procedures that might increase muscle damage, such as active physiotherapy.

Coagulopathy While coagulopathy can be a secondary result of cardiovascular collapse after envenoming by a wide range of animals, by far the most common cause is snakebite (see Table 5). Antivenom is the preferred treatment, giving enough to neutralise expected venom load. In general, replacement therapy (FFP, cryoprecipitate) is unnecessary.

Great care is required in avoiding iatrogenic bleeding, through injudicious insertion of canulae. Beware femoral punctures, and subclavian and jugular line insertions and arterial blood gas sampling. For established coagulopathy, where repeat venous sampling is required to titrate antivenom therapy against response, an indwelling line, such as a long line through the cubital vein, may be advantageous.

Necrosis The single most important aspect of care for necrotic bite wounds is good wound care; keeping the wound clean, elevated and avoiding early surgical debridement (if a recluse spider bite). Particularly with necrotic arachnidism, ulcers may be indolent, slow healing, suggestive of vascular impairment. A number of unfortunate patients have had limb amputations for intractable bite ulcers whose impaired healing is falsely ascribed to peripheral vascular disease. Early debridement and grafting most often fails and should generally be avoided. Infection should be treated with antibiotics targeted to the causative organism, thus culture and sensitivity testing should be routine. Infection Infection is always possible after any penetrating injury, such as a bite or sting. Though uncommon, tetanus does occasionally occur in venomous bites and stings, so tetanus prophylaxis should be routine. Avoid injections in snakebite, however, until any coagulopathy is resolved. In most cases, prophylactic antibiotics are unnecessary. If secondary infection occurs, endeavor to culture the organism and so target antibiotic therapy. If this is impractical, assume a wide possibility of organisms and use an antibiotic combination appropriate to provide wide coverage.

Follow up While mild envenoming without complications may not warrant follow up, major envenoming usually does. In particular, patients who have received antivenom should be informed of the symptoms of serum sickness, so that they will report for early assessment should this complication arise. Both major physical and emotional sequelae of envenoming may occur and require extensive follow up. Venomous snakes Venomous snakes are the single most important cause of envenoming globally, because of the high rate of major morbidity and mortality. Most snakes are non-venomous, with the exception of Australia, where venomous species predominate. Many people may have difficulty distinguishing venomous from non venomous species and anxiety may cause symptoms that mimic those of true envenoming. There are four Families of venomous snakes. Colubrids Most colubrid snakes lack either fangs or venom glands. A few species have fangs towards the back of the mouth (see Figure 15), associated with well developed venom glands and potent venom. A number of other colubrids may have enlarged teeth and salivary glands producing toxic secretions, thus may cause envenoming. Venomous colubrids account for only a small fraction of major snakebites. The most important species are listed in Table 6. The approximate global distribution of colubrids (all species, not just venomous species) is shown in Figure 16.

Elapids

Elapids, or cobra type snakes, are a diverse Family, all of whose members are venomous, with both developed venom glands and fangs (see Figure 17). Major groups of elapids include cobras, kraits, mambas, coral snakes, sea snakes and Australian and New Guinea species (Figures 18-20). Historically, elapid envenoming has been considered as primarily neurotoxic, with minimal local effects; this is almost entirely incorrect. While many elapids can cause paralysis, some may also cause coagulopathy, myolysis, primary or secondary renal failure and many African and Asian cobras cause severe local necrosis. A few cobras actually spit their necrotic venom towards the eyes of victims. The major species groups are listed in Table 7. The approximate global distribution of elapids is shown in Figure 21.

Atractaspids Atractaspid snakes were, until recently, included with vipers. They are restricted to Africa and the Middle East. They are predominantly burrowing snakes and the dangerous species (from Genus Atractaspis) have sideways striking fangs and unusual venom, that contains endothelin like toxins, the sarafotoxins. The approximate global distribution of atractaspids is shown in Figure 22.

Vipers Vipers probably cause the highest percentage of global snakebite mortality. They are widely represented, found even up to nearctic regions, but are absent from New Guinea and Australia. They have highly evolved envenoming structures, with a mobile fang that folds against the roof of the mouth when not in use. This enables long fang lengths compared to other types of venomous snakes (see Figure 23). There are two subfamilies. Viperinae includes the old world vipers, such as European adders, African vipers such as puff adders and Gaboon vipers, Russell’s vipers and the saw scaled or carpet vipers (Figures 24-27). These latter two groups are undoubtedly the cause of many deaths in Africa and Asia. Crotalinae covers the pit vipers, those species with infrared sensing pit organs on the head, enabling the snake to detect and strike warm blooded prey in pitch darkness. Species groups include rattlesnakes, moccasins, bushmasters and other South American vipers, and the Asian terrestrial and arboreal pit vipers (Figures 28-31). Traditionally, viper envenoming has been characterised as coagulopathic and locally necrotic; as with elapids, this simplistic overview is quite inaccurate. Many viper species will cause local swelling and even bruising or necrosis at the bite site, but a minority may cause minimal local effects. Coagulopathy is a feature of some viper bites, but not all. A few cause primary renal failure. Several species cause predominantly paralysis, while a few others cause myolysis. The major species are listed in Table 8. The approximate global distribution of viperids is shown in Figure 32.

Venomous lizards There are only two species of venomous lizards, both closely related, in the Family Helodermatidae. They are found only in parts or arid northern Mexico and adjacent parts of south western USA. They have primitive venom glands in the lower jaw. Venom is innoculated through injuries inflicted by the teeth during a bite; there are no true fangs. The venom is multicomponent. Clinically it causes intense local pain, assisted by the mechanical injury of the bite. The jaws are strong and it may be difficult to prise the lizard off. The pain may last several hours and there is often local

swelling. The wounds do not develop necrosis. Uncommonly there may be systemic effects, notably hypotension, which may be severe and appears to be a direct venom effect, resulting in shock. Paralysis, myolysis, coagulopathy and renal damage do not occur, although the latter two might develop as secondary complications in severe shock. There is no antivenom available. Treatment is directed to pain relief and symptomatic therapy and treatment of shock and its complications, if these arise.

Venomous arthropods There are a vast number of arthropod species, inhabiting almost all parts of the globe. A considerable number are venomous, but relatively few can cause significant envenoming of humans. Morbidity and secondary allergy is a far bigger problem than mortality from arthropod envenoming.

Spiders There are many thousands of species of spiders, nearly all of which are venomous, but only a few are capable of envenoming humans significantly. Spiders may be present in high concentrations; numbers exceeding 2 million per hectare have been reported in the UK. Spiderbite is probably very common. Where incidences have been studied, as in Australia, the number of cases is 5 to 10 times higher than snakebite, but most of the bites are of minor medical significance. Of the relatively few species that can inflict significant injury to humans, most fall into just four groups; the widow spiders (Genus Latrodectus); the recluse spiders (Genus Loxosceles); the banana spiders (Genus Phoneutria); and the Australian funnel web spiders (Genera Atrax and Hadronyche). There is a fifth group, those spiders, other than recluse spiders, causing local necrosis (necrotising arachnidism), but the species responsible are generally poorly documented and vary with geographic region. Those spiders known to have caused injury to humans are listed in Table 10. The management of spiderbite varies with the type of spider involved. Antivenom is available for envenoming by spiders known to cause problems, as listed earlier. A Discussion of all types of spiderbite is beyond the scope of this chapter. A summary of features and management for important species is given below.

Widow spiders (latrodectism) Widow spiders are globally distributed and probably the most common cause of medically significant spider bites. They are sexually dimorphic, the female being far larger than the male (Figure 33). Only the female is likely to cause significant envenoming. The venom contains a mixture of related complex -latrotoxin, appearsαprotein neurotoxins, the latrotoxins, only one of which, to be active in humans, in whom it causes widespread neurotransmitter release. Most widow spider bites are minor, with 20% or less resulting in significant envenoming. In this latter group, the bite is most often felt, but is usually not severely painful. A variable time later, from 10 minutes to several hours, but usually within 60 minutes, the bite site becomes progressively painful, sometimes associated with local sweating or erythema. The pain becomes severe and gravitates proximally to involve regional lymph nodes and produce a severe regional pain syndrome. The rate of progression is quite variable, from less than one hour, to more than 24 hours. Untreated the pain may spread further, giving rise to severe chest pain (mimicing myocardial ischaemia) or abdominal pain (mimicing acute abdomen), often associated with marked localised or generalised sweating, mild to severe hypertension, nausea, occasionally vomiting and general malaise. Rarely pulmonary oedema may ensue. Where pain

involves the face and head, particularly with bites in or near to these regions, the severity of the pain may result in marked facial grimacing; “facies latrodectisma”. Localised or generalised muscle spasms occur in some cases. True flaccid muscle paralysis does not occur, but some patients complain of muscle weakness. There are few laboratory abnormalities in latrodectism, but a raised white cell count is common and rarely a mild rise in CK is seen. Without treatment, latrodectism can cause distressing symptoms for days, weeks or even months. While a few deaths have been reported, these are most likely due to secondary complicatiuons rather than primary venom toxicity and given the high number of cases of loxoscelism, fatality is quite rare. Latrodectism is not associated with local tissue injury or necrosis at the bite site. In those cases with significant regional or systemic envenoming, antivenom is the best treatment option. Several antivenoms are available, depending on the geographic region. All are equine. Australian CSL Red Back Spider Antivenom (RBSAV)has been tested with a variety of major widow spider venoms, including those from Australia, North America and Europe, and found to be effective for all (this testing remains unpublished at time of writing this chapter and was not conducted by CSL). It is possible some other widow spider antivenoms may also have a wide spectrum of use, but this is untested. Experience in Australia with the CSL RBSAV, which has been used in tens of thousands of patients, has shown this product to be safe and effective, in contrast to some similar widow spider antivenoms in other regions. The following advice on antivenom administration is therefore based on the CSL RBSAV.

Antivenom should be used in all cases with significant systemic envenoming and if there is severe regional envenoming, notably severe pain, as this is usually unresponsive to standard analgesia. In contrast to most other antivenoms, this antivenom appears effective if given IM. Give a single ampoule IM, with epinephrine (adrenaline) and resuscitation facilities ready, in case of anaphylaxis (rare with this antivenom). Wait two hours; if there has been minimal response or a relapse, give a second ampoule. Repeat the procedure, up to three ampoules. Occasionally, particularly where treatment has been delayed or the patient is large, higher doses are required. Five ampoules is the usual maximum, but higher doses have occasionally been used. If envenoming is severe, consider the IV route. The antivenom appears effective even when commenced late, even days, occasionally weeks after the bite. While the theoretical basis for this is obscure, the finding is established by clinical experience with numerous cases. Nonantivenom treatments are generally far less effective; IV calcium gluconate or chloride and pharmaceuticals such as diazepam have been used with mixed success; they should not be considered in preference to antivenom.

Recluse spiders (loxoscelism) and necrotic arachnidism Recluse spiders, also known as brown recluse, fiddleback or violin spiders, genus Loxosceles, are globally distributed, but most cases of significant envenoming are reported from the Americas, southern Europe and southern Africa. The spiders are small, delicate, usually with a characteristic violin shaped marking on the dorsal cephalothorax (Figure 34). These spiders may be present in houses, yet rarely seen, because of their cryptic habits. They are most active at night, when most bites occur, often while the victim is asleep in bed. Their venom is complex and incompletely understood, but can cause direct tissue injury at the bite site, with marked necrosis, occasionally extending well beyond the bite area. Microvascular damage, thrombosis and occlusion, chemotaxis of neutrophils, releasing cytotoxic components and direct cellular injury are all postulated as mechanisms involved in the local necrosis. The percentage of bites resulting in necrosis is unknown, but certainly less than 100%. The bite is usually

not felt and often the spider is not seen, thus diagnosis of loxoscelism is often presumptive. A variable time later, often many hours, the bite area will become painful, red, then progressively discolour, often with a violaceous colour, or suggestion of bruising. Blisters may form, containing clear fluid or blood tinged fluid. The central area may become increasingly dark, dry, suggesting a dry gangrene eschar. This progression may take from 2 to 7 days. The eschar, on separation, will reveal underlying necrosis. In the early stages of the illness, the patient often suffers non-specific systemic symptoms, such as fever, sweats, nausea, malaise, usually resolving after about 48 hours. The area of necrosis may extend over days to weeks and is usually very slow to heal. It is often painful, but not always so and there are cases where the whole process of necrosis and ulceration is pain free, at least in the first week or so. Secondary infection is a significant problem once ulceration has become established. Venom has been detected in the ulcerated area for at least 28 days post bite, possibly explaining why early debridement often results in extending the lesion. This syndrome of local and non-specific systemic effects is classified as cutaneous loxoscelism. More rarely, there may be a specific systemic syndrome associated, classified as viscerocutaneous loxoscelism, characterised by all the features of the cutaneous form, plus a major and potentially lethal systemic illness, with intravascular haemolysis, haemorrhage into major organs, DIC and renal failure. This form has been associated with 30% mortality, even with antivenom treatment. It is rare in North American cases of loxoscelism, but more common in South America. Necrotic arachnidism is more common and widespread than loxoscelism, though loxoscelism is undoubtedly the most common cause of necrotic arachnidism globally. A few other species of spiders are suspected of causing necrosis (see Table 10). Their venoms are generally not characterised. The pattern of non-loxosceles necrotic arachnidism is generally similar to loxoscelism, but without the viscerocutaneous form. For all forms of necrotic arachnidism, including loxoscelism, it is apparent that overdiagnosis occurs; a variety of other conditions, including infections, allergy, drug reactions, other venomous bites, vascular disease, secondary effects of systemic diseases such as diabetes mellitus, may cause a clinical picture similar to necrotic arachnidism. The patient is not well served by mislabelling such problems as “necrotic arachnidism”, as the opportunity for appropriate and effective treatment may be missed. Equally, these and similar diseases may be invoked as a diagnosis, when necrotic arachnidism is the real cause, resulting in detrimental early surgical intervention and later unnecessary amputation of viable limbs, presumed “non-viable due to vascular disease”. In Australia there is a common belief in the community and amongst members of the medical profession that a common house spider, the white tailed spider, Lampona cylindrata, is a frequent cause of necrotic arachnidism. This belief is not supported by evidence; reported bites by this spider do not result in extensive necrosis, indeed there are only 5 cases where even minor ulceration has occurred and in at least 3 of these the identity of the spider is suspect. In all other confirmed cases, no tissue injury has occurred. Further, venom research has failed to demonstrate any necrotic activity in this venom. It is therefore inappropriate to label cases of suspected necrotic arachnidism in Australia as “white tailed spider bites”. Treatment of loxoscelism and necrotic arachnidism is contoversial. Antivenom (for loxoscelism) is only available in parts of South America, notably Brazil (IV Instituto Butantan Polyvalent Spider Antivenom; Soro anti-aracnídico polivalente), where it is reported as effective at reducing the extent of tissue injury, but studies elsewhere have not reproduced this effectiveness in animal models. Pharmaceutical reduction in chemotaxis, using dapsone, has been advocated and if used early may reduce tissue injury, but adverse drug toxicity has cast doubt on this treatment. Steroids have not been shown beneficial. As mentioned earlier, surgical debridement within the first 3-5 weeks of the bite may extend and worsen the necrotic lesion and skin grafting is usually unsuccessful within the first 1-3 months.

Hyperbaric oxygen therapy (HBO) is advocated by some physicians, with limited research giving equivocal and contadictory results on its benefit. Experience in Australia with HBO in necrotic arachnidism has been more positive, but not yet confirmed by clinical trials. HBO appears to be effective at reducing or abolishing local pain associated with the necrosis and probably reduces the extend and hastens recovery of the necrotic area, but does not show benefit in all patients. Overall, the most effective treatment for loxoscelism and necrotic arachnidism, is good wound care, targeted antibiotic therapy if secondary infection occurs, and avoidance of early surgical debridement or grafting. Banana spiders Banana spiders, of the genus Phoneutria, are found principally in South America, particularly Brazil. They are large robust looking spiders (see Figure 35) and are common in some Brazilian urban areas, where they dominate as a cause of significant spiderbite. Their venom contains excitatory neurotoxins (Na+ channel activators), resulting in a syndrome of systemic envenoming characterised by local and generalised pain, local swelling, sweating, hyper lachrymation and salivation, piolerection, hypertension, muscle spasm, priapism, nausea, vomiting and rarely, cardiac arrhythmias and pulmonary oedema. Death is very rare and local wound necrosis is not a problem. The most effective treatment is IV Instituto Butantan Polyvalent Spider Antivenom (Soro anti-aracnídico polivalente), but is generally reserved for those with moderate to severe envenoming, characterised by clear systemic effects such as hypertension (or hypotension), vomiting, salivation, priapism, marked sweating, cardiac arrhythmia, or pulmonary oedema. Dosage is 2-5 ampoules, depending on severity of envenoming. For local pain in all cases, a regional anaesthetic block is effective, though infiltration of 2% lignocaine or similar SC is also effective in many cases.

Australian funnel web spiders Australian funnel web spiders are primitive mygalomorph spiders of the Family Hexathelidae, genera Atrax (3 species) and Hadronyche (30+ species), restricted to wetter areas of eastern and southern Australia (Figures 36-38). They are generally large spiders with long fangs, found in burrows with typical silk funnel-like entrances, most often on the ground, though a few species are arboreal. Mature male spiders leave their burrows to mate and are therefore more commonly encountered by humans. Bites may occur by stepping on the spider, or by close contact with a spider which has entered shoes or clothing left on the ground, indoors or out. They can survive prolonged periods in swimming pools. Unfortunately, several major urban centres, notably parts of Sydney and surrounds, are built on major habitat for funnel web spiders. Worse still, at least for the Sydney funnel web spider, Atrax robustus, it is the more frequently encountered male spider which is most toxic. In the past most reported funnel web spider bites and fatalities occurred in the Sydney region, but there are now confirmed cases and fatalities from a wider geographic range (most of eastern New South Wales and SE Queensland) and a wide range of species, including several Hadronyche species. This clinical experience and venom research now suggests that possibly all species of funnel web spiders may cause severe envenoming in humans. This greatly extends the area and population at risk. Mitigating this is the rarity with which these spiders are encountered outside the range of recorded major bites, as listed above. For those species examined, the venom appears similar, containing polypeptide excitatory neurotoxins that result in widespread neurotransmitter release and a “ catecholamine storm”. Most funnel web spider bites are minor, but cause local pain, partly due to mechanical trauma from the large fangs. The venom is acidic, also causing pain. In cases developing systemic envenoming, there is rapid progression to

systemic effects, with potentially lethal envenoming occurring within 60 minutes of the bite in some cases. Fatalities have occurred as soon as 15 minutes post bite. First seen is perioral tingling, then tongue spasms, nausea, vomiting, abdominal pain, profuse sweating, salivation and lachrymation, tachycardia, hypertension and severe dyspnoea secondary to pulmonary oedema. Cerebral hypoxia may lead to confusion or coma. Generalised fits have been reported, in one case being “status epilepticus”, resulting in ultimately fatal cerebral injury. The pulmonary oedema can be extreme and was a common cause of death. Those surviving this stage sometimes developed generalised muscle spasms, progressing to insidious hypotension and death due to cardiac arrest. First aid for suspected funnel web spider bite is important as it may both delay onset of envenoming and allow local inactivation of venom. The approved method is the pressure immobilisation bandage, as used for Australian snakebite (see First Aid section). All cases should be admitted for observation, as late envenoming can occur. If there is any evidence of systemic envenoming, then CSL Funnel Web Spider Antivenom should be given IV without delay. The starting dose is 2 ampoules, or 4 if severe envenoming and further doses may be needed in severe cases, titrated against response. Apparent recovery, then relapse with pulmonary oedema suggests re-envenoming, requiring further antivenom, but beware overhydration as an alternate cause of late pulmonary oedema. Anaphylaxis is unlikely with this antivenom, because of the catecholamine storm, but serum sickness has been reported in a single case. The antivenom is rabbit IgG. In the absence of antivenom, severe envenoming may prove lethal despite full intensive care treatment. Intubation and positive pressure mechanical ventilation may help control pulmonary oedema. Pharmaceutical manipulation has generally proved unhelpful, with the exception of atropine and occasionally isoprenaline, while beta blockers are considered contraindicated. Scorpions Of the numerous scorpion species, only those in the Family Buthidae cause significant envenoming in humans. Several buthid scorpions are potentially lethal and their stings result in hundreds of thousands of cases of envenoming and thousands of deaths each year. They are therefore far more dangerous than spiders overall, though none would be considered as more dangerous than Australian funnel web spiders. The medically important types of scorpion are listed in Table 11. Scorpions envenom by using a sting in their tail. Their venom contains mixtures of potent toxins, particularly proteins, notably excitatory neurotoxins targeting neuronal ion channels (Na+, K+, Ca++). The clinical effects of scorpion envenoming vary between species, but in general stings cause immediate marked pain, sometimes associated with local erythema, pruritis or hyperaesthesia. When systemic envenoming ensues, it usually does so rapidly, often within an hour. Systemic features may include hyperexcitability, tachy- or bradycardia, hyperthermia, restlessness or uncoordinated movements of limbs or eyes, profuse sweating, lachrymation and salivation, nausea, vomiting or diarrhoea, abdominal pain or distension, dyspnoea, pulmonary oedema, cough, hypoor hypertension, cardiac arrhythmias, shock, convulsions, ataxic gait, muscle fasciculation or coma. Local sting site necrosis is not usually a problem, with the occasional exception of stings by Hadrurus species. Most stings occur at night, often when the person stands, sits or lies upon a scorpion. Children are most likely to develop severe or fatal envenoming. The treatment of scorpion envenoming is controversial and varies both with species and country. In most regions where potentially lethal species exist, specific antivenom is available and there appears ample evidence to support its effectiveness, but in some countries, notably Israel, there are physicians who decry its use. Antivenom choice will depend on the species and country, as will initial and subsequent dosage, but in all cases it is most effective if given early and IV, with the usual precautions against anaphylaxis. There is continuing unresolved argument about the

relative merits of Fab versus F(ab)2 versus whole IgG antivenoms for scorpion envenoming. In the absence of antivenom, or as adjunctive therapy, IV hydration (especially in shock), inotropes etc for control of blood pressure, diazepam and related drugs for muscle spasm or involuntary muscle movement, and airway maintenance may all be useful. Prazosin, in particular, is favoured by some clinicians and is reported as effective in controlling systemic envenoming by Indian scorpions, without use -blockers are likely to worsen envenoming and are of antivenom. contraindicated. Atropine may potentiate the pulmonary oedema, so is not generally recommended, but may be required if there is severe bradycardia. Neostigmine, steroids, barbiturates and narcotics are either of no proven value or are potentially hazardous.

Insects There are a vast array of insect species whose bite or sting can harm humans, often through transmission of disease. Hymenopteran insects (bees, wasps, ants) include many species with stings and venom glands. Their venom mostly contains peptides, components such as melittin, apamin, histamine, serotonin and dopamine. While these may induce both local and systemic effects in sufficient quantity, most stings inject too little to induce major toxicity. Multiple stings, particularly from honey bee species (eg. “Africanised” bees) and some large wasps (European wasps, hornets etc), can cause systemic toxicity, often causing haemolysis, with secondary renal failure, DIC and secondary organ failure and shock. Particularly in children, this can be rapidly fatal. In most fatal cases the number of stings exceeds 1,000, though significant toxicity is possible with fewer stings. The other major effect of hymenopteran stings is acute allergy, specifically anaphylaxis in individuals previously stung, who have developed IgE to venom components. Far more humans die from anaphylactic reactions to hymenopteran venom than sucumb to toxicity from multiple stings. In North Carolina (1972-89) 42.4% of all animal injury deaths were caused by insect stings, almost entirely due to anaphylactic reaction to a hymenopteran sting (17.4% honey bees; 8.7% wasps; 7.6% yellow jackets; 2.2% hornets). The common honey bee, Apis mellifera, is a prime cause of such sting allergy, but it may occur with stings from other species, notably “native” bees, common wasps (European wasps, hornets etc) and a few species of primitive stinging ants (eg. Inch and jumping ants in Australia; Myrmeciinae, genus Myrmecia). These latter ants have particularly potent and allergenic venom and are a significant cause of major hymenopteran allergy in SE Australia. Desensitisation is appropriate for individuals with a history of major systemic reactions to stings, but venom for such therapy is generally only available for honey bee sting allergy. Some ants lack stings, but can bite, their saliva causing local pain or irritation, or spray venom from the abdomen. For most species this is minor, but for some, such as fire ants genus Solenopsis, an introduced pest species in North America, the effects may be significant, their sting causing local burning, pruritis and blistering due to dialkylpiperidines and other venom alkaloids. A number of beetles (coleopterans) may cause local tissue injury as a result of their bite, spraying saliva or abdominal or prothoracic gland contents. The latter is most important in toxic reactions. Most prominent of these are the blister beetles (Meloidae), the principal toxin being cantharidin (“Spanish fly”), which causes blistering of the skin and local dermatitis, for which there is no specific treatment. Contrary to mythology, this toxin is not an aphrodisiac and if swallowed causes inflammation of the urinary tract and is lethal in doses as low as 15mg. A number of other beetles may cause local skin irritation, blistering or dermatitis, notably whiplash rove beetles (Staphylinidae; genus

Paederus), which cause a delayed (by 12-48 hours) erythematous rash, followed by a wheal, then small blisters, which weep for several days, before resolving into a pruritic scab. The blistering stage is very painful. The causative toxin, paederin, is a highly toxic alkaloid, more potent than latrotoxin (from widow spiders) or parathion (an organophosphate). As with necrotic arachnidism, by the time envenoming is apparent, tissue injury is well established. No specific treatment is available, steroids are of no value and good conservative wound care and targeted treatment of any secondary infection is the most appropriate management. Lepidopterans (butterflys and moths) also use defensive toxins that may injur humans. The most widespread type of lepidopteran injury, is Erucism, caused by a wide variety of both butterfly and moth larvae. This usually occurs through skin contact with the hair or body of larval forms (caterpillars), resulting in pruritic or painful skin lessions, which in severe cases may blister or ulcerate and occasionally involve substantial areas and may be accompanied by a systemic illness, characterised by fever, malaise, muscle spasms, nausea and vomiting, local or regional neuritis and, rarely, paralysis. Lepidopterism, in contrast, is caused by contact with shed venomous scales from female moths of the genus Hylesia. It may affect all exposed areas of skin, as the scales may contaminate the atmosphere. In the first stage (foreign body syndrome) there is an itchy sensation in affected skin, which after a few hours becomes intensely pruritic, the resultant scratching releasing the toxins, causing local erythema and the onset of the second stage (toxic syndrome). This latter develops 6-12 hours post exposure, with severe pruritis, especially in flexures, papulous erythematous patches, with spreading of the toxins, via sweating, to eventually involve most of the skin, including mucous membranes (conjunctivitis), often associated with a systemic illness, consisting of malaise, fever, nausea and vomiting and muscular spasms. This may progress to secondary infection of affected skin or severe allergic reactions on subsequent exposure. A few caterpillars may cause other toxic effects, notably coagulopathy, as a result of skin contact. There are no specific treatments for lepidopteran injuries. The most important measure is to determine the causative organism and ensure its removal from the local environment. Numerous other insects may bite humans or emit noxious substances which may be allergenic. Amongst the bugs (Hemiptera), there are the “bed bugs” and the assasin bugs; the latter may inflict painful stings which may result in local tissue injury and transmit disease.

Millipedes and Centipedes Millipedes contain paired exocrine glands in each segment, which secrete toxins when the animal is threatened. A wide variety of toxins are involved, the type depending on species of millipede, but they include benzoquinones, hydrogen cyanide, benzaldehyde, phenol, monoterpenes and peptides. These toxins can induce local pain, pruritis or dermatitis. Centipedes have paired venom glands with fangs at the head and their bite can cause severe pain. Large specimens may also macerate the skin and secondary infection can occasionally result in extensive local tissue damage. For neither group are there specific treatments. Cleaning affected skin, good wound care, targeted treatment of secondary infection and analgesia for prolonged local pain are appropriate.

Venomous mammals

The only venomous mammal of note is the Australian monotreme (egg laying mammal), the platypus. The male has venomous spurs on the hind limbs. When injudiciously handled these may puncture the skin, resulting in extreme local pain and extensive swelling, both of which may persist for days to weeks. There is no significant systemic illness. In the absence of specific treatment, management is best directed to adequate analgesia, which may necessitate regional nerve block, control of swelling by elevation of the stung limb and targeted treatment of any secondary infection. Venomous Fish Spiny Fish A variety of fish have venom gland ensheathed spines, either on fins (dorsal, ventral, lateral or tail fins) or on or behind the head (eg. Catfish) (Table 12). For most species the venom has not been studied, but for the most dangerous species, the stonefish (Scorpaenidae; Synanceiinae; Synanceia), the venom apparatus, venom and clinical effects are well understood and may act as a model for other venomous spiny fish. The stonefish has 13 dorsal spines with venom gland sheaths. The spines have groves to facilitate venom flow up towards the tip. When the spine is activated, by pressure from an “assailant’s” skin (such as the sole of a foot, when a human accidentally steps on the fish) it penetrates the skin and the venom gland is compressed, forcing venom up the groves, deeply into the tissue underlying the skin (Figure 39). When a stonefish is stepped on, several spines may penetrate the foot simultaneously. A similar mechanism occurs with other spiny venomous fish species, such as lateral fin spines puncturing the hand when a fish is picked from a net. Stonefish venom contains a number of potent toxins, including a neurotoxin, stonustoxin, but the clinical effects are generally related to the severe local pain at the sting site, so severe that collapse may ensue. This may be associated with nausea and hypotension. The affected limb will show marked swelling and often a blue discolouration around the sting site. This is not indicative of impending necrosis; tissue injury is not a feature of stonefish envenoming. Stings by other spiny venomous fish, though generally not as severe as stonefish, also produce marked local pain, often with swelling. A common feature of envenoming by these fish is the heat labile nature of their venom. Immersion of the stung limb in hot water (but not so hot as to cause thermal injury!) usually produces rapid relief of pain, but only while in the water. If, after 1-2 hours, removal from the water is still associated with return of intense pain, then analgesia, including regional nerve block in severe cases, may be required. The wound should be inspected for broken spine(s), which should be removed, if present. Contrast radiography or skilful ultrasound may help determine if a retained spine is embeded. If found, surgical exploration should only be attempted if performed early and where there is a high likelihood of success without extending tissue injury. Otherwise, surgical exploration should be avoided. In the case of stonefish stings, there is a specific antivenom (CSL Stonefish Antivenom) which is effective at resolving pain and other symptoms. The dose is 1 ampoule IM or IV for 1-2 spine wounds, 2 ampoules for 3-4 spine wounds and 3 ampoules for more than 4 spine wounds. While this antivenom is not approved for other venomous spiny fish stings, there is anecdotal evidence that it may be effective for some species such as bullrouts (Notesthes species) and lionfish or butterfly cod (Pterois species).

Stingrays

Stingrays are cartilagenous fish (like sharks) with a unique body shape, including a long tail, equipped with a venom gland ensheathed spine. There are relatively few studies of stingray venom, but it appears to be pain producing and heat labile, as seen in spiny fish venom. Stingray injuries are common in seaside regions and consist of 2 components; the mechanical trauma of the sting, plus the venom effects. It is the former which is generally most important. The injury occurs when a human comes too close to a stingray, which whips its tail around in defense. This most often is the result of the victim running into shallow, sandy bottomed seawater, or stepping out of a small boat into similar water; the stingray, resting or hiding on the sandy bottom is surprised and reacts (Figure 40). The spine is driven at speed and with great force into the victim, sometimes resulting in deep or lengthy laceration, which may extend into deep structures. This may result in damage to nerves, tendons, muscle or blood vessels. Death has occurred from exsanguination after severing a major vessel. There are rare cases of puncture of the abdomen or thorax, with potentially catastrophic consequences, including a case of direct heart puncture. In addition to blood loss, shock, loss of some limb function, there is marked pain from this mechanical injury. This is worsened by the effect of the venom on the spine, which is intensely painful. It may occasionally cause systemic effects, but often reported cardiac effects, principally arrhythmias, are probably rare or generally of little clinical concern. Treatment is directed first at control of the mechanical injury, with stemming of blood loss. If the wound is extensive it should be surgically explored early and any residual spine removed, but the wound should be left open and allowed to close by secondary intention. Infection may be common in stingray injuries, so antibiotic therapy is often indicated. Immersion in hot water, as for fish stings, is often helpful in relieving pain, at least in less severe injuries, but in cases with more sever or persistent pain, consider systemic analgesia or regional nerve block. Venomous molluscs Octopuses Only the blue ringed octopuses (genus Haplochlaena) of Australian and adjacent Pacific waters are capable of envenoming humans significantly. Their saliva contains tetrodotoxin, a potent paralytic neurotoxin (Figure 26). Bites almost always occur when the octopus is removed from the water and placed on exposed skin. The bite can be virtually painless. Envenoming can develop rapidly, with paralytic symptoms within 10 minutes and life threatening paralysis and hypotension within 20-30 minutes. However, effective envenoming is rare, most bites being minor. Local tissue injury or infection is not a problem. First aid is the pressure immobilisation bandage method used for Australian snakebite and maintenance of cardiorespiratory function. Hospital treatment consists of intubation, ventilation and control of hypotension. There is no antivenom.

Cone shells Only a few cone shells are capable of effectively envenoming humans. The poison tipped radula tooth is fired at the victim (Figure 42), who has usually picked up the cone shell because of its attractive colouration. The puncture is often painful, but not always so. The venom contains an array of highly active peptides, principally known as conotoxins, which have many effects. Clinically the most important is progressive flaccid paralysis, potentially lethal. First aid is the pressure immobilisation bandage method used for Australian snakebite and maintenance of cardiorespiratory function. Hospital treatment consists of intubation, ventilation and control of hypotension. There is no antivenom.

Venomous echinoderms Many species of echinoderms (Asteroidea, sea stars; Echinoidea, sea urchins; not Holothuria, sea cucumbers ) can cause injury to humans, firstly by mechanical trauma from spines, secondly by local envenoming from venom on the spines. Sea stars generally cause contact dermatitis after handling, but one, the crown of thorns starfish, can cause severe local pain, oedema, bleeding and potentially, secondary infection, but not consistent or severe systemic effects. Subsequent stings may result in marked allergic response. First aid is immersion in hot water (see fish stings). Usually only simple analgesia is required, as the pain, though severe, is short lived. Spine fragments may be embedded, but are hard to find and surgical exploration is generally inadvisable. Prophylactic antibiotics are generally not appropriate; treat infection if it occurs. Sea urchins usually cause injury when handled, most often a mechanical injury from spines, but envenoming from the spines of some species can cause severe local pain, with redness and swelling. Discolouratrion of the wounds may occur, but does not necessarily indicate developing necrosis, though secondary infection and ulceration may occur. Hot water immersion is useful first aid, plus wound cleaning. Medical treatment is as for sea stars. No antivenoms are available.

Venomous cnidarians Jellyfish Jellyfish are both numerous in terms of species diversity and abundance and jellyfish stings are very common. One expert has estimated 2 million stings each summer in Chesapeake Bay alone, just by one species. All jellyfish have stinging cells (nematocysts), either in their tentacles on their body (bell). When these contact a biological membrane, such as human skin, they are triggered to fire, everting their stinging tubule and injecting venom (Figure 43). In some cases much of this venom will directly enter capillaries and the circulation, causing rapid, catastrophic envenoming (Australian box jellyfish). However, most jellyfish stings cause only minor local irritation or short lived local pain, often with wheal formation. Application of a local cold pack is effective first aid for most jellyfish stings. The Australian box jellyfish and related species of chirodropid jellyfish from the Indian and Pacific oceans can cause massive and occasionally lethal envenoming. The sting is immediately very painful, sufficient to cause collapse. There is usually typical ladder-like tentacle contact erythema, which may progress to necrosis. Within minutes of major stings, systemic envenoming will ensue, with cardiorespiratory collapse. Without vigorous first aid this may prove fatal. Application of copious amounts of vinegar over the sting site will deactivate unfired nematocysts, preventing further envenoming, while use of the pressure immobilisation bandage may decrease rate of systemic envenoming.Antivenom, given IM or IV (equine, minimal incidence of adverse effects), may provide benefit, both for systemic and local effects, but its value is the subject of controversy. However, since it has essentially no adverse medical effects, its use is still advocated by most authorities for moderate to severe stings. Secondary infection of sting tracks may require antibiotics. The irukandji jellyfish, also of Australian northern waters and the adjacent IndoPacific oceans, may cause severe, but a quite different form of envenoming. These often tiny jellyfish sting most from the bell and the sting may go unnoticed. About 30 minutes later the victim will experience severe ascending muscle pains in the back and elsewhere which may be associated with a variable systemic illness, akin to a “catecholamine storm”, with pulmonary oedema in severe cases. Medical treatment is supportive as there is no antivenom.

Hydrozoans The most important hydrozoan is a jellyfish-like colony organism, the blue bottle or Portuguese man-o-war. It is typified by the “bell”, which is inflated with air and acts as a float on the surface, with tentacles dangling beneath. Stings generally cause mild to moderate local pain, erythema or wheals and mild oedema. Less often there are systemic symptoms such as nausea and occasionally a syndrome like mild to moderate irukandji syndrome (see above). There is also a likelihood of sensitisation, with allergioc reaction tio further stings. There are also rare cases of local vasospasm and necrosis. First aid is application of a local cold pack. Medical treatment is symptomatic, as there is no antivenom. Coral Coral cuts and abrasions cause both a painful mechanical injury, potentially subject to secondary infection, and local envenoming, also painful. It is the former injury which is usually of most concern. First aid consists of cleaning the wound by gentle scrubbing with a stiff brush in warm fresh water. This procedure should be repeated medically, under anaesthesia if necessary, to ensure all coral fragments are cleaned from the wound.

Anemones Most anemone stings are minor, but severe envenoming rarely occurs, with at least one reported death, after 9 days, as a result of liver failure. Other reported systemic effects include renal failure and extensive necrosis. In most cases, however, symptoms are purely local, with stinging or burning pain which may be immediate or delayed up to one hour. There may be local oedema, erythema, wheal formation, blanching or vesicle formation. Local necrosis or ulceration may follow and the wound may remain painful for days or weeks. Currently recommended first aid is to wash the wound with sea water, apply local cold packs and use oral analgesics. Medical care is symptomatic. No antivenoms are available. Non-venomous animals An overview of non-venomous animal bites Non-venomous animal bites are frequent and are a significant trauma burden on developed nations health facilities, particularly dog bites. They are also probably frequent in developing nations, but statistics are less available. First aid All bites or related injuries from non-venomous animals are potentially significant, either through local or more extensive trauma, through the possibility of significant secondary infection and because of the psychological effects of the trauma. It follows that all cases should be considered for first aid. For minor wounds simple cleaning of the puncture wound may suffice, prior to medical assessment. For more severe wounds, standard first aid will apply, depending on the nature of the injury (ie tissue defect, protective bandage; major bleeding, local compress ± tourniquet; limb fracture, immobilisation; trunk, spine, head injury, immobilisation).

Medical management Most bites or related non-venomous animal injuries will require at least some assessment and treatment, even if all that is required is tetanus booster. Assessnot just for physical trauma, but for potential psychological trauma, a likely sequelae of an animal attack. Diagnosis This is generally straightforward, a clear history of an animal attack being available in most non-fatal cases. The type of animal, circumstances of the attack, location, time and date, number of attacks or number of animals involved should all be documented, for both medical and legal reasons. Particular note should be taken where there is a rabies risk (dogs, bats, some other species in certain regions). The injury should be assessed along standard lines, noting punctures (depth, number, location), lacerations or other tissue disruption, evidence of blunt trauma (eg blows from large animals such as horses hoofs), evidence of internal injuries, evidence of secondary effects (bleeding, shock, impaired conscious state), evidence of specific tissue injury (to blood vessels, nerves, tendons, muscle etc). Ensure allergies are documented early (especially to antibiotics or sticking plaster).

Critical Care Major trauma from animal attacks can be lethal or result in a critical situation, particularly if there is shock or major neurological injury. Standard critical care applies.

Pharmaceutical treatment Essentially all animal attacks causing injury are a risk for tetanus; a booster is the minimum required treatment. Appropriate treatment for rabies applies where this is a risk (see below). Broad spectrum antibiotics will be required in most cases, if there is evidence of secondary infection or if the nature of the injury makes infection likely; perform culture and sensitivities to target therapy.

Rabies Even in the USA, numbers at risk of rabies are significant (18,000 cases/yr requiring prophylaxis), though confirmed cases of rabies are rare (about 10/yr) and in many parts of the tropical and developing world, rabies is a significant risk after animal bite, particularly dogs. In the USA animals responsible for rabies include skunks (43%), raccoons (27.7%), foxes (2.5%) and domestic animals (12.8%). Bats are also a potential source of rabies. Suspected rabid wounds should be thoroughly cleaned, debrided, left open, and active immunisation of highly suspicious cases considered.

Surgical treatment This will depend on the nature of the injuries. Injudicious surgical exploration of minor wounds should be avoided. Surgical management of trauma from animal attacks will depend on the nature of the injuries. Specific details will be found elsewhere in this textbook.

Complications These will depend on the nature of the injuries, but secondary infection is a major risk. Long term psychological effects from even quite minor animal attacks can occur and should be specifically addressed from an early stage of management of injuries.

Follow Up Apart from follow up for specific injuries, routine follow up over the first few days for secondary infection is advisable in all cases. Follow up after a week or more for psychological problems will be justified, at least in selected cases, based on the early psychological response to the attack.

Animal bites Human bites Human beings bite each other in love and combat. Management is based upon experience with closed fist injuries otherwise their management is similar to animal bites. Most bites occur after altercations and when the injured is intoxicated with alcohol. A history may be difficult to obtain and presentation may be delayed. They are not unusual in institutions. They usually involve young males, especially closed fist injuries. Young children may bite each other and penetrating tooth bites of the scalp and face may be a problem in young patients. There are three main types: •

Closed/clenched fist injury and the incised capsule of the bite may act like a trap-door. Also the inoculated extensor tendon and sheath transfers the bacterial load proximally as they relax after striking. Normal incision and drainage will not clear this load.

•

Chomping injury to the finger. When the finger is bitten, it may appear to be minor but the tendons and sheaths are close to the skin and infection may go deep.

•

Puncture-type wounds to other parts of the body such as the scalp where a subgaleal infection may result especially in children with thin scalp tissue.

Where a closed fist has been bitten or been used to punch a mouth, the metacarpal head may be mistaken for a tooth in the wound. Infection is the main concern. Contaminating organisms are usually a mixture of Gram positive and Gram neagative anaerobes: Staphylococcus aureus, Eikenella corrodens, Streptococcus species and -lactamase-producing anaerobic bacteria. Management is meticulous wound care: thorough cleansing, lavage, debridement, wound excision, leaving the wound open, delayed primary closure, and repair of extensor tendon. The organisms in secondary infection are identified and treated with broad-spectrum oral antibiotic and some form of splinting. Check tetanus status. Antibiotics (for all but simple clean wounds seen within 12 hours) are: Procaine penicillin 1gm IM and amoxycillin/potassium clavulanate 500/125 mg (child: 40/10mg/kg/day up to adult dose, in 3x divided doses) orally, 8-hourly for 5 to 10 days. If allergic to pencillin then use = metronidazole 400mg (child: 25mg/kg/day up to adult dose, in 3 divided doses orally), 12hourly for 5 to 10 days and doxycycline 100 mg orally, daily for 5 to 10 days (not in children under 8 years of age or

pregnancy or breast-feeding) or co-trimoxazole 160/800mg (child: 8/40 mg/kg/day up to adult dose, in 2 x divided doses) orally, 12-hourly for 5 to 10 days or a cephalosporin. Complications of such injuries are: •

cellulitis with swelling, erythema and ascending lymangiitis; no pus, no fluctuation; caused by Streptococcus pyogenes; treat with elevation, antibioitcs and splint

•

tendon sheath infections caused by S. aureus and gram negatives (20% cases); with Kanavel's classical signs of infection of pain/fusiform swelling/flexed digit/pain on passive extension

•

deep space infections (in thenar or midplamar spaces; treated by I&D, exclude extension elsewhere)

•

felon

•

scar formation with reduced hand function

•

ear cartilage damage may be slow to heal.

Domestic animals Domestic animals, notably dogs and to a lesser extent, cats, are the major cause of animal attacks and injuries in most regions. In Switzerland, a rate of 325 per 100,000 population per year has been reported for animal attacks, 605 due to dogs and 25% due to cats. In the USA more than one million dog attacks are treated each year but cat bites/scratches requiring medical attention are less frequent (only 5% of cases). However, deaths are proportionately less frequent than for other animal attacks; in North Carolina (1972-1989) dog bites accounted for only 15% of animal attack fatalities, compared to horses (21.7%) and insect sting allergy (45.7%).

Dogs All bites represent 1% of emergency department admissions. Of these 80 – 90% are dog bites. Young boys are the most common victims, with the face, head and neck being the sites of choice. Conversely, the legs (33%), fingers and hands (32%), and arms (18%) are more commonly attacked in adults. The mechanism of injury is usually a combination of puncture, compression, tensile and shearing forces, capable of inflicting superficial and deep injuries. These include soft tissue laceration and avulsion, tendon and neurovascular injury, joint disruption and bony fracture. The contaminated nature of these bites mean these injuries are likely to be further complicated by superimposed infection. Although infection only occurs in 5% of cases, untreated it can impose significant morbidity. Infection may result in cellulitis, tenosynovitis, septic arthritis, abscess, lymphangitis, osteomyelitis, and in extreme cases, septicaemia. It must be detected and treated early to avoid these complications. Patients at high risk of infection include those over the age of 50 years, the immunocompromised (e.g. asplenia, alcoholism), wounds with delayed presentation (8 hours or longer), wounds involving hands, feet or the face, and deep crush/puncture wounds. Infections are often polymicrobial due to heavy bacterial colonization of the oral cavity. Causative organisms include Pasteurella species (P .canis and P .multicoda), streptococci, staphylococci, Capnocytophaga canimorsus and

anaerobes. Capnocytophaga canimorsus is particularly devastating in immunocompromised patients with the potential to cause sepsis and multisystems organ failure. It is important in the history to inquire about the period of delay in presentation and about immunocompromising conditions to assess the patient’s likelihood of infection. The patient’s tetanus immunisation status must also be determined. Examination should assess the site, size and depth of the wound, and damage to deeper structures including nerves, tendon, bone and joints. Adequate examination of deep wounds necessitates exploration under anaesthesia in theatre. Radiological examination may also be required if there is evidence of infection or any suspicion of foreign body or bone fractures. Most dog bites are treated in the emergency department and discharged with follow up. These patients should be advised about signs of infection and to promptly seek medical assistance if infection develops. Admission is required for extensive injuries and wounds complicated by infection or deep tissue involvement. The mainstay of treatment is thorough wound irrigation, debridement, excision of devitalised tissue, thorough wound irrigation and antibiotics. The importance of thorough wound toileting and tissue debridement cannot be understated as these two simple measures alone have been shown to substantially reduce the rate of wound infection. The child should be taken to theatre and the wounds cleaned meticulously to remove any foreign body. The wound should be washed out with copious amounts of normal saline and the edges freshened up. Any devitalised tissue should be removed. In most instances it is possible to perform primary anastomosis with this regime. A mistake made in dog bites is to clean the wound in the emergency department and place sutures. Such treatment will almost certainly result in a secondary infection. The child that has been bitten by a dog has usually sustained some psychological trauma and the child needs to be assessed regularly by the local doctor. Prevention is important in the management of dog bites in children. Very young children and dogs do not mix and they need to be supervised at all times. The appropriate use of antibiotics is important.

Wounds that are not obviously infected, but which are at high risk, or wounds that are complicated by only local cellulitis should have:

Procaine penicillin (child : 50mg/kg up to) 1.0g IM, as a single dose, followed by Amoxycillin/Clavulanate (child : 22.5mg/kg up to) 875/125mg PO bd for 5 days.

Wounds that are infected should have wound cultures before commencing antibiotics. Severe and penetrating injuries require: Metrnoidazole (child : 10mg/kg up to) 400mg PO bd for 5 to 10 days, PLUS either Cefotaxime (child 50mg/kg up to) 1g IV tds or Ceftriaxone (child : 50mg/kg up to) 1g IV daily for 5 to 10 days. Alternatively, as a single agent: Ticarcillin/Clavulanate (child : 50mg/kg up to) 3.1g IV qid for 5 to 10 days. For patients with penicillin hypersensitivity :

Metrnoidazole (child : 10mg/kg up to) 400mg PO bd for 5 to 10 days, PLUS either Doxycycline (child older than 8 years: 2mg/kg up to) 100mg PO, daily for 5 to 10 days or Cotrimoxazole (child: 4/20mg/kg up to) 160/800mg PO bd for 5 to 10 days Ciprofloxacin (child: 10mg/kg up to) 500mg PO bd for 5 to 10 days The standard schedule for tetanus should also be followed. The method of wound closure will depend its site, size and absence or presence of infection. Wounds that are clean may be primarily closed, particularly those to the scalp, face, torso and extremities other than hands and feet. Wounds that are infected must have the infection treated first and before delayed primary closure. Wounds that leave a significant defect may be repaired with skin flaps or left to heal by secondary intention.

Cats Cats may bite or scratch, most wounds being minor, more severe cases often associated with stray female cats. Infected bites or scratches most commonly are due to Pasteurella multocida. The wound should be cleaned and for deep bites, consider puncture excision and irrgiation.

Pet rabbits, hamsters, guinea pigs, rats Manage as for cat bites.

Buffalo, cattle and related herbivores While not causing significant bites or stings, ruminants such as water buffalo and cattle can cause major injuries and fatalities. In North Carolina (1972-89) 9.8% of deaths were attributable to cattle. Injuries included goring from horns, fractured neck, intracranial haemorrhage, multiple trauma and crush injuries, particularly of the chest. Similar injuries are reported following attacks by wild ruminants, notably water buffalo and related species in Africa and Asia. If there is no externally evident trauma, significant internal trauma may be missed, with potentially lethal consequences. The large size, weight and power of these animals should not be underestimated and all cases of injury carefully evaluated, to exclude internal crush or related injuries. In one reported case of bull gore injury, impact from a horn cover blow to the face resulted in a severe orbital blowout fracture, the eye being displaced into the maxilla, with permanent visual loss. Injuries from riding bulls may also be severe, notably severe head injuries, spinal injuries and crush injuries from trampling. Horses and related animals Horses are well known causes of major trauma and fatalities. In North Carolina (1972-89) they accounted for 21.7% of animal injury fatalities, more than caused by dogs. Fatal cases are the result of kicks, usually to the head or chest, and falls, though crush injuries are involved in some cases. Non-fatal injuries reflect similar mechanisms, with facial trauma, intracranial injury, spinal injury and blunt trauma to chest or abdomen being prominent. Horse relatives such as zebra can also cause injury, usually from either kicks or trampling.

Pigs While pigs might not be considered dangerous, they can cause severe and fatal injuries. In North Carolina (1972-89) they caused 2.2% of animal injury fatalities. In one case the victim had a crushed chest and numerous soft tissue injuries from pig bites. In another victim there were tearing and shredding injuries of the scalp and trunk and one leg had been amputated by the pigs. In non fatal cases, both crush injuries and significant lacerations from bites may be expected. Incidence of infection is undocumented, but likely to be high.

Other animals A wide variety of wild animals may potentially cause injury to humans. Only a few selected groups which are the more common (though still rare overall) causes are detailed here. Data on epidemiology of injuries from wild animals is scant, as are published case series or reports on the nature of injuries and their management. Therefore the following information should not be considered comprehensive, but rather indicative of some of the problems that may be encountered. For all wild predatory animals in many regions of the world, rabies should be considered.

Big cats Very few “big cats” are reported as attacking humans and causing significant trauma or death. In Africa, only lions are a major risk. Leopards, cheetahs and other big cats uncommonly attack and almost never kill humans, with rare exceptions such as a rogue leopard that killed 67 people. Lions will readily attack, particularly if in abnormal or stressful environments, such as artificial wildlife parks. Adult lions can exceed 200kg and are powerful predators that usually strike at the neck, head or trunk of their victim. There is a preference for attacking the anterior neck, to strangulate, with consequent injury to the larynx, trachea, pharynx and other adjacent structures. The resultant trauma is often rapidly fatal. In non-fatal cases, injuries can be expected from both the teeth, which may penetrate quite deeply or rip, and from the claws, which may rip tissue. For areas which have been forcibly bitten, some degree of crush injury may also be expected. Secondary wound infection should be anticipated and shock is likely in most cases, often associated with significant blood loss. Leopards also commonly attack the throat, while cheetahs are more likely to cause limb injuries. In parts of Asia where tigers remain present (parts of India, Siberia, a few regions within Indonesia) they occasionally attack or kill humans, with similar effects to African lions. Even rarer, but with similar potential, are Indian lions. North American mountain lions are smaller and less likely to attack, but do rarely cause injuries, generally similar in nature, but less severe than those caused by African lions. At least in California, there is evidence of increasing frequency of attacks by mountain lions.

Wolves and wild dogs and related animals Data on wild dog and wolf caused injuries to humans are not readily available, but it may be assumed that in most cases, injuries will be similar to those caused by dogs, notably injuries caused by bites, either teeth puncture and lacerations, or tearing injuries. To this must be added the potential for more severe injuries as the result of simultaneous attack by several animals, with severe tearing injuries as animals pull in different directions, the victim being subjected to a “tug of war”. Whole limbs could conceivably be wrenched off by this mechanism. In addition to the traumatic injury, secondary infection is likely and in many regions, rabies should also be considered.

Other wild animals similar to dogs or causing similar injuries include foxes, which may bite repeatedly and rapidly; badgers, whose sharp teeth may cause severe slicing injuries; skunks, which cause small chewing bites; biturnongs, which have needle sharp teeth; wolverines, very powerful animals capable of causing massive local trauma, including torn or ruptured deep structures and major fractures. Bears Bears are medium to large predators (up to 400kg) with powerful jaws, sharp teeth and often long sharp claws on powerful limbs. Despite their large size, bears can move quickly (up to 48km/hr). Some species, such as the grizzly bear of North America, are reputed to be inclined to attack humans. Bear attacks, at least in North America, are reported as “becoming more frequent”, though the actual risk remains very low (0.1-0.4 per 100,000 Park visitors/yr in Alberta, Canada). Polar bears are even more powerful and may also attack and kill humans. Injuries are caused by the teeth, with both puncture and tearing injuries; tearing injuries from the claws; blunt trauma from blows from the limbs; crush injuries from grasping with the forelimbs or by sitting or standing on the victim and injuries from severe shaking of the victim. They can fracture or amputate limbs. In fatal cases, severe head and neck injuries, spinal fractures and multiple lacerations are prominent. Early surgical debridement and irrigation is advisable.

Hippopotamus The hippopotamus is a large African herbivore reputed to be the leading cause of fatalities from wild animals in Africa, despite the fact it is a herbivore. A hippo may weigh up to 3,000kg and though most agile in water, where it can submerge for 6 minutes, even on land, where it feeds on grasses at night, it can attain speeds of 40km/hr. The ferocity and danger of these animals is encapsulated by the fact that they nearly always win encounters with crocodiles, themselves most powerful predators. Hippos regularly attack boats approaching too close or anyone standing between them and water or their young. Risk activities are boating or swimming near hippos and walking in hippo grazing areas at night. The long sharp canines can cause devastating injuries, even bisecting adult humans with a single bite, while being trampled by a charging hippo can result in very severe crush injuries. Non-fatal bites can result in massive puncture wounds, blood loss and shock, internal organ damage and fractures, such as fractured limb bones and crush injuries, such as to major vessels. Infection of wounds has not been a problem in most reported cases, but antibiotic cover was used in most (IV penicillin, gentamycin and metronidazole). Immediate soft tissue and fracture debridement and copious wound irrigation is advised.

Elephants and rhinoceros Elephant injuries are uncommon, most often caused by rogue males or females defending young, and generally consist of blunt trauma and crush injuries, which are occasionally lethal. Rhinoceros are nowhere common, but most likely to be encountered in the wild in Africa, rather than India or parts of SE Asia. While the African white rhino is larger (up to 2200kg), it is the black rhino (up to 850kg) which is more likely to attack humans. It can charge at 40km/hr or more and injuries may result from goring by the horn or trampling, with potentially severe crush injuries.

Other mammals

Of the many other mammals that may occasionally bite or otherwise injure humans, a few are of some significance. Primates, especially monkeys in regions such as India (8.8% of all animal bites; 1987-91), may be a significant source of bites, which will be similar to human or dog bites, with a propensity for local infection. Rats may also cause bites, particularly to young children at night, usually to the hands or face. In Western Australia, on a tourist island (Rottnest Island) bites from quokkas, a small species of wallaby, are common (72 cases in 9 months), most injuries being simple incisions or puncture wounds involving digits (83% involved the index finger) which had a low likelihood of infection, partly because the quokka’s mouths lacked pathogenic bacteria.

Crocodiles and alligators Crocodiles and alligators are ancient reptiles, successful ambush predators in wetlands and waterways and a significant cause of major wild animal attacks and fatalities to humans in several regions, including parts of Africa, Asia, South America, northern Australia and SE USA. The jaw and teeth structure of crocodiles and alligators does not permit chewing functions, therefore prey must be torn into bite sized pieces. These animals use several methods to achieve this, of relevance in understanding the injuries they may cause humans. Firstly, they tend to grip their prey, then rotate their body rapidly in a spiral motion, dismembering the prey. This can cause massive injuries to humans and amputate limbs easily. Secondly, they may use decomposition to help predigest prey, thus teeth are likely to be coated with bacteria from decaying corpses of past meals. When they first grip their victim, they will usually try and drag them into water, before twisting or thrashing. Rapid sideways thrashing of the head is designed to quickly kill or immobilise the victim. The powerful tail may also be used to strike the victim. The jaws are capable of exerting enormous pressure and may cause severe crush injury to body parts bitten. While alligators and caimans may occasionally attack humans, such events are rare. Large species of crocodiles, such as those in parts of Africa, SE Asia, India and Northern Australia are more likely to view humans as legitimate prey. Even so, attacks not common, even in Africa (51 deaths over 52 months, 1990-94, in Korogwe District, Tanzania; 60 cases admitted to a single hospital over 4 years, 1 case fatal, in southern Malawi). In Northern Australia, 16 crocodile attacks were reported over 10 years (1981-91), with 4 fatalities. This was considered an underestimate, as attacks and deaths in aboriginal communities were often unreported. From this Australian experience, the range of injuries expected in survivors of crocodile attacks includes multiple fractures, multiple and severe lacerations, secondary blood loss and shock, visceral trauma (hepatic laceration in one case) and puncture wounds. To this should be added crush injuries, flail chest, amputations and secondary wound infections, the latter occurring in 6 of 11 cases. Both aerobes (Pseudomonas, Proteus, Staphylococcus) and anaerobes (Aeromonas, Enterococcus, Clostridium) may be involved and life threatening infections may ensue, particularly after extensive crush injuries. In 4 fatal cases death was due to transection, in two cases at L4-5, in one case at T7 and in one case at C5, as decapitation. Management involves early meticulous surgical exploration and debridement of wounds, anticipating wounds will be deeper than superficially apparent and that underlying crush injuries are likely. Wounds should generally be nursed open and allowed to heal by secondary intention. Tetanus prophylaxis is mandatory and prophylactic broad spectrum antibiotics are adviseable, such as ceftazidime plus penicillin plus metronidazole. In Australian crocodile attacks, where infection by Pseudomonas pseudomallei is likely, attempts to culture this organism should be made (Ashdown’s selective medium which contains 4mg/ml of gentamicin). Ceftazidime (120 mg/kg/day) is appropriate therapy for this type of infection, known as meliodosis. For infections following American alligator bites, Aeromonas hydrophilia and Clostridium sp. are particular risks.

Pythons and boas There are few reports of human injuries from boas and pythons, yet these snakes are popular in captivity in western nations and bites to keepers are probably quite common. These snakes, though non-venomous, have numerous long, sharp recurved teeth that may penetrate deeply and on digits, may reach to bone. Local infection is probably common and potentially severe, as bites are most commonly to the fingers or hand. Osteomyelitis and severe cellulitis may occur. For a deep bite from a large specimen, IV antibiotics may be adviseable. These snakes kill their prey by crushing the body and by asphyxiation. In humans attacked by large specimens, where the snake has wrapped around the neck and body, look for crush injuries and effects of hypoxia, in addition to bite injuries.

Sharks and rays Stingray injuries are both mechanical and toxic and are covered in the section of this chapter on venomous animals, including discussion of mechanical trauma. Sharks of at least 32 species have been implicated in attacks on humans, with up to 100+ attacks worldwide reported each year, of which only the minority are fatal. The incidence of attacks has been estimated as only 1 in 5 million on Atlantic east coast USA. Sharks have widely opening jaws with numerous razor sharp serrated teeth. Most bites occur in shallow water close to shore, around dawn or dusk. The majority of bites are “tentative”, resulting in injuries ranging from small lacerations to removal of sizeable portions of tissue from limbs. The lower limbs are most often attacked. While sharks are powerful predators, injuries seem related more to cutting, slicing and tearing, rather than the crush injuries caused by some other animal bites. However, major fractures are seen in attacks to limbs. When serious feeding bites are made, the victim is usually gripped then either thrashed or tossed, sometimes bodily out of the water. Further bites will occur, often proving rapidly lethal, through body or head transection or blood loss from massive deep lacerations or limb amputation. In survivors of both types of shark attack, extensive lacerations and critical blood loss can be expected. The latter may prove rapidly lethal and mandates early, vigorous control of bleeding and resuscitation. The use of pneumatic splints or MAST suits is often advocated. Once the initial bleeding and shock are controlled, urgent attention should be paid to surgical debridement of wounds. Where possible, preoperative assessment of sensory function in injured areas is advisable, to assist localising possible nerve injuries or transections for tagging or repair in theatre. Primary closure of wounds is advocated by some. Secondary problems, such as infection (eg. by organisms such as Mycobacterium marinum), hypovolaemic renal failure and DIC may occur.

Bony fish A variety of large fish may potentially attack humans, such as barracudas, moray eels, gropers , swordfish and needlefish. The latter is a particular risk to night divers using headlights, which may attract these fish, causing them to spear the diver in the face or head. This may cause very severe injuries or death. For the other fish, bites are the only risk, except swordfish, which may cause shark-bite like lacerations with their serrated snout. Bites result in lacerations. Management is similar to that for shark attacks.

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