Snake bite in southern Africa: diagnosis and management Docs/Snake bite in Southern Africa-Diagnosis and...Snake bite in southern Africa: diagnosis and management There are three groups

2016/11/22, 17)08Muller

Page 1 of 53http://www.cmej.org.za/index.php/cmej/rt/printerFriendly/2546/2581

Continuing Medical Education, Vol 30, No 10(2012)

Snake bite in southern Africa: diagnosis andmanagement

There are three groups of venomous snakes in southern Africa– cytotoxic, neurotoxic and haemotoxic.GJ Müller, BSc, MB ChB, Hons BSc (Pharm), MMed (Anaes), PhD(Tox)Dr Müller is part-time consultant in the Division ofPharmacology, Department of Medicine, Faculty of Medicine andHealth Sciences, Stellenbosch University. He is the founder ofthe Tygerberg Poison Information Centre.H Modler, Dip Pharm (Pharmacy), BSc, MB ChB, MMed (Anaes)Dr Modler is an anaesthetist in private practice, as well as apart-time lecturer and external examiner in pharmacology atthe Department of Anaesthesia, Stellenbosch University and theColleges of Medicine of South Africa.CA Wium, MSc Medical SciencesMs Wium is a principal medical scientist employed as atoxicologist in the Tygerberg Poison Information Centre, Divisionof Pharmacology, Department of Medicine, Faculty of Medicineand Health Sciences, Stellenbosch University.DJH Veale, PhD PharmacologyDr Veale is the former director of the Tygerberg PoisonInformation Centre and currently a consultant clinicalpharmacist and lecturer in pharmacology and toxicology.C J Marks, BSc Pharmacy, MSc Medical SciencesMs Marks is the director of the Tygerberg Poison InformationCentre, Division of Pharmacology, Department of Medicine,Faculty of Medicine and Health Sciences, StellenboschUniversity.Correspondence to: Gert Müller ([email protected])

Venomous snakes in southern Africa can, in broad terms, bedivided into 3 groups: cytotoxic, neurotoxic and those that caninduce haemostatic toxic effects. However, significant overlap ofthese effects may occur. Some snake species may, for example,display both cytotoxicity and neurotoxicity.See Table 1 at end of article for classification, distribution,habitat and clinical toxinology of venomous snakes of southernAfrica.The identification of the snake responsible for the bite is usuallydifficult, unless a dead snake is brought into hospital with itsvictim and can be reliably identified. Descriptions of the snakeand the circumstances of the bite may suggest a speciesdiagnosis, but this is not often a satisfactory basis for specific

2016/11/22, 17)08Muller


treatment.In most cases of snake bite appropriate clinical managementrequires reliable identification of a distinctive clinical syndromebased on epidemiological, clinical and laboratory data. Asyndromic approach is, therefore, recommended in the majorityof cases.

Main clinical syndromesFive main clinical syndromes of snake envenoming arerecognised in southern Africa:• marked local pain and progressive swelling associated withprominent cytotoxic skin changes with coagulable blood• progressive paralysis (neurotoxicity), with negligible or minorlocal swelling• incoagulable blood, with negligible to mild local swelling• moderate to marked local swelling, associated withneurotoxicity• mild to moderate swelling, with negligible or absent systemicsymptoms.

Marked local pain and progressive swellingassociated with prominent cytotoxic skin changeswith coagulable bloodSnakes responsible for this syndrome include:• The major adders, e.g. Bitis arietans (puff adder) and B.gabonica (gaboon adder) (Figs 1 and 2).• Spitting cobras, e.g. Naja mossambica (Mozambique spittingcobra, M’fesi), N. nigricollis (black-necked spitting cobra), N.nigricincta (barred, zebra spitting cobra) and N. nigricinctawoodi (black spitting cobra) (Figs 3 - 5).• The rinkhals, Hemachatus haemachatus. Although mildneurotoxic effects have been mentioned to occur in rinkhalsbite, these have not been well documented (Fig. 6).(It should be noted that extensive cytotoxicity with insignificantneurotoxicity has been described after South African greenmamba bites.)For further information with regard to the classification,morphology, habitat and distribution of the above-namedsnakes, see Table 1 and Figs 7 and 8.The toxins of cytotoxic snake venom are digestive hydrolases(proteolytic enzymes and phospholipases) and polypeptides thatdestroy cell membranes, skeletal muscle and other tissues.These effects increase the permeability of the vascularendothelium, which leads to local swelling, blistering andoedema. Irreversible death of tissues may occur(necrosis/gangrene).

Clinical featuresThe local effects of bites by spitting cobras are essentiallysimilar to those of large adder bites. Swelling usually begins

2016/11/22, 17)08Muller


early, often within 10 - 30 minutes. It may become extensive,involving the entire limb and even adjacent areas of the trunk,especially in children. Regional lymph nodes may becomeenlarged and painful within 30 - 60 minutes. The aggressiveand progressive cytotoxic nature of envenoming is usuallyevident within hours of the bite. Blisters and bullous skinlesions, fluid or blood filled, and ecchymoses often develop, atfirst near the fang marks, but may later extend beyond the bitesite within 6 - 24 hours.‘Skip lesions’ (areas of necrosis separated by strips ofapparently normal skin caused by proximal spread of venom inlymphatic vessels) are characteristic of spitting cobra bites (Fig.10). Spitting cobras frequently enter dwellings at night andoften bite victims while asleep.Extravasations of plasma may cause hypovolaemia, which maylead to hypovolaemic shock, especially in children. The localcytotoxic effects may progress to necrosis, with spontaneoussloughing of dead tissue. Compartmental syndromes maydevelop, especially involving the anterior tibial compartmentafter bites of the feet and ankles, or forearm, in bites of thehand or wrist. This complication may lead to ischaemic necrosisof the compartmental muscles and nerve damage. Late (2 - 3days post bite) haemostatic disturbances, especiallythrombocytopenia, have been described in puff adder andgaboon adder bites.Gaboon adder bites may be accompanied by cardiovascularabnormalities, including hypotension, cardiac dysrhythmias andshock. Fortunately these bites are rare.Fig. 9 (a - d) shows the local toxic effects of a puff adder bite.Fig. 10 shows the effects of spitting cobra bites.

Special investigationsAbnormal blood biochemistry, such as raised serumconcentrations of creatine kinase and other muscle-derivedenzymes, is commonly found in severe envenoming because oflocal muscle damage. Neglected major adder bites may becomplicated by rhabdomyolysis, with release of muscle contentsinto the plasma (myoglobinaemia), manifesting withmyoglobinurea, which may lead to compromised renal function.Thrombocytopenia is also a potential complication. Specialinvestigations should therefore include urinalysis, urea, serumcreatinine, electrolytes, and full blood count (including the bloodclotting profile).Snake venom ophthalmia is eye envenoming that occurs whenvenom is spat into the eyes (see under ancillary treatment).Antivenom is available for bites of the abovementioned snakes(SAIMR Polyvalent Snakebite Antiserum SAVP).

Progressive paralysis (neurotoxicity), withnegligible or minor local swellingSnakes responsible for this syndrome include:• Neurotoxic cobras: Naja anchietae (Anchieta’s Egyptian

2016/11/22, 17)08Muller


cobra), N. annulifera (banded or snouted cobra), N.melanoleuca (forest, black and white-lipped cobra) and N. nivea(Cape cobra) (Figs 11 and 12). See Fig. 13 for distribution ofneurotoxic cobras and Table 1 for classification and otherinformation.• Mambas: Dendroaspis polylepis (black mamba) and D.angusticeps (common, eastern green, white mouthed mamba).It should be noted that extensive cytotoxicity with insignificantneurotoxicity has been described after South African greenmamba bites (Figs 14 and 15). See Fig. 16 for distribution ofmambas and Table 1 for classification and other information.The venoms of neurotoxic cobras contain polypeptides thatcompete with acetylcholine for binding at post-synaptic nicotinicreceptors at skeletal muscle nerve junctions, leading to acurare-like paralysis. Mamba venom, in addition to its effects onpost-synaptic nicotinic receptors, also contains polypeptidetoxins, which facilitate the release of acetylcholine from thenerve endings (dendrotoxins), as well as toxins which inhibitsynaptic acetylcholinesterases (fasciculins). Neurotoxins thatblock muscarinic receptors have also been described in mambavenom. See Fig. 4 in the article on scorpion sting with regard tothe mechanisms of action of neurotoxic venoms on theperipheral nervous system.

Clinical featuresNeurotoxicity is characterised by progressive, descending flaccidparalysis. Early symptoms and signs include transientparaesthesia of the tongue and lips, blurred and double visionand ptosis, pupillary abnormalities (e.g. dilated pupils), externaland internal ophthalmoplegia and paralysis of facial musclesand other muscles innervated by the cranial nerves, leading todysarthria, dysphonia, and dysphagia. There is an increase inoro-pharyngeal secretions due to difficulty in swallowing. This isfollowed by progressive, descending paralysis, and finallyrespiratory failure. As respiratory distress increases, the patientbecomes anxious, sweaty and cyanosed and will die unlessgiven ventilatory support. Neurotoxic snakes can cause life-threatening paralysis and death within 1 - 8 hours. Respiratoryfailure is usually the primary cause of death. Fig. 17 depictsptosis after a Cape cobra bite.In addition to the above neurotoxic effects, patients bitten bymambas may present with trembling, skeletal musclefasciculations and signs of autonomic nervous systemstimulation (due to increased acetylcholine activity in thesynaptic cleft – see mechanisms above). Early features arevomiting, chest and limb pains and excessive salivation. Cardiacdysrhythmias have also been described in mamba bite victims.Patients bitten by elapid neurotoxic snakes may present withpain at the bite site and varying degrees of minor local swelling.However, in some envenomed patients the bite site is difficult tolocate/identify. Necrosis and other local cytotoxic effects do notusually develop to any significant degree. Fig. 18 shows minimallocal swelling with Cape cobra bite, while Fig. 19 demonstratesthat in some cases of Cape cobra envenomed patients the bitesite is difficult to locate/identify.

2016/11/22, 17)08Muller


Special investigations, where appropriate, should includearterial blood gas and other respiratory function tests and anECG.

Differential diagnosis of neurotoxic snake biteThe diagnosis of elapid neurotoxic snake bite, especially whenthe patient is unaware of being bitten or where the culprit hasnot been identified, may occasionally be difficult. Clinicalconditions that should be considered in the differential diagnosisinclude scorpionism and latrodectism. See Table 1 in thescorpion sting article for a comparison of major symptoms andsigns of scorpionism, latrodectism and neurotoxic cobra bite. Inneurotoxic/cytotoxic berg adder bite the cytotoxic component ofenvenoming is quite prominent when compared with theminimal local effects of elapid neurotoxic snake bite.Antivenom is available for bites of the abovementioned snakes(SAIMR Polyvalent Snakebite Antiserum SAVP).

Incoagulable blood, with negligible to mild localswellingSnakes responsible for this syndrome include:• boomslang (Dispholidus typus) (Figs 20 and 21)• South eastern Savanna vine/bird/twig snake (Thelotorniscapensis)• Oate’s savanna vine snake (Thelotornis capensis oatesi).Fig. 21 demonstrates the position of boomslang fangs. See Fig.22 and Table 1 for distribution of boomslang and bird snake.Venom of the boomslang has potent pro-coagulant effects byactivating factors II (prothrombin), X and possibly also IX.Severe consumptive coagulopathy develops within several hours(4 - 24 hours) after the bite. See Fig. 23, in which the bloodcoagulation cascade is depicted.

Clinical featuresPatients may present with nausea, vomiting, abdominal pain,headache, dizziness and fainting. Persistent oozing of bloodfrom fang punctures or other wound sites is often observed.Although bleeding may occur within 6 - 24 hours after a bite,systemic haemostatic symptoms and signs may be delayed formore than 24 hours, even days after the bite. Bleeding usuallymanifests as gingival bleeding, epistaxis, purpura,haematemesis, melaena, haematuria, extensive ecchymoses,and in severe cases, subarachnoid or intracerebralhaemorrhage. Severe consumptive coagulopathy may lead tomultiple organ failure.There is local pain with insignificant ormild local swelling.Special investigations reveal incoagulable blood, defibrination,elevated fibrinogen degradation products, thrombocytopeniaand anaemia. Incoagulable blood is a cardinal sign ofconsumptive coagulopathy. To confirm this, the ‘20 minutewhole blood clotting test’ is a simple, rapid test of bloodcoagulability, which can be performed at the bedside andcorrelates well with the fibrinogen concentration. A fewmilliliters of blood taken by venepuncture is placed in a new,

2016/11/22, 17)08Muller


clean, dry glass vessel and left undisturbed at roomtemperature for 20 minutes, then tilted once to see whether ornot the blood has clotted. Other more sensitive laboratory testsinclude prothrombin time (often reported as INR), thrombin andfibrinogen levels, activated partial thromboplastin times andmeasurement of fibrinogen degradation products and D-dimerconcentrations. Other laboratory investigations should includeurinalysis, full blood count, urea and electrolytes and serumcreatinine.Antivenom is available for boomslang bite (SAIMR BoomslangSnakebite Antiserum SAVP). No antivenom is available forvine/bird twig (Thelotornis) snake bites.

Moderate to marked local swelling, associated withneurotoxicitySnakes responsible for this syndrome include:• berg adder (Bitis atropos) (Fig. 24)• other small/dwarf adders (side-winding adder – B. peringueyiand desert mountain adder – B. xeropaga).See Fig. 25 and Table 1 for distribution and classification of thedwarf adders.Phospholipase A2 neurotoxins are responsible for the toxiceffects of these snake venoms. The neurotoxins actpresynaptically, initially releasing acetylcholine, followed by aninterference with or blockade of its release.

Clinical featuresAfter initial pain and the development of local swelling,paraesthesiae of the tongue and lips, blurring of vision and theloss of the sense of smell (anosmia) and taste, and dysphagiadevelop, often within 2 - 3 hours of the bite. External andinternal ophthalmoplegia are characterised by ptosis, fixeddilated pupils and loss of eye movements and accommodation.Muscle weakness and respiratory failure are commoncomplications (in >50% of cases) and typically develop late (6 -36 hours after the bite), often at a stage when not anticipatedor expected.Hyponatraemia, attributable to a natriuretic hormone-like toxinpresent in the venom, is also a frequent complication. Ittypically develops late (24 - 36 hours post bite). If undetectedthis may lead to unexpected convulsions (see further undermanagement).Ophthalmoplegia and anosmia may take quite a long time toresolve (weeks to months).The local effects include moderate to marked local swelling.Swelling may involve more than half the bitten limb. Blisteringand necrosis may develop in the region of the bite site.Extensive cytotoxic skin changes and compartmental syndromesare not expected to develop.Fig. 26 shows ptosis after a berg adder bite and Fig. 27 a bergadder bite demonstrating local swelling. Fig. 28 shows localnecrotic changes after a berg adder bite.Recommended special investigations should include urinalysis,

2016/11/22, 17)08Muller


urea and electrolytes, full blood count, oxygen saturation andother respiratory function tests. Specific attention should begiven to the plasma sodium level. The sodium level should berecorded at regular intervals until hyponatraemia is noted oruntil such time as hyponatraemia has been excluded, e.g. at 4days after envenoming.No antivenom is available for berg adder and other dwarf adderbites.

Mild to moderate swelling, with negligible orabsent systemic symptomsSnakes responsible for this syndrome include:• night adder (Causus rhombeatus) (Fig. 29)• burrowing asp (Atractaspis bibronii) (Fig. 30)• Natal black snake (Macrelaps microlepidotus)• some dwarf adders, e.g. horned adder (Bitis caudalis) (Fig.31).

Figs 32 and 33 show the distribution of the night adders,burrowing asp and the Natal black snake.

Clinical featuresAssociated symptoms and signs include local pain, regionallymphadenopathy and fever. Swelling rarely involves more thanhalf of the bitten limb. Blistering and necrosis may develop atthe bite site. Extensive cytotoxic skin changes andcompartmental syndromes are not expected to develop. Bitesby the Natal black snake are said to have resulted in collapseand loss of consciousness.Minor envenoming by spitting cobras and major adders shouldbe considered in the differential diagnosis in cases where thesnake has not been identified. Special investigations shouldinclude urinalysis and a full blood count.No antivenom is available for bites of the above-mentionedsnakes.For information with regard to envenoming by the lesser knownor poorly documented venomous snakes (e.g. garter and coralsnakes) consult Table 1.

Management of snake bite

First aid and general management• While instituting first aid procedures, organise transport to getthe patient to a medical facility as soon as possible. Use a cellphone and other forms of communication to call for help. Alertthe medical facility or doctor ahead of arrival.• Reassure the victim, who may be terrified.• Remove constricting clothing, rings, bracelets, bands, shoes,etc. from the bitten limb/area.

2016/11/22, 17)08Muller


• Immobilise the whole patient.• Avoid the many harmful and time-wasting traditional first-aidtreatments such as cauterisation, local incision or excision,tattooing, immediate prophylactic amputation of the bitten digit,suction by mouth or vacuum pumps or ‘venom-ex’ apparatuses,instillation of chemical compounds such as potassiumpermanganate, application of petrol, ice packs, ‘snake stones’and electric shocks. The above measures are contraindicated asthey are potentially harmful and none has any proven benefit.• In suspected neurotoxic cobra or mamba bite, especially if thepatient is far from medical help, apply a tight crepe bandageover and proximal to the bite site. This procedure may reducerapid distribution of the venom. Avoid crepe or other bandagingin all cytotoxic bites.• The classic ‘pressure-immobilisation technique’ demandsspecial equipment and training and is considered not practicablefor general use in South Africa.• A tight arterial tourniquet should NEVER be used! The dangersof tourniquets include the development of ischaemia andgangrene if they are applied for more than about 1½ hours.• Since species diagnosis is important, the dead snake shouldbe taken along to hospital. However, if the snake is still at large,do not risk further bites.• In suspected neurotoxic snake bites, the patient should beassessed regularly (e.g. every 10 - 15 minutes) for thedevelopment of complications of neurotoxicity.• Cardiopulmonary resuscitation (CPR) may be needed. Thisincludes clearance of the airway, oxygen administration by facemask or nasal catheters, and establishment of intravenousaccess. If the patient is unresponsive and no respiratorymovement is detectable, start CPR. In case of respiratorydistress/failure: clear the airway, lift the chin, give oxygen byface mask or nasal catheters with or without assisted ventilationand consider the need for endotracheal intubation. Shocked,hypotensive patients should be given intravenous fluids. Pressoragents, such as dopamine or phenylephrine may need to beadministered.• Give analgesia by mouth if required: paracetamol(acetaminophen) or paracetamol/codeine combinations arepreferred. Aspirin and other non-steroidal anti-inflammatoryagents should be avoided in patients with haemostaticdisorders. When using parenteral opioids in neurotoxic snakebite, respiratory function should be monitored closely.• In the cases of berg adder bite, hyponatraemia should not betreated by means of fluid restriction, but rather by a titratedinfusion of hypertonic saline. In this respect the administrationof normal saline may prove useful as a means of partiallymeeting both fluid and salt requirements.• In cases where the snake has not been identified it isrecommended that asymptomatic patients be admitted to amedical facility for observations for 12 - 24 hours.

Antivenom treatment

2016/11/22, 17)08Muller


Two snakebite antivenoms are available:• Polyvalent antivenom (SAIMR Polyvalent Snakebite AntiserumSAVP) is supplied in 10 ml ampoules. Venoms of the followingsnakes are used as antigens in the preparation of the polyvalentantivenom: puff adder, gaboon adder, rinkhals, green mamba,Jameson’s mamba, black mamba, Cape cobra, forest cobra,snouted cobra and Mozambique spitting cobra. Polyvalentantivenom is ineffective AND SHOULD NOT BE USED intreatment of bites caused by the berg adder, other dwarfadders, night adders, the burrowing asp and back-fangedsnakes (boomslang and vine snake).• Boomslang antivenom (SAIMR Boomslang SnakebiteAntiserum SAVP) is supplied in 10 ml ampoules. It is effectiveagainst the venom of boomslang, but not against the venom ofthe vine snake (bird of twig snake).Antivenom neutralises a fixed amount of venom. Since snakesinject the same amount of venom into adults and children, thesame dose/volume of antivenom must be administered tochildren as in adults.Antivenom is not always necessary: some patients are bitten bynon-venomous snakes and 10 - 50% of those bitten byvenomous snakes are not envenomed (so called ‘dry bites’).Indications for antivenom treatment after bites by South Africansnakes:• neurotoxicity• abnormal blood clotting parameters, incoagulable bloodand/or spontaneous systemic bleeding• rapidly progressive and/or extensive swelling involving morethan half the bitten limb within a few hours after the bite• cardiovascular abnormalities such as hypotension, shock andcardiac arrhythmias.

PrecautionsSkin testing for sensitivity is not recommended, since it isunreliable and only delays urgent administration of antivenom.Administration of antivenom may be associated with acute life-threatening adverse reactions (anaphylaxis), pyrogenic(feverish) reactions, or late immune complex disease (serumsickness). Most acute/severe allergic reactions occur during thefirst hour after antivenom administration and only a negligiblenumber occur more than 6 hours post administration.There is no absolute contraindication to antivenom treatmentwhen a patient has life-threatening systemic envenoming.However, patients with an atopic history and those with ahistory of previous reactions to equine antisera have anincreased risk of severe antivenom reactions. In these cases,pretreatment with subcutaneous adrenaline, 0.25 ml of a 1:1000 (250 µg) solution in adults is justified to prevent ordiminish the reaction. In children the dose of adrenaline is 0.01mg/kg. Some experts recommend prophylactic adrenaline in allpatients. Patients in whom adrenaline is relativelycontraindicated include those with a history of ischaemic heart

2016/11/22, 17)08Muller


disease or stroke, uncontrolled hypertension andtachyarrhythmias.Premedication with antihistamines may dampen minor allergicreactions but will not prevent serious allergic/anaphylactoidreactions. Hydrocortisone takes several hours to act and isineffective as a prophylactic agent against acute reactions.Slow infusion of the antivenom, rather than administration bybolus, is recommended as a method of reducing seriousantivenom reactions (be aware of acute fluid overload inchildren).

Dose and methods of administrationChildren should be given the same dose of antivenom as adults.Antivenom should be given as soon as possible once signs ofsystemic or severe local envenoming are evident. Although thepolyvalent antivenom is more effective when given early (within6 hours after the bite) it may be administered up to 24 - 48hours or later in serious envenomations − it is never too late togive antivenom.Antivenom is most effective when given intravenously. It shouldbe diluted in isotonic fluid and infused over 30 - 60 minutes (inmost cases a 200 ml volume container is adequate).Intramuscular injection is not recommended. Do not injectantivenom into or around the wound.The recommended intravenous dose of polyvalent antivenom inserious cytotoxic snake bite (puff adder, gaboon adder) is 50 -100 ml (5 - 10 ampoules). In neurotoxic snake bite (mambas,neurotoxic cobras) the recommended dose is 80 - 120 ml (up to200 ml in severe cases of mamba bites). A follow-up dose mayoccasionally be required in black mamba bites.The recommended dose of boomslang antivenom is 20 ml (2ampoules) intravenously in isotonic fluid given over 30 minutes.A follow-up dose of 10 ml may sometimes be necessary.

Response to antivenom treatmentNeurotoxic signs improve slowly after several hours (2 - 6hours), often unconvincingly. It must be emphasised that theadministration of polyvalent antivenom in the acute phase ofneurotoxic snake envenoming will usually not preventprogression of neurotoxic effects, most notably respiratoryparalysis, and consequently the patient will not survive withoutlife support. Respiratory support is the only life-savingtreatment modality in neurotoxic snake envenoming. However,intravenous administration of adequate doses of antivenom willdecrease the time course of muscle paralysis and recovery.Similarly, in cytotoxic envenoming, administration of polyvalentantivenom will not reverse but may limit further tissue damage.However, in boomslang bite the haemostatic effects are rapidlyreversed by boomslang antivenom at any time after the bite.

Treatment of antivenom reactions

2016/11/22, 17)08Muller


Early serious reactions may begin 3 - 60 minutes after startingintravenous administration. Adrenaline (epinephrine) 0.1% (1:1000) should be given intramuscularly in a dose of 0.5 - 1.0 mlfor adults and 0.01 mg/kg for children. This should be followedby a slow intravenous injection of an H1 antagonist(antihistamine) such as promethazine at a dose of 25 - 50 mgin adults. It is contraindicated in children <2 years of age. In children 5 - 10 years old the dose ofpromethazine is 6.25 -12.5 mg and in children 10 - 16 years ofage 12.5 - 25 mg (or 0.125 - 0.5 mg/kg).Late (serum sickness type) reactions occur 5 - 24 (average 7)days after treatment. It presents with itching, urticaria, fever,arthralgia, peri-articular swellings, proteinuria and sometimesneurological symptoms. Antihistamines are used for milderattacks, but in severe cases a short course of prednisoloneshould be given.

Ancillary treatmentAlthough most local effects of snakebite are attributable directlyto cytolytic and other activities of the venom itself, the bite mayintroduce pathogenic bacteria. The risk of local infectionsgreatly increases if the wound has been incised with anunsterile instrument or tampered with in some other way. Thewound should be cleaned with an antiseptic. Blisters and tensebullae should be aspirated only if rupture seems imminent.Snake-bitten limbs should be nursed in the most comfortableposition but should not be elevated excessively if there is tenseswelling or suspicion of incipient intracompartmental syndrome,as this increases the risk of ischaemia. Debrided tissue,serosanguinous discharge and pus should be cultured and thepatient treated with appropriate antimicrobials.Expert surgical advice should be sought where applicable.

Compartmental syndromesThese are uncommon and over-diagnosed but require urgentattention. The clinical appearance of snake-bitten limbs oftensuggests that there is a compartmental syndrome. There maybe severe pain, tense swelling, cold cyanosed skin, pain onpassive stretching of the muscles and apparently absent pulses.However, these appearances are usually misleading. When theintracompartmental (tissue) pressure is measured directly (e.g.with a Stryker monitor) pressures are usually found to be belowthe threshold of danger for ischaemic necrosis of theintracompartmental muscles. Should conservative treatmentfail, full-length fasciotomy should be performed, providing thereis no coagulopathy or gross thrombocytopenia. It should bementioned that animal studies have shown that fasciotomy isineffective in saving envenomed muscles. Provided thatadequate antivenom treatment is given as soon as possibleafter the bite, fasciotomy is rarely if ever needed.Necrotic tissue should be debrided by a surgeon. Skin graphsmay be necessary.

2016/11/22, 17)08Muller


Haemostatic abnormalitiesRecovery of normal haemostatic function may be accelerated bygiving fresh whole blood, fresh frozen plasma, cryoprecipitatesor platelet concentrates.NB: Heparin and antifibrinolytic agents should never be used insnake bite patients. Heparin does not inhibit the abnormalthrombin generated by snake venoms and it exaggerates,sometimes fatally, the haemostatic disturbances.Acute renal failure may be caused by haemorrhage, ischaemiaresulting from hypotension, effects of blood clottingabnormalities, renal vasoconstriction, pigment nephropathycaused by haemoglobinuria or myoglobinuria, directnephrotoxicity and immune complex glomerulonephritis causedby serum sickness reactions to antivenom. If the urine outputfalls below 400 ml in 24 hours, central venous pressure shouldbe monitored and a urethral catheter inserted. Cautiousrehydration with isotonic fluids can be followed by a high doseof furosemide. If these measures fail, dialysis may be indicated.

Anticholinesterase therapy as an option forneurotoxic cobra biteNeuromusclar blockade by post-synaptic neurotoxins (e.g.neurotoxic cobra venom) may be partly overcome by the use ofanticholinesterase drugs. Although anticholinesterase may assistin management, this should not replace antivenom therapy andshould also not take priority over respiratory support. It may beof particular benefit to patients allergic to antivenom.Anticholinesterase therapy is, however, not recommended inbites by snakes with presynaptic acting neurotoxins, such asmamba or neurotoxic adders. A test dose of edrophonium toassess whether anticholinesterase therapy may be of benefit isgenerally recommended. However, edrophonium is not availablein South Africa. Neostigmine is therefore used throughout.The administration of anticholinesterases requires the co-administration of an anticholinergic drug to block potentiallyserious muscarinic effects, such as bradycardia, bronchospasmand an increase in secretions. Two anticholinergic drugs areavailable for this purpose, namely, atropine and glycopyrrolate.Glycopyrrolate is the preferred anticholinergic. It gainedpopularity because it produces less tachycardia than atropine, itis a much more potent antisialagogue and does not cross theblood-brain barrier. It should be noted that reversal of blockadeis difficult with concomitant respiratory acidosis. Hypoventilationhas to be addressed to decrease the PaCO2 before neostigmineand glycopyrrolate will be optimally effective.The recommended average dosing regimen for the reversal ofnon-depolarising neuromuscular blockade in adults isneostigmine 2.5 mg and glycopyrrolate 0.6 mg (or atropine 1mg) given together as a bolus. The same dosage regimen isrecommended to overcome snake bite-induced postsynapticblockade. It is generally recommended that the dose ofglycopyrrolate (Robinul) be 0.2 mg (1 ml) for each 1.0 mg ofneostigmine. In children the dosage schedule of neostigmine forthe reversal of non-depolarising neuromuscular blockade is 0.03

2016/11/22, 17)08Muller


- 0.07 mg/kg, maximum 2.5 mg). The average dose ofglycopyrrolate with neostigmine is 0.010 - 0.015 mg/kg. (Therecommended dose of atropine with neostigmine in children is0.02 - 0.03 mg/kg.) Patients who respond convincingly bydemonstrating increased muscle strength and/or improvementof ptosis can be maintained on neostigmine 0.5 - 2.5 mg every1 - 3 hours intravenously up to 10 mg per 24 hours for adults or0.01 - 0.04 mg/kg every 2 - 4 hours for children. Again, thedose of glycopyrrolate should be 0.2 mg (1ml) for each 1.0 mgof neostigmine.

Snake venom ophthalmiaSnake venom ophthalmia is caused when venom is spat into theeyes. The spitting elapid species in southern African (Najamossambica, N. nigricollis, N. nigricincta and Hemachatushaemachatus) can cause intense conjunctivitis and bullouscorneal erosions, complicated by secondary infection, anterioruveitis, corneal opacities and permanent blindness.First aid treatment consists of irrigating the eye or otheraffected mucous membrane as soon as possible, using largevolumes of water or any other available bland fluid such as milk.A single application of local anaesthetic eye drops to overcometightly closed eyelids (blepharospasm) may be used to facilitateirrigation. Topical or systemic antivenom treatment should notbe applied or given. Corneal abrasions can be excluded byfluorescein staining/slit lamp examination. If there are noabrasions, treat with antibiotic eye ointment and an eye pad.Resolution should occur within 24 - 48 hours. If corneal erosionsare present, antibiotic eye drops/ointment, mydriatics and aneye pad should be applied. Daily slit lamp examinations arerecommended until resolved. An ophthalmologist should beconsulted in all cases.

Further reading available at www.cmej.org.za

2016/11/22, 17)08Muller


Fig. 1. Puff adder (Bitis arietans). A very large, heavy-bodiedsnake, maximum total length exceeding 190 cm. Its colour mayvary from brown, reddish to orange to very dark, withdistinctive pale back edged U or V markings (chevron-likepatterns) along the dorsum becoming annular rings around thetail. The belly is pale. When threatened it inflates its body andhisses loudly. Bites are common. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 2. The large adders (vipers) have large, hinged, tubularfangs that can fold back into a protected sheath against the roofof the mouth. When attacking, the fangs are forced forward,enabling a deep penetrating injection of venom. (Photo: JohnVisser.)

2016/11/22, 17)08Muller


Fig. 3. Mozambique spitting cobra (Naja mossambica). Averagelength 80 - 130 cm. Above it is black grey to olive brown. Belowit is pale or salmon pink, sometimes yellowish with crossbars,half-bars and blotches on the throat and anterior third of thebelly. Bites are common. Spits and bites. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 4. Barred or zebra cobra (Naja nigricincta). Average length100 - 120 cm. There are between 50 and 85 black crossbars ona brown or pinkish background. These crossbars usually encirclethe body. The head is uniformly black both dorsally andventrally. (Photo: Tony Phelps.)

2016/11/22, 17)08Muller


Fig. 5. Black spitting cobra (Naja nigricincta woodi). Averagelength 120 - 150 cm; uniformly black. Spits and bites. (Photo:John Visser.)

2016/11/22, 17)08Muller


Fig. 6. Rinkhals (Hemachatus haemachatus). Average length 1m. Colour variable, but normally olive to dark brown or dullblack above and below with one or two white crossbars on thethroat. Specimens in the south-western and eastern Capedisplay numerous orange-yellow crossbands. (Photo: JohnVisser.)Neglected major adder bites may be complicated byrhabdomyolysis, with release of muscle contents into theplasma (myoglobinaemia), manifesting with myoglobinurea,which may lead to compromised renal function.

2016/11/22, 17)08Muller


Fig. 7. Distribution of the major adders in southern Africa. Allcomposite maps have been compiled by GJ Müller withreference to the locations published in Spawls S and Branch B:The Dangerous Snakes of Africa. London: Southern BookPublishers, 1995 and Visser J: Dangerous Snakes andSnakebite, published by John Visser (no date).

Fig.8. Distribution of the spitting cobras and rinkhals insouthern Africa.

2016/11/22, 17)08Muller


Fig. 9a. Puff adder bite. Progression of local cytotoxic effects 6hours post bite.

2016/11/22, 17)08Muller


Fig. 9b. Puff adder bite. Progressive local swelling 6 hours postbite.

2016/11/22, 17)08Muller


Fig. 9c. Puff adder bite 12 hours post bite.

2016/11/22, 17)08Muller


Fig. 9d. Puff adder bite 18 - 24 hours post bite. Swellinginvolving the whole limb extending to the lower abdomen. Notethe ecchymotic skin lesions.

2016/11/22, 17)08Muller


Fig. 10. A single bite on the left hand inflicted by a barredspitting cobra 2 weeks previously was responsible for the ‘skip’lesions on the shoulder and chest. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 11. Cape cobra, ‘geelslang’, ‘bruinkapel’ (Naja nivea). Theaverage length is 150 - 180 cm. The colour of the Cape cobra isextremely variable, ranging from bright yellow, brown, reddishbrown to black. Lighter copper-coloured specimens often havebrown speckles. Undersurface yellowish white. All colour phasesusually occur in one locality. Like all Elapidae, it spreads animpressive hood when confronted. Envenomings common in thesouth eastern regions of the country. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 12. The Elapidae have rigid, hollow, short fixed fangs in thefront of the mouth. (Photo: John Visser.)

Fig. 13. Distribution of neurotoxic cobras and the sea snake insouthern Africa.

2016/11/22, 17)08Muller


Fig. 14. Black mamba (Dendroaspis polylepis). It is moreheavily built than other mambas. Average length is 240 - 300cm. It is coloured greyish brown to olive brown and neverentirely black. Its name is derived from the colour of the insideof the mouth, which is blue-black. Undersurface uniform olivegreen. (Photo: John Visser.)

Fig. 15. Green mamaba (Dendroaspis angusticeps). Average

2016/11/22, 17)08Muller


length 180 - 200 cm. It is coloured uniformly bright green withundersurface pale green. The mouth lining is bluish white.(Photo: John Visser.)

Fig. 16. Distribution of mambas in southern Africa.

Fig. 17. Demonstration of ptosis after a Cape cobra bite.

2016/11/22, 17)08Muller


Fig. 18. Cape cobra bite. The area shown on the foot of aparalysed patient 4 days after the bite, demonstrating minimalswelling. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 19. Patient was completely paralysed 4 hours after a Capecobra bite, requiring respiratory support. Note that the bitemark is difficult to locate on the right ankle.

2016/11/22, 17)08Muller


Fig. 20. Boomslang (Dyspholidus typus). Average length 120 -150 cm. It has a short chunky head with very large emeraldgreen eyes. The colour may vary from green, brown, black toreddish, with a lighter belly. When cornered, they inflate theanterior part of the body. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 21. The colubridae (back-fanged snakes) have small,grooved fangs that are situated far back in the mouth below theeye. Species include the boomslang and vine snake. (Photo:John Visser.)

Fig. 22. Distribution of boomslang and bird snake in southernAfrica.

2016/11/22, 17)08Muller


Fig. 24. Berg adder (Bitis atropos). The berg adder is a stoutlybuilt viper, average length 30 - 40 cm. Greyish-olive to darkbrown, with two rows of triangular black dorsal markings and anoff-white belly with grey infusions. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 23. Blood coagulation cascade.

Fig. 25. Distribution of dwarf adders in southern Africa.

2016/11/22, 17)08Muller


Fig. 26. Ptosis in berg adder bite. The patient is contracting thefrontalis muscle in an attempt to open his eyes.

2016/11/22, 17)08Muller


Fig. 27. Prominent swelling of lower limb after berg adder biteon base of big toe.

2016/11/22, 17)08Muller


Fig. 28. Berg adder bite 6 days post bite showing local necroticchanges.

2016/11/22, 17)08Muller


Fig. 29. Night adder (Causus rhombeatus). Average length 30 -60 cm. The head has a distinct dark brown or black forwardpointing V-shaped mark. There are 20 - 30 dark, pale-edgedrhombic blotches along the back. The belly is pearly white toyellowish or light grey. (Photo: John Visser.)

2016/11/22, 17)08Muller


Fig. 30. Burrowing asp or southern stilletto snake (Atractaspisbibronii). Average length 30 - 40 cm. Dorsally it is uniformlypurple-brown to black. Below it is creamy white or dark brownto black. When the snake bites, the fangs are exposed out ofthe side of the mouth and are then hooked or jabbed into thevictim with a backward jerk of the head. (Photo: Tony Phelps.)

2016/11/22, 17)08Muller


Fig. 31. Horned adder (Bitis caudalis). Average length 22 - 26cm. Colour variable. Bluish-grey with two series of dark brownblotches over the back and sides in the northern areas. Olivebrown with darker blotches in the central Cape. Reddish inNamibia. Belly always white. (Photo: John Visser.)

Fig. 32. Distribution of the night adders.

2016/11/22, 17)08Muller


Fig. 33. Distribution of the burrowing asp and the Natal blacksnake.

In a nutshell• Five main clinical syndromes of snake envenoming arerecognised in southern Africa:• marked local pain and progressive swelling associated withprominent cytotoxic skin changes with coagulable blood• progressive neurotoxicity (paralysis), with negligible or minorlocal swelling• incoagulable blood, with negligible to mild local swelling• moderate to marked local swelling associated withneurotoxicity• mild to moderate swelling with negligible or absent systemicsymptoms.• Neurotoxic snakes can cause life-threatening paralysis anddeath within 1 - 8 hours. Respiratory failure is usually theprimary cause of death.• Polyvalent antivenom is available for the management ofmamba, neurotoxic cobra, spitting cobra and major adder bites.Monovalent antivenom is used in the management ofboomslang bite.• Since snakes inject the same amount of venom into adultsand children, the same dose/volume of antivenom must beadministered to children as in adults.• The administration of polyvalent antivenom in the acute phaseof neurotoxic snake envenoming will usually not preventprogression of neurotoxic effects, most notably respiratoryparalysis, and consequently the patient will not survive withoutlife support.• Respiratory support is the only life-saving treatment modalityin neurotoxic snake envenoming.• Administration of antivenom may be associated with acutelife-threatening anaphylactoid reactions.

2016/11/22, 17)08Muller


Table 1. Venomous snakes of southern Africa: classification, distribution,habitat and clinical toxinology

Family andspecies

Commonname

Distribution(see figures) Clinical toxinology

Atractaspididae

(GenusAtractaspis)

Africanburrowingadders orasps(burrowingor molevipers oradders,sidestabbingor stilettosnakes),Natalblacksnake

Approximately15 speciesdistributedthroughoutsub-SaharanAfrica

Most cause local pain,swelling and lymphadenitisonly; blistering, local necrosisdescribed; life-threateningand fatal cases have beenrecorded

The burrowing asps are fossorial, living mostlyunderground in deserted termite mounds, under stonesor logs, or in soft soil or sand. They are mostly grey,black or brown and most are relatively small (30 - 70cm). They are nocturnal and usually emerge on warm,wet summer evenings, especially after heavy rains. Whenthe snake bites (strikes) the fangs are exposed out of thesides of the mouth and are then hooked or jabbed intothe victim with a backward jerk of the head. They areextremely irritable, striking in sideways swings andsweeps, and showing annoyance by flattening the body.Accidental bites usually occur at night when the victimtreads on the snake.

Atractaspisbibronii

Southern,Bibron’sburrowingasp

Semi-desert,savanna andwoodland ofsouthernAfrica, fromKenyathrough toeasternTanzania,Malawi,Zambia,Zimbabwe,Botswana,eastern partsof SouthAfrica

Local pain, swelling,lymphadenitis, necrosis

Macrelapsmicrolepidotus

Natalblacksnake

East coast ofSouth Africa:riverine forestand urban

Local pain, swelling; seriouscases recorded

2016/11/22, 17)08Muller


gardens

Colubridae

Commonsnakes orrear-fangedsnakes

WidedistributionthroughoutAfrica

Venom of some capable ofinducing fatal haemostaticdefects

The back-fanged snakes have fixed, grooved rear fangsthat are situated quite far back in the mouth. Althoughonly the boomslang and the vine snakes have causedfatal bites, all back-fanged colubrids should be regardedas potentially dangerous to man and must be handledwith caution.

Dispholidustypus

Boomslang(‘treesnake’)

Widedistributionthroughoutsub-Saharanopenbushveld andsavanna

Venom contains enzymeswhich activate prothrombinand factor X, leading to aconsumptive coagulopathy,severe hypofibrinogenaemiaand fatal bleeding ifuntreated

Thelotorniscapensiscapensis

South-easternsavannavine snake

Trees andshrubs inlowland forestto moistsavanna andarid savanna:south-westernZimbabweand south-easternBotswana,south throughnorthernSouth Africaand Swazilandto southernMozambiqueand KwaZulu-Natal

Same as for boomslang (seeabove)

Thelotorniscapensisoatesi

Oates’savannavine snake

Trees andshrubs inlowland forestto moistsavanna andarid savanna:southernAngola andnorthernNamibia, westthroughnorthernBotswana,Zambia andsouth-eastKatanga to

Same as for boomslang (seeabove); no cases recorded

2016/11/22, 17)08Muller


Zimbabwe,westernMozambiqueand Malawi

Elapidae

The majority of elapids are long and slender. The rinkhalsand the cobras are easily identified, since they usuallyrear their heads and spread a hood. Some have the abilityto spit venom. There is a relatively high incidence ofserious spitting cobra bites in Africa. The black mambamay also spread a narrow hood when threatened.Compared with vipers, elapids possess relatively short (upto about 10 mm long) fixed front (proteroglyphous)fangs. In the case of mambas, the fangs are mounted atthe very front of the maxilla, and can rotate at theirarticulation with the pre-frontal bone.

Cobras,rinkhals,mambas,coral,shield,nose,garter andsea snakes

Wide distributionthroughout Africa

Potently neurotoxicand cytotoxic;common cause offatal snake bite

Family andspecies

Commonname

Distribution (seefigures)

Clinicaltoxinology

Neurotoxiccobras (genusNaja)

Najaanchietae

Anchieta’sEgyptian cobra

Arid savanna:Namibia, Angola,north-westernBotswana, south-west Zambia

Potentlyneurotoxic; seebelow as for N.nivea

Najaannulifera Banded cobra

Arid and moistsavanna: northernSouth Africa,eastern Botswanaand Zimbabwe


Najamelanoleuca

Forest, blackand white-lipped cobra

Forrested areas ofWest and CentralAfrica, southernEast Africa andeastern coast ofSouth Africa


Naja nivea Cape cobra

Karoo scrub, aridsavanna, Namibdesert: westernpart of SouthAfrica, southernNamibia and

Potentlyneurotoxic,causing flaccidparalysis andrespiratoryfailure; fatalitiescommon due to

2016/11/22, 17)08Muller


Botswana respiratoryarrest

Spitting orcytotoxiccobras (genusNaja)

Najamossambica

Mozambiquespitting cobra,M’fesi

Moist savanna andlowland forest:south-east Africa,from Pemba tonorthern SouthAfrica and Namibia

Potentlycytotoxic; spitsand bites;severe localpain, swelling,tissue necrosis,often extensive;eye envenoming

Najanigricollis:speciesunder review

Najanigricollisnigricollis

Black-neckedspitting cobra

Savanna, fromWest Africa tosouthern Sudanand southwards,through West Africato Angola

Potentlycytotoxic; spitsand bites; as inN. mossambica

Najanigricincta

Barred, zebraspitting cobra

Namib desert andKaroo scrub:southern coastalAngola andnorthern Namibia


Najanigricinctawoodi

Black spittingcobra

Dry savanna:southern Namibia,Northern Cape anddown to WesternCape Province ofSouth Africa


Coral/shield-nose snakes(genusAspidelaps)

Relatively small, robust elapids easily recognised by themuch enlarged, shield-like rostral scale on the snout. 60- 80 cm in size. A relatively thick-bodied elapid colouredblack and orange or greyish with blackish bands. Itrears up, spreads a narrow hood and hisses in defence.

Aspidelaps lubricus. Threecoral snake sub-speciesrecognised: Aspidelapslubricus lubricus (southernrace), Aspidelaps lubricusinfuscatus (central race) andAspidelaps lubricus cowlesi(northern race)

Desert and aridsavanna: south-western SouthAfrica, throughNamibia tosouthern Angola

Local pain,swelling,lymphangitis;mildlyneurotoxic; bitesnot welldocumented

Aspidelaps scutatus. Threeshield-nose snake subspecies

Sandy and stonyregions in Namibdesert, moist and

Detailscontradictory;local pain,

2016/11/22, 17)08Muller


(races) recognised: Aspidelapsscutatus scutatus (westernrace), Aspidelaps scutatusfulafula (eastern race) andAspidelaps scutatusintermedius (central race)

arid savanna,across northernregions of southernAfrica, fromNamibia across toMozambique

swelling andlymphangitis insome of thebites; neurotoxicin others, withone fatality

Mambas(genusDendroaspis)

Large, agile, slender diurnal elapid snakes with a longflat-sided head, a medium-sized eye and a round pupil.Scales are smooth and narrow. All except the blackmamba (Dendroaspis polylepis) are arboreal.Colouration varies from light green to olive brown anddark grey. 1.5 - 3.5 m in size. Coffin-shaped head. Theblack mamba may spread a narrow hood.

Family andspecies

Commonname


Clinicaltoxinology

Dendroaspisangusticeps

Common,eastern green,white-mouthedmamba

Forests or bush oneastern coast ofAfrica, from Kenyato South Africa

Local pain,swelling,lymphangitis,peripheralgangrene;mildlyneurotoxic; onefatal case

Dendroaspispolylepis Black mamba Savanna of eastern

and southern Africa

Potentlyneurotoxic;nausea,vomiting,sweating,involuntarymusclecontractions orfasciculations;respiratoryparalysis maydevelop within 1- 2 hours;cardiacdysrhythmiashave beendescribed; highincidence offatal cases

Garter snakes(genusElapsoidea)

Taxonomyunderrevision;severalsubspecies

Small fossorial, nocturnal elapid snakes, with very shorttails, cylindrical bodies, with no distinct neck and abluntly rounded rostral scale as in other burrowingspecies. Most have an average length of 25 - 50 cm.The young are brightly banded (except for one species),the bands fading as they grow. Sluggish when exposedand do not bite if handled gently.

Angolan or half-Savanna: Senegalto northern Uganda

2016/11/22, 17)08Muller


Elapsoideasemiannulata

bandedgarter snake

and a separatesouthern populationfrom Angola toMozambique

Local pain,swelling andlymphangitis

Elapsoideasundevallii

Sundevall’sgarter snake

Karoo scrub to aridsavanna, moistsavanna, grasslandand lowlandforest: southernAfrica

Local pain,swelling andlymphangitis;neurotoxic?

Other Elapidae

Hemachatushaemachatus Rinkhals

Wide variety ofhabitats;grassland,moist savanna,lowland forest:eastern regionsof SouthAfrica; isolatedpopulation insouth-westernZimbabwe

Bites and spits; localswelling andbruising. Mildlyneurotoxic?

Pelamisplaturus

Pelagic, yellow-bellied seasnake

East coast ofAfrica, fromDjibouti toCape Town

Neurotoxic andmyotoxic;myoglobinuria; bitesare rare

Viperidae Adders andvipers

Approximately45 speciesdistributedthroughoutAfrica

Cytotoxic,haemostaticdisorders,neurotoxic; commoncause of life-threatening and fatalsnake bite in Africa

Vipers or adders are relatively thick bodied, sluggish,mainly terrestrial snakes which have long, curved,cannulated and fully erectile fangs which fold downagainst the upper jaw in a mucous membrane sheathwhen the snake is not striking.

Large adders(genus Bitis)

Wide head and narrow neck. The tail appears oddlyshort in females and only less so in males. The fourlarger species have a total length of 80 cm – 2 m. Thepuff adder is the most widespread and unmistakable;body stout and massive; brown or greyish with well-marked chevron markings. Medically, one of the mostimportant snakes in Africa. The small adders ofsouthern Africa have an average length of 20 - 50 cm.

Wide variety ofhabitat,savanna andopengrassland,

Potently cytotoxic;severe local pain,

2016/11/22, 17)08Muller


Bitis arietansarietans Puff adder

except in highmontanegrasslands,true desert andrainforest:widespreadthroughoutsub-SaharanAfrica, absentin African rainforests

extensive swellingand blistering,compartmentalsyndrome, necrosis,hypovolaemia,shock; bloodcoagulationabnormalities

Bitisgabonica

Gaboon adderor viper,forest puffadder

Tropical forestsof West,Central andEast Africa,and easternparts ofsouthern Africa

Local effects asabove;cardiovascular andhaemostaticabnormalities maydevelop

Family andspecies

Commonname


Clinicaltoxinology

Small (dwarf)adders(genus Bitis)

Bitis atropos Berg adder

Montanefynbos andgrasslands:mountainsof easternZimbabwe,Drakensbergmountainsdown tomountainsof south-westernCape

Cytotoxic and neurotoxic;local pain, swelling andlymphangitis,ophthalmoplegia, anosmia,hyponatraemia, life-threatening respiratorydepression in some cases

Bitis caudalis Hornedadder

Aridsavanna anddesert: aridregionsof south-west Africa,extendingeastwardsthroughBotswana tonorthernSouth AfricaandsouthernZimbabwe

Local pain and swelling (thismay be extensive withnecrosis) lymphangitis

Peringuey’s Local pain, swelling and

2016/11/22, 17)08Muller


Bitisperingueyi

adder,side-windingadder

Namibdesert,Namibia

lymphangitis;ophthalmoplegia and otherminor neurotoxic effectsobserved

Bitisschneideri

Namaquadwarfadder,Schneider’sadder

Vegetatedcoastalsand:coastalregions ofsouthernNamibia andnorthernCapeProvince

Local pain, swelling andlymphangitis

Bitisxeropaga

Desertmountainadder

Sparselyvegetatedrockyhillsides andmountainslopes:southernNamibiaandadjacentsmall areaacrossOrangeRiver intoSouth Africa

Local pain and swelling;ophthalmoplegia and otherminor neurotoxic effectsobserved; hyponatraemia

Other small adders (vipers) considered venomous, but for which no biteshave been recorded: Bitis albanica (Albany adder): isolated population in theAlgoa Bay region, eastern Cape, South Africa; Bitis armata (Southern adder):two isolated populations on the coast of the Western Cape, South Africa;Bitis cornuta (many-horned adder, hornsman): coastal regions of south-western and western South Africa to southern Namibia, Bitis heraldica(Angolan adder): high parts of central Angola; Bitis inornata (plain mountainadder): isolated populations in the Graaff Reinet region of the Eastern Cape,South Africa; Bitis rubida (red adder): southern to south-western part ofSouth Africa: Cederberg, through Little Karoo and foothills of the Roggeveldand Komsberg.

Night adders(genusCausus)

The night adders are small (<1 meter) and despite theirname they are active by day and by night. They are notadder-like, and are fairly stout with the head being onlyslightly distinct from the neck. The venom fangs areshort with no hinge action compared with the genusBitis. They have round pupils (most adders have verticaleye pupils) and they have large scales on top of thehead (most vipers have small scales). They are notgiven to standing their ground, but when angry, theyhiss and puff ferociously, inflating the body to greatextent. They may also raise the forepart of the body offthe ground and slide forward with the neck flattened,looking quite cobra-like.

2016/11/22, 17)08Muller


Caususdefilippii

Snoutednightadder

Moist anddry savannaand coastalthicket:easternAfrica, fromKenya andTanzania,Malawi,Zambia,ZimbabweandMozambiqueto north-easternSouth Africa

Local pain, swelling,lymphangitis and localnecrosis

Caususrhombeatus

Easternrhombicnightadder

Savanna,fromeasternNigeria,throughCentralAfrica, downto easternhalf ofSouth Africa

Local pain, swelling,lymphangitis and localnecrosis

Further readingAshe S, Blaylock R, Chisale MGP, et al. Guidelines for thePrevention and Clinical Management of Snakebite in Africa.World Health Organization, Regional Office for Africa,Brazzaville, 2010.Blaylock RSM. Snake bites at Triangle Hospital January 1975 toJune 1981. Cent Afr J Med 1982;28:1-11.Blaylock R.S.M. Femoral vessel entrapment and compartmentsyndromes following snakebite. S Afr J Surg 2003;41(3):72-73.Blaylock R. Epidemiology of snakebite in Eshowe, KwaZulu-Natal, South Africa. Toxicon 2004;43(2):159-166.Blaylock RS, Lichtman AR, Potgieter PD. Clinical manifestationsof Cape cobra (Naja nivea) bites. Two cases. S Afr Med J1985;68(5):342-344.Broadley DG, Wüster W. A review of the southern African ‘non-spitting’ cobras (Serpentes: Elapidae: Naja). Afr J Herpetology2004;53:101-122.Bush SP. Snakebite suction devices don't remove venom: theyjust suck. Ann Emerg Med 2004;43(2):187-188.Coetzer PWW, Tilbury CR. The epidemiology of snakebite inNorthern Natal. S Afr Med J 1982;62:206-212.Davidson RA. Case of African Cobra bite. Brit Med J1970;4:660.Hardy DL. A review of first aid measures for pit viper bite inNorth America with an appraisal of ExtractorTM suction and stungun electroshock. In Campbell JA, Brodie ED, eds. Biology of the

2016/11/22, 17)08Muller


Pit Vipers. Tyler, Texas, Selva 1992:405-414.Harvey AL. Snake Toxins. International Encyclopedia ofPharmacology and Therapeutics. New York: Pergamon Press,1991.Kasilo OMJ, Nhachi CFB. A retrospective study of poisoning dueto snake venom in Zimbabwe. Hum Exp Tox 1993;12:15-18.Lath NK, Patel MM. Treatment of snake venom ophthalmia.Centr Afr J Med 1984;30(9):175-176.Khandelwal G, Katz KD, Brooks DE, Gonzalez SM, Ulishney CD.Naja Kaouthia: two cases of Asiatic cobra envenomations. JEmerg Med 2007;32(2):171-174.Malasit P, Warrell DA, Chanthavanich P, et al. Prediction,prevention and mechanism of early (anaphylactic) antivenomreactions in victims of snake bites. BMJ 1986;292:17-20.Marsh NA, Whaler BC. The Gaboon viper (Bitis gabonica): itsbiology, venom components and toxinology. Toxicon1984;22(5): 669-694.McNally T, Conway GS, Jackson L, et al. Accidental envenomingby a Gaboon viper (Bitis gabonica): the haemostaticdisturbances observed and investigation of in vitro haemostaticproperties of whole venom. Trans Roy Soc Trop Med Hyg1993;87:66-70.Meier J, White J. Handbook of Clinical Toxicology of AnimalVenoms and Poisons. CRC Press, 1995.Näreoja K, Kukkonen JP, Rondinelli S, Toivola DM, Meroluoto J,Näsman J. Adrenoceptor activity of muscarinic toxins identifiedfrom mamba venoms. Br J Pharmacol 2001;164:538-550.Punde DP. Management of snake-bite in rural Maharashtra: a10-year experience. Nat Med J India 2005;18(2):71-75.Sano-Martins IS, Fan HW, Castro SC et al. Reliability of thesimple 20 minute whole blood clotting test (WBCT20) as anindicator of low plasma fibrinogen concentration in patientsenvenomed by Bothrops snakes. Toxicon 1994;32:1045-1050.Singh G, Pannu HS, Chawla PS, Malhotra S. Neuromusculartransmission failure due to common krait (Bungarus caeruleus)envenomation. Muscle & Nerve 1999;22(12):1637-1643.Spawls S, Branch B: The Dangerous Snakes of Africa. London:Southern Book Publishers, 1995.Strover HM. Observations on two cases of snake bite by Najanigricollis mossambica. Cent Afr J Med 1973;19(1):12-13.Sutherland SK, Coulter AR, Harris RD. Rationalisation of first-aidmeasures for elapid snake bite. Lancet 1979;1:183-186.Warrell DA, Ormerod LD. Snake venom ophthalmia andblindness caused by the spitting cobra (Naja nigricollis) inNigeria. Am J Trop Med Hyg 1976;25:525-529.Warrell DA, Ormrod LD, Davidson NMcD. Bites by the puff adder(Bitis arietans) in Nigeria, and value of antivenom. Br Med J1975;4:697-700.Warrell DA, Ormrod LD, Davidson NMcD. Bites by the nightadder (Causus maculatus) and burrowing vipers (genusAtractaspis) in Nigeria. Am J Trop Med Hyg 1976;25:517-524.Wilkinson D. Retrospective analysis of snakebite at a rural

2016/11/22, 17)08Muller


hospital in Zululand. S Afr Med J 1994;84(12):844-847.

Documents

Snake bite in southern Africa: diagnosis and management Docs/Snake bite in Southern Africa-Diagnosis and...Snake bite in southern Africa: diagnosis and management There are three groups