Snakebite Treatment Protocol Swaziland Antivenom Foundation

1. Detailed Clinical Assessment and Species Diagnosis 1.1. History A precise history of the time and circumstance of the bite and the progression of local and systemic symptoms and signs is of the utmost importance. Five initial questions should be asked i. “In which part of your body have you been bitten?” Look where the patient points. There may be evidence that the patient has been bitten by a snake (for example: fang marks), with signs of local envenoming (for example: local swelling, bruising or continuing bleeding from the fang punctures), but also evidence of pre-hospital treatment (for example: impressions made by a tourniquet or incision marks that may be bleeding, suggesting that the blood is incoagulable). The snakebite may not have been recognized by the victim, if it occurs at night during sleep, or in the dark, or in water. In such cases, suspicion of the diagnosis will depend on typical signs such as fang puncture marks, progressive swelling, bleeding gums or descending paralysis.

ii. “What time were you bitten?” Assessment of the severity of envenoming depends on the length of time between the actual bite and when the patient seeks treatment. The patient seeks treatment so soon after the bite that symptoms and signs of envenoming have not yet developed. Or, the patient may arrive so late after the bite that the only signs are of late complications of envenoming (for example: gangrene, pneumonia or renal failure).

iii. “Where is the snake that bit you?” or “What did the snake look like?” The snake responsible for a bite may be killed and brought to hospital with the victim. If the snake is available, its identification can be extremely helpful but only if there is someone competent who can identify the snake (for assistance contact Thea 76025088 ). If it is obviously a harmless species (or not a snake at all), the patient can be quickly reassured, given an injection of tetanus toxoid and discharged from hospital immediately.

Descriptions of the snake by bite victims or onlookers are often unreliable and misleading but it is worth asking about the snake’s size, colouring, markings and behaviour. The surroundings where the bite occurred and the time when it happened can also suggest a particular species: • Cobras may rear up and spread a characteristic hood and hiss; puff adders make a loud blowing sound • Dangerous tree snakes include Black mamba, Boomslang and Vine snake. • Any green tree snake longer than about 1 m is likely to be a Boomslang (juvenile Boomslang are not green). All snakes that are green and shorter than 80cm are totally harmless. • Bites inflicted on sleeping persons in their huts at night are likely to have been caused by Mozambique spitting cobras • Bites in and near rivers, lakes and marshy areas are also most likely to be caused by Mozambique spitting cobras. • Bites at night are generally caused by Puff adders, Mozambique spitting cobras or Night adders

iv. “How are you feeling now?” The patient’s current symptoms can point to what is likely to be the most important effect of envenoming (for example: faintness or dizziness indicating hypotension or shock; breathlessness indicating incipient respiratory failure). Do not ask leading questions! Patients should be asked to describe their symptoms and should then be questioned directly about the extent of local pain, swelling, tenderness, tender painful enlarged lymph nodes draining the bite area, bleeding from the bite wounds, at sites of other recent injuries and at sites distant from the bite (gums, nose etc), motor and sensory symptoms, vomiting, fainting and abdominal pain. The time after the bite when these symptoms appeared and their progression should be noted. Details of pre-hospital treatment (tourniquets, ingested and applied herbal remedies etc) should also be recorded as these may, themselves, be responsible for some of the symptoms.

v. “Have you ever been bitten before and did you receive antivenom?” If the patient has been bitten before he/she may have an allergic reaction to the VENOM. Snake handlers will very often have a severe reaction to the venom. This must not be confused with anaphylaxis as urgent and large quantities of AV will be required. If the patient has received antivenom before, there is an increased risk of anaphylaxis.

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2. Examination A. Immediately and clearly draw a ring around the bite site with a permanent marker and record the time B. The patient should be monitored every 30 - 60 minutes. Record the symptoms as well as the progress of swelling and the time.

Figure 1: Record progress of swelling every 30 minutes.

2.1. Tooth and Fang marks The absence of visible fang marks does not exclude snakebite. Often, with the Black mamba, there is no evidence of a distinct puncture wound and a tiny scratch from a Boomslang is enough to cause a serious reaction as the venom is extremely potent. There may be slight bruising or the puncture wound may resemble a pimple. Two or more distinct, separate puncture marks suggests a bite by a venomous snake. The pattern of fang punctures is very rarely helpful as marks made by accessory fangs, palatine maxillary and mandibular teeth may complicate the pattern and there may have been multiple bites and scratches. The greater the distance between the fang marks, the larger the snake.

All© Thea Litschka-Koen Figure 2 (left): Simunye, Swaziland. A typical bite from a non -venomous snake Figure 3 (second from left): Big bend, Swaziland. Two clear fang marks by a venomous snake with blistering 3 hours after envenomation Figure 4 (third from left): Siteki, Swaziland. Severe envenomation by a Black mamba. No clear fang mark, only slight bruising Figure 5 (second from right) : Siteki Swaziland. Severe envenomation by a black mamba the bite site only showing a tiny spot with no bruising Figure 6 (second from right): Nelspruit, South Africa. Severe envenomation by a Boomslang.

2.2. Local Signs Local swelling and enlargement and tenderness of regional lymph nodes are often the earliest signs of envenoming, but swelling may be caused or aggravated by a venous tourniquet or traditional remedies. Local swelling, caused by cytotoxic snakes, like the adders and spitting cobras, are usually visible within two hours of the bite, but there have been exceptions to this rule. Symptoms and signs of severe systemic envenoming from the two Haemotoxic snakes (Boomslang and Vine snakes) can be delayed for 15 hours or more. Most often there will be negligible local swelling. With neurotoxic envenomation by the Black mamba and snouted cobra, there will be little or no swelling.

All© Thea Litschka-Koen Figure 8 (left): Siteki, Swaziland. Mozambique spitting cobra 2 hours after envenomation. S welling, typical bruised area, no bleeding from bite site. Figure 9 (second from left): Simunye, Swaziland. Mozambique spitting cobra 6 hours after envenomation. Typical bruised area “dam” with blisters forming around the discoloured area. Figure 10 (centre): Mhlume, Swaziland. Puff adder bite 5 hours after envenomation. Typical random blistering with bleeding from the blisters and bite site. Figure 11 (second from right) : Siteki Swaziland. Black mamba bite. Swelling was caused by tourniquet and self inflicted wounds. Figure 12 (right): Big Bend, Swaziland. A non-venomous bite but severe swelling caused by self inflicted cuts and herbal potion rubbed into the wounds.

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2.3. Bleeding Persistent bleeding from the fang marks, other recent wounds and venepuncture sites suggest that the blood is in-coagulable (Haemotoxic envenomation by the Boomslang or Vine snake). The gums should be examined thoroughly as these are usually the first sites of spontaneous systemic bleeding.

©David Dr. Warrell ©David Dr. Warrell Figure 13 (left): Haemotoxic envenomation showi ng bleeding of the gums. Figure 14 (second from left): Haemotoxic envenomation.

2.4. Shock The signs of shock are blurred vision, dizziness, fall in blood pressure; collapse; cold, cyanosed and sweaty skin; and impaired consciousness, sometimes occurring very soon after the bite; these symptoms may be transient, recurrent, persistent, progressive, delayed and life threatening. The foot of the bed should be raised and an intravenous infusion of isotonic saline or a plasma expander such as haemaccel, gelofuse, dextran or fresh frozen plasma should be started immediately.

2.5. Neurotoxicity/paralysis The earliest symptoms of neurotoxicity after bites from the Black mamba or Snouted cobra are often a metallic taste, paresthesia of the lips (black mamba bite), blurred vision, a feeling of heaviness of the eyelids and drowsiness. The victim will raise the eyebrows and pucker the forehead before ptosis is observed. Respiratory muscle paralysis with imminent respiratory failure is suggested by dyspnoea, distress, restlessness, sweating, exaggerated abdominal respiration and cyanosis. Coma is usually the result of respiratory or circulatory failure.

2.6. Monitoring of snake-bitten patients Patients bitten by snakes should, ideally, be observed in hospital for at least 24 hours after the bite. The intensive care unit or a high dependency bed is appropriate but rarely possible. In an open ward, the patient should be placed close to the nursing station and in full view of the medical staff. The following should be checked at least once every hour and action taken if there is any deterioration: i. Level of consciousness. ii. Metallic taste, llight-headedness, dizziness, bitter taste in mouth, paraesthesiae of the tongue, lips and mouth , headache, dull pain in the abdomen, severe thirst and dry mouth, increased / severe sweating, weak limbs and poor co-ordination, nausea and vomiting, fasciculation’s , gooseflesh , increased salivation , difficulty to cough, dysphasia, hoarseness, ataxia, nosebleed, flushed face, warm / cold skin, shock, hypotension, dysphagia, ptosis. Pupillary abnormalities, inability to open or clench the jaw, inability to protrude tongue, slurred speech, chest tightness (similar to asthma), paradoxical respiration, hypotension, tachycardia, bradycardia, flaccid paralysis - limbs hang limp, victim is conscious but cannot respond, altered mental state. iii. Pulse rate and rhythm. iv. Blood pressure. Measure while lying supine and after sitting up or being propped up in bed to assess any postural drop in pressure, suggesting hypovolaemia. v. Respiratory rate. vi. Extent of local swelling and tenderness (best marked gently on the skin with black marker pen with time and date). vii. New symptoms or signs.

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3. Syndromic Management of Snakebite. Table 1: Syndromic Management of Snakebite Syndrome Species Symptoms: Not all signs and symptoms will necessarily develop, even with sever envenomation. Painful Mozambique Accounts for most venomous bites in Swaziland. Intense pain (strong, dull or sharp) within minutes after the bite Progressive spitting cobra intensifies. Local swelling commences within minutes, gradually becoming more severe. Necrosis occurs in 90% of bites Swelling Mfeti and tissue destruction is usually severe but superficial. Necrosis usually involves only the skin and subcutaneous (PPS) connective tissues. Regional lymphadenopathy is only present when the swelling reaches that area, or is secondary to sepsis. There is no bleeding at the bite site and there are no bleeding complications. The symptoms are distinctive. A Caused by darkened area develops at the bite site, indicating necrosis. This area will later be depressed compared with the swelling Cytotoxic around it. Blisters are formed around the darkened necrotic area approximately 72 + hours after the bite. There may be venom “skipping legions”, areas of necrosis separated by strips of apparently normal skin caused by proximal spread of venom in lymphatic vessels. Patients may become drowsy due to hypovolaemic shock Compartment syndrome will never be a complication. Puff adder Intense pain (strong, dull or sharp) within minutes after the bite intensifies. Local swelling com mences within minutes, Libululu gradually becoming more severe. Bleeding from the bite site and signs of bleeding may be found at the bite site, in gums, nose, blood, vomit and urine. The bite site area appears red, purple, blue or darkly discolored. Blood blisters may develop randomly 6-48 hours after envenomation. With time, necrosis is common. Diarrhoea and vomiting may be experienced. General shock (due to extravasation and bleeding) usually develops insidiously and if unnoticed and untreated, could result in death. This sudden, and often fatal collapse, is frequently found in a patient who seemed to be “recovering and doing quite well”. Patients may become drowsy due to hypovolaemic shock. Compartment syndrome in 2% of cases only. Progressive Black mamba If envenomation has occurred, the symptoms usually manifest within 15 minutes to 2 hours following the bite . Pain at the Weakness Imamba bite site can be absent, minimal or mild. Swelling will be absent, minimal to mild in most cases. Light-headedness, vertigo, (PW ) dizziness, bitter taste in the mouth, paraesthesiae of the tongue, lips and mouth and later the whole body , headache, dull pain in the abdomen, severe thirst and dry mouth, increased / severe sweating, weak limbs and poor co-ordination, nausea Caused by and vomiting, fasciculation’s , other involuntary muscle spasms , g ooseflesh , increased salivation which might be very Neurotoxic thick and “stringy”, difficulty to cough, dysphasia as throat constricts /is painful, hoarseness, ataxia, nosebleed, flushed venom face, warm / cold skin, shock, hypotension, dysphagia, ptosis. Pupillary abnormalities, inability to open or clench the jaw, inability to protrude tongue, slurred speech, chest tightness (similar to asthma), broken neck syndrome, paradoxical respiration, hypotension, tachycardia, bradycardia, flaccid paralysis - limbs hang limp, victim is conscious but cannot respond, respiratory distress or weakness, altered mental state causing hallucinations and confusion, abnormal or morbid excitement, paralysis of sphincters causes incontinence of urine and faeces, evacuation of bowels, recurrent episodes of paralysis despite antivenom treatment, quiet period with a fixed stare before coma sets in.

Snouted cobra If envenomation has occurred, the symptoms usually manifest within 15 minutes to 6 hours following the bite . Phemphetfwane Bites are uncommon or unconfirmed as a neurotoxic envenomation is usually attributed to the Black mamba. There is local pain and swelling, much more so than with the Black mamba, which may involve more than half the bitten limb. Blisters may form but there will be little or no necrosis. Vomiting and continuous gagging is an early systemic symptom. Classical neurotoxic symptoms appear as early as 30 minutes after the bite and can evolve to the point of fatal respiratory paralysis within 2-16 hours of the bite, despite the use of antivenom and mechanical ventilation. There are signs of progressive descending paralysis, starting with ptosis, external ophthalmoplegia (causing diplopia, i.e. double vision) and weakness of the muscles innervated by the cranial nerves so that the victim cannot open the mouth, clench the jaws, protrude the tongue, swallow, protect the airway from secretions, speak, flex the neck and eventually cannot breathe. When the respiratory muscles become affected, the pattern of breathing is initially abdominal or “paradoxical” (the abdomen expands during inspiration due to contraction of the diaphragm). Respiratory distress increases, the patient becomes anxious, sweaty and cyanosed and will die unless ventilated artificially.

Mixed Rinkhals The Rinkhals is found in the cooler, Middle and Highveld regions of Swaziland. Bites are rare and symptoms include PPS and Phemphetfwane mild to moderate local swelling and bruising, drowsiness, nausea, vomiting, vertigo, mild pyrexia, dyspnoea, tightness PW of the throat and chest, paralysis of the tongue and vocal cords, blurring of vision, weakness of the arms and legs, unconsciousness. Bleeding Boomslang These snakes are not aggressive and bites are very rare. Their venom is extremely potent and a glancing bite or scratch (B) Indlondlo can lead to envenomation. Persistent bleeding from fang marks, nausea, vomiting, colicky abdominal pain, headache, Caused by bleeding from the bite site, old and recent wounds such as venepuncture, bleeding from the gums and nose, hot and cold Haemotoxic Vine snake fever, increased sweating, spontaneous gingival bleeding, epistaxis (nosebleed), haematemesis (vomiting blood), melaena venom Lununkhu (black “tarry” faeces associated with gastrointestinal haemorrhage), subarachnoid or intracerebral haemorrhage, haematuria (blood in urine), extensive ecchymoses’Mental confusion, yellow vision due to blood in the eyes, hypotension, multiple organ failure, convulsions, unconsciousness and coma.

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4. Indications for antivenom Antivenom is indicated in all cases of systemic and severe local envenoming Table2: Indications for antivenom treatment after bites by African snakes: Systemic Envenoming Local Envenoming by species causing local necrosis

1. Neurotoxicity 1. Bites on fingers or toes (with swelling) 2. Spontaneous systemic bleeding 2. Bites on small limbs of babies and small children (with swelling) 3. Incoagulable blood (20MWBCT) 3. Extensive swelling (more than half the bitten limb) 4. Cardiovascular abnormality: 4. Rapidly progressive swelling a. Hypotension a. Swelling extends more than 2.5cm per hour. b. Shock b. Swelling of the whole hand or foot in 1 hour after c. Arrhythmia envenomation. d. Abnormal electrocardiogram c. Swelling extends to elbow or knee in 3-4 hours after envenomation. d. Swelling of whole limb in 8 hours after envenomation.

4.1. Antivenom dosage Antivenom needs to be given in a large enough doses to neutralise ALL of the injected venom. Under-dosing with antivenom leads to poor patient outcomes, undermines confidence in antivenom effectiveness, and may lead to prolonged hospitalisation which ultimately exceeds the cost of an initial treatment with a therapeutically effective volume of antivenom. Guidelines for initial dosage based on clinical studies for bites by snakes found in Swaziland (Table 2). In most cases, manufacturers’ recommendations given in the package insert are based on mouse assays which may not correlate with clinical findings. The initial dose of antivenom, however large, may not completely neutralize the depot of venom at the site of injection or prevent redistribution of venom from the tissues. Patients should therefore be observed for at least 48 hours even if they show a good clinical response to the initial dose of antivenom. Continuing absorption of venom from the bite-site depot and redistribution of venom from the tissues may cause recurrent neurotoxicity or haemostatic problems after therapeutic antivenom has been eliminated. This process may be enhanced by resuscitation: correction of hypovolaemia and restoration of blood pressure may improve tissue perfusion at the bite site, resulting in further absorption of venom from the site of injection.

4.1.1. Minimal Initial antivenom dosage Table 2: Guide to initial dosage for Swaziland snakes. Do NOT compromise; give enough antivenom to neutralize the venom! PPS: P ainful Progressive Swelling Syndrome PW: P rogressive Weakness Syndrome B : B leeding Syndrome

Table: 3 Initial dosage If symptoms Additional Syndrome Venom Species Responsible Comments Antivenom persist after Antivenom 20ml Repeat with 20ml every hour PPS Cytotoxic Mozambique spitting cobra; 100ml Polyvalent 1 Hour until symptoms stop. Repeat with 20ml every hour PPS Cytotoxic Puff adder; Rinkhals 50ml Polyvalent 1 Hour 20ml until symptoms stop. Repeat with 20ml every hour PW Neurotoxic Black mamba, Snouted cobra 80ml Polyvalent 1 Hour 20ml until symptoms stop. Cytotoxic & 20ml Repeat with 20ml every hour Mixed PPS & B Puff adder 50ml Polyvalent 1 Hour Haemotoxic until symptoms stop. Mixed PPS & Cytotoxic & 20ml Repeat with 20ml every hour Rinkhals 50ml Polyvalent 1 Hour PW Neurotoxic until symptoms stop. Boomslang; Repeat with 10ml every 6 B Syndrome Haemotoxic 20ml Monovalent 6 hours 10ml Vine snake hours until symptoms stop Note: Very often snakebite victims arrive at hospital with a tourniquet in place. If antivenom treatment is necessary, it should be started before the tourniquet is loosened as there is a risk of sever envenoming when the venom in the occluded limb is released into general circulation. The tourniquet should be removed slowly and re-applied if any adverse reactions are noticed 5 | Eswatini Antivenom Foundation - This document may not be copied or distributed in any way . Amended: April 2019

4.2. Timing of antivenom treatment An emergency doctor should be able to recognize the signs and symptoms of snakebite envenomation and make an early decision to start antivenom therapy to limit the extent of tissue damage, blood changes or paralysis. Antivenom should be given as soon as possible once signs of systemic or severe local envenoming are evident. It is almost never too late to try antivenom treatment for persistent systemic envenoming; it has proved effective in reversing coagulopathy 10 days or more after Boomslang bites. When patients arrive in hospital with a tourniquet or other constricting band in place, antivenom treatment, if it is thought necessary, should be started before these are loosened or there is a risk of severe envenoming when the venom in the occluded limb is released into the general circulation.

4.3. Pre-treatment for possible anaphylaxis caused by antivenom To prevent or diminish possible anaphylaxis, pre-treat with intramuscular adrenaline. Patients in whom adrenaline is relatively contraindicated include those with a history of ischaemic heart disease or stroke, uncontrolled hypertension and tachyarrhythmias.

Table: 4 Age Dose <6yrs 0.15mg 6-12yrs 0.2mg >12yrs Adult dose (0.25 -0.5mg) Adult 0.25mg – 05mg

Premedication with antihistamines may dampen minor allergic reactions but will not prevent serious allergic/anaphylactoid reactions. Hydrocortisone takes several hours to act and is ineffective as a prophylactic agent against acute reactions.

4.4. Antivenom administration The earlier antivenom is administered, when indicated, the greater the clinical benefit to the patient will be both in terms of the potential to save life and limb. Antivenom is most effective when given intravenously at a rate of about 10 ml per minute, or diluted in isotonic fluid and infused over 15-30 minutes. A paediatric burette is a useful device for mixing a diluted solution of antivenom (50/50). This method works well for both adults and children. The incidence and severity of antivenom reactions was the same with these two methods. The advantage of intravenous infusion is ease of control, but intravenous “push” injection requires less expensive equipment, is quicker to set up and ensures that someone remains at the patient’s side during the crucial first 10-15 minutes after the start of treatment, when early reactions are most likely to occur. The patient should be kept talking if s/he is able to do so. Uncover the neck, chest or back to check for the development of a rash. Listen carefully to hear if there is a change to the pitch of the voice or if they start to clear their throat or cough. One of the first signs is intensely itchy scalp, the palms of the hands as well as the soles of the feet.

All© Thea Litschka-Koen

Figure 15 (left) : Mhlume Swaziland. The advantage of administering antivenom IV push is that the doctor is close at hand. Figure 16 (right) : Siteki Swaziland. Minimal equipment is required.

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4.5. Neurotoxic Envenomation Neostigmine: inhibits the action of acetylcholinesterase and may prevent paralysis progression and in some cases reverse the symptoms. Atropine should always be administered with neostigmine to reduce some of the side effects, such as bowel discharge. Neostigmine is to be administered i.v.i. Adult dose 2.5 mg. Paediatric dose is 2.5 mg Neostigmine diluted to a volume of 5 ml. Neostigmine/Atropine can be administered every 2-4 hours, if there has been significant improvement after the first dose.

Table: 5 AGE BODY WEIGHT i.v.i. DOSE VOL. ml 1-3 Years Under 11 kg 0.5 mg 1.0 ml 4-7 Years 11-15 kg 0.75 mg 1.5 ml 8-11 Years 16-20 kg 1.0 mg 2.0 ml 12-15 Years 20-40 kg 2.0 mg 4.0 ml

Atropine: To be used for excessive salivation (Black Mamba bites), and to reduce some of the side effects, such as bowel discharge. Atropine to be administered immediately after neostigmine. Adult dose 12 years > 0.6 mg i.v.i. Paediatric dose (1 ml/600 mcg) diluted to 3 ml. The below dose can be administered for excessive oral secretions, not to be administered if BP> 150 mmHg and/or HR > 100 bpm. Atropine can be administered every 2-4 hrs.

Table: 6 AGE BODY WEIGHT i.v.i. DOSE VOL. ml 1-3 Years Under 11 kg 0.2 mg 1.0 ml 4-7 Years 11-15 kg 0.3 mg 1.5 ml 8-11 Years 16-20 kg 0.4 mg 2.0 ml

4.6. Snakebite and Antivenom in pregnancy During the last trimester of pregnancy avoid the supine hypotensive syndrome by resuscitating the mother while she sits up, or place her in the left lateral decubitus position or raise the left hemipelvis. Envenoming by the Puff adder causes a bleeding diathesis and may cause ante-partum haemorrhage and precipitate miscarriage at any stage of pregnancy. Pregnant women should be questioned about and examined for evidence of vaginal bleeding and, in the third trimester, foetal heart rate and uterine contractions should be monitored. Foetal bradycardia may indicate foetal envenoming. Late deceleration of foetal heart rate in relation to uterine contractions indicates foetal distress. Envenomed pregnant women are at risk of ante- and post-partum haemorrhage, premature labour, foetal distress and stillbirth. Early adequate antivenom treatment is indicated, its benefits outweighing the risks to the mother and foetus e.g. of anaphylactic antivenom reaction Envenomed pregnant woman are at risk and early and adequate antivenom treatment is indicated, as its benefits outweigh the risks to the mother and foetus. Pregnant patients may develop uterine vasoconstriction during compensated hypovolaemic shock even though maternal vital signs may appear normal. As a result, the foetus may become hypoxic while the mother has normal tissue oxygenation. Adequate fluid resuscitation and oxygenation of the mother are therefore essential. Uterine and foetal heart rate monitoring are recommended to detect asymptomatic premature labour and foetal distress. If there is coagulopathy, retroplacental haemorrhage may occur, causing high maternal and foetal mortality. Early, adequate doses of antivenom are therefore essential if there is any suggestion of antihaemostatic disorders. Labour (for example, induced by the snakebite) in a woman with snake venom-induced haemostatic abnormalities may be complicated by massive post-partum haemorrhage.

4.7. Snakebite and Antivenom in children Children may be more prone to morbidity and mortality due to the higher dose of venom they receive relative to their body weight compared to adults. The indications for antivenom arise sooner in children, which tends to mitigate this. The dose of antivenom administered is the same as for an adult as antivenom is designed to neutralize a fixed venom dose, which the snake injects indiscriminately into humans large or small. Venous access may be a problem. The intraosseous route may be required. Due to high venom: mass ratio both morbidity and mortality are higher than in adults. Swelling travels further and faster up their bodies, coagulopathies occur sooner as does weakness and respiratory failure due to a faster evolution of envenomation. Frequent reassessment of snake bitten children is necessary. 7 | Eswatini Antivenom Foundation - This document may not be copied or distributed in any way . Amended: April 2019

4.8. Snakebite in the elderly The elderly are no different than younger patients when it comes to snakebite. However, they may be more prone to hypotension, therapeutic fluid overload and adverse effects of adrenaline (epinephrine) and are more likely to be suffering from intercurrent and unrelated chronic illnesses such as hypertension and other cardiovascular diseases, chronic obstructive bronchitis and diabetes mellitus. These possibilities should be taken into account in treatment. 5. Medical Management summary of Bleeding syndrome SAVP Monovalent Antivenom is manufactured for Boomslang envenomation. Monovalent Antivenom has the greatest benefit should a patient have a severe coagulopathy with active bleeding. There is no place for heparin, fibrin stabilising drugs, fibrinolytics or thrombolytics. Venominduced ‘thrombin’ is far less susceptible to heparin than physiological thrombin. (Blaylock 2005) The Monovalent Antivenom is very effective, even when given many hours or days after the bite and the positive effects of the treatment is rapid, even in a very sick patient. The initial dose of two ampoules should be injected intravenously, the serum should be at room temperature and the injection given very slowly, with the patient recumbent (lying down) during the injection, and for at least one hour afterwards. The dose of serum required depends on the amount of venom injected by the snake, not on the size or mass of the victim, and should not be reduced in the case of children. If bleeding continues for more than two hours after the first dose, a further injection of one or two ampoules may be given.

5.1. Test of haemostasis: 20-minute whole blood clotting test (20WBCT) Incoagulable blood is a cardinal sign of consumption coagulopathy from envenoming by puff adders, Boomslang and Vine snake. For clinical purposes, the 20WBCT has proved reliable. This is a simple, rapid, “all-or-nothing” test of blood coagulability which can be done at the bedside and correlates well with fibrinogen concentration (Warrell et al, 1977; Sano-Martins et al, 1994). A few milliliters of blood taken by venepuncture is placed in a new, clean, dry, glass vessel left undisturbed at room temperature for 20 minutes; then tipped once to see if the blood has clotted or not. The vessel must be glass rather than plastic in order to activate blood coagulation via Hageman factor (FXII). Glass vessels may not activate coagulation if they have been cleaned with detergent or are wet.

6. Response to antivenom treatment Use of antivenom in patients with well established cytotoxicity or advanced neurotoxicity may appear not to be particularly effective, due to the inability of antivenom to rapidly reverse the local effects of cytotoxins or the profound respiratory depression of paralysed patients. A common reason for apparent ineffectiveness is inadequate dosage. Clinicians should be realistic in their expectations of what antivenom can and cannot do. It is important to remember that the role of antivenom is to neutralise injected venom. Antivenom does not repair destroyed tissues or nerve cells. Neutralising the injected venom may prevent further progression of cell injury, but will not undo the damage that has already been done. Early administration of antivenom leads to the best clinical outcomes

A favourable response can be expected within 15 minutes to 6 hours, when adequate quantity of antivenom has been administered (otherwise a second antivenom dose might be indicated). For other problems (local necrosis and some paralyses) the effect is a great deal less spectacular. Polyvalent antivenom will not reverse damaged already caused by cytotoxic venom, but will be limit further tissue damage. If adequate dose of antivenom has been given, response can be expected: • Appropriate administration of antivenom can stop the progression of swelling. • Neurotoxic effects begin to improve within 30 minutes but complete recovery takes much longer. In the event of acute neurotoxic envenoming (respiratory paralysis), antivenom will NOT prevent progression of neurotoxic effects. In this case, respiratory support is the ONLY life-saving treatment. By administering adequate dose of antivenom, the time the victim requires artificial respiration, is shortened dramatically. Some patients have required up to 12 days artificial ventilation, but have recovered completely. • The blood pressure normalises within an hour • Cardiac arrhythmias improve rapidly. • Cardiovascular effects such as hypotension and sinus bradycardia may respond within 10-20 minutes. • Spontaneous systemic bleeding usually stops within 15-30 minutes and blood coagulability is restored within about six hours. The 20MWBCT test should be used to monitor the dose of antivenom in patients with coagulopathy. If the blood remains incoagulable 6 hours after the first antivenom dose, the dose should be repeated and so on, every 6 hours, until blood coagulability is restored.

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7. Reactions to Antivenom treatment 7.1. Early reactions Antivenoms can cause adverse reactions, ranging in severity from mild cutaneous eruptions to life-threatening anaphylaxis. Symptoms are usually mild and include urticaria, vomiting, fever, bronchospasm, angiooedema and hypotension. The risk of a potentially severe reaction to antivenom should be balanced against the imperative need to neutralise circulating venom.

Clinicians should prepare to treat adverse anaphylaxis before administration of antivenom. Adequate supplies of adrenaline should be drawn up and ready for use, and resuscitation equipment, drugs and volume expanders kept close at hand. Premedication with adrenaline is helpful as it is effective in reducing incidence of antivenom reactions caused by antivenom. However premedication with antihistamines and hydrocortisone has been found to be ineffective (Fan et al, 1999; Seneviratne et al, 2000). Steroids are of no value and interfere with the venom /antivenom reaction.

The following symptoms are life threatening: shortness of breath, caryngeal swelling, bronchospasm and cyanosis (skin turns blue), respiratory arrest, cardiovascular collapse and coma.

The patient should be kept talking if s/he is able to do so. Uncover the neck, chest or back to check for the development of a rash. Listen carefully to hear if there is a change to the pitch of the voice or if they start to clear their throat or cough. One of the first signs is intensely itchy scalp, the palms of the hands as well as the soles of the feet. Establishing a victim’s allergy profile is also vital. Ask the following questions: 1. Are you allergic to any medication like penicillin, etc.? 2. Have you had antivenom treatment before? 3. Do you suffer from asthma or hay fever? 4. Have you had infantile eczema? 5. Are there any other allergies that you know of, like foods (peanuts), bee stings etc. 6. Have you ever been bitten by a snake before – if yes – what snake?

If any one of the above questions is answered “Yes”, be prepared for a possible reaction. 7.1.1. Treatment of anaphylaxis. 1. Stop Antivenom 2. Adrenalin: Give appropriate dose (1:1000) IM into anterolateral aspect of the thigh if the patient develops progressive systemic features. Repeat every 5-15 minutes if there is no improvement. 3. Oxygen: Give high flow volume mask ~8-10L/min via mask 4. Maintain a patent airway: Position in semi-Fowler’s to assist breathing. Monitoring respiratory parameters and vital signs continuously 5. Always be ready for Intubation should condition progress to obstruction 6. Establish IV access: Give 1-2 litres of crystalloid if hypotensive. Keep Systolic Blood pressure >90mmHg 7. IV adrenaline: Try and avoid IV adrenaline because of its hazardous potential unless you have all equipment for monitoring. 8. Antihistamine: Promethazine 25mg IM is sufficient. 9. Corticosteroids: Give 200mg Hydrocortisone 200mg IV slowly 10. Bronchodilators: Salbutamol together with ipratropium should be given every 15-20 minutes if bronchospasm is a major feature. 11. Glucagon: This is given if patient is not responding to adrenalin 12. Admit for Observation overnight in case of recurrence Antivenom treatment should be continued unless there was full blown anaphylactic shock.

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7.2. Pyrogenic reactions Pyrogenic reactions result from pyrogen contamination of the antivenom during manufacture. They begin within 1-2 hours after treatment. There is an initial chill with cutaneous vasoconstriction, gooseflesh and shivering. Temperature rises sharply during the rigors and there is intense vasodilatation, widening of the pulse pressure and eventual fall in mean arterial pressure. In children, febrile convulsions may occur at the peak of the fever. Patients should be laid flat to prevent postural hypotension. Their temperature should be reduced by fanning, tepid sponging and antipyretic medicines such as paracetamol (15 mg/kg) given by mouth, suppository or via nasogastric tube.

Serum Sickness Late (serum sickness type) reactions occur 5-24 (average 7) days after treatment. There is itching, urticaria, fever, arthralgia, peri-articular swellings, proteinuria and sometimes neurological symptoms. Antihistamines are used for milder attacks, but in severe cases, including those with neurological symptoms, a short course of prednisolone should be given.

8. Ancillary Treatment 8.1. Treatment of local envenoming 8.1.1. Tetanus toxoid: It is appropriate to give a prophylactic booster dose of tetanus toxoid to all snakebite victims. This is also a safe and useful “placebo” for those who are not envenomed but need the reassurance of being given some sort of therapy.

8.1.2. Wound infection: Although most local effects of snakebite are attributable directly to cytolytic and other activities of the venom itself, the bite may introduce bacteria, and the risk of local infections greatly increases if the wound has been incised with an unsterile instrument, tampered with in some other way or if it contains necrotic tissue. The potential risk of tetanus must be addressed by boosting immunity (see above). The pattern of bacterial flora may vary in different countries (Theakston et al, 1990). Antibiotic treatment should be delayed until there are definite signs of infection, such as a hot reddened fluctuant local swelling resembling an abscess or if the wound is necrotic. Appropriate blind antibiotic treatment is with chloramphenicol or amoxicillin with clavulanic acid. Prophylactic antibiotics are not appropriate (Jorge et al, 2004) unless the wound has been grossly interfered with or is frankly necrotic.

8.1.3. Care of the bitten limb: the wound should be cleaned with an antiseptic. Blisters and bullae should be left intact. Snake-bitten limbs should be nursed in the most comfortable position but should not be elevated excessively if there is tense swelling or suspicion of incipient intracompartmental syndrome as this increases the risk of ischaemia. The wound should be examined frequently for evidence of necrosis: blistering, blackening or depigmentation of the skin, loss of sensation and a characteristic smell of putrefaction.

8.1.4. Debridement of necrotic tissue: necrotic tissue should be debrided by a surgeon under general or local anaesthesia after 5-7 days. Skin appearances may be deceptive, for necrosis can undermine apparently normal skin. Large areas may be denuded of skin; recovery can be accelerated by applying split skin grafts immediately after debridement provided that the wound is not infected. Debrided tissue, serosanguinous discharge and pus should be cultured and the patient treated with appropriate antimicrobials. Fluctuant areas, suggestive of an underlying abscess, should be aspirated and opened for drainage. Inexperienced surgeons may mistake bruised for necrotic muscle. In some cases, muscle fibers damaged by snake venom myotoxins may regenerate if the muscle sheath is left intact and so debridement should be restrained. 8.1.5. Compartment syndromes: these are uncommon and over-diagnosed but require urgent attention. The clinical appearance of snake-bitten limbs often suggests that there is a compartment syndrome. There may be severe pain, tense tender swelling, cold cyanosed anaesthetic skin, pain on passive stretching of the muscles and apparently absent pulses. However, these appearances are usually misleading and when the intracompartmental (tissue) pressure is measured directly (for example with a Stryker monitor) pressures are found to be below the threshold of danger for ischaemic necrosis of the intracompartmental muscles. Compartment syndromes of hands and feet tend to self decompress via the bite site. If a compartment syndrome in a limb is suspected, the pressure should be measured directly as this is the only reliable way of confirming raised intracompartmental pressure and justifying fasciotomy. However, many surgeons seem reluctant to measure the pressure. The normal intracompartmental pressure is 0-10 mmHg. An intracompartmental pressure of more than 45 mmHg is usually associated with compartment syndrome, but there may be a risk of intracompartmental ischaemia at lower pressures if mean arterial pressure1 (perfusion pressure; mean arterial pressure = diastolic pressure + 1/3 [systolic – diastolic pressure] ) is reduced, for example, in an elevated limb (Matsen, 1980). If the pressure is raised but mean arterial pressure is more than 30 mmHg higher than intracompartmental pressure, the patient may be treated conservatively for one hour with the appropriate antivenom and intravenous mannitol 100 g (500 ml of 20% solution in adults, less for children) (Mars et al, 1991; Mars and Hadley, 1998). Should conservative treatment fail, open full length fasciotomy should be performed providing there is no coagulopathy or gross thrombocytopenia. However, animal studies have shown that fasciotomy is ineffective in saving envenomed muscles (Garfin et al, 1994). Provided that adequate antivenom treatment is given as soon as possible after the bite, fasciotomy is rarely if ever needed ( Warrell and Rollinson, 2000 ). However, bites involving the finger pulps are frequently complicated by necrosis. Expert surgical advice should be sought, especially if the thumb or index finger is involved. 10 | Eswatini Antivenom Foundation - This document may not be copied or distributed in any way . Amended: April 2019

8.1.6. Vessel entrapment syndrome: this is uncommon and is usually due to massive swelling compressing the femoral vessels beneath the inguinal ligament. It presents as a cool, blistercovered leg with absent distal pulses (Blaylock, 2003). Provided there is no coagulopathy and the leg is still viable, division of the inguinal ligament and multiple fasciotomies are required.

8.1.7. Nerve entrapments (e.g. median carpal tunnel syndrome, femoral nerve i.e. meralgia paraesthetica) are treated conservatively.

8.1.8. Muscle haematomas (e.g. iliacus haemorrhage causing unilateral weakness of hip flexion as in patients with haemophilia) are treated conservatively after correction of the haemostatic disorder with antivenom and, in some cases, clotting factors.

8.1.9. Vascular thromboses: Deep vein thrombosis may be suspected when the swelling of a leg fails to subside after 2-3 weeks. Arterial and venous thromboses are rare complications reported after bites by vipers. Arterial thrombosis is suspected when agonizing pain develops rapidly in a limb, there is a sharply demarcated cold distal area and arterial pulses prove undetectable even by doppler. Once haemostatic abnormalities are corrected, the limb might be investigated by arteriography with the possibility of angioplasty, thrombectomy or reconstructive arterial surgery.

8.1.10. Amputation of doomed digits and limbs is the last resort but the decision must be made and agreed upon by the patient and family before life- threatening septicaemia, gas gangrene or tetanus supervenes.

8.1.11. Late complications of local envenoming : these include incapacitating and deforming hypertrophic and keloid scars, muscle and tendon contractures, equinus deformity, destroyed or arthrodesed joints, osteomyelitis, chronic ulceration with or without malignant change and consequences of intracompartmental syndromes such as Volkmann's ischaemic contracture. These are treated according to standard guidelines. 9. Haemostatic abnormalities Once adequate doses of antivenom have been given to neutralize venom antihaemostatic factors, recovery of normal haemostatic function may be accelerated by giving fresh whole blood, fresh frozen plasma, cryoprecipitates or platelet concentrates. However, this is unnecessary unless traumas such as imminent childbirth or emergency surgery are anticipated. The risk of contamination of blood and its products with HIV, HTLV-1, hepatitis viruses and other pathogens greatly restricts their use in many parts of Africa. NB: Heparin and antifibrinolytic agents should never be used in snake bitten patients. Heparin does not inhibit the abnormal thrombin generated by snake venoms and it exaggerates, sometimes fatally, the haemostatic disturbances ( Warrell et al, 1976d ).

10. Hypotension and shock Specific antivenom can reverse the direct myocardial and vasodilating effects of some venoms, but in patients who have leaked large amounts of blood and plasma into the bitten limb and elsewhere, a plasma expander is needed to correct hypovolaemia. As an emergency, the foot of the bed can be raised to improve cardiac filling while an intravenous infusion is set up. Ideally, central venous pressure should be monitored to prevent fluid overload. Other causes of hypotension, such as a massive concealed haemorrhage or effects of venom toxins on the physiological mechanisms controlling blood pressure (e.g. ACE-inhibiting and bradykininpotentiating peptides should be considered.

11. Snake venom opthalmia Spitting cobras can cause intense conjunctivitis and bullous corneal erosions complicated by secondary infection, anterior uveitis, corneal opacities and permanent blindness. First aid treatment consists of irrigating the eye or other affected mucous membrane as soon as possible using large volumes of water or any other available bland fluid such as tea or milk. To facilitate irrigation, a single application of local anaesthetic eye drops to overcome tightly closed eyelids may be used. Unless a corneal abrasion can be excluded by slit lamp examination or fluorescein staining, the patient should be treated as for a corneal injury with a topical antimicrobial agent (tetracycline and chloramphenicol). Topical or systemic antivenom treatment is not indicated. It has been said that 1 in 1000 (0.1%) adrenaline eye drops or 10% phenylephrine eye drops relieve the burning sensation instantaneously. However, these eye drops can cause a rise in blood pressure and tachycardia and should be used with caution in older patients.

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Flowchart 1: Management of venom opthalmia

First aid: Immediate irrigation with water or other bland solution (open and close the eyes under water )

Medical practitioner :

A single application of local anaesthetic eye drops to overcome tightly

closed eyelids facilitates irrigation. Fluorescein staining .

Fluorescein staining

Slit lamp

Corneal erosions

Absent Present

Antibiotic eye ointment Antibiot ic eye drops/ointment Eye pad Mydriatic Resolution within 24 – 48 hours Eye pad Daily slit lamp examination until cured

Antivenom (dilute) topically or systemically IS NOT INDICATED. Steroids (topical or systemic) ARE CONTRAINDICATED. Encourage patients not to rub herbal, home or traditional remedies in their eye. VENOM ELSEWHERE : In the mouth: wash out with water or other bland solution. On the skin: wipe or wash off.

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Flowchart 2: Swaziland Snakebite Authority – Treatment Protocol

PPS Syn drome PW Syndrome PPS/PW Syndrome B Syndrome Syndrome Painful, Progressive Swelling Progressive Weakness Mixed Cytotoxic & Bleeding Venom Type Cytotoxic Venom Neurotoxic Venom Neurotoxic Venom Haemotoxic Venom

IV Fluids IV Fluids IV Fluids IV Fluids Supportive Elevate limb Protect airway by mask Blood or Blood Treatment Analgesia * Analgesia * or ventilation Protect airway component therapy ‡

Sev ere pain, Metallic taste; profuse Drowsiness, nausea, Fang punctures do not Swelling >15cm/hour; stop bleeding, severe Severe sweating; paraesthesiae; vomiting, vertigo, mild Swelling to elbow or knee by excessive salivation, pyrexia, dyspnoea, headaches, dizziness, envenomation 3-4 hours. Swelling of whole anticipated shortness of breath, general weakness. fainting or convulsions. limb in 8 hours. Bleeding difficulty swallowing, abnormalities. ptosis, fasiculations

To prevent or diminish possible anaphylaxis, pre-treat with IM adrenaline, 0.5 ml of a 1:1 000 (250 µg) solution in adults and 0.01mg/kg for children 10-15 minutes before starting antivenom treatment.

Insert IV line (not same limb as bite). Doctor to administer antivenom personally. No test dose needed.

Polyvalent Polyvalent Polyvalent Monovalent Antivenom Type IV Push 1 ampoule/min IV Push 1 ampoule/min. IV Push 1 ampoule/min IV Push 1 ampoule/min Or diluted 50/50 in Atropine Or diluted 50/50 in Or diluted 50/50 in isotonic fluid infused Neostigmine isotonic fluid infused isotonic fluid infused over 15-30 minutes. (see page 7: 4.5) over 15-30 minutes. over 15-30 minutes.

Puff adder: 50ml – 100ml Black mamba; Rinkhals: Boomslang: STARTING Snouted cobra Vine snake: dose of Mozambique spitting No antivenom available. antivenom IV. cobra: 100ml + 80ml -200ml 50ml 20ml

Monitor progression of Monitor neurological Monitor progression of If the blood remains swelling every hour. symptoms closely. If swelling every hour. incoagulable 6 hours If swelling continues there no improvement If swelling continues after the first administer 2 additional after 30 minutes, administer 2 additional antivenom dose, repeat Additional ampoules of AV until administer an additional 4 ampoules of AV until dosage, until blood Antivenom swelling stops vials. Repeat as swelling stops. coagulability is necessary. restored.

The patient should be kept talking if able. Uncover ches t to check for rash. Listen carefully for change to the pitch of the voice , clear ing throat or cough,

intensely itchy scalp, the palms of hands or soles of the feet. Refer to point 7.11 for Treatment of Anaphylaxis.

* Analgesia: Paracetamol (acetaminophen) or codeine phosphate. Not aspirin or non -steroidal anti -inflammatory medicines which can cause bleeding. ‡ Heparin, antifibrinolytics and thrombolytics are of no value and may be dangerous. ¥ Small doses may lead to recurrence of symptoms.

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Flowchart 3: Indications for Antivenom

Indications for Antivenom

Clinical syndromes of envenomation (There may be overlap between syndromes)

Painful progressive Progressive weakness Bleeding swelling (PPS) (PW) (B)

Severe envenomation anticipated

Rapidly progressive swelling

Swelling extends 15cm or

more per hour. The triad of pins and Fang punctures do not stop needles, profuse bleeding and/or severe Swelling of the whole hand sweating and excessive headaches, dizziness, or foot in 1 hour after salivation (mamba) or fainting or convulsions envenomation. metallic taste

Swelling extends to elbow or knee in 3-4 hours after envenomation.

Severe or life-threatening envenomation present

Swelling of whole limb in 8 hours after envenomation Active systemic bleeding (not bruising of the bitten Swelling threatening the Shortness of breath due to limb alone) airway weakness - with no PPS (Black mamba) Non-clotting blood after Associated unexplained 20 minutes in an unused, shortness of breath Inability to swallow saliva new, dry, clean test tube. Use blood from a healthy Associated unexplained Generalised weakness person as a control. shortness of breath with PPS (Snouted cobra) Significant laboratory Very tense limb evidence of a blood clotting (compartment syndrome) abnormality. or compressed major blood vessel (vessel entrapment)

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12. Snakes of Swaziland 12.1. Highly Venomous Snakes of Swaziland The “7 Deadly Sins” of Swaziland for which either polyvalent or monovalent antivenom should be used, are: 1. Black Mamba ( Dendroaspis polylepis ) - iMamba 2. Snouted or Savannah Cobra (Naja annulifera) - Phemphetfwane 3. Mozambique Spitting Cobra (Naja mossambica) - Mfeti 4. Rinkhals (Hemachatus haemachatus) - Phemphetfwane 5. Puff Adder (Bitis arietans) - Libululu 6. Boomslang (Dispholidus typus) - Indlondlo 7. Twig, Bird or Vine Snake (Thelotornis capensis) - Lununkhu

12.2. Venomous and Dangerous: Rarely Seen One or more deaths have been attributed to the following snakes, not normally regarded as deadly, but in exceptional circumstances they could be. Antivenom is not effective. 8. Berg Adder (Bitis atmpos) 9. Shield Nosed Snake (Aspidelaps intermedius) 10. Zambezi Garter snake ( Elapsoidea boulengeri ) 11. Sundervall’s Garter snake ( Elapsoidea sundevalli ) 12. De Coster’s Garter snake ( Elapsoidea sundevalli )

12.3. Mildly Venomous Snakes of Swaziland Although classified as mildly venomous, the following snakes may cause severe pain and may need medical attention. Antivenom is not affective 13. Stiletto Snake / Bibron’s burrowing asp (Atractaspis bibronii) 14. Night Adder ( Causus rhombeatus) 15. Snouted Night Adder ( Causus defilippii )

12.4. Mildly venomous (mostly asymptomatic) Many other snakes classified as Mildly Venomous cause almost no pain, swelling or discomfort. Antivenom is not effective. 16. Eastern Tiger Snake (Telescopus semiannulata semiannulata) 17. Herald Snake (Crotaphopeltis hotamboeia) 18. Marbled Tree snake/ Cat-eyed Tree snake (Dipsadoboa aulica) 19. Short-snouted Whip snake ( Psammophis brevirostris ) 20. Western Stripe-bellied Sand snake ( Psammophis subtaeniatu s) 21. Olive Grass Snake (Psammophis mossambicus) 22. Crossed Whip snake ( Psammophis crucifer ) 23. Black-headed Centipede-eater ( Aparallactus capensis ) 24. Reticulated Centipede-eater ( Aparallactus lunulatus ) 25. Spotted Skaapsteker (Psammophylax rhombeatus) 26. Spotted Harlequin snake ( Homoroselaps lacteus ) 27. Striped Harlequin snake ( Homoroselaps dorsalis ) 28. Natal Purple-glossed snake ( Amblyodipsas concolor ) 29. Common Purple-glossed snake ( Amblyodipsas polylepis )

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12.5. Non-venomous Snakes of Swaziland Swaziland’s non-venomous snakes are harmless as they do not have venom glands and pose no danger to man at all. 30. Brown House snake ( Lamprophis capensis ) - umdlumi 31. Spotted Bush snake ( Philothamnus semivariegatus ) 32. Eastern Natal Green snake ( Philothamnus natalensis natalensis ) 33. Common Wolf snake ( Lycophidion capense ) 34. Common Egg-eater ( Dasypeltis scabra ) 35. Aurora House snake ( Lamprophis aurora ) 36. Olive House snake ( Lamprophis inornatus ) 37. Yellow-bellied House snake ( Lamprophis fuscus ) 38. Swazi Rock snake ( Lamprophis swazicus ) 39. Spotted Rock snake ( Lamprophis guttatus ) 40. Dusky-bellied Water snake ( Lycodonomorphus laevissimus ) 41. Common Brown Water snake ( Lycodonomorphus rufulus ) 42. Floodplain Water snake ( Lycodonomorphus obscuriventris ) 43. East African Shovel-snout ( Prosymna stuhlmannii ) 44. Sundervall’s Shovel-snout ( Prosymna sundevalli ) 45. Semiornate snake ( Meizodon semiornatus ) 46. Green Water snake ( Philothamnus hoplogaster ) 47. Western Natal Green snake ( Philothamnus natalensis occidentalis ) 48. Common Slug-eater ( Duberria lutrix ) 49. Variegated Wolf snake ( Lycophidion variegatum ) 50. Southern File snake ( Mehelya capensis ) – iMamba lukhonkhotse 51. Black File snake ( Mehelya nyassae ) 52. Southern Brown Egg-eater ( Dasypeltis inornata ) 53. Schlegel’s Blind snake ( Phinotyphlops schlegelii ) 54. Bibron’s Blind snake ( Typhlops bibronii ) 55. Long-tailed Worm snake ( Leptotyphlops longicaudus ) 56. Peter’s Worm snake ( Leptotyphlops scutifrons ) 57. Incognito Worm snake ( Leptotyphlops incognitos ) 58. Tello’s Worm snake ( Leptotyphlops telloi ) 59. Cape Worm snake ( Leptotyphlops conjunctus conjunctus ) – umtfwana wenyoka lengaboni

There are two exceptions with regard to non-venomous snakes. Both these snakes have no venom but can inflict a nasty bite which may need stitches. 12.6. Non-venomous and Possibly Dangerous 60. Southern African Python ( Python natalensis ) - inhlatfu 61. Mole snake ( Pseudaspis cana ) - imboma

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13. Characteristics of Swaziland’s venomous snakes 13.1. Highly venomous snakes of Swaziland 13.1.1. Black mamba (Dendroaspis polylepis) – “Imamba” Found throughout Swaziland. A long slender snake that on average, reaches 2.0 - 2.8 m with larger individuals reaching 3.0m. Maximum 4.3 meters (KZN). The head has vertical sides with the distinctive coffin shape. The colour is never pitch black although it can become very dark, almost black, just before shedding. The normal colour is a light to dark grey, light black or various shades of brown or olive, with lighter banding on the rear part of the body. The underside is white in colour, and can be plain or sometimes heavily spotted towards the tail. The inside of the mouth is inky-black. This snake is shy, nervous, alert and tries to avoid contact with humans. It does NOT attack unprovoked as is often reported, and is NOT an aggressive snake. The belief that it will “chase or hunt” its victim is totally untrue. When approached it will lift the head well off the ground to obtain a better view, flatten the neck into a slight hood, hiss a hollow sounding hiss, and gape the mouth showing the black lining of the mouth. Any closer approach could result in the snake lunging forward to bite, sometimes striking twice in quick succession. Black Mambas rarely give a dry-bite. They do not hold on and chew, but deliver a quick bite and release immediately. Many locals believe that a snake that bites twice will remove all the venom with the second bite, this is not true, in fact, it will envenomate with each bite. It is active during the day, normally emerging from about 7:00 in the morning to bask in the sun for about 1 - 2 hours, after which it will move away to forage for prey. It will return to its refuge, which can be a hole in the ground, or under a large rock outcrop, or a hollow tree, from about 15:00 to 17:00. They will live undisturbed in the same hollow log or termite mound for up to 8 years. Mambas will often enter houses or building when foraging for prey. They are often attracted to human dwellings because of the presence of rats, mice and chickens. The estimated maximum speed of a mamba is probably 15 to 20 km/h over a short distance, not 40 km/h as is believed. Venom: Predominantly Neurotoxic (PPW Syndrome)

Figure 17 (left) : Black mamba ( Dendroaspis polylepis ), Simunye Swaziland. Figure 18 (right) : Black mamba ( Dendroaspis polylepis ), two male mambas in combat

Figure 19 (left) : Black mamba, Simunye Swaziland showing fangs, venom and black buccal lining. Figure 20 (centre): Black mamba ( Dendroaspis polylepis ), Simunye Swaziland showing venom glands. Figure 21 (right) : Black Mamba, Simunye Swaziland with raised body, small hood.

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13.1.2. Snouted cobra (Naja annulifera) – “Phemphetfwane” This non-spitting cobra is slender averaging 1.2m but can reach 2m or longer when it becomes quite thickset and robust. The head is distinct from the neck. Large specimens have bulging temporal muscles. The colour is variable but more often grey, brown or light brown on the back with a lighter yellow underside, which is usually heavily mottled. Easily identified by the broad, dark honey-coloured band on the throat. When threatened it will left the head off the ground and spread an impressive hood. These snakes are very defensive and they will strike readily and repeatedly whilst possibly making a hissing sound. A banded phase occurs throughout the range of the species but has to date not been found in Swaziland. The banding is hardly discernable in hatchlings, but by the time a snake attains a length of 600 mm, it is black with seven to nine yellow bands on the body and one or two on the tail. The light bands are usually about half the width of the dark ones and may be divided by a narrow black transverse line. The yellow bands may encircle the body, but are frequently mottled with black ventrally. Venom: Predominantly Neurotoxic and mildly Cytotoxic

Figure 22 (left): Snouted cobra Naja annulifera Simunye, Swaziland showing the honey -coloured band on the throat Figure 23 (centre): Snouted cobra Naja annulifera Simunye, Swaziland showing the broad hoot and large temporal muscles. Figure 24 (right): Juvenile Snouted cobra Naja annulifera Simunye, Swaziland heavily mottled below

13.1.3. Mozambique spitting cobra ( Naja mossambica) – “Mfeti” Found throughout Swaziland, they are common and responsible for the majority of serious envenomations in Swaziland. A medium length snake averaging 1.2m – 1.5m, very rarely growing larger 1.6 m. The colour is light to dark grey. The skin between the scales is black, giving it a fish-net stocking appearance on the dorsal (top) side. The ventral is light orange to with from one to three irregular black bands on the throat. Although it becomes more active at night, it is also often found during the day. It will eat almost anything and is fond of frogs, toads, rodents, birds and their eggs, nestlings as well as other snakes. Given the slightest opportunity it enters a residence, especially when doors and windows are left open. The most common encounter with this cobra would be venom spat in the eyes but most reported snakebites are attributed to this snake. Bites to sleeping people are also regularly reported. Venom: Cytotoxic

Figure 25 (left): Mozambique spitting cobra Naja mossambica Simunye, Swaziland with typical salmon coloured throat and black bands.

Figure 26 (right): Mozambique spitting cobra Naja mossambica Simunye, Swaziland making a hood and spraying venom.

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13.1.4. Rinkhals (Hemachatus haemachatus) - “Phemphetfwane” Found in the cooler regions of Swaziland. A small to medium size snake usually 90cm to 1.2m in length but it can reach 1.5m. The snake is closely related to the true cobras but differs from them in having keeled dorsal scales and it produces live young but in all other respects in acts like a cobra, being able to rear up and spread a hood. The colour is usually a light grey when young, turning darker and becoming black when about 1m in length. The ventral part is normally dark brown or shiny black with one to three white bands on the throat. A banded phase occurs throughout the range of the species. This snake is active during the day. It starts its day with a basking session, usually from about 8 to 9 am, after which it will start moving around in search of prey. It loves raiding chicken runs, eating eggs as well as small chicks, and is often found near homesteads in search of prey or water. This snake will usually flee but if cornered it will face its attacker, rear the front of the body off the ground and spread a broad hood, exposing the black with white bands on the throat. From this position it will lung forward and spray its venom at an attacker, the body hitting the ground and at the same time the snake emits a loud hiss. If the threat from an attacker is kept up, the snake may drop to the ground, turn the front of the body over, open the mouth and lay there as if dead. A very effective ploy, fooling many people as well as dogs. It will later “come to life” again and move off. Venom: Neurotoxic and Cytotoxic

Figure 27 (left): Rinkhals ( Hemachatus haemachatus ) Simunye, Swaziland with typical black throat and white bands. Figure 28 (centre): Juvenile banded phase Rinkhals ( Hemachatus haemachatus ), Simunye Swaziland, shaming death. Figure 29: Rinkhals (Hemachatus haemachatus ) Simunye, Swaziland acting “dead”.

13.1.5. Puff adder (Bitis arietans) – “Libululu” Found throughout Swaziland. A short fat snake with adults averaging between 0.9m to 1.2m The head is triangular, broad and very distinct from the neck The colour can vary from light to dark brown to black with yellow or cream V shapes (chevrons) down the back. The ventral part is light-cream or yellow. This very common snake is responsible for a large majority of snakebites in Swaziland as it tends to remain immobile as a form of defence whereas other snakes will move away. Mainly active at night but does also emerge during the day to bask in the sun. Most commonly seen in spring and autumn. It is often found around human habitation where it will hunt for prey. The name puff adder comes from this snake’s habit of inhaling air and expelling it forcefully through the nostrils to produce a loud hiss. This is a warning that the snake’s patience is running out, and if ignored the snake will form an S shape and strike out at remarkable speed. Venom: Predominantly Cytotoxic but with possible Haemotoxic symptoms combined

Figure 30 (left): Puff adder (Bitis arietans ) Simunye, Swaziland with chevr on markings on the back Figure 31 (centre): Puff adder (Bitis arietans ) Simunye, Swaziland. Fangs can grow up to 5mm in length Figure 32 (right): Puff adder ( Bitis arietans ), Simunye Swaziland, venom gland.

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13.1.6. Boomslang (Dispholidus typus) – “ Indlondlo” Found throughout Swaziland. A long slender snake growing to 1.8m in length. It can be identified by the blunt head and very large eye. Because if the bright green colour of the males it is often mistaken for a Green mamba which are NOT found in Swaziland. The females normally grey or brown and the males are bright green. It is more often than not confused with the Green mamba which is not found in Swaziland, or other harmless green snakes. Their bellies are light yellow, green or cream. Juveniles are grey with a brown head and white jaw. The most distinctive feature of the juvenile Boomslang is the large bright green eye. The juvenile Boomslang are often mistaken for the Vine/Twig/Bird snakes. This snake is active during the day and often found in fruit trees where they hunt for birds. It is not true that snakes eat fruit or bees. It avoids human contact and rarely bites but will demonstrate its displeasure by inflating the front part of the body when molested to almost twice its normal size. From this position it may strike out, often at a sideways angle. Although venom may not be injected in this instance, the venom is so potent that even a tiny scratch could cause serious symptoms. If the snake is allowed to hang on and “chew” the consequences are usually dire. The fange marks presented on a victim can be very confusing as they more often than not have two or three fangs on the one side and one or two on the other side. Their fangs are situated just below the eye (see fig 30). Venom: Predominantly Haemotoxic

Figure 33 (left): Male Boomslang (Dispholidus t ypus ) Simunye, Swaziland. Males are green in colour. Figure 34 (second from left): Male Boomslang (Dispholidus typus ), Swaziland. Fangs are situated below the eye. There are often two fangs on each side. Figure 35 (centre): Natal green snake (Philothamnus natalensis) often mistaken for a Green mamba which is NOT found in Swaziland Figure 36 (second from right): Female Boomslang ( Dispholidus typus ) Simunye, Swaziland. Females are brown in colour. Figure 37 (right): Juvenile Boomslang ( Dispholidus typus ) Simunye, Swaziland. They are often mistaken for a Vine snake but can be identified by the distinctive large green eye.

13.1.7. Twig Bird or Vine Snake (Thelotornis capensis) – “Lununkhu” A very slender snake with a long, thin tail. The colour is various shades of grey resembling a twig. The head is lance-shaped and can be green, emerald or brown with black spots. The eye has a horizontal pupil and is keyhole-shaped. This arboreal snake is active during the day when it will move around in search of its favourite prey like lizards and chameleons. It will also hunt reed frogs and will raid bird’s nests for hatchlings. This snake will then be mobbed by the parents in defence of their young and are occasionally killed by these birds. It is an inoffensive snake which has never been implicated in any legitimate snakebite’s. Reptile enthusiasts are most at risk. When annoyed, it will inflate the front part of the body, similar to the Boomslang. From this position it will strike sideways towards its attacker. This snake must bite and chew to get the fangs into play and should not be allowed this opportunity as there is no antivenom available to treat its bite. Venom: Predominately Haemotoxic

Figure 38 (left): Vine/Twig/Bird snake (Thelotomis capensis ) Simunye, Swaziland inflating its neck as a warning. Figure 39 (second from left): Vine/Twig/Bird snake (Thelotomis capensis ) Simunye, Swaziland. Distinctive keyhole shaped eye. Figure 40 (centre, second from right and right): Vine/Twig/Bird snake (Thelotomis capensis ) Simunye, Swaziland. Colour variations.

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13.2. Venomous snakes of Swaziland 13.2.1. Berg adder (Bitis atropos) Very seldom seen in Swaziland as it is only found in certain remote locations. Average total length 30–40 cm (maximum 60 cm). This small, stoutly built viper is greyish, reddish, olive to dark brown with two rows of triangular black dorsal markings and lateral rows of square markings. The belly is off-white with grey infusions. It does not have the raised ridges above the eyes. It is a very rare snake, only found on the high mountains in the Bulembu and Malolotja area. Venom: Neurotoxic and Cytotoxic

Figure 41: Berg adder ( Bitis atropos ). Not a Swaziland specimen.

13.2.2. Shield Nosed Snake/ Shield Cobra (Aspidelaps scutatus) Very seldom seen in Swaziland. Short and stocky with very obvious large scale covering the tip of the snout which they use to bulldoze through loose sand. Adult length is 40-45 cm but can reach 75 cm. The colour is very variable but usually salmon pink or creamish or orange-brown with indistinct blotches on the back. The head and neck are black, but the throat is usually white with possible black band around the neck. The underside is white or yellowish. Venom: Unknown but possibly neurotoxic

Figure 42 (left): Shield nosed snake (Aspidelaps scutatus ). Not a Swaziland specimen. Figure 43 (right): Deceased Shield nosed snake (Aspidelaps scutatus Sihhoye), Swaziland. Large scale covering the snout.

13.2.3. Zambezi Garter snake ( Elapsoidea boulengeri ) Very seldom seen in Swaziland. Above, dark chocolate brown to black with 8-17 narrow white bands on the back and up to 3 white bands on the tail. Juvenile have a white head and are black above with 12-17 white to pale yellow bands on the body and tail. The belly is usually dark grey or brown, but may occasionally be white. Adult length 50-60 cm. Venom : A cobra type venom that may cause immediate pain and stiffness of the affected limb. The symptoms are usually short lived and severe effects have not been recorded.

. Douglas .

©M

Figure 44 (left) : Juvenile Zambezi Garter snake ( Elapsoidea boulengeri ), Mpumalanga, South Africa. Figure 45 (right) : Zambezi Garter snake ( Elapsoidea boulengeri )

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13.2.4. Sundervall’s Garter snake ( Elapsoidea sundevalli ) / De Coster’s Garter snake ( Elapsoidea sundevalli decosteri ) Both species are very seldom seen in Swaziland. Sundervall’s Garter snake ( Elapsoidea sundevalli ) The adults are slate grey with a reddish brown tinge and have 19-34 pale bands on the body and 2-4 pale bands on the tail. The belly scales are yellowish and may have darker mottling. In juveniles, the head and belly are pale and the body and tail distinctly banded with chocolate brown to black and white to cream bands. The white bands fade with age.

De Coster’s Garter snake ( Elapsoidea sundevalli decosteri ) Juvenile species have 19-21 white edged pale brown bands on a darker background on the body. There are also 3-4 of these bands on the tail. The belly scales on the lower flanks are white. These bands fade with age and eventually disappear completely.

Venom: The venom has been little studied and only a few case histories have been documented. Known symptoms include nausea, vomiting, pain, swelling, blurred vision and loss of consciousness.

Figure 46 (left and right) : Sundervall’s Garter snake ( Elapsoidea sundevalli ), South Africa.

13.2.5. Stiletto Snake / Bibron’s burrowing asp (Atractaspis bibronii) Found commonly throught Swaziland. Burrowing asps are found in a wide variety of habitats. They are fossorial (burrowing), living mostly underground in deserted termite mounds, under stones or logs, or in soft soil or sand. They are coloured predominantly grey, black or brown. Most are relatively small (30–70 cm in length). They are glossy, with a head indistinct from the neck. A very short tail ends abruptly, giving the snake a “two-headed” appearance.. The head is short with tiny dark looking eyes. These snakes are nocturnal and usually emerge on warm, wet summer evenings, especially after heavy rains. When the snake strikes, one fang is protruded out of the side of the mouth and is then hooked or jabbed into the victim with a backward jerk of the head (“side swipe”). They are extremely irritable, striking in sideways swings and sweeps (multiple bites), and showing annoyance by flattening the body. Accidental bites usually occur at night when the victim treads on the snake in a gutter or water-logged path after heavy rain or when incorrectly identified as non-venomous and handled. These snakes are easily confused with several species of non-venomous black snakes. Even experienced snake enthusiasts find it difficult identify. There are two characteristics you can look out for: 1. When threatened, they make a distinct stiletto shape by burrowing their heads into the ground 2. They show annoyance by flattening the body It is impossible to pick this snake up by hand, you will get bitten. Use a Snake Glove or better yet, a snake tong or hook. Venom: Cytotoxic (antivenom is ineffective)

© Warrell A David Figure 47 (left): Southern (Bibron’s) Stiletto snake ( Atractaspis bibronii ), showing unique fangs. Figure 48 (centre): Southern (Bibron’s) Stiletto snake ( Atractaspis bibronii ), showing typical warning behaviour. Not a SD specimen. Figure 49 (right): Southern (Bibron’s) Stiletto snake ( Atractaspis bibronii ), a nondescript small black snake, often underestimated.

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13.2.6. Night adder ( Causus rhombeatus) The night adders are small (less than 100 cm) and, despite their name, are active by day and by night. They are not adder-like, and are fairly tubby. The most obvious feature is the V mark on the top of the head. The point of the V extends up to the centre of the eyes. The venom fangs are short compared to those of genus Bitis (Puff adder) but the length of their venom glands are impressive. They have round pupils (most adders have vertical slit eye pupils). When threatened, they hiss and puff ferociously, inflating the body to a great extent. They may also raise the forepart of the body off the ground and slide forward with the neck flattened, looking quite cobra-like. Venom: Mildly Cytotoxic

Figure 50 (left): Night adder Causus rhombeatus Simunye, Swaziland. Figure 51 (centre): Night adder (Causus rhombeatus ) Simunye, Swaziland. Distinguishing V shaped mark on the head. Figure 52 (right): Night adder (Causus rhombeatus ) Simunye, Swaziland. Showing exceptionally long venom glands.

13.2.7. Snouted Night Adder ( Causus defilippii ) Average total length 20-35 cm (maximum 42 cm). It has a relatively thick body, with pointed upturned snout. The colour is brownish, greenish or greyish, with a dorsal series of dark rhomboidal markings, extending to dark stripes on the flanks. As with the night adder, it has a prominent dark V-shaped mark on the top of the head, the apex of which extends to between the eyes. As with the Night adder Causus rhombeatus, hen threatened, they hiss and puff ferociously, inflating the body to a great extent. Venom: Mildly Cytotoxic

Figure 53 (left): Snouted Night adder (Causus defilippii ) Simuny e, Swaziland. Figure 54 (right): Snouted Night adder (Causus defilippii ) Simunye, Swaziland. Distinguishing pointed upturned snout.

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Annex 1

Essential Medicines and Supplies for Managing Snakebite at a District Hospital

In order for health workers to deal effectively with cases of snakebite, it is important that certain essential supplies are available in their health facilities and that they are trained in the best methods for using them. Below is a list of recommended essential supplies for the management of snakebite. It can be modified to suit the needs of local health workers, depending on their specific training and aptitude in dealing with snakebite victims.

1. Antivenom 2. Tetanus toxoid 3. Epinephrine (adrenaline) injection 0.1% (1:1,000) (1 mg/ml) 4. Parenteral antihistamine and hydrocortisone 5. Pain killers e.g. paracetamol and codeine NOT aspirin or nonsteroidal anti-inflammatory agents 6. Antipyretics (paracetamol tablets, syrups and suppositories) 7. Local anaesthetic agents (1-2% lidocaine) 8. Intravenous (IV) fluids e.g. normal saline (0.9% NaCl) 9. Vasopressor drug e.g. phenalephrine, adrenaline and nonadrenalin 10. Atropine and edrophonium or neostigmine (Prostigmin) for “Tension Test” 11. Fresh frozen plasma or cryoprecipitates 12. Blood platelets 13. Oxygen cylinders with spanners, gauges, necessary connectors 14. Antibiotics (chloramphenicol, benzylpenicillin, flucloxacillin, metronidazole, gentamicin, amoxicillin-clavulanic acid) 15. Laryngoscope (adult and paediatric sizes) with spare batteries and bulbs 16. Cuffed endotracheal tubes (various sizes) 17. Ambu bag with connectors to endotracheal tube and face mask that fit 18. Face masks and oral airways 19. Suction apparatus and catheters 20. Urine dip sticks 21. New, clean, dry glass vessels for 20WBCT 22. Syringes, needles, intravenous cannulae 23. IV administration set 24. Sticking plaster 25. Scissors 26. Splints 27. Uretheral catheters 28. Bathroom type weighing scales 29. Stretchy, elasticated crepe bandage and splint

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Annex 2 Emergency Reference

Adrenalin: is to be administered IM 10 minutes prior to starting antivenom. Adult dose 0.25 mg. Paediatric dose (1:1000 Adrenalin), 0.25 mg diluted to a volume of 2.5 ml.

AGE BODY WEIGHT s.c.i. DOSE VOL. ml 1-3 Years Under 11 kg 0.10 mg 1.0 ml 4-7 Years 11 -15 kg 0.15 mg 1.5 ml 8-11 Years 16 -20 0.20 mg 2.0 ml

Neostigmine: is to be administered i.v.i. Adult dose 2.5 mg. Paediatric dose is 2.5 mg Neostigmine diluted to a volume of 5 ml. Neostigmine/Atropine can be administered every 2-4 hrs, if there has been significant improvement after the first dose.

AGE BODY WEIGHT i.v.i. DOSE VOL. ml 1-3 Years Under 11 kg 0.5 mg 1.0 ml 4-7 Years 11 -15 kg 0.75 mg 1.5 ml 8-11 Years 16 -20 kg 1.0 mg 2.0 ml 12 -15 Years 20 -40 kg 2.0 mg 4.0 ml

Atropine : to be administered immediately after neostigmine. Adult dose 12 years > 0.6 mg i.v.i. Paediatric dose (1 ml/600 mcg) diluted to 3 ml. The below dose can be administered for excessive oral secretions, not to be administered if BP> 150 mmHg and/or HR > 100 bpm. Atropine can be administered every 2-4 hrs.

AGE BODY WEIGHT i.v.i. DOSE VOL. ml 1-3 Years Under 11 kg 0.2 mg 1.0 ml 4-7 Years 11 -15 kg 0.3 mg 1.5 ml 8-11 Years 16 -20 kg 0.4 mg 2.0 ml

Antivenom Polyvalent: to be administered IV Push, one vial a minute or diluted to 200 ml at 180 drops per minute (15-30 minutes) Monovalent: to be administered slowly 1 vial per minute Minimal Initial antivenom dosage Table: 3 Initial dosage If symptoms Additional Syndrome Venom Species Responsible Comments Antivenom persist after Antivenom 20ml Repeat with 20ml every hour PPS Cytotoxic Mozambique spitting cobra; 100ml Polyvalent 1 Hour until symptoms stop. Repeat with 20ml every hour PPS Cytotoxic Puff adder; Rinkhals 50ml Polyvalent 1 Hour 20ml until symptoms stop. Repeat with 20ml every hour PW Neurotoxic Black mamba, Snouted cobra 80ml Polyvalent 1 Hour 20ml until symptoms stop. Cytotoxic & 20ml Repeat with 20ml every hour Mixed PPS & B Puff adder 50ml Polyvalent 1 Hour Haemotoxic until symptoms stop. Mixed PPS & Cytotoxic & 20ml Repeat with 20ml every hour Rinkhals 50ml Polyvalent 1 Hour PW Neurotoxic until symptoms stop. Boomslang; Repeat with 10ml every 6 B Syndrome Haemotoxic 20ml Monovalent 6 hours 10ml Vine snake hours until symptoms stop

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Metoclopramide: Paediatric dosage: Age Dosage IV Frequency <6yrs 0.1mg/kg TID 6-14yrs 2.5 – 5mg/kg TID >14yrs 10mg TID

AIRWAY MANAGEMENT (Adult or Child) In case of a Mamba bite • Apnoeic patient • Ensure anatomical alignment (Open Airway) • Apply cricoid pressure • Ensure Initial Oxygenation • Secure Airway (depends on skill and availability of equipment) • Tracheal intubation or Laryngeal Mask Airway • Failure to secure way and adequate ventilation • Return to basic airway Technique • Unable to ventilate • Consider surgical Airway • Needle Cricothyroidotomy or Surgical Cricothryroidotomy • Ventilate

Vitamin K : for all patients who present with an ongoing coagulopathy six hours post the administration of antivenom. Adult and Paediatric: Vitamin K (1ml/1 mg) i.v.i. slow push over 5 minutes.

Sedation and Induction: Patient is placed on 100% O2 prior to commencement. Initiate sedation approx. 5 minutes prior to induction. Administer pressor approx. 1 minute prior to induction. Tidal Vol: 8-10 ml/kg Midazolam: 0.1 mg/kg (Paed max single dose 2.5 mg) Fentanyl: 1.5 mcg/kg Suxamethonium (succinylcholine) : 1.5 mg/kg

Paediatric Vital Signs AGE HR BP mmHg RR bpm Premature 120 -170 55 -75/35 -45 40 -70 0-3 month 100 -150 65 -85/45 -55 35 -55 3-6 month 90 -120 70 -90/50 -65 30 -45 6-12 month 80 -120 80 -100/55 -65 25 -40 1-3 years 70 -110 90 -105/55 -70 20 -30 3-6 years 65 -110 95 -110/60 -75 20 -25 6-12 years 60 -95 100 -120/60 -75 14 -22 12> years 55 -85 110 -135/65 -85 12 -18

Paediatric Fluid Maintenance Calculation WEIGHT Method A: Daily iv Requirements (ml/ 24 hours ) Method B: Hourly iv Requirements (ml/hour)

3-10 kg 100ml/kg 4ml/kg 10 -20 kg 1000ml + (50ml/kg for each kg over 10kg) 40ml + (2ml/kg/hr for each kg over 10 kg)

>20 kg 1500ml + (20ml/kg for each kg over 20 kg) 60ml + (1ml/kg/hr for each kg over 20 kg)

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Paediatric Fluid Maintenance Chart - Based on Weight

Weight kg Total Fluid Intake ml/hr Weight kg Total Fluid Intake ml/hr 3 12 20 60 4 16 25 65 6 24 30 70 8 32 35 75 10 40 40 80 12 44 45 85 14 48 50 90 16 52 55 95 18 56 60 and above 100

Endotracheal Tube Size Guide Size Recommended Patient Size Recommended Patient 2.5 Pre -term neonates 5.5 8 to < 10 years 3.0 ≥3 kg to < 8 months 6.0 Large child 3.5 8 months to 2 years 7.0 Adult Female 4.0 2 to < 4 years 8.0 Adult female/male 4.5 4 to < 6 years 9.0 Adult Male 5.0 6 to <8 years

First-aid for snakebite, Venom dependant. First-aid is site and situation specific. Species Venom First-Aid Antivenom Mozambique Spitting Cobra Elevation. Antivenom is Cytotoxic (Naja mossambica ) Do not use a pressure bandage or tourniquet Effective Puff Adder Cytotoxic and to a less Elevation. Antivenom is (Bitis arietans arietans ) extent, Haemotoxic Do not use a pressure bandage or tourniquet Effective Rinkhals Cytotoxic and to a lesser Keep limb lower than heart. Antivenom is (Hemachatus haemachatus ) extent, Neurotoxic Do not use a pressure bandage or tourniquet Effective

Stiletto Snake Elevation. Antivenom is Cytotoxic (Atractaspis bibronii ) Do not use a pressure bandage or tourniquet Ineffective.

Night Adder Cytotoxic and to a less Elevation. Antivenom is (Causus rhombeatus ) extent, Haemotoxic Do not use a pressure bandage or tourniquet Ineffective. Berg Adder Antivenom is Cytotoxic and Neurotoxic Pressure Bandage (Bitis atropos ) Ineffective. Black Mamba Pressure Bandage but if more than 30 minutes from a Antivenom is Neurotoxic (Dendroaspis polylepis ) hospital, Broad Tourniquet Effective Snouted Cobra Neurotoxic and to a lesser Pressure Bandage but if more than 45 minutes from a Antivenom is (Naja annulifera ) extent, cytotoxic hospital, Broad Tourniquet Effective Intermediate Shield Cobra Antivenom is (Aspidelaps scutatus Neurotoxic Pressure Bandage Ineffective. intermedius ) Boomslang Antivenom is Haemotoxic Pressure Bandage (Dispholidus typus ) Effective Vine Snake Antivenom is Haemotoxic Pressure Bandage (Thelotornis capensis capensis ) Ineffective

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Species – Venom – Syndrome & Description

Species Venom Syndrome Description Cytotoxic venom is generally composed of several digestive Mozambique enzymes and spreading factors, which result in local and systemic Spitting Cobra injury. Clinically, local effects progressing from pain and swelling (Naja to ecchymosis (bleeds under the skin) and bullae (watery blisters). mossambica ) Painful Progressive Swelling Severe generalized bleeding is not common. Cytotoxic PPS Syndrome Puff Adder Pain and swelling occurs almost immediately after the bite from a (Bitis arietans cytotoxic snake and gradually becomes worse, in the next few hours. arietans ) (Within 4 to 6 hours it will be more pronounced) It is often described as “cold fire”. Later shock develops and this may cause death. Non -spitting cobra and Black mamba envenomation is an extrem ely Black Mamba variable process. Most species cause profound neurological (Dendroaspis abnormalities (e.g., cranial nerve dysfunction, abnormal mental polylepis ) Progressive Weakness Syndrome status, muscle weakness, paralysis, and respiratory arrest).

Neurotoxic PW Syndrome Symptoms include mild to moderate pain and swelling. Snouted Cobra

(Naja annulifera ) Mamba bites are considered more serious than bites from other

elapid species. This is due to greater volumes of injected venom and

more rapid onset of neurotoxic symptoms. Mortality is also higher. This type of venom is slow in comparison with the other two types mentioned. Effects can be seen after as little as 1 hour but can take a few days to manifest. The venom causes irregularities in the victim’s blood, preventing it from clotting. A bleeding tendency Boomslang occurs starting with all the mucous membranes and progress to nose (Dispholidus bleeds, bruises, blood is found in the urine and vomiting of blood. typus ) Bleeding Syndrome Anaemia and shock may develop and eventually kidney failure may

Haemotoxic B Syndrome set in. Slight pain and discomfort and haemorrhage at sight of bite, Vine Snake dizziness and headaches are known to occur. (Thelotornis

capensis Death usually follows after 2 to 5 days. Antivenom can be capensis) administered after a few days and still work effectively however the kidneys would have been damaged by then. In the event that the antivenom is not obtained in time, whole blood and fresh freeze- dried plasma should be administered Mixed Symptoms include mild to moderate pain and swelling. Rinkhals Neurotoxic Mixed PPS & PW Syndrome Although mild neurotoxic effects have been mentioned to occur (Hemachatus and in Rinkhals bite, these have not been well documented. haemachatus) Cytotoxic Symptoms are predominantly cytotoxic.

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References/Further reading Blaylock RSM (1982). Snake bites at Triangle Hospital January 1975 to June 1981. Cent Afr J Med 28:1-11. Blaylock RSM (1999). Antibiotic use and infection in snakebite victims. S Afr Med J 89(8):874–76. Blaylock RSM (2000). Antibacterial properties of KwaZulu-Natal snake venoms. Toxicon 38 (11):1529–34. Blaylock RSM (2001). Normal oral flora from some Southern African snakes. Onderstepoort Journal of Veterinary Research 69:175–82. Blaylock RSM (2002). Acute adverse reactions to South African manufactured snakebite antivenom. Current Allergy & Clinical Immunology 15:107–13. Blaylock RSM (2003). Femoral vessel entrapment and compartment syndromes following snakebite. S AfrJ Surg 41(3):72–3. Blaylock R (2004). Epidemiology of snakebite in Eshowe, KwaZulu-Natal, South Africa. Toxicon 43 (2):159–66. Blaylock RS (2004). Snakebites. In: Kamel R, Lumley J (eds). Tropical Surgery, Westminster Publishing Ltd, London, pp. 1149–52. Blaylock RS (2005). The identification and syndromic management of snakebite in South Africa, SA Fam Pract 47:48–53. Blaylock RSM, Tilbury CR, Branch WR (2002). Anaphylaxis following exposure to snake venoms in South Africa. Current Allergy and Clinical Immunology 15(2):65–8. Broadley DG, Wüster W (2004). A review of the southern African “non-spitting” cobras (Serpentes: Elapidae: Naja). Afr J Herpetology 53:101–22. Chappuis F et al (2007). Protection against snake bites by sleeping under a bed net in south-eastern Nepal. Am J Trop Med Hyg 77(1):197–9. Coetzer PWW, Tilbury CR (1982). The epidemiology of snakebite in Northern Natal. S Afr Med J 62:206–212. Davidson RA (1970). Case of African Cobra bite. Brit Med J 4:660. Dobiey M, Vogel G (2007). Venomous snakes of Africa. Frankfurt am Main, Edition Chimaira. (and review by DG Broadley. African Journal of Herpetology 56(2):179–81. Kurnik D, Haviv Y, Kochva E (1999). A snake bite by the burrowing asp, Atractaspis engaddensis. Toxicon 37:223-7. Lath NK, Patel MM (1984). Treatment of snake venom ophthalmia. Centr Afr J Med. 30 (9):175-6. Malasit P et al (1986). Prediction, prevention and mechanism of early (anaphylactic) antivenom reactions in victims of snake bites. BMJ 292:17-20. Mars M, Hadley, GP (1998). Raised intracompartmental pressure and compartment syndromes. Injury 29(6):403–11. Mars M, Hadley GP, Aitchison JM (1991). Direct intracompartmental pressure measurement of snakebites in children. S Afr Med J 80:227-8. Matsen FA (1980). Compartmental Syndromes. Grune and Stratton, New York. Müller GJ (2005). African Snakes In: Brent J et al, eds, Critical Care Toxicology: The Diagnosis and Management of the Critically Poisoned Patient. Elsevier Mosby, Philadelphia, pp. 1159–70. Norris RL et al (2005). Physicians and lay people are unable to apply pressure immobilization properly in a simulated snakebite scenario. Wilderness Environ Med. 16(1):16–21. Oram S et al (1963). Renal cortical calification after snake bite. Br Med J 22;1(5346):1647–8. Sano-Martins IS et al (1994). Reliability of the simple 20 minute whole blood clotting test as an indicator of low plasma fibrinogen concentration in patients envenomed by Bothrops snakes. Toxicon 32:1045–50. Schire L, Muller GJ, Pantanowitz L (1996). The Diagnosis and Treatment of Envenomation in South Africa. South African Institute for Medical Research, Johannesburg. Sezi CL, Alpidovsky VK, Reeve MI (1972). Defibrination syndrome after snakebite. East Afr Med J 49:589–596. Simpson ID et al (2008). The Ebbinghaus retention curve: training does not increase the ability to apply pressure immobilisation in simulated snake bite-implications for snakebite first aid in the developing world. Trans R Soc Trop Med Hyg [Epub ahead of print]. Strover HM (1967). Report on a death from Black Mamba bite (Dendroaspis polylepis). Cent Afr J Med 13(8):185-6. Strover HM (1973). Observations on two cases of snake bite by Naja nigricollis ss mossambica. Cent Afr J Med 19(1):12–13. Sutherland SK, Coulter AR, Harris RD (1979). Rationalisation of first-aid measures for elapid snakebite. Lancet i:183–186. Tilbury CR (1982). Observations on the bite of the Mozambique spitting cobra (Naja mossambica mossambica). S African Med J 61(9):308-13. Tilbury CR, Branch WR (1989). Observations on the bite of the southern burrowing asp (Atractaspis bibronii) in Natal. S Afr Med J. 75:327–31. Visser J, Chapman DS (1978). Snakes and snakebite. Venomous Snakes and Management of Snakebite in Southern Africa. Purnell, Cape Town. Warrell D (1999). Snakebite in sub-Saharan Africa, African Health July: 5–9. Warrell DA (2008). Unscrupulous marketing of snakebite antivenoms in Africa and Papua New Guinea: choosing the right product-“What’s in a name?” Trans R Soc Trop Med Hyg Mar 20; [Epub ahead of print]. Warrell DA, Ormerod LD (1976). Snake venom ophthalmia and blindness caused by the spitting cobra (Naja nigricollis) in Nigeria. Am J Trop Med Hyg 25:525–29. Warrell DA, Ormrod LD, Davidson N McD (1975). Bites by the puff adder (Bitis arietans) in Nigeria, and value of antivenom. Br Med J 4:697–700. Wilkinson D (1994). Retrospective analysis of snakebite at a rural hospital in Zululand. S Afr Med J 84 (12):844–47. World Health Organization (1981). Progress in the characterization of venoms and standardization of Antivenoms. WHO Offset Publication No 58. World Health Organization, Geneva.

World Health Organization (2010). WHO/SEARO Guidelines for the prevention and clinical management of snake bites in the Africa. WHO/AFR/EDM/EDP/10.01

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