Management of Animal bites :- Poisonous snake bite

Basic First Aid :

• Immediately seek medical assistance especially if the area changes color, begins to swell or is painful
• Don’t try to capture the snake. Try to remember its length, eyes, color and shape. If it’s safe you can try to take a photo with a camera or phone as it may aid snake identification
• Keep the person calm and still to stop further spreading of venom. Remind the victim that most snake bites are not fatal
• If the bite is on the limbs, immediately remove any rings, bracelets, shoes or watches. In case swelling occurs loosen any tight clothing to avoid cutting off blood supply that may lead to gangrene, which can be fatal or result in amputation of the limb. Splint or use a sling on the bitten limb to restrict movement
• Have the person lie down, if possible, so that the bite is at or below the level of his heart. Raising it can cause venom to travel through the body quicker; Having it hanging, can increase swelling.
• Clean the wound and cover it with a clean, dry dressing
• Don’t use a tourniquet or apply ice because it may cause tissue ischemia and gangrene respectively
• Do not give aspirin, ibuprofen or other pain relievers to the victim
• Avoid the many harmful and time-wasting traditional first-aid treatments such as local incision or excision of puncture sites, suction by mouth, administration of potassium permanganate as they are potentially harmful and none has any proven benefit.
• In suspected neurotoxic cobra or mamba bite, especially if the patient is far from medical help apply a broad pressure crepe bandage or clothe over the bite, starting from below the bite. Immobilize the bitten limb with a sling but the tightness should allow for some blood flow.

Notice to Doctor :

• Assess for signs of poisoning: difficulty swallowing or breathing, muscle weakness or paralysis, or bleeding disorders.
Administer anti-tetanus inj if none has been given in the last 5years.
• Administer polyvalent antivenom and other anti-inflammatory agents if necessary.
• The bandages should be left in position until appropriate antivenom and resuscitation equipment has been assembled.
• Avoid crepe or other bandaging in all cytotoxic bites.
• Assess regularly (q 10-15 min) patents suspected of neurotoxic snake bites for the development of complications.
• Start CPR if the patient is unresponsive and no respiratory movement is detectable.
• Administer intravenous fluids (preferably normal saline) to shocked, hypotensive patients. Vasopressor agents, such as dopamine ,noradrenaline or phenylephrine may need be administered if there is inadequate response.
• Control pain with paracetamol or or paracetamol/codeine combinations (monitor for respiratory depression)

Toxicology:

Most of venom content is protein. Each venom contains hundreds of different proteins: enzymes (constituting 80-90% of viperid and 25-70% of elapid venoms), non-enzymatic polypeptide toxins. Venom enzymes include digestive hydrolases, hyaluronidase, and activators or inactivators of physiological processes, such as kininogenase. other common venom enzymes includes L-amino acid oxidase, phosphomono- and diesterases, 5’-nucleotidase, DNAase, NAD-nucleosidase, phospholipase A2 and peptidases (World Health Organization, 2010).
Zinc metalloproteinase haemorrhagins: these enzymes damage vascular endothelium resulting in bleeding.
Venoms of Vipers and some Elapids contain serine proteases and other procoagulant enzymes that are thrombin-like or activate factor X, prothrombin and other clotting factors. These enzymes causes clotting and fibrin formation in the blood stream. However, most of the fibrin clot is broken down immediately by the body’s own plasmin fibrinolytic system. Occasionally within 30 minutes of the bite, the levels of clotting factors are so depleted that blood becoming incoagulable (“consumption coagulopathy”) (World Health Organization, 2010).
Phospholipase A2 (lecithinase): Damages mitochondria, red blood cells, leucocytes, platelets, peripheral nerve endings, skeletal muscle, vascular endothelium, and other membranes, produces presynaptic neurotoxic activity, opiate-like sedative effects, leads to the autopharmacological release of histamine and anti-coagulation.
Acetylcholinesterase:Although found in most elapid venoms, it is rarely involved clinically. Hyaluronidase promotes the spread of venom through tissues.
Proteolytic enzymes (metalloproteinases, endopeptidases or hydrolases) and polypetide cytotoxins Increases vascular permeability resulting in oedema, blistering, bruising and necrosis at the site of the bite.
Venom polypeptide toxins (“neurotoxins”) such as (α) neurotoxins (a-bungarotoxin) bind to acetylcholine receptors at the motor endplate. Presynaptic (β) neurotoxins such as β-bungarotoxin, crotoxin, and taipoxin release acetylcholine at the nerve endings at neuromuscular junctions and then damage the endings, preventing further release of transmitter
Snake venom is categorized according to the primary action of venom:
1. Cytotoxins contain digestive hydrolases (proteolytic enzymes), phospholipases and polypeptides that destroy cell membranes, skeletal muscle and other tissues thereby increasing the permeability of the vascular endothelium. The results of increased vascular permeability is local swelling, hypovolaemia (may cause hypovolemic shock) and blistering which may lead to irreversible death of tissues (necrosis/gangrene). Spontaneous sloughing of dead tissue may then ensue (Muller et al 2012).
• Examples of snakes producing cytotoxic venoms: Spitting cobra,Puff adder, night adders, Gaboon adder, rinkhals, Hemachatus haemachatus.
2. Hemotoxins affects activation factors II(prothrombin), IX and X leading to severe consumptive coagulopathy which develops within 4-24 hrs (Muller et al 2012).
• Examples of snakes producing hemotoxins:boomslang,savanna twig/vine snakes).
3. Neurotoxin such as neurotoxic cobras contain polypeptides that competitively inhibit cholinergic nicotinic receptors at neuromuscular junctions leading to a curare-like paralysis. Mamba venom, in addition, contains polypeptide toxins with parasympathomimetic activitiy which facilitate the release of acetylcholine from the nerve endings (dendrotoxins), as well as anti- acetylcholinesterases (fasciculins).
• Examples of snakes producing neurotoxins: Non spitting cobras-Anchieta’s Egyptian cobra , banded or snouted cobra, forest, black and white-lipped cobra and Cape cobra; Mambas-black mamba and green mamba (Muller at al 2012).
4. Mixed Cytotoxic and neurotoxic venoms
• Examples snakes producing mixed poisons: Rinkhal, berg adder, peringueys’s adder, desert mountain adder, garter snakes, shield-nose snake (STG for South Africa, 2012)
Lymphatic system plays a key role in transport of toxins from the periphery to the circulation. In fact, adenopathy in nodes draining the bite site is mostly an early sign of absorption of venom.

Clinical Manifestation:

• Most snakes are rarely identified, clinician’s early recognition of systemic envenomation or toxidromes below,for prompt interventions is crucial in reducing morbidly and mortality from envenomation ( (STG for South Africa, 2012).
• The general manifestation of systemic envenomation includes the following:
– Difficulty in breathing
– Difficulty in swallowing or speaking
– Diplopia and ptosis
– Progressive weakness
– Cardiovascular derangement (hypotension, shock, arrhythmias)
– Spontaneous bleeding or abnormal blood clotting parameters
– Progressive tissue necrosis or swelling involving more than half the bitten limb within a few hours after the bite or progresses to the elbow/knees within 4 hrs
The clinical presentation of two major class of snakes- Elapid and Viperids
1. Elapid snakes (Cobra, Mamba)
Their venoms may contain both neurotoxins and cytotoxins.
Clinical manifestations
The early manifestation includes (within 15 min):
• Severe pain at puncture site
• Blisters
• Large areas of skin destruction near the puncture site.
• Descending paralysis of the muscles in the face, lips, tongue and throat that results in diplopia, ptosis, slurred speech and difficulty in swallowing
• Muscle weakness
• Headache
• Cold skin
• Frequent nausea & vomiting
• Dizziness.
The delayed manifestation includes (after 15min)
• Paralysis of neck and limb muscles
• Paralysis of respiratory muscles
• Low blood pressure and slow pulse
• Coma.
. 2. Viperid snakes (Puff adders, Rattlesnakes, Boomslang, Savanna twig snake)
Their venoms affect the blood, circulatory system and cause severe skin and muscle damage.
Clinical manifestations
• Pain near the puncture site
• Swelling near the bite site that spreads quickly to the whole limb
• Nausea and vomiting
• Sweating
• Spontaneous hemorrhage: bleeding gums, nose bleeding
• Constant oozing of blood from puncture sites
• Abdominal pain and diarrhea
• Blood in vomit, urine and stools.
• Sloughing of the skin which then permits secondary infections
• Kidney damage
• Lung oedema,
Snake venom ophthalmia (Eye envenomation) causes intense conjunctivitis and bullous corneal erosions, complicated by secondary infection, anterior uveitis, corneal opacities and permanent blindness (Muller et al 2012)
Laboratory investigation
• Heamotoxic venoms: Full blood count including clotting profile eg 20min whole blood clotting test
• Neurotoxic venoms: ABGs, Respiratory function tests, ECG
• Cytotoxic venoms: Raised creatine kinase and other muscle derived enzymes
• Kidney function tests –Serum creatinine, Electrolites
Coagulation parameters, CBC with platelet counts should be repeated periodically if Hemotoxins are suspected-in moderate to severe hematoxicity Coagulation parameters (PT 50-100 seconds, PTT 75-100 seconds, platelets 20,000-50,000/µL, fibrinogen < 50 mcg/mL)

Clinical Management :

The patient’s vital signs should be monitored frequently the first 48 hours after the bite for evidence of hypotension, bradycardia, or circulatory shock
• Before referring neurotoxic snake bites, apply a simple firm pressure bandage (preferably crepe bandage for limb bites) over and above the bitten area to partially occlude the capillaries and lymphatic vessels. In addition, immobilize joints on either side of the bitten area using sling (hand) and splint to restrict venom absorption.
•After one complete vial has been infused remove the splints and crepe bandage slowly over a period 10 minutes. If symptoms progress rapidly, reapply the bandage, wait 10 minutes, and then again release the bandage slowly over 10 minutes while antivenom administration is continuing
• Keep the victim and the limb completely at rest.
• Cleanse wound with a disinfectant such as chlorhexidine 0.05% and provide a prophylactic such as oral Co-amoxiclav for 5 days. Administer tetanus toxoid IM 0.5ml (STG South Africa,2012;Muller et al 2012)
• Relieve pain with paracetamol or opioids in severe cases (monitor for respiratory function depression by opiods). Subcutaneous. intramuscular or even intravenous pethidine, initial adult dose 50-100 mg; children 1-1.5 mg/kg; or morphine, initial adult dose 5-10 mg; children 0.03-0.05 mg/kg. Avoid NSAIDS which might aggravate haemostatic disorders or renal failure (STG for South Africa,2012)
• Give IV fluids preferably normal saline (250ml/hr) to support perfusion. Pressor agents, such as dopamine or phenylephrine may be administered.
• Administration of antivenom may cause life-threatening allergic reactions: prophylaxis is indicated for hypersensitive patients (15-30min early):
 IM adrenaline 0.25ml of 1:1000 or 0.01mg/kg in children.
 IM Hydrocortisone 100mg- delayed onset of action.
 IM antihistamine(H1)- suppresses minor allergic reactions but not prevent serious.
Should anaphylactoid reactions occur (sweating, nausea, vomiting, urticuria and hypotension) immediately discontinue the administration of antivenom, and treat symptoms with Iv adrenaline 0.1% (1:1000) 0.5-1ml and 0.01 mg/kg for children + Slow Iv promethazine 25-50mg in adults (contraindicated in children <2 years. As soon as the patient is stabilized, continue the antivenom infusion at a slower rate. (i.e. 120ml/hour) (STG for South Africa,2012, Muller, 2012).
• In case of delayed (after 5-24 days) hypersensitivity ie serum sickness presenting as itching, urticaria, fever, arthralgia, peri-articular swellings, proteinuria and sometimes neurological symptoms:
 Antihistamines (mild forms) and short course prednisolone (severe cases) (STG for South Africa,2012, Muller, 2012).
• For symptomatic patients or those bitten by confirmed venomous snakes should obtain immediately directly observed polyvalent antivenin 20ml – 150 mls depending on severity and venom type, in 100mls-500mls of normal saline: Administer the diluted antivenom at a rate as tolerated by the patient beginning at as slow infusion (≥1 ml/min) in the first 15min, thereafter increased gradually to about 250mls in 1 hr. Repeat after 2hrs if symptoms do not resolve. Further antivenom doses may be repeated every 6hrs until patient turns asymptomatic (STG for South Africa,2012) • Administer antivenin subcutaneously around the bite site in case of cytotoxins to prevent gangrene development.
• The patient should be monitored closely and blood products including whole blood, packed RBC’s platelets, cryoprecipitate, and fresh frozen plasma should be given when indicated(Fadare JO and Afolabi OA, 2012).
If the patient has evidence of respiratory paralysis, insert endotracheal tube or laryngeal mask airway. If there is evidence of respiratory failure, assist ventilation manually by anaesthetic (Ambu) bag or mechanical ventilator.
 In case anticholinergic syndrome is observed use IV bolus Neostigmine 2.5mg (children 0.03 – 0.07 mg/kg, maximum 2.5 mg) given together with atropine 1 mg or preferably glycopyrrolate 0.6 mg to counter severe muscarinic effects, such as bradycardia and bronchospasm . If symptoms improve demonstrated by increased muscle strength and/or improvement of ptosis repeat neostigmine 2.5 mg every 1 – 3 hours up to 10 mg/ 24 hours for adults. The paediatric maintenance dose is 0.01 – 0.04 mg/kg every 2 – 4 hours for children (Muller et al 2012).
For venom ophthalmia:
 Immediately irrigate the eye with large amounts of normal saline and consult an opthalmologist
 In case of a tightly closed eyelids administer eye drops of local anaesthtetic to facilitate irrigation  Do not administer Topical or systemic antivenom treatment  Examine for corneal abrasions by fluorescein staining/slit lamp examination.  In case of corneal erosions, administer antibiotic eye drops/ointment, mydriatics and apply an eye pad
 Daily slit lamp examinations are recommended until resolved.
• In case of puncture wounds overlying a bone, perform radiological imaging
• In case of acute kidney failure
 Perform haemodialysis or peritoneal dialysis.
 Expert surgical advice should be sought where necessary. Fasciotomy should not be carried out unless or until haemostatic abnormalities have been corrected. (Muller et al 2012).

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