SNAKE BITES

Case

• 5 year old girl was brought to ED with alleged snake bite over her left leg

• Occurred at 2pm and arrived to ED at 3pm• Child was playing near her house in Paya Jaras

when she was suddenly bitten by a small cobra like snake

• No bleeding or LOC• Left lower leg becomes painful and tender

The Culprit

• Upon arrival to ED, child appears alert and concious

• Not in shock, comfortableO/E• Pink, well hydrated, cooperative, not

tachypnoeic• Systemic examination was normal• HR 89, BP 110/56, SpO2 100% on air

• Noted 2 bite marks over Lt lateral maleolus with erythematous skin changes surrounding it measuring 5x5cm

• Her left leg was not oedematous• Pulses were palpable, able to move her toes,

sensation intact• The left leg was splinted for immobilization

• Admission to ward, noted 6 hours after bite , Lt lower foot was swollen and had bluish discoloration

• Swelling was increasing and has encroached mid shin, tender++, limited ROM

• FBC TW 9, Hb 12.3, PLT 256,PT/ApTT normal• She was also having spiking temperature

After 8 hours

• At 11pm, she was administered 1 vile of monovalen antivenom

• Subsequenlty started on IV Augmentin• On the following day, noted that swelling was

static and fever was slowly subsiding• BP remains stable• Serial FBC and coagulation profile remains

normal• Child remains alert and comfortable

• At D3 of bite, swelling has reduced and child was able to move her lower limbs

• She was also able to ambulate • Currently still in ward awaiting swelling to

resolve• No systemic involvement subsequently

Introduction

• Snakebite is a serious medical problem in Malaysia

• From 1978 to 2000, there were 55000 cases of snakebites recorded in the hospitals in Malaysia

• The mortality rate of snakebite in Malaysia is only 0.3 per 100000 population but the local necrotic effects of some venoms can cause prolonged morbidity or even crippling deformity

Types of snakes• In Malaysia and the coastal waters of the region, there are

at least 18 different species of venomous front fanged land snakes and more than 22 different species of sea snakes

• These venomous snakes belong to the following 5 subfamilies:1. Crotalinae: represented by the two genera Calloselasma and Trimeresurus.2. Elapinae: represented by the five genera Naja, Bungarus, Ophiophagus, Maticora and Calliophis;3. Laticaudinae, represented by the genus Laticauda4. Hydrophiini, represented by the six genera Enhydrina, Kerilia, Hydrophis, Thalassophis, Pelamis and Kolpophis5. Ephalophiini, represented by the only genus Aipysurus.

• not all snakes are venomous• In Malaysia there are approximately 40 species of

venomous snakes (18 land snakes, all 22 of sea snakes) belonging to two families:

- Elapidae – have short, fixed front fangs. The family includes cobras, kraits, coral snakes and sea snakes.

- Viperidae – have a triangular shaped head and long, retractable fangs. The most important species in Malaysia are Calloselasma rhodostoma (Malayan pit viper) and Trimeresurus genus (green viper)

• The Malayan pit vipers are common in the northern part of Peninsular Malaysia but are not found in Sabah and Sarawak

• Epidemiological studies showed that in Malaysia, bites were mainly due to four species of land snakes :

1)Calloselasma rhodostoma (Malayan pit viper), 2)Naja naja (Asian common cobra),3)Trimeresurus purpureomaculatus (shore pit viper) 4)Trimeresurus wagleri (Wagler’s pit viper)

Biochemical composition of Snake Venoms

• Dried snake venom contains mainly proteins (70-90%) and small amounts of metals, amino acids, peptides, nucleotides, carbohydrates, lipids and biogenic amines

• The protein components include enzymes and non-enzymatic proteins/polypeptides

• The main toxins in the venoms of elapid snakes (cobras, kraits and sea snakes) include: polypeptide postsynaptic neurotoxins, cardiotoxins and phospholipases A that may exhibit presynaptic neurotoxicity or myotoxicity

• The main toxins of crotalid (pit viper) snake venoms, on the other hand, are thrombin-like enzymes, hemorrhagic proteases and platelet-aggregation inducers

Elapid Venom Poisoning

• Elapid venoms (cobras, kraits and sea snakes) generally exhibit neurotoxicity and cardiotoxicity

• The earliest symptom of systemic elapid poisoning is a feeling of drowsiness or intoxication, which starts from 15 min to 5 hr after cobra bites

• Difficulty in opening the eyes (bilateral ptosis: eyelids may remain completely closed though the patient usually remains conscious until respiratory failure is advanced), speaking, opening the mouth, moving the lips and in swallowing follows within 1 to 4 hrs

• Breathing becomes increasingly difficult. In severe poisoning, respiratory failure sets in rapidly

Neurotoxicity

Neurotoxins block transmission at the NM junctionFlaccid/Respiratory paralysisAnticholinesterase drugsUnphysiologic drowsiness

• The neurotoxic effects are mainly at the postsynaptic level of the neuromuscular junction where the neurotoxins block acetylcholine receptors, thereby producing muscular paralysis and respiratory failure

• The major neurotoxins are usually basic polypeptides

• Cardiotoxicity is caused by polypeptide cardiotoxin that affects both excitable and non-excitable cells, causing irreversible depolarization of the cell membrane and consequently impairing the structure and function of various cells, thus contributing to muscle paralysis and leading to circulatory and respiratory failure and systolic arrest

• Cobra venom also causes extensive local necrosis, which requires treatment

• The local necrosis is presumably caused by the combine action of cardiotoxin and phospholipase A2

• Sea snake venoms contain both polypeptide neurotoxins (homologous to elapid neurotoxins) and myotoxins, which are basic phospholipase A2.

• The venom causes respiratory failure (neurotoxic effect), myonecrosis, myoglobinemia and acute renal failure

Renal failure/rhabdomyolysis

ATN: hypotension/hypovolemia, DIC, direct toxic effect on tubules, hemoglobinuria, myoglobinuria

Generalized rhabdo: Release of myoglobin, muscle enzymes, uric acid, K (presynaptic neurotoxins)

Local necrosis

Increased vascular permeabilitySwelling and brusingMyotoxins and cytotoxinsIschemia/ thrombosisVenom ophthalmia

Pit Viper Venom Poisoning(Viperidae)

• The venom of pit vipers causes local swelling, necrosis and systemic bleeding. Hemorrhage is the outstanding symptom of systemic pit viper poisoning

• Clotting defect usually accompanies hemorrhage. The commonest and earliest hemorrhagic manifestation is hemoptysis, which may be seen as early as 20 minutes after the bite

• Bleeding from the gum is less common and follows later after the bite

• Discoid ecchymoses appear in the skin an hour or so later

• Bleeding into the brain or other vital organ may be fatal.

• In severe cases, loss of blood may lead to hypovolemic shock

• In Malayan pit viper bite, the clotting defect is primarily due to thrombocytopenia aggravated by defibrination syndrome

Hypotension/shock

VasodilationDirect action of venom on myocardiumBleeding/hypovolemiaVipers: profound hypotension within minutes (ACE inhibitors)

• Defibrination syndrome is due mainly to the action of ancrod and partly to the activation of fibrinolysis causing fibrinogenolysis.

• Ancrod is a thrombin-like enzyme that acts directly on fibrinogen, releasing only fibrinopeptide A and fibrin monomers that form microclots.

• The microclots formed are easily lysed by plasmin digestion.

• Thus, ancrod causes continual microcoagulation of fibronogen but the microclots are virtually simultaneously lysed.

• In the presence of sufficient amount of ancrod, the rate of consumption of fibrinogen may exceeed its rate of synthesis in the liver, resulting in defibrination syndrome characterized by non-clotting blood.

• Thrombocytopenia is presumably due to the actions of platelet aggregation inducers.

• Aggregoserpentin, a non-enzymatic protein with molecular weight of 28160 has been purified, it activates platelets through the activation of endogenous phospholipase A2 or C.

• Anti-platelet protease may be also be involved.

• Hemorrhage is presumably due to the action of some metalloproteases that cause damage to vascular endothelium.

• L-amino acid oxidases and platelet aggregation inhibitor may also play a role in the hemorrhagic action of the venom.

Coagulopathy

Procoagulants and anticoagulantsIntravascular coagulation, consumption coagulopahty ThrombocytopeniaBleeding from old and recent wounds, gingiva, epistaxis, hematemesis, melena

Recovery times

• In the absence of necrosis, pain after viper bites rarely exceeds 2 weeks.

• When necrosis develops (in about 10% of cases) pain may remain severe for a month.

• Swelling usually resolves completely in 2-3 weeks. • Healing time of local necrotic lesions varies

greatly according to the extent of the lesion and the treatment given, but may requires 1-6 months or longer.

• In patients who do not receive specific antivenin, systemic symptoms generally subside more quickly than local symptoms.

• Neurotoxic symptoms usually resolve in 2-3 days.

• Hemorrhagic effects in viper bites are also short-lived and rarely exceed a week but the coagulation defect may persist for 3-4 weeks

Management

• The aims are to retard absorption of venom, provide basic life support and prevent further complications

Management Principles in Snake Venom Poisoning

General management of snakebite poisoning includes the following measures:

• adequate reassurance• immobilize the patient, particularly the bitten limb. If a tourniquet

has been applied, it should be released upon admission to hospital• Treatment of local lesion: the site of the bite and blisters should be

let strictly alone. Sloughs should be excised when local necrosis is obvious

• Treatment of shock• Tetanus prophylaxis: Tetanus antitoxin should be given in victims in

whom local necrosis developed• Specific antivenom should be given to patient with systemic

poisoning• All bitten patients, even without symptom of poisoning, should be

admitted to hospital for observation of at least 24 hours.

First Aid

In Hospital

Antivenom treatment

• Antivenom is the only specific treatment for envenomation.

• Give as early as indicated for best result. • However, it can be given as long as the signs

of systemic envenomation are still present• For local eff ect, anti venom is probably not

effective if given more than a few hours after envenomation

• Monospecific (monovalent) antivenoms are more effective and less likely to cause reactions than polyspecific (polyvalent) antivenoms.

• At present, however, monospecific antivenoms are available only against the three common types of Malaysian poisonous snakes (anti-Malayan pit viper, anti-Malayan cobra and anti-Enhydrina schistosa).

When to start antivenom?

Precautions

Antivenom reactions

Anticholinesterase

Supportive Treatment