SNAKE BITE AND ITS MANAGEMENT

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INTRODUCTION

The Indian subcontinent is home to more than 230 species of snakes of which some are poisonous. In 4 families of venomous snakes, 6 species are responsible for snakebites & are medically important in India.

They are :-

1.Elapidae.    Represented by   * Cobras    a. King Cobra (Ophiphagushannah)

                                                                           b. Common Cobra (Naja Naja)

                                                       * Krait. (Bungarus ceruleus)

2. Hydrophilidae - Seasnakes.

3. Viperidae - Russel viper/Saw scaled vipers.

4. Atractasipidae.

            Here the epidemiology, pathogenesis, clinical features and managements are discussed.

EPIDEMIOLOGY

It is widely agreed that India contributes the largest share to the annual worldwide mortality due to snake bite. Figures of mortality range from 15000,to 40,000/year in India. Hospital records the sole source of most snakebite likely to over represent the more seriously envenomed patients. As in developing countries like India 80% of victims first consult traditional healers, so population survey gives most accurate picture of diagnosis than hospital record. First of all it was SWAROOP STUDY which reported about 200,000 bites/yr and 15,000 deaths as far as back in 1954. based on epidemiologic survey of 26 villages with a total population of 19,000 in Burdwan Dist. of W.B. HARI et all worked out an annual incidence of 0.16% and mortality of 0.061%. Myanmar has the highest snake bite mortality in the world. Maharastra has highest incidence of snakebites i.e 70bites per 100,000 population/year, with mortality of 2.4/ 100,000 per year. Bengal, Tamilnadu , UP & Kerala, are  other states with large no of snake bites.  Chippaux study shows marked increased frequency   of   - illegitimate bite in Developed countries and hazardous bite in developing countries.

Age & Sex

Though all age groups of both sexes are the victims majority  are 11-50 years of male suggesting special risk in outdoor activities. Males are victimized twice or thrice than females.

Time & Seasonal variation:-

Maximum incidence between 4.00pm to midnight (varies with outdoor activities). During rainfall & epidemics after floods and natural disaster.

Site of bite:-

Most frequent site of bite – Lowerlimb(2/3^rd ) of which 50% occur in feet alone.

Host factors:-

Occupational hazards- for farmers, harder,  hunter & fisherman.

Morbidity & mortality:-

Depends upon the species of snake involved as estimated fatal dose of the venom varies with species.

 Severity of Envenoming:-

Depends upon the dose of venom injected, composition & potency of venom, number & depth of bites, age of the victim, site of bite, nature, timing & quality of first aid & medical treatment.

PATHOPHYSIOLOGY OF OPHITOXEMIA:-

Most complex of all poisons are mixture of enzymatic & nonenzymatic compound, nontoxic proteins including carbohydrates & metals.

Enzymes – It is a constitute of 20 different enzymes including phospholipase. A₂ B, C, D, hydrolases, phosphatases, proteases, esterase, Acetyl choline esterase, transaminase, hyaluronidase, phosphodiesterase DNAse RNAse etc.

Nonenzymatic compounds are               - Neurotoxins

                                                             - Haemorrhagins.

Different species have different proportion of most of it. So they are formerly categorized as neurotoxic, haemotoxic, myotoxic but strict categorization is not essential

·          Neurotoxins     

Cobra – Cobrotoxin & bungarotoxin causes postsynaptic blokage (at moter end plate release of Ach).

Krait – B bungarotoxin causes pre synaptic blockage

Viper – Acetylcholine esterase causes breaksdown of Ach.

·          Cardiotoxins

Cobra & Taipan – cardiotoxins causes myocardial depression and cardiac arrythmias.

·          Vasculotoxins

 Viper – Viper venom – affects coagulation pathways at several points. Activates factors V, IX, X, XII,  platelets & protein C & fibrinolysins.

Haemorrahgins – damages endothelium to produce spontaneous bleeding, potentiates platelet aggregation & favours  vasodilation.

·          Myotoxins

Sea snake  - Myotoxins produces muscle necrosis, myoglobinuria, hyperkalaemia.

·          Nephrotoxins

Vipers – Indirectly damage renal system and causes prolonged hypotension, hypovolumia  and hyperkalaemia/DIC/direct  damage/rhabdomyolysis.

·          Locally affecting toxins are protease, phoshpolipase 2, polypeptide toxins, hyaluronidase, histamine/brady kinin, hydrolanse

·          Proteolysis

(Damages RBC, leucocytes & platelet membranes & vascular endothelium & other membranes.)

       Increase Vascular permeability – Local effects, (swelling, edema inflammation, gangrene).

Systemic effects.

                              (Hypoalbuminemia)  (hypotension) (shock)

CLINICAL FEATURES

              I.      Snake bites with no manifestations:

Confirmed bites with no manifestations – Drybites by poisonous snakes and bite by non poisonous snakes, Large no of studies show that a lot of poisonous bites do not  cause symptoms, Banerjee – noted 80% of victims have no evidence of envenomations.  Reid also states that over 50% of individual bitten by poisonous snakes escape with hardly any feature of poisoning, Stainly’s 117 out of 200 cases showed envenomation, Lamb states that 30% of cobra bites are superficial.

           II.      Local  manifestations :-

Physiological trauma is the earliest. Local reactions are marked in both families of elapidae and viperadae ( krait is the exception). Local reactions are noted within 6-8 mins but may have onset upto 30min & develop upto 24 hrs. Local pain , with radiation & tenderness and the development of small reddish wheal are first to occur followed by oedema, swelling & appearance of bullae progressing  rapidly involving trunk. Tingling, numbness over tongue, parasthesia around wound local bleeding including petechial & purpuric rash – more common in viperbites.  Regional lymphadenopathy is an early & reliable sign. Intercompartmental syndrome- occur in 10% of cases. Necrosis of skin, subcutaneous tissue & muscle causes increased intercompartmental pressure  which leads to  pain & anasthesia on stretching of intercompartmental muscles.  Severe pain, absence of arterial pulses and cold segment of limbs is due to thrombosis of major arteries which may lead to  dry gangrene. All the above features of local reactions are evident in elapidae but the gangrene is mostly wet gangrene. In rare instances patients may have – Raynaud’s phenomenon/ secondary infection/ tetanus/ gas gangrene.

III.    Systemic Menisfestations:

The most common and earliest symptom following snake bite is fright of unpleasant & rapid death. Victim attempts flight  which unfortunately results in enhanced systematic absorption of venom leading to  psychological shock & even death . Fear may cause transient pallor, sweating & vomiting.

Time of onset of systemic poisoning in cobra – 5 min to 10 hrs, Viper – 20 min to several hrs and Sea snake – almost always within 2 hrs.

Systemic manifestations depend predominantly on the constituents of the venom of that particular species as neurotoxin (cobras & kraits) haemorrhagin(vipers) myotoxin(sea snake), but strict categorization is not valid.

a)             Neurotoxic features  

Usually within 6 hrs  but may be delayed.  Symptoms are  usually preceded  by preparalytic syndromes which includes vomiting, blurred vision, drowsiness , heaviness of head, tingling sensation of mouth. Paralysis first appears as bilateral ptosis followed by bilateral opthalmoplegia, followed by paralysis of muscles of palate jaw, tongue , larynx , neck & muscles of deglutition . Muscles innervated by cranial nerves are involved earlier. Pupils react to light till terminal stage. Reflexes are not affected usually & preserved till late stages. Muscles of diaphragm are involves late which accounts for terminal respiratory paralysis.  Onset of coma is variable ( may progress to coma in 2hrs).

b)            Cardiotoxic features:-

Include tachycardia, hypotension, & ECG changes. 25% of viperbite include rate/rhythm/bloodpressure fluctuation. Sudden cardiac arrests may occur due to dyselectrolytemia. Though nondyselectrolytemia MI has also been seen.

c)             Haemostatic abnormalities:-

One case of nonbacterial thrombotic endocarditis-reported from, PGI Chandigarh. Bleeding from the punctured wound is the earliest feature, Blood do not coagulate due to consumption coagulopathy &haemorrhagins produce widespread bleeding detected as bleeding gum, nose, GIT (haematemesis & melaena), Urinary bladder (haematuria). Consequent to bleeding hypotension & shock occurs. Intracerebral haemorrhage may occur. Subarachnoid haemorrhage is reported in 5 in 200 cases of  Saini’s series in Jammu,(most were elderly).

d)             Nephrotoxicity:-

In a series of study of Clarke out of 40 viper bites renal failure was detected in 3. The extent of renal abnormalities is correlated with the amount  of coagulation defect . However renal defect persisted for several days after coagulation defect normalized, suggesting that multiple factors are involved in venom induced ARF.

e)             Hypotension syndromes :-

Due to increased capillary permeability – menifested by serous effusions/ pulmonary edema/ haemoconcentration/hypoalbuminemia/shock.

f)               Pregnency outcomes:-

 Almost all pregnant abort or present with APH/PPH.

g)             Rare outcomes-

Hypopitutarism, bilateral thalamichaematoma, hysteric paralysis.

LABORATORY DIAGNOSIS:-

·      History- Patient usually gives history of snakebite but it may be absent in kraitbite        (painless). Although fangmarks are essential fatal envenoming do occur without identifiable marks.

·      Cell counts – Neutrophillic Leucolytosis

-       Anaemia

-       Thrombocytopenia

-       Haematocrit – Initially ( haemoconcentration), Later ( haemolysis).

·      Coagulation profile          -  Prolonged clotting time

-         Prolonged  prothrombin time.

-         Fibrin Degradation products ( >80 mg/dl).

·       Simple bedside test  

(1)    Tourniquet test – Torniquet pressure of 100 – 120 mm of Hg is applied for 5 minutes – (+ve) if >5purpuric spots.

(2)    Whole blood clotting test :- 5ml of blood taken in clean, dry test tube- undisturbed for 20 min – seen for clotting.

(3)    Clot quality observation test (Clot retraction test):- seen for clotting after one hour

·      Urine Analysis

All snake bite patients should be advised to evacuate bladder at first aid & urine  examined for microscopic haematuria. It could also reveal proteinuria, haemoglobinuria or myoglobinuria.

·      Features of Azotemia  S.Urea , S.creatinire may be raised.

·      Metabolic parameters:- Hyperkalaemia, Hypoxemia, Respiratory acidosis may occur

·      Myotoxicity is evidenced by – Raised Sr.CPK, & transaminase .

·      ECG shows – Nonspecific alteration in rate, rhythm, predominently bradycardia, menifestation of hyperkalemia.

·      X-ray chest – To rule out pulmonary edema/Infarction/bronchopneumonia/pleural effusion

·      CT scan - May be required if suspision of Intracerebral bleeding,

·      Immunodiagnosis

Detection of venom antigens in bodyfluids –

            Used for -    Pathophysiology

-        Assessment of first aid

-        Antivenom dose monitoring.

ELISA test – (venom detection kits) - Highly sensitive but not specific.

MANAGEMENT

1. First aid:-

Reassurance (to flight & fright response), Immobilisation of bitten limb, No tampering of the wound is best (Reid).  Aim should be to transfer the patient to nearest hospital as quickly as passively as comfortably as possible.

Controversial first aid methods which are :-

·                Local incision, excision of bitten skin , cauterization, amputation of digits

It has been proved from animal studies  that all these methods do not decrease systemic envenomation, rather potentates bleeding introduces infection damage tissues.

·                Suction by mouth as shown in Indian cinema has been rejected by its questionable efficacy while some advocate large amount of venom can be aspirated by this method if approached within seconds.

·                Introduction of chemicals are worthless ( Nowhere recommended  in any textbooks& therapeutics,  rather rejected by Mansoon)

2. Use of tourniquets, compressionpads, bandages (controversial):-

Manson – Tight tourniquets have been responsible for terrible morbidity &  mortality in snake bite victims & should not be used .

Sautherland (Australia)- advocated a pressure  immobilization method by crepe bandaging proved effective in limiting absorption of venom ( applies p.of 55of hg). It is just tightly as sprained ankle starting from toes & fingers & incorporating a splint. It should be binded so tightly that only lymphatic circulation is obliterated not arterial. One finger should be introducible between the affected part & tourniquet. Use of tourniquets may be dangerous as they can cause gangrene, fibrinolysis, bleeding from occluded limbs, peripheral nerve palsy, compartmental ischaemia , intensification of local reaction. So general consensus in Western countries is to use crepebandage  & splints in Elapidae and  Sea snakes bites and to be avoided in Viperbites, which are responsible of intense  local reactions. Clinical trials are needed to prove the efficacy of tourniquets & Compression bandage. The patient should be transferred in Lt. Lateral decubitus position to prevent aspiration.

3. Drugs :-

Reid advocated pain relief with placebo was as effective as NSAIDS. Gellert- experienced that codeine sulfate should be given to calm the patient & to reduce autonomic hyperactivity. Vomiting – can be treated with chlorphromazine ( 25-50mg IV infusion.) Others symptoms like syncope , shock, angioedema if supervene 0.1% adrenaline S/C can be given as first aid .

4. Specific Therapy :-

A. ANTIVENOM :-

Decision – In the management of snakebite, the most important clinical decision is whether to give antivenom therapy. For only a minority of snakebite patient need it. It may produce severe reactions & it is expensive & often in short supply.

Preparation:- They are prepared by immunizing horses with venom of poisonous snakes & extracting serum & purifying it . They may be species specific monovalent form/ poly valent form . Supplied as dry powder & reconstituted with DW or NS.

INDIA – C.R.I. Kasaulli – Antivenom against  4 medically important species are available.

Hopkins institute Pune – Against 30 species are available.

INDICATIONS OF ANTIVENOM TREATMENTS 

a)       Systemic envenoming

Neurotoxicity (ptosis, opthalmoplegia), incoagulable blood indicating consumption coagulopathy / DIC, spontaneous systemic bleeding ( from gingival sulci , nose), hypotension ( shock), generalised rhabdomyolysis. ( stiff tender painful muscles darkurine, myoglobinuria), impaired consciousness.

b)      Severe  local envenoming

Extensive local swelling ( > ½ of bitten limb), rapidly evolving local swelling, bites on fingers and toes, wider range of indication are prescribed in wealthy countries.

Contraindications Atopic patients & those previously had reaction with equine antiserum.

Prediction of antivenom reaction :- Hypersensitivity testing by intradermal or S.C. injection of diluted antivenom have no predictive  value for early and late antivenom reactions. However these tests delay the start of treatment & are not without risk.

Prevention of antivenom reactions:-

Desert et all advocated in their trial that significant reduction in ASV reactions (from 12.5 to 30%) if the patients are given adrenaline subcutaneously (0.1% of adrenaline).

It is a dictum that it is never too late to give antivenom as long as signs of venom persists (it can be given from 2 days of seasnake bite to many days after viperbite proved by Saini’s study) .

Average requirements of dose in various studies:-

Suggestive tentative schedule:-

·          Over various parts of the country recommended doses are:-

Viper – Initial dose – 20 to 100 ml

            Repeat dose – 20 to 50 ml every (4-6) hr till CT is normal

            Recurrence of coagulation defect – 20 to 50 ml.

Cobra/Krait – Initial dose – 200 ml preferred (100 ml effective)

                        Repeat dose – (50-100)ml 4 to 6 hrly - Until neurotropic sign disappear

King Cobra – (100-150) ml Monospecific ASV

Fab based Antivenom alt. to IgG

Dart et al 99   (1) It largely reduces the antivenom reaction

(2) Effectively reverses coagulation abnormalities.

However it requires repeated doses as ½ life is<12 hrs

Antivenom Reactions

B. HYPOTENSION SHOCK – Fresh blood is ideal

-         Ionotropic support

-         I.V Hydrocortisone ( in delayed hypotension )

C. NEUROTOXICITY

·          Bulbar, respiratory paralysis – cuffed endotracheal intubation / tracheostomy.

·          Complete respiratory