Prevention

By Sandhya

If possible, avoid areas with snakes. Snakebites tend to happen most during warm weather and when the weather is beginning to cool off. When temperatures drop during the evening and night, snakes are attracted to buildings or other objects that hold heat from the day.

Before you visit, hike, or camp in a new area, do the following:

• Learn about the snakes that may live in the area.
• Learn the proper first aid for a snake bite.
• Know where the closest medical facility is in case of an emergency.
• Take a mobile phone with you.
• Leave snakes alone. Do not try to kill a snake or get a closer look. Stay at least 6 feet away from any snakes you see.

While Camping/Trekking :

• Wear long pants and boots.

• If you are camping in an area that has snakes with long fangs, layering with multiple pairs of pants help

• Stay on hiking paths

• Be cautious and alert when you climb rocks.

• Do not pick up firewood or rocks unless you are sure that you are out of a snake's striking distance.

• While walking through knee-high-grass, disturb the grass ahead with a stick to ensure that there are no snakes.

• Keep your bags/haversacks and boots above the ground. Preferably closed to deny entry to snakes, these are good overnight shelters for snakes.

• Before you wear your boots, hold its sole from toe side and bang the heel side on the ground several times to disturb any snake or biting and stinging insects inside and let it go.

• During summer, when there is a scarcity of water, snakes may be attracted to cool spots near tents. So do not wet the soil around tents.

• Make sure that you keep your tent zipped anytime that you aren't going into or out of it. If you are in your tent and want to see outside, make sure that your tent has a mesh window or door that you can zip and still see outside.

• Rats or other small animals are attracted to leftover food at night. Snakes are likely to follow rat tracks. Make sure that your leftover food is thrown far away at a designated area or buried.

• Remember that most snakes can swim very fast.

At Home

• Drain-pipe openings of your kitchen and bathrooms should have fixed mesh caps (not hinged) to deny easy entry to snakes, which may stray in while chasing rats or to hide in a cool and dark place.

• All windows should be fitted with mesh.

• The bottom of doors should have rubber lining, on the outside, to stop the gap, so to prevent any snake creeping in.

• There should not be any vegetation (such as creeper, bush or small tree) touching the walls of the house, which can help a snake to climb to windows and any ventilators.

• Disinfectants with pungent smells, like phenyl may be regularly used to wipe the floor and in the drains. Snakes avoid unpleasant smell.

• Use torchlight at night – all local poisonous snakes are active in the evening and at night.

Note:

• Snakes usually don't bite you without alarm:

- Cobra – lifts vertically front part of the body (1/3), opens hood, makes hiss, rushes to the aim.

- Vipers - make a spiral from a tail, bend like zigzag front part of the body, and make a strong hiss.

• If you meet a snake, go back slowly, don't do sudden movements, do not turn your back to the snake, do not run, and give the possibility for a snake to go away

• If you spot a snake, avoid it by walking slowly around it. Remember that snakes have a strike zone of 1/2 to 1/3 of their body length.
  

References:

http://www.livestrong.com/article/11036-prevent-snakebites-camping/

http://www.auroville.org/comingtoav/snakebite.htm

http://www.med.umich.edu/1libr/aha/aha_snakebit_crs.htm

http://www.bt.cdc.gov/disasters/snakebite.asp

TYPE OF POISONOUS SNAKE

BY SYUKRIAH

Pictures will be available on friday pcl..

Here are the five families of snakes that account for the majority of species:

• Colubridae -- The Colubridae family of snakes (known as colubrids) is by far the largest family, accounting for nearly two-thirds of the world's snakes. The vast majority of colubrids are non-venomous, though a few rear-fanged colubrid species are able to produce venom (such as the lyre snake of California). But even the venomous members of the Colubridae family are considered harmless to humans. So it's safe to say that colubrids, as a whole, pose no threat to humans.

• Boidae -- The Boidae family of snakes (known as boids) includes python and boa species. The three largest types of snakes in the world -- the anaconda, the reticulated python, and the African rock python -- are all members of the Boidae family. But smaller species like the royal python / ball python are also found in this family of snakes. All boids are non-venomous, powerful constrictors. Thus, they rely on strength instead of venom to kill their prey.

• Elapidae -- The Elapidae family of snakes (known as elapids) includes cobras, mambas, coral snakes and taipans. All elapids are venomous, and some of the most venomous snakes in the world are found within this family. Elapids produce a neurotoxic venom that attacks the central nervous systems (breathing) of their prey).

• Viperidae -- The Viperidae family of snakes (known as viperids) includes rattlesnakes, vipers, adders and other species. All types of snakes in the Viperidae family are venomous. In the United States, most venomous snakes species fall within this family (including all rattlesnakes, the copperhead, and the water moccasin). The coral snake (and elapid) is one of the only venomous snakes in the U.S. that is not in the Viperidae family. Nearly all members of this family produce hematoxic venom that attacks the tissue and blood of their prey.

• Hydrophiidae -- As the name suggests, the Hydrophiidae family includes sea snakes. Most sea snakes are venomous, and some species produce an incredibly powerful venom, a drop of which could kill a grown man. Fortunately for humans, sea snakes are reluctant to bite unless provoked (though you should still leave them alone).

http://www.reptileknowledge.com/articles/article9.php

Pathophysiology of Snake Bite

Daksha

Snake’s Venom

Venom is produced and stored in paired glands below the eye. It is discharged from hollow fangs located in the upper jaw. Fangs can grow to 20 mm in large rattlesnakes. Venom dosage per bite depends on the elapsed time since the last bite, the degree of threat the snake feels, and the size of the prey. The nostril pits respond to the heat emission of the prey, which may enable the snake to vary the amount of venom delivered.

Coral snakes have shorter fangs and smaller mouths. This allows them less opportunity for envenomation than the crotalids, and their bites more closely resemble chewing rather than the strike for which the pit vipers are famous. Both methods inject venom into the victim to immobilize it quickly and begin digestion.
Venom is mostly water. Enzymatic proteins in venom impart its destructive properties. Proteases, collagenase, and arginine ester hydrolase have been identified in pit viper venom. Neurotoxins comprise the majority of coral snake venom. Specific details are known for several enzymes as follows: (1) hyaluronidase allows rapid spread of venom through subcutaneous tissues by disrupting mucopolysaccharides; (2) phospholipase A2 plays a major role in hemolysis secondary to the esterolytic effect on red cell membranes and promotes muscle necrosis; and (3) thrombogenic enzymes promote the formation of a weak fibrin clot, which, in turn, activates plasmin and results in a consumptive coagulopathy and its hemorrhagic consequences.

Enzyme concentrations vary among species, thereby causing dissimilar envenomations. Copperhead bites generally are limited to local tissue destruction. Rattlesnakes can leave impressive wounds and cause systemic toxicity. Coral snakes may leave small wounds that later result in respiratory failure from the typical systemic neuromuscular blockade.

The local effects of venom serve as a reminder of the potential systemic disruption of organ system function. One effect is local bleeding; coagulopathies are not uncommon with severe envenomations. Another effect, local edema, increases capillary leak and interstitial fluid in the lungs. Pulmonary mechanics may be altered significantly. The final effect, local cell death, increases lactic acid concentration secondary to changes in volume status and requires increased minute ventilation. The effects of neuromuscular blockade result in poor diaphragmatic excursion. Cardiac failure can result from hypotension and acidosis. Myonecrosis raises concerns about myoglobinuria and renal damage.


PATHOPHYSIOLOGY OF OPHITOXAEMIA

Snake venom, the most complex of all poisons is a mixture of enzymatic and non-enzymatic compounds as well as other non-toxic proteins including carbohydrates and metals. There are over 20 different enzymes including phospholipases A2, B, C, D hydrolases, phosphatases (acid as well as alkaline), proteases, esterases, acetylcholinesterase, transaminase, hyaluronidase, phosphodiesterase, nucleotidase and ATPase and nucleosidases (DNA & RNA). The non-enzymatic components are loosely categorized as neurotoxins and haemorrhagens. Different species have differing proportions of most if not all of the above mixtures- this is why poisonous species were formerly classified exclusively as neurotoxic, haemotoxic or myotoxic. The pathophysiologic basis for morbidity and mortality is the disruption of normal cellular functions by these enzymes and toxins. Some enzymes such as hyaluronidase disseminate venom by breaking down tissue barriers. The variation of venom composition from species to species explains the clinical diversity of ophitoxaemia. There is also considerable variation in the relative proportions of different venom constituents within a single species throughout its geographical distribution, at different seasons of the year and as a result of ageing.

The various venom constituents have different modes of action. Ophitoxaemia leads to increase in the capillary permeability which may cause loss of blood and plasma volume into the extravascular space. This accumulation of fluid in the interstitial space is responsible for edema. The decrease in the intravascular volume may be severe enough to compromise circulation and lead on to shock. Snake venom also has direct cytolytic action causing local necrosis and secondary infection, a common cause of death in snake bite patients. The venom may also have direct neurotoxic action leading to paralysis and respiratory arrest, cardiotoxic effect causing cardiac arrest, myotoxic and nephrotoxic effect. Ophitoxaemia also causes alteration in the coagulation activity leading to bleeding which may be severe enough to kill the victim.

References:
http://emedicine.medscape.com/article/168828-overview
http://priory.com/med/ophitoxaemia.htm

Diagnosis and Investigation

Jesslyn & CarrMen

Diagnosis

3 principle diagnosis questions:

1. Is this a snakebite, or some other condition
2. If it is a snakebite, is there significant envenoming present and to what extent
3. Lastly, what type of snake was responsible?

Steps that get you to the diagnosis questions above:

1. The patient’s history and account of the injury
2. Observation of fang marks
3. Snake identification (if possible)
4. Progressive symptoms of envenomation all point to poisonous snakebite

Confirm that it’s a poisonous snake bite?
1. Puncture marks (usually on limbs). These may be difficult to see, and may consist of a single or double puncture or scratch marks or multiple punctures. They may be bleeding or oozing
2. Regional tender lymphadenopathy (NB this may also be present after bites from non-venomous snakes, and is not by itself an indication for antivenom)

Presentation of envenomation may include:
headache, nausea, vomiting
abdominal pain
collapse, unconsciousness, coma
painful, tender muscles
blurred vision
irritability, confusion
dark urine (myoglobinuria, haematuria)
weakness/paralysis
respiratory failure (neurotoxicity)
hypotension
cardiorespiratory arrest

Differential diagnosis
Of venomous snakebite
· non-venomous snakebite - leaves scratches, not punctures
· bite or sting by other venomous creature (arthropod)
· ascending neuropathy e.g. Guillain-Barre Syndrome
· AMI
· anaphylaxis
· hypoglycaemia/hyperglycaemia
· drug overdose
· closed head injury

Laboratory Investigations

Samples for venom detection and for pathology obtained to :

· Identify the genus of snake as the composition of particular venoms influences the clinical presentation of particular snakebites.
· Give the appropriate antivenom.
· Alert clinicians to particular features characteristic of envonomation.

However, fang marks alone are not an indication for the use of antivenom ( some snakes don’t give out enough ). This is when laboratory investigations come in handy.

* Antivenoms should not be used unless there is evidence of systemic envenomation

Although lab tests are of little value in the diagnosis of snake envenomation, nevertheless they are useful for monitoring the patient and deciding about specific interventions and prognosis.

They should include:
· a full blood count
· electrolytes
· glucose
· creatinine
· serum amylase
· creatinine phosphokinase (CPK)
· prothombin time (PT)
· partial thromboplastin time (PTT)
· fibrinogen and fibrin degradation products (FDP's).Looking into the tests…

Specific investigations

(a) The 20-min whole blood clotting test (20 WBCT): The 20 WBCT is a simple bedside test of coagulopathy to diagnose viper envenomation and rule out elapid bite. It requires a new clean, dry test tube made up of simple glass that has not been washed with any detergent. A few milliliters of fresh venous blood is drawn and left undisturbed in the test tube for 20 min; the tube is then tilted gently. If the blood is still liquid after 20 min, it is evidence of coagulopathy and confirms that the patient has been bitten by a viper. Cobras or kraits do not cause antihemostatic symptoms.

(b) Enzyme linked immunosorbent assay (ELISA): ELISA tests are now available to identify the species involved, based on antigens in the venom. These tests, however, are expensive and not freely available and thus have limited value in diagnosis; at present, they find use mainly in epidemiological studies.

Non-specific investigation
· Hemogram: The hemogram may show transient elevation of hemoglobin level due to hemoconcentration (because of the increased capillary leak) or may show anemia (due to hemolysis, especially in viper bites). Presence of neutrophilic leucocytosis signifies systemic absorption of venom. Thrombocytopenia may be a feature of viper envenomation.
· Serum creatinine: This is necessary to rule out renal failure after viper and sea snake bite.
· Serum amylase and creatinine phosphokinase (CPK): Elevated levels of these markers suggests muscle damage (caution for renal damage).
· Prothrombin time (PT) and activated partial thromboplastin time (aPTT): Prolongation may be present in viper bite. (repeated within 12hrs)
· Fibrinogen and fibrin degradation products (FDPs): Low fibrinogen with elevated FDP is present when venom interferes with the clotting mechanism. (repeated within 12hrs)
· Arterial blood gas and electrolyte determinations: These tests are necessary for patients with systemic symptoms.
· Urine examination: Can reveal hematuria, proteinuria, hemoglobinuria, or myoglobinuria. (Arterial blood gases and urine examination should be repeated at frequent intervals during the acute phase to assess progressive systemic toxicity).
*Include free protein, haemoglobin, myoglobin
*Arterial blood gas tested if an signs of respiratory compromise are evident
· Electrocardiogram (ECG): Nonspecific ECG changes such as bradycardia and atrioventricular block with ST-T changes may be seen. (suggested for patients >50 and patients with history of heart disease)
· Electroencephalogram (EEG): Recently, EEG changes have been noted in up to 96% of patients bitten by snakes. These changes start within hours of the bite but are not associated with any features of encephalopathy. Sixty-two percent showed grade I changes, 31% cases manifested grade II changes (moderate to severe abnormality), and the remaining 4% showed severe abnormality (grade III). These abnormal EEG patterns were seen mainly in the temporal lobes.

Blood changes include anaemia, lecuocytosis (raised white cell count) and thrombocytopenia (low platelet count). The peripheral blood film may show evidence of haemolysis especially in viperine bites. Clotting time and prothrombin time may be prolonged and a low fibrinogen may be present.

Blood should be typed and crossmatched on the first blood drawn from the patient, as both direct venom and anti-venom effects can interfere with later cross matching. Some specialised centers can identify species of snake involved.

Commonly hyperkalaemia and hypoxaemia with respiratory acidosis may be seen, particularly with neuroparalysis.

Imaging Studies
Baseline chest radiograph in patients with pulmonary edema
Plain radiograph to rule out retained fang(s)




References
Springhouse 2005, Professional Guide to Diseases (Eighth Edition), Lippincott Williams & Wilkins.
Springhouse 2003, Handbook of Diseases, 2003 Lippincott Williams & Wilkins.
M. William Schwartz MD; et al 2008, The 5-Minute Pediatric Consult , Lippincott Williams & Wilkins.
http://www.toxinology.com/fusebox.cfm?staticaction=snakes/ns-sndiag01.htm
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2700615
http://www.aafp.org/afp/20020401/1367.html
http://emedicine.medscape.com/article/168828-diagnosis
http://www.emedicinehealth.com/snakebite/page4_em.htm
http://www.nda.ox.ac.uk/wfsa/html/u16/u1606_02.htm
http://www.wrongdiagnosis.com/s/snake_bite/diagnosis.htm
http://www.wrongdiagnosis.com:80/s/snake_bite/book-diseases-7a.htm
http://emedicine.medscape.com/article/168828-diagnosis
http://www.avru.org/compendium/biogs/A000065b.htm

Pathophysiology & Complications of Snake Bite

Prepared by: Arma

Neurotoxin
Neurotoxins play a key role in immobilizing prey through paralysis, disorientation and depressed respiration.
Venoms often contain different neurotoxins that work synergistically to cripple the nervous system. Neurotoxins can be classified according to their site of action: pre-synaptic neurotoxins block neurotransmission by affecting acetylcholine transmitter release; post-synaptic neurotoxins are antagonists of the acetylcholine receptor. Together these neurotoxins effectively block skeletal neuromuscular transmission by crippling receptors, while at the same time acting to destroy any neurotransmitter that might compete with the toxin for receptor binding. Venoms often contain several post-synaptic neurotoxins, each with a high affinity for a nicotinic receptor subtype - in this way the venom can cripple as many receptors as possible. The post-synaptic neurotoxins are found only in elapids and sea snakes (Hydrophiidae). In the many-banded krait, a pre-synaptic toxin is -bungarotoxin, while post-synaptic toxins are  and -bungarotoxins.

There are two types of acetylcholine receptors (AchR): muscarinic-type, which are primarily neuronal, and nicotinic-type, which are either neuronal or muscle-type. The venom from the many-banded krait (Bungarus multicinctus) contains toxins that can bind to each type of receptor: the -bungarotoxins act primarily on nicotinic AchRs at the neuromuscular junction, the -bungarotoxins act primarily on nicotinic AchRs in neuronal tissue, and there are also muscarinic AchR-binding toxins. These toxins show almost irreversible binding to the receptors, competitively inhibiting acetylcholine binding and, consequently, inhibiting the acetylcholine-induced electrical response.

b-Bungarotoxin is much more lethal than either a- or k-bungarotoxin. b-Bungarotoxin is a pre-synaptic toxin that acts on the (pre-synaptic) motor nerve terminals to block the release of acetylcholine. The action of b-bungarotoxin is complex. It has phospholipase A2 activity, which functions to hydrolyse phosphatidylcholine, in this case the phospholipids in the nerve membrane. Yet b-bungarotoxin displays both phospholipase-dependent and –independent activities. b-Bungarotoxin is thought to bind to and block Shaker-type potassium channels; the subsequent block of transmitter release is probably due to phospholipase A2-mediated destruction of the nerve terminal. Animals die as a consequence of respiratory failure.

Acetylcolinesterase (AchE) plays a key role in cholinergic nerve transmission, acting to breakdown acetylcholine to choline and acetate, which is important in controlling a receptor’s response. Snake venom makes use of AChE to breakdown any neurotransmitter that might compete with a- or k-bungarotoxin for binding to AchRs. Venom AChE contains an additional exon over endogenous AChE, which generates a soluble form of the enzyme that is suitable for its venomous use.

Neurotixin can cause:
- Neurotoxic paralysis may also begin within the first hour of snake bites and is seen first as ptosis, then blurred vision and diplopia, followed by facial weakness and dysarthria. In severe cases, weakness of the limbs, paralysis of respiration, and fixed and dilated pupils may be observed.
- Ptosis which is also called "drooping eyelid." It is caused by the damage of nerves that control the muscle responsible for raising the eyelid.
- Circumoral parethesia- An abnormal touch sensation, such as burning or prickling, often in the absence of an external stimulus. A sagging or prolapse of an organ or part, paralysis of the oculomotor nerve.
- Muscle paralysis by blocking the nicotinic acetylcholine receptors at the post-synaptic motor endplates, or they affect the mode of neurotransmitter release at the presynaptic motor nerve endings.
- The most common eye symptom - ophthalmoplegia, paresis of the right medial rectus muscle; incomplete motion of each eye on upward, downward and inwardgaze, due to dysfunctions of oblique muscles, which is considered as a rare complication.
-Restriction in mouth opening- indicate trismus (sea snake envenoming) or more often paralysis of pterygoid muscles
-Respiratory paralysis occurs when the muscles associated with breathing become do weak to function properly. Breathing becomes difficult and severe cases can result in death if breathing assistance is not delivered

Myolisis
It is generally systemic rather than local. Systemic myolisis may take several hours, occasionally more than 24 hours, to become clinically apparent. Features include muscle pain, tenderness and weakness, elevated plasma creatine kinase, which may be grossly elevated and myoglobinuria.

Cardiac toxicity
Viper’s venom can cause cardiac dysrhythmias or arrest in envenomed patient. This effect is not common. It is more commonly as a secondary effect of other processes such as hyperkalemia secondary effect to severe myolisis.

Local tissue injury
It is variable in extent and presentation. Local pain may be severe, and often is associated with moderate to marked swelling that may ultimately involve in the entire bitten limb. Local oozing, bleeding, blistering and discolouration may occur. The extent of necrosis varies from none, to superficial skin loss in the bite area, to widespread skin loss. The development of necrosis often occurs over days. One of the biggest hazards from the tissue injury is hypovolemic shock secondary to massive fluid shifts, particularly apparent in younger children in whom this complication can prove rapid lethal.

References:
http://www.ebi.ac.uk/interpro/potm/2004_6/Page1.htm
http://www.nlm.nih.gov/medlineplus/ency/article/001018.htm
http://www2.merriam-webster.com/cgi-bin/mwmednlm
http://www.health-glossary.com/1001-circumoral-paresthesia.html
http://jkms.org/Synapse/Data/PDFData/0063JKMS/jkms-19-631.pdf

http://books.google.com.my/books?id=BfdighlyGiwC&pg=PA1579&lpg=PA1579&dq=respiratory+paralysis+and+snake+venom&source=bl&ots=Krc8xQp5_d&sig=w5r4uONEpuMFHIXbVM8nVbZP7pc&hl=en&ei=5A9vSpqmB9K9kAWA_8HBBQ&sa=X&oi=book_result&ct=result&resnum=6
http://priory.com/med/ophitoxaemia.htm#LOCAL%20MANIFESTATIONS
http://www.wrongdiagnosis.com/r/respiratory_paralysis/intro.htm