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