• Is produced by the permeable vessels, caused by venom, allowing fluid and blood to extravasate
• Is the first objective sign of envenomation and should trigger full attention
• Can progress to become profound enough to cause hypovolemic shock
• Decreases slowly with treatment, which makes it a poor indicator of clinical improvement
• Creates skin problems relative to the extent of the edema – Skin loses elasticity, stretches, and fissures. Generally superficial, fissures can be sources of secondary infection

• May occur with edema
• May indicate, by speed of its progression, the severity of envenomation
• Caused by bleeding into skin due to coagulopathy induced by envenomation

• May be filled with clear serous fluid (vesicles) or with blood (bullae)
• Usually develop in the bite area but may be seen over the entire extremity

• Vomiting
• Convulsions
• Abdominal Pain
• Metallic or Minty Taste*

• Caused by pre- and/or postsynaptic neurotoxins – Presynaptic paralysis usually involves terminal axon damage. Reversal requires regeneration of axons, which takes days, weeks, or even months
• May take 1 to 12 hours to become evident
• Is progressive, often first seen in cranial nerves – Is easily missed if not specifically sought in exam
• Is also evidenced early by ptosis, ophthalmoplegia, dysarthria, and/or dysphagia
• Can lead to respiratory failure – Paralyzes the diaphragm last - up to 24 hours postbite

• Hypo- or hypertension
• Bradycardia
• Tachycardia

*Likely due to the metalloproteinases in the venom.

• Coagulopathy is insidious, beginning with persistent bleeding from the bite wound
• Hemorrhage is evidenced by bleeding gums, hematemesis, melena, or hematuria
• Punctures by line insertions or surgery may result in prolonged and significant bleeding