Introduction

• The adder, or viper (Vipera berus ), is the only venomous snake in UK.
• Snake bite envenomation occurs in approximately 50% of bites.
• Cases of envenomation generally occur between February and October, peaking in June to August, and should always be treated as an emergency.
• Adder bites can be life-threatening where systemic envenoming occurs.

Pathogenesis

Etiology

• Venom constituents are complex, containing a mixture of enzymes, proteins and peptides. Further details on the enzymatic activities of adder venom can be found in Siigur et al, 1979. The genomic DNA sequences encoding the phospholipases A2 from the venoms of a number of European vipers have been sequenced, together with genes encoding a number of neurotoxins (Guillemin et al, 2003).

Pathophysiology

• Only ~50% of bites by exotic venomous snakes inject sufficient venom to cause clinical envenoming (Warrell, 2005). Macintire et al (2005) state that 20% of snakebites are "dry", ie contain little or no toxic venom. The percentage of dry adder bites is uncertain.
• If injected, the complex nature of adder venom is largely responsible for the range of physiological and clinical effects reported:
  • An immediate drop in systemic blood pressure is commonly seen. This arises through arterial vasodilation, followed by increased peripheral vascular resistance, decreased cardiac output, hypoproteinemia and increased PCV. The hypoproteinemia and hypovolemia probably arise due to increases in vascular permeability and loss of circulating fluid and protein.
  • Bradykinin release may be seen resulting in vasodilation.
  • Phospholipase A2, present in many viperid venoms, can cause release of prostaglandins. This can lead to further vasodilation and hypotension. Phospholipase A2 has significant anticoagulant properties.
  • Anticoagulation effects may be seen resulting in clinical features of a bleeding diathesis.
  • Renal failure can result for a variety of reasons, including myoglobinuria, hemoglobinuria and hypovolemic shock.
  • Serious complications include ventricular arrhythmias, cardiac failure, acute renal failure, DIC Disseminated intravascular coagulation and airway obstruction.
  • Disseminated intravascular coagulation (DIC) can result in hemorrhage, shock, collapse and, sometimes, death.

Timecourse

• The signs of envenomation may appear within minutes, or be delayed up to an hour.
• If no swelling apparent within 2 hours then envenomation has not occurred.
• The swelling will gradually increase in size and become hemorrhagic.
• Swelling may become necrotic with overlying skin sloughing.
• Death due to heart Acute heart failure , renal Kidney: chronic kidney disease (CKD) and hepatic failure Liver: chronic disease - overview (if occurs) is within 5-7 days.
• Death may occur acutely due to development of DIC Disseminated intravascular coagulation.

Diagnosis

Treatment

Prevention

Outcomes