Marine envenomations can cause nociceptive, inflammatory, and necrotic tissue injuries. For treatment, hot water immersion (HWI) has become established. The mechanism of action of such therapy has not been scientifically confirmed; however, prevailing opinion attributes it to venom denaturation. Using established bioheat models, we evaluated the theory of protein denaturation as HWI’s mechanism of action. Heat transfer in a human limb was described using the Pennes equation, where the results of the numerical solution were validated by agreement with the analytical solution and with simulations in Ansys; all numerical results were within a ±0,9 min range. Within the temperature range of 40°C–46°C and for exposure times up to 180 min, the model does not predict the occurrence of deep dermal burns, whereas above 47°C, the safe window decreases exponentially. At Tv = 46°C, the predicted denaturation times are 4,1 min–5,2 min (lacerations), 4,1 min–51,8 min (moderately deep injuries), and 6,2 min–76,9 min (puncture to the bone), depending on the anatomical location. Parametric analysis showed that perfusion prolongs the denaturation time but vasoconstrictive venom components lower it; assuming a 50 % reduction in perfusion, the increase in td ranges from 3,0 % (lacerations) to 31,9 % (puncture to the bone). Burn formation time depends on the values of the kinetic parameters used; at Tv = 47°C, the predicted onset of deep dermal burns ranges from 46,0 min (Stoll) to 141,4 min (Henriques). Burn formation is from 4,3 % (finger, 47°C) to 15,7 % faster (sole, 50°C) in hairy compared to glabrous skin. The study shows that, with the use of HWI, it is physically possible to achieve protein denaturation in venom before deep dermal burns form. This confirms the biophysical plausibility of the proposed mechanism of action of HWI therapy.
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