Pathophysiology of Decompression Sickness

Investigation of the potential for vascular bubble formation in a repetitively diving dolphin

“…subarachnoidal hemorrhage) observed in other mass strandings of beaked whales either putatively or known to be associated with the presence of MFA sonar (Evans, 2002;Ketten, 2005). The observed presence of intravascular bubbles and tissue separation representative of bubble formation within tissues is consistent with the presentation of decompression insults in laboratory animals and humans (Gersh et al, 1944;Shim et al, 1967;Kitano and Hayashi, 1981;Francis and Mitchell, 2003). The presence of fat emboli is consistent with initial formation of N 2 bubbles in fat bodies, such as bone marrow, and/or a possible activation of complement in the immune system that accompanies intravascular bubble formation (Kitano and Hayashi, 1981;Francis and Mitchell, 2003).…”

“…The observed presence of intravascular bubbles and tissue separation representative of bubble formation within tissues is consistent with the presentation of decompression insults in laboratory animals and humans (Gersh et al, 1944;Shim et al, 1967;Kitano and Hayashi, 1981;Francis and Mitchell, 2003). The presence of fat emboli is consistent with initial formation of N 2 bubbles in fat bodies, such as bone marrow, and/or a possible activation of complement in the immune system that accompanies intravascular bubble formation (Kitano and Hayashi, 1981;Francis and Mitchell, 2003). The relationship between the magnitude of the fat embolic response and the degree of the decompression insult remains uncertain and there is evidence that fat emboli can form without any of the debilitating effects associated with decompression sickness [DCS (Shim et al, 1967)].…”

Pharmacological Interventions to Decompression Sickness in Rats: Comparison of Five Agents

“…The pressure reduc tion results in bubbles of inert gas, usually nitrogen, within body tissues. Originally, it was believed that the bubbles caused mechanical damage to cells by displac ing and deforming adjacent structures, tearing vessels, or obstructing vessels, leading to ischemia (22). How ever, the full spectrum of pathology found in DCS can not be explained solely by the hypothesis of bubble induced mechanical obstruction of the vasculature (16).…”

Intravenous Lidocaine as Adjunctive Therapy in the Treatment of Decompression Illness

“…Although the exact pathophysiology of decompression illness remains unclear, current studies support activation of the coagulation and complement systems, with promotion of interstitial edema and microvascular sludging with progressive local ischemia as contributing mechanisms. 7,8 Lidocaine has been shown to reverse many of these effects 2-5,9 , to reduce intracranial hypertension associated with arterial gas embolism 3 , to increase spinal cord blood flow 9 , and to preserve nerve conduction in isolated nerves. 10 Conflicting results have been obtained in studies evaluating recovery of somatosensory evoked potentials after experimental air embolism.…”