This paper reviews the pathophysiology and therapy of the multiorgan failure which occurs with submersion injury of children.

This paper reviews the pathophysiology and therapy of the multiorgan failure which occurs with submersion injury of children. First, the influence of hypothermia, the pulmonary, cardiovascular, neurologic and renal changes and the blood gas, acid-base and bloodvolume and serum electrolyte disturbances are discussed in detail. The therapeutic procedures are separated in the cardiopulmonary resuscitation at the scene of the accident and in the management of the children within the hospital where all near-drowned children should be taken. The intensity of the treatment at the hospital depends on the level of consciousness and on the respiratory and cardiovascular problems of the near-drowned child. For the treatment of comatose children with abnormal patterns of respiration and cardiovascular derangements the routine management and a more aggressive approach to therapy are presented. The rational for the aggressive therapy is to improve cerebral salvage. The urgency for an extensive monitoring system is underlined.

Most pharmaceuticals, toxic compounds, mutagens, and carcinogens undergo metabolism in the human body. Differences in drug metabolizing enzymes cause differences in susceptibility towards effects or side effects of these compounds. This chapter presents a comparison of epoxide hydratase (EH) activity in human individuals. Activities were measured in biopsy samples of liver, which is the main site of drug metabolism, and of lung, which is an organ that is continually exposed to potential enzyme inducers and to carcinogenic compounds. EH was studied in native lymphocytes, cultured lymphocytes, and fibroblasts in which environmental influences can be controlled and the genetic differences can be discriminated from environmental effects. The chapter explains that EH activity varies from organ to organ and, in some organs, from individual to individual. This is apparent in liver and lung, which are organs heavily exposed to foreign compounds. The much smaller variation in control liver and in cells in culture under uniform environmental conditions indicates that epigenetic factors are essential for the differences.

Epoxide hydratase activity with benzo[a]pyrene 4,5-oxide and glutathione S-transferase activity with 2,4-dinitrochlorobenzene as substrates were determined in cultured fibroblasts from skin biopsies of different donors and from several biopsies of the same donor. Variation of the results from experiment to experiment was reduced by the use of a reference cell strain and expression of the results as activities relative to those of the reference cells. Epoxide hydratase activity varied 2.3-fold in 39 cultures from the same subject (the variation coefficients were 0.22 and 0.15, respectively). The results indicate that, at least in skin fibroblasts, genetically caused interindividual differences in epoxide hydratase activities do not exist or are negligibly small or very rare. Glutathione S-transferase activity varied more in cultures from different donors (variation coefficient = 0.22) than in different cultures from the same donor (variation coefficient = 0.08), but the highest and the lowest activities only differed by a factor of 2.3. No significant differences in either enzyme activity were observed between males, females, subjects without tumours, lung carcinoma bearers and melanoma patients.