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SUMMARY
Erythrocyte disorders from physical or chemical agents occur via such processes as red cell volume expansion within hypotonic solutions, erythrocyte membrane damage from biotoxins, damage to the spectrin skeleton from insults such as heat, and eryptosis associated with oxidizing agents such as oxygen, arsine gas, and chlorates. Erythrocyte damage also can be induced by other agents that lack well defined mechanisms of action (see Table 52–1). These processes include erythrocyte damage caused by lead, copper, and radiation, as well as neocytolysis, a phenomenon once thought unique to microgravity, but subsequently observed in individuals demonstrating altitude induced polycythemia upon transition to normoxic conditions.
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Abbreviations and Acronyms:
AsH3, arsenic hydride (arsine gas); EDTA, ethylenediaminetetraacetic acid; G6PD, glucose-6-phosphate dehydrogenase; NADPH, reduced nicotinamide adenine dinucleotide phosphate.
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MECHANISTICALLY DESCRIBED ERYTHROCYTE DAMAGE
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Chemical and physical agents causing erythrocyte disorders within the context of enzyme deficiency, unstable hemoglobins, cell fragmentation or immune dysfunction are discussed in Chaps. 46 to 51 and 54. The present chapter deals with drugs, toxins, and other physical agents that can cause red cell disorders, which are not discussed elsewhere within this text.
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ERYTHROCYTE VOLUME EXPANSION AND HYPOTONIC LYSIS
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When large amounts of distilled water gain access to the systemic circulation, either by intravenous injection or when used as an irrigating solution during surgery, hemolysis will occur.1 Severe hemolysis may also result from water inhalation in near-drowning.2 Occasionally self-induced hypotonic lysis secondary to water intoxication from polydipsia in the setting of psychiatric illness or hazing rituals occurs.3 In all cases, hemolysis follows expansion of the erythrocyte volume, transition to a spherical shape and ultimately cell rupture.4
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DAMAGE TO THE RED BLOOD CELL MEMBRANE
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Bee5,6 and wasp7,8,9 stings, as well as contact with caterpillar bristle from Lonomia obliqua,10 are associated with severe hemolysis. In addition, spider and scorpion bites occasionally are followed by hemolytic anemia and hemoglobinuria.11,12,13,14,15,16 The spiders usually responsible are Loxosceles laeta and Loxosceles recluse. In such cases, sphingomyelinase D is one of the causative toxins. The venom preferentially hydrolyzes band 3 of the red cell membrane protein.17 Band 3 has dual functions of ion exchange and anchoring of the cell membrane to the underlying cellular skeleton.18 It appears disruption of the structural role is responsible for cell lysis.
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One of the most intriguing mechanisms of membrane damage is that induced by a class of pore-forming cytotoxins, usually from Bacillus cereus.19 Toxins using similar mechanisms of hemolysis are found in marine organisms including jelly fish (Chironex fleckeri),20 sea cucumbers (Cucumaria echinata),21 and sea anemones (Stichodactyla helianthus).22 X-ray crystallography reveals these toxins ...