Studies in Acute Iron Poisoning III. The Hemodynamic Alterations in Acute Experimental Iron Poisoning

Acute Effects of Iron on Contractile Function in Isolated Rabbit Myocardium

“…The current concept of the pathogenesis of Fe-induced shock is derived primarily from animal experi ments [Reissmann und Coleman, 1955;Reissmann et ah, 1965;Bronson and Sisson, 1960;Whitten et ah, 1965;Whitten t1 ah, 1968], This concept proposes that Fe poisoning initially produces venous pooling and decreased cardiac filling which then results in a decline in cardiac output and circula tory shock. However, the data from studies which included direct measure ments of cardiac filling pressures do not support the hypothesis that an Fe-mediated decrease in cardiac filling is sufficient to account for the hemo dynamic consequences of severe Fe toxicity [ Whitten et al, 1968;Artman et al, 1982]. Therefore, we postulated that depression of myocardial contrac tility may contribute significantly to the pathogenesis of Fe-induced shock [Artman et al, 1982].…”

“…However, in experiments in which cardiac filling pressures were measured following a lethal dose of Fe, all animals demonstrated marked and progressive declines in cardiac out put which were not related to declines in central venous or left ventricular end-diastolic pressure [ Whitten et al, 1968;Artman et al, 1982]. Thus, the concept that venous dilation is the event of primary hemodynamic signifi cance in severe Fe toxicity does not appear to be supported by studies incorporating the direct measurement of cardiac filling pressures.…”

Acute Iron Poisoning—Clinical Features and Management

“…This is an example where complications of treatment were worse than the ingestion of iron. Whitten (1966) reported two cases and some dog experiments which showed that hypotension followed rapid administration of intravenous desferrioxamine.…”

“…Shock frequently follows ingestion of toxic amounts of iron salts. Blood and especially plasma volume decrease and cardiac output falls (Whitten, Chen and Gibson 1968). There is increased capillary permeability and blood and fluids may be lost into the gut through the damaged mucosa.…”

“…Urinary iron excretion is greater with intravenous than with oral desferrioxamine (Leikin, Vossough and Mochir-Fatemi 1967). The oral route is now not recommended as desferrioxamine forms ferrioxamine with iron which is absorbed readily through the injured gut and is toxic at higher dose levels causing hypovolaemia, hypotension and anuria (Whitten, Chen and Gibson 1966).…”