Abstract
The earliest case of oxalic-acid poisoning, reported by Royston, occurred in England, in 1814. Since then, the number of deaths due to oxalic acid and its soluble salts has so increased that today it ranks among the first three poisons in the number of fatalities. A. W. Blyth states that in the five years between 1912 and 1916, there were 448 deaths in England and Wales due to oxalic acid.
The duration of a case of oxalic-acid poisoning is usually between 2 and 14 days. There is one case on record by Ogilvie (Lancet, 1845) however where death occurred within 3 minutes.
Oxalic acid acts locally as a corrosive and also as a systemic poison. Locally it is more or less destructive to the mucous membrane with which it comes in contact. The lips, tongue, pharynx and esophagus are discolored yellowish white, sometimes marked with patches of a reddish hue. The mucous surface of the stomach is coarsely corrugated and presents a bright red color both in the elevations and depressions; this may change to brown or even black by postmortem action. In some cases the mucous surface is in part or in whole pale, opaque or translucent, and marked by a coarse ramiform vascularity of the submucous tissue. The mucous membrane is soft, pulpy, eroded in patches, thrown into folds, and is easily detached. Perforation is rare.
The systematic effects are attested by falling of the blood pressure, arhythmia and retardation of the pulse, slow breathing, paralytic symptoms and fibrillary muscular contractions. Some consider it a poison acting on the extracardiac ganglia. The red blood corpuscles are destroyed, with consequent fatty degeneration of the tissues. The activity of the muscles is diminished consequent upon loss of irritability.
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