Solution (source code)

= Solution

\b[<Oxalic acid poisoning> may produce corrosive gastrointestinal injury, early circulatory collapse and later <kidney> injury; no single post-mortem appearance proves the diagnosis.] The severity of local injury and systemic poisoning need not be identical in every case.

After ingestion, burning pain in the mouth, throat or upper abdomen may be followed by <vomiting>, sometimes containing <blood>, abdominal tenderness and <diarrhoea>. Weakness, a small rapid <pulse>, cold clammy skin and collapse may develop. A dilute preparation may produce less obvious surface injury than concentrated <oxalic acid>, while still giving systemic poisoning. Current chemical safety information recognizes both corrosive effects and disturbance of <calcium> balance.<Oxalic Acid: International Chemical Safety Card 0529>[Ingestion hazards and effects of short-term exposure]{ref}

The absorbed <oxalate> can bind <calcium> and form <calcium oxalate>. A fall in ionized <calcium> can contribute to neuromuscular disturbance and cardiac instability, but <hypocalcaemia> must not be asserted to occur in every case or inferred from a symptom alone. If the person survives the early illness, <acute kidney injury> can follow. In modern pathological investigations, <calcium oxalate> crystals in renal tubules and associated tubular damage provide a mechanism for this later complication.<Plasma Oxalic Acid and Calcium Levels in Oxalate Poisoning>[1967, five patients: plasma oxalate, calcium and tissue deposits]{ref}<Acute Renal Failure Following Oxalic Acid Poisoning: A Case Report>[Clinical course and renal biopsy: tubular injury with oxalate crystals]{ref}

At <autopsy>, examine the mouth, <oesophagus> and <stomach> for corrosive changes. Depending on concentration and survival, the <mucous membrane> may be pale or discoloured, inflamed, eroded, haemorrhagic or softened; blood-stained contents and severe gastric damage may be present. Perforation is possible, but is not a necessary finding. The pre-examination report <Case of Criminal Poisoning with Oxalic Acid, in Which Perforation of the Stomach Took Place by Henry Duncan Littlejohn> documents a particular severe example with marked softening and perforation. It is evidence that these changes can occur, rather than a description that every fatal case must reproduce.<Case of Criminal Poisoning with Oxalic Acid, in Which Perforation of the Stomach Took Place by Henry Duncan Littlejohn>[1861, pp.13–20: examination of the damaged stomach]{ref}

Examine the <kidneys> as well as the gastrointestinal tract; histological tubular changes and crystals may matter especially after delayed death. Nevertheless, <calcium oxalate> deposition is not unique to direct ingestion of <oxalic acid>, and gross corrosive damage is not unique to this poison. Preserve material for controlled <toxicological analysis>, and interpret the chemical findings alongside the history and pathological distribution. The older classification of <oxalic acid> as a “narcotic” does not adequately explain the corrosive, electrolyte and renal mechanisms now recognized.