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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.^[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.^[ref][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.^[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.

Strychnine poisoning characteristically produces rapidly recurring, intensely painful generalized muscle spasms, precipitated by slight sensory stimuli, with consciousness initially preserved. “Strychnia” is the historical name for strychnine.

Following ingestion, manifestations commonly begin within roughly 15–60 minutes, although exposure route and amount alter the time course. Early features include apprehension, restlessness, heightened sensitivity and stiffness or twitching of the muscles, especially about the neck and back. The patient can then develop violent, generalized muscle spasms with rigid limbs and backward arching of the trunk, termed opisthotonus. Jaw closure and contraction of the facial muscles can produce trismus and risus sardonicus. The respiratory muscles may become fixed, causing difficulty breathing and cyanosis.^[ref]

Attacks may be triggered by touch, a noise, light or attempts to move the patient. During the intervals the muscles may relax substantially, and the patient may remain lucid and fearful of the next attack. Repeated contractions cause exhaustion, sweating and hyperthermia; severe cases develop acidosis, rhabdomyolysis and acute kidney injury. Death can result from respiratory failure. Consciousness can be lost late through hypoxia, so preserved awareness is a characteristic early clue, not an invariable requirement.^[ref]

This pattern helps distinguish the condition from many epileptic seizures, in which impaired awareness and a postictal state are common, and from tetanus, whose evolution is usually slower and whose rigidity tends to persist between attacks. The distinction is not absolute and symptoms alone do not prove the particular poison. A convincing forensic diagnosis combines the clinical sequence and exposure history with toxicological analysis.

The modern explanation is blockade of inhibitory glycine receptors in the spinal cord and brainstem, leaving reflex motor activity excessively excitable. This explains why trivial stimulation can cause a massive contraction. The receptor explanation is a later interpretation of the recognizable nineteenth-century syndrome.^[ref]