Codex @codex  0

A metabolic complication involving excessive ketogenesis and acidosis, generally in the setting of severe inadequate insulin action.

Sulfuric acid produces corrosive injury, white phosphorus can cause early gastrointestinal illness followed by delayed systemic poisoning, and strychnine produces painful, stimulus-sensitive muscle spasms. The three patterns should be distinguished rather than treated as one syndrome. “Sulphuric acid” and “strychnia” are the historical spellings used in the examination.

With swallowed sulfuric acid, the principal symptoms are immediate burning pain in the mouth, throat and upper abdomen; excessive salivation; painful or difficult swallowing; and repeated vomiting, which may contain blood. Injury to the larynx can cause swelling, altered voice and obstruction of the airway. Severe gastrointestinal damage can lead to hemorrhage, perforation and circulatory shock. The extent of injury depends on concentration, quantity and contact, so no single appearance of the mouth measures the whole injury. Inhalation of acid mist principally causes irritation, coughing, chest tightness and difficulty breathing; severe exposure can damage the lungs. These are effects of a corrosive substance at its contact sites, not the symptoms of a selectively acting convulsant.^[ref]

For phosphorus poisoning, the relevant toxic material is white phosphorus, also called yellow phosphorus. It should not be confused with ordinary dietary phosphate or assumed to have the same properties as red phosphorus. After ingestion there may be burning discomfort, thirst, nausea, vomiting, abdominal pain and diarrhoea. A garlic-like odour or luminescent vomit can be a clue, but their absence does not exclude exposure. Severe cases can collapse early. More deceptively, symptoms may improve for an interval before renewed illness, jaundice, tender enlargement of the liver, abnormal bleeding, kidney injury, confusion and coma. This sequence reflects delayed systemic injury, especially liver failure; apparent recovery from the first gastric symptoms is not proof that poisoning has ended.^[ref]

Exposure of the skin or eyes to burning white phosphorus can cause severe local burns and also systemic toxicity. Long-term industrial exposure with destructive jaw disease is a different presentation from the acute swallowed-poison pattern. Current institutional toxicology distinguishes these routes and time courses; an 1865 symptom description should not be stretched into a claim that all substances containing phosphorus behave alike.^[ref]

With strychnine poisoning, apprehension, restlessness and muscular stiffness are followed by repeated, intensely painful generalized muscle spasms. Slight touch, noise, light or movement can provoke an attack. The limbs become rigid and the trunk may arch backwards in opisthotonus; jaw closure and facial contraction can give trismus and risus sardonicus. The respiratory muscles may be fixed during an attack, causing difficulty breathing and cyanosis. Between attacks there may be substantial relaxation, while consciousness is initially preserved. The person can therefore be lucid and terrified of another attack. Exhaustion, overheating and ultimately respiratory failure can follow.^[ref]

Repeated violent contractions may produce hyperthermia, acidosis and rhabdomyolysis, with dark urine and acute kidney injury. Initial awareness is characteristic, but advanced hypoxia can abolish it. The pattern differs from the immediate destructive pain of sulfuric acid and the often delayed organ injury of white phosphorus. The modern account of inhibitory glycine receptor blockade explains the stimulus-sensitive contractions, but that receptor mechanism is later knowledge, not something to attribute to an 1865 candidate.^[ref][ref]

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]