Past exam of the medicine course of the University of Oxford / 1864 / Second examination / Forensic medicine and hygiene (No. IV.)

Original volume: Examination papers for the Degree of Bachelor of Medicine by the University of Oxford (1864–1867). Open the original paper in the scanned volume.

Original questions are transcribed from the public-domain edition. Credit: Wellcome Collection; original supplied by Royal College of Physicians, London. Source and public-domain rights statement.

By what symptoms would you seek to form a diagnosis between intoxication from alcoholic drinks, and concussion of the brain ?

Neither the smell of alcohol nor a drunken appearance excludes concussion or a more serious head injury. The useful distinction comes from the history, a complete examination and repeated assessment; alcohol intoxication and head injury may occur together.

First establish the order of events. Witnesses may describe drinking followed by progressive slurring, unsteadiness and drowsiness, or a blow or fall followed immediately by altered consciousness, confusion or a gap in human memory. Ask about the amount and timing of the drink, the mechanism of injury and any interval of apparent recovery. A person may have fallen because of alcohol intoxication, and subsequently have suffered a head injury. Conversely, an injured person may be mistakenly described as drunk because of slurred speech and an unsteady gait.

Examine the level of consciousness, orientation, speech, human memory and ability to follow commands. In alcohol intoxication, disinhibition, slurred speech, incoordination, vomiting and increasing drowsiness can occur; severe poisoning can progress to coma and impaired breathing. After concussion, confusion, amnesia, headache, dizziness, nausea and vomiting may occur, with or without an observed loss of consciousness. Thus vomiting or drowsiness alone does not decide the diagnosis.^[ref][ref]

Look for a scalp wound, swelling or other evidence of impact, and examine the pupils, their reaction to light, limb movements and any focal neurological deficit. Unequal pupils, one-sided weakness, a worsening level of consciousness or a seizure should prompt concern for significant traumatic brain injury, rather than be dismissed as ordinary drunkenness or uncomplicated concussion. The absence of an external wound does not exclude an internal injury. Nor are a flushed face, a particular pulse or the smell of drink sufficiently specific to settle the question.

The defensible diagnostic conclusion may initially be uncertainty requiring observation and investigation. Current guidance specifically requires important traumatic brain injury to be excluded before depressed consciousness is attributed to intoxication. Modern computed tomography and measurement of blood glucose can resolve problems that an 1864 bedside examination could not; these are later diagnostic aids, not equipment to attribute to the examination's period.^[ref]

How would you proceed for the purpose of testing the contents of the stomach of a person suspected of having been poisoned by Arsenic ?

Keep an untouched portion, use clean apparatus and reagent blanks, separate the suspected arsenic from the organic material, and confirm it by independent chemical reactions. A coloured deposit alone would be inadequate evidence.

Record the container, seal and condition of the stomach contents before opening. Examine and describe the material, including any visible particles, without assuming that a white powder is arsenic trioxide. Retain an unaltered portion for a repeat examination. Because a solid poison may settle, examine representative liquid and solid portions separately rather than testing only the clear upper liquid. Label each portion and each subsequent extract so that a positive reaction can be traced back to its source.

A practicable historical preliminary separation is the Reinsch test. Warm a portion with hydrochloric acid and a clean strip of copper; a dark coating suggests deposition of a substance requiring further identification. Carry out a parallel blank with the same copper, chemical acid, water and apparatus. A coating may be caused by substances other than arsenic, and contaminated copper or reagents can create a false accusation. Wash and dry a coated strip, then heat it in a small tube: an arsenical deposit can give a sublimate of arsenic trioxide, whose crystals can be examined with a microscope. The deposit and sublimate, rather than their mere colour, are the material for confirmation.^[ref]

On a separate suitably prepared portion, the Marsh test provides another mode of separation. The original James Marsh apparatus collected a hydrogen mixture for deposition tests; a heated-tube implementation separates collection from the subsequent heating zone. Zinc and dilute chemical acid generate hydrogen; arsenic in a suitable chemical form is converted to volatile arsine, and heating the gas in a narrow tube can produce a metallic mirror. First run the generator with the actual reagents alone, until their freedom from arsenic has been demonstrated. Keep the sample out of the gas outlet, and distinguish chemical deposition from mechanical carry-over. The apparatus separates a volatile derivative from much of the organic matrix, which explains its analytical value. Arsine is extremely toxic: this is a description of historical analytical principles, not a procedure for an uncontained demonstration.^[ref]

A mirror is not uniquely arsenical: antimony can form stibine and give a misleading deposit. Recover or oxidize the material and use additional reactions, such as formation of yellow arsenic trisulfide under appropriate acidic conditions, together with the characteristic oxide sublimate. Separate aliquots, suitable controls and agreement between chemically distinct tests are more persuasive than repeatedly observing the same ambiguous stain. Organic material must be removed or treated by a controlled preparation that neither introduces nor loses arsenic; indiscriminate charring or heating can invalidate the examination.

Finally distinguish detection from interpretation. A demonstrated arsenical compound supports exposure, but the amount, distribution and circumstances determine its significance. A negative test on the stomach contents alone does not exclude poisoning after absorption or expulsion of the poison. Further organs or excretions could be examined if available, but no positive finding in such material is assumed here.

What are the symptoms of a poisonous dose of Belladonna and of Hydrocyanic Acid ?

Poisoning by belladonna characteristically combines delirium with dry secretions and dilated pupils; poisoning by hydrocyanic acid can cause very rapid collapse with failure of breathing. The two patterns are distinctive descriptions, not infallible diagnoses from one symptom.

With belladonna, expect dryness of the mouth and throat, difficulty swallowing, blurred vision and mydriasis. The skin may become hot, dry and flushed; the pulse is often rapid. Restlessness, confusion, visual hallucinations and agitated delirium may be prominent: the person may talk incoherently or pick at imaginary objects. Reduced intestinal activity and urinary retention can accompany the dryness. Severe poisoning can proceed to seizures, depressed consciousness, coma and circulatory failure. This is now understood chiefly as an antimuscarinic poisoning syndrome produced by alkaloids including atropine, which oppose the action of acetylcholine at muscarinic receptors.^[ref]

Hydrocyanic acid is hydrogen cyanide, historically also called prussic acid. Depending on the route and amount, early complaints may include dizziness, headache, anxiety, nausea, weakness and a sense of suffocation. Rapid breathing may give way to slow or failing breathing, followed by seizures, coma, circulatory collapse and death. A sufficiently large exposure may be so rapid that an elaborate sequence of preliminary symptoms is not observed. There is no single obligatory interval from exposure to collapse.^[ref]

In modern terms, cyanide impairs cellular use of oxygen, including inhibition of cytochrome c oxidase in cellular respiration. An apparently oxygenated colour therefore cannot exclude serious poisoning. A bitter-almond odour is an unreliable clue: it may be absent or not perceived, and no examiner should intentionally smell a suspect sample. The historical term “narcotic poison” does not mean that either belladonna or hydrogen cyanide acts like an opioid. The receptor and cellular explanations above are present scientific interpretations, rather than molecular explanations available in 1864.^[ref]

What are the symptoms of poisoning by Oxalic Acid, and what the post mortem appearances ?

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.

What evidence would satisfy you that an infant found dead had not breathed ?

An undecomposed infant with uniformly unaerated lungs provides evidence supporting absence of breathing, but a negative lung flotation test cannot establish with certainty that no breath was ever taken. The strength of the conclusion depends on the whole investigation.

First establish the circumstances of discovery, apparent maturity, preservation and any manipulation of the body. Reliable observations during and immediately after delivery would be particularly valuable, but none are supplied here and none should be invented. Record whether artificial respiration was attempted and whether putrefaction has begun. Both can affect the interpretation of gas in the lungs.

At examination, lungs that remain small, dense and unexpanded, rather than aerated and expanded, support the hypothesis of no established pulmonary ventilation. In the historical hydrostatic procedure, test the lungs in water, followed by individual lobes and representative pieces; record differences between regions. Uniform sinking in a fresh, unmanipulated body is more consistent with lack of aeration than a mixed result. Inspection and section of the tissue help distinguish an apparently unexpanded lung from one containing localized gas. This is a method of assembling evidence, not a claim that any particular infant in the question has those findings.

The logical limitation is essential. Breathing can have been brief or ineffective, and diseased or incompletely expanded lungs may sink despite prior life and breathing. A modern prospective autopsy study recorded four false-negative flotation results among 208 examined newborns: the lungs sank despite evidence of prior life. That observation disproves an absolute rule equating sinking with never having breathed; it is not a universal accuracy estimate for all forensic populations.^[ref]

Conversely, floating tissue need not prove spontaneous breathing: putrefaction or introduced air during artificial respiration may produce gas. Historical case-record research also documents why investigators combined the flotation result with the other findings and circumstances.^[ref]

Thus several concordant observations can justify the cautious opinion that no effective breathing has been demonstrated and that absence of breathing is the best-supported explanation. They do not justify certainty from a single negative test. Finally, the absence of breathing and the absence of every sign of life are different propositions: an assessment of live birth cannot simply be replaced by a test of lung buoyancy.

What are the several ways by which a room, or a ward, may be ventilated ?

The several methods are natural ventilation by wind or buoyancy, mechanical supply, mechanical extraction, and combinations of these. Each must provide both a route for clean outdoor air to enter and a route for used air to leave.

For natural ventilation, opening windows on different sides permits cross ventilation when the wind creates a suitable pressure difference. Even one window can exchange air, but the amount and distribution are more dependent on conditions. Openings at different heights use the stack effect: warmer, less dense indoor air tends to rise and leave through an upper opening, drawing replacement air through a lower one. A flue or ventilating shaft can extend this route. A fireplace may assist extraction through its chimney, provided replacement air enters and combustion products are carried safely away.

Permanent inlets, adjustable window openings and outlet shafts can make these principles more controllable. Their positions should distribute fresh air through the occupied part of the ward instead of allowing it to pass directly from inlet to outlet. An open door into an adjoining foul space is not necessarily a source of clean air. Florence Nightingale's pre-1864 discussions emphasize outside air, openings and the relation between ventilation and warmth; admitting fresh air need not mean exposing a patient to an avoidable cold draught.^[ref][ref]

With mechanical extraction, a fan or other air-moving apparatus removes indoor air, while planned inlets admit replacement air. With mechanical supply, the apparatus introduces outdoor air, and outlets allow displacement of the used air. A balanced installation provides both mechanically. Natural openings can also be combined with mechanical assistance. Heating the incoming air can reduce chilling without making it necessary to recirculate all the used air.

What matters is the actual airflow through the room, including its direction. Outlet flow can be investigated with an anemometer; short-circuiting between nearby openings and stagnant regions must be considered. Moving the same indoor air around does not by itself supply fresh air. Nor does a perfume remove a source of contamination. Source removal, sufficient exchange and reasonable temperature control belong together; windows or fans are means to those ends, not proof that they have been achieved.

What impurities have been detected in the air of sick rooms ?

Sick-room air may contain excess carbon dioxide and water vapour, volatile products from excreta and soiled materials, suspended dust, and infectious aerosols; defective drains or combustion can add further contaminants. Their sources and evidential significance differ.

Breathing adds carbon dioxide and water vapour; washing, damp bedding and evaporation add further moisture. Ammonia and other volatile products may arise from excreta, soiled linen or decomposing material. Suspended dust can include textile fibres, skin particles and other organic matter. These are plausible objects of chemical or microscopic examination, rather than a single substance called “hospital poison”.

The sources need to be stated conditionally. Defective drainage can introduce sewer gases, including hydrogen sulfide; fires, smoky stoves or gas lighting can introduce combustion products such as carbon monoxide, smoke and, with appropriate fuel, sulfur dioxide. Such gases are not inevitable constituents of every sick-room atmosphere. Carbon monoxide is especially important because smell is not a reliable warning of its presence.^[ref][ref]

There were already quantitative methods for some constituents in 1864. A measured volume of air could be brought into contact with a known alkaline absorbent and the absorbed carbon dioxide determined; Chemical News volume 9 (1864) describes baryta-based air analysis. Humidity can be investigated with a psychrometer, and collected dust examined microscopically. Detection of Ammonia requires suitable chemical controls, rather than identification by a disagreeable smell alone.^[ref]

Present science further distinguishes infectious particles from nonspecific dust and gases. Some patients release pathogen-bearing aerosols, but their presence and infectivity cannot be established merely from a high carbon dioxide measurement, an odour or an unidentified microscopic particle. Modern environmental microbiology also requires sampling methods appropriate to the organism and a clear purpose; routine indiscriminate sampling is not a universal test of ward safety. This later understanding should be kept separate from the varied nineteenth-century theories of miasma.^[ref]

How is Typhoid Fever said to be propagated ?

The important transmission chain is from an infected person's intestinal discharges to another person's mouth, especially through contaminated drinking water, food or hands. In the terminology of 1864, the specific infectious material was associated with the bowel discharges of typhoid fever.

William Budd's 1861 argument makes this a disease propagated from preceding cases. Excreta enter a privy, drain or sewer; contamination can then reach a water supply, food or domestic surroundings and expose another person. Soiled linen and attendants' hands can also carry faecal material into the ingestion pathway. A shared polluted supply can therefore distribute infection to people who have never met the original patient. Removing and safely disposing of the discharges, protecting the supply and preventing transfer to food interrupt successive parts of this chain.^[ref]

This contemporary explanation should be distinguished from the competing suggestion that decomposing organic matter spontaneously generates typhoid fever. A sewer can transmit infection because it receives infected excreta; its smell is not itself proof of the causal material or of a primary inhalation route. The question's historical wording reflects a period of dispute, rather than an obligation to present all competing beliefs as equally correct.

The present explanation identifies Salmonella Typhi and faecal–oral transmission. People who are ill, convalescent or asymptomatic carriers can shed the organism; contaminated food and water convey it to another person. This specific bacteriological account is later knowledge, corroborating the route without attributing modern identification methods to 1864. Typhoid fever must also be distinguished from typhus, which has a different transmission history and biology.^[ref]

Under what conditions is drinking water usually contaminated by Lead?

The source may be a pipe, cistern, service connection or fitting. Robert Christison's pre-examination experiments addressed the action of different waters on metallic lead: very pure waters, including distilled water or rainwater, could attack it, whereas salts in many natural waters modified the process. This provides a contemporary basis for treating the character of the supply, as well as the material of the cistern or pipe, as important.^[ref]

The dissolving tendency is called plumbosolvency. In modern chemical terms, low pH and low alkalinity can favour the release of lead. Dissolved oxygen supports corrosion of the metal; dissolved carbon dioxide affects both acidity and carbonate chemistry. Carbonate deposits can provide a partly protective surface layer, while conditions favouring their dissolution can increase release. It is therefore misleading to say simply that all carbon dioxide prevents contamination or that all waters containing it dissolve lead to the same degree. Water hardness and alkalinity are related features of many waters but are not interchangeable quantities.^[ref]

Long contact, especially stagnation overnight or through disuse, can increase contamination. Warmer conditions, changes in the supply chemistry, disturbance of an old pipe and the condition of accumulated deposits can also matter. Water can carry dissolved lead or particles containing lead; an old apparently coated pipe is not an assurance that release has ceased. Modern supplies may additionally encounter lead-bearing solder or brass, which should be recognized as a present comparison rather than assumed to be the construction of a particular 1864 installation.^[ref]

A clear appearance and acceptable taste cannot exclude lead. Investigate the actual plumbing materials and analyse appropriately collected samples, recording the period of standing and other conditions instead of inventing a concentration. The most direct way to remove the source is replacement of lead-bearing components; treatment that controls corrosion is chemistry-dependent and is not equivalent to a universal guarantee from a hard-water scale. These considerations answer when contamination is likely without imposing an unsupported period numerical threshold.

Can you state any diseases which make butchers' meat wholly unfit for human food ?

Anthrax, generalized suppurative or septic disease, and generalized tuberculosis are clear examples of conditions requiring rejection of the whole carcass; extensive parasitic disease supplies further examples. The reason for whole-carcass condemnation is systemic disease or distribution too extensive to be dealt with as an isolated local lesion.

With anthrax, infection is not a harmless change confined to one removable piece of meat. Infected animal products also pose risks during handling, and eating infected raw or undercooked meat can cause gastrointestinal anthrax. The appropriate conclusion is exclusion from the food supply, not a promise that ordinary preparation will make a suspect carcass acceptable.^[ref]

Generalized pyemia or septicaemia, with disseminated infection, multiple suppurative foci or systemic deterioration, likewise makes trimming one visible lesion an inadequate response. Generalized tuberculosis, particularly with widespread lesions or associated wasting, differs from an isolated local abnormality. For a clearly identified modern comparison, current United States meat-inspection rules require condemnation for generalized tuberculosis and for disease presenting a food-poisoning risk, expressly including septicaemia and pyemia. Those are current comparative criteria, not rules to attribute to English law in 1864.^[ref]

Parasitic meat was already a concrete contemporary concern. On Poisoning by Diseased Pork by Julius Althaus, published in 1864, discusses trichinellosis from infected pork. Trichinella larvae in muscle can be missed by casual naked-eye inspection; the historical importance of the microscope is that apparently ordinary flesh can contain parasites. Widespread infestation cannot be assumed to be confined to an easily discarded patch. Cysticerci in meat are another foodborne parasitic hazard, but exact inspection and disposition depend on the organism and distribution, and should not be invented as a universal 1864 statutory rule.^[ref][ref]

A useful biological distinction is that eating viable cysticerci in beef or pork can cause intestinal taeniasis; human cysticercosis follows ingestion of Taenia solium eggs. These are different routes and disease stages, so one should not describe cysticercosis as simply the direct result of eating pork containing cysticerci.^[ref][ref]

The contemporary English legal framework is independently verifiable. Section 2 of the Nuisances Removal Act for England (Amendment) Act 1863 empowered inspection and seizure of food appearing diseased, unsound, unwholesome or unfit, followed by a justice's disposal order where unfitness was established. It did not supply a disease-by-disease table equating every local lesion with whole-carcass rejection. Thus the answer gives diseases and the medical reason for excluding the whole animal, while keeping localized lesions, generalized disease and legal procedure distinct.^[ref]