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The chief physiological routes are abrupt failure of blood circulation, failure of pulmonary ventilation or gas exchange, or catastrophic failure of the central control of those functions. Historical clinical accounts used labels such as syncope, asphyxia and medical coma in explaining deaths; these terms describe broad physiological failures rather than identifying the underlying diseases.^[ref] A brief faint or ordinary medical coma is not itself necessarily fatal.

In primary circulatory failure, effective delivery of blood to the brain stops. Modern examples include ventricular fibrillation, pulseless ventricular tachycardia, severe bradyarrhythmia and asystole. They may arise in coronary artery disease, after myocardial infarction, in cardiomyopathy, or from inherited cardiac ion channel disorders. An electrical cause may leave little distinctive gross evidence at autopsy. These modern mechanisms refine the broad historical description of cardiac syncope.^[ref]

Mechanical interruption of blood circulation gives another group: massive haemorrhage, rupture of an aortic aneurysm, cardiac tamponade, and large pulmonary embolism. The immediate deficit differs in each. Haemorrhage removes circulating volume; cardiac tamponade prevents adequate filling; pulmonary embolism obstructs flow through the pulmonary circulation. All can end with critically low cardiac output even if some electrical activity persists.^[ref]

Respiratory failure includes obstruction of the airway by a foreign body, laryngeal oedema or aspiration; drowning; and depression of breathing by drugs or major brainstem injury. Oxygen delivery then fails and secondary cardiac arrest follows. Carbon monoxide poisoning and cyanide poisoning illustrate related failure of oxygen transport or use: not every hypoxic death is caused by physical obstruction of an airway.^{[ref][ref][ref]}

A major intracranial haemorrhage or rapidly developing brain herniation can destroy or compress the pathways maintaining consciousness and breathing. A severe disturbance of electrolytes, especially potassium, may instead act directly on the heart's electrical function. A fatal seizure can involve respiratory and circulatory mechanisms; sudden unexpected death in epilepsy remains a diagnosis requiring exclusion of other causes, not merely recognition of a history of epilepsy.^[ref]

The practical distinction is between mode, immediate mechanism and underlying cause. For example, rupture of an aneurysm can cause haemorrhage, then circulatory failure, then irreversible hypoxic-ischaemic brain injury. A complete explanation identifies that chain. Inspection, histology, examination of the airway and heart, and appropriately interpreted toxicology may establish it; an unexplained sudden death cannot be assigned a precise cause from its suddenness alone.

Obstruction of major pelvic or thigh veins raises pressure in the channels draining the limb; fluid then accumulates in the tissues as oedema. Severe outflow obstruction can also impede lymphatic drainage. The pale, tense appearance accounts for “alba”. It differs from phlegmasia cerulea dolens, in which more complete obstruction, including collateral channels, produces a congested blue limb and can threaten arterial perfusion. A historical case description cannot automatically be assigned one modern diagnosis solely from its name.

The central causal mechanisms are slowed venous flow, injury to the vessel wall and increased tendency of the blood to clot. Pregnancy promotes hypercoagulability and pelvic venous compression; childbirth can add tissue injury, immobility and infection. Prior venous thrombosis, thrombophilia, prolonged immobility, operative delivery and severe systemic illness further increase risk. It is not confined to the puerperium or even to women. The serious consequences are extension of the thrombus, detachment into the pulmonary arteries as a pulmonary embolism, and chronic obstruction or valvular damage producing post-thrombotic syndrome.^[ref]

An historically informed explanation should recognise that nineteenth-century arguments concerned the relative importance of venous obstruction, phlebitis, lymphatic disease and puerperal illness. Rest, support and elevation of the limb, pain relief and local soothing applications belonged to the period's conservative repertoire. These could ease symptoms but did not provide effective anticoagulation. Neither the “milk leg” name nor the observation of puerperal infection establishes that every case is caused by milk displacement or by infected clot. The thrombotic and infective questions must be distinguished.

Current management begins with clinical assessment and compression ultrasonography. A normally patent vein collapses under appropriate transducer pressure; a thrombosed segment often fails to compress. Doppler ultrasonography adds information about flow, and suspected pelvic disease may require further imaging. A negative initial study does not close a strongly suspicious case; repeat or additional imaging may be needed. Fever and systemic illness prompt assessment for infection, while breathlessness, chest pain or collapse require urgent assessment for pulmonary embolism.^[ref]

Unless contraindicated, therapeutic low-molecular-weight heparin is the usual treatment during pregnancy. It limits further clot formation while the body's own processes deal with the existing thrombus; it is not an instant mechanical solvent. Management also provides analgesia, elevation and appropriate mobilisation once stable, with fitted compression for symptoms when suitable. Prolonged compulsory bed rest is not a general modern remedy. A threatened limb or suspected massive pulmonary embolism needs immediate specialist escalation; routine thrombolysis for every swollen leg would expose patients to unjustified haemorrhage.

For confirmed pregnancy-associated venous thromboembolism, treatment usually continues through the rest of pregnancy and for at least six weeks after birth, with at least three months' treatment in total; the delivery plan must account for bleeding and anaesthesia. Antibiotics address a demonstrated or strongly suspected infective complication, not uncomplicated venous thrombosis itself.^[ref]