The face is flushed, and wears a drawn, anxious expression, and the eyes are bright.  A characteristic sweetish odour, which has been compared to that of new-mown hay, can be detected in the breath and may pervade the patient.  The appetite is lost; there may be sickness and vomiting and profuse diarrhoea; and the patient emaciates rapidly.  The skin is continuously hot, and has often a peculiar pungent feel.  Patches of erythema sometimes appear scattered over the body.  The skin may assume a dull sallow or earthy hue, or a bright yellow icteric tint may appear.  The conjunctivae also may be yellow.  In the latter stages of the disease the pulse becomes small and fluttering; the tongue becomes dry and brown; sordes collect on the teeth; and a low muttering form of delirium supervenes.

Secondary infection of the parotid gland frequently occurs, and gives rise to a suppurative parotitis.  This condition is associated with severe pain, gradually extending from behind the angle of the jaw on to the face.  There is also swelling over the gland, and eventually suppuration and sloughing of the gland tissue and overlying skin.

Secondary abscesses in the lymph glands, subcutaneous tissue, or joints are often so insidious and painless in their development that they are only discovered accidentally.  When the abscess is evacuated, healing often takes place with remarkable rapidity, and with little impairment of function.

The general symptoms may be simulated by an attack of malaria.

Prognosis.—­The prognosis in acute pyaemia is much less hopeless than it once was, a considerable proportion of the patients recovering.  In acute cases the disease proves fatal in ten days or a fortnight, death being due to toxaemia.  Chronic cases often run a long course, lasting for weeks or even months, and prove fatal from exhaustion and waxy disease following on prolonged suppuration.

Treatment.—­In such conditions as compound fractures and severe lacerated wounds, much can be done to avert the conditions which lead to pyaemia, by applying a Bier’s constricting bandage as soon as there is evidence of infection having taken place, or even if there is reason to suspect that the wound is not aseptic.

If sepsis is already established, and evidence of general infection is present, the wound should be opened up sufficiently to admit of thorough disinfection and drainage, and the constricting bandage applied to aid the defensive processes going on in the tissues.  If these measures fail, amputation of the limb may be the only means of preventing further dissemination of infective material from the primary source of infection.

Attempts have been made to interrupt the channel along which the infective emboli spread, by ligating or resecting the main vein of the affected part, but this is seldom feasible except in the case of the internal jugular vein for infection of the transverse sinus.