The acidosis following anaesthesia is of intense importance, and is met with in two well-marked forms: -

(1) Acute. This is apparently quite sudden in its onset, intense restlessness, or in children screaming, supervening from eight to thirty hours after operation; but these symptoms are in reality preceded by a semi-comatose condition, which is usually attributed to the anaesthetic, and so much valuable time is lost in commencing the treatment. Rapid pulse, slight icteric tinge of the conjunctiva, a hay-like odour of the breath, persistent vomiting, and a rise of temperature combine to indicate the gravity of the condition, and examination of the urine reveals the presence of acetone and diacetic acid. Death takes place in from twelve hours to four days, and then the urine may contain leucin and tyrosin. This acute type occurs chiefly in children who have suffered from cyclic vomiting or some congenital lesion, although it may also arise in septic abdominal cases in badly fed adults.

(2) Subacute. This variety is much more common, and its presence is manifested by a rapid pulse and vomiting, often prolonged from two to four days, and the severity of which is proportional to the amount of acetonuria.

In delayed chloroform poisoning, the oxidation process is diminished in intensity, and the fats not being properly oxidised, their acids accumulate in large amounts. These acids increase the autolysis, and if this has had a good start and become fairly pronounced, then the exhibition of alkalis can only neutralise them, and does not suffice to repair the damage done to the tissues. As hepatic changes are frequently present, it is surmised that the liver is chiefly responsible for the formation or distribution of the acetone bodies. Embden has demonstrated by perfusing a recently excised liver with normal blood that acetone is found in the hepatic vein and must therefore have been formed in the liver. This cannot happen in normal liver, so that profound changes must be present either in the shape of damaged cells or a diminished blood supply. In either case this means imperfect functioning and lessened oxygenation, and the fatty acids, being imperfectly oxidised, exhaust the store of alkalis, impair hepatic activity, and interfere with the glycogenic function, while in the effort to obtain the much-needed energy, the fats in the subcutaneous tissues are attacked. After death the glycogen is almost exhausted from the liver, and it is known that starvation and limitation of carbohydrates can deplete the store of glycogen.

Acidosis, therefore, may be said to be due to a lack of carbohydrates in the food, or a lack of ability to use the carbohydrates, or, still further, an increased capacity for consuming the fat of the food or the body. Its pathology is still somewhat uncertain, but what is fairly clear is that the body is incapable of completely metabolising fats excepting in the presence of carbohydrates.