often been found, and have been regarded as causative in some cases. A peculiar form of diabetes with hepatic disease and general icteroid staining (hemochromatosis) of the skin and other tissues has been described under the title diabète bronzé. Skin eruptions (eczema, furuncles, carbuncles) are frequent in certain forms of diabetes, and gangrene of the extremities is common. Pneumonia and pulmonary tuberculosis are among the frequent developments of late stages of the disease. Chronic endocarditis, neuritis, and cataract are comparatively rare lesions. The blood in diabetes is less alkaline than normal and contains an excess of solid matter, particularly when great polyuria has led to inspissation.

Oxaluria. This term is, strictly speaking, applicable only to increase of oxalic acid in the urine, but is usually employed for cases in which crystals of oxalate of lime are found abundant in the urine. The normal maximum of oxalic acid is 20 mgr. for twenty-four hours. It has been sometimes held that oxaluria is a result of deficient oxidation of the carbohydrates or of the albumins of the body, but this theory has not been established. True oxaluria determined by chemical estimation of the total excretion of oxalic acid has been found in jaundice and in some cases of diabetes. The authors who have argued in favor of a specific disease marked by nervous symptoms and oxaluria based their observations on the presence of an excess of oxalate sediment, rather than on chemical examinations. Increased sediment occurs in certain instances of gout in which the oxalates alternate with uric acid or coexist with this. In these cases, as in cases of oxalate calculus in the kidney or bladder, the important causative factor is most probably some alteration in the constitution of the urine, such as conversion of monosodic phosphate into the disodic phosphate, that reduces the solvent power of the urine for oxalate of lime.

Phosphaturia. This term should be restricted to increased excretion of phosphoric acid, rather than to the presence of increased phosphate sediment in the urine. The latter may be due simply to want of acidity of the urine. The daily maximum of phosphoric acid with ordinary diet is from 3.5 to 4 g. The term phosphaturia might also be applied to cases in which no absolute excess of phosphoric acid is found, but in which this substance is relatively in excess when compared with the excretion of nitrogen. The normal proportions are from 17 to 20 parts of phosphoric acid for 100 parts of nitrogen. Phosphaturia in the sense just described has been found in some cases of inanition. Decided increase in the phosphatic excretion, absolute as well as relative, occurs in some cases of diabetes; also in cases of tuberculosis and disease of the bones, such as ostitis and osteomyelitis. In considering the question of phosphatic excretion in the urine it is important to remember that the greatest portion of phosphoric acid is derived from the food, only minor quantities coming from the metabolic consumption of tissues. Further, it must be remembered that much of the phosphoric acid of metabolism is excreted through the bowel. The term diabetes phosphaticus has been used by Teissier for phosphaturia in the sense of increased total excretion, and four varieties have been described: (a) cases with polyuria and marked nervous symptoms; (b) cases preceding or accompanying pulmonary diseases, especially tuberculosis; (c) cases in which phosphaturia alternates with or coexists with glycosuria; and (d) cases in which oxaluria, polyuria, and slight albuminuria are present and in which there is some relationship with gout.

The nature of the metabolic disturbances in phosphaturia are obscure. Sometimes the disorder of metabolism seems to be merely quantitative, in other cases doubtless qualitative.

FEVER.

Definition. It is not easy to define this term accurately, though we may regard as fever a condition in which the temperature of the body is elevated above the normal (98.6° F.; 37° C.) and in which the tissue-metabolism is altered in the direction of increased consumption. There are cases in which the latter is insignificant or wanting, and there are other instances in which the temperature remains normal or subnormal under influences that ordinarily provoke fever. It is doubtful whether mere elevation of temperature, such as occurs in experimental injury of certain parts of the brain, constitutes fever; but unquestionably it would be improper to apply this term to conditions of excessive tissuedestruction without elevation of temperature.

Nature. It is important, first, to consider the regulation of the temperature in health. In the normal individual heat is produced in the body by constant oxidation and other metabolic activities, and the excess is dissipated by radiation from the surface and the heating or evaporation of excreta. These processes of heat-production and heat-dissipation are regulated in an orderly manner under the influence of the nervous system. Special centers for the production, dissipation, and regulation of heat have been described by the physiologists, though their location and method of operation still remain in doubt. Whatever the exact mechanism may be found to be, it is quite certain that in some way the nervous system exercises a control over production and discharge of heat.

The excessive heat of fever may conceivably be due to excess of heat-production, to diminution of the dissipation, to both of these conditions, or to increase of both with greater excess of production. In most instances of fever in man it appears that production and dissipation are both increased, though the latter is insufficient. At the onset heat-dissipation may for a time be diminished. The increased production results from increased oxidation and other metabolic processes. A study of the respiratory exchange of gases shows that oxygen is consumed in greater quantity than normally, and the quantity of CO2 is correspondingly increased. The excess may amount to as much as 20 per cent., but in part this increased oxidation is due to the stimulation. of muscular contractions in rigor, etc. Investigation of the excreta shows at the same time evidences of more or less rapid and extensive tissue-waste. The quantity of nitrogen eliminated is in excess of that consumed in the food, and wasting of the tissues results. The albuminous elements suffer particularly in the metabolic wasting, the decrease of fat being more especially dependent on insufficiency of food.

Etiology. The causes of fever doubtless vary greatly. Di

rect exposure to heat does not affect the temperature more than a fraction of a degree in healthy persons, unless the surrounding temperature is very great. Ordinarily the heat-regulating mechanism maintains a proper adjustment. Excessive heat may, however, bring on fever, as in the case of sunstroke. Here, it has been held that the heat leads to direct disturbances of the nervousregulating apparatus; but recent investigations seem to show that there are first produced toxic substances which secondarily influence the heat-centers of the brain. In another class of cases still more direct disturbance of heat-regulation seems to occasion fever. Among these cases are the instances of fever in hysteria and other nervous diseases.

In the great majority of cases of fever it is quite certain that toxic substances are the cause of the febrile disturbances. These substances may be of quite different sorts. In the case of infections it is known that certain substances contained within the bacteria. themselves may cause fever, and that products of the growth of the micro-organisms may have the same effect. The latter are probably of albuminous nature. Other albuminous bodies resulting from normal or disturbed metabolism, independent of the action of bacteria, such as albumoses, peptone, tissue-fibrinogen, etc., may be equally potent; and various ferments, such as pepsin, fibrinferment, diastase, etc., are known to have the same power. These facts explain the multiplicity of causes capable of producing fever, as any chemical, mechanical, or bacterial injury of the tissues may liberate toxic substances, which in turn act upon the nervous system and occasion the phenomena of fever.

Pathologic Physiology.-Fever is accompanied by or leads to a variety of disorders. The appetite is lost, there is excessive thirst, emaciation is habitual, and the functions of the various organs are more or less disturbed. To a large extent these results are doubtless due to the presence of toxic substances in the blood and to other changes in this fluid. There is always a tendency to inspissation of the blood, the number of corpuscles being augmented (relatively) and the specific gravity increasing. This is not, however, invariably the case, as destruction of the solid matters of the blood may exceed the loss of liquid. The alkalinity of the blood is more or less reduced by the production of various acids in the increased tissue-destruction. A common or possibly characteristic metabolic process is the hydration of the albuminous tissues with formation of albumoses. There is little accurate knowledge of the toxic substances in the blood. The original poisons that caused the fever may be toxic for the entire organism, and other poisons may be produced by the elevation of temperature and the disturbed metabolism.

Pathologic Anatomy.-Definite morbid changes may occur in the various tissues of the body, notably the muscles, heart, liver,

and kidneys. Among these changes are cloudy swelling, fatty degeneration, and coagulation-necrosis. It is unlikely that these changes are the direct result of the increased temperature. More probably they result from the action of toxic substances generated in the course of the fever.

Conservative Effects of Fever.-While fever occasions many disturbances and leads to various pathologic consequences, it is not improbable that there is a certain measure of usefulness in it. Some authors have called attention to the fact that rapid reduction of the temperature under the influence of antipyretics is often followed by harmful consequences. This does not necessarily prove the usefulness of the fever, as the antipyretics are all capable of harm in themselves. A more definite proof of the uses of fever is that obtained by subjecting infected animals to high temperatures or to febrile conditions, and then studying the progress of the infection. Under these circumstances it has been found that the course of various infections, such as with the Diplococcus pneumonie, the bacillus of typhoid fever, and other organisms, is much milder and the consequences less serious than in animals not placed under the same conditions. These results agree very well with experiments with bacteria outside the animal body. For example, it is known that many of the bacteria are influenced unfavorably in their growth and virulence by excessive temperatures (104° to 107.6° F.; 40° to 42° C.). Whether in the body the temperature affects the micro-organisms directly or indirectly through the production of antitoxic substances, or in other ways, remains unsettled. It is not unlikely that increased circulation and respiration favor the elimination of the toxins that cause the fever. Increased toxicity of the urine has been found, but the methods employed are open to criticism.

CHAPTER III.

DISTURBANCES OF THE CIRCULATION OF THE BLOOD.

GENERAL DISTURBANCES.

THE circulation of the blood is maintained by the rhythmic contractions of the auricles and ventricles of the heart, aided by the elasticity of the arteries; by the compression of the veins by the muscles; and by the suction of the inspiratory movements of the chest.

General disturbances of the circulation result from lessened or

excessive heart-power, from arterial disturbances, or from changes in the quantity or character of the blood. Muscular and respiratory weakness may be contributing causes.

Weak Heart.-There are various forms of heart-disease that may lead to disordered circulation. The muscle itself may be weakened from overstrain, the fevers or other diseases, the action of poisons or insufficient nourishment, as in the anemias, or from narrowing of the coronary artery. The muscle may be soft and cloudy, fatty, or hardened by sclerotic changes. There may be no evident muscular disease, but merely functional weakness of the intracardiac ganglia. The valves or orifices of the heart may be diseased, and regurgitation or obstruction of the blood-flow results. Sometimes blood-clots form within the heart and similarly cause obstruction of the current. Finally, pericardial effusions or adhesions or tumors pressing upon the heart may seriously disturb its action.

The result of the weakened state of the heart must be the accumulation of blood in the venous system. The place of engorgement depends upon the part of the heart specially weakened. If the left ventricle fails, the blood backs into the left auricle and the lungs. As long as the right heart maintains its power the venous congestion goes no further; but when this fails repletion of the right auricle and of the systemic veins ensues. When the right heart is first at fault general venous congestion is an earlier manifestation. In all cases the arterial pressure falls and the blood-current is slowed, whereas the venous pressure is increased.

Sudden and complete failure of the heart causes anemia of the brain and syncope, which may prove fatal if not instantly relieved. Hypostatic Congestion.-In cases of serious weakness of the heart, in which it is quite unable to maintain an active circulation, the blood tends by the force of gravity to sink to dependent parts. This condition is known as hypostatic congestion. It occurs very frequently in low fevers and quite commonly just before slow death resulting from any cause. Dilatation of the vessels from vasomotor paresis, general muscular weakness, and the failure of vigorous inspiratory efforts are secondary causes.

The blood accumulates in the skin of the back, especially about the buttocks. The skin is of a livid color, but is bloodless over the bony points; the tissues tend to become sodden from transudation of liquid from the blood-vessels. Sloughing and gangrene (bedsores) may result. Internally, hypostatic congestion affects the lungs particularly, and a form of pneumonia may follow.

Post-mortem lividity is allied to hypostatic congestion. After death the blood gravitates to the dependent parts and accumulates