Drops of fat may be seen floating on fluid or semifluid blood after many operations and compound injuries, and the possibility of escape of fat--or, more accurately, its suction into the vessels from which this blood has escaped--is easily appreciable. But it has also been shown that absorption of fat is possible even from serous surfaces, and that fat embolism may occur when fluid fat has been passed into the heart through the thoracic duct, although more slowly. Oil drops are also found in the interior of the tissues, while in a piece of lung spread out in water in the visible vessels highly refracting fatty material may be noted. _Fatty infarction_, particularly in the lower lobes, is sometimes plainly visible to the naked eye. Under a low objective, especially with osmic-acid staining, the presence of fat is easily demonstrated. The essential danger in case of fat embolism is of so clogging the pulmonary capillaries that oxygenation shall become so imperfect as to lead to absolute asphyxiation from carbonic dioxide poisoning. When this fact is understood, the cyanosis, the rapid breathing, the overaction of the heart, etc., are easily and correctly interpreted. Fat embolism by itself cannot cause inflammation nor infection, nor sepsis in any sense. It may, however, lead to ecchymoses in conjunction with fatty infarcts in the organs most affected. The minute hemorrhages are easily explained by the bursting of the capillaries in the attempt to force blood through them. Fatty emboli, however, take the same course as do septic--are carried first to the right side of the heart and distributed over the lungs; are, if the patient lives, forced through the lungs into the systemic circulation, and are then carried to the brain, kidneys, etc. The first symptoms are referable to the plugging of the pulmonary capillaries; the secondary symptoms to the systemic disturbance. =Symptoms.=--Pallor of countenance with facial expression of anxiety and distress, followed by cyanosis and contracted pupils, are seen. Patients are usually first excited, sometimes more or less disturbed, then become somnolent, and, finally, comatose in the fatal cases. The respiration rate increases from normal up to 50 or 60, and breathing is sometimes stertorous. Dyspnea, increasing in intensity until it becomes agonizing, sometimes marks these cases. Occasionally foam, possibly blood, proceeds from the mouth, as in edema of the lungs. Sometimes hemoptysis occurs. The pulse becomes weak, frequent, and irregular, while toward the close it is fluttering. Temperature is not notably disturbed, at least not typically. These symptoms set in usually within thirty-six to seventy-two hours after the lesion which has caused them. I have, however, known death to occur in one or more cases within eighteen hours after reception of injury.