TRANSACTIONS OF SECTION I. 553 
by Caspar in 1850 hardly exceeding fifty. The present case occurred in the 
General Hospital, Birmingham, in October 1913, in a boy aged eight, admitted 
under the care of Mr. Woodman. He was a healthy lad who had been run over 
by a light motor van. Laparotomy disclosed a rupture of the liver about two 
inches long and one and a half inch deep close to the fissure of the gall bladder. 
The abdominal cavity contained about two pints of blood-stained fluid. There 
was no other lesion. Neither the shock nor the amount of blood lost was serious. 
The operation lasted half an hour, anesthesia having been initiated by chloroform 
and ether mixture for four minutes, and maintained thereafter by ether alone. 
The total amount of chloroform administered did not exceed two drachms. He 
recovered completely from the narcosis and did well for a time, but symptoms 
suggestive of septic poisoning supervened, and he died in about forty hours. 
On post-mortem examination no peritonitis or other inflammatory condition was 
found, nothing, in short, beyond the rupture and a markedly fatty state of 
the liver, to which the fatal toxemia could be ascribed. Microscopically an 
intense degree of fatty degeneration combined with a peripheral fatty infiltration 
existed in every lobule throughout the organ, but somewhat more severe in the 
neighbourhood of the rupture. Though there was no actual cell necrosis, the 
nuclei mostly staining well, the cytoplasm was markedly degenerated and had 
lost its power of retaining fat within its intimate structure. Its ‘masked’ fat 
had become visible in the form of numerous fine granules and globules within 
the hepatic cells, particularly those in the inner parts of the lobules—a condition 
of true fatty degeneration. ‘Towards the peripheral parts, on the other hand, 
the fat globules were fewer and larger—an infiltration instead of a degeneration. 
The peripheral cells had retained their normal function of infiltrating fat, and a 
larger supply being available, had produced a high degree of fatty infiltration. 
All the fat present readily absorbed the ordinary stains for fat, and, by giving 
the typical red-colour with Nile blue, was shown to be neutral fat. In short, 
the condition of the liver, while resembling phosphorus poisoning most closely, 
presented appearances similar to those resulting from the action of other 
poisons, notably those of the pyogenic organisms and of acute yellow atrophy. 
All these poisons damage the liver cells, producing granular and fatty degenera- 
tion often combined with fatty infiltration, if their intensity be not too great. 
But they all differ from delayed chloroform in that their results are certain, 
provided that the dose be sufficient, whereas in the case of chloroform the 
results are extremely capricious, hardly arising even in one case for every 
thousand in which they do not appear. That is, if the chloroform be inhaled, 
but if given by the mouth or subcutaneously, they follow as certainly as after 
the other poisons. This anomaly is not at present capable of explanation, 
except on the assumption of an individual idiosyncrasy, and, though individual 
susceptibility to certain drugs is an admitted phenomenon, it can hardly be 
regarded as satisfactory. A better explanation may be forthcoming with an 
increase in our knowledge of the physiological action of chloroform. The severe 
and persistent vomiting which is such a characteristic symptom of the disease, 
and the hemorrhagic inflammation of the gastric mucosa sometimes found, sug- 
gest that either chloroform or a toxic derivative thereof is secreted into the 
stomach and absorbed by the portal vein, but, even if true, it does not explain 
the capricious incidence of the disease. Ina considerable number of the recorded 
cases, the liver has already been damaged by pre-existing abdominal or other 
disease, and the chloroform may be held to act as the last straw, but in others, 
as in the present case, it has been healthy. But it is not difficult, as experi- 
ments show, to produce, and that rapidly, an extreme degree of fatty change 
within the liver under a variety of conditions, and it is possible that some 
other factor than the chloroform, not yet recognised, may be the cause of the 
disease. On experimental grounds alone it seems certain that ether cannot cause 
it. Though as yet unexplained, it seems probable that delayed chloroform 
poisoning does exist as a separate entity, and, though rare and fatal in its 
severer forms, may be not uncommon and transient in milder forms. 
Professors OSBORNE and Mitroy also took part in the Discussion. 
