1222 



THE TROPICAL HEMOGLOBINURIAS 



principally in the blood of the liver and kidney, and to a less extent in that of 

 the spleen. The lysaemia produces hgemoglobinaemia, which is best demon- 

 strated by receiving the blood into hypertonic citrate solution and then centri- 

 iugalizing, when the serum is observed to be of an orange, rarely of a reddish, 

 colour. The amount of haemoglobin present in this condition was estimated 

 by Christophers and Bentley to be from i to 3*75 per cent, of that present in 

 normal blood. This haemoglobin quickly appears in the urine as oxyhsemo- 

 globin, which may become methsemoglobin on standing. All the haemo- 

 globin probably does not escape by the kidney, for there is evidence of increased 

 production of bile, and it is possible that only such quantity as the liver is 

 incapable of converting into bile appears in the urine. It is, however, by no 

 means certain whether the pigment escapes only by the glomeruli or through 

 the tubules, or by both, and it is also uncertain whether the haemoglobin can 

 pass through the cells of a normal kidney. 



Barratt and Yorke, on the other hand, find that the haemoglobinuria is not 

 dependent upon haemolysinaemia, but that it is due to a haemoglobinaemia the 

 origin of which they were unable to determine. 



They, supported by de Haan, consider that the suppression of 

 urine is due to a mechanical blocking of the renal tubes by the forma- 

 tion of large, firm, coarsely granular casts in the ducts of Bertini. 

 Plehn, however, ascribes this suppression to a nervous inhibition of 

 the glomerular secretion. Many authors ascribe the suppression to 

 nephritis caused by the disease. Recently the subject has been 

 reinvestigated by Yorke and Nauss, who support the mechanical 

 theory, and find that it is considerably facilitated^by any factor 

 which tends to lower the blood-pressure, and by that means the 

 secretion of water by the glomeruli, but that if the blood-pressure 

 is kept up by the injection of saline solutions, the tendency to 

 suppression is decreased. This is of importance in guiding the 

 treatment of the condition. 



Morbid Anatomy. — ^There are three cardinal features in the 

 morbid anatomy of a case which has died during blackwater fever, 

 and these are: (i) Jaundice of the tissues ; (2) Non-coagulated blood ; 

 (3) Swollen congested kidneys. In addition, there may be the signs 

 of acute or chronic malaria in the liver, spleen, and bone-marrow. 



On making the post-mortem, the yellow staining of the skin and 

 organs is most marked. The kidneys are enlarged, dark red to black 

 in colour, while microscopically they show degeneration of the 

 epithelium of the convoluted and other tubules, the lumen of which 

 is filled with granular material, while the glomeruli may contain 

 granular material, and show desquamated capsular cells. 



The liver is enlarged, and the gall-bladder full of inspissated bile. 

 Microscopically, areas of necrosis, with thrombi in the sublobular 

 veins and quantities of hsemosiderin in the cells, many of which may 

 be in a state of fatty degeneration, are to be seen. 



The stomach and small intestine are often hypersemic, and the 

 bone-marrow is yellowish, and either fluid or gelatinous. 



The Blood. — ^The blood is thin and watery, and there may be 

 hgemoglobinaemia and cholsemia, with lessened tonicity. The red 

 cells and haemoglobin are greatly reduced, and the former may 

 include shadow cells and small fragments of cells, and deep staining 

 round cells (spherocytes) in the early stages, and later may show 



