The primary cause of splenomegaly would seem to
be a gastro -enteritis with repression of the glandular
digestive activities. In many cases the gastroenteritis is brought about by great mental strain.
The changed stomach and bowel condition sets up
fermentative and putrefactive processes giving rise
to vomiting, flatulence, distention and colic pain,
flatus, diarrhoea, frequent micturition. The putrefactive processes are set up by Bacilli of the typhoid
group which are facultative anaerobic and thus will
draw oxygen.from the surrounding tissue such as haemoglobin and be thus the cause of a slight chlorosis.
The intra and extra cellular toxins enter the portal
vein and mixing with the portal blood enters the
spleen. Some constituent is fixed by the connective
tissue cells there and neutralized. The 'aggressin'
element destroys the white blood corpuscle and the
serum complement the red blood corpuscle.
The destruction of the red blood corpuscle alters
the viscosity of the bile in the smaller bile ducts
and produces haemohepatogenous jaundice. The escape
of the toxins into the general circulation alters the
lining endothelium of the vessels and the coagulability
of the serum of the blood so that you have haemorrhages
especially from the ill- supported mucous membranes.
The irregular pyrexia means an irregular toxaemia.
The poisoning process may be repeated in the liver
with atrophy of the liver cells and ultimately ascites
from portal pressure.
Removal of the spleen throws into greater act - icity all lymphoid tissue of the body which may or
may not increase. If it does not increase then in
all likelihood this tissue is equal to the toxic
qualities present. If it does increase it may be due
to greater glandular capacity but more likely to a connective tissue hyperplasia such as is found in the
spleen and liver and which brings splenomegaly in
close similarity or proximity to Hodgkin's disease.
Finally. Idiopathic splenic enlargement.
Hanti's disease and splenic anaemia are one and the
same disease, all being dependent upon a bowel toxaemia
and differing only in the degree and intensity of the
putrefactive processes in the bowel.