408 



STOMACH AND INTESTINE. 



of the stomach, long known to occur in ill- 

 nourished infants, or in cases of hydrocephalus 

 or brain disease, point just as decidedly to 

 the influence of an abnormal state of nutri- 

 tion in favouring this state. 



Lastly, there are many cases of acute dis- 

 ease, in which the softened stomach is more 

 or less coloured by blood that has stagnated 

 in its walls, where we have the additional dif- 

 ficulty of determining whether this congested 

 condition preceded or followed death. 



Hyperoemia. The hyperaemia of the diges- 

 tive canal constitutes an abnormal state, the 

 correct appreciation of which is of great pa- 

 thological importance. Of course, even the 

 loosest interpretation of the term would limit 

 it to an increase in the quantity of blood pre- 

 sent in the vessels of the alimentary tube ; and 

 would thus exclude a condition which is ca- 

 pable of being confounded with it : namely, 

 a transudation of the mere colouring matter 

 of the blood from neighbouring parts. 



But there are many circumstances which 

 render it very difficult exactly to determine 

 the amount of true hyperaemia present in any 

 segment of the digestive canal after death. 



Thus, while there is little doubt that hyper- 

 aemia is a stage of almost all the processes 

 ordinarily regarded as inflammatory, as \vell 

 as of those which result in the deposit of 

 adventitious growths, the examination of the 

 digestive canal after death shows that this 

 condition by no means accurately coincides 

 with these processes. On the contrary, it is 

 often absent in the very cases in which the 

 symptoms during life might best entitle us to 

 expect it. And conversely, it is often present 

 where death has been the result of accident, 

 or of disease no way referable to the organ 

 which is the seat of the congestion. We are 

 therefore bound to conclude: (1.) that the 

 presence of hyperaemia in any part of the di- 

 gestive canal does not necessarily prove this 

 part to have been the seat of disease during 

 life ; and, (2.) that the absence of hyperaemia 

 in the dead structure does not disprove its 

 previous presence in the living organ. And 

 we have therefore to inquire: (1.) What 

 causes can produce it in the healthy tube? 

 (2.) What circumstances can efface it from 

 the diseased tube ? And (3.), what are the 

 marks by which we may recognize hyperaemia 

 in the corpse, as a true and characteristic relic 

 of diseased action during life ? 



It is to the phenomena of death, as this 

 process usually affects the organs of circu- 

 lation, that we must first look for an answer 

 to the above questions. A very cursory 

 allusion to these phenomena may suffice to 

 indicate, in what manner they can by turns 

 imitate, modify, or efface the state of true 

 hyperaemia occurring during life. The rigor 

 mortis of the dying arteries flushes and dis- 

 tends the capillaries beyond them with an ab- 

 normal quantity of blood. The degree, date 



dicate that although it is probably preceded and 

 assisted by an unhealthy state of the tissues of the 

 stomach, the gastric juice is at least the chief im- 

 mediate agent of the change. 



and extent of this arterial contraction in dif- 

 ferent vessels, will obviously be capable of 

 imparting almost any moderate amount of 

 distention or congestion to the terminal net- 

 works they respectively supply. And at a 

 later period after death, the gravitation of the 

 now stagnant blood may distend the vessels 

 of any dependent part of the body. But the 

 congestion of one part implies other things 

 being equal the drain of some others which 

 are immediately contiguous to it. And hence 

 the very occurrences which can cause mode- 

 rate hyperaemia in a healthy segment of in- 

 testine, may at the same time produce a cer- 

 tain amount of anaemia in another ; and, may 

 therefore diminish and, when moderate, re- 

 move a state of simple congestion due to 

 disease. 



It would be easy to accumulate instances 

 of the fact last alluded to. The state of 

 really intense, though healthy, hyperaemia, 

 which is present during the periodic activity 

 of the stomach or other parts of the canal, 

 rarely leaves any traces after death, unless in 

 animals who are examined very speedily after 

 this event, and before these new adjustments 

 of its circulating fluids have had time to take 

 place. In like manner, the increased vascu- 

 larity of the intestines which accompanies 

 cholera or diarrhoea is often just as com- 

 pletely effaced after death: disappears, in 

 short, in the same manner in which the red- 

 ness of erysipelas and various other cutaneous 

 disorders rapidly fades away in the first few 

 moments that immediately follow the last 

 breath. 



But, even with all allowances for such 

 sources of error, the condition of hyperaemia 

 is one of the highest significance in the patho- 

 logy of the digestive canal. It is, generally, 

 an important sign of disease. And, with 

 proper attention to its collateral circumstances, 

 its import need rarely be misinterpreted. 

 Thus, as regards the extent of the process, 

 an intense and minute congestion is almost 

 always morbid ; and is obviously much less 

 likely to be removed by the phenomena of 

 death, than one of more moderate hyperaemia. 

 Again, a long duration of the abnormal vascu- 

 larity, as in the hyperaemia of chronic disease^ 

 generally brings about such a definite and per- 

 manent enlargement of the vessels concerned, 

 as evidently tends to enable them better to 

 resist the action of these cadaveric changes. 

 In other instances, a similar result appears to 

 be produced by a process of exsudation 

 around the vessels; and by changes in the 

 structure of these tubes themselves. It must, 

 however, be confessed, that we do sometimes 

 meet with specimens of tolerably intense con- 

 gestion of a part of the alimentary canal, 

 where it is only from the presence or absence 

 of corresponding symptoms during life, that 

 we can conjecture whether the state of hyper- 

 aemia has preceded or followed death. 



Of course, the mere hyperaemia of any net- 

 work of capillaries may be determined in two 

 ways : either by an increased afflux, or by 

 a diminished reflux, of the blood. But the 



