|SURNAME:||Wainwright||FORENAMES:||Francis||BORN:||c1806||AT:||.||OCCUPATION[S]:||.||RELIGION/DENOMINATION:||.||FATHER:||.||MOTHER:||.||SIBLINGS:||Brother William Wainwright, 4LD
Brother John Wainwright, of Carnew Wicklow
|OTHER RELATIONS:||.||NOTES:||.||1st REGIMENT NO:||398||2nd REGIMENT NO:||.||ENLISTED:||07 12 1826 Dublin||ATTESTED:||.||HEIGHT AT ENLISTMENT:||.||TROOP NO:||Feb 1827: Depot Troop
Jun 1827: Troop 2
1831: Troop 2
|TROOP CAPTAIN:||1831: Captain Harcourt Master||RANK:|| 1827: Private
1829: Private, Corporal
1830: Corporal, Sergeant
|PROMOTIONS:||06 03 1829 From Private to Corporal
24 01 1830 From Corporal to Sergeant
|REDUCTIONS:||.||DESERTIONS:||.||COURT MARTIALS:||.||GIVEN UP TO:||.||GOOD CONDUCT BADGES:||.||MEDALS:||.||EMBARKATIONS:||16 02 1827 England||DISEMBARKATIONS:||12 06 1827 Bombay India||CAMPAIGNS:||.||OTHER DUTIES:||.||TRANSFERRED FROM:||.||TRANSFERRED TO:||.||DIED:||14 10 1832 Kirkee India aged 26 years. See autopsy report below||BURIED:||14 10 1832 Kirkee India||WILL:||.||BENEFICIARY:||.||NEXT OF KIN:||.||PRIZE MONEY:||.||NOTES:||.||AUTOPSY REPORT:|| CASE No. 5. Abscesses in the liver-diseased large intestines.
FRANCIS WAINWRIGHT, Sergeant, 4th Light Dragoons, AEt. 26; 5 years in India. Never had hepatitis nor dysentery.
June 21st, 1832, had febrile symptoms, oppression across the chest and slight cough, which were removed by leeches, &c. Discharged cured, June 30th.
Re-admitted October 3rd, 1832. Seized on the previous day with sense of cold, faintishness, retching, vomiting, and vertigo; followed by heat, pain at left hypochondre, stretching across to the right. Respiration difficult, anxiety, pulse quick, rather strong.
- 4th, pain severe last night; pulse 96, rather feeble, with a degree of sharpness: the pain is under the ensiform cartilage; secretions from the bowels foetid, unnatural.
- 5th, occasional retching; pain on turning and inspiring.
- 6th, pain when he moves; bowels acted on; evacuations of various colours.
- 7th, pain returned in the night, more on the right side; oppressed breathing and anxiety; can only lie on his back; no unnatural heat hiccup. Was bled thrice freely, leeched frequently; blistered; took purgatives. After the 7th, occasional vomiting; frequent irritable pulse; sometimes damp cold skin; occasional flushes of heat; occasional apparent amendment. Took camphor, opiates, wine. Latterly he was affected by hickup, but experienced relief from pain. Died October 13th.
It appeared that on the day previous to admission, this patient, who was remarkable for his bodily strength, after an exertion in throwing a heavy weight, felt sudden and violent pain across the hypochondria; was seized with vomiting; and he continued drinking cold water in his barrack-room, and came into hospital the following day. Habits somewhat intemperate.
Inspection, ten hours after death. Much fat in the integuments of the abdomen. The liver occupied the epigastrium and greater portion of left hypochondre; the stomach completely concealed. All the convexity of the left lobe of the liver, where opposed to the disphragm, adhered firmly to that muscle. Part of the convexity of the right lobe towards the great fissure was also adherent to the diaphragm; there was one large abscess in the left lobe, closely approximated to that part of the diaphragm where the adhesions had been formed. In fact, the upper wall of the abscess was in parts solely formed by the peritoneum of the liver and by the diaphragm; there was a similar abscess in the right lobe, but the diaphragm did not form the upper wall for so great an extent as on the other side; there were two other smaller abscesses in both lobes; the contents of the large abscesses were in part honey-coloured serum, which flowed out with the thinner parts of the pus. About 1 lb. of the thinner secretions in both abscesses. On making a section of the abscesses, they shewed internally a massive flocculent aspect, caused by the firm adherence of the thicker parts of the secretion to the lining membrane of the sac. It appeared as if the bonds of adhesion to the walls of the sac were by means of the normal vessels of the liver, which traversing or hanging loosely into the cavity of the sac became a nucleus to which the secretions adhered. The membrane lining the sac was not thick, but firm, and when the secretions were scraped from it shewed a rough granulated surfacel; the rest of the liver pale, distinctly mottled red and white: in the language of Andral, hypertrophy of the white substance. The lower lobe of left lung adhered, but not firmly, to the diaphragm: that of right lung did not so, though part of the adhesions of the liver were to that part of the diaphragm opposed to the right lung. The mucous coat of the stomach towards the pylorus dotted red, otherwise natural - no very marked lesion - no peritoneal inflammation.
In the coecum, ascending colon, and commencement of the transverse, there were round defined ulcers from the size of a split pea to that of a shilling; they had all defined prominent mucous edges. In the coecum there was the greatest number of these ulcers, there the ulcerated surface exceeded the non-ulcerated. The bottoms of all these ulcers consisted of partially condensed, opaque cellular tissue, adhering closely to the muscular tunic; in some few of them there was a thick purulent secretion. In the coecum here and there a dark-grey colour was observed, with that exception no discoloration round the ulcers. The mucous coat surrounded the ulcers was softened, and thinned; it peeled easily from the cellular tissue - the site of ulcer shewing a round, slightly elevated surface, prominent at the edges, more depressed within their circumference, each still somewhat above the surrounding cellular level. These edges were cellular tissue, which I had denuded of its mucous covering, which latter superimposed had formed the rounded edge of the ulcer. The disease then was ulceration, and removal of the mucous coat within the circumference of the defined edge. Where the mucous coat was removed, there slight hypertrophy and closer interlacement of the fibrils of the intercellular tissue existed, forming a firm bottom to the ulcer; - the elevated edge, a frame work of mucous coat. Beyond the ulcers the cellular tissue undiseased.
In the coecum, where the ulcers were so close to each other, the whole cellular tissue may be said to have been somewhat implicated - more certainly so at the site of the ulcer, but the diseased action extending beyond, communicated with that thickening dependant upon some other ulcer, and thus involved the whole cellular tissue.
At the middle of the transverse colon, the ulcers were fw, small, and like small pox-pits. In the descending colon, white granules like a millet seed - enlargement of the mucous follicles, the rest of the great bowels sound. Two feet of the ileum slit up - no disease. The coecum, and ascending and transverse colon contained a considerable quantity of consistent, dark-coloured feculence. Lungs and heart healthy.
Remarks. The cause of the acute symptoms in this case probably escapes us: there were no results of recent inflammatory action to account for them; they were not the symptoms either of abscess in the liver or ulcerated colon. Moreover, we must surely consider the lesions in both these organs to have existed much prior to the date of the fatal illness, to have existed, very much in the condition found after death, at a time when the patient was in the full enjoyment of health and remarkable for bodily strength: they were perhaps connected with the slight illness in June. It may be supposed that the feat of strength on the 2nd instant in some manner, though unrecognized, affected the already diseased organs. This case contrasts well with No. 2 [John Ryan]. The lesions in both were very much the same, yet how different the symptoms. In the one, according to my manner of viewing it, the changes took place and the health remained little disturbed. In the other each successive change had a symptom to mark the date of its occurrence.
It is contrasts as this which mark the true position of Medical Science: there are two other points of practical interest connected with this case. 1st. The evacuations were foetid and watery, very much similar to those frequently seen in remittent fevers, called bilious, and attributed to some error of the liver. Here they were connected with unsuspected ulcerated bowels. Case No. 8 [William Whitaker] is another reason for not losing sight of this circumstance. 2nd. It is probable that while the mucous lining was in a state of disease in this case, that the bowels were performing their functions well; at all events we have the distinct co-existence of ulcerated large bowels and healthy feculence. In the records of pathology, there are many cases where defecation during life has been well performed, and yet the large bowels were found ulcerated after death: these facts ought to be borne in mind, and keep us from too hastily concluding that the return of healthy evacuations in dysentery is a necessary index that the disease has been cured.
It is a too common belief that when the function of an organ which has been diseased is again naturally performed, the tissues of the organ have resumed their normal condition. The fact would seem to be that the amount of perfectibility which renders an organ efficient to meet every legitimate demand is far superior to that which fits it to play its part under ordinary circumstances. The ulcers were probably in the mucous follicles: the implication of the sub-cellular tissue bearing relation to the amount of disease of the mucous coat was thinned in some places. A condition similar [according to one view] to the portions of lower level in the colon of No. 2. [John Ryan] and coecum of No. 4. [John Garness]
|BL SOURCES:||IOR/N/3/10||OTHER SOURCES:||Transactions of the Medical and Physical Society of Calcutta, Vol. 7, 1835||LINKS:||.|
4th Light Dragoons Index