ANOCI-ASSOCIATION IN THE PREVENTION OF SHOCK AND POST-OPERATIVE DISCOMFORTS: AN EXPERIENCE OF 143 CASES
Authors: H. B. Butler, E. W. Sheaf
Journal: BMJ (1914)

PtEVE VNTION OF SHOCK.TNRITuUWm s ;f -ULY 18, 19141, r~~~~~~~~~~~~~~~~~~~~~MZDICAL JOUBN94L.I3 the cause', providing tllis is done before tlle development of adenoluata or cysts.Glands containing these will subside as a 'whole' but tlie adenomiata-or' cysts are left.The administration of iodine may cause a slight diminu-' tion in their size, but they have not disappeared even after ei hteen months', treatmnent.Cysts and adenomata shotld' be treated along-the usual surgical lines.Tile symptoms of excessive secretion at first rapidly diminish'after removal of the cause,' and then more slowly pari.pacszb with the diminution in' tlle size of the gland.Any excitement will for tlle moment bring these symptoms again into evidence.If the disease has progressed so far tlhat the various organs have beconle degenerated, only partial recovery can be made.The patient may be left with a dilated heart, permanent albuminuria or glycosuria,>or -vith some weakness of tlle nervous system, either central, periplheral, or sympathetic, leading to feeble mentality, paralysis of a nerve, or some vasomotor disturbance.These require appropriate treatment.Acute Exophthalmic Goitre.Tfhese cases arise from the effect of a toxaemia actiDg on a gland that.isalready hypertrophied and lhas led to liyperthyroidis,m or typical.exophthalmic goitre.Th6 added stimulus gives rise t,o an acute exacerbatiou which miay rapidly lead to death.Treatiment is a mlatter of difficulty, as the five cases quoted slhow.Medicinal measures may prove unavailing, removal of tlle toxaemia nlay be impracticable, anld any attempt to remove a portion of the gland may prove fatal.CASE Iv.-A.L., male, 30, developed an acute catarrhali.sinfection before involution was complete from exophthalmic goitre and died in a few weeks despite all medical remedies.CAS-E v.-F.H., male, 30.An extention of a catarrhlalis infection on exophthalmic goitre caused death in five days despite medical remedies.CASE XXII.-S.L., female, 28.Developed an acute catarr7lali.sinfectioll on medium type exophthalmic goitre and went rapidly down hill.An attempt to remove half the thyroid under Crile's alnaesthesia proved fatal.CASE XXI-I.-V.D., female, 25.Developed acute exophthalmic goitre onl endemic goitre and teeth infectioni.She lost 26 lb. in weight, but recovered under miiediciinal treatment after appearing moriturus for some weeks.Slhe niow exlhibits the combination of myxoedema and degeneration of various organs from exophthalmic goitre.CASE XXIV.-M.It., female, 51.An acute exophthalmic goitre developed from the effect of acute c(atslarhalis oni exoph- thalmic goitre 'from chronic catarrhialis alnd teeth infection.Recovery after partial thyroidectomy under Crile's anaesthiesia.Such cases can only be treated on their own merits.CONCLUSIONS AND SL-M1MARY.Endemic goitre is caused by the toxins froom tlle atypical formis of B. coli.Tlle mnutants are usually con- veyed by water.Tlhoy becomue indigenous in the intestine, and different mutants of B. coli are to be found in tlle faec'es of cases of endemic goitre.The muLtants are but -arely present iii .thefaeces of normal individu,als or in the faeces of individuals goitrous from othler causes.It is possible to conceive circumstances wllich place the B. coli under abnormal conditions in the intestine itself, and lead to mutation and the temporary appearance of miutcants in the faeces of normal individuals.Tllh mutants set up an apyrexial toxaemia, which stimulates tlle tllyroid, so leading to a colloid hyperplasia and eventually to enlargement of the glancl.Tlhe whole process can be imitated in the laboratory, an(d ,endemic goitre induced in guinea-pigs by feeding witl siuall'doses of the mutants.