521

20 hours after recovery from paralysis, so that it would seemthat regeneration of the ganglion cells takes place sometimeswithin 20 hours after disappearance of the symptoms of

paralysis. But we hope at some future time to study morecarefully the process of regeneration in the ganglion cellseither with cobra venom or with one of the other snake

poisons.In concluding, we wish to express our indebtedness to

Dr. J. Lindsay Steven for the use of his laboratory andapparatus in carrying out a part of this investigation. Oneof us (W. K. H.) has also to acknowledge aid from theCarnegie Trlzst in the form of a grant towards the expensesincurred in this investigation.

THE

RESPIRATORY AND CARDIAC REFLEX IN-DUCED BY PERIPHERAL IMPRESSIONS

ON THE PUDIC NERVE DURINGANÆSTHESIA.

BY ALEXANDER WILSON, F.R.C.S. ENG.,SENIOR ADMINISTRATOR OF ANÆSTHETICS TO THE ROYAL INFIRMARY,

MANCHESTER; SURGEON TO THE MANCHESTER ANDSALFORD LOCK HOSPITAL.

IN his " Address in Surgery" to the British MedicalAssociation Sir William Macewen refers to the familiar

spasm of the glottis produced during anaesthesia by forcibledilatation of the sphincter ani or irritation of the partssupplied by the pudic nerve. In these circumstances this

spasm is part, often the only surviving part, of an expulsiveeffort and has, I think, been recognised-as such for sometime. The causes which give rise to it are of a kind whichin normal circumstances tend to initiate expulsive efforts.Chief of these are any sudden increase in the intra-abdominal pressure-e.g., distension of the bladder or

rectum, the reduction of large hernias of old standing, theintroduction of the hand or large sponges into the abdominalcavity, dilatation of the sphincter ani and occasionally ofthe os uteri, &c. It may also be produced by any peripheralirritation, especially in young subjects. Its occurrence inthe course of surgical interference comes about in the

following manner.Expulsive efforts are performed through the agency of the

respiratory and other nerve centres in response to stimuli

reaching them from certain organs and conveyed by variousnerves, chief of which are the branches of the pudic nerve.Irritation of one of these nerves produces an impression onthe centre more or less equivalent to its normal stimulus andevokes a reflex response, just as irritation of the optic nervegives the sensation of a flash of light. During narcosisnormal stimuli conveyed to the nerve centres by a distendedbladder or rectum or abnormal stimulation by forcible dilata-tion of the sphincter ani or irritation of the pudic nerveresult in an expulsive effort. The completeness of this effortdepends upon the degree of narcosis ; that is, upon thenumber of unparalysed nerve centres that are left to carryout the act. This becomes evident when the constitution ofthe nervous system and its mode of reaction towardsanesthetics are considered.The nervous system as a whole is composed of numerous

nerve centres or nerve mechanisms which appear and reachtheir maturity at different periods in the evolution ofthe race and growth of the individual. The highest andmost complex of these functions are latest developed andleast able to resist disease or depressing conditions. Thisalso holds good as regards their response to the action ofchloroform and other anaesthetics. The continued inhalationof chloroform induces a progressive paralysis of the variousnerve centres, beginning with the highest, most complex, andlatest acquired functions, and ending with paralysis of thefundamental functions of respiration and circulation. Whatis true of the nervous system as a whole is equally true ofits more complicated reflex mechanisms which react toanaesthetics in a similar manner. Each reflex mechanismconsists of a fundamental and accessory elements, whichlatter by their cooperation assist in the performance of thereflex without being absolutely essential to it. Thus in

every such reflex there are associated several nerve centresthe coordinate action of which is necessary for the complete

development of the reflex. Under the influence of deepen-ing anaesthesia these associated accessory centres are the firstto be paralysed, but the essential factor in the reflex resistslongest and is the last to disappear.An expulsive effort is a mixed reflex intimately associated

with respiration but requiring for its most effectual per-formance the assistance of various nerve centres. Intrinsi-

cally it is an expiration, more or less forcible, necessarilyassociated with closure of the glottis. This sudden closureor spasm of the glottis is an essential or fundamental portionof the reflex and constitutes: the feature which differentiatesit from an ordinary expiration. This being so, the act ofclosing the glottis, as a fundamental factor in the reflex,should longest resist the anesthetic, and this proves to bethe case. Under the influence of the anesthetic the asso-ciated nerve centres gradually become paralysed, the responseto stimuli becoming less and less complete as fewer nervecentres participate in the action. Ultimately when thenarcosis has become profound the essential fundamentalportion of the reflex, the closure of the glottis, alone sur-vives. Finally, this, too, may be abolished and then theonly response to stimulation is evidenced by an alteration inthe respirations through the effect of the stimulus on

the unparalysed respiratory centre. Under varying degreesof narcosis every variety of expulsive effort may beseen from a complete effort accompanied with closureof the lips, alteration of the facial expression, and

"bearing down" in slight anesthesia, to the faintest

laryngeal stertor or mere catch in the breath in deep narcosis.The spasm cannot be safely abolished because it arises fromthe respiratory centre, which strongly resists the action ofanesthetics.When spasm of the glottis arises as the consequence of

peripheral irritation its mechanism would appear to be asfollows. Sudden acute pain in the conscious subject is metby an involuntary deep inspiration, followed by closure ofthe glottis and fixation of the chest preparatory to anexclamation or other effort. What occurs in the conscioussubject tends equally to occur in the unconscious or semi-conscious individual, but a number of centres being paralysedthe action is not complete or properly coordinated, hence thestertor. As regards the alteration in the pulse there are twofactors. The procedures inducing the above abortive ex-

pulsive efforts are all painful and as such cause a certainamount of shock and so may influence the circulation.Further, the circulation is intimately associated with, andin a measure dependent upon, the respiratory movements.Any modification of these, especially such as increase theintrathoracic pressure, as do expulsive efforts, of necessityalter the pulse and will account for the majority of thecases.

It is interesting to note that forcible dilatation of thesphincter ani has been suggested as a remedy in chloroformaccidents, the object being to stimulate respiration. Ofcourse, in the conscious subject an expulsive effort is pre-ceded by a deep inspiration but in a state of narcosis

sufficiently profound to induce respiratory paralysis thiswould not take place. It is questionable if at any stage ofnarcosis other than a very slight one this almost involuntarypreliminary inspiration could be elicited by dilatation of thesphincter ani.Manchester.

A CASE OF LATENT PORTAL CIRRHOSISWITH SUDDEN ONSET OF HÆMAT-EMESIS AND RAPIDLY FATAL

TOXÆMIA.

BY ROBERT M. MCQUEEN, L.R.C.P. LOND.,M.R.C.S. ENG.,

CLINICAL ASSISTANT AT THE VICTORIA HOSPITAL FOR SICK CHILDRENAND THE GROSVENOR HOSPITAL FOR WOMEN AND CHILDREN.

The following case is of interest from the great rarity ofthe concurrence of these conditions, the suddenness and

rapidity of the symptoms without any prodromal signs in acase of cirrhosis which had been latent for many years, andthe post-mortem examination revealing a healthy conditionof the abdominal viscera. ’

On April 26th, 1904, was called to see the patient, a stout,healthy man, aged 56 years. He had been perfectly well rp

522

to the previous day, but now complained of malaise anddrowsiness with a feeling of "fulness in the stomach."Examination proved negative ; no pain or abdominal tender-ness could be made out. The temperature was normal andthe pulse was 76 and soft. Simple gastric sedatives wereprescribed. On the next morning at 3 A.M. I was called tosee him. When I arrived I found that he had vomited abouta quart of blood consisting of small recent clots. He wasnow in a semi-comatose condition and very irritable andresisted any attempts at physical examination. Later inthe day a large motion consisting of altered blood was

passed and with considerable difficulty the following pointswere revealed by examination. In the epigastrium a hardtumour was felt of about the size of the closed fist ; it wassemi-resonant and apparently the surface was smooth, butowing partly to the patient’s mental condition and partly tothe fatness of the abdominal walls its relation to the livercould not be definitely made out. The edge of the liverwas felt in the right flank about two fingers’ breadth belowthe costal margin. There were no prominence of the super-ficial abdominal veins, no evidence of ascites, and no oedemaof the extremities. The patient was not jaundiced, the

tongue was clean, and the breath had no characteristicodonr. The temperature was 99° F. and the pulse was

84, soft and regular. The arteries were normal. Examina-tion of the thorax was negative. Later he became deliriousand finally comatose but recovered consciousness after anintravenous transfusion of a quart of normal saline solution.Urine was freely passed during this period of consciousness.There were no trace of albumin and no reaction with ferricchloride. The specific gravity was 1030. Unfortunatelythe improvement of his mental condition was only temporary,In about eight hours his pulse rose suddenly to 132 andsuspecting the possibility of another hsemorrbage one and ahalf drachms of adrenalin chloride were administered bythe mouth. Within half an hour the pulse had fallen to 96with decided improvement in his condition. On the next

day the patient rapidly lost consciousness again, the pulseremaining at 96. The weakness gradually increased. Sixhours before death the temperature rose to 102’6, four hourslater it was 104- 2°, and it was maintained at that point whendeath occurred.

Post-morterra examination.—Rigor mortis was present. Therewas about an inch of fat on the abdominal walls. There wereno enlarged veins and no signs of jaundice. The abdominal

cavity was free of fluid. The tumour felt in the epigastriumwas found to be the left lobe of the liver which was

moderately enlarged. The liver was "hobnailed." The rightlobe was of about the normal size and shape. It cut with in-creased resistance : on section it showed signs of coarse

cirrhosis of a multilobular type. The fibrous tissue was innarrow strands and evenly distributed throughout the organ.The gall-bladder was distended with normal bile, but nocalculi were present. The spleen was much softer thanusual and about double the normal size. There was noevidence of gastritis in the stomach beyond a small amountof mucus on the walls and it was not dilated ; petechisewere found at the cardiac end on the lesser curvature, overan area about two inches by one inch, together with two orthree small erosions at the same spot, but no evidence oferoded vessels was found. Only one inch of the oesophaguswas examined ; the veins were very prominent. The kidneyswere healthy. It is to be regretted that only a partial post-mortem examination could be made.The patient, a hypochondriac whose previous medical

history was uneventful, had, so far as it could be ascertained,always enjoyed good health and not suffered from any ill-ness. After his death I was able to obtain a history of freeindulgence in alcohol for a year or two which, however, wassaid to have ceased some seven years or more ago. Sincethen he had been a moderate liver, though there is reasonto believe that for about a fortnight before this illness hehad drunk to excess and had suffered great mental distress.Three months previously I had examined him thoroughly butcould not find any sign of local or general disease. Therehad at no time been any epistaxis, nausea, or dyspepsia,beyond occasional attacks of flatulence ; neither had vomit-ing occurred and the bowels were always very regular-infact, up to the onset of his illness there had been no reasonto regard him otherwise than as a healthy man with atendency to corpulence.The chief interest of this case lies (1) in the conjunction

of hasmatemesis and toxaemia, the latter being possiblyexaggerated by the hsematemesis ; (2) the latent hepatic

condition ; and (3) the fulminating quality of the symptomswhen they arose, all of which rendered diagnosis extremelydifficult. That toxasmia from somc cause or other was

present appeared probable from the absence of any definite,evidence of an organic cerebral lesion, but with the excep-tion of hsematemesis and what subsequently proved to be

enlargement of the liver the signs upon which to base a

diagnosis were purely negative. The urine was free from

sugar and albumin. The heart and the radial vessels were

healthy and there were no signs of renal disease. Probablyin this case an acute process had been set up in the liver

by the last bout of drinking, and this, together with thedecrease in the coagulability of the blood produced by thealcohol, would account for the rapidity and the combinationof the symptoms.As has been pointed out already, the peculiar feature of

interest in this case of latent cirrhosis is the sudden andsimultaneous appearance of hasmatemesis, which is usuallyan early symptom, and of toxasmic coma, usually a terminalevent in portal cirrhosis. The most satisfactory explanationwould appear to be that sudden and complete insufficiencyof the liver supervened, probably as the result of recentexcessive alcoholism. Gilbert and Carnot,’ who speakof this condition as "anhepatie," mention among itsmanifestations " multiple haemorrhages, delirium, andcoma." " It is possible that the small erosions in thestomach were due to the toxic action of the alcohol andtheir existence might account for the occurrence of the ex-tensive local hasmorrhage instead of multiple extravasations.Latent cirrhosis was thought of and that diagnosis was heldtentatively. Less difficulty might have been experiencedhad an alcoholic history been forthcoming earlier, but itsabsence at that time, together with the rare combination ofhasmatemesis and toxasmia, militated against the theory ofhepatic cirrhosis and it is owing to this unusual combinationthat I venture to place this case on record.

I am indebted to Dr. H. D. Rolleston for his kind

suggestions.Carlogan-garr1ens, S.W.

THE

MEDICAL TREATMENT OF DEEP-SEATEDHÆMORRHAGE.

BY FRANCIS HARE, M.D.,CONSULTING PHYSICIAN TO THE BRISBANE GENERAL HOSPITAL;

VISITING PHYSICIAN AT THE DIAMANTINA HOSPITAL FORCHRONIC DISEASES, BRISBANE ; LATE INSPECTOR-

GENERAL OF HOSPITALS FOR QUEENSLAND.

IT is generally admitted that most therapeutic advanceshave originated more or less accidentally in observation-that is, inductively, not deductively. The therapeutic pro-cedure advocated in this paper, should it be accepted as anadvance, is one of the exceptions to the above general rule.It was suggested by physiological considerations and onlythereafter put to the clinical test.

It may be stated as not open to question that haemorrhage,whether arterial or capillary, depends essentially upon theexistence of a certain blood pressure in the bleeding areaand that the indication for medical treatment consists in

reducing this localised blood pressure. Such we mighthope to achieve : (1) by promoting vaso-constriction ofthe arterioles supplying the bleeding area; or (2) bypromoting fall of blood pressure through widespreadvaso-dilation in other areas. It is to the first of thesemethods that attention is commonly directed. In cases

where the bleeding area is accessible to local treat-ment-for example, in certain cases of hæmatemesis—thepromotion of localised vaso-constriction, as by ice pills,adrenalin, &c., may be very successful. But frequently thebleeding area is inaccessible to direct local treatment. Thenin order to promote localised vaso-constriction we are forcedto fall back upon remedies which promote vaso-constrictiongenerally. Until lately ergot was the remedy usually usedfor this purpose, but now that far more powerful vaso-constrictor adrenalin is coming into general use. As regardsergot, though I have used it conscientiously for many yearsin cases of inoperable deep-seated haemorrhage yet I couldnever assure myself that it was of real advantage except, of

1 Les Fonctions Hépatiques, p. 273.