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whether there is a panacea for dental ills. The vagariesof the single case must be assessed by the dental surgeonto the best of his ability, and the treatment variedaccordingly.

CHLOROFORM IN OBSTETRICS

No-oNE would willingly reopen the old controversy 1about whether to use or not to use chloroform in labour, 1but Sheehan’s’ paper on acute yellow’ atrophy and 1delayed chloroform poisoning should not be overlookedeither by habitual devotees of chloroform or by those iwho use it but rarely and then with misgivings. Both 1true acute yellow atrophy and obstetric yellow atrophy, 1which is a definite and separate entity, can be associated jwith labour without chloroform anaesthesia ; they aresimilar clinically but the former arises from a gross livernecrosis and is very rare in pregnancy, the latter from a 4gross fatty change in the liver with an entire absence of -

necrosis. Sheehan describes delayed chloroform poisoning =as being far commoner in obstetric than other types of patients, and maintains that this is not generally realisedbecause the liver lesion is not always recognised as dueto chloroform and is ascribed to the obstetric complica-tions. Three types of lesion are associated with threetypes of patient. In the first there is an isolated celllesion with a distinctive necrosis of scattered individualliver cells. This is the rarest form of delayed chloroformpoisoning and occurs as the result of overdose in a healthysubject. Sheehan describes two .cases, one dying 18hours and the other 2 days after chloroform anesthesiafor delivery. The commonest type is the second, a mid-zonal necrosis. Of the nine cases cited by Sheehan all hada long labour before the administration of chloroformbegan (a mean of 31 days). Two of the patients diedwithin a day of having chloroform ; the others developedtypical delayed chloroform poisoning and died 3-5

days after the administration. Some of theFe patientshad relatively short anaesthesia, the longest being45 min., and there was no clear relation between theamount of chloroform used and the severity of theillness. All of them had been almost starved for a few

days before the chloroform was given and were probablyin a condition of starvation acidosis, in which there is anitrogen retention apparently due to oliguria from

pressure on the trigone and ureteric orifices.2 The third

type, with a central necrosis, was found in two patients,each of whom had hyperemesis; they aborted withchloroform without preliminary intravenous glucose anddied 3-4 days later with the clinical picture of delayedchloroform poisoning. These patients have a meta-bolic disturbance which includes both an acidosis and agross ursemia, apparently related to the anhydraemia.The gross fatty infiltration of the liver seen in delayedchloroform poisoning in children apparently does notarise in obstetrics. Sheehan concludes that a healthypregnant woman is normally resistant to chloroform, andthe risk of liver damage from chloroform anaesthesia insuch a patient is therefore remote, but that this risk is veryreal in patients who have a gross metabolic disturbancebefore their anaesthetic begins. The common factor inall cases, and one which is easily obviated and treated,is a starvation acidosis. He urges that as much atten-tion should be given to the anaesthetic as to the obstetricproblems. The history of the few days prior to anoes-thesia is all-important, for, as Sheehan says, " the patientwho has been left in labour for a few days withoutadequate treatment is extremely susceptible to whatmay be regarded rather as a poisoning by delayedchloroform than as a delayed poisoning by chloroform."He accounts for the greater frequency of delayed chloro-fôrm poisoning in obstetric hospitals than in domiciliarymidwifery on the ground that it is to the hospitals thatpatients are brought for delivery when there has been

1. Sheehan, H. L. J. Obstet. Gynœc. 1940, 47, 49.2. Crawford, M. D. Ibid, 1939, 46, 540.

long delay in labour and when starvation acidosis hastherefore developed. If the history of the previous twoor three days is studied he maintains that almost

every case can be foreseen before the anaesthetic isbegun, and that the general prohibition of the use

of chloroform for fear of delayed poisoning is whollyunnecessary. Those who advocate chloroform in obste-trics can therefore point triumphantly to this article asvindicating their opinion, provided adequate precautionsare taken. Sheehan does not touch on the incidence ofimmediate fatalities under chloroform anaesthesia andthese are responsible for the opinion of many that theuse of chloroform is unjustified because they cannot beforeseen, and because experience on the part of theanaesthetist cannot prevent them. Nevertheless, suddendeath under chloroform in the labouring woman isextremely rare. These patients and these alone lookforward eagerly to the arrival of the anaesthetist, andhence in them there is no fear of the anaesthetic itself,and therefore no outpouring of adrenaline into the blood-stream during induction. And it is the simultaneousaction of adrenaline and chloroform on the heart whichseems most likely to lead to fatal ventricular fibrillation.8

SEROUS FLUID

TEXTBOOK accounts of the different pathologicalfluids found in serous cavities tend to be clear-cutbecause most of them are a legacy accepted withoutcriticism from older authors, but the clinician has goodreasons for disillusion. When a pathogenic organism isisolated, or, more rarely, when a diagnostic group oftissue cells is seen, diagnosis is simple, but commonly theevidence is only circumstantial and not too trustworthy.Paddock’s 4 review of more than 1500 fluids collected over25 years is one of the few critical analyses of the accepteddata. Apart from looking at a fluid the usual starting-point is the specific gravity and it is often held that 1016is the dividing line between dropsical (transudative) andinfected (exudative) fluids. Paddock found that 313cardiac fluids from the pleural cavity had an averagespecific gravity of 1010 but 10% were 1016 or more ;while tuberculous fluids averaged 1020, with 10% 1016or less. In ascites 95% of cirrhotic fluids were in thetransudative range while neoplastic fluids both from thepleura and peritoneum were evenly divided between theexudative and transudative specific gravities. A curious

discrepancy exists between cardiac fluids from the chestand those from the abdomen, a third of the latter havinga specific gravity of 1016 or more, with a correspondinglyhigh protein content. It seems then that the boundary -between the specific gravities of transudates and exudatesis a broad elastic band rather than a sharp, line. The

cytological and biochemical findings in aspirated fluidsare also variable though there are a few general indica-tions to help in the individual case. Erythrocyte countsof over 10,000 per c.mm. were found by Paddock intwo-thirds of neoplastic fluids and in a third of cirrhoticand pulmonary-infection fluids, ’but the possibility of

damage by the puncturing needle may lead to doubt ofthe accuracy of all such figures. White-cell counts aremore useful, but in 85% of fluids associated with acutepulmonary infection, in 73% with tuberculosis and in42% of neoplastic fluids there was a total count of morethan 1000 per c.mm. The high polymorphonuclearleucocytosis in pyogenic infections is a great aid but theremay be such a neutrophilia in non-infected cirrhoticfluids and in early tuberculous effusions, and Paddockrecords 9 proved cases of tuberculosis with more thanhalf the cells polymorphonuclear. It follows that evenwith the most familiar pictures one has to be on guard ininterpreting cellular findings. The same can be said ofthe protein content of the various types of effusions.

3. See Macintosh, R. R. and Pratt, F. B. Essentials of General Anæs-thesia, Oxford, 1940, p. 174.

4. Paddock, F. K. New Engl. J. Med. 1940, 223, 1010.