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TREATMENT OF PNEUMOCOCCAL MENINGITIS

J. W. D. GOODALL.African Hospital,

Zomba, Nyasaland.

8.,-I have read with interest the article by Dr.Gibson and Dr. James. Excluding 3 deaths within

twenty-four hours of the start of treatment, they haveobtained a recovery-rate of 100%.My experience in Nyasaland has been very different.Since April, 1951, I have had 10 cases of pneumococcal

meningitis under my care ; 6 were in children betweentwo and twelve years of age, the remainder being in adults.I have had only 2 recoveries, 1 a child and 1 an adult.Treatment consisted in a daily intrathecal injection of50,000 units of penicillin with 100,000 units intramuscularlysix-hourly. This was supplemented with Sulphatriad ’ orsulphadiazine 1 g. four-hourly after an initial loading dose.All these patients had been ill for three or four days beforecoming to hospital. They usually improved at first ; butafter a week the theca became blocked, and in 2 cases

penicillin was administered by cisternal puncture with noimprovement.

I have tried intrathecal streptomycin and oral chlor-amphenicol with no better results. Up to date I havefound no means of improving on our 80% mortality-rate.As far as I am aware, most doctors in Central Africahave had similar experience ; and Dr. E. R. Cullinan,who recently visited Nyasaland, informed me that hehad gained the same impression in other parts of Africaduring his tour as Nuffield visitor.

I have never given penicillin in as large a daily dosageas the 1,600,000 units used by Dr. Gibson and Dr. James.I would not like to increase the intrathecal dose, as evenwith 50,000 units convulsions have occurred.

1. Gibson, C. D., James, D. G. Lancet, 1952, ii, 1203.2. Dreyfuss, F., Ikin, E. W., Lehmann, H., Mourant, A. E. Ibid,

p. 1010.3. Scriver, J. B., Waugh, T. R. Canad. med. Ass. J. 1930, 23, 375.4. Beck, J. S. P., Hertz, C. S. Amer. J. clin. Path. 1935, 5, 325.

SEARCH FOR SICKLE-CELL TRAIT

LIE-INJO LUAN ENG.

University of Indonesia,Department of Parasitologyand General Pathology,Salemba 6, Djakarta.

SiR,-I read with great interest the article byDr. Dreyfuss and his colleagues 2 on the search for sickle-cell trait in Yemenite Jews.A few months ago I had the same difficulties that these

investigators describe. Using the moist stasis methodof Scriver and Waugh 3 I investigated more than 200Indonesian patients (taken at random from the GeneralCentral Hospital at Djakarta). Of the 216 patientsexamined in this way, 2 were found positive for sicklingof the blood. Moreover, a private patient of mine withabdominal crisis was also found positive. -

Assuming that the method of Scriver and Waugh wasspecific and that a positive result indicated a sickle-cell trait or sickle-cell anemia, I believed that I had

found the sickle-cell trait in Indonesians. However,further examinations of the blood of the same patientsgave inconsistent results. Sometimes I obtained positiveresults and at other times negative results in the samepatients. I have since found more positive tests for

sickling with the same lack of consistency.As a routine all the slides to be used were cleaned in

bichromate/sulphuric-acid mixture for two days, then washedin running water. They were then placed in distilled waterfor twenty-four hours and finally transferred to absolutealcohol, where they remained until use.On one occasion I used a batch of slides which had been

treated as described above except for the cleaning withchromic acid. This batch of slides gave many positive resultswith blood of different patients taken at random from thehospital. However, using another batch of slides thesesame patients gave negative results. I collected the slideswhich gave positive tests and examined my own blood onthem. As a control, slides which had given negative resultswith the blood of the same patients were also tested withmy blood. All the slides which gave positive tests with thedifferent patients’ blood gave also positive tests with myhlood, and all the negative ones gave a negative result.B- the test-tube method of Beck and Hertz my blood and

that of these patients did not show sickling. Addition ofascorbic acid (2% or 5%) or bisulphite (2%) to the blood underliquid paraffin did not give sickling. Using the other sides ofthe slides with a positive preparation I could get the bloodof all my laboratory workers to sickle. I concluded that

something on the slide (a chemical substance ?) caused thesickling. Sometimes the whole preparation showed a full

development of the abnormal cells, but very often the sicklingappeared in localised areas. The sickling usually appearedafter twenty-four hours (sometimes earlier or later) butnever immediately as in the test with glue. õ It was furtherfound that incubation was not necessary, and a positiveresult could also be found without sealing the preparationand without preliminary stasis of the blood.

If a slide with positive test is washed not too vigorouslywith water, the same slide can again give a positive testwith any blood ; but after vigorous washing and brushingthe test becomes negative. Moreover, washing in bichromatesolution did not assure that a slide would not give an

erratic result.

I am of the opinion that the method of Scriver andWaugh, without control, should not be used as a routinetest ; for it is very difficult to be sure that a slide is

entirely free from the sickling substance, which (evenin traces) causes sickling of the blood of any person.When I read the article by Caminopetros 6 on sickle-

cell anomaly as a sign of Mediterranean anaemia, I

suspected that the factor described above caused thesickling in most of his tests, though perhaps not in all.If so, the difference between the findings of Dr. Camino-petros and those of Dr. Choremis 7 on the sickle-cell

. trait in Athens can easily be understood.. The same

suspicion arose when I read the article by Dr. Dreyfussand his colleagues.A more detailed description of my investigation will be

published later.

5. Isaacs, R. Science, 1950, 112, 716.6. Caminopetros, J. Lancet, 1952, i. 687. See also Ibid, pp. 1068, 1212.7. Choremis, C. Ibid, p. 1069; Ibid, ii, 42.

DEATH AFTER ANÆSTHETIC WITHHYPOTENSION

G. L. ALEXANDER.

Sin,—Dr. Bodman’s example of modern anaesthesia(Nov. 29) and Dr. Belfrage’s comment (Dec. 13) suggestthis question : How many such patients would be aliveand well today had they had chloroform on a bit of lint ?In the old rag-and-bottle days did we really kill as manyas now succumb to " advances " in anaesthesia ? Q .

I have spent twenty-five years in the tropics, inAfrica and on ships, where chloroform, given by anuntrained nurse or dispenser, is the only general anaes-thetic available ; and well it serves. us. Yet, I am told,there are persons with the D.A. who have never given itin their lives.And another thing ; what was the cost of all this,

compared with that of a few drachms of chloroform ?

CARTRIDGE-TYPE HYPODERMIC SYRINGE

SiR,-The introduction of the cartridge-type hypo-dermic syringe is an obvious sequel to the use of a similarinstrument in dental surgery for many years.The method is hardly suitable for intravenous injection as

the plunger cannot be deliberately withdrawn. The accidental,. recoil " of the plunger following injection is well illustratedby the simple test of injecting a small amount into a bottleof ink. The quantity of ink which flows up the needle andenters the phial on the release of the plunger has to be seento be believed.

Attention has alreadv been drawn to this drawback indental journals, for it is obvious that cross-infection could

easily result if a cartridge left over from a half dose wereused on a second patient.