gastric acidity and its significance

2
1035 GASTRIC ACIDITY AND ITS SIGNIFICANCE tourniquet, pierce the full vein with a needle. Let it bleed a drop or two, catching the drops on wool. Gently lay the patient down backwards on the couch, affix the syringe to the needle (which is now in an empty vein), draw blood into the syringe (to make sure the needle is still in the vein), and inject. The tourniquet moreover is unpleasant for nervous patients, especially when pumped up to the arbitrary level of 180 mm. Hg. These " dodges also save time. I note that Mr. Bennett-Jones uses exclusively sodium salicylate 30 per cent. Sicard’s work was done exclusively with this. But, from long experience with various sclerosing fluids, I have come to the conclusion that different fluids are indicated in different types of veins and also in different types of patients. I largely use lithium salicylate 35 per cent. with 1 per cent. Ethocaine (an injection fluid we owe to R. Maingot), which has all the advantages of sodium salicylate and none of its disadvantages. It has however one drawback that I recently pointed out (Brit. Med. Jour., 1935, ii., 229)-viz., that clots seem to get bigger even ten weeks after an injection and lead occasionally to ulcers many weeks later. Therefore I avoid this fluid in superficially placed or thin-walled veins. Quinine is, I think, the most constant fluid to be effective; but patients do not like its associated momentary flushing of the face, buzzing head, and palpitation. Sodium morrhuate is most useful for small superficial veins, and its froth for skin venules. But it has its dangers in susceptible people (see Brit. Med. Jour., 1933, i., 430, 674). I would commend to Mr. Bennett-Jones the value of firm pressure over a large strip of the vein, for three days subsequent to its injection, of a firm wad of wool held in position by Elastoplast. In this way one secures smaller clots, a greater likelihood of occlusion, and, I am convinced, less chance of ultimate recanalisation. I am, Sir, yours faithfully, Liverpool, April 21st. STUART McAuSLAND. STUART MCAUSLAND. GASTRIC ACIDITY AND ITS SIGNIFICANCE To the Editor of THE LANCET SiB,—In an article under this title in your issue of Jan. 4th Prof. F. L. Apperly states that it was he who with Crabtree showed in 1931 that the CO 2 content of the fasting blood plasma governed the acidity of the gastric contents after a test-meal in any one individual, and that the CO content of the plasma was responsible for the differences in gastric acidity existing between different individuals. I wish to call attention to the fact that this observa- tion was made and described first by me (Klin. Woch., 1924, iii., 1951), and that I subsequently enlarged on this subject in several other publications (A New Approach to Dietetic Therapy, Metabolism of Water and Minerals and Its Disturbances, Boston, 1933, &c.). I showed, in addition, that in reality it is the concentration of all the acid substances in the blood rather than that of CO alone that, in accordance with the rules of physico chemistry, influences the concentration of hydrochloric acid in the gastric cavity. The acid substance of the blood which is quantitatively most important is CO and since the variations in the concentration of this acid are the most common occurrences, in most (but not all) cases a parallel behaviour might be found between its concentration in the blood and the gastric acidity. In addition to the concentration of the acid substances in the blood I showed that there is another factor that influences the concentration of hydro- chloric acid in the gastric cavity. This is the permeability of the membrane formed by those cells of the mucosa of the fundus of the stomach in which the production of hydrochloric acid takes place. If the permeability of this membrane decreases, as may occur as a consequence of a chronic gastritis, a low hydrochloric acid concentration or, in other words, a hypochlorhydria or achlorhydria may be found, notwithstanding the presence of a high CO 2 concentration in the blood or, generally speaking, in spite of a " hyperacidemia." (This relationship is similar to the association of a high urea-nitrogen content in the blood with a low urea-nitrogen content in the urine as a consequence of decreased permeability of kidney cells in chronic glomerulonephritis.) The existence of a chronic gastritis and the consecutive decrease in the permeability of the gastric mucosa would explain the seeming contradiction (to which Dr. Hurst calls attention in your issue of Jan. 18th, p. 168) that notwithstanding there is a high C02 content of the blood the hyperchlorhydria postulated by Apperly is absent in bronchial asthma. Another statement made by Apperly is that " there is a direct relationship between the red cell content of the blood and gastric acidity." This observation also was first published by me in the year 1924 (Zeits. f. d. ges. exper. Med., 1924, xli., 342, &c.). I described my findings in a statement that the higher the percentual volume of the red blood-cells in the whole blood ("hematocrit value ") the higher the gastric acidity. The existence of this relationship was explained by the observation that both the haematocrit figure and the gastric acidity are governed by the concentration of the acid substances in the blood. Mention should be made, however, that the behaviour of the red blood-cells is identical with that of acid substances in the blood, so that not only are these former influenced by the concentration of the latter. but that the red blood-cells in their turn influence the concentration of the acid substances in the blood, hence influence the gastric acidity as well. Consequently, a hypochlorhydria or achlorhydria may follow if there is a decrease in the red blood- cell content of the blood, an occurrence which I described in 1924 as " hematogenous hypochlorhydria or achlorhydria " (ibid., 1924, xliii., 247) and to which Apperly’s anaemic achlorhydria corresponds. It would appear, therefore, that Hurst goes too far in his contention that the red blood-cells do not influence the gastric acidity. In the production of the hydrochloric acid concentration in the stomach, however, consideration must not be given to the presence and physiological significance of only one acid substance, such as the erythrocytes, but to the concentration of all the acid substances. Thus the acids of the blood represented by the red blood-cells may be decreased on account of anaemia and yet the sum total of all the acids may be normal or higher than normal. This would explain the observation that anaemia may exist without achlorhydria or with normal hydrochloric acid concentration or even with hyperchlorhydria, the existence of such cases contradicting, as pointed out by Hurst, the assertion of Apperly that, when the red blood-cell content of the blood falls to about one-half or two-thirds normal, free acid disappears from the stomach. I am, Sir, yours faithfully, New York City, March 14th. EUGENE F6LDES. EUGENE FRÖLDES.

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1035GASTRIC ACIDITY AND ITS SIGNIFICANCE

tourniquet, pierce the full vein with a needle. Let itbleed a drop or two, catching the drops on wool. Gentlylay the patient down backwards on the couch, affix thesyringe to the needle (which is now in an empty vein),draw blood into the syringe (to make sure the needle isstill in the vein), and inject.The tourniquet moreover is unpleasant fornervous patients, especially when pumped up to thearbitrary level of 180 mm. Hg. These " dodgesalso save time.

I note that Mr. Bennett-Jones uses exclusivelysodium salicylate 30 per cent. Sicard’s work wasdone exclusively with this. But, from long experiencewith various sclerosing fluids, I have come to theconclusion that different fluids are indicated indifferent types of veins and also in different types ofpatients. I largely use lithium salicylate 35 per cent.with 1 per cent. Ethocaine (an injection fluid we oweto R. Maingot), which has all the advantages ofsodium salicylate and none of its disadvantages.It has however one drawback that I recently pointedout (Brit. Med. Jour., 1935, ii., 229)-viz., that clotsseem to get bigger even ten weeks after an injectionand lead occasionally to ulcers many weeks later.Therefore I avoid this fluid in superficially placed orthin-walled veins. Quinine is, I think, the mostconstant fluid to be effective; but patients do notlike its associated momentary flushing of the face,buzzing head, and palpitation. Sodium morrhuateis most useful for small superficial veins, and itsfroth for skin venules. But it has its dangers in

susceptible people (see Brit. Med. Jour., 1933, i.,430, 674).

I would commend to Mr. Bennett-Jones the valueof firm pressure over a large strip of the vein, forthree days subsequent to its injection, of a firm wadof wool held in position by Elastoplast. In this wayone secures smaller clots, a greater likelihood ofocclusion, and, I am convinced, less chance of ultimaterecanalisation.

I am, Sir, yours faithfully,

Liverpool, April 21st. STUART McAuSLAND.STUART MCAUSLAND.

GASTRIC ACIDITY AND ITS SIGNIFICANCE

To the Editor of THE LANCET

SiB,—In an article under this title in your issue ofJan. 4th Prof. F. L. Apperly states that it was hewho with Crabtree showed in 1931 that the CO 2content of the fasting blood plasma governed theacidity of the gastric contents after a test-mealin any one individual, and that the CO content of theplasma was responsible for the differences in gastricacidity existing between different individuals. Iwish to call attention to the fact that this observa-tion was made and described first by me (Klin.Woch., 1924, iii., 1951), and that I subsequentlyenlarged on this subject in several other publications(A New Approach to Dietetic Therapy, Metabolismof Water and Minerals and Its Disturbances, Boston,1933, &c.). I showed, in addition, that in reality it isthe concentration of all the acid substances in theblood rather than that of CO alone that, in accordancewith the rules of physico chemistry, influences theconcentration of hydrochloric acid in the gastriccavity. The acid substance of the blood which is

quantitatively most important is CO and since thevariations in the concentration of this acid are themost common occurrences, in most (but not all)cases a parallel behaviour might be found betweenits concentration in the blood and the gastric acidity.

In addition to the concentration of the acidsubstances in the blood I showed that there is anotherfactor that influences the concentration of hydro-chloric acid in the gastric cavity. This is the

permeability of the membrane formed by those cellsof the mucosa of the fundus of the stomach in whichthe production of hydrochloric acid takes place. Ifthe permeability of this membrane decreases, as

may occur as a consequence of a chronic gastritis,a low hydrochloric acid concentration or, in otherwords, a hypochlorhydria or achlorhydria may befound, notwithstanding the presence of a high CO 2concentration in the blood or, generally speaking,in spite of a

"

hyperacidemia." (This relationshipis similar to the association of a high urea-nitrogencontent in the blood with a low urea-nitrogen contentin the urine as a consequence of decreased permeabilityof kidney cells in chronic glomerulonephritis.) Theexistence of a chronic gastritis and the consecutivedecrease in the permeability of the gastric mucosawould explain the seeming contradiction (to whichDr. Hurst calls attention in your issue of Jan. 18th,p. 168) that notwithstanding there is a high C02content of the blood the hyperchlorhydria postulatedby Apperly is absent in bronchial asthma.Another statement made by Apperly is that " there

is a direct relationship between the red cell contentof the blood and gastric acidity." This observationalso was first published by me in the year 1924

(Zeits. f. d. ges. exper. Med., 1924, xli., 342, &c.).I described my findings in a statement that the

higher the percentual volume of the red blood-cellsin the whole blood ("hematocrit value ") the higherthe gastric acidity. The existence of this relationshipwas explained by the observation that both thehaematocrit figure and the gastric acidity are governedby the concentration of the acid substances in theblood. Mention should be made, however, that thebehaviour of the red blood-cells is identical with thatof acid substances in the blood, so that not only arethese former influenced by the concentration of thelatter. but that the red blood-cells in their turninfluence the concentration of the acid substances inthe blood, hence influence the gastric acidity as well.Consequently, a hypochlorhydria or achlorhydriamay follow if there is a decrease in the red blood-cell content of the blood, an occurrence which Idescribed in 1924 as "

hematogenous hypochlorhydriaor achlorhydria " (ibid., 1924, xliii., 247) and to whichApperly’s anaemic achlorhydria corresponds.

It would appear, therefore, that Hurst goes toofar in his contention that the red blood-cells do notinfluence the gastric acidity. In the productionof the hydrochloric acid concentration in the stomach,however, consideration must not be given to the

presence and physiological significance of only oneacid substance, such as the erythrocytes, but to theconcentration of all the acid substances. Thus theacids of the blood represented by the red blood-cellsmay be decreased on account of anaemia and yet thesum total of all the acids may be normal or higherthan normal. This would explain the observationthat anaemia may exist without achlorhydria or withnormal hydrochloric acid concentration or even

with hyperchlorhydria, the existence of such cases

contradicting, as pointed out by Hurst, the assertionof Apperly that, when the red blood-cell contentof the blood falls to about one-half or two-thirdsnormal, free acid disappears from the stomach.

I am, Sir, yours faithfully,New York City, March 14th. EUGENE F6LDES.EUGENE FRÖLDES.

1036 PUBLIC HEALTH

PROPHYLACTIC ENUCLEATION OF LOWERWISDOM TOOTH FOLLICLES

To the Editor of THE LANCETSIR,-I am sure that the medical profession as

a whole will be grateful to Mr. Bowdler Henry forbringing forward such an easy and entirely satisfactoryprocedure to cope with what is often a menacenamely, a badly impacted unerupted lower molartooth. By such a prophylactic measure as Mr. Henryhas introduced, all the numerous risks which are

attendant upon maleruption are eliminated. Surgeonsare familiar with some of the complications whichfollow the extraction of a badly unerupted thirdmolar and it has been my lot to be called into consulta-tion several times when fracture of the jaw hasresulted from attempts to remove such a tooth.I can vouch that prophylactic enucleation is entirelyfree from trauma, and is quite a simple operation ;one only wonders why such an easy remedy had notbeen thought of years ago.

I am, Sir, yours faithfully,CECIL P. G. WAKELEY.

Queen Anne-street, W., April 22nd.CECIL P. G. WAKELEY.

PURPURA HÆMORRHAGICA FOLLOWINGMEASLES

To the Editor of THE LANCET

SIR,-Your last issue contained an account ofpurpura complicating scarlet fever, and it may beof interest to put on record a case in which itfollowed measles.A girl, aged 4, was admitted to this hospital on

April 8th, with the provisional diagnosis of ,. black

measles." It appeared that she had a measles rashon March 29th ; on April 7th she came out with ahaemorrhagic rash and passed blood in the faeces andurine. She had widespread petechial and purpurichaemorrhages all over the body and sordes of

coagulated blood. The hands were a deep dark blue,the face pale and the child obviously poorly. Temp.,

99° F. ; pulse-rate, 120. She was given 20 c.cm. ofwhole blood from her father, as well as glucose andsaline intramuscularly. Both punctures bled veryfreely, but curiously when 20 c.cm. of scarlatinalantitoxin was given, also intramuscularly, the

puncture did not bleed. She passed a dark tarrystool; the urine was bright red with blood. Blood-

platelets numbered 35,000 per c.mm. ; otherwisethere was nothing strikingly abnormal in the blood.Prof. J. F. Wilkinson was consulted and advisedintensive vitamin-C therapy, both oral and hypo-dermic ; ascorbic acid was used, and in addition

eight lemons were given daily. She continued to

pass blood until April 15th, when both faeces andurine were clear. The skin gradually cleared, butpeeled profusely and serum continued to ooze in

places. She is making good progress towards

complete recovery. On April 24th the blood-plateletswere up to 100,000 per c.mm., and the generalcondition has improved considerably.

I am, Sir, yours faithfully,W. EDGE,

Medical Superintendent, Ladywell SanatoriumApril 27th. and Isolation Hospital, Salford.

W. EDGE,Medical Superintendent, Ladywell Sanatorium

and Isolation Hospital, Salford.

OMNIPRATICIENS

To the Editor of THE LANCETSIR,-I have just observed that in a circular

emanating from the publishers of a medical book inParis they state that " Tous les medecins (omni-praticiens et specialistes) doivent avoir ce petitvolume sur leur bureau." The word " omniprati-ciens " is new to me, and I suppose is nearer akinto the English " general practitioner

" than was theold expression " medecin praticien." I have no

knowledge of how far the new word is generally usedin France, but it is certainly compact if it means" general practitioner

" as in English, and it may be

quite useful to our own doctors visiting France ifthey wish to describe their position concisely inmodern language.-I am, Sir, yours faithfully,London, April 24th. BLANCUS.

PUBLIC HEALTH

Revised Milk DesignationsTHE Milk (Special Designations) Order, 1936, was

made available last Saturday and will come into forceon June 1st. It supersedes the two draft orderswhich have been issued and lays down the new

system of milk grading.The grades at present in force are :-CertifiedGrade A (tuberculin tested)Grade A[Grade A (pasteurised)]Pasteurised.

There is no necessity for producers to conform tothe standards established for these grades, and mostmilk sold to the public is undesignated. The newregulations make no change in this policy: they donot require that all milk shall be graded. Insteadthey continue the plan by which designations are

given as a mark of commendation for efforts to reacha better standard.

The new scheme is simpler than the old, and

essentially there are only three grades :—

Tuberculin-testedAccreditedPasteurised.

Additional descriptions may, however, be added by

producers who are suitably qualified. If tuberculin-tested milk has been bottled on the farm-like thepresent Certified milk-it may be described as.

tuberculin-tested (certified) ; if it has been pasteurisedit will be called tuberculin-tested (pasteurised).Furthermore accredited milk may be described as.

"farm bottled." Hence the varieties available tothe public (not necessarily in order of merit) will be-

Tuberculin-tested (certified)Tuberculin-tested (pasteurised)Tuberculin-testedAccredited (farm bottled)AccreditedPasteurised

and, of course, undesignated milk.It will be observed that all tuberculin-tested milk

will now be described as such-whether or not theterm " certified " is applied in addition. The oldrequirements were that certified milk should containnot more than 30,000 bacteria per c.cm. and Grade A(T.T.) not more than 200,000; and until the end ofthis year the latter standard will hold good for thenew T.T. grade. After that time the bacterialplate-count will be discontinued in favour of a

methylene-blue reduction test (see THE LANCET,April llth, p. 866). In addition, no coliform bacillishould be found in 0-01 millilitre-a requirementsimilar3 to that for Grade A (T.T.). Tuberculin-