ACID-BASE DIAGRAMS

160 ACID-BASE DIAGRAMS

SIR,-Iam glad that Dr. van Ypersele de Strihou (May 29, p. 1134) has found the [H+]/Pco2 plot valuable in teaching and evaluation of clinical respiratory acid-base problems over the past four years. I thank him for pointing to the experimental evidence that the significance band for acute hypocapnia is indeed a linear extrapolation of the acute hypercapnic band. I differ, however, in suggesting that the [H +]/PC02 relationship in arterial blood is linear in primary metabolic acid-base disturbances. The accompanying figure shows the 95% confidence limits of this linear relationship, based on 143 observations from 13 reports in: (1) patients suffering from untreated renal failure,1-6 diabetic ketoacidosis, 2, or cholera 8; (2) in normal subjects taking oral bicarbonate,3,9-12 ammonium chloride,5,12,13 or ethacrynic acid,14 over several days. I have excluded cases who may have had lung disease, [H+] values over 80 nmole per litre, and also cases shortly after hxmodiallySiS.4 The [H+]/Pco2 relationships in Dr. van Ypersele de Strihou’s own careful studies of 1. 2. 3. 4.

5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Weller, J. M., Swan, R. C., Merrill, J. P. J. clin Invest. 1953, 32, 729. Moller, B. Acta med. scand. 1959, 165, suppl. no. 348. Bradley, R. D., Semple, S. J. G. J. Physiol., Lond. 1962, 160, 381. Cowie, J., Lambie, A. T., Robson, J. S. Clin. Sci. 1962, 23, 397. Albert, M. S., Dell, R. B., Winters, R. W. Ann. intern. Med. 1967, 66, 312. Lambie, A. T., Anderton, J. L., Cowie, J., Simpson, J. D., Tothill, P., Robson, J. S. Clin. Sci. 1965, 28, 237. Zimmet, P. Z., Taft, P., Ennis, G. C., Sheath, J. Br. med. J. 1970, iii, 610. Pierce, N. F., Fedson, D. S., Brigham, K. L., Mitra, R. C., Sack, R. B., Mondal, A. Ann. intern. Med. 1970, 72, 633. Stone, D. J J. appl. Physiol. 1962, 17, 33. Falchuk, K. H., Lamb, T. W., Tenney, S. M. ibid. 1966, 21, 393. Bergofsky, E. H., Lehr, D. E., Fishman, A. P. J. clin. Invest. 1962, 41, 1492. Fend, V., Vale, J. R., Broch, J. A. J. appl. Physiol. 1969, 27, 67. Chiesa, A., Stretton, T. B., Massond, A. A. E., Howell, J. B. L. Clin. Sci. 1969, 37, 689. Goldring, R. M., Cannon, P. J., Heinemann, H. O., Fishman, A. P. J. clin. Invest. 1968, 47, 188.

arterial blood in 19 patients with chronic renal failure 15 before dialysis can also be satisfactorily described by a linear relationship, [H+]= 73-1-0-90 (PC02)’ which lies well within the 95 % confidence limits shown in the figure. I am sorry that Professor Semple (June 12, p. 1246) so far remains unconvinced of the teaching value of the [H+]/Pco2 plot. Regrettably, I cannot accede to his defence of the venous total plasma CO2 content, [C02], as an indication of acid-base status for most cases. Two examples may illustrate my suspicion that this most familiar acidbase variable may perpetuate diagnostic error. A hyperventilating patient with chronic renal failure could have a [C02] of 17-5 mmole per litre with an arterial PC02 of 30 mm. Hg due to his mild primary metabolic acidosis, yet if the hyperventilation were due to hysteria, or even pulmonary oedema, this same [C02] could be associated with an arterial PC02 of 20 mm. Hg, with a primary respiratory alkalosis and an [H+] of 20 nmole per litre. More serious confusion arises in respiratory disturbances where the bicarbonate and [CO2] isopleths run more or less parallel to the significance bands. Thus a [C02] of 27-28 mmole per litre, at the upper end of the normal range, is compatible with a primary acute respiratory disturbance varying from severe hyperventilation (Pco, 22 mm. Hg) to life-threatening ventilatory failure with a Pco2 over 80 mm. Hg. One hopes that the extremes of this range will be recognised clinically, but there is a vast area of clinical diagnostic imprecision and potential therapeutic disaster concealed by this " normal [C02] ". This is no mere theoretical possibility, for a patient with severe asthma may quickly traverse this gamut on his way to the grave. I am sure that Professor Semple would also avoid such pitfalls by arteriblood analysis, when the results will almost certainly be expressed as the two coordinates of the [H+],/Pco2 plot. Why not use them as such ? I accept that one will be measured as pH, but I had hoped to make clear that I use [H+] as a measure of hydrogen-ion activity (synonymous with AH+ or aH+) and not the unknown, immeasurable, and possibly irrelevant hydrogen-ion concentration. Simplicity of use suggests that " antilog " graph paper be used for the [H+]/Pco2 plot, so that pH readings can be entered directly, and I am exploring this possibility. My mathematically naive suggestion that inverted log graph paper would suffice I is not borne out by experiment ! to readers for this misapologise your take. Derivation of [H+] from the venous [COz] (with analysis errors of ±0-5 mmole per litre), and PC02 (with analysis errors of ::L3 mm. Hg 16), leads to an uncertainty of between 8 and 16 nmole per litre in [H+], which could be of considerable importance in some

therapeutic regimens. 17 May I finally add to my heresy by suggesting that clinicians (including medical students) might dispense altogether with the in-vitro CO2 dissociation curves, which are largely an artefact created by the technical limitations previously imposed on physiological chemists. However, I suggest that the clinician must know the differ15. Van

Acid-base diagram of arterial blood, with 143 values from the literature in patients with primary metabolic acid-base disturbances, as described in text, with - - - the 95 % confidence limits of the linear regression; [H+] =86-8+1-17 Pco2.

16. 17.

Ypersele de Strihou, C., Frans, A. Nephron, 1970, 7, 37. Flenley, D. C., Millar, J. S., Rees, H. A. Br. med. J. 1967, ii, 349. Flenley, D. C. Scott. med. J. 1970, 15, 61.

161 ence

between the

acute

respiratory acidosis, clearly

and chronic in-vivo lines in shown on the H+ /Pco2 plot.

Department of Medicine,

Royal Infirmary, Edinburgh.

DAVID C. FLENLEY.

SERVICES FOR THE MENTALLY HANDICAPPED

SIR,-It should be understood that the white-paper, Services for the Mentally Handicapped, is essentially a political document, approximately two-thirds of which is devoted to general statements about the mentally handicapped which only a handful of reactionaries would seriously object to, and the remainder a statement of intent. The dramatic expenditure figure of E100 million is made up of E40 million already allocated plus normal capital and Better

contribute three sessions each to the mental deficiency field, and little or possibly no previous experience in subnormality may be required, the whole concept of this report may well fall into disrepute. At a recent meeting of the R.M.P.A. (now the Royal College of Psychiatry), Edward of State for Scotland, posed the Taylor, Under-Secretary " Who gives continuity of responsibility throughquestion, out the whole life of the mentally retarded child and adult ? ". He pointed out that this is the guidance and support most frequently requested by parents. Perhaps such a person should not be psychiatrically (or medically) qualified; certainly, if present trends continue, he is unlikely to be a psychiatrist or paediatrician. Need I add that the Under-Secretary’s question was unanswered ? T. L. PILKINGTON.

Edinburgh.

available from National Health Service a piece of window dressing. It is generally accepted that a very large number of

revenue resources

funds, and is largely

patients in mental-subnormality hospitals do not require medical nursing care and, with the help of rehabilitative programmes and the availability of suitable local-authority services, could be absorbed into the community. Opinions differ as to what should be the appropriate environment for the remainder, but there can be little dispute that in other than exceptional cases children should not be kept in long-stay institutions. The suggestion which emerges from the white-paper that non-ambulant children require hospital care is not borne out by experience. A great many children in Spastics Society schools are non-ambulant. In fact, many non-ambulant children in subnormality hospitals could, with the help of physiotherapy and stimulating regimens, become partially ambulant. In some respects perhaps the most disquieting features of the Government’s determination to keep the long-stay hospitals are the waste of medical and nursing skills which are in such short supply, and the pouring of large sums of money into a hospital system which, judged by the standards of more progressive countries, is largely irrelevant to the needs of the mentallv handicapped. Spastics Society, 12 Park Crescent, London W1N 4EQ.

JAMES LORING, Director.

STAFFING OF MENTAL SUBNORMALITY HOSPITALS SIR9 The Scottish Home and Health Department’s report on the staffing of mental deficiency hospitals,1 published in December, 1970, is currently under consideration by various bodies. This document contains some fairly radical proposals. From the medical point of view it challenges the concept of mental deficiency (subnormality) as a specialty in its own right, and proposes a system of For the

joint appointments. Para.

37 states: two main specialities of psychiatry and pxdiatrics, these joint appointments should include a substantial number of sessions in the mental deficiency service, so that the latter is not seen as a minor commitment which might consequently be

neglected. Some of this report’s recommendations have been antithe Eastern and South-Eastern Regional Hospital Boards (Scotland), so that now about half the total mental deficiency consultants in Scotland hold joint appointments. (It should be remarked that a similar system is appearing in England and Wales.) If, however, the logical conclusion of this principle is represented by some situations, whereby several senior posts only

cipated by

1. The

Staffing of Mental Deficiency Hospitals: report of a joint sub-committee of the Scottish Home and Health Department and the Scottish Health Services Council. H.M. Stationery Office, 1970. See Lancet, 1971, i 92.

PERNICIOUS ANÆMIA WITH IRON DEFICIENCY

SIR,-I

interested to note that in the two cases of anxmia reported by Professor Girdwood and

was

pernicious his colleagues (March 13, p. 528), iron-deficiency anaemia was the presenting feature. I have seen two patients who had a similar presentation. The first patient’s iron-deficiency anaemia completely masked the hxmatological picture of pernicious anaemia, and the second patient’s iron-deficiency anaemia relapses each time iron supplements are withdrawn. Case 1.-A 72-year-old man was admitted to hospital because of angina of effort. He was pale, but there were no other abnormal findings on physical examination. Investigations were as follows: ml.; red-cell count 4-2 corpuscular volume (M.c.v.) 71 c.;-t; mean corpuscular haemoglobin concentration (M.c.H.c.) 28%; white-cell count (W.B.C.) 4200 per c.mm., normal differential; serum-iron 31 jj.g. per 100 ml.; total iron-binding capacity (T.I.B.C.) 980 !Jog. per 100 ml.

Haemoglobin (Hb.)

million per c.mm.;

8-6 g. per 100

mean

Faecal occult bloods were negative. Barium meal and revealed no disease. Sigmoidoscopy was negative. Intestinal malabsorption was excluded. Inquiry into diet revealed a daily intake of iron of 10-12 mg. He was treated with oral iron, and repeat investigations five months later were as follows:

enema

Hb. 15-6 g. per 100 ml.; red-cell count 4-8 million per c.mm.; 104 c.p.; M.C.H.C. 31%; w.i3.c. 4200 per c.mm.; plateletcount 164,000 per c.mm.; film showed anisocytosis, ovalocytosis, and macrocytosis; megaloblastic bone-marrow; histamine-fast achlorhydria; parietal-cell antibodies positive; intrinsic-factor antibodies negative; serum-folate 10’1ng. per ml. (normal); serum-B 12 70 pg. per ml. (low); Schilling test, 24-hour urinary excretion 2% (normal 12-30%).

M.c.v.

Case 2.-A girl presented at the age of 10 with myxcedema and was found to have an iron-deficiency anaemia (Hb 10-8 g. per 100 ml.; M.C.H.C. 34%; M.c.v. 60 c.[L; w.B.c. 7800 per c.mm.; platelet-count per c.mm.; serumiron 60 .g. per 100 ml.; T.LB.C. 390 g. per 100 ml.). (Her case has been reported previously.) Parietal-cell antibodies were positive; intrinsic-factor antibodies were negative ; serum-B12 was 584 pg. per ml. A biopsy specimen showed gastric atrophy. There was little rise in haemoglobin on thyroxine alone, but it did rise on iron therapy which was given intermittently. There was no evidence of bloodloss and the girl had not menstruated. She now has diabetes mellitus. Both these patients had atrophic gastritis in association with parietal-cell antibodies. This gastritis may be the cause of the iron-deficiency ansemia in our patients, since

200,000

1.

Vaterlaws, A.

L. Archs Dis. Childh. 1969, 44, 710.