670

openings presented a perfect conduit for the swift transmissionof a sclerosing solution from the superficial to the deep venoussystem.

It would be interesting to know how long each patientof Mr. Fegan’s was followed after delivery, how she faredafter the pregnancy, and how the varicosities looked whena previously treated patient became pregnant again.

Toledo, Ohio,U.S.A. BERT SELIGMAN.

UNUSUAL POLIOMYELITIS

SIR, The evidence given by Colonel Foster (March 7)concerning a patient with an unusual neurological illness,certainly does not justify the conclusion that the illnesswas caused by the strain of poliovirus type 1 isolated, letalone " that poliomyelitis has in some way been modifiedor altered in its clinical manifestations ".

Enteroviruses are frequently found in the fxces of

healthy individuals and, moreover, now that vaccinationwith live attenuated strains of poliovirus is widely practisedin this country, it is not surprising that sometimes a strainof poliovirus is isolated coincidentally from a patientsuffering from an illness which is not poliomyelitis.

Central Public Health Laboratory,Colindale Avenue,London, N.W.9. C. E. D. TAYLOR.

EFFECT OF pH ON THE FUNCTIONAND GLUCOSE METABOLISM OF THE HEART

SIR,-Prompted by the communication from Dr. Opieand others (Sept. 14) I report the following case ofneonatal asphyxia.The mother, a 24-year-old primigravida, had had recurrent

vaginal " spotting " since the 20th week of pregnancy. A

fairly considerable hxmorrhage heralded the onset of labour to36 weeks. There was accompanying foetal tachycardia, butsubsequently the fcetal heart-rate remained between 140-150per minute throughout the first-stage. 7 hours after the onsetof labour, the cervix was dilated to 4 cm. A marginal placentaprxvia was diagnosed, and, since contractions were good andthe foetal head was low, the membranes were ruptured. 50minutes later forceps delivery was performed under regionalblock. Other than an infusion of 5% dextrose in water, themother received no medication during labour. 5 minutesbefore delivery, the foetal heart-rate dropped to 50 beats perminute. The mother was given oxygen by mask (there hadbeen no fall in maternal blood-pressure).The infant, male, weighed 2270 g. The cord was not around

his neck. He was apnoeic, unresponsive to stimuli, and flaccid.His heart was beating slowly but regularly, and the Apgarscore was 1 at 1 minute. At about 1 minute, an endotrachealtube was passed, and mouth-to-tube intermittent positive-pressure respiration was started, oxygen being passed into theresuscitator’s mouth. The lungs were expanded easily, andafter 3-4 insufflations the heart-rate rose to 140-150 perminute-a rate which was maintained for many hours-andthe infant was pink all over.At the time of delivery, a loop of cord was secured beween

clamps. Blood was drawn from the umbilical vessels and the

syringes were sealed with mercury. Blood was taken from amaternal vein 4 minutes after delivery. At 68 minutes, bloodwas withdrawn from a femoral artery. The improvement inacid-base balance and the satisfactory oxygenation (see table)persuaded us to leave well alone. 3 hours after delivery asecond sample of blood was taken from a femoral artery. Theinfant was apparently developing hypocarbia in an attempt tocorrect his metabolic acidosis. The regimen advised byUsher 1-3 for the respiratory distress syndrome was instituted.A solution of 10% glucose to which was added sodium bi-carbonate (60 mEq. per litre) was infused through the umbilicalvein, at a rate which would provide 100 ml. solution per kg.body-weight per 24 hours.At 5 hours the infant’s condition seemed improved, but a

third sample of arterial blood showed that the metabolicacidosis was not being relieved, and that the carbon-dioxidetension was still falling. The concentration of bicarbonate inthe infusion solution was increased, therefore, to 120 mEq. perlitre, and insulin was added (10 units per 500 ml. solution).The initial rate of infusion was maintained.At 20 hours the acid-base state was improving. Our assay

of blood-sugar takes an hour to complete. On returning to theward with the result, I found that the infant had collapsed20 minutes previously; he was limp and gasping. The infusionhad been stopped, because the infant was thought to be dying.As a forlorn gesture, 5 ml. of 50% glucose was injected into theumbilical vein at 23 hours. Respirations became a little moreregular, but there was no other response. At 25 hours a finalsample of blood was withdrawn, probably from a femoralvein. There was further marked recovery from the acidosis,and the blood-sugar concentration was satisfactory, but therewas no change in the clinical condition of the infant, and hedied 35 hours after delivery.Postmortem examination (Dr. Manglano) was not fruitful.

The lungs had been completely aerated, though the upperlobes were congested. The portal vein was not thrombosed.There was no macroscopic evidence of haemorrhage on thebrain surface. Microscopic examination remains to be

performed.The case raises several interesting points:The period of severe intrauterine asphyxia must have been

long; yet there was no evidence of foetal distress (the brady-cardia during the final few minutes is likely to have been dueprimarily to pressure on the foetal skull).

Despite an arterial blood pH of 6-628, the circulatory systemseemed unimpaired. This supports the contention of Opie etal. that " the myocardium is relatively resistant to the effects ofalterations in pH ".The administration of insulin was a mistake resulting from

an inadequate reading of Usher’s papers. Usher states thatinsulin is given only when, in additon to severe asphyxia, thereis severe hyperkalxmia and electrocardiographic evidence ofdisordered cardiac activity.The episode of hypoglycsemia in an infant who was receiving

an intravenous (or perhaps one should say, intrahepatic)infusion of glucose, was startling. There were possibly threecontributory elements : (1) the insulin (the infant receivedapproximately 3-4 units of insulin in 19 hours); (2) the fall in

1. Usher, R. H. Pediat. clin. N. Amer. 1961, 8, 525.2. Usher, R. H. N.Y. State J. Med. 1961, 61, 1677.3. Usher, R. H. Postgrad. Med. 1962, 31, 44.

* Kipp 12a=more_flector, t Astrup Radiometer. t Modified Marks method: glucose oxidase. § P. & 1. flame-photometer. 11 Approximate values,All assays performed in duplicate.