594

HaeMATOLOGICAL HISTORY OF MOTHER AND CHILD

Coombs test was negative in the serum of both mother andbaby. *Follow-up.-The purpura disappeared spontaneously and

completely in the baby after six or seven days, and all furtherblood examinations were normal.

Discussion

Since 1924 thrombocytopenia purpura in the newbornhas been reported at intervals. In all the publishedcases the baby was born with purpura, which fadedgradually in the first days of life. Landolt (1948)differentiated between three groups of congenital pur-pura, of which the first two disappear spontaneously :(1) the more important affects children born of motherswho have either Werlhof’s disease (thrombocytopenicpurpura) or secondary purpura ; and (2) purpuraaffecting babies whose mothers had no haemorrhagicdisease.

Robson and Walker (1951) published an unusual case inwhich the mother was healthy at the time of the birth butstarted having haemorrhagic manifestations three weeks aftergiving birth to a baby with generalised purpura ; only thendid the undiagnosed Werlhof’s disease of the mother becomeobvious.

A third group of thrombocytopenia, often lasting along time, is due to congenital hypoplasia of the

megakaryocytes.Our observation is -of interest because of the presence

of anti-platelet agglutinins in the serum of both themother and her baby-a finding which has not previouslybeen published. These agglutinins disappear spon-

We are indebted to Dr. J. J. Van Loghem and Dr. A. J. SauerAmsterdam, for their help in controlling the antibody reactions.

Platelet-counts and anti-platelet agglutinins in mother and baby

taneously from the baby but persist in the mother. Theanti-platelet agglutinins can continue to be formed andpass through the placental barrier even after splenectomy.

REFERENCES

Ackroyd, J. F. (1949) Clin. Sci. 8, 269.Broch, O. J. (1941) Nord. Med. 10, 1542.Collins, D. C. (1950) Circulation, 2, 438.Evans, R. S., Takahashi K., Duane, R. T., Payne, R., Liu, C. K.

(1951) Arch. intern. Med. 87, 48.Hirsch, E. O., Dameshek, W. (1950) Amer. J. Med. 9, 828.Kissmeyer-Nielsen, F. (1953) Vox Sanguinis, 3, 123.Landolt, R. F. (1948) Helv, pœdiat. acta, 3, 3.Larson, R. K. (1953) Blood, 8, 16.Nolthenius, C. T., Hoorweg, P. G., Van Loghem, J. J. (1953) Vox

Sanguinis, 3, 27.Norcross, J. W. (1950) New Engl. J. Med. 242, 53.Nudelman, P. L., Leff, I. L., Howe, C. D. (1948) J. Amer.med. Ass.

137, 1219.Robson, H. N., Walker, C. H. M. (1951) Arch. Dis. Childh. 26, 175.Verstraete, M., Vandenbroucke, J. (1955) Acta hœmat. 13, 129.

SODIUM-NITRITE POISONING TREATED

BY EXCHANGE TRANSFUSION

NORMAN G. KIRBYM.B. Birm.

CAPTAIN R.A.M.C. ; LATE SURGICAL REGISTRAR, BIRMINGHAMACCIDENT HOSPITAL

SODIUM nitrite is an exceedingly deadly poison, and allproducts containing it should be marked prominently assuch, and at least an approximate formula should begiven of their contents. Machine-oil containing sodiumnitrite is increasingly used and is widely obtainable fromengineering firms.

Case-record

A girl, aged 11, was admitted on May 28, 1954, fifty minutesafter having taken one mouthful of an unknown machine-oil,some of which she spat out. A sample of this oil was broughtalong; but attempts to obtain the formula from the workswhere it was being used and the dealers from whom it wasbought were unsuccessful.

On admission the patient was unconscious, pale, andextremely cyanosed. Her pulse and respirations were feeble,and she did not respond to painful stimuli. When intravenousnikethamide 3 ml. was given, the venous blood was seen tobe thick and chocolate-brown ; methsemoglobinsemia wasdiagnosed. In view of this and of the patient’s rapid deteriora-tion a replacement blood-transfusion was started.

Treatnaent and Pr’og1"ess.- While the anaesthetist administeredoxygen and did gastric lavage, an intravenous transfusionwas started of group-0 Rh-negative blood which was not cross-matched until later. The median cubital vein was opened forvenesection, but rapid clotting made this very difficult, Tohasten the withdrawal of blood the radial artery was partiallydivided at the wrist. Rapid clotting persisted until about1250 ml. of blood had been transfused ; it was so rapid thata nurse had to keep wiping away clots to maintain blood-flowfrom both vein and artery. When 1000 ml. of blood had beentransfused and the patient’s condition had begun to improve

595

thirty to forty, minutes after admission, the West MidlandForensic Science Laboratory, to which a sample of the oilhad been sent, reported that it contained ’36-5% of sodiumnitrite, 7’5% of an emulsifying agent, and 56-0% of water.Sodium nitrite 7-8 mg. per 100 ml. was present in t’he stomachwashings. Spectroscopy showed methsemoglobinaemia.Altogether 1700 ml. of blood was transfused. The patient wasnursed in an oxygen tent for forty-eight hours. Pyrexia andincreased pulse-rate persisted for four days. Radiography ofthe chest showed no abnormality. The urine was normal.Procaine benzylpenicillin 300,000 units twice daily andascorbic acid 300 mg. daily were started on admission andcontinued for twelve days.Examination of the blood next day showed normal oxyhaemo-

globin and Hb 15 g. per 100 ml. The following day the Hbwas 17-4 g. per 100 ml. A white-cell count showed granulo-cytopenia (see figure), the polymorphs decreasing from 51%on May 31 to 19 % on June 3, and was not normal until June 7-i.e., the tenth day. Turk’s cells and " toxic " granules inthe polymorphs were present on June 3 but not afterwards.On June 11 the blood picture, including absolute values, waswithin normal limits ; and the patient was discharged fourteendays after the accident.

Follow-up.-On June 18 a white-cell count showed 8300

perc.mm. (metamyelocytes 1%, polymorphs 50’5%). Elevenweeks after admission the blood picture was normal, with

White-cell counts.

Hb 14-1 g. per 100 ml., white cells 6000 per c.mm. (poly-morphs 44%). The child looked well and had been normallyactive after a fortnight’s convalescence. Sixteen w,eeks afteradmission her blood picture remained normal, with Hb 14-7 g.per 100 ml. and white cells 8000 per c.mm. (polymorphs 54%).

Discussion

Sodium nitrite is absorbed rapidly, its effects startingfive to twenty minutes after ingestion. Absorption startssublingually, causing vasodilatation and, in large doses,syncope and methaemoglobinaemia. The methaemoglobinis the stable oxidised form of haemoglobin with the ironin the trivalent ferric state. This form is only slowlybroken down in the body and thus is of little value

’in supplying oxygen to the tissues. There is also ashift of the oxygen dissociation-curve to the left,making the oxygen less readily available to thetissues.Ascorbic acid in doses of about 500 mg. daily is of

value in the chronic mild cyanotic case, but severe casesof either chronic or acute methaemoglobinaemia requiremore rapid action. Intravenous methylene-blue 1-2

mg. per kg. of body-weight is reported to be effective inthe methaemoglobinaemia following ingestion of nitritesin drinking-water by infants, but in acute poisoningwith a moribund patient it is quicker and more satis-factory to start an exchange transfusion. The removal ofthe methsemoglobin together with any nitrite still circu-lating and the substitution of transfused blood will lessenthe degree of bone-marrow damage with the resultingneutropenia. No time should be wasted in waiting forexperts in exchange transfusion ; the doctor who firstsees the patient should give it.

Conclusion

In severe cases of sodium-nitrite poisoning an imme-diate exchange transfusion may be life-saving and is themethod of choice.

Prolonged observation of the case is subsequentlyneeded because of the danger of neutropenia and agranu-locytosis despite a good general clinical condition, whichis misleading.

I wish to thank Mr. J. S. Horn for permission to publish ;Mr. Ruscoe Clarke for advice and encouragement ; Dr. S.Sevitt for hmraatological reports ; and Prof. J. M. Webster,of the West Midland Forensic Science Laboratory, for thespeedy analysis of the mixture and for advice about after-treatment.

RUPTURE OF THE DUODENAL STUMP

AFTER GASTRECTOMY

G. F. HENSONM.B. Lond., F.R.C.S.

SENIOR SURGICAL REGISTRAR, PADDINGTON GENERAL HOSPITAL,LONDON

POLYA gastrectomy is one of the commonest majoroperations. The risks associated with it have consider-

ably diminished in the last fifteen years, but still a fewof the patients die and one of the commonest causesof death is rupture of the duodenal stump. For thisreason many methods of closing the stump have beendevised.

In some cases in which leakage subsequently takesplace the duodenum has been difficult to close (e.g.,in patients with an adherent ulcer of the posteriorduodenal wall) ; but in others, leakage follows a simplestraightforward operation in which no difficulty whateverwas experienced in closing the duodenal stump apparentlysecurely. This state is almost invariably the sequelto operations for gastric ulcer or for malignant disease,when the duodenal stump occasionally ruptures. Insuch cases the rupture is often attributed to an inabilityof the patient’s tissues to heal, and malnutrition isblamed ; but in many of these cases no disorder ofnutrition or imbalance of fluid or electrolytes can befound.

Aird (1949), Wangensteen (1941), and Tanner (1954)have emphasised that distension of the duodenal stumpdue to obstruction of the afferent jejunal loop may bethe most important factor in rupture of the duodenalstump in such cases. Usually after leakage it is difficultat operation to be certain about pre-existing distensionof the afferent loop. The following case is reportedbecause there was clinical evidence of such a derange-ment, and it was clearly confirmed at operation, theafferent loop with the duodenal stump being distendedvirtually to the point of rupture of the stump.

Case-reportA married woman, aged 35, was admitted to Paddington

General Hospital with a history of ten years’ typical duodenaldyspepsia and one previous attack of melsena. She hadalready undergone medical treatment with temporary benefit,but her symptoms had now recurred.On examination she was rather pale but otherwise looked

fit, and no abnormality was detected on ordinary clini-cal examination. Further investigation, however, showedmoderate ansemia and radiological evidence of a posterior-wall duodenal ulcer. After correction of her anaemia shewas operated on.Operation.-The abdomen was opened through an upper

right paramedian incision and’ the presence of the ulcerconfirmed. Without undue difficulty a high partial gastrectomyof the Polya-Hoffmeister-Finsterer type was done, but theabdomen was closed with stab drainage down to the site ofthe closed duodenal stump because this was not deemedperfect.