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SUMMARY

A series of 105 cases of perforated peptic ulcer arereviewed.

Of these, 103 patients were operated on, of whom4 died.

It is suggested that recent advances in anaesthesiaand postoperative care were mainly responsible for

reducing the mortality to this figure from the 29%found in a former survey.

I wish to thank the medical superintendent for permissionto publish this article ; and the members of the staff whoseefforts have so largely been responsible for the happy resultsobtained in most of these cases.

REFERENCES

Baritell, A. L. (1947) Surgery, 21, 24.McClure, R. D. (1940) in Frank Howard Lahey Birthday Volume,June 1, 1940. Springfield, Ill.

Martz, H., Foote, M.N. (1940) Amer. J. Surg. 48, 634.Monro, A. K. (1945) Post-grad. med. J. 21, 228.Sangster, A. H. (1939) Lancet, ii, 1311.Varco, R. L. (1946) Surgery, 19, 303.

POLYARTERITIS NODOSAREPORT OF A CASE

R. D. TONKINM.D. Lond.,M.R.C.P.

CHIEF MEDICAL ASSISTANT

AND REGISTRAR,WESTMINSTER

HOSPITAL

R. J. V. PULVERTAFTO.B.E.,

M.D. Camb., F.R.C.P.PROFESSOR OF CLINICAL

PATHOLOGY IN THE UNIVERSITY

OF LONDON AT WESTMINSTER

HOSPITAL

IT is curious that the presence of palpable skin nodulesand eosinophilia should still be regarded as the essential

diagnostic criteria of polyarteritis nodosa because formany years now the various authorities who havereviewed the subject (Strong 1928, Curtis and Coffey1934, Harris et al. 1939, and Miller and Daley 1946)have all shown that in only a small proportion of casesis either of these features present.

’

Furthermore, few people realise that polyarteritisnodosa by no means carries the high mortality originallyascribed to it. Over half the patients recover, andthis recovery may include complete resolution of the

pathological lesions in the arteries.-

Believing that the condition is about to take greaterprominence in clinical diagnosis, we offer a brief outlineof a further proved case.

CLINICAL RECORD

Mrs. A., aged 25, was admitted to Westminster Hospitalon Feb. 2, 1947, in a state of coma, with a history of havinghad two fits within the past two hours. She had complainedof abdominal pain over the preceding three weeks, and thishad been unrelieved by alkalis. In the early hours of themorning of Feb. 2 she had a fit lasting a few minutes, afterwhich she recovered consciousness. A second fit followedclosely on the first.An hour later, on admission to hospital, she presented

the clinical picture of " rousable " cerebral irritation, but

without any localising signs. Apart from incontinence, therewere two outstanding clinical findings-hypertension (165/100)and massive albuminuria. There was slight fever, but of fargreater significance was the fact that she showed a tachy-cardia out of proportion to this fever, and irregularity ofrhythm. There was also early papillcedema of the left opticdisc. The other systems were normal. -

Next day she had a succession of ten epileptiform attacksat intervals of about 1/4 hour. These ceased after the intra-muscular administration of soluble phenobarbitone gr. 3.She exhibited an irregular pyrexia over the next few days,

but improved gradually to the point of cooperation. However,the disproportionate tachycardia and the heavy albuminuriapersisted, and the hypertension became progressively moreevident, there being a rise in the diastolic pressure to 130 mm.,a level which persisted until her death three weeks later.Macroscopic haematuria was present on two occasions, andrepeated microscopy of the urine in the interval revealeda moderate pyuria with some red cells and a few hyaline

Fig. I-Macroscopical appearance of kidneys (half-scale).

and granular casts. The blood-urea level was only 25 mg.per ’100 ml.Within a few days it became apparent that she had

developed a peripheral neuritis involving the left foot. Theknee-jerk was weak, the ankle-jerk absent, and the plantarresponse lost in consequence of a cutaneous sensory lossover the foot and extending up the outer side of the lower leg.The Wassermann reaction was negative, and the cerebro-

spinal fluid was normal im pressure and content. Radio-

graphy revealed no abnormality in skull, but some enlargementof the left cardiac border ; the lung fields were clear.

Electrocardiography gave confirmatory evidence of wide.spread myocardial involvement : there were multiple pre-mature beats in the presence of a rapid nodal rhythm, andarising from various foci. Serial tracings were taken and therewas a constant change. One taken three weeks later showeddefinite right axis deviation, in spite of the fact that the out-standing clinical finding was that of systemic hypertension.The r waves were large and the r-B, interval prolonged.

Over the next week or so the hypertension and the albu-minuria remained unchanged, the blood-urea rose to 60 mg.per 100 ml., the disproportionate tachycardia persisted, andthe leucocyte-count remained raised in the region of 16,000per c.mm. (polymorphs 89%). ). There was no eosinophilia.The patient repeatedly asserted that she had no headache,

and she was in fact remarkably free from any subjectivecomplaints. Her indifference to her predicament as a whole, andto the paralysis of the left foot in particular, was noteworthy.On the 16th day she developed acute left heart-failure

with presystolic gallop, and extensive pulmonary oedema,but responded very satisfactorily to digitalisation. However,five days later her general condition began to deteriorate

rapidly. The blood-pressure rose even further (200/130),epileptiform attacks came on again, and papilloedema becameunmistakable in both eyes. A blood-count showed a persistenceof the leucocytosis at 18,000 per c.mm. (polymorphs 91%),

Fig. 2-Section of kidney, showing multiple small infarcts.

292

and blood-urea remained at 60 mg. For the last few daysof life continuous inorphinisation was required to controlthe epileptiform attacks. The blood-pressure rose further, untilas a result of myocardial failure it fell shortly before death.The total duration of illness was about seven weeks. The

patient maintained a tachycardia throughout her illness, andthat this was constantly disproportionate to the temperature.

POST-MORTEM FINDINGS

The outstanding macroscopical finding was extensiveinfarction in the kidneys (fig. 1). The infarcts were both oldand recent and caused contraction and gross lobulation of thekidneys. Fig. 2 is a section of one of the kidneys, andstrikingly demonstrates the secondary effects of the vascularlesions. It shows multiple infarcts, surrounded by a zone ofhypersemia, with areas of normal kidney tissue intervening.The heart showed considerable hypertrophy of the left

ventricle and minute white nodules just under the visceralpericardium and arranged along the track of small superficialblood-vessels (fig. 3) ; microscopy revealed that these con-sisted of a fibrous reaction round the vessels where the wallshad given way as a result of fibrinoid necrosis. There wasalso a small area of infarction in the muscle of the left ventricle

Fig. 3-Surface of heart, showing nodules along course ofsmall pericardial vessels.

at the apex. The main branches of the coronary arteries werenormal.The spleen showed a solitary healed infarct. No signifi-

cant abnormality was discovered in the brain.The microscopical appearances were essentially similar

in all parts, but were best illustrated in the small myocardialand renal vessels. At points along the course of the arteriolesareas of necrosis in the walls were found, and segments of thecircumference were absent. Thrombosis occurred withinthe vessel, and at the point of a local breach in the wall theneighbouring tissues had been invaded. Various stages ofthis process were seen in different sections : in some placesfibrinoid necrosis of the wall and early thrombus formation ;in others organisation of thrombus and surrounding inflam-mation. Most of the lesions, however, were in the stage of"

healing " ; the thrombus within the vessel was well organisedand in some cases had even recanalised, and considerablefibrosis surrounded the lesions.

Fig. 4 shows a section of a subpericardial vessel cut

diagonally. The vessel wall has given way in several places,thrombosis has occurred, and there is much fibrous reactionround the lesions. Portions of the original vessel wall remainintact. Fig. 5 shows a further stage of healing, in that thethrombus has been recanalised.

In the parts of the kidney which were not involved in theinfarction the glomeruli were normal-i.e., there was noassociated glomerulonephritis. This is by no means uncommonin cases of manifest polyarteritis nodosa.

DISCUSSION

Though the lesions in polyarteritis nodosa are extremelylocalised and constant they are very widespread andprofuse. Hundreds of small arterioles in all parts of

Fig. 4-Oblique section through pericardial arteriole, showing severalareaswherewall has necrosed and thrombus has invaded neighbouringtissue.

the body are occluded, with consequent production ofmany small infarcted areas. Since any organ in the

body may be involved, the symptoms are protean;and it is this that makes diagnosis during life so difficult.Many observers have attempted to classify polyarteritis

nodosa into different types ; but, as Miller and Daley(1946) point out, it is questionable whether this is

helpful. Nevertheless it is necessary to have some basicframework on which to develop a clinical picture, forit is scarcely scientific to say that a diagnosis of poly-arteritis nodosa must be considered when a plethora ofsymptoms is present not conforming to any establishedsyndrome.

’

Harris et al. (1939) demonstrated by necropsy thatpathologically the kidneys are the organs most ofteninvolved ; they found lesions in 87% of cases. Poly-arteritis nodosa is therefore a diagnosis that should beconsidered in any case which presents with a

"

nephriticsyndrome " (in its broadest sense), and in which thereare one or more additional and apparently incongruousfeatures. The more important of these features are

(1) fever ; (2) persistent tachycardia disproportionateto the rise in temperature ; (3) cardiac arrhythmia, orother evidence of an acute toxic myocardial process,especially a changing electrocardiogram ; (4) peripheralneuritis ; (5) persistent moderate polymorph leuco-

cytosis ; (6) recurrent polyarthritis ; (7) abdominal pain;and (8) transient pulmonary infiltrations.

Fig. 5-Cross-section through small arteriole, showing later stage of organisation of thrombus and recanalisation.

293

Though the term " nephritic syndrome " has beenused here as the basic framework upon which to developthe clinical description, in any particular case thealbuminuria, the hypertension, the oedema, or all three,may be absent. The two features which we regard asthe most important, and the most often encountered,are (1) a disproportionate tachycardia, especially if

supported by electrocardiographic evidence of wide-

spread myocardial involvement ; and (2) a persistentmoderate polymorph leucocytosis without any other

adequate explanatory cause. These two features were

emphasised by Lamb (1914).SUMMARY

Attention is drawn to the fact that polyarteritisnodosa only carries a 50% mortality, and that skinnodules and eosinophilia, previously regarded as

pathognomonic, are uncommon.A case is reported in which the clinical manifestations

were observed for seven weeks and the diagnosis wasconfirmed post mortem.The clinical picture may be pleomorphic, but there

is almost always clinical evidence of renal involvement.Two other diagnostic " signposts " are a disproportionatetachycardia and other evidence of myocardial involve-ment, and a persistent moderate polymorph leucocytosis.Our thanks are due to Sir Adolphe Abrahams for permission

to publish the case and for much help and advice, and Mr.E. F. King for opinion on the fundal changes.

REFERENCES

Curtis, A. C., Coffey, R. M. (1934) Ann. intern. Med. 7, 1345.Harris, A. W., Lynch, G. W., O’Hare, J. P. (1939) Arch. intern. Med.

63, 1163.Lamb, A. R. (1914) Ibid, 14, 481.Miller, H. G., Daley, R. (1946) Quart. J. Med. 15, 255.Strong, G. F. (1928) Canad. med. Ass. J. 19, 534.

MINIMAL REQUIREMENTS FOR MASSRADIOGRAPHY

F. C. S. BRADBURYM.D. Belf., B.Hy., D.P.H.

CENTRAL CONSULTANT TUBERCULOSIS OFFICER, LANCASHIRECOUNTY COUNCIL

DOUBT has arisen about the value of mass radiographyin that the return may not be commensurate with the

expense, as foreseen from the beginning by manyin the tuberculosis service. One obvious method of

preventing this result is to use mass radiography solelyfor selected groups in whom tuberculosis is expected tobe more than ordinarily prevalent. This is the method

usually followed at present. A drawback to the exclusiveuse of this method is that mass radiography wouldcome to be associated with susceptibility to tuberculosis,and to be singled out for mass radiography would betantamount to being labelled a tuberculosis suspect.This seriously limits the use of mass radiography.A better method, which could include the foregoing,

would be to make sure that by adequate propaganda4 high proportion of the examinees in any group to besurveyed could be expected to attend for examination.There are two reasons behind this statement. First,the common-sense argument that there must be someminimal effectiveness of mass radiography below whichthe procedure is not worth while. Some would perhapsplace this minimum at a single person and say that ifa survey discovers one tuberculous person it has beenworth while ; but it is not difficult to reject this extremeview. Secondly, it may be expected that if two-thirdsof a large group of people agree to participate in a mass-radiography survey and a third decline, the reasonswhich caused the third to decline will lead to the existenceof more cases of tuberculosis per 1000 in the abstaininggroup than in the two-thirds who participate. In otherwords, the greater the proportion of persons examinedin any group, the greater will be the percentage incidence

INCIDENCE OF TUBERCULOSIS IN RELATION TO PERCENTAGE

OF PERSONS EXAMINED

of tuberculosis discovered, because it will more andmore approximate to the true percentage incidence inthe whole group.That this is no mere speculation is shown by the

figures relating to the last five surveys carried out bythe Lancashire county council no. 1 mass radiographyunit (see table). ,

The question now arises whether any lower limit canbe fixed to the effectiveness of mass radiography, belowwhich its use cannot reasonably be justified. Clearlysuch a limit must be arrived at from practical con-sîderations. I suggest that, to be worth while from thestandpoints of cost, man-power, and effective controlof infection, a mass-radiography survey should discovermore tuberculosis than it leaves undiscovered. To placethe limit any lower than this would incur the risk ofactual harm being done by a mass-radiography surveyowing to the false sense of security which might reasonablyattach to a group which had been so inadequatelysurveyed that the greater part of its initial content oftuberculosis still remained undiscovered. -

If it is accepted that the limit of effectiveness of asurvey is the discovery of at least half the tuberculosisin any group, it can be shown that the proportion ofpersons who must be examined to satisfy this requirementis about 70%. This figure is derived from the foregoingtable in the following manner : , ,

It is noted from the table that the variation in the amountof tuberculosis detected by mass radiography is almost

directly proportional to the percentage response. This’meansthat if 100% response gave 10 tuberculous persons per 1000examined, a 40% response would give 4 tuberculous personsper 1000 examined, and the degree of adequacy with which apartial examination represents the percentage incidence, oftuberculosis in the entire group will vary with the squareof the percentage examined. Hence if 100% examinationgives all the detectable tuberculosis, 70% response will give(70)2

or 49% of the total tuberculosis in the entire group-100i.e., 70% of the total because only 70% ,are examined ; andthis figure is again reduced to 70% of itself because theexpected incidence of tuberculosis is only 70% of the incidencein a representative sample.

It is possible to obtain a similar result by calculationfrom the known incidence of tuberculosis in the generalpopulation, without the information given by the pre-ceding table, but the calculation is too complicated forgeneral use.

In view of the loss of time associated with the dis-mantling, transportation, re-erection, and testing of theapparatus each time it is moved, it is scarcely practicableto arrange a survey for less than about 4000 persons,except as part of a larger survey.

SUMMARY ’

There is a lower limit to the efficiency of mass

radiography, below which it becomes uneconomical. Itis suggested that a practical measure of this lowerlimit would be the point where mass radiography leavesundiscovered more tuberculosis than it discovers.On this basis it is shown that not less than 70% of

any group to be surveyed should actually be examined.