PURPURA AND INTUSSUSCEPTIONBY

H. WOLFSOHN, M.D., M.R.C.P., D.C.H.(From the Fulham Hospital, London)

As early as 1808 Willan described visceral crisesoccurring with purpura. Henoch published hisclassical paper in 1874, after which date abdominalpurpura became associated with his name. Thefirst report of intussusception with purpura appearsto have been that of Vierhuff (1893). Since then,as far as can be ascertained, this combination hasbeen reported only nineteen times. It is for thisreason and because of the many interesting pointsthis conclition raises that a further case is recorded.

Case ReportA male child aged four years and eight months

was admitted to hospital on Nov. 12, 1946. Amonth earlier he had had an attack of abdominalpain an(i vomiting which subsided rapidly andwhich was labelled 'chill on the liver.' Otherwisehis earlier childhood had been uneventful exceptfor measles, whooping cough, and tonsillitis. Hewas an only child. Both his parents were healthyand had not suffered from any of the 'allergicdiseases.Four days before admission he complained of

pain in his left knee and the mother noticed thatthere was much swelling. The next day his rightelbow became swollen and painful. He was thentaken to his doctor, who diagnosed rheumatic feverand prescribed sodium salicylate. On Nov. 12 theswelling of his left knee had subsided but his rightelbow and right wrist were painful. At noon onthis day he suddenly developed severe abdominalpain, which was soon followed by vomiting. At thesame time purpuric spots were observed on buttocksand right arm and he was transferred to hospitalas a possible case of Henoch's purpura. His bowelshad been regular until then, and no blood wasnoticed in the stool passed that morning.On examination he was found to be normally

developed and thin. He was apyrexial and quitealert. His skin was of striking pallor, but theconjunctival mucosa was well coloured.

Joints. He complained of no pain in the joints,and all movements were unrestricted and painless.There was some swelling of his right elbow, andpogsibly also of the right wrist.

Rash. A crop of petechial haemorrhages wasfound on his buttocks which, according to themother, had been larger and more distinct a few

hours previously. On the outer side of the swollenright elbow he had an extensive ecchymosis, and inthe right cubital fossa there was one definite purpuricspot. He also had a boil on his right thigh. Nourticarial lesions were seen.Abdomen. Liver and spleen were not palpable.

In the right iliac fossa a hard irregular mass was f.ltwhich was very slightly tender. It could be readilymoved up and down but less easily sideways. Itappeared to be in the peritoneal cavity. It occupiedmost' of the right iliac fossa. A knob on its out-rside was attached to the main mass. On rectalexamination semi-solid yellow faeces without bloodwere found, and no other abnormality was detected.Cardiomuscular, respiratory, lymphatic, and centralnervous systems appeared normal.

INVESTIGATIONS. The Mantoux test, 1-10,000,was negative. Red blood cells numbered 6,180,000per c.mm. of blood; haemoglobin was 120 per cent.,colour index 0 9, white cells 18,100 per c.mm.,polymorphs 76 per cent., lymphocytes 20 per cent.,monocytes 4 per cent., and blood platelets 238,000per c.mm.tThere was a trace of albumin in the urine; no

red blood cells were seen. Culture was sterile, andthere was a yellow reduction of Benedict'ssolution.

Bleeding time was 21 minutes, coagulation time31 minutes, and the tourniquet test negative.A tentative diagnosis of purpura with rheumatic

(Schonlein's) and abdominal (Henoch's) symptomswas made, but in view of the abdominal massthe possibility of intussusception could not beexcluded.

PROGRESS. On Nov. 13 he vomited watery fluidonce during the night. He had no appetite andbecame more dehydrated. The abdominal lumpcould still be felt. Intravenous therapy (glucosesaline and plasma) was begun. Next day he wasstill vomiting and the petechiae were paler. At theadvice of the paediatric consultant, expectanttreatment was continued.On Nov. 15 his general condition had deteriorated,

anorexia, vomiting, and dehydration being marked.There' had been no bowel action since admission.The cardiac rate was now 150 per minute, althoughtemperature was still normal. The vomit containedupper intestinal contents. The abdomen was moredistended; and the lump, unchanged in size andshape, was slightly more tender. Purpura was still242

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PURPURA AND INTUSSUSCEPTIONpresent but only very faintly. In.spite of dehydra-tion there was now frequency of micturition and theurine gave an orange reaction to Benedict's solutionand contained ketone 'bodies. Capillary bloodsugar at 4 p.m. was 313 mg. per cent. The occur-rence of diabetic symptoms was considered to bedue to a temporary toxic exhaustion of islet function.As conservative measures, continued over three

days,. had not resulted in any improvement, as theabdominal mass had remained unchanged duringthe time of observation, and as the child had-becomeextremely ill from acute intestinal obstruction,laparotomy was decided on. The intravenous dripwas carried on throughout the operation and duringthe next two days. Penicillin (15,000 units everythree hours) was given intramuscularly, and solubleinsulin in doses oftwenty units at 4 p.m., at 5.30 p.m.,and again at 7 a.m. the next day, when his urinestilLgave a green reaction to Benedict's solution.

OPERATION. At operation (under nitrous oxideand ether anaesthesia) blood-stained fluid appearedwhen the peritoneum was opened. An irreducibleileo-ileal intussusception was found, with its apexabout six inches from the ileo-caecal valves. Thiswas resected from four inches above to two inchesbelow the intussusception and a side-to-sideanastomosis performed to restore' the continuity ofthe gut. Rapid examination of the peritonealcontents showed no purpuric haemorrhages. Thewound was closed in layers. The removed specimenconsisted of about eight inches of intussusceptedsmall intestine causing haemorrhagic infarction.On Nov. 16 the general condition was much better.

The pulse was full and good, and there was nofurther vomiting. At 3.30 p.m. the child becamesuddenly worse and failed to respond to questions.He was unable to swallow and had a squint and aright plantar extensor response. As this attackoccurred so rapidly, and more than eight hoursafter his last dose of soluble insulin, it was notconsidered to be due to hypoglycaemia, particularlyas his intravenous glucose saline infusion was stillin progress. The blood sugar was, however, notexamined. The possibility of a purpuric intra-cerebral haemorrhage was dismissed as unlikely.The attack was probably due to a small cerebralembolus. On the next day he was gradually regain-ing consciousness, and by Nov. 18 was fullyconscious, talking, and swallowing well, with noabnormal neurological signs. At this and subse-quent examin,tions there were no reducingsubstances in the urine. The temperature was1000 F., and there was pneumonic consolidationin the right upper lobe. Sulphadiazine was begunin addition to penicillin, and the intravenous dripdiscontinued.On Nov. 20 the chest was beginning to clear, the

abdomen was soft, and the temperature 990 F.There was pain and swelling in both wrists and theleft elbow, but no rash. Sodium salicylatw, gr. 15four-hourly,. was begun. By Nov. 23 the painsand swelling in the joints had subsided, but there

were petechial spots on both elbows. He vomitedafter taking salicylate, so this was changed to.aspirintablets and to calcium aspirin gr. 10, three times #iday. Sulphadiazine was discontinued.On Nov. 24 the rash round the elbows had become

more profuse. Some spots were truly petechial,others were raised. At night the temperature wasstill 990 F. By Nov. 25 there was swelling andbruising of the right metacarpo-phalangeal joint ofthe right thumb, with recurrence of swelling ofrightwrist and dorsum of the right hand. There wasmore purpura also on the left elbow, but no otherpetechiae were seen. The chest was now clinicallyclear, and penicillin and all salicylates were stopped.He was afebrile.On Nov. 29 he complained of abdominal pain

and pain in the right lower chest. There were noabnormal signs. On Dec. 11 a swelling appearedover left tempero-mandibular joint, and also overthe right frontal region and in the right knee joint..The temperature had risen to 1020 F. by next morn-ing, but gradually fell to normal by Dec. 17. Theright testis was tender and slightly enlarged. Aradiograph of the skull showed nothing abnormal.By Dec. 17 he was afebrile and symptom-free,

the bowels were regular, the abdomen soft, andthere were no signs or symptoms in the joints andno urticarial or purpuric eruptions. The bloodsedimentation rate was 40 mm. in the first hour.On Dec. 31 he was transferred to Queen Mary's

Hospital, Carshalton. Radiography of chest, joints,and long bones revealed nothing abnormal. Theblood sedimentation rate varied between 35 mm.and 1-0 mm. per hour up till the middle of March,1947, and has been normal since then. He has hadseveral short febrile episodes, one accompanied byabdominal pain, two by finger sepsis, and one byneck pain radiating in turn to either ear. He hasreceived dental treatment and has had aspirinadministered for several weeks. No further purpurahas been noted.

In July, 1947, there was a further attack ofabdominal pain, accompanied on one occasion bypassage of bright red blood. There were no otherpurpuric manifestations, and he was symptom-freeafter two days.

Analysis of this and Previously Reported CasesSex. Of the twenty cases under review, sixteen

occurred in boys. The large preponderance of boysis significant and exaggerates a similar sex irregularityfound amongst patients with so-called Henoch'spurpura without added complications. McKechnie(1911) in fact states that all his cases of Henoch'spurpura at Vancouver occurred in boys, althoughother observers have described this condition alsoin girls. Non-purpuric intussusception also is saidto be two to three times more common in malesthan in females (Mitchell-Nelson, 1946). The maleincidence of 80 per cent. in the present series maytherefore be explained by either condition alone or

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ARCHIVES OF DISEASE IN CHILDHOOD

by the combination of intussusception andpurpura.Age. The average age of the twenty cases is

91 years. Excluding the four adults of 21, 31, 29,and 21, the average age of the remaining sixteenchildren becomes nearly six years, which is a figurevery much higher than that of intussusceptionwithout purpura. Indeed not one patient was underthree years old, whereas the non-purpuric intus-susception occurs most commonly in young childrenunder three. On the other hand the age distributiontallied well with that of anaphylactoid purpuragenerally. This fact is important and supports thesupposition that purpura is the primary condition.

Symptomatology. The initial symptoms and signsdescribed in these cases differ in no way from thoseof non-thrombocytopenic purpura with abdominalsymptoms. Their duration before intestinalobstruction becomes manifest is very variable.Most of the children were ' not well ' for a few daysto a few weeks before the onset ofintestinal blockage.Dobeli's (1908) patient gave the longest history.For about five years he had had abdominal andjoint pains which were considered to be due to leadpoisoning or rheumatism. Gara's (1912) patientsuffered from 'purpura simplex' for two yearsbefore intestinal symptoms developed. At theother extreme is Gamstedt's (1933) patient, in whomonly three days after the onset of symptoms anirreducible intussusception was found at lapar-otomy.

JoINT PAINS. In eleven out of seventeen patients-joint pains and swellings were described, eighteenmonths to two days before the obstruction. A notunusual story is that the joint symptoms subsidedrapidly with or without salicylates and that theintussusception occurred shortly afterwards. Thishappened in the present case and in the one reportedby Robinson (1910) and Dobeli (1908).PURPURA. Purpura in some form or other was

invariably present, and indeed its presence formspart of the diagnosis. Sutherland (1909) regardeda case of Still's (1909) where no haemorrhagicmanifestations were described as one of anaphylac-toid purpura. Nowadays, however, we wouldclassify this particular patient as having sufferedfrom chronic recurrent intussusception. In thisseries in practically every patient some cutaneousmanifestations were obvious: at times a few isolatedpin-point petechiae around the elbow joints or overthe buttocks, at times larger ecchymoses, were seen.Haematuria is mentioned in four of the cases.Nose bleeds and vomiting of blood were recordedonly once. An interesting symptom, which is notusually referred to in this connexion, is pain,swelling, and sometimes discoloration of thescrotum, which are described by Lett (1908b),Lederer (1913), Tonking (1910), and in my patient.

INTUSSUSCEPTION. Of particular clinical interestand of vital importance is the diagnosis of intus-susception in this condition. Sutherland. referringto intussusception and abdominal purpura, stated

in 1909, ' We do not seem to possess any reliablemeans of distinguishing these two affections, andeven now, nearly forty years later, the problem isstill equally difficult. Far more patients withpurpura and abdominal symptoms are suspectedof intussusception and are operated on than areactually found to have this condition. Very manycases of this kind have been reported in the literature,and many more have undoubtedly occurred, forexample, Bailey (1930), Burrows (1904), Sutherland(1904), FitzWilliams(1908). The most tragic of theseis probably that of Sutherland's; he, having advisedlaparotomy on one of his patients, who turned outto have no intussusception, refrained from operatingon a very similar case shortly afterwards, and thechild died from peritonitis due to intestinal invagina-tion. A similar disaster was fortunately, but onlybarely, avoided in my own case.

There is not one symptom which clearlydifferentiates the two conditions. Bailey (1930),discusses the differential diagnosis between non-purpuric intussusception and Henoch's purpura, andAlthausen et al. (1937), try to clarify the matter bytabulating the essential symptoms and signs. Theyounger age, abdominal tenderness disappearingbetween colics, absence of bleeding (haematemesis,petechiae, haematuria, and joint symptoms), andparticularly the presence of a sausage shaped massare all in favour of intussusception. None of thesepointers are of course relevant to our presentproblem, where both phenomena are present at thesame time. An abdominal mass has been feltfrequently in uncomplicated purpura, and may havebeen due to bleeding into the intestinal wall (Greig,1908), or lumen (FitzWilliams, 1908), to haemorrhageinto the mesentery (Lett, 1908a), or omentum, tolocalized oedema and extravasation of fluid intothese organs, to faecal masses, or even to theimagination of the observer. On the other hand,in the present series were at least six cases where no'tumour was felt but the intussusception was dis-covered by operation (Hall, 1908; Collinson, 1910;de Lavergne, 1927), autopsy (Sutherland, 1909;Gara, 1912) or when passed per rectum (Lederer,1913). Even vomiting was absent three times(Lett, 1908; Dobeli, 1908; Robinson, 1910). Thepresence or absence of blood in the stools also is oflittle significance. Reviewing all the cases, one canonly say that a sudden worsening of the conditionof a purpuric patient, if accompanied by severecolicky abdominal pain and vomiting, by absoluteconstipation (or the passage of bright red bloodwithout faecal material or flatus), and by theappearance of an abdominal lump which changeslittle on repeated examination, should provide astrong indication for laparotomy. If this dictumis followed many children will be unnecessarilysubmitted to laparotomy, as has hitherto occurred.But the risk of an unnecessary operation must bevery much smaller than that of leaving an intus-susception untouched (Schwartzman, 1940).

All the patiertts in the present series have had

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245PURPURA AND INTUSSUSCEPTION I

TABLE OF REPORTED CASES OF PURPURA WITH INTUSSUSCEPTION

Site ofCase Author Sex and Joint Purpura Vomit- Blood Haema- Mass Intussus- Treatment Result and RemarksNo. Age Symptoms ing p.r. turia ception

1 Vierhuff m. 29 + Ileo-caecal. No operation. Intussuscepted piece of bowel1(1893) passed per rectum. Re-

covery.

21 Lett (1906) M. 3 + + 0 + 0 R. Loin. Ileo-caecal. Reduced. Recurrence of intussuscep-Ileo-ileal No operation. tion three days after reduc-

tion of first. Died.

3 Hall (1908) M. 5k ± + + 0 0 0 Ileo-ileal. Resection. Died.

4 Dobeli M. 8 + + 0 + + Left hypo- ? Sigmoid Enemas of Recovered. Frequent re-(1908) chrondrium colon, glycerine and lapses of intestinal obstruc-

at intervals, oil. tion, purpura, and intestinalmasses. Presence of intus-susception not proved.

5 Sutherland F. 7 0 + +4 + i 0 Ileo-caecal. No operation. Died. General peritonitis at(1909) with necropsy.

blood.

6 Morse and F. 7 ± + + + 0 RIPF. Ileo-colic. Reduction. Recovery. Recurrence ofStone (1909) vomittmg, purpura, mntes-

tinal bleeding. At laparo-tomy. nothing abnormal.

7 Collinson M. 4 + + ± 0 0 0 Ileo-ileal. Insertion of Resection 3 days after(1910) - Paul's tubes. preliminary operation.

Recovery.

81 Tonking M. 5k + + + 0 Above .l1eo-ileal. Reduction. Recovery..(1910) umbilicus.

9 Robinson M. 5 + ± 0 + Below Ileo-ileal. Reduction Affected bowel also resected(1910) umbilicus, and resetion. because of mesenteric throm-

bosis and gangrene. Re-covery.

10 McKechnie M. 10 0 + + + + Right of Ileo-ilesl. Reduction. Died several months later(1911) umbilicus, from nephritis.

11 Gara (1912) M. 5 0 + + + + Right of Jeo-caecal. No operation. Died.after umbilicus.enema. Not felt

afterwards.

12 Lederer M. 12 + + + + 0 0 ? Necrotic peeof intussuscepted intestine(1913) passed%5ewi.e:ks after onset of symptoms.

13 Barling M. 4 0 ± + + Epigastric. Ileo-colic. Resection. Recovered.(1913)

14 de Lavergne M. 21 0 + + + 0 0 Ileo-ileal. Resection. IDied.andGuillemin(1927)

15 Caizergues F. 3 IIleo-ileal. Reduction. Recovered.(1929)

16 Ballin and M. 31 + + + + Right of Ileo-caecal. Reduction. Death 31 months later fromMorse umbilicus. haematuria, nephritis, pur-

(1930) 1pr. At autopsy manysub-peritoneal haenmrhaeleading to ulceration, per-foration, and peritonitis.

17 Gamstedt F. 7 0 ± + 0 0 Ileo-ileal. Resection. Recoveay.(1933)

18 Gray (1936) M. 21 + +I ± + + Ileo-caecal. Reduction. Recovery. Six days afterreduction once more devel-oped signs, of intestinal

I ~~~~~~obstruction. At operationkinking of terminal ileumover gangrenous patch incaecum. Lateral anasto-mosis performed.

19 Schwartz- m. 3 0 + + + 0 Indefinite. Ileo-caecal. Resection. Died day after operation.man (1940) Family history of allergy.

20 lWolfsohn M. 4 + + ± 0 0 R.IF. Ileo-ileal. Resection. Recovery.(1947)

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ARCHIVES OF DISEASE IN CHILDHOODsome purpuric symptoms for a few days before theonset of intestinal obstruction. If, with the aboveindication, laparotomy is undertaken but nointussusception is discovered, the most likelyfindings will be purely those of so-called Henoch'spurpura. According to Holubec (1935), this maybe complicated by duodenal perforation or appendi-citis, and either of these may therefore have givenrise to the serious symptoms. Alternatives, particu-larly in the slightly older age group, may be whatSheppard Siegal (1945) describes as benignparoxysmal peritonitis, where a reversible inflam-matory reaction occurs in the peritoneum, joint-lining, and other endothelial membranes. Some ofSiegal's patients came to laparotomy. Furtherdifferential diagnoses to be considered are severeconstipation, appendicitis (Holubec, 1935. Whit-more and Peterson, 1946), intestinal obstruction ofother types, and acute regional ileitis (Mailer, 1938).Barnes and Duncan (1941) actually made the latterdiagnosis at laparotomy, but when the abdomenwas reopened ten days later no abnormality wasdetected and purpuric manifestations made themalter the diagnosis to one of anaphylactoid purpura.

Treatment and Outcome (see table)Of the twenty cases under review, fifteen came to

operation. Ofthe remainder, in two (cases 1 and 12)the piece of intussuscepted intestine sioughed awayand was passed per rectum. In two (cases 5 and 11)the diagnosis was only made at necropsy, and inone (case 4) we have no absolute proof that a trueinvagination actually occurred. Lett's patient(case 2) had a further intussusception three daysafter the reduction of the first. This had to be leftowing to the child's condition, and he died. Gray'spatient (case 18) developed signs of obstru6tion sixdays after the reduction, and this was due to kinkingof the terminal ileum over a patch of gangrenouscaecum. The patient recovered after a lateralanastomosis had overcome the blockage. Case 6had to be reopened a week after the reduction of anileo-colic intussusception because of a recurrenceof abdominal pain, vomiting, and bleeding, but noabnormality whatever was found at this secondoperation. Immediate resection had to be performedon seven occasions, with four resulting recoveries.In one of these (case 9) the invaginated bowel couldbe reduced but had to be excised owing to thepresence *of mesenteric thrombosis and resultinggangrene. One child had the affected loop resectedthree days after an initial ileotomy and he recovered(case 7). Two patients (cases 10 and 16) died severalmonths after successful operation, one fromnephritis, the other, who also had nephritis, fromperitonitis due to the perforation of haemorrhagicintestinal ulcers. Altogether twelve of the twentypatients recovered and, as far as is recorded, nofurther recurrence of either intussusception or evenpurpuric symptoms occurred later than a year afterthe abdominal catastrophe.

DiscussionThe nature of anaphylactoid purpura has been

frequently discussed and the present case will throwno further light on the subject. In common withmost reported cases, our patient presented nofamily or past history of allergic disease. Noprecipitating factor could be elicited to account forhis illness, and no eosinophilia was encountered.At first it was thought that purpura may have beenthe response to the administration of salicylates,but when aspirin and saJicylates were given on athird occasion during his convalescence no adversereaction occurred. At any rate salicylates do notusually lead to this kind of purpura in susceptiblesubjects.

Several theories have been advanced to explainwhy intussusception should occur in these patients.The first assumption is that purpura and intus-susception occur independently, and that eachhappens without being influenced by the other.Against this view must be held the rarity of eachof the two conditions, so that the chances of asimultaneous occurrence of both must beinfinitesimally small. Furthermore, the age incid-ence of intussusception in the present series issignificantly higher than is found with non-purpuriccases. This argument can be used also against thesecond possibility, that intussusception is theprimary condition and that purpura follows as asecondary, presumably toxic, complication. Dobeli(1908) believed that a gastro-intestinal -disorder,such as peptic ulceration, intussusception, orenteritis, could be found in most cases if looked for,and that through absorption of bacteria or toxinsabdominal purpura resulted. He stated that onlyby dealing with the underlying disorder couldpurpura be cured. All the data, however, speakagainst this idea. In practicaUy every one of thetwenty cases in this series there was a clear onsetof intestinal obstruction, and this was invariablypreceded (and not followed) by evidence of purpura.In my own patient rheumatic symptoms andpetechiae occurred three and one days before severeabdominal pain and vomiting developed. Duringconvalescence this boy had several bouts of purpurabut intussusception apparently did not recur. Evenin the case described by Dobeli himself, haemor-rhagic manifestations appeared some time beforethe onset of abdominal pain and masses, and hisdiagnosis of chronic recurrent intussusception ofthe sigmoid flexure was never proved. His maywell have been a case of purely abdominal purpura.Moreover, Dobeli's theory fails to explain thegreat frequency of the intestinal diseases he mentionswithout the co-existence of purpura.

This leaves the third and most likely possibilitythat intussusception develops as a complication ofpurpura. It has been assumed that a blood clotin the bowel lumen may act mechanically by itsweight and thus cause this portion to be invaginated.This seems an inadequate explanation. Hall (1908),thought,that the straining from vomiting during the

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PURPURA AND INTUSSUSCEPTION 247

gastro-intestinal crisis of Henoch's purpura couldlead to intussusception, and Althausen et al. (1937)consider amongst numerous causes of intussuscep-tion the presence of spasm in the intestinal segmentabove a partial hold-up, this spasm correspondingto the colicky pains experienced by the patient.Most observers agree that either extravasation ofserous fluid, or especially haemorrhage into themucous, submucous, muscular or subperitonealcoats of an intestinal segment are the main pre-cipitating factors to produce the invagination.Intense congestion would invariably ensue. Theactual intussusception could thus be the result ofthickening of the bowel wall from haemorrhage,oedema, and congestion, this leading to partialobstruction, and a secondary paralysis of theaffected intestinal segment with spasm and over-action of the portion above it. This theory appearsto fit most of the known facts and agrees withmany of the operative findings.

SummaryA case of purpura with intussusception followed

by resection and recovery is described, and theliterature of similar cases is reviewed. Thesymptomatology, etiology, diagnosis, and treatmentof this condition are discussed.

I am grateful for the co-operation and advicereceived from Mr. J. Leebody, F.R.C.S.E., theSuperintendent of Fulham Hospital, and fromMr. H. L. Cochrane, F.R.C.S., who operated onmy patient, and whose interest never failed. Mythanks are also due to Sister Myra Collins for thecontinuous watch and nursing-care which con-tributed so largely to the patient's recovery.

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29, 253.Burrows, H. (1904). Brit. J. Child. Dis., 1, 28.Caizergues, J. F. (1929). Nourisson, 17, 99.Collinson, F. W. (1910).. Lancet, 1, 716.Dobeli, E. (1908). Cor-BI. Schweiz. Aerzte, 38, 201,-240,

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26, 287.Robinson, H. B. (1910). Lancet, 2, 1,008.Schwartzman, J. (1940). Arch. Pediatr., 57, 389.Siegal, S. (1945). Ann. intern. Med., 23, 1.Still, G. F. (1909). Common Disorders of Childhood.

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(1909). Lancet, 1, 1,817.Tonking, J. H. (1910). Ibid., 2, 802.Vierhuff, J. (1893). St. Petersb. med. Wschr., N.F.,

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