PYLORIC SPASM SIMULATING CONGENITAL HYPERTROPHIC STENOSIS

794

PYLORIC SPASM SIMULATING CONGENITAL HYPERTROPHIC STENOSIS REPORT OF A CASE

ELIZABETH LATE

DE

C. FALLE

M.B. Lond., D.C.H. REGISTRAR, CHILDREN’S UNIT,

E.M.S.

SECTOR

THOUGTi the textbooks state that the differential of congenital hypertrophic stenosis and pyloric spasm rests on the presence or absence of a tumour, and that pure pyloric spasm never gives rise to symptoms severe enough to endanger life, the case reported here appears to be one of pure spasm.

diagnosis

CASE-RECORD

girl, aged 6 weeks, with 4 weeks’ history of vomiting, was admitted with her mother to the children’s unit, Old Windsor Emergency Hospital, on Feb. 5, 1945. She was a first-born child, weighing 7 lb. 14 oz. at birth. Delivery had been normal at full term. Satisfactory 4-hourly breast-feeding had been instituted. There had been some regurgitation of food since birth, and for 4 weeks vomiting immediately after every feed, the food dribbling out. Stools had been infrequent for the last 7 days but were still soft and yellow. 6 lb. 15 oz. Slight dehydration. Obvious loss of weight. - After a feed the epigastrium was distended, peristalsis was visible, a firm pyloric tumour was palpable, and there was projectile vomiting. Stools very small, yellow, relaxed, and curdy with mucus. Treatment.-Six 3-hourly breast-feeds of 3 oz. and midnight feed of 3 oz. of half-strength Hartmann’s solution ; ’Pylostropin’ gr. 1/gso (sublingual lamella) 20 min. before fivefeeds ; and daily gastric lavage. Progress.-Vomiting continued after every feed but was never bile-stained. Occasional small green relaxed stools. Gastric residue increased from 0-2 oz. of thick curds. Operation (Feb. 10).-At laparotomy under local anaesthesia, the pylorus looked and felt perfectly normal. There was no sign of tumour, dilatation, or collapse of duodenum or jejunum, or any abnormality in upper abdomen. No surgical treatment was attempted, and the abdomen was A

’

.E’.MM/MMOM’tt.—Weight

-

closed.

P6sto,perative Progress.-During the next 9 days the was put back on the breast 3-hourly. As the breast-

child milk

given

to fail, the feeds were complemented with halfPhenobarbitone gr. 1/8 was National dried milk. thrice daily. Vomiting persisted and was sometimes

began

cream

Stools were still infrequent (every other day), later small and relaxed. Weight was only just maintained with subcutaneous saline 4 oz. on alternate days. Bismuth Meal (Feb. 19).-Almost complete obstruction at pylorus-i.e., typical radiological appearance of hypertrophic pyloric stenosis. After 11/2 hours there was still a large residue in stomach in spite of copious vomit. Very little bismuth passed into small intestine, and first and second parts of duodenum appeared very narrow. Further Progress.-Nine 2-hourly 3-oz. feeds daily of breastmilk alternating with Nestle’s sweetened condensed milk, 1 part to 4 of water. Pylostropin given again. March 3:-. body-weight maintained without vomiting much less ; subcutaneous saline ; stools 2-4 daily, small, yellow, and digested ; gastric residue 2i/oz. daily of very thick mucus and curds. March 5 : breast-milk failed ; half-cream National dried milk given. March 9 : vomits smaller ; gastric residue reduced to 1/2 oz. of fine curds. March 15-25 : severe attack of diarrhoea and vomiting due to bilateral staphylococcal otitis media. March 26 : both ear-drums healed ; stools pasty but 6 small vomits daily ; glyceryl trinitrate gr. 1/400 by mouth 5 min. after feeds. March 28 : only 2 or 3 small regurgitations daily ; 2 yellow pasty stools daily ; negligible gastric residue. April 22 : feeds gradually changed to fullstrength full-creamCow and Gate.’ April 29 : weight 10 lb. May 6: weight 10 lb. 51/2 oz. May 11: bismuth

projectile.

meal. On

May 11 radiography was repeated, glyceryl trinitrate being given before this feed. Delay at pylorus still very considerable, but more bismuth passed into intestines. Stomach quarter-full after 4 hours. Large bismuth residue found at ensuing gastric lavage. On May 15 a further meal was given, 5 min. after glyceryl trinitrate gr. 1/400. It passed much more freely through pylorus. Stomach almost empty after 4 hours. No residue found at ensuing gastric lavage. Much bismuth passed in stools. On May 23 the infant was discharged from hospital. Weight 11 lb. 61/2 oz. Glyceryl trinitrate gr. 3/1600 thrice daily prescribed. Progress as Outpatient.-June 6 : weight (clothed) 13 lb. 21/’2 oz. ; glyceryl trinitrate reduced to gr. lJ4oo twice daily. July 4 : weight 15 lb. 2 oz. ; glyceryl trinitrate

not

discontinued. DISCUSSION

This case presented as a typical pyloric stenosis. The child had all the classical symptoms and signs (with the possible exception of her .sex), and these signs were observed separately by three doctors. It was our custom to treat medically at first all infants in whom pyloric stenosis had been diagnosed. They all had daily gastric lavage, some preparation of atropine methyl nitrate (in this case pylostropin), and subcutaneous saline sufficient to correct their daily loss of fluids by vomiting. Only if their condition did not improve during the first week and after correcting any dehydration did we proceed to surgical treatment. In the present did not case the condition (see figure) respond to medical treatment, and therefore a laparotomy was undertaken. To the surgeon’s consternation there was neither visible_ nor palpable thickening of the pylorus ; nor was there organic obstruction of the lumen. Stimulated by the success of organic nitrates, as used by Elaine Field1 in cardiospasm, glyceryl trinitrate was tried. Its effect was immediate and dramatic : the infant gained 15 oz. in three days, and never looked back. It was therefore astonishing that radiography on May 11 showed practically no change from the radiological appearances on Feb. 15 ; but on May 15, after the third bismuth meal, the therapeutic effects of glyceryl trinitrate were plainly 1. Field, C. E.

Lancet, 1944, ii, 848.

795

visible. At the age of nine months the child reached the correct weight for her age and was progressing on a normal diet. We have since tried glyceryl trinitrate for proved hypertrophic pyloric stenosis with no success. -

I wish to thank Dr. Charles Pinckney for his criticism and permission to publish this case.

INTRACEREBRAL CALCIFICATION IN A MICROCEPHALIC D. CAPPON M.B. Lond.

With illustrations

plate A Eurasian female baby, aged 9 months, seen in private practice in India, was brought to me by her father, who was worried about the child’s listlessness on

and backwardness. The child was very microcephalic, unable to sit up for any length of time, took little or no interest in her surroundings, and was a weak feeder. Her emotional response was poor ; she hardly smiled or gurgled, and her cry was feeble. It was difficult to examine the patient satisfactorily, because the parents, who were both Eurasian, were overanxious and diffident. No stigmata of mental deficiency, telangiectasis, naevi, abnormal pigmentations, or Pringle’s facial adenomata were seen, and the child certainly was not blind, though retinoscopy was not done. Nothing relevant was disclosed in the family history. Radiograms of the skull (figs. 1 and 2) presented a most unusual picture. An abnormally small skull showed a curious pattern of intracerebral calcification, apparently involving mainly the brain substance round the lateral ventricles. Thinking that this might be an unusual manifestation of tuberous sclerosis or of the Sturge-Wever syndrome, I referred the radiograms and notes to Dr. F. Parkes Weber. Meanwhile the patient and her parents and myself were leaving India; so it was impossible to investigate the patient further. Dr. Parkes Weber writes as follows : " The radiograms reveal symmetrical calcification in the the exact pattern of which has apparently not hitherto been described. If the two large circles in the anteroposterior view are due to calcification in the walls of grossly dilatedlateral ventricles in the child’s microcephalic brain, the brain must be very deficient in quantity. substance " In the differential diagnostic toxoplasmosis must certainly be considered. This disease, when present in infants, causes extensive destruction in the brain and spinal cord ; large foci of calcification appear within the necrotic areas ; 80% of toxoplasmic infants have internal hydrocephalus, which is either present at birth -or develops shortly afterwards : and periventricular infiltration with lymphocytes and plasma cells and, ependymal ulceration are often found. Unfortunately in the present child the eyes were not examined for chorioretinal atrophy. On the whole, though the pattern of calcification differs from any of the published descriptions, there is much to be said in favour of the diagnosis of infantile toxoplasmosis. Nevertheless, it must not be forgotten that symmetrical cerebral calcification, particularly1 of the basal ganglia, has been found in other conditions. " An excellent leading article on human toxoplasmosis in the Journal of the American Medical Association2 furnishes a valuable bibliography."

brain,

_

"

’

,

Efforts

being made to follow up this it further.

are

investigate

case

and

I am grateful to Dr. Dessa for the radiograms and for the stimulus of interest in the case, and to Dr. Parkes Weber for his comments. 1.

Love,

J.

G., Camp,

13, 225.

J.

D., Eaton, L.

2. J. Amer. med. Ass. 1947,

133, 852.

M.

Proc. Mayo Clin. 1938,

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