:Indian ft. Pediat., 24 I 143, 1957

INTIRACRANIAL INJURY D U R I N G BIRTH *

Nlvnm'rA Sr,.y

Calculla

l n t r a c r a n i a l in iury is the greatest p rob lem in the neonala l per iod

i m m e d i a t e l y fol lowing bir th. I a m presen t ing the result of a s tudy of in t racrania l i rr i tat ion after

b i r t h b r o u g h t on by in t racrania l in iury sustained by the infant dur ing bir th. T h e s tudy was m a d e in the L a d y I)ufferin Hospital , Ca lcu t t a du r ing the per iod 1st July to 30th Sep tember , 1956.

TABLE I

Incidence of Intracranial Injury in Lady Dufferin Hospital., Calcutta; •from 1st July to 30th September 1956.

Per cent Disease No. of total

c a s e s

Delayed labour with natural delivery .. I1 0-8

Forceps delivery

Precipitate labour

Asphyxia

Normal delivery i ;

Caesarian section

.. 7 0.5

• . 10 0.7

• . 1 3 1.0

.. 7 0"5

.. 1 07

Fatality Mortality rate

%

6 54'5

4 57"5

4, 40"0

11 84-6

4 57"5

1 100'0

To tal .. 49 3.7 30 61-2

T h e total n u m b e r of live bir ths f rom 1st J u l y to 30th Sep tember , 1956 1,307. T a b l e I shows tha t the inc idence of in t racrania l in jury is very

:high, be ing 3"7% of total cases and tha t it is a c c o m p a n i e d by a h igh mor ta l i ty itlae fatal i ty ra te be ing 61-2%.

In de layed l abour there is p ro longed pressure on the foetal head causing venous congest ion. I f the delay is due to d i spropor t ion be tween the foetal ~ e a d and m a t e r n a l pelvis as is often the case, m o u l d i n g occurs. This, if excessive, causes u n d u e stress on the dura l septa, t en to r i um cerebelli and ~ cerebri l ead ing to rup tu re . I f the tear involves a blood vessel it will ~_~use h a e m o r r h a g e . ~ I n forceps del ivery u h i c h is usual ly done for delayed l abour requi r ing ~ t a n c e , the re will be all tile changes m e n t i o n e d previously and m a d d m o n

~-~flq'rom the Lady Dufferin Hospital, Calcutta. Received for publication on January 22, 1957.

N

144 India. Journal of Pedialrics li

. | ~ 1 . there may be injury caused by mechanical prcss,~r¢" of th(" tbrc(zps b,,m,: on ih(. foetal sk,,ll.

In precipilate labour thr: changes in the- shape of th(: head i.~ very quick wlth great('r danger of intracranial damage.

In asphyxia there is g('n.-.ralised vcr,(ms congestion including the head .1 brain ' " ' may injure the latter. -~ n W l I I C l l

' i 'he foetus is always subjected l(~ a ce.rtain am(rant (d" t rauma (luring birth and it is very difficult to (lraw th¢- line between physiological and pathological birth injury. .qometimcs ,:yen after an apparent ly normal delivery the baby dewzlops signs (£ intracranial irritation.

A baby born by caf-sarian section sometimes develops intracranial irritation, the case of which is not known exactly. "Fhe sudden change in pressure from inside the uterus to outside may contribute to it.

T A B L E II

Effect ~f Premalurily r,n Mortali(),

New-born infants Incidence Per cent of Morta l i ty Fatal i ty total cases rate

. . . . . . . . . . . . . . . . . . . . . .

Mature . . . . . . 40 3.[) 23 57-7%

Premature . . . . 9 0-6 7 77.7%

Total . . . . . . 49 3.7 30 61.2%

Table 2 shows that mortali ty is higher when intracranial injury occurs in premature infants, the fatality rate being 77-7°. . while in mature infants it is less, the fatality rate being 57.70/0 .

The new-born baby is more likely to have intracranial haemorrhage than older infants because of capillary fragility and of low pro thrombin concentrat ion in the blood. Both these factors are more marked in the premature. The increased fragility is due to immatur i ty and a greater degree of anoxia in the tissues. The lowering of pro thrombin after bir th is also more marked in the premature than in the full term infant.

CLINICAL FEATURES

Signs and symptoms may be present at bir th or develo p soon after. Sometimes they may be delayed until the fourth to the tenth day. The symptoms are main ly somnolence and motor excitability. There are periods of drowsiness al ternat ing with restlessness. There may be twitching movements of the nmscles of one or more limbs. Sometimes it may spread all over the body and end in a convulsion. There may be spasticity of the voluntary muscles. The eyes may be wide opened with a staring expression. The baby does not suck or swallow satisfactorily. Difficulty in breathing is present in almost all cases. Respirat ion is shallow, irregular and marked

Sen--Inlracranial Injury During Birth 145

by periods of a lmoea . "I'h*:re may be cyanot ic attacks. Respi ra t ion may bccoln(: rapid gradual ly becoming slow~:r. T h e respirat~ry symptoms are due to d,.:prcssion of the respiratory centru. 'l'lqcr< may b c a rise ,~t t empera tu re duc to d is turbance o l the hea t regula t ing centre. ' i h e cry is weak and whining . A sudden shrill cry known as the: cepha l ic cry may })f: heard but is very rare. The reflexes are absent , thr'. rncst ~r.,j,.~r~a,,~" - , , , '" ~,' I ,,.; ,,., , ~, Moro's reflex. T h e ant~-rior fimtanc.lle may tm lensf: or bu lg ing if" the h'sion is supral~:ntorial with it, creased tension. In lesions in the in l ra tcntor ia l !bssa the an ter ior lbntan~:lle is of normal tension. "l'hcso clinical t;".alur(:s were soon in our series, the individual signs being more or less marked it, different cases. O ne feature we not iced, not men t i oned by o ther workers, is the occurrence of abdomina l distension in a lmost all cases. This may be due to anoxia causing di la tat ion of tho smooth muscles inc lud ing those in the intestinal walls.

In p rema tu re s the clinical signs are usually slightly de layed in appearance and are ma in ly respiratory. Moto r excitabil i ty is less m a r k e d than in full t e rm babies. T h e delay may be due to a compa ra t i ve insensit ivity of the nervous sys tem because of i m m a t u r i t y of the tissues and of grea te r degree of anoxia .

DIAGNOSIS

This is m a d e f rom the clinical features. L u m b a r p u n c t u r e is not of much value because a large h a e m o r r h a g e m a y not c o m m u n i c a t e wi th the suba rachno id space, whereas even a small h a e m o r r h a g e m a y show blood in the cerebrospinal fluid. T h e differential diagnosis includes congeni ta l mal format ions of the brain. In t h e m the onset is de layed and the respirator}' symptoms are absent .

PROGNOSIS

In t r ac r an i a l in jury carries a very h igh rnortali ty. Most of the cases are fatal wi th in the first three days. I f the baby lives longer t h a n three days the chances of survival are p ropor t iona te ly greater ; 63-3% of deaths in our series occur red wi th in the first three davs.

TREATMENT

T h e baby should be kept quiet , w a r m and h a n d l e d little. Oxygep. should be given w h e n there are respiratory" symptoms . Sedatives should be given to keep the baby quiet . We have found Pot. b rom. and Chloral fairly satisfactory. T h e head end should be raised to relieve o e d e m a by gravity'. Cardiac s t imulan ts should be given to p r o m o t e bet ter b lood flow. V i t amins K and C should be given to decrease h y p o p r o t h r o m b i n a e n a i a and capi l lary fragility respectively. Ant ibiot ics should be given to p reven t secondary infection. Atelectasis and aspi ra t ion p n e u m o n i a are Very c o m l n o n complicat ions.

14,6 lndian ,7oumal cCf Pediatrics

"[ ) IBf ;USSION

l n l r ac ran i a l injury is a very impor t an t cause, of dea th in the neonata l per iod, s t and ing only next to p rematur i ty , l ) u r i n £ the per iod of ou r s tudy 13.3% ot" neona ta l deaths were caused by in t rac ran ia l in ju ry while 68"8% were due to p rcma tu r i ty .

l ) u r i n g the process of bir th the foetal head unde rgoes m o u l d i n g d u r i n g its passage t h rough the bi r th canal. I t ia also subjected to pressure wi th each u te r ine cont rac t ion . I f the. m o u l d i n g is exc¢-ssiw" a.s may occur ira cases of d i spropor t ion be tween the foetal head and the m a t e r n a l pelvis the dura l septa are subjected to u n d u e strain and may rupture.. 7It" the tear involves a blood vessel, h a e m o r r h a g e will occur the extent o[" w h i c h will d e p e n d on the size ot" the vessel. T h e s y m p t o m s are more m a r k e d if the h a e m o r r h a g e is in the infra tentor ia l fossa as there almost all the space is occupied by b ra in tissue. In asphyxia there is generalised venous congest ion inc lud ing the brain. Anoxia increases the fragility of the blood vessels wh ich m a y cause cerebra1 oedema, ext ravasa t ion of blood and small haemor rhages . I t m a y also cause vasomotor paralysis resul t ing in congest ion and d i la ta t ion of the b lood vessels. T h e r e is re laxat ion of the smoo th muscles which m a y lead to card iac d i l a ta t ion and to a b d o m i n a l dis tension by re laxing the muscles in the walls o f the gut.

I t is very difficult clinically to differentiate be tween cerebral o e d e m a a n d in t rac ran ia l h a e m o r r h a g e as the clinical freatures are the same. I n those due to cerebra l o e d e m a the s y m p t o m s m a y appea r after a short in terval a n d there is be t te r prognosis t h a n in in t racrania l h a e m o r r h a g e which very of ten ends fatally and in "which the symptoms are present a t birth. Moro ' s reflex wh ich is indica t ive of in t racrania l d a m a g e is absent f rom bi r th in in t rac ran ia l h a e m o r r h a g e bu t is present for a short whi le before d isappear- ing in cases of cerebral oedema . T h e most accura te m e t h o d of different ia t ing these condi t ions , however , is by autopsy. We were able to do p o s t m o r t e m e x a m i n a t i o n in only three cases. F r ank h a e m o r r h a g e was seen in two while in the th i rd case venous conges t ion wi th m a r k e d d i la ta t ion of the veins as seen in asphyxia , was present . T h e special i m p o r t a n c e of in t racrania l in ju ry is due to its h igh fatality rate, and to the fact that a large pe rcen tage of those who survive develop sequelae, i.e. men ta l defect, cerebral palsies wi th or w i t h o u t a the to id m o v e m e n t and hydrocepha lus . T h e h igh fatality rate is well shown in our series, be ing 61 .2%.

In our chi ldren 's clinic we have seen several cases wi th menta l defect and wi th cerebral plasv giving a history of d i m c u h birth.

REFERENCES ;

Tile fi~llowing books were used in the preparation of the paper: Management of the Newborn.--A.. H. PARSt~LEE. Diseases of Childl~n.---PA'rERsoN and MONCRIEVV, Edward Arnold & Co. 1949. Text Books of Pediatrlcs.--MIwcHEtm-NELso~, W. B. Saunders & Co,, 1950. Year Book of Pediatrics.--Ed. By H. G. POXCrIER, The Tear Book PuElishers Chicago, 1951, 1954-1955.