Ind. 3 t. Pediat., 23: 157, 1956

THE PROBLEM OF ASPHYXIA IN THE NEWBORN*

NIVEDITA SEN

Calcutta

Asphyxia neona to rum is the first and a major problem that presents

itself immediate ly ffter an infant is born. I t is the period of anoxia in the newborn before it starts b rea th ing properly. Asphyxia is said to exist if the brea th ing t ime is more than one minute . Crying t ime of more that two minutes is also a poor reaction as well as failing to ma in t a in breath-

ing normal ly after it has been initiated. Anoxia can be classified into two m a i n groups : - -

1. Extrinsic anoxla, L e. anoxia arising in the foetus while still inside

the uterus due to defects in its envi ronment . 2. Intr insic anoxia, i. e. anoxia arising due to defects in the foetus it-

self. This paper presents the results of a study of the incidence and morta l i ty

of asphyxia in the newborn in Lady Duffer in Hospital, Calcutta, from I st

October, 1955 to Decem0ber, 1955 when the total n u m b e r of live bi~:ths was 1,400.

Tab le 1 shows that the incidence and morta l i ty of this condit ion is higher in the intrinsic group.

TABLE 1 Incidence of Asphyxia Neonatorum in Lady Dufferin Hospital, Calcutta, fi'om 1st October 1955 to

31st December 1955

Disease No. Per cent of Mortal~,ty Fatality rate total cases %

Extrinsic Anoxia .. 53 3'78 19 35.84 Intrinsic Anoxia .. 73 5'22 36 49.31

Total .. 126 9'00 55 43'65

By s tudying these groups in greater detail the following figures are obta ined : -

TABLE 2 Extrinsic Anoxia

Disease No. Per cent of Mortality Fatality rate total cases ~

Maternal analgesia Maternal anaesthesia Maternal toxaemia Placental insufficiency True knots in the cord Maternal anaemia Early rupture of

membranes

2

i i 2 1 3

.. 31

0 . 1 4 . . . .

1:00 "i 28-~'7 0.14 2 100'00 0"07 0'21 "fi 66.66

2.21 11 35.48

Total .. 53 3-78 19 35.84

* From ~he Lady Dufferin Hospital, Calcutta. Paper Read at the Seventh AU-India Pediatric Conference, Indore, February 24, 1956.

158 Indian ffournal of Pediatrics

Table 2 shows that the incidence is high where there is early rupture of membranes and maternal toxaemia, while the mortali ty is highest in those with placental insufficiency, the fatality rate being 100 per cent indicating frequency of the former two "and severity of the last group.

Analgesics during labour narcotize the foetal brain if given within a short time of delivery, h6nce the central nervous system of these infants does not respond to sensory ~imuE after birth or takes time to do so. The two patients reported in this series had morphine and pethedine respectively less than two hours before delivery. No case of maternal anaesthesia has been included because all mothers who required it had instrumental deli- very, causing greater 'damage to the foetus. I t too acts in the same way as analgesics narcotizing the respiratory centre.

In the group termed "maternal toxaemia" are included eclampsia and pre-eclampsia cases, The toxins occurring in these two conditions de- press tl~e respiratory corltre and either prevent or delay the response to sensory stimuli after birth.

Placental insufficiency may occur if the placenta is partially separated from the uterus while the foetus'is still inside. This causes anoxia by 'd imi- nishing the foetal blood supply as may happen in placenta praevia or in retroplacental haematoma. This may be severe enough to be incompatible with life, the foetus dying shortly before or soon after birth. Two cases of placenta praevia are reported in this series, th e babies dying soon after birth, and three cases of'still births due to the same ca, use during this period.

True knots in the cord, by impeding the blood flow may diminish the blood supply and act in the same way. This paper reports one case in which the knot was'not too tight and the baby revived after resuscitation.

In maternal anaemia, because of a low haemoglobin content, less oxygen is supplied to the foetus producing anoxia which if severe enough may cause death. In this series the maternal haemoglobin in three cases was 10 per cent, 15 per cent and 25 per cent respectively, the first two babies dying soon after birth.

I f the membranes rupture early, the beneficial effect of the amniotic fluid during labour is lost. This, by equalising the pressure, protects the foetal head from injury. In its absence there is local congestion of the foetal head and brain which causes local anoxia, and may even cause intra- cranial haemorrhage. There were thirty-one cases of this type, of which eleven died indicating the severity of the condition.

Table 3 shows t h a t the incidence of intrinsic anoxla is high in cases of" prematuri ty and intracranial injury while the mortality is highest in prema- tures and in infants with blockage of the respiratory" tract, the fatality rates being 82.14 per cent and 40 per cent respectively.

I f the cord is tight around the neck, it may cause congestion and anoxia of the foetal head by strangulation, which may be severe enough to cause death. In the milder cases the resptratory centre may be affected interfer- ing with post-natal respiration. In this series there were eleven such cases of which two died soon after birth,

Sen--Problem of Asphyxia in the .Newborn

TABLE 3

Intrinsic Anoxia

159

Disease No. Per cent of ~r Fatality rate total cases %

Cord tight around the neck II 0.78 2 18.18 Intracranial injury .. 24 1-71 7 29.16 Developmental detect . . . . . . . . . . Insufficiency of foetal

red blood ceils . �9 Prematurity 28 2[()0 23 82"14 Blockage of respiratory tract

by foreign material .. l0 0.71 4 40.00

Total .. 73 5-21 36 4~9:31

Iaa intracranial injury there may be intracranial congestion and haemor- rhage which may produce local anoxia and affect the respiratory centre, causing difficulty in respiration after birth. When there is a developmental defect the respiratory centre may be imperfectly developed or not deve- loped. In the latter case life may be possible inside the uterus with the maternal blood supplying nutrition and oxygen through the placenta, but impossible outside the uterus.

I f the foetal red blood cells are reduced in number, as may occur in erythroblastosis foetalis the oxygen carrying capacity of the foetal blood may not be sufficient for its needs resulting in foetal anoxia and respiratory dif- ficulty after birth.

Prematuri ty is a large group where asphyxia is of very common occur-

rence. This is because the respiratory centre being immature, has a higher threshold for sensory stimuli and secondly due to immaturi ty of the lungs, the air-sacs are not properly developed. The capillaries have not yet reached the surface of the walls of the air-sacs causing difficulty in exchange of oxygen between the blood and the air. Survival is inversely proportional to the degree of immaturi ty. In this series out of twenty- eight cases twenty-three died within three days of birth.

Blockage of the respiratory tract is caused commonly by aspiration of blood, mucus and amniotic fluid from the mouth and throat. Aspiration may occur while the foetus is still inside the uterus, if the environment is abnormal enough to cause anoxia in the foetus as has been described in the extrinsic group. Foreign material in the air-passages by mechanical blockage may interfere with the passage of air to and from the air-sacs. I f the respira- tory centre is depres~d the gag reflex is also depressed allowing foreign material to be aspirated much more easily than in normal infants. In some cases breathing is initiated normally after birth, the difficulty appearing later and may be severe enough to cause death, which suggests the possibility of hyaline membrane. In this series out of ten such eases four ended fatally.

160 Indian aTournal of Pediatrics

CLINICAL FEATURES

In mild asphyxia the colour of the infant is normal ; the respiration is irregular, heart sounds are normal and muscle tone is good.

In asphyxia of a medei'ate degree the infant is cyanosed ; the respira- tion is irregular and shallow ; heart sounds are weak anu muscle tone is poor. Frothy fluid sometimes blood-stained may come out of the mouth and nose.

Ir~ the severe type there: is pallor ; the respiration is very shallow, irre- gular, and infrequent heart sounds are very weak and the baby is absolu- tely limp. In some cases breathing may start normally but attacks of cyanosis and dyspnoca occur later. Sometimes there may be haemorrhage due to the rupture of congested and distended capillaries which may be prolonged due to a low. prothrombin levcl.

TREATMENT

The baby should be handled very gently. Over t rea tment is some- times worse than no treatment. Mucus should be sucked out of the mouth and throat, preferably before the first gasp when there is danger of its being sucked in. Oxygefl should be given and the baby should be kept warm. Cardiac and respiratory stimulants, i .e. coramine and lobe!ine should be given. Forcing oxygen or air intratracheally under positive pressure should be avoided as the air-passages being very. delicate are easily ruptured es- pecially at the junction of the alveoli and alveolar ducts. The air-sacs cannot be inflated either by positive or by negative pressure. More recently, intragastric oxygen is being administered to those who fail to be resuscitated by the usual methods and has been spoken of highly. We have not had any experience ha this method. Positive pressure oxygen air-lock, a rocker for asphyxia, mist oxygen therapy and postural drainage are other methods which have been tried but have not been used in this hospital. Vitamin K should be given to avoid a low prothrombin level and antibiotics should be given since infection easily enters the respiratory tract of those requiring resuscitation.

After a baby is born, it has to adjust itself in various ways in order to become adapted to an extra-uterine existence. One and the most important is the change-over of respiration from the placenta to the lungs. The reflexes which bring this about develop in the foetus before birth but start to function after. A chemical stimulating mat~riaI is produced inside the cells of the respiratory centre which, having reached sufficient concen- tration, stimulate the centre to function. Adequate amounts of oxygen must be present also. A mild degree of anoxia stimula.~es the centre which becomes c~epressed if the anoxia is too marked. At the same time an in- hibitory influence is exerted by the higher centres on the respiratory centre. The latter is also stimulated after birth by sensory impulses from the skin. When the combination of this sensory stimulus and the stimulating material

Sen--Problem of Asphyxia in the Newborn 161

becomes strong enough to overcome the inhibition of the higher centres, breathing is initiated. Sometimes due to various reasons the baby becomes asphyxiated. In quite a number of such infants the anoxia starts M the foetus before it is born and that contributes to a large extent to the continua- tion and perhaps increase of the anoxia after the birth process is completed. The respiratory centre is depressed due to anoma and fails to respond to sensory stimuli after birth. Mild degrees of anoxia which stimulate the respi- ratory centre, may make the foetus gasp while still inside the uterus, thus aspirating amniotic fluid into the air passages. Anoxia also depresses the gag reflex facilitating aspiration of blood, mucus and a~aniotic fluid from the mouth after birth. These form a mechanical obstruction to the entry of air into the air sacs as well as promote the formation of hyaline membrane in the air-passages. According to one theory this membrane forms when the fluid portion of the amniotic fluid is absorbed and the air entering the air- passages forces the solid portion, i.e. protein, fat ahd squamous cells against the walls. The cells gradually lose their nuclei; become a homogeneous mass, acidophil in reaction, and form a membrane lining the bronchioles and alveolar ducts which may seal off the opening into the air-sacs f~rming a permanent obstruction. I f the extent of this membrane become~ too great, continuation of normal respiration is not possible. Symptoms due to hyaline membrane usually start a few hours after birth, after respiration has become established and is more conmaon in the premature. Though several of the cases in this series have been'suggestive of this condition, confirmation of the diagnosis was not possible since post-mortem examination was not carried out.

Anoxia causes congestion as well as damage to the capillary walls in- creasing their permeability. This results in fluid exuding into the alveoli and bronchi and in marked cases completely filling the air-sacs. Anoxia prevents air from entering the sacs or if even air does enter the sac, there is a fluid wall between the air and the blood in the capillaries impending the exchange of oxygen and ( ] 0 2 between them. This is more marked in the premature and was noticed in many of these cases. Moist sounds appeared in the lungs several hours after birth and persisted till death. Cardiac stimulants help in such cases promoting better blood flow and absorption of the fluid. Atropine may be tried.

I t is evident from this study that a large number of newborn babies suffer from asphyxia due to various causes, the incidence being nine per cent in this series. The mortali ty is high, the fatality rate being 43.65 per cent in these cases. Those who survive are likely to develop undesirable after-effects such as spasticity and idiocy in later life due to permanent damage to the brain.

In treatment of asphyxia the co-operation of the obstetrician and the pediatrician is necessary. The former can do much to prevent asphyxia by efficiently treating maternal diseases during pregnancy and minimising premature births as well as by using the least amount of analgesics and anaesthetics during delivery. The role of the pediatrician comes in after the baby is born, and has already been described.